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1001 Cards in this Set

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1. The driving force of the ventilator (Datex-Ohmeda 7000, 7810, 7100, and 7900) on the anesthesia workstation is accomplished with A. Compressed oxygen B. Compressed air C. Electricity alone D. Electricity and compressed oxygen
1. (A) The control mechanism of standard anesthesia ventilators, such as the Ohmeda 7000, uses compressed oxygen (100%) to compress the ventilator bellows and electric power for the timing circuits. Some ventilators (e.g., North American Dräger AV-E and AV-2+) use a Venturi device, which mixes oxygen and air. Still other ventilators use sophisticated digital controls that allow advanced ventilation modes. These ventilators use an electric stepper motor attached to a piston (Miller: Miller’s Anesthesia, ed 8, p 757; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 160–161; Miller: Basics of Anesthesia, ed 6, pp 208–209).
2. Select the correct statement regarding color Doppler imaging. A. It is a form of M-mode echocardiography B. The technology is based on continuous wave Doppler C. By convention, motion toward the Doppler is red and motion away from the Doppler is blue D. Two ultrasound crystals are used: one for transmission of the ultrasound signal and one for reception of the returning wave
2. (C) Continuous wave Doppler—Continuous wave Doppler uses two dedicated ultrasound crystals, one for continuous transmission and a second for continuous reception of ultrasound signals. This permits measurement of very high frequency Doppler shifts or velocities. The “cost” is that this technique receives a continuous signal along the entire length of the ultrasound beam. It is used for measuring very high velocities (e.g., as seen in aortic stenosis). Also, continuous wave Doppler cannot spatially locate the source of high velocity (e.g., differentiate a mitral regurgitation velocity from aortic stenosis; both are systolic velocities). Pulsed Doppler—In contrast to continuous wave Doppler, which records the signal along the entire length of the ultrasound beam, pulsed wave Doppler permits sampling of blood flow velocities from a specific region. This modality is particularly useful for assessing the relatively low velocity flows associated with transmitral or transtricuspid blood flow, pulmonary venous flow, and left atrial appendage flow or for confirming the location of eccentric jets of aortic insufficiency or mitral regurgitation. To permit this, a pulse of ultrasound is transmitted, and then the receiver “listens” during a subsequent interval defined by the distance from the transmitter and the sample site. This transducer mode of transmitwait- receive is repeated at an interval termed the pulse-repetition frequency (PRF). The PRF is therefore depth dependent, being greater for near regions and lower for distant or deeper regions. The distance from the transmitter to the region of interest is called the sample volume, and the width and length of the sample volume are varied by adjusting the length of the transducer “receive” interval. In contrast to continuous wave Doppler, which is sometimes performed without two-dimensional guidance, pulsed Doppler is always performed with two-dimensional guidance to determine the sample volume position. Because pulsed wave Doppler echo repeatedly samples the returning signal, there is a maximum limit to the frequency shift or velocity that can be measured unambiguously. Correct identification of the frequency of an ultrasound waveform requires sampling at least twice per wavelength. Thus, the maximum detectable frequency shift, or Nyquist limit, is one half the PRF. If the velocity of interest exceeds the Nyquist limit, “wraparound” of the signal occurs, first into the reverse channel and then back to the forward channel; this is known as aliasing (Miller: Basics of Anesthesia, ed 6, pp 325–327).
3. When the pressure gauge on a size “E” compressedgas cylinder containing N2O begins to fall from its previous constant pressure of 750 psi, approximately how many liters of gas will remain in the cylinder? A. 200 L B. 400 L C. 600 L D. Cannot be calculated
3. (B) The pressure gauge on a size “E” compressed-gas cylinder containing liquid N2O shows 750 psi when it is full and will continue to register 750 psi until approximately three fourths of the N2O has left the cylinder (i.e., liquid N2O has all been vaporized). A full cylinder of N2O contains 1590 L. Therefore, when 400 L of gas remain in the cylinder, the pressure within the cylinder will begin to fall (Miller: Basics of Anesthesia, ed 6, p 201; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 12–13).
4. What percent desflurane is present in the vaporizing chamber of a desflurane vaporizer (pressurized to 1500 mm Hg and heated to 23° C)? A. Nearly 100% B. 85% C. 65% D. 45%
4. (D) Desflurane is unique among the current commonly used volatile anesthetics because of its high vapor pressure of 664 mm Hg. Because of the high vapor pressure, the vaporizer is pressurized to 1500 mm Hg and electrically heated to 23° C to give more predicable concentrations: 664/1500 = about 44%. If desflurane were used at 1 atmosphere, the concentration would be about 88% (Barash: Clinical Anesthesia, ed 7, pp 666–668; Miller: Basics of Anesthesia, ed 6, pp 202–203; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 60–64).
5. If the internal diameter of an intravenous catheter were doubled, flow through the catheter would be A. Decreased by a factor of 2 B. Decreased by a factor of 4 C. Increased by a factor of 8 D. Increased by a factor of 16
5. (D) Factors that influence the rate of laminar flow of a substance through a tube are described by the Hagen- Poiseuille law of friction. The mathematic expression of the Hagen-Poiseuille law of friction is as follows: ˙ (� P) V = �r4 Anesthesia Equipment and Physics 11 where ˙V is the flow of the substance, r is the radius of the tube, ΔP is the pressure gradient down the tube, L is the length of the tube, and μ is the viscosity of the substance. Note that the rate of laminar flow is proportional to the radius of the tube to the fourth power. If the diameter of an intravenous catheter is doubled, flow would increase by a factor of two raised to the fourth power (i.e., a factor of 16) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 377–378).
6. A size “E” compressed-gas cylinder completely filled with N2O contains how many liters? A. 1160 L B. 1470 L C. 1590 L D. 1640 L
6. (C) The World Health Organization requires that compressed-gas cylinders containing N2O for medical use be painted blue. Size “E” compressed-gas cylinders completely filled with liquid N2O contain approximately 1590 L of gas. See table from Explanation 10 (Miller: Basics of Anesthesia, ed 6, p 201; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 12).
7. Which of the following methods can be used to detect all leaks in the low-pressure circuit of all contemporary anesthesia machines? A. Negative-pressure leak test B. Common gas outlet occlusion test C. Traditional positive-pressure leak test D. None of the above
7. (D) Anesthesia machines should be checked each day before their use. For most machines, three parts are checked before use: calibration for the oxygen analyzer, the low-pressure circuit leak test, and the circle system. Many consider the low-pressure circuit the area most vulnerable for problems because it is more subject to leaks. Leaks in this part of the machine have been associated with intraoperative awareness (e.g., loose vaporizer filling caps) and hypoxia. To test the low-pressure part of the machine, several tests have been used. For the positive-pressure test, positive pressure is applied to the circuit by depressing the oxygen flush button and occluding the Y-piece of the circle system (which is connected to the endotracheal tube or the anesthesia mask during anesthetic administration) and looking for positive pressure detected by the airway pressure gauge. A leak in the low-pressure part of the machine or the circle system will be demonstrated by a decrease in airway pressure. With many newer machines, a check valve is positioned downstream from the flowmeters (rotameters) and vaporizers but upstream from the oxygen flush valve, which would not permit the positive pressure from the circle system to flow back to the low-pressure circuit. In these machines with the check valve, the positive-pressure reading will fall only with a leak in the circle part, but a leak in the low-pressure circuit of the anesthesia machine will not be detected. In 1993, use of the U.S. Food and Drug Administration universal negative-pressure leak test was encouraged, whereby the machine master switch and the flow valves are turned off, and a suction bulb is collapsed and attached to the common or fresh gas outlet of the machine. If the bulb stays fully collapsed for at least 10 seconds, a leak did not exist (this needs to be repeated for each vaporizer, each one opened at a time). Of course, when the test is completed, the fresh gas hose is reconnected to the circle system. Because machines continue to be developed and to differ from one another, you should be familiar with each manufacturer’s machine preoperative checklist. For example, the negative-pressure leak test is recommended for Ohmeda Unitrol, Ohmeda 30/70, Ohmeda Modulus I, Ohmeda Modulus II and II plus, Ohmeda Excel series, Ohmeda CD, and Datex-Ohmeda Aestiva. The Dräger Narkomed 2A, 2B, 2C, 3, 4, and GS require a positive-pressure leak test. The Fabius GS, Narkomed 6000, and Datex-Ohmeda S5/ADU have self-tests (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 83–85; Miller: Miller’s Anesthesia, ed 8, pp 752–755). Check valve Oxygen flush Machine outlet valve Suction bulb –65 cm Suction bulb Leak Machine outlet Check valve Oxygen flush valve 0 cm Negative Pressure Leak Test 12 Part 1 Basic Sciences
8. Which of the following valves prevents transfilling between compressed-gas cylinders? A. Fail-safe valve B. Check valve C. Pressure-sensor shutoff valve D. Adjustable pressure-limiting valve
8. (B) Check valves permit only unidirectional flow of gases. These valves prevent retrograde flow of gases from the anesthesia machine or the transfer of gas from a compressed-gas cylinder at high pressure into a container at a lower pressure. Thus, these unidirectional valves will allow an empty compressed-gas cylinder to be exchanged for a full one during operation of the anesthesia machine with minimal loss of gas. The adjustable pressure-limiting valve is a synonym for a pop-off valve. A fail-safe valve is a synonym for a pressure-sensor shutoff valve. The purpose of a fail-safe valve is to discontinue the flow of N2O (or proportionally reduce it) if the O2 pressure within the anesthesia machine falls below 30 psi (Miller: Miller’s Anesthesia, ed 8, p 756).
9. The expression that for a fixed mass of gas at constant temperature, the product of pressure and volume is constant is known as A. Graham’s law B. Charles’ law C. Boyle’s law D. Dalton’s law
9. (C) Boyle’s law states that for a fixed mass of gas at a constant temperature, the product of pressure and volume is constant. This concept can be used to estimate the volume of gas remaining in a compressedgas cylinder by measuring the pressure within the cylinder (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 4).
10. The pressure gauge on a size “E” compressed-gas cylinder containing O2 reads 1600 psi. How long could O2 be delivered from this cylinder at a rate of 2 L/min? A. 90 minutes B. 140 minutes C. 250 minutes D. 320 minutes
10. (C) U.S. manufacturers require that all compressed-gas cylinders containing O2 for medical use be painted green. A compressed-gas cylinder completely filled with O2 has a pressure of approximately 2000 psi and contains approximately 625 L of gas. According to Boyle’s law, the volume of gas remaining in a closed container can be estimated by measuring the pressure within the container. Therefore, when the pressure gauge on a compressed-gas cylinder containing O2 shows a pressure of 1600 psi, the cylinder contains 500 L of O2. At a gas flow of 2 L/min, O2 could be delivered from the cylinder for approximately 250 minutes (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 4; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 10–12). CHARACTERISTICS OF COMPRESSED GASES STORED IN “E” SIZE CYLINDERS THAT MAY BE ATTACHED TO THE ANESTHESIA MACHINE Characteristics Oxygen N2O CO2 Air Cylinder color Green* Blue Gray Yellow* Physical state in cylinder Gas Liquid and gas Liquid and gas Gas Cylinder contents (L) 625 1590 1590 625 Cylinder weight empty (kg) 5.90 5.90 5.90 5.90 Cylinder weight full (kg) 6.76 8.80 8.90 Cylinder pressure full (psi) 2000 750 838 1800 *The World Health Organization specifies that cylinders containing oxygen for medical use be painted white, but manufacturers in the United States use green. Likewise, the international color for air is white and black, whereas cylinders in the United States are color-coded yellow. From Miller RD: Basics of Anesthesia, ed 6, Philadelphia, Saunders, 2011, p 201, Table 15-2.
11. A 25-year-old healthy patient is anesthetized for a femoral hernia repair. Anesthesia is maintained with isoflurane and N2O 50% in O2, and the patient’s lungs are mechanically ventilated. Suddenly, the “low-arterial saturation” warning signal on the pulse oximeter gives an alarm. After the patient is disconnected from the anesthesia machine, he undergoes ventilation with an Ambu bag with 100% O2 without difficulty, and the arterial saturation quickly improves. During inspection of your anesthesia equipment, you notice that the bobbin in the O2 rotameter is not rotating. This most likely indicates A. Flow of O2 through the O2 rotameter B. No flow of O2 through the O2 rotameter C. A leak in the O2 rotameter below the bobbin D. A leak in the O2 rotameter above the bobbin
11. (B) Given the description of the problem, no flow of O2 through the O2 rotameter is the correct choice. In a normally functioning rotameter, gas flows between the rim of the bobbin and the wall of the Thorpe tube, causing the bobbin to rotate. If the bobbin is rotating, you can be certain that gas is flowing through the rotameter and that the bobbin is not stuck (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 43–45). Anesthesia Equipment and Physics 13 N2O Oxygen supply failure alarm Pipeline pressure Cylinder gauge pressure gauge N2O cylinder supply N2O pipeline supply N2O O2 O2 Check valve “Fail-safe” valve Flowmeters Low-pressure circuit Flow-control valve Pressure regulator Calibrated vaporizers Check valve (or internal to vaporizer) Second stage O2 pressure regulator O2 pipeline supply O2 cylinder supply Oxygen flush valve Machine outlet (common gas outlet)
12. The O2 pressure-sensor shutoff valve requires what O2 pressure to remain open and allow N2O to flow into the N2O rotameter? A. 10 psi B. 30 psi C. 50 psi D. 100 psi
12. (B) Fail-safe valve is a synonym for pressure-sensor shutoff valve. The purpose of the fail-safe valve is to prevent the delivery of hypoxic gas mixtures from the anesthesia machine to the patient resulting from failure of the O2 supply. Most modern anesthesia machines, however, would not allow a hypoxic mixture, because the knob controlling the N2O is linked to the O2 knob. When the O2 pressure within the anesthesia machine decreases below 30 psi, this valve discontinues the flow of N2O or proportionally decreases the flow of all gases. It is important to realize that this valve will not prevent the delivery of hypoxic gas mixtures or pure N2O when the O2 rotameter is off, because the O2 pressure within the circuits of the anesthesia machine is maintained by an open O2 compressed-gas cylinder or a central supply source. Under these circumstances, an O2 analyzer will be needed to detect the delivery of a hypoxic gas mixture (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 37–40; Miller: Basics of Anesthesia, ed 6, pp 199–200).
13. A 78-year-old patient is anesthetized for resection of a liver tumor. After induction and tracheal intubation, a 20-gauge arterial line is placed and connected to a transducer that is located 20 cm below the level of the heart. The system is zeroed at the stopcock located at the wrist while the patient’s arm is stretched out on an arm board. How will the arterial line pressure compare with the true blood pressure (BP)? A. It will be 20 mm Hg higher B. It will be 15 mm Hg higher C. It will be the same D. It will be 15 mm Hg lower
13. (C) It is important to zero the electromechanical transducer system with the reference point at the approximate level of the heart. This will eliminate the effect of the fluid column of the transducer system on the arterial BP reading of the system. In this question, the system was zeroed at the stopcock, which was located at the patient’s wrist (approximate level of the ventricle). The BP expressed by the arterial line will therefore be accurate, provided the stopcock remains at the wrist and the transducer is not moved once zeroed. Raising the arm (e.g., 15 cm) decreases the BP at the wrist but increases the pressure on the transducer by the same amount (i.e., the vertical tubing length is now 15 cm H2O higher than before) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 276–278; Miller: Miller’s Anesthesia, ed 8, pp 1354–1355).
14. The second-stage O2 pressure regulator delivers a constant O2 pressure to the rotameters of A. 4 psi B. 8 psi C. 16 psi D. 32 psi
14. (C) O2 and N2O enter the anesthesia machine from a central supply source or compressed-gas cylinders at pressures as high as 2200 psi (O2) and 750 psi (N2O). First-stage pressure regulators reduce these pressures to approximately 45 psi. Before entering the rotameters, second-stage O2 pressure regulators further reduce the pressure to approximately 14 to 16 psi (Miller: Miller’s Anesthesia, ed 8, p 761). 14 Part 1 Basic Sciences
15. The highest trace concentration of N2O allowed in the operating room (OR) atmosphere by the National Institute for Occupational Safety and Health (NIOSH) is A. 1 part per million (ppm) B. 5 ppm C. 25 ppm D. 50 ppm
15. (C) NIOSH sets guidelines and issues recommendations concerning the control of waste anesthetic gases. NIOSH mandates that the highest trace concentration of N2O contamination of the OR atmosphere should be less than 25 ppm. In dental facilities where N2O is used without volatile anesthetics, NIOSH permits up to 50 ppm (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 81).
16. A sevoflurane vaporizer will deliver an accurate concentration of an unknown volatile anesthetic if the latter shares which property with sevoflurane? A. Molecular weight B. Oil/gas partition coefficient C. Vapor pressure D. Blood/gas partition coefficient
16. (C) Agent-specific vaporizers, such as the Sevotec (sevoflurane) vaporizer, are designed for each volatile anesthetic. However, volatile anesthetics with identical saturated vapor pressures can be used interchangeably, with accurate delivery of the volatile anesthetic. Although halothane is no longer used in the United States, that vaporizer, for example, may still be used in developing countries for administration of isoflurane (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 61–63; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 72–73). VAPOR PRESSURES Agent Vapor Pressure mm Hg at 20° C Halothane 243 Sevoflurane 160 Isoflurane 240 Desflurane 669
17. A 58-year-old patient has severe shortness of breath and “wheezing.” On examination, the patient is found to have inspiratory and expiratory stridor. Further evaluation reveals marked extrinsic compression of the midtrachea by a tumor. The type of airflow at the point of obstruction within the trachea is A. Laminar flow B. Turbulent flow C. Undulant flow D. Stenotic flow
17. (B) Turbulent flow occurs when gas flows through a region of severe constriction such as that described in this question. Laminar flow occurs when gas flows down parallel-sided tubes at a rate less than critical velocity. When the gas flow exceeds the critical velocity, it becomes turbulent (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 488–489).
18. Concerning the patient in Question 17, administration of 70% helium in O2 instead of 100% O2 will decrease the resistance to airflow through the stenotic region within the trachea because A. Helium decreases the viscosity of the gas mixture B. Helium decreases the friction coefficient of the gas mixture C. Helium decreases the density of the gas mixture D. Helium increases the Reynolds number of the gas mixture
18. (C) During turbulent flow, the resistance to gas flow is directly proportional to the density of the gas mixture. Substituting helium for oxygen will decrease the density of the gas mixture, thereby decreasing the resistance to gas flow (as much as threefold) through the region of constriction (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 498–499, 1286–1287; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 230–234).
19. A 56-year-old patient is brought to the OR for elective replacement of a stenotic aortic valve. An awake 20-gauge arterial catheter is placed into the right radial artery and is then connected to a transducer located at the same level as the patient’s left ventricle. The entire system is zeroed at the transducer. Several seconds later, the patient raises both arms into the air until his right wrist is 20 cm above his heart. As he is doing this the BP on the monitor reads 120/80 mm Hg. What would this patient’s true BP be at this time? A. 140/100 mm Hg B. 135/95 mm Hg C. 120/80 mm Hg D. 105/65 mm Hg Anesthesia Equipment and Physics 3
19. (C) Modern electronic BP monitors are designed to interface with electromechanical transducer systems. These systems do not require extensive technical skill on the part of the anesthesia provider for accurate use. A static zeroing of the system is built into most modern electronic monitors. Thus, after the zeroing procedure is accomplished, the system is ready for operation. The system should be zeroed with the reference point of the transducer at the approximate level of the aortic root, eliminating the effect of the fluid column of the system on arterial BP readings (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 276–278).
20. An admixture of room air in the waste gas disposal system during an appendectomy in a paralyzed, mechanically ventilated patient under general volatile anesthesia can best be explained by which mechanism of entry? A. Positive-pressure relief valve B. Negative-pressure relief valve C. Soda lime canister D. Ventilator bellows
20. (B) Waste gas disposal systems, also called scavenging systems, are designed to decrease pollution in the OR by anesthetic gases. These scavenging systems can be passive (waste gases flow from the anesthesia machine to a ventilation system on their own) or active (anesthesia machine is connected to a vacuum system, then to the ventilation system). Positive-pressure relief valves open if there is an obstruction between the anesthesia machine and the disposal system, which would then leak the gas into the OR. A leak in the soda lime canisters would also vent to the OR. Given that most ventilator bellows are powered by oxygen, a leak in the bellows will not add air to the evacuation system. The negative-pressure relief valve is used in active systems and will entrap room air if the pressure in the system is less than −0.5 cm H2O (Miller: Miller’s Anesthesia, ed 8, p 802; Miller: Basics of Anesthesia, ed 6, pp 212; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 101–103).
21. The relationship between intra-alveolar pressure, surface tension, and the radius of an alveolus is described by A. Graham’s law B. Beer’s law C. Bernoulli’s law D. Laplace’s law
21. (D) The relationship between intra-alveolar pressure, surface tension, and the radius of alveoli is described by Laplace’s law for a sphere, which states that the surface tension of the sphere is directly proportional to the radius of the sphere and pressure within the sphere. With regard to pulmonary alveoli, the mathematic expression of Laplace’s law is as follows: T = (1/2) PR Anesthesia Equipment and Physics 15 where T is the surface tension, P is the intra-alveolar pressure, and R is the radius of the alveolus. In pulmonary alveoli, surface tension is produced by a liquid film lining the alveoli. This occurs because the attractive forces between the molecules of the liquid film are much greater than the attractive forces between the liquid film and gas. Thus, the surface area of the liquid tends to become as small as possible, which could collapse the alveoli (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 493–494; Miller: Miller’s Anesthesia, ed 8, p 475).
22. Currently, the commonly used vaporizers (e.g., GEDatex- Ohmeda Tec 4, Tec 5, Tec 7; Dräger Vapor 19.n and 2000 series) are described as having all of the following features EXCEPT A. Agent specificity B. Variable bypass C. Bubble through D. Temperature compensated
22. (C) Because volatile anesthetics have different vapor pressures, the vaporizers are agent specific. Vaporizers are described as having variable bypass, which means that some of the total fresh gas flow (usually less than 20%) is diverted into the vaporizing chamber, and the rest bypasses the vaporizer. Tipping the vaporizers (which should not occur) may cause some of the liquid to enter the bypass circuit, leading to a high concentration of anesthetic being delivered to the patient. The gas that enters the vaporizer flows over (does not bubble through) the volatile anesthetic. The older (now obsolete) Copper Kettle and Vern-Trol vaporizers were not agent specific, and oxygen (with a separate flowmeter) was bubbled through the volatile anesthetic; then, the combination of oxygen with volatile gas was diluted with the fresh gas flow (oxygen, air, N2O) and administered to the patient. Because vaporization changes with temperature, modern vaporizers are designed to maintain a constant concentration over clinically used temperatures (20° C-35° C) (Barash: Clinical Anesthesia, ed 7, pp 661–672; Miller: Basics of Anesthesia, ed 6, pp 202–203; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 60–64).
23. For any given concentration of volatile anesthetic, the splitting ratio is dependent on which of the following characteristics of that volatile anesthetic? A. Vapor pressure B. Molecular weight C. Specific heat D. Minimum alveolar concentration (MAC) at 1 atmosphere
23. (A) Vaporizers can be categorized into variable-bypass and measured-flow vaporizers. Measured-flow vaporizers (nonconcentration calibrated vaporizers) include the obsolete Copper Kettle and Vernitrol vaporizers. With measured-flow vaporizers, the flow of oxygen is selected on a separate flowmeter to pass into the vaporizing chamber, from which the anesthetic vapor emerges at its saturated vapor pressure. By contrast, in variable-bypass vaporizers, the total gas flow is split between a variable bypass and the vaporizer chamber containing the anesthetic agent. The ratio of these two flows is called the splitting ratio. The splitting ratio depends on the anesthetic agent, the temperature, the chosen vapor concentration set to be delivered to the patient, and the saturated vapor pressure of the anesthetic (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 68–71).
24. A mechanical ventilator (e.g., Ohmeda 7000) is set to deliver a tidal volume (VT) of 500 mL at a rate of 10 breaths/min and an inspiratory-to-expiratory (I:E) ratio of 1:2. The fresh gas flow into the breathing circuit is 6 L/min. In a patient with normal total pulmonary compliance, the actual VT delivered to the patient would be A. 500 mL B. 600 mL C. 700 mL D. 800 mL
24. (C) The contribution of the fresh gas flow from the anesthesia machine to the patient’s VT should be considered when setting the VT of a mechanical ventilator. Because the ventilator pressure-relief valve is closed during inspiration, both the gas from the ventilator bellows and the fresh gas flow will be delivered to the patient’s breathing circuit. In this question, the fresh gas flow is 6 L/min, or 100 mL/sec (6000 mL/60 sec). Each breath lasts 6 seconds (60 sec/10 breaths), with inspiration lasting 2 seconds (I:E ratio = 1:2). Under these conditions, the 500 VT delivered to the patient by the mechanical ventilator will be augmented by approximately 200 mL. In some ventilators, such as the Ohmeda 7900, VT is controlled for the fresh gas flow rate in such a manner that the delivered VT is always the same as the dial setting (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 79–81).
25. In reference to Question 24, if the ventilator rate were decreased from 10 to 6 breaths/min, the approximate VT delivered to the patient would be A. 600 mL B. 700 mL C. 800 mL D. 900 mL
25. (C) The ventilator rate is decreased from 10 to 6 breaths/min. Thus, each breath will last 10 seconds (60 sec/6 breaths), with inspiration lasting approximately 3.3 seconds (I:E ratio = 1:2) (i.e., 3.3 seconds × 100 mL/sec). Under these conditions, the actual VT delivered to the patient by the mechanical ventilator will be 830 mL (500 mL + 330 mL) (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 79–81).
26. A 65-year-old patient is mechanically ventilated in the intensive care unit (ICU) after an open nephrectomy. How far should the suction catheter be inserted into the endotracheal tube for suctioning? A. To the midlevel of the endotracheal tube B. To the tip of the endotracheal tube C. Just proximal to the carina D. Past the carina
26 (B) Endotracheal tubes frequently become partially or completely occluded with secretions. Periodic suctioning of the endotracheal tube in the ICU assures patency of the artificial airway. There are hazards, however, of endotracheal tube suctioning. They include mucosal trauma, cardiac dysrhythmias, hypoxia, increased intracranial pressure, colonization of the distal airway, and psychologic trauma to the patient. To reduce the possibility of colonization of the distal airway it is prudent to keep the suction catheter within the endotracheal tube during suctioning. Pushing the suctioning catheter beyond the distal limits of the endotracheal tube also may produce suctioning trauma to the tracheal tissue (Tobin: Principles and Practices of Mechanical Ventilation, ed 3, p 1223).
27. If the anesthesia machine is discovered Monday morning to have run with 5 L/min of oxygen all weekend long, the most reasonable course of action before administering the next anesthetic would be to A. Administer 100% oxygen for the first hour of the next case B. Place humidifier in line with the expiratory limb C. Avoid use of sevoflurane D. Change the CO2 absorbent
27. (D) CO can be generated when volatile anesthetics are exposed to CO2 absorbers that contain NaOH or KOH (e.g., soda lime) and have sometimes produced carboxyhemoglobin levels of 35%. Factors that are involved 16 Part 1 Basic Sciences in the production of CO and formation of carboxyhemoglobin include (1) the specific volatile anesthetic used (desflurane ≥ enflurane > isoflurane ≫ sevoflurane = halothane), (2) high concentrations of volatile anesthetic (more CO is generated at higher volatile concentrations), (3) high temperatures (more CO is generated at higher temperatures), (4) low fresh gas flows, and especially (5) dry soda lime (dry granules produce more CO than do hydrated granules). Soda lime contains 15% water by weight, and only when it gets dehydrated to below 1.4% will appreciable amounts of CO be formed. Many of the reported cases of patients experiencing elevated carboxyhemoglobin levels occurred on Monday mornings, when the fresh gas flow on the anesthesia circuit was not turned off and high anesthetic fresh gas flows (>5 L/min) for prolonged periods of time (e.g., >48 hours) occurred. Because of some resistance of the inspiratory valve, retrograde flow through the CO2 absorber (which hastens the drying of the soda lime) will develop, especially if the breathing bag is absent, the Y-piece of the circuit is occluded, and the adjustable pressure-limiting valve is open. Whenever you are uncertain as to the dryness of the CO2 absorber, especially when the fresh gas flow was not turned off the anesthesia machine for an extended or indeterminate period of time, the CO2 absorber should be changed. This CO production occurs with soda lime and occurred more so with Baralyme (which is no longer available), but it does not occur with Amsorb Plus or DrägerSorb Free (which contains calcium chloride and calcium hydroxide and no NaOH or KOH) (Barash: Clinical Anesthesia, ed 7, p 676; Miller: Basics of Anesthesia, ed 6, pp 212–215; Miller: Miller’s Anesthesia, ed 8, pp 789–792).
28. According to NIOSH regulations, the highest concentration of volatile anesthetic contamination allowed in the OR atmosphere when administered in conjunction with N2O is A. 0.5 ppm B. 2 ppm C. 5 ppm D. 25 ppm
28. (A) NIOSH mandates that the highest trace concentration of volatile anesthetic contamination of the OR atmosphere when administered in conjunction with N2O is 0.5 ppm (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 81).
29. The device on anesthesia machines that most reliably detects delivery of hypoxic gas mixtures is the A. Fail-safe valve B. O2 analyzer C. Second-stage O2 pressure regulator D. Proportion-limiting control system
29. (B) The O2 analyzer is the last line of defense against the inadvertent delivery of hypoxic gas mixtures. It should be located in the inspiratory (not expiratory) limb of the patient’s breathing circuit to provide maximum safety. Because the O2 concentration in the fresh-gas supply line may be different from that of the patient’s breathing circuit, the O2 analyzer should not be located in the fresh-gas supply line (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 209–210).
30. A ventilator pressure-relief valve stuck in the closed position can result in A. Barotrauma B. Hypoventilation C. Hyperventilation D. Low breathing circuit pressure
30. (A) The ventilator pressure-relief valve (also called the spill valve) is pressure controlled via pilot tubing that communicates with the ventilator bellows chamber. As pressure within the bellows chamber increases during the inspiratory phase of the ventilator cycle, the pressure is transmitted via the pilot tubing to close the pressure-relief valve, thus making the patient’s breathing circuit “gas tight.” This valve should open during the expiratory phase of the ventilator cycle to allow the release of excess gas from the patient’s breathing circuit into the waste-gas scavenging circuit after the bellows has fully expanded. If the ventilator pressure-relief valve were to stick in the closed position, there would be a rapid buildup of pressure within the circle system that would be readily transmitted to the patient. Barotrauma to the patient’s lungs would result if this situation were to continue unrecognized (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 34, 79–80). Anesthesia Equipment and Physics 17
31. A mixture of 1% isoflurane, 70% N2O, and 30% O2 is administered to a patient for 30 minutes. The expired isoflurane concentration measured is 1%. N2O is shut off, and a mixture of 30% O2 and 70% N2 with 1% isoflurane is administered. The expired isoflurane concentration measured 1 minute after the start of this new mixture is 2.3%. The best explanation for this observation is A. Intermittent back pressure (pumping effect) B. Diffusion hypoxia C. Concentration effect D. Effect of N2O solubility in isoflurane 4 Part 1 Basic Sciences 50 0 5 PCO2 (mm Hg) 10 15
31. (D) Vaporizer output can be affected by the composition of the carrier gas used to vaporize the volatile agent in the vaporizing chamber, especially when N2O is either initiated or discontinued. This observation can be explained by the solubility of N2O in the volatile agent. When N2O and oxygen enter the vaporizing chamber, a portion of the N2O dissolves in the liquid agent. Thus, the vaporizer output transiently decreases. Conversely, when N2O is withdrawn as part of the carrier gas, the N2O dissolved in the volatile agent comes out of solution, thereby transiently increasing the vaporizer output (Miller: Miller’s Anesthesia, ed 8, pp 769–771).
32. The capnogram waveform above represents which of the following situations? A. Kinked endotracheal tube B. Bronchospasm C. Incompetent inspiratory valve D. Incompetent expiratory valve
32. (D) The capnogram can provide a variety of information, such as verification of exhaled CO2 after tracheal intubation, estimation of the differences in Paco2 and Petco2, abnormalities of ventilation, and hypercapnia or hypocapnia. The four phases of the capnogram are inspiratory baseline, expiratory upstroke, expiratory plateau, and inspiratory downstroke. The shape of the capnogram can be used to recognize and diagnose a variety of potentially adverse circumstances. Under normal conditions, the inspiratory baseline should be 0, indicating that there is no rebreathing of CO2 with a normal functioning circle breathing system. If the inspiratory baseline is elevated above 0, there is rebreathing of CO2. If this occurs, the differential diagnosis should include an incompetent expiratory valve, exhausted CO2 absorbent, or gas channeling through the CO2 absorbent. However, the inspiratory baseline may be elevated when the inspiratory valve is incompetent (e.g., there may be a slanted inspiratory downstroke). The expiratory upstroke occurs when the fresh gas from the anatomic dead space is quickly replaced by CO2-rich alveolar gas. Under normal conditions, the upstroke should be steep; however, it may become slanted during partial airway obstruction, if a sidestream analyzer is sampling gas too slowly, or if the response time of the capnograph is too slow for the patient’s respiratory rate. Partial obstruction may be the result of an obstruction in the breathing system (e.g., by a kinked endotracheal tube) or in the patient’s airway (e.g., chronic obstructive pulmonary disease or acute bronchospasm). The expiratory plateau is normally characterized by a slow but shallow progressive increase in CO2 concentration. This occurs because of imperfect matching of ventilation and perfusion in all lung units. Partial obstruction of gas flow either in the breathing system or in the patient’s airways may cause a prolonged increase in the slope of the expiratory plateau, which may continue rising until the next inspiratory downstroke begins. The inspiratory downstroke is caused by the rapid influx of fresh gas, which washes the CO2 away from the CO2 sensing or sampling site. Under normal conditions, the inspiratory downstroke is very steep. The causes of a slanted or blunted inspiratory downstroke include an incompetent inspiratory valve, slow mechanical inspiration, slow gas sampling, and partial CO2 rebreathing (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 248).
33. Select the FALSE statement. A. If a Magill forceps is used for a nasotracheal intubation, the right nares is preferable for insertion of the nasotracheal tube B. Extension of the neck can convert an endotracheal intubation to an endobronchial intubation C. Bucking signifies the return of the coughing reflex D. Postintubation pharyngitis is more likely to occur in female patients
33. (B) The complications of tracheal intubation can be divided into those associated with direct laryngoscopy and intubation of the trachea, tracheal tube placement, and extubation of the trachea. The most frequent complication associated with direct laryngoscopy and tracheal intubation is dental trauma. If a tooth is dislodged and not found, radiographs of the chest and abdomen should be taken to determine whether the tooth has passed through the glottic opening into the lungs. Should dental trauma occur, immediate consultation with a dentist is indicated. Other complications of direct laryngoscopy and tracheal intubation include hypertension, tachycardia, cardiac dysrhythmias, and aspiration of gastric contents. The most common complication that occurs while the endotracheal tube is in place is inadvertent endobronchial intubation. Flexion, not extension, of the neck or a change from the supine position to the head-down position can shift the carina upward, which may convert a midtracheal tube placement into a bronchial intubation. Extension of the neck can cause cephalad displacement of the tube into the pharynx. Lateral rotation of the head can displace the distal end of the endotracheal tube approximately 0.7 cm away from the carina. The complications associated with extubation of the trachea can be immediate or delayed; of the immediate complications associated with extubation of the trachea, the two most serious are laryngospasm and aspiration of gastric contents. Laryngospasm is most likely to occur in patients who are lightly anesthetized at the time of extubation. If laryngospasm occurs, positive-pressure bag and mask ventilation with 100% O2 and forward displacement of the mandible may be sufficient treatment. However, if laryngospasm persists, succinylcholine should be administered intravenously or intramuscularly. Pharyngitis is another frequent complication after extubation of the trachea. It occurs most commonly in female individuals, presumably because of the thinner mucosal covering over the posterior vocal cords in comparision with male individuals. This complication usually does not require treatment and spontaneously resolves in 48 to 72 hours. Delayed complications associated with extubation of the trachea include laryngeal ulcerations, tracheitis, tracheal stenosis, vocal cord paralysis, and arytenoid cartilage dislocation (Miller: Miller’s Anesthesia, ed 8, p 1655). 18 Part 1 Basic Sciences
34. Gas from an N2O compressed-gas cylinder enters the anesthesia machine through a pressure regulator that reduces the pressure to A. 60 psi B. 45 psi C. 30 psi D. 15 psi
34. (B) Gas leaving a compressed-gas cylinder is directed through a pressure-reducing valve, which lowers the pressure within the metal tubing of the anesthesia machine to 45 to 55 psi (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 27–34).
35. Eye protection for OR staff is needed when laser surgery is performed. Clear wraparound goggles or glasses are adequate with which kind of laser? A. Argon laser B. Nd:YAG (neodymium:yttrium-aluminum-garnet) laser C. CO2 laser D. None of the above
35. (C) CO2 lasers can cause serious corneal injury, whereas argon, Nd:YAG, ruby, or potassium titanyl phosphate lasers can burn the retina. Use of the incorrect filter provides no protection! Clear glass or plastic lenses are opaque for CO2 laser light and are adequate protection for this beam (contact lenses are not adequate protection). For argon or krypton laser light, amber-orange filters are used. For Nd:YAG laser light, special green-tinted filters are used. For potassium titanyl phosphate:Nd:YAG laser light, red filters are used (Miller: Miller’s Anesthesia, ed 8, pp 2328–2331).
36. Which of the following systems prevents attachment of gas-administering equipment to the wrong type of gas line? A. Pin index safety system B. Diameter index safety system C. Fail-safe system D. Proportion-limiting control system
36. (B) The diameter index safety system prevents incorrect connections of medical gas lines. This system consists of two concentric and specific bores in the body of one connection, which correspond to two concentric and specific shoulders on the nipple of the other connection (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 20, 27–28).
37. A patient with aortic stenosis is scheduled for laparoscopic cholecystectomy. Preoperative echocardiography demonstrated a peak velocity of 4 m/sec across the aortic valve. If her BP was 130/80 mm Hg, what was the peak pressure in the left ventricle? A. 145 mm Hg B. 160 mm Hg C. 194 mm Hg D. 225 mm Hg
37. (C) The modified Bernoulli equation defines the pressure drop (or gradient) across an obstruction, narrowing, or stenosis as follows: ΔP = 4V2 Where ΔP is the pressure gradient; V is the measured velocity across the stenosis using Doppler echocardiography. In this example, ΔP = 4 × 42 = 64. The peak pressure in the left ventricle is 130 + 64 = 194 mm Hg (Kaplan: Kaplan’s Cardiac Anesthesia: The Echo Era, ed 6, pp 315–382).
38. The dial of an isoflurane-specific, variable bypass, temperature-compensated, flowover, out-of-circuit vaporizer (i.e., modern vaporizer) is set on 2%, and the infrared spectrometer measures 2% isoflurane vapor from the common gas outlet. The flowmeter is set at a rate of 700 mL/min during this measurement. The output measurements are repeated with the flowmeter set at 100 mL/min and 15 L/min (vapor dial still set on 2%). How will these two measurements compare with the first measurement taken? A. Output will be less than 2% in both cases B. Output will be greater than 2% in both cases C. Output will be 2% at 100 mL/min O2 flow and less than 2% at 15 L/min flow D. Output will be less than 2% at 100 mL/min and 2% at 15 L/min
38. (A) The output of the vaporizer will be lower at flow rates less than 250 mL/min because there is insufficient pressure to advance the molecules of the volatile agent upward. At extremely high carrier gas flow rates (>15 L/min), there is insufficient mixing in the vaporizing chamber (Miller: Miller’s Anesthesia, ed 8, pp 777–778).
39. Which of the following would result in the greatest decrease in the arterial hemoglobin saturation (Spo2) value measured by the dual-wavelength pulse oximeter? A. Intravenous injection of indigo carmine B. Intravenous injection of indocyanine green C. Intravenous injection of methylene blue D. Elevation of bilirubin
39. (C) Pulse oximeters estimate arterial hemoglobin saturation (Sao2) by measuring the amount of light transmitted through a pulsatile vascular tissue bed. Pulse oximeters measure the alternating current component of light absorbance at each of two wavelengths (660 and 940 nm) and then divide this measurement by the corresponding direct current component. Then the ratio (R) of the two absorbance measurements is determined by the following equation: R AC660 / DC660 AC940 / DC940 = Using an empiric calibration curve that relates arterial hemoglobin saturation to R, the actual arterial hemoglobin saturation is calculated. Based on the physical principles outlined above, the sources of error in Spo2 readings can be easily predicted. Pulse oximeters can function accurately when only two hemoglobin species, oxyhemoglobin and reduced hemoglobin, are present. If any light-absorbing species other than oxyhemoglobin and reduced hemoglobin are present, the pulse oximeter measurements will be inaccurate. Fetal hemoglobin has a minimal effect on the accuracy of pulse oximetry because the extinction coefficients for fetal hemoglobin at the two wavelengths used by pulse oximetry are very similar to the corresponding values for adult hemoglobin. In addition to abnormal hemoglobins, any substance present in the blood that absorbs light at either 660 or 940 nm, such as intravenous dyes used for diagnostic purposes, will affect the value of R, making accurate measurements of the pulse oximeter impossible. These dyes include methylene blue and indigo carmine. Methylene blue has the greatest effect on Sao2 measurements because the extinction coefficient is so similar to that of oxyhemoglobin (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 261–262). Anesthesia Equipment and Physics 19
40. Each of the following statements concerning nonelectronic conventional flowmeters (also called rotameters) is true EXCEPT A. Rotation of the bobbin within the Thorpe tube is important for accurate function B. The Thorpe tube increases in diameter from bottom to top C. Its accuracy is affected by changes in temperature and atmospheric pressure D. The rotameters for N2O and CO2 are interchangeable
40. (D) Rotameters consist of a vertically positioned tapered tube that is smallest in diameter at the bottom (Thorpe tube). Gas enters at the bottom of the Thorpe tube and elevates a bobbin or float, which comes to rest when gravity on the float is balanced by the fall in pressure across the float. The rate of gas flow through the tube depends on the pressure drop along the length of the tube, the resistance to gas flow through the tube, and the physical properties (density and viscosity) of the gas. Because few gases have the same density and viscosity, rotameters cannot be used interchangeably (Barash: Clinical Anesthesia, ed 7, pp 655–657; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 43–45).
41. Which of the following combinations would result in delivery of a lower-than-expected concentration of volatile anesthetic to the patient? A. Sevoflurane vaporizer filled with desflurane B. Isoflurane vaporizer filled with sevoflurane C. Sevoflurane vaporizer filled with isoflurane D. All of the above would result in less than the dialed concentration Anesthesia Equipment and Physics 5
41. (B) Saturated vapor pressures depend on the physical properties of the liquid and the temperature. Vapor pressures are independent of barometric pressure. At 20° C the vapor pressures of halothane (243 mm Hg) and isoflurane (240 mm Hg) are similar, and at 1 atmosphere the concentration in the vaporizer for these drugs is 240/760, or about 32%. Similarly, the vapor pressure for sevoflurane (160 mm Hg) and enflurane (172 mm Hg) are similar, and at 1 atmosphere the concentration in the vaporizer for these drugs is 160/760, or about 21%. If desflurane (vapor pressure of 669 mm Hg) is placed in a 1-atmosphere pressure vaporizer, the concentration would be 669/760 = 88%. Because the bypass flow is adjusted for each vaporizer, putting a volatile anesthetic with a higher saturated vapor pressure would lead to a higher-than-expected concentration of anesthetic delivered from the vaporizer, whereas putting a drug with a lower saturated vapor pressure would lead to a lower-than-expected concentration of drug delivered from the vaporizer (Barash: Clinical Anesthesia, ed 7, pp 661–672). VAPOR PRESSURE AND MINIMUM ALVEOLAR CONCENTRATION Halothane Enflurane Sevoflurane Isoflurane Desflurane Methoxyflurane Vapor pressure 20° C mm Hg 243 172 160 240 669 23 MAC 30-55 yr 0.75 1.63 1.8 1.17 6.6 0.16 MAC, minimum alveolar concentration.
42. At high altitudes, the flow of a gas through a rotameter will be A. Greater than expected B. Less than expected C. Less than expected at high flows but greater than expected at low flows D. Greater than expected at high flows but accurate at low flows
42. (D) Gas density decreases with increasing altitude (i.e., the density of a gas is directly proportional to atmospheric pressure). Atmospheric pressure will influence the function of rotameters because the accurate function of rotameters is influenced by the physical properties of the gas, such as density and viscosity. The magnitude of this influence, however, depends on the rate of gas flow. At low gas flows, the pattern of gas flow is laminar. Atmospheric pressure will have little effect on the accurate function of rotameters at low gas flows because laminar gas flow is influenced by gas viscosity (which is minimally affected by atmospheric pressure), not by gas density. However, at high gas flows, the gas flow pattern is turbulent and is influenced by gas density. At high altitudes (i.e., low atmospheric pressure), the gas flow through the rotameter will be greater than expected at high flows but accurate at low flows (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 43–45, 230–231).
43. A patient presents for knee arthroscopy and tells his anesthesiologist that he has a VDD pacemaker. Select the true statement regarding this pacemaker. A. It senses and paces only the ventricle B. It paces only the ventricle C. Its response to a sensed event is always inhibition D. It is not useful in a patient with atrioventricular (AV) nodal block
43. (B) Pacemakers have a three- to five-letter code that describes the pacemaker type and function. Given that the purpose of the pacemaker is to send electric current to the heart, the first letter identifies the chamber(s) paced: A for atrial, V for ventricle, and D for dual chamber (A + V). The second letter identifies the chamber where endogenous current is sensed: A,V, D, and O for none sensed. The third letter describes the response to sensing: O for none, I for inhibited, T for triggered, and D for dual (I + T). The fourth letter describes programmability or rate modulation: O for none and R for rate modulation (i.e., faster heart rate with exercise). The fifth letter describes multisite pacing (more important in dilated heart chambers): A, V or D (A + V), or O. A VDD pacemaker is used for patients with AV node dysfunction but intact sinus node activity (Miller: Miller’s Anesthesia, ed 8, pp 1467–1468).
44. All of the following would result in less trace gas pollution of the OR atmosphere EXCEPT A. Use of a high gas flow in a circular system B. Tight mask seal during mask induction C. Use of a scavenging system D. Allow patient to breathe 100% O2 as long as possible before extubation
44. (A) Although controversial, it is thought that chronic exposure to low concentrations of volatile anesthetics may constitute a health hazard to OR personnel. Therefore, removal of trace concentrations of volatile anesthetic gases from the OR atmosphere with a scavenging system and steps to reduce and control gas leakage into the environment are required. High-pressure system leakage of volatile anesthetic gases into the OR atmosphere occurs when gas escapes from compressed-gas cylinders attached to the anesthetic machine (e.g., faulty yokes) or from tubing delivering these gases to the anesthesia machine from a central supply source. The most common cause of low-pressure leakage of anesthetic gases into the OR atmosphere is the escape of gases from 20 Part 1 Basic Sciences sites located between the flowmeters of the anesthesia machine and the patient, such as a poor mask seal. The use of high gas flows in a circle system will not reduce trace gas contamination of the OR atmosphere. In fact, this could contribute to the contamination if there is a leak in the circle system (Miller: Miller’s Anesthesia, ed 8, pp 3232–3234).
45. The greatest source for contamination of the OR atmosphere is leakage of volatile anesthetics A. Around the anesthesia mask B. At the vaporizer C. At the CO2 absorber D. At the endotracheal tube
45. (A) Although there is insufficient evidence that chronic exposure to low concentrations of inhaled anesthetics may pose a health hazard to those in the OR, precautions are made to decrease the pollution of inhalation anesthetics there. This includes ventilating the room adequately (air in the OR should be exchanged at least 15 times an hour), maintenance of anesthetic system scavenging systems to remove anesthetic vapors, and a tight anesthetic seal with no leakage of gas into the OR atmosphere. Although periodic equipment maintenance should be performed to make sure the anesthetic equipment is operating properly, leakage around an improperly sealed face mask as well as the face mask not applied to the face during airway manipulations (placement of an airway) poses the greatest risk of OR contamination from inhaled anesthetics (Barash: Clinical Anesthesia, ed 7, pp 62–64; Miller: Basics of Anesthesia, ed 6, pp 211–212; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 130–145; Miller: Miller’s Anesthesia, ed 8, pp 3232–3234).
46. Uptake of sevoflurane from the lungs during the first minute of general anesthesia is 50 mL. How much sevoflurane would be taken up from the lungs between the 16th and 36th minutes? A. 25 mL B. 50 mL C. 100 mL D. 500 mL
46. (C) The amount of volatile anesthetic taken up by the patient in the first minute is equal to the amount taken up between the squares of any two consecutive minutes (square root of time equation). Thus, if 50 mL is taken up in the first minute, 50 mL will be taken up between the first (1 squared) and fourth (2 squared) minutes. Similarly, between the fourth and ninth minutes (2 squared and 3 squared), another 50 mL will be absorbed. In this example, we are looking for the uptake between the 16th (4 squared) and 36th (6 squared) minutes, which would be 2 consecutive minutes squared, or 2 × 50 mL = 100 mL (Miller: Miller’s Anesthesia, ed 8, pp 650–651).
47. Which of the drugs below would have the LEAST impact on somatosensory evoked potentials (SSEPs) monitoring in a 15-year-old patient undergoing scoliosis surgery? A. Midazolam B. Propofol C. Isoflurane D. Vecuronium
47. (D) In evaluating SSEPs, one looks at both the amplitude or voltage of the recorded response wave and the latency (time measured from the stimulus to the onset or peak of the response wave). A decrease in amplitude (>50%) and/or an increase in latency (>10%) is usually clinically significant. These changes may reflect hypoperfusion, neural ischemia, temperature changes, or drug effects. All of the volatile anesthetics and the barbiturates cause a decrease in amplitude as well as an increase in latency. Propofol affects both latency and amplitude and, like other intravenous agents, has a significantly less effect than “equipotent” doses of volatile anesthetics. Etomidate causes an increase in latency and an increase in amplitude. Midazolam decreases the amplitude but has little effect on latency. Opioids cause small and not clinically significant increases in latency and a decrease in amplitude of the SSEPs. Muscle relaxants have no effect on SSEPs (Miller: Miller’s Anesthesia, ed 8, pp 1514–1517; Miller: Basics of Anesthesia, ed 6, pp 505–506).
48. Which of the following is NOT found in the lowpressure circuit on an anesthesia machine? A. Oxygen supply failure alarm B. Flowmeters C. Vaporizers D. Vaporizer check valve
48. (A) The anesthesia machine, now more properly called the anesthesia workstation, has two main pressure circuits. The higher-pressure circuits consist of the gas supply from the pipelines and tanks, all piping, pressure gauges, pressure reduction regulators, check valves (which prevent backward gas flow), the oxygen pressuresensor shutoff valve (also called the oxygen failure cutoff or fail-safe valve), the oxygen supply failure alarm, and the oxygen flush valve—or, simplistically, everything up to the gas flow control valves and the machine common gas outlet. The low-pressure circuit starts with and includes the gas flow control valves, flowmeters, vaporizers, and vaporizer check valve and goes to the machine common gas outlet. See also figure for explanation to Question 12 (Barash: Clinical Anesthesia, ed 7, pp 641–650; Miller: Basics of Anesthesia, ed 6, pp 198–204).
49. Frost develops on the outside of an N2O compressedgas cylinder during general anesthesia. This phenomenon indicates that A. The saturated vapor pressure of N2O within the cylinder is rapidly increasing B. The cylinder is almost empty C. There is a rapid transfer of heat to the cylinder D. The flow of N2O from the cylinder into the anesthesia machine is rapid
49. (D) Vaporization of a liquid requires the transfer of heat from the objects in contact with the liquid (e.g., the metal cylinder and surrounding atmosphere). For this reason, at high gas flows, atmospheric water will condense as frost on the outside of compressed-gas cylinders (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 12–13; Miller: Basics of Anesthesia, ed 6, p 201).
50. The LEAST reliable site for central temperature monitoring is the A. Pulmonary artery B. Skin on the forehead C. Distal third of the esophagus D. Nasopharynx
50. (B) Temperature measurements of the pulmonary artery, esophagus, axilla, nasopharynx, and tympanic membrane correlate with central temperature in patients undergoing noncardiac surgery. Skin temperature does not reflect central temperature and does not warn adequately of malignant hyperthermia or excessive hypothermia (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 137; Miller: Miller’s Anesthesia, ed 8, pp 1643–1644).
51. Of the following medical lasers, which laser light penetrates tissues the most? A. Argon laser B. Helium–neon laser (He–Ne) C. Nd:YAG (neodymium:yttrium-aluminum-garnet) laser D. CO2 laser
51. (C) Laser refers to Light Amplification by the Stimulated Emission of Radiation. Laser light differs from ordinary light in three main ways. First, laser light is monochromic (possesses one wavelength or color). Second, laser Anesthesia Equipment and Physics 21 light is coherent (the photons oscillate in the same phase). Third, laser light is collimated (exists in a narrow parallel beam). Visible light has a wide spectrum of wavelengths in the 385- to 760-nm range. Argon laser light, which can penetrate tissues to a depth of 0.05 to 2.0 mm, is either blue (wavelength 488 nm) or green (wavelength 514 nm) and is often used for vascular pigmented lesions because it is intensively absorbed by hemoglobin. Helium–neon laser light is red, has a frequency of 632 nm, and is often used as an aiming beam because it has very low power and presents no significant danger to OR personnel. Nd:YAG laser light is the most powerful medical laser and can penetrate tissues from 2 to 6 mm. Nd:YAG laser light is in the near infrared range, with a wavelength of 1064 nm, has general uses (e.g., prostate surgery, laryngeal papillomatosis, coagulation), and can be used with fiberoptics. CO2 laser light is in the far infrared range, with a long wavelength of 10,600 nm. Because CO2 laser light penetrates tissues poorly, it can vaporize superficial tissues with little damage to underlying cells (Barash: Clinical Anesthesia, ed 7, pp 212–214; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 776–777; Miller: Miller’s Anesthesia, ed 8, pp 2598–2601).
52. The reason Heliox (70% helium and 30% oxygen) is more desirable than a mixture of 70% nitrogen and 30% oxygen for a spontaneously breathing patient with tracheal stenosis is that A. Helium has a lower density than nitrogen B. Helium is a smaller molecule than O2 C. Absorption atelectasis is decreased D. Helium has a lower critical velocity for turbulent flow than does O2
52. (A) Normal gas flow is laminar within the trachea, but with tracheal stenosis, airflow is more turbulent. Resistance during turbulent flow depends on gas density, and helium has a lower gas density than nitrogen. Thus, there is less work of breathing when helium is substituted for nitrogen. Remember, though: the higher the concentration of helium, the lower the concentration of oxygen (Miller: Miller’s Anesthesia, ed 8, p 2545).
53. The maximum Fio2 that can be delivered by a nasal cannula is A. 0.30 B. 0.35 C. 0.40 D. 0.45
53. (D) The Fio2 delivered to patients from low-flow systems (e.g., nasal prongs) is determined by the size of the O2 reservoir, the O2 flow, and the patient’s breathing pattern. As a rule of thumb, assuming a normal breathing pattern, the Fio2 delivered by nasal prongs increases by approximately 0.04 for each L/min increase in O2 flow up to a maximal Fio2 of approximately 0.45 (at an O2 flow of 6 L/min). In general, the larger the patient’s VT or the faster the respiratory rate, the lower the Fio2 for a given O2 flow (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 1282–1283).
54. General anesthesia is administered to an otherwise healthy 38-year-old patient undergoing repair of a right inguinal hernia. During mechanical ventilation, the anesthesiologist notices that the scavenging system reservoir bag is distended during inspiration. The most likely cause of this is A. An incompetent pressure-relief valve in the mechanical ventilator B. An incompetent pressure-relief valve in the patient’s breathing circuit C. An incompetent inspiratory unidirectional valve in the patient’s breathing circuit D. An incompetent expiratory unidirectional valve in the patient’s breathing circuit 6 Part 1 Basic Sciences
54. (A) APL valve Ventilator relief valve Frequency Flow Volume Intake valve 22 Part 1 Basic Sciences In a closed scavenging system interface, the reservoir bag should expand during expiration and contract during inspiration. During the inspiratory phase of mechanical ventilation, the ventilator pressure-relief valve closes, thereby directing the gas inside the ventilator bellows into the patient’s breathing circuit. If the ventilator pressure-relief valve is incompetent, there will be a direct communication between the patient’s breathing circuit and the scavenging circuit. This will result in delivery of part of the mechanical ventilator VT directly to the scavenging circuit, causing the reservoir bag to inflate during the inspiratory phase of the ventilator cycle (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 130–132).
55. Which color of nail polish would have the greatest effect on the accuracy of dual-wavelength pulse oximeters? A. Red B. Yellow C. Blue D. Green
55. (C) The accurate function of dual-wavelength pulse oximeters is altered by nail polish. Because blue nail polish has a peak absorbance similar to that of adult deoxygenated hemoglobin (near 660 nm), it has the greatest effect on the Spo2 reading. Nail polish causes an artifactual and fixed decrease in the Spo2 reading as shown by these devices. Turning the finger probe 90 degrees and having the light shining sidewise through the finger is useful when there is nail polish on the patient’s fingernails (Miller: Miller’s Anesthesia ed 8, p 1547).
56. The minimum macroshock current required to elicit ventricular fibrillation is A. 1 mA B. 10 mA C. 100 mA D. 500 mA
56. (C) Leakage electric currents less than 1 mA are imperceptible to touch. The minimal ventricular fibrillation threshold of current applied to the skin is about 100 mA. If the current bypasses the high resistance of the skin and is applied directly to the heart via pacemaker, central line, etc. (microshock), currents as low as 100 μA (0.1 mA) may be fatal. Because of this, the American National Standards Institute has set the maximum leakage of electric current allowed through electrodes or catheters in contact with the heart at 10 μA (Barash: Clinical Anesthesia, ed 7, p 192; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 17; Miller: Miller’s Anesthesia, ed 8, p 3226).
57. The line isolation monitor A. Prevents microshock B. Prevents macroshock C. Provides electric isolation in the OR D. Sounds an alarm when grounding occurs in the OR
57. (D) The line isolation monitor gives an alarm when grounding occurs in the OR or when the maximum current that a short circuit could cause exceeds 2 to 5 mA. The line isolation monitor is purely a monitor and does not interrupt electric current. Therefore, the line isolation monitor will not prevent microshock or macroshock (Brunner: Electricity, Safety, and the Patient, ed 1, p 304; Miller: Miller’s Anesthesia, ed 8, pp 3221–3223).
58. Kinking or occlusion of the transfer tubing from the patient’s breathing circuit to the closed scavenging system interface can result in A. Barotrauma B. Hypoventilation C. Hypoxia D. Hyperventilation
58. (A) A scavenging system with a closed interface is one in which there is communication with the atmosphere through positive-pressure and negative-pressure relief valves. The positive-pressure relief valve will prevent transmission of excessive pressure buildup to the patient’s breathing circuit, even if there is an obstruction distal to the interface or if the system is not connected to wall suction. However, obstruction of the transfer tubing from the patient’s breathing circuit to the scavenging circuit is proximal to the interface. This will isolate the patient’s breathing circuit from the positive-pressure relief valve of the scavenging system interface. Should this occur, barotrauma to the patient’s lungs can result (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 130–137).
59. The reason a patient is not burned by the return of energy from the patient to the ESU (electrosurgical unit, Bovie) is that A. The coagulation side of this circuit is positive relative to the ground side B. Resistance in the patient’s body attenuates the energy C. The exit current density is much less D. The overall energy delivered is too small to cause burns
59. (C) Electrocautery units, or electrosurgical units (ESUs), were invented by Professor W. T. Bovie and were first used in 1926. They operate by generating ultra-high frequency (0.1-3 MHz) alternating electric Anesthesia Equipment and Physics 23 currents and are commonly used today for cutting and coagulating tissue. Whenever a current passes through a resistance such as tissue, heat is generated and is inversely proportional to the surface area through which the current passes. At the point of entry to the body from the small active electrode or cautery tip, a fair amount of heat is generated. For the current to complete its circuit, the return electrode plate or dispersive pad (incorrectly but commonly called the ground pad) has a large surface area, where very little heat develops. The dispersive pad should be as close as is reasonable to the site of surgery. If the current from the ESU passes through an artificial cardiac pacemaker, the pacemaker may misinterpret the current as cardiac activity and may not pace, which is why a magnet placed over the pacemaker will turn off the pacemaker sensor, putting the pacemaker in the asynchronous mode, and should be available (if the pacemaker’s sensory mode is not turned off preoperatively). In addition, automatic implantable cardioverter-defibrillators (AICDs) may misinterpret the electric activity as ventricular fibrillation and defibrillate the patient. AICDs should be turned off before use of an ESU (Barash: Clinical Anesthesia ed 7, pp 204–206; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 19–22).
60. Select the FALSE statement regarding noninvasive arterial BP monitoring devices. A. If the width of the BP cuff is too narrow, the measured BP will be falsely lowered B. The width of the BP cuff should be 40% of the circumference of the patient’s arm C. If the BP cuff is wrapped around the arm too loosely, the measured BP will be falsely elevated D. Frequent cycling of automated BP monitoring devices can result in edema distal to the cuff
60. (A) Automated noninvasive BP (ANIBP) devices provide consistent and reliable arterial BP measurements. Variations in the cuff pressure resulting from arterial pulsations during cuff deflation are sensed by the device and are used to calculate mean arterial pressure. Then, values for systolic and diastolic pressures are derived from formulas that use the rate of change of the arterial pressure pulsations and the mean arterial pressure (oscillometric principle). This method provides accurate measurements of arterial BP in neonates, infants, children, and adults. The main advantage of ANIBP devices is that they free the anesthesia provider to perform other duties required for optimal anesthesia care. Additionally, these devices provide alarm systems to draw attention to extreme BP values, and they have the capacity to transfer data to automated trending devices or recorders. Improper use of these devices can lead to erroneous measurements and complications. The width of the BP cuff should be approximately 40% of the circumference of the patient’s arm. If the BP cuff is too narrow or if the BP cuff is wrapped too loosely around the arm, the BP measurement by the device will be falsely elevated. Frequent BP measurements can result in edema of the extremity distal to the cuff. For this reason, cycling of these devices should not be more frequent than every 1 to 3 minutes. Other complications associated with improper use of ANIBP devices include ulnar nerve paresthesia, superficial thrombophlebitis, and compartment syndrome. Fortunately, these complications are rare (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 88–91; Miller: Basics of Anesthesia, ed 6, pp 321–322; Miller: Miller’s Anesthesia, ed 8, pp 1347–1348).
61. When electrocardiogram (EKG) electrodes are placed for a patient undergoing a magnetic resonance imaging (MRI) scan, which of the following is true? A. Electrodes should be as close as possible and in the periphery of the magnetic field B. Electrodes should be as close as possible and in the center of the magnetic field C. Placement of electrodes relative to field is not important as long as they are far apart D. EKG cannot be monitored during an MRI scan
61. (B) EKG monitoring is often not used during MRI scans because artifacts are very common (abnormalities in T waves and ST waves), and heating of the wires during the scan would potentially burn the patient. However, EKG can be used if the electrodes are placed close together and toward the center of the magnetic field and the wires are insulated from the patient’s skin and straight. In addition, the wires should not be wound together in loops (because this can induce heating of the wires), and worn or frayed wires should not be used (Barash: Clinical Anesthesia, ed 7, p 884; Miller: Miller’s Anesthesia, ed 8, p 2655).
62. The pressure gauge of a size “E” compressed-gas cylinder containing air shows a pressure of 1000 psi. Approximately how long could air be delivered from this cylinder at the rate of 10 L/min? A. 10 minutes B. 20 minutes C. 30 minutes D. 40 minutes
62. (C) A size “E” compressed-gas cylinder completely filled with air contains 625 L and will show a pressure gauge reading of 2000 psi. Therefore, a cylinder with a pressure gauge reading of 1000 psi is half-full, containing approximately 325 L of air. A half-full size “E” compressed-gas cylinder containing air can be used for approximately 30 minutes at a flow rate of 10 L/min (see definition of Boyle’s law, Question 9) (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 10–12; Miller: Basics of Anesthesia, ed 6, pp 199–201).
63. The most frequent cause of mechanical failure of the anesthesia delivery system to deliver adequate O2 to the patient is A. Attachment of the wrong compressed-gas cylinder to the O2 yoke B. Improperly assembled O2 rotameter C. Fresh-gas line disconnection from the anesthesia machine to the in-line hosing D. Disconnection of the O2 supply system from the patient
63. (D) Failure to oxygenate patients adequately is an important cause of anesthesia-related morbidity and mortality. All of the choices listed in this question are potential causes of inadequate delivery of O2 to the patient; however, the most frequent cause is inadvertent disconnection of the O2 supply system from the patient (e.g., disconnection of the patient’s breathing circuit from the endotracheal tube) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 121; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 43–47).
64. The esophageal detector device A. Uses a negative-pressure bulb B. Is especially useful in children younger than 1 year of age C. Requires a cardiac output to function appropriately D. Is reliable in morbidly obese patients and parturients
64. (A) The esophageal detector device (EDD) is essentially a bulb that is first compressed and then attached to the endotracheal tube after the tube is inserted into the patient. The pressure generated 24 Part 1 Basic Sciences is about –40 cm of water. If the endotracheal tube is placed in the esophagus, then the negative pressure will collapse the esophagus, and the bulb will not inflate. If the endotracheal tube is in the trachea, then the air from the lung will enable the bulb to inflate (usually in a few seconds, but sometimes more than 30 seconds). A syringe that has a negative pressure applied to it has also been used. Although initial studies were very positive about the use of the EDD, more recent studies show that up to 30% of correctly placed endotracheal tubes in adults may be removed because the EDD has suggested esophageal placement. Misleading results have been noted in patients with morbid obesity, late pregnancy, status asthmaticus, and copious endotracheal secretion, wherein the trachea tends to collapse. Its use in children younger than 1 year of age has shown poor sensitivity and poor specificity. Although a cardiac output is needed to get CO2 to the lungs for a CO2 gas analyzer to function, a cardiac output is not needed for an EDD (Miller: Miller’s Anesthesia, ed 8, p 1654).
65. The reason CO2 measured by capnometer is less than the arterial Paco2 value measured simultaneously is A. Use of ion-specific electrode for blood gas determination B. Alveolar capillary gradient C. One-way values D. Alveolar dead space
65. (D) The capnometer measures the CO2 concentration of respiratory gases. Today this is most commonly performed by infrared absorption using a sidestream gas sample. The sampling tube should be connected as close as possible to the patient’s airway. The difference between the end-tidal CO2 (Etco2) and the arterial CO2 (Paco2) is typically 5 to 10 mm Hg and is due to alveolar dead space ventilation. Because nonperfused alveoli do not contribute to gas exchange, any condition that increases alveolar dead space ventilation (i.e., reduces pulmonary blood flow, as by pulmonary embolism or cardiac arrest) will increase dead space ventilation and the Etco2-to-Paco2 difference. Conditions that increase pulmonary shunt result in minimal changes in the Paco2–Etco2 gradient. CO2 diffuses rapidly across the capillary-alveolar membrane (Barash: Clinical Anesthesia, ed 7, pp 704–706; Miller: Miller’s Anesthesia, ed 8, pp 1551–1553).
66. Which of the following arrangements of rotameters on the anesthesia machine manifold is safest with leftto- right gas flow? A. O2, CO2, N2O, air B. CO2, O2, N2O, air C. Air, CO2, O2, N2O D. Air, CO2, N2O, O2 Anesthesia Equipment and Physics 7
66. (D) The last gas added to a gas mixture should always be O2. This arrangement is the safest because it ensures that leaks proximal to the O2 inflow cannot result in the delivery of a hypoxic gas mixture to the patient. With this arrangement (O2 added last), leaks distal to the O2 inflow will result in a decreased volume of gas, but the Fio2 of anesthesia will not be reduced (Miller: Basics of Anesthesia, ed 6, pp 201–202; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 43–45).
67. A Datex-Ohmeda Tec 4 vaporizer is tipped over while being attached to the anesthesia machine but is placed upright and installed. The soonest it can be safely used is A. After 30 minutes of flushing with dial set to “off” B. After 6 hours of flushing with dial set to “off” C. After 30 minutes with dial turned on D. Immediately
67. (C) Most modern Datex-Ohmeda Tec or North American Dräger Vapor vaporizers (except desflurane) are variable-bypass, flow-over vaporizers. This means that the gas that flows through the vaporizers is split into two parts, depending on the concentration selected. The gas goes through either the bypass chamber on the top of the vaporizer or the vaporizing chamber on the bottom of the vaporizer. If the vaporizer is tipped, which might happen when a filled vaporizer is switched out or moved from one machine to another machine, part of the anesthetic liquid in the vaporizing chamber may get into the bypass chamber. This could result in a much higher concentration of gas than that dialed. With the Datex-Ohmeda Tec 4 or the North American Dräger Vapor 19.1 series, it is recommended to flush the vaporizer at high flows with the vaporizer set at a low concentration until the output shows no excessive agent (this usually takes 20-30 minutes). The Dräger Vapor 2000 series has a transport (T) dial setting. This setting isolates the bypass from the vaporizer chamber. The Aladin cassette vaporizer does not have a bypass flow chamber and has no tipping hazard (Miller: Miller’s Anesthesia, ed 8, p 771).
68. In the event of misfilling, what percent sevoflurane would be delivered from an isoflurane vaporizer set at 1%? A. 0.6% B. 0.8% C. 1.0% D. 1.2%
68. (A) Accurate delivery of volatile anesthetic concentration is dependent on filling the agent-specific vaporizer with the appropriate (volatile) agent. Differences in anesthetic potencies further necessitate this requirement. Each agent-specific vaporizer uses a splitting ratio that determines the portion of the fresh gas that is directed through the vaporizing chamber versus that which travels through the bypass chamber. VAPOR PRESSURE, ANESTHETIC VAPOR PRESSURE, AND SPLITTING RATIO Halothane Sevoflurane Isoflurane Enflurane Vapor pressure at 20° C 243 mm Hg 160 mm Hg 240 mm Hg 172 mm Hg VP/(BP−VP) 0.47 0.27 0.47 0.29 Splitting ratio for 1% vapor 1:47 1:27 1:47 1:29 BP, blood pressure; VP, vapor pressure. Anesthesia Equipment and Physics 25 The table shows the calculation (fraction) that when multiplied by the quantity of fresh gas traversing the vaporizing chamber (affluent fresh gas in mL/min) will yield the output (mL/min) of anesthetic vapor in the effluent gas. When this fraction is multiplied by 100, it equals the splitting ratio for 1% for the given volatile agent. For example, when the isoflurane vaporizer is set to deliver 1% isoflurane, one part of fresh gas is passed through the vaporizing chamber while 47 parts travel through the bypass chamber. One can determine on inspection that when a less soluble volatile agent like sevoflurane (or the obsolete volatile agent enflurane, for the sake of example) is placed into an isoflurane (or halothane) vaporizer, the output in volume percent will be less than expected; how much less can be determined by simply comparing their splitting ratios 27/47 or 0.6. Halothane and enflurane are no longer used in the United States, but old halothane and enflurane vaporizers can be (and are) used elsewhere in the world to accurately deliver isoflurane and sevoflurane, respectively (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 72–73).
69. How long would a vaporizer (filled with 150 mL volatile) deliver 2% isoflurane if total flow is set at 4.0 L/min? A. 2 hours B. 4 hours C. 6 hours D. 8 hours
69. (C) Two percent of 4 L/min will be 80 mL of isoflurane per minute. VAPOR PRESSURE PER MILLILITER OF LIQUID Halothane Enflurane Isoflurane Sevoflurane Desflurane mL vapor per mL liquid at 20° C 226 196 195 182 207 Given that 1 mL of isoflurane liquid yields 195 mL of anesthetic vapor and by applying the calculation (195 mL vapor/1 mL liquid isoflurane) × (150 mL isoflurane liquid) = 29,250 mL isoflurane vapor, it follows that (29,250 mL ÷ 80 mL/min = 365 minutes). Three hundred sixty-five minutes is around 6 hours (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 65–70).
70. Raising the frequency of an ultrasound transducer used for line placement or regional anesthesia (e.g., from 3 MHz to 10 MHz) will result in A. Higher penetration of tissue with lower resolution B. Higher penetration of tissue with higher resolution C. Lower penetration of tissue with higher resolution D. Higher resolution with no change in tissue penetration
70. (C) The human ear can perceive sound in the range of 20 Hz to 20 kHz. Frequencies above 20 kHz, inaudible to humans, are ultrasonic frequencies (ultra = Latin for “beyond” or “on the far side of”). In regional anesthesia, ultrasound is used for imaging in the frequency range of 2.5 to 10 MHz. Wavelength is inversely proportional to frequency (i.e., λ = C/f [λ = wavelength, C = velocity of sound through tissue or 1540 m/sec, f = frequency]). Wavelength in millimeters can be calculated by dividing 1.54 by the Doppler frequency in megahertz. Penetration into tissue is 200 to 400 times wavelength, and resolution is twice the wavelength. Therefore, a frequency of 3 MHz (wavelength 0.51 mm) would have a resolution of 1 mm and a penetration of up to 100 to 200 mm (10-20 cm), whereas 10 MHz (wavelength 0.15 mm) corresponds to a resolution of 0.3 mm but a penetration depth of no more than 60 to 120 mm (6-12 cm) (Miller: Miller’s Anesthesia, ed 8, pp 1398–1405; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 979).
71. The fundamental difference between microshock and macroshock is related to A. Location of shock B. Duration C. Voltage D. Lethality
71. (A) Microshock refers to electric shock located in or near the heart. A current as low as 100 μA passing through the heart can produce ventricular fibrillation. Pacemaker electrodes, central venous catheters, pulmonary artery catheters, and other devices in the heart are necessary prerequisites for microshock. Because the line isolation monitor has a threshold of 2 mA (2000 μA) for alarming, it will not protect against microshock (Miller: Miller’s Anesthesia, ed 8, p 3226).
72. Intraoperative awareness under general anesthesia can be eliminated by closely monitoring A. Electroencephalogram B. BP/heart rate C. Bispectral index (BIS) D. None of the above
72. (D) Intraoperative awareness or recall during general anesthesia is rare (overall incidence is 0.2%, for obstetrics 0.4%, for cardiac 1%-1.5%) except for major trauma, which has a reported incidence as high as 43%. With the electroencephalogram, trends can be identified with changes in the depth of anesthesia; however, the sensitivity and specificity of the available trends are such that none serve as a sole indicator of anesthesia depth. Although using the bispectral index monitor may reduce the risk of recall, it, like the other listed signs as well as patient movement, does not totally eliminate recall (Miller: Miller’s Anesthesia, ed 8, pp 1527–1528).
73. A mechanically ventilated patient is transported from the OR to the ICU using a portable ventilator that consumes 2 L/min of oxygen to run the mechanically controlled valves and drive the ventilator. The transport cart is equipped with an “E” cylinder with a gauge pressure of 2000 psi. The patient receives a VT of 500 mL at a rate of 10 breaths/min. If the ventilator requires 200 psi to operate, how long could the patient be mechanically ventilated? A. 20 minutes B. 40 minutes C. 60 minutes D. 80 minutes
73. (D) The minute ventilation is 5 L (0.5 L per breath at 10 breaths/min) and 2 L/min to drive the ventilator for a total O2 consumption of 7 L/min. A full oxygen “E” cylinder contains 625 L. Ninety percent of the volume of the cylinder (≈560 L) can be delivered before the ventilator can no longer be driven. At a rate of 7 L/min, this supply would last about 80 minutes (Miller: Basics of Anesthesia, ed 6, pp 201, 209; Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 29–33, 37; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 10–11). 26 Part 1 Basic Sciences
74. A 135-kg man is ventilated at a rate of 14 breaths/min with a VT of 600 mL and positive end-expiratory pressure (PEEP) of 5 cm H2O during a laparoscopic banding procedure. Peak airway pressure is 50 cm H2O, and the patient is fully relaxed with a nondepolarizing neuromuscular blocking agent. How can peak airway pressure be reduced without a loss of alveolar ventilation? A. Increase the inspiratory flow rate B. Take off PEEP C. Reduce the I:E ratio (e.g., change from 1:3 to 1:2) D. Decrease VT to 300 and increase rate to 28
74. (C) After eliminating reversible causes of high peak airway pressures (e.g., occlusion of the endotracheal tube, mainstem intubation, or bronchospasm), adjusting the ventilator can reduce the peak airway pressure. Increasing the inspiratory flow rate would cause the airway pressures to go up faster and would produce higher peak airway pressures. Removing PEEP would lower peak pressure at the expense of alveolar ventilation. Changing the I:E ratio from 1:3 to 1:2 will permit 8% (25% inspiratory time to 33% inspiratory time) more time for the VT to be administered and will result in lower airway pressures. Decreasing the VT to 300 and increasing the rate to 28 would give the same minute ventilation but not the same alveolar ventilation. Recall that alveolar ventilation equals (frequency) times (VT minus dead space), and because dead space is the same (about 2 mL/kg ideal weight), alveolar ventilation would be reduced, in this case to a dangerously low level. Another option is to change from volume-cycled to pressure-cycled ventilation, which produces a more constant pressure over time instead of the peaked pressures seen with fixed VT ventilation (Barash: Clinical Anesthesia, ed 7, pp 1593–1596; Miller: Miller’s Anesthesia, ed 8, pp 3064–3074).
75. The pressure and volume per minute delivered from the central hospital oxygen supply are A. 2100 psi and 650 L/min B. 1600 psi and 100 L/min C. 75 psi and 100 L/min D. 50 psi and 50 L/min
75. (D) The central hospital oxygen supply to the ORs is designed to give enough pressure and oxygen flow to run the three oxygen components of the anesthesia machine (patient fresh gas flow, anesthesia ventilator, and oxygen flush valve). The oxygen flowmeter on the anesthesia machine is designed to run at an oxygen pressure of 50 psi, and for emergency purposes the oxygen flush valve delivers oxygen at 35 to 75 L/min (Miller: Basics of Anesthesia, ed 6, pp 199–201).
76. During normal laminar airflow, resistance is dependent on which characteristic of oxygen? A. Density B. Viscosity C. Molecular weight D. Temperature
76. (B) Within the respiratory system, both laminar and turbulent flows exist. At low flow rates, the respiratory flow tends to be laminar, like a series of concentric tubes that slide over one another with the center tubes flowing faster than the more peripheral tubes. Laminar flow is usually inaudible and is dependent on gas viscosity. Turbulent flow tends to be faster, is audible, and is dependent on gas density. Gas density can be decreased by using a mixture of helium with oxygen (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 54–56).
77. If the oxygen cylinder were being used as the source of oxygen at a remote anesthetizing location and the oxygen flush valve on an anesthesia machine were pressed and held down, as during an emergency situation, each of the items below would be bypassed during 100% oxygen delivery EXCEPT A. O2 flowmeter B. First-stage regulator C. Vaporizer check valve D. Vaporizers 8 Part 1 Basic Sciences
77. (B) Anesthesia workstations have high-pressure, intermediate-pressure, and low-pressure circuits (see figure in the explanation for Question 12). The high-pressure circuit is from the oxygen cylinder to the oxygen pressure regulator (first-stage regulator), which takes the oxygen pressure from a high of 2200 psi to 45 psi. The intermediate-pressure circuit consists of the pipeline pressure of about 50 to 55 psi and goes to the second-stage regulator, which then lowers the pressure to 14 to 26 psi (depending on the machine). The low-pressure circuit then consists of the flow tubes, vaporizer manifold, vaporizers, and vaporizer check valve to the common gas outlet. The oxygen flush valve is in the intermediate-pressure circuit and bypasses the low-pressure circuit (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 34–36; Miller: Basics of Anesthesia, ed 6, p 200).
78. After induction and intubation with confirmation of tracheal placement, the O2 saturation begins to fall. The O2 analyzer shows 4% inspired oxygen. The oxygen line pressure is 65 psi. The O2 tank on the back of the anesthesia machine has a pressure of 2100 psi and is turned on. The oxygen saturation continues to fall. The next step should be to A. Exchange the tank B. Replace pulse oximeter probe C. Disconnect O2 line from hospital source D. Extubate and start mask ventilation
78. (C) Two major problems should be noted in this case. The first obvious problem is the inspired oxygen concentration of 4%, a concentration that is not possible if the gases going to the machine are appropriate unless the oxygen analyzer is faulty. Given the dire consequences of a hypoxic gas mixture, one must assume the oxygen analyzer is correct and work on the premise that the O2 pipeline is supplying a gas other than oxygen. Second, the oxygen line pressure is 65 psi. The pipeline pressures are normally around 50 to 55 psi, whereas the pressure from the oxygen cylinder, if the cylinder is turned on, is reduced to 45 psi. For the oxygen tank to deliver oxygen to the patient, the pipeline pressure needs to be less than 45 psi, which in this case will occur only when the pipeline is disconnected. Although we rarely think of problems with hospital gas lines, a survey of more than 200 hospitals showed about 33% had problems with the pipelines. The most common pipeline problems were low pressure, followed by high pressure and, very rarely, crossed gas lines (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 34; Miller: Miller’s Anesthesia, ed 8, p 756).
79. The correct location for placement of the V5 lead is A. Midclavicular line, third intercostal space B. Anterior axillary line, fourth intercostal space C. Midclavicular line, fifth intercostal space D. Anterior axillary line, fifth intercostal space
79. (D) There are many ways to monitor the electric activity of the heart. The five-electrode system using one lead for each limb and the fifth lead for the precordium is commonly used in the OR. The precordial lead placed in the V5 position (anterior axillary line in the fifth intercostal space) gives the V5 tracing, which, combined with the standard lead II, are the most common tracings used to look for myocardial ischemia (Miller: Miller’s Anesthesia, ed 8, pp 1429–1434).
80. The diameter index safety system refers to the interface between A. Pipeline source and anesthesia machine B. Gas cylinders and anesthesia machine C. Vaporizers and refilling connectors attached to bottles of volatile anesthetics D. Both pipeline and gas cylinders interface with anesthesia machine
80. (A) See also Question 36. The diameter index safety system provides threaded, noninterchangeable connections for medical gas pipelines through the hospital as well as to the anesthesia machine. The pin index safety system has two metal pins in different arrangements around the yoke on the back of anesthesia machines, Anesthesia Equipment and Physics 27 with each arrangement for a specific gas cylinder. Vaporizers often have keyed fillers that attach to the bottle of anesthetic and the vaporizer. Vaporizers not equipped with keyed fillers occasionally have been misfilled with the wrong anesthetic liquid (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 49–50).
81. Each of the following is cited as an advantage of calcium hydroxide lime (Amsorb Plus, Drägersorb) over soda lime EXCEPT A. Compound A is not formed B. CO is not formed C. More absorptive capacity per 100 g of granules D. It does not contain NaOH or KOH
81. (C) Calcium hydroxide lime does not contain the monovalent hydroxide bases that are present in soda lime (namely, NaOH and KOH). Sevoflurane in the presence of NaOH or KOH is degraded to trace amounts of compound A, which is nephrotoxic to rats at high concentrations. Soda lime normally contains about 13% to 15% water, but if the soda lime is desiccated (water content <5%—which has occurred if the machine is not used for a while and the fresh gas flow is left on) and is exposed to current volatile anesthetics (isoflurane, sevoflurane, and especially desflurane), CO can be produced. Neither compound A nor CO is formed when calcium hydroxide lime is used. With soda lime and calcium hydroxide lime, the indicator dye changes from white to purple as the granules become exhausted. The two major disadvantages of calcium hydroxide lime are the expense and the fact that its absorptive capacity is about half that of soda lime (10.2 L of CO2/100 g of calcium hydroxide lime versus 26 L of CO2/100 g of soda lime) (Miller: Miller’s Anesthesia, ed 8, pp 787–789; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 36–38; Miller: Basics of Anesthesia, ed 6, pp 212–214).
82. 160 80 0 1 second ART 166/56 (82) NIBP 126/63 (84) The arrows in the figure above indicate A. Respiratory variation B. An underdamped signal C. An overdamped signal D. Atrial fibrillation
82. (B) The aim of direct invasive monitoring is to give continuous arterial BPs that are similar to the intermittent noninvasive arterial BPs from a cuff, as well as to give a port for arterial blood samples. The displayed signal reflects the actual pressure and the distortions from the measuring system (i.e., the catheter, tubing, stopcocks, and amplifier). Although the signal is usually accurate, at times we see an underdamped or an overdamped signal. In an underdamped signal, as in this case, exaggerated readings are noted (widened pulse pressure). In an overdamped signal, readings are diminished (narrowed pulse pressure). However, the mean BP tends to be accurate in both underdamped and overdamped signals (Miller: Miller’s Anesthesia, ed 8, pp 1347–1359).
83. During a laparoscopic cholecystectomy, exhaled CO2 is 6%, but inhaled CO2 is 1%. Which explanation could NOT account for rebreathing CO2? A. Channeling through soda lime B. Faulty expiratory valve C. Exhausted soda lime D. Absorption of CO2 through peritoneum
83. (D) Rebreathing of expired gases (e.g., stuck open expiratory or inspiratory valves), faulty removal of CO2 from the CO2 absorber (e.g., exhausted CO2 absorber, channeling through a CO2 absorber, or having the CO2 absorber bypassed—an option in some older anesthetic machines), or addition of CO2 from a gas supply (rarely done with current anesthetic machines) can all increase inspired CO2. The absorption of CO2 during laparoscopic surgery when CO2 is used as the abdominal distending gas will increase absorption of CO2 but will not cause an increase in inspired CO2 (Miller: Miller’s Anesthesia, ed 8, pp 1551–1559; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 42).
84. Helium A. Black B. Brown C. Blue D. Gray
84. (B) Medical gas cylinders are color coded, but the colors may differ from one country to another. In the United States, if there is a combination of two gases, the tank would have both corresponding colors; for example, a tank containing oxygen and helium would be green and brown. The only exception to the mixed gas color scheme is O2 and N2 in the proportion of 19.5% to 23.5% O2 mixed with N2, which is solid yellow (air) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 7). GAS COLOR CODES Gas United States International Air Yellow White and black CO2 Gray Gray Helium Brown Brown Nitrogen Black Black N2O Blue Blue Oxygen Green White Data from Ehrenwerth J, Eisenkraft JB, Berry JM: Anesthesia Equipment: Principles and Applications, ed 2, Philadelphia, Saunders, 2013. 28 Part 1 Basic Sciences
85. Nitrogen A. Black B. Brown C. Blue D. Gray
85. (A) Medical gas cylinders are color coded, but the colors may differ from one country to another. In the United States, if there is a combination of two gases, the tank would have both corresponding colors; for example, a tank containing oxygen and helium would be green and brown. The only exception to the mixed gas color scheme is O2 and N2 in the proportion of 19.5% to 23.5% O2 mixed with N2, which is solid yellow (air) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 7). GAS COLOR CODES Gas United States International Air Yellow White and black CO2 Gray Gray Helium Brown Brown Nitrogen Black Black N2O Blue Blue Oxygen Green White Data from Ehrenwerth J, Eisenkraft JB, Berry JM: Anesthesia Equipment: Principles and Applications, ed 2, Philadelphia, Saunders, 2013. 28 Part 1 Basic Sciences
86. CO2 A. Black B. Brown C. Blue D. Gray
86. (D) Medical gas cylinders are color coded, but the colors may differ from one country to another. In the United States, if there is a combination of two gases, the tank would have both corresponding colors; for example, a tank containing oxygen and helium would be green and brown. The only exception to the mixed gas color scheme is O2 and N2 in the proportion of 19.5% to 23.5% O2 mixed with N2, which is solid yellow (air) (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, p 7). GAS COLOR CODES Gas United States International Air Yellow White and black CO2 Gray Gray Helium Brown Brown Nitrogen Black Black N2O Blue Blue Oxygen Green White Data from Ehrenwerth J, Eisenkraft JB, Berry JM: Anesthesia Equipment: Principles and Applications, ed 2, Philadelphia, Saunders, 2013. 28 Part 1 Basic Sciences
87. Best for spontaneous ventilation. Match the figures below with the correct numbered statement. Each lettered figure may be selected once, more than once, or not at all. A B C D E F FGF FGF FGF FGF FGF FGF
87. (A) There are six different types of Mapleson breathing circuits (designated A through F). These circuits vary in arrangement of the fresh-gas-flow inlet, tubing, mask, reservoir bag, and unidirectional expiratory valve. These systems are lightweight, portable, and easy to clean; they offer low resistance to breathing, and, because of high fresh gas inflows, they prevent rebreathing of exhaled gases. In addition, with these breathing circuits, the concentration of volatile anesthetic gases and O2 delivered to the patient can be accurately estimated. The reservoir bag enables the anesthesia provider to provide assisted or controlled ventilation of the lungs. The unidirectional expiratory valve functions to direct fresh gas into the patient and exhaled gases out of the circuit. In the Mapleson A breathing circuit, the unidirectional expiratory valve is near the patient, and the fresh-gas-flow inlet is proximal to the reservoir bag. This arrangement is the most efficient for elimination of CO2 during spontaneous breathing. However, because the unidirectional expiratory valve must be tightened to permit production of positive airway pressure when the gas reservoir bag is manually compressed, this breathing circuit is less efficient in preventing rebreathing of CO2 during assisted or controlled ventilation of the lungs. The structure of the Mapleson D breathing circuit is similar to that of the Mapleson A breathing circuit except that the positions of the fresh-gasflow inlet and the unidirectional expiratory valve are reversed. The placement of the fresh-gas-flow inlet near the patient produces efficient elimination of CO2, regardless of whether the patient is breathing spontaneously or with controlled ventilation. The Bain anesthesia breathing circuit is a coaxial version of the Mapleson D breathing circuit except that the fresh gas enters through a narrow tube within the corrugated expiratory limb of the circuit. The Jackson-Rees breathing circuit is a modification of the Mapleson E breathing circuit and is called a Mapleson F breathing circuit. In the Jackson-Rees breathing circuit, the adjustable unidirectional expiratory valve is incorporated into the reservoir bag, and the fresh-gas-flow inlet is close to the patient. This arrangement offers the advantage of ease of instituting assisted or controlled ventilation of the lungs, as well as monitoring ventilation by movement of the reservoir bag during spontaneous breathing (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 109–117; Miller: Miller’s Anesthesia, ed 8, pp 780–781). 29
88. Best for controlled ventilation. Match the figures below with the correct numbered statement. Each lettered figure may be selected once, more than once, or not at all. A B C D E F FGF FGF FGF FGF FGF FGF
88. (D) There are six different types of Mapleson breathing circuits (designated A through F). These circuits vary in arrangement of the fresh-gas-flow inlet, tubing, mask, reservoir bag, and unidirectional expiratory valve. These systems are lightweight, portable, and easy to clean; they offer low resistance to breathing, and, because of high fresh gas inflows, they prevent rebreathing of exhaled gases. In addition, with these breathing circuits, the concentration of volatile anesthetic gases and O2 delivered to the patient can be accurately estimated. The reservoir bag enables the anesthesia provider to provide assisted or controlled ventilation of the lungs. The unidirectional expiratory valve functions to direct fresh gas into the patient and exhaled gases out of the circuit. In the Mapleson A breathing circuit, the unidirectional expiratory valve is near the patient, and the fresh-gas-flow inlet is proximal to the reservoir bag. This arrangement is the most efficient for elimination of CO2 during spontaneous breathing. However, because the unidirectional expiratory valve must be tightened to permit production of positive airway pressure when the gas reservoir bag is manually compressed, this breathing circuit is less efficient in preventing rebreathing of CO2 during assisted or controlled ventilation of the lungs. The structure of the Mapleson D breathing circuit is similar to that of the Mapleson A breathing circuit except that the positions of the fresh-gasflow inlet and the unidirectional expiratory valve are reversed. The placement of the fresh-gas-flow inlet near the patient produces efficient elimination of CO2, regardless of whether the patient is breathing spontaneously or with controlled ventilation. The Bain anesthesia breathing circuit is a coaxial version of the Mapleson D breathing circuit except that the fresh gas enters through a narrow tube within the corrugated expiratory limb of the circuit. The Jackson-Rees breathing circuit is a modification of the Mapleson E breathing circuit and is called a Mapleson F breathing circuit. In the Jackson-Rees breathing circuit, the adjustable unidirectional expiratory valve is incorporated into the reservoir bag, and the fresh-gas-flow inlet is close to the patient. This arrangement offers the advantage of ease of instituting assisted or controlled ventilation of the lungs, as well as monitoring ventilation by movement of the reservoir bag during spontaneous breathing (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 109–117; Miller: Miller’s Anesthesia, ed 8, pp 780–781). 29
89. Bain system is modification of. Match the figures below with the correct numbered statement. Each lettered figure may be selected once, more than once, or not at all. A B C D E F FGF FGF FGF FGF FGF FGF
89. (D) There are six different types of Mapleson breathing circuits (designated A through F). These circuits vary in arrangement of the fresh-gas-flow inlet, tubing, mask, reservoir bag, and unidirectional expiratory valve. These systems are lightweight, portable, and easy to clean; they offer low resistance to breathing, and, because of high fresh gas inflows, they prevent rebreathing of exhaled gases. In addition, with these breathing circuits, the concentration of volatile anesthetic gases and O2 delivered to the patient can be accurately estimated. The reservoir bag enables the anesthesia provider to provide assisted or controlled ventilation of the lungs. The unidirectional expiratory valve functions to direct fresh gas into the patient and exhaled gases out of the circuit. In the Mapleson A breathing circuit, the unidirectional expiratory valve is near the patient, and the fresh-gas-flow inlet is proximal to the reservoir bag. This arrangement is the most efficient for elimination of CO2 during spontaneous breathing. However, because the unidirectional expiratory valve must be tightened to permit production of positive airway pressure when the gas reservoir bag is manually compressed, this breathing circuit is less efficient in preventing rebreathing of CO2 during assisted or controlled ventilation of the lungs. The structure of the Mapleson D breathing circuit is similar to that of the Mapleson A breathing circuit except that the positions of the fresh-gasflow inlet and the unidirectional expiratory valve are reversed. The placement of the fresh-gas-flow inlet near the patient produces efficient elimination of CO2, regardless of whether the patient is breathing spontaneously or with controlled ventilation. The Bain anesthesia breathing circuit is a coaxial version of the Mapleson D breathing circuit except that the fresh gas enters through a narrow tube within the corrugated expiratory limb of the circuit. The Jackson-Rees breathing circuit is a modification of the Mapleson E breathing circuit and is called a Mapleson F breathing circuit. In the Jackson-Rees breathing circuit, the adjustable unidirectional expiratory valve is incorporated into the reservoir bag, and the fresh-gas-flow inlet is close to the patient. This arrangement offers the advantage of ease of instituting assisted or controlled ventilation of the lungs, as well as monitoring ventilation by movement of the reservoir bag during spontaneous breathing (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 109–117; Miller: Miller’s Anesthesia, ed 8, pp 780–781). 29
90. Jackson-Rees system. Match the figures below with the correct numbered statement. Each lettered figure may be selected once, more than once, or not at all. A B C D E F FGF FGF FGF FGF FGF FGF
90. (F) There are six different types of Mapleson breathing circuits (designated A through F). These circuits vary in arrangement of the fresh-gas-flow inlet, tubing, mask, reservoir bag, and unidirectional expiratory valve. These systems are lightweight, portable, and easy to clean; they offer low resistance to breathing, and, because of high fresh gas inflows, they prevent rebreathing of exhaled gases. In addition, with these breathing circuits, the concentration of volatile anesthetic gases and O2 delivered to the patient can be accurately estimated. The reservoir bag enables the anesthesia provider to provide assisted or controlled ventilation of the lungs. The unidirectional expiratory valve functions to direct fresh gas into the patient and exhaled gases out of the circuit. In the Mapleson A breathing circuit, the unidirectional expiratory valve is near the patient, and the fresh-gas-flow inlet is proximal to the reservoir bag. This arrangement is the most efficient for elimination of CO2 during spontaneous breathing. However, because the unidirectional expiratory valve must be tightened to permit production of positive airway pressure when the gas reservoir bag is manually compressed, this breathing circuit is less efficient in preventing rebreathing of CO2 during assisted or controlled ventilation of the lungs. The structure of the Mapleson D breathing circuit is similar to that of the Mapleson A breathing circuit except that the positions of the fresh-gasflow inlet and the unidirectional expiratory valve are reversed. The placement of the fresh-gas-flow inlet near the patient produces efficient elimination of CO2, regardless of whether the patient is breathing spontaneously or with controlled ventilation. The Bain anesthesia breathing circuit is a coaxial version of the Mapleson D breathing circuit except that the fresh gas enters through a narrow tube within the corrugated expiratory limb of the circuit. The Jackson-Rees breathing circuit is a modification of the Mapleson E breathing circuit and is called a Mapleson F breathing circuit. In the Jackson-Rees breathing circuit, the adjustable unidirectional expiratory valve is incorporated into the reservoir bag, and the fresh-gas-flow inlet is close to the patient. This arrangement offers the advantage of ease of instituting assisted or controlled ventilation of the lungs, as well as monitoring ventilation by movement of the reservoir bag during spontaneous breathing (Ehrenwerth: Anesthesia Equipment: Principles and Applications, ed 2, pp 109–117; Miller: Miller’s Anesthesia, ed 8, pp 780–781). 29
91. A 29-year-old man is admitted to the intensive care unit (ICU) after a drug overdose. The patient is placed on a ventilator with a set tidal volume (Vt) of 750 mL at a rate of 10 breaths/min. The patient is making no inspiratory effort. The measured minute ventilation is 6 L and the peak airway pressure is 30 cm H2O. What is the compression factor for this ventilator delivery circuit? A. 2 mL/(cm H2O) B. 3 mL/(cm H2O) C. 4 mL/(cm H2O) D. 5 mL/(cm H2O)
91. (D) A volume-cycled ventilator set to deliver a volume of 750 mL at a rate of 10/min would deliver a minute ventilation of 7.5 L. The measured minute ventilation, however, is only 6 L; therefore, 1.5 L must be absorbed by the breathing circuit. This volume is known as the compression volume. If one divides the volume by 10 (number of breaths/min), then one determines the compression volume/breath. This number (mL) can be further divided by the peak inflation pressure (cm H2O) to determine the actual compression factor, which in this case is 5 mL/(cm H2O) (Miller: Basics of Anesthesia, ed 6, p 208; Ehrenwerth: Anesthesia Equipment Principles and Applications, p 364). Compression volume = (V V )/ Respiratory rate Peak airway pressure (cm H O) delivered measured 2 ˙ − ˙ = 5 mL/(cm H2O)
92. A 62-year-old man is brought to the ICU after elective repair of an abdominal aortic aneurysm. His vital signs are stable, but he requires a sodium nitroprusside infusion at a rate of 10 μg/kg/min to keep the systolic blood pressure below 110 mm Hg. The Sao2 is 98% with controlled ventilation at 12 breaths/min and an Fio2 of 0.60. After 3 days, his Sao2 decreases to 85% on the pulse oximeter. Chest x-ray film and results of physical examination are unchanged. Which of the following would most likely account for this desaturation? A. Cyanide toxicity B. Thiocyanate toxicity C. Methemoglobinemia D. Thiosulfate toxicity
92. (C) The metabolism of nitroprusside in the body requires the conversion of oxyhemoglobin (Fe++) to methemoglobin (Fe+++). The presence of sufficient quantities of methemoglobin in the blood will cause the pulse oximeter to read 85% saturation regardless of the true arterial saturation. Cyanide toxicity is also a possibility in any patient who is receiving nitroprusside. Cyanide toxicity should be suspected when the patient develops metabolic acidosis or becomes resistant to the hypotensive effects of this drug despite a sufficient infusion rate. This can be confirmed by measuring the mixed venous Pao2, which would be elevated in the presence of cyanide toxicity. Thiocyanate toxicity is also a potential hazard of nitroprusside administration in patients with renal failure. Patients suffering from thiocyanate toxicity display nausea, mental confusion, and skeletal-muscle weakness (Miller: Miller’s Anesthesia, ed 8, pp 1545, 2228; Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 782–783).
93. Maximizing which of the following lung parameters is the most important factor in prevention of postoperative pulmonary complications? A. Tidal volume (Vt) B. Inspiratory reserve volume C. Vital capacity D. Functional residual capacity (FRC)
93. (D) (Please see diagram and table for explanation with Question 102.) FRC is composed of expiratory reserve volume plus residual volume. It is essential to maximize FRC in the postoperative period to ensure that it will be greater than closing volume. Closing volume is that lung volume at which small-airway closure begins to occur. Maximizing FRC, therefore, reduces atelectasis and lessens the incidence of arterial hypoxemia and pneumonia. Maneuvers aimed at increasing FRC include early ambulation, incentive spirometry, deep breathing, and intermittent positive-pressure breathing (Barash: Clinical Anesthesia, ed 7, p 279).
94. An 83-year-old woman is admitted to the ICU after coronary artery surgery. A pulmonary artery catheter is in place and yields the following data: central venous pressure (CVP) 5 mm Hg, cardiac output (CO) 4.0 L/min, mean arterial pressure (MAP) 90 mm Hg, mean pulmonary artery pressure (PAP) 20 mm Hg, pulmonary artery occlusion pressure (PAOP) 12 mm Hg, and heart rate 90. Calculate this patient’s pulmonary vascular resistance (PVR). A. 40 dyne-sec/cm5 B. 80 dyne-sec/cm5 C. 160 dyne-sec/cm5 D. 200 dyne-sec/cm5
94. (C) PVR = (PAP PAOP) CO mean� � 80 where PVR is the pulmonary vascular resistance, PAPmean is the mean pulmonary artery pressure, PAOP is the mean pulmonary capillary occlusion pressure, and CO is the cardiac output. PVR = (20� ) � 80 = 160 dyne-sec/cm5 12 4 The normal range for PVR is 50 to 150 dyne-sec/cm5 (Miller: Miller’s Anesthesia, ed 8, pp 1460–1461).
95. A 72-year-old man with a history of myocardial infarction 12 months earlier is scheduled to undergo elective repair of a 6-cm abdominal aortic aneurysm under general anesthesia. When would this patient be at highest risk for another myocardial infarction? A. During placement of the aortic cross-clamp B. Upon release of the aortic cross-clamp C. 24 hours postoperatively D. On the third postoperative day
95. (D) For reasons that are not fully understood, patients who have sustained a myocardial infarction and subsequently undergo surgery are most likely to have another infarction on the third postoperative day (Miller: Respiratory Physiology and Critical Care Medicine 37
96. Calculate the body mass index (BMI) of a man 200 cm (6 feet 6 inches) tall who weighs 100 kg (220 lb). A. 20 B. 25 C. 30 D. 35
96. (B) Calculation of BMI for adults (>20 years of age) can help identify patients who are underweight (BMI <18.5), normal weight (BMI 18.5-24.9), overweight (BMI 25-29.9), class 1 obesity (BMI 30-34.9), class 2 obesity (BMI 35-39.9), class 3 obesity (BMI 40-49.9), and the superobese (BMI >50). BMI = mass (kg) (Height)2 (meters ) BMI = 100 25 (2)2 = All major organ systems are affected as a consequence of obesity. The greatest concerns for the anesthesiologist are, however, related to the heart and lungs. Cardiac output must increase about 0.1 L/min for each extra kilogram of adipose tissue. As a consequence, obese patients frequently are hypertensive, and many ultimately develop cardiomegaly and left-sided heart failure. FRC is reduced in obese patients, and management of the airway often can be difficult (Miller: Miller’s Anesthesia, ed 8, pp 2200–2201).
97. The normal FEV1/FVC ratio is A. 0.95 B. 0.80 C. 0.60 D. 0.50
97. (B) The forced expiratory volume in 1 second (FEV1) is the total volume of air that can be exhaled in the first second. Normal healthy adults can exhale approximately 75% to 85% of their forced vital capacity (FVC) in the first second, 94% in 2 seconds, and 97% in 3 seconds. Therefore, the normal FEV1/FVC ratio is 0.75 or higher. In the presence of obstructive airway disease, the FEV1/FVC ratio less than 70% reflects mild obstruction, less than 60% moderate obstruction, and less than 50% severe obstruction. This ratio can be used to determine the severity of obstructive airway disease and to monitor the efficacy of bronchodilator therapy (Barash: Clinical Anesthesia, ed 7, p 279).
98. Direct current (DC) cardioversion is not useful and, therefore, NOT indicated in an unstable patient with which of the following? A. Supraventricular tachycardia in a patient with Wolff-Parkinson-White syndrome B. Atrial flutter C. Multifocal atrial tachycardia (MAT) D. New-onset atrial fibrillation
98. (C) MAT is a non-reentrant, ectopic atrial rhythm often seen in patients with chronic obstructive pulmonary disease (COPD). It is frequently confused with atrial fibrillation but, in contrast to atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia, DC cardioversion is ineffective in converting it to normal sinus rhythm. Ectopic atrial tachydysrhythmias are not amenable to cardioversion because they lack the re-entrant mechanism, which is necessary for successful termination with electrical counter shock (Miller: Miller’s Anesthesia, ed 8, pp 3191–3193).
99. During the first minute of apnea, the Paco2 will rise A. 2 mm Hg/min B. 4 mm Hg/min C. 6 mm Hg/min D. 8 mm Hg/min
99. (C) During apnea, the Paco2 will increase approximately 6 mm Hg during the first minute and then 3 to 4 mm Hg each minute thereafter (Miller: Basics of Anesthesia, ed 6, p 61).
100. Potential complications associated with total parenteral nutrition (TPN) include all of the following EXCEPT A. Ketoacidosis B. Hyperglycemia C. Hypoglycemia D. Hypophosphatemia
100. (A) TPN therapy is associated with numerous potential complications. Blood sugars need to be carefully monitored because hyperglycemia may develop due to the high glucose load and require treatment with insulin, and hypoglycemia may develop if TPN is abruptly stopped (i.e., infusion turned off or mechanical obstruction in the IV tubing). Other complications include electrolyte disturbances (e.g., hypokalemia, hypophosphatemia, hypomagnesemia, hypocalcemia), volume overload, catheter-related sepsis, renal and hepatic dysfunction, thrombosis of the central veins, and nonketotic hyperosmolar coma. Increased work of breathing is related to increased production of CO2 most frequently due to overfeeding. Acidosis in these patients is hyperchloremic metabolic acidosis resulting from formation of HCl during metabolism of amino acids. Ketoacidosis is not associated with TPN therapy (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 331).
101. O2 requirement for a 70-kg adult is A. 150 mL/min B. 250 mL/min C. 350 mL/min D. 450 mL/min
101. (B) The O2 requirement for an adult is 3 to 4 mL/kg/min. The O2 requirement for a newborn is 7 to 9 mL/ kg/min. Alveolar ventilation (Va) in neonates is double that of adults to help meet their increased O2 requirements. This increase in Va is achieved primarily by an increase in respiratory rate as Vt is similar to that of adults (i.e., 7 mL/kg). Although CO2 production also is increased in neonates, the elevated Va maintains the Paco2 near 38 to 40 mm Hg (Barash: Clinical Anesthesia, ed 7, pp 1181–1182).
102. The FRC is composed of the A. Expiratory reserve volume and residual volume B. Inspiratory reserve volume and residual volume C. Inspiratory capacity and vital capacity D. Expiratory capacity and Vt
102. (A) A comprehensive understanding of respiratory physiology is important for understanding the effects of both regional and general anesthesia on respiratory mechanics and pulmonary gas exchange. The volume of gas remaining in the lungs after a normal expiration is called the functional residual capacity. The volume of gas remaining in the lungs after a maximal expiration is called the residual volume. The difference between these two volumes is called the expiratory reserve volume. Therefore, the FRC is composed of the expiratory reserve volume and residual volume (Barash: Clinical Anesthesia, ed 7, pp 278–279; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 776–777). 38 Part 1 Basic Sciences LUNG VOLUMES AND CAPACITIES Measurement Abbreviation Normal Adult Value Tidal volume Vt 500 mL (6-8 mL/kg) Inspiratory reserve volume IRV 3000 mL Expiratory reserve volume ERV 1200 mL Residual volume RV 1200 mL Inspiratory capacity IC 3500 mL Functional residual capacity FRC 2400 mL Vital capacity VC 4500 mL (60-70 mL/kg) Forced exhaled volume in 1 sec FEV1 80% Total lung capacity TLC 5900 mL 1200 2400 3600 4800 6000 0 Lung volume (mL) RV ERV VT IRV IC FRC VC TLC
103. Which of the following statements correctly defines the relationship between minute ventilation ( ˙V E ), dead space ventilation ( ˙V D), and Paco2? A. If ˙V E is constant and ˙V D increases, then Paco2 will increase B. If ˙V E is constant and ˙V D increases, then Paco2 will decrease C. If ˙V D is constant and ˙V E increases, then Paco2 will increase D. If ˙V D is constant and ˙V E decreases, then Paco2 will decrease
103. (A) The volume of gas in the conducting airways of the lungs (and not available for gas exchange) is called the anatomic dead space. The volume of gas in ventilated alveoli that are unperfused (and not available for gas exchange) is called the functional dead space. The anatomic dead space together with the functional dead space is called the physiologic dead space. Physiologic dead space ventilation (Vd) can be calculated by the Bohr dead space equation, which is mathematically expressed as follows: V /V = (Pa P ) Pa D T CO ECO CO 2 2 2 − where Vd/Vt is the ratio of Vd to Vt, and a and e represent arterial and mixed expired, respectively. Of the choices given, only the first is correct. A large increase in Vd will result in an increase in Paco2 (Barash: Clinical Anesthesia, ed 7, pp 275–277; West: Respiratory Physiology, ed 9, pp 19–21; Miller: Miller’s Anesthesia, ed 8, pp 446–447).
104. A 22-year-old patient who sustained a closed head injury is brought to the operating room (OR) from the ICU for placement of a dural bolt. Hemoglobin has been stable at 15 g/dL. Blood gas analysis immediately before induction reveals a Pao2 of 120 mm Hg and an arterial saturation of 100%. After induction, the Pao2 rises to 150 mm Hg and the saturation remains the same. How has the oxygen content of this patient’s blood changed? A. It has increased by 10% B. It has increased by 5% C. It has increased by less than 1% D. Cannot be determined without Paco2
104. (C) The oxygen content of blood can be calculated with the following formula: O2 content = 1.39 × [Hgb] × arterial saturation + (0.003 × Pao2) First oxygen content = (1.39 × 15 × 1.0) + 0.003 × 120 = 21.21 mL / dL Second oxygen content = (1.39 × 15 × 1.0) + 0.003 × 150 = 21.30 mL/dL The difference in the oxygen content is 0.09 mL/dL. This represents a change of 0.42% (Miller: Basics of Anesthesia, ed 6, p 57 ). Respiratory Physiology and Critical Care Medicine 39
105. Inhalation of CO2 increases ˙V E by A. 0.5 to 1 L/min/mm Hg increase in Paco2 B. 2 to 3 L/min/mm Hg increase in Paco2 C. 3 to 5 L/min/mm Hg increase in Paco2 D. 5 to 10 L/min/mm Hg increase in Paco2
105. (B) The degree of ventilatory depression caused by volatile anesthetics can be assessed by measuring resting Paco2, the ventilatory response to hypercarbia, and the ventilatory response to hypoxemia. Of these techniques, the resting Paco2 is the most frequently used index. However, measuring the effects of increased Paco2 on ventilation is the most sensitive method of quantifying the effects of drugs on ventilation. In awake unanesthetized humans, inhalation of CO2 increases minute ventilation ( ˙V E) by approximately 2 to 3 L/min/mm Hg increase in Paco2. Using this technique, halothane, isoflurane, desflurane-O2, desflurane-N2O, and N2O cause a dose-dependent depression of the ventilation (Miller: Basics of Anesthesia, ed 6, pp 93–94).
106. What is the O2 content of whole blood if the hemoglobin concentration is 10 g/dL, the Pao2 is 60 mm Hg, and the Sao2 is 90%? A. 10 mL/dL B. 12.5 mL/dL C. 15 mL/dL D. 17.5 mL/dL
106. (B) (See also explanation to Question 104.) The amount of O2 in blood (O2 content) is the sum of the amount of O2 dissolved in plasma and the amount of O2 combined with hemoglobin. The amount of O2 dissolved in plasma is directly proportional to the product of the blood/gas solubility coefficient of O2 (0.003) and Pao2. The amount of O2 bound to hemoglobin is directly related to the fraction of hemoglobin that is saturated. One gram of hemoglobin can bind 1.39 mL of O2. The mathematical expression of O2 content is as follows: O2 content = 1.39 × [Hgb] × SaO2 + (0.003 × PaO2) where [Hgb] is the hemoglobin concentration (g/dL), Sao2 is the fraction of hemoglobin saturated with O2, and (0.003 × Pao2) is the amount of O2 dissolved in plasma. In this case (1.39 × 10 × 0.9) + (0.003 × 60) = 12.51 + 0.18 = 12.69 or approximately 13 mL/dL (Miller: Basics of Anesthesia, ed 6, p 57 ).
107. Each of the following will cause erroneous readings by dual-wavelength pulse oximeters EXCEPT A. Carboxyhemoglobin B. Methylene blue C. Fetal hemoglobin D. Methemoglobin
107. (C) The presence of hemoglobin species other than oxyhemoglobin can cause erroneous readings by dualwavelength pulse oximeters. Hemoglobin species such as carboxyhemoglobin and methemoglobin, dyes such as methylene blue and indocyanine green, and some colors of nail polish will cause erroneous readings. Because the absorption spectrum of fetal hemoglobin is similar to that of adult oxyhemoglobin, fetal hemoglobin does not significantly affect the accuracy of these types of pulse oximeters. High levels of bilirubin have no significant effect on the accuracy of dual-wavelength pulse oximeters but may cause falsely low readings by nonpulsatile oximeters (Miller: Miller’s Anesthesia, ed 8, pp 1545–1547).
108. �0.5 0 1 2 3 4 5 6 7 8 9 10 0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 Pressure (kPa) D C B A Volume (L) In the diagram above, curve “D” represents A. Emphysema B. Chronic bronchitis C. Normal lungs D. Fibrotic lungs
108. (D) This graph depicts lung volumes as a function of pressure or compliance; one kPa is roughly equal to 10 cm H2O. Curve A shows an enormous volume with a small pressure (i.e., emphysema). Curve B depicts chronic bronchitis or asthma. The compliance curve is roughly the same as the normal lung, curve C, but volumes have increased. Curve D depicts stiff noncompliant lungs as seen with fibrosis or ARDS (Miller: Miller’s Anesthesia, ed 8, pp 447–448).
109. The P50 for normal adult hemoglobin is approximately A. 15 mm Hg B. 25 mm Hg C. 35 mm Hg D. 45 mm Hg Respiratory Physiology and Critical Care Medicine 31
109. (B) P50 is the Pao2 required to produce 50% saturation of hemoglobin. The P50 for adult hemoglobin at a pH of 7.4 and body temperature of 37° C is 26 mm Hg (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 788–789; Miller: Basics of Anesthesia, ed 6, p 56).
110. During a normal Vt (500-mL) breath, the transpulmonary pressure increases from 0 to 5 cm H2O. The product of transpulmonary pressure and Vt is 2500 cm H2O-mL. This expression of the pressurevolume relationship during breathing determines what parameter of respiratory mechanics? A. Lung compliance B. Airway resistance C. Pulmonary elastance D. Work of breathing
110. (D) The work of breathing is defined as the product of transpulmonary pressure and Vt. The work of breathing is related to two factors: the work required to overcome the elastic forces of the lungs, and the work required to overcome airflow or frictional resistances of the airways (Barash: Clinical Anesthesia, ed 7, pp 266–268; Miller: Miller’s Anesthesia, ed 8, p 1563).
111. An oximetric pulmonary artery catheter is placed in a 69-year-old man who is undergoing surgical repair of an abdominal aortic aneurysm under general anesthesia. Before the aortic cross-clamp is placed, the mixed venous O2 saturation decreases from 75% to 60%. Each of the following could account for the decrease in mixed venous O2 saturation EXCEPT A. Hypovolemia B. Bleeding C. Congestive heart failure D. Sepsis
111. (D) The normal mixed venous O2 saturation is 75%. Physiologic factors that affect mixed venous O2 saturation include hemoglobin concentration, arterial Pao2, cardiac output, and O2 consumption. Anemia, hypoxia, decreased cardiac output, and increased O2 consumption decrease mixed venous O2 saturation. During sepsis with adequate volume resuscitation, the cardiac output is increased and maldistribution of perfusion (distributive shock) results in an elevated mixed-venous O2 saturation. Mixed venous O2 saturation (Svo2) is related to a number of factors, as shown in this equation: Sv V 13.9 Q Hgb O O O 2 2 = Sa − 2 ˙ ˙ ( ( where Hgb is hemoglobin concentration, 13.9 is a constant (O2 combining power of Hgb [mL/10 g]), ˙Q is cardiac output, and ˙V O2 is the oxygen consumption (Miller: Miller’s Anesthesia, ed 8, pp 1386–1387 ). 40 Part 1 Basic Sciences
112. The normal vital capacity for a 70-kg man is A. 1 L B. 2 L C. 5 L D. 7 L
112. (C) The volume of gas exhaled during a maximum expiration is the vital capacity. In a normal healthy adult, the vital capacity is 60 to 70 mL/kg. In a 70-kg patient, the vital capacity is approximately 5 L (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 776; Barash: Clinical Anesthesia, ed 7, p 278).
113. A 32-year-old man is found unconscious by the fire department in a room where he has inhaled 0.1% carbon monoxide for a prolonged period. His respiratory rate is 42 breaths/min, but he is not cyanotic. Carbon monoxide has increased this patient’s minute ventilation by which of the following mechanisms? A. Shifting the O2 hemoglobin dissociation curve to the left B. Increasing CO2 production C. Causing lactic acidosis D. Decreasing Pao2
113. (C) Carbon monoxide inhalation is the most common immediate cause of death from fire. Carbon monoxide binds to hemoglobin with an affinity 200 times greater than that of oxygen. For this reason, very small concentrations of carbon monoxide can greatly reduce the oxygen-carrying capacity of blood. In spite of this, the arterial Pao2 often is normal. Because the carotid bodies respond to arterial Pao2, there would not be an increase in minute ventilation until tissue hypoxia was sufficient to produce lactic acidosis (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 554–555; Miller: Miller’s Anesthesia, ed 8, pp 2679–2680; West: Respiratory Physiology, ed 9, pp 80–82).
114. An acute increase in Paco2 of 10 mm Hg will result in a decrease in pH of A. 0.01 pH unit B. 0.02 pH unit C. 0.04 pH unit D. 0.08 pH unit
114. (D) Respiratory acidosis is present when the Paco2 exceeds 44 mm Hg. Respiratory acidosis is caused by decreased elimination of CO2 by the lungs (i.e., hypoventilation) or increased metabolic production of CO2. An acute increase in Paco2 of 10 mm Hg will result in a decrease in pH of approximately 0.08 pH unit. The acidosis of arterial blood will stimulate ventilation via the carotid bodies, and the acidosis of cerebrospinal fluid will stimulate ventilation via the medullary chemoreceptors located in the fourth cerebral ventricle. Volatile anesthetics greatly attenuate the carotid body–mediated and aortic body–mediated ventilatory responses to arterial acidosis, but they have little effect on the medullary chemoreceptor– mediated ventilatory response to cerebrospinal fluid acidosis (Miller: Basics of Anesthesia, ed 6, pp 339–340, 343).
115. You are taking care of a patient in shock in the ICU, and, after adequate fluid resuscitation, you decide to add a vasoactive medication. Each of the following initial infusion rates is correct EXCEPT A. Dopamine 2 to 10 μg/kg/min B. Norepinephrine 0.1 to 0.5 μg/kg/min C. Vasopressin 0.01 to 0.04 units/kg/min D. None of the above; they all are reasonable starting doses
115. (C) Dopamine can be infused at low doses (2-5 μg/kg/min), moderate doses (5-10 μg/kg/min), or high doses (10-20 μg/kg/min). Many feel that if dopamine is needed at rates greater than 10 μg/kg/min, one should use epinephrine or norepinephrine infusions instead. Epinephrine and norepinephrine infusion rates are commonly started at 0.1 to 0.5 μg/kg/min. Although many cardiovascular drugs are based on a μg/kg/min dose, vasopressin is not. The starting vasopressin dose is 0.01 to 0.04 unit/min (American Heart Association: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, pp S774–S775; Kaplan: Cardiac Anesthesia, ed 6, pp 1000, 1034–1035; Miller: Basics of Anesthesia, ed 6, pp 675–676).
116. A 44-year-old patient is hyperventilated to a Paco2 of 24 mm Hg for 48 hours. What [HCO3 −] would you expect (normal [HCO3 −] is 24 mEq/L)? A. 10 mEq/L B. 12 mEq/L C. 14 mEq/L D. 16 mEq/L
116. (D) Respiratory alkalosis is present when the Paco2 is less than 36 mm Hg. There are three compensatory mechanisms responsible for attenuating the increase in pH that accompanies respiratory alkalosis. First, there is an immediate shift in the equilibrium of the [HCO3 −] buffer system, which results in the production of CO2. Second, alkalosis stimulates the activity of phosphofructokinase, which increases glycolysis and the production of pyruvate and lactic acid. Third, there is a decrease in reabsorption of [HCO3 −] by the proximal and distal renal tubules. These three compensatory mechanisms result in a maximum decrease in [HCO3 −] of approximately 5 mEq/L for every 10 mm Hg decrease in Paco2 less than 40 mm Hg (Miller: Basics of Anesthesia, ed 6, p 340; Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 1154–1155).
117. The diagram below depicts which mode of ventilation? 30 20 10 0 A. Spontaneous ventilation B. Controlled ventilation C. Assisted ventilation D. Assisted/controlled ventilation
117. (D) Mechanical ventilation of the lungs can be accomplished by various modes. These modes are categorized as controlled, assisted, assisted/controlled, controlled with positive end-expiratory pressure (PEEP), and assisted/controlled using intermittent mandatory ventilation (IMV). Assisted/controlled modes of mechanical ventilation are used in patients when the muscles of respiration require rest because minimal breathing efforts are required. With the assisted/controlled mode of ventilation, positive-pressure ventilation is triggered by small breathing efforts produced by the patient. The airway pressure tracing shown is typical of that of a patient requiring assisted/controlled ventilation (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 207–208). Respiratory Physiology and Critical Care Medicine 41
118. A 35-year-old morbidly obese patient is discharged after gastric bypass surgery. She is readmitted 4 days later after she falls and twists her ankle. She is noted in the emergency room (ER) to be in atrial fibrillation and is hypotensive but only complains of leg pain. She is admitted to the hospital, and temperature on admission is 38.6° C and heart rate is 105 beats/min. The next step in management of her dysrhythmia should be A. Ibutilide B. Procainamide C. Echocardiographic study D. DC cardioversion
118. (C) The first step in evaluating any patient with a tachycardia is to determine if the patient is hemodynamically stable or unstable (serious signs or symptoms are chest pain or congestive heart failure due to the tachycardia). In the unstable patient, DC cardioversion should be performed for rapid heart rate control regardless of the duration of atrial fibrillation. In this case, where the patient is reasonably stable, the three major goals in the management of atrial fibrillation should be considered. These goals are control of ventricular rate, assessment of anticoagulation needs, and conversion to sinus rhythm. In addition, the underlying cause of atrial fibrillation should be sought and treated. Because this patient is febrile and may be dehydrated, an intravenous (IV) line for fluid resuscitation should be initiated. Because we do not know when atrial fibrillation developed (after 48 hours, embolic events may occur with conversion to sinus rhythm), it would be best not to convert the atrial fibrillation to sinus rhythm using either ibutilide or procainamide until the patient is adequately anticoagulated. Adequate anticoagulation should usually be therapeutic for at least 3 weeks. In marginal cases where the duration of atrial fibrillation is uncertain, cardiac consultation and transesophageal echocardiography to exclude atrial thrombus should be performed before cardioversion. This patient should undergo cardiac echocardiographic study to look for intra-atrial thrombus and to determine the ejection fraction (EF) of the ventricle. After adequate hydration, rate control could be improved with calcium channel blockers or β-blockers in patients with preserved left ventricular function (EF > 40%) or with digoxin, diltiazem, or amiodarone if EF is less than 40% (2010 AHA Guidelines for CPR and Emergency Cardiovascular Care: Circulation 122 (Suppl 3) S750–S756). 42 Part 1 Basic Sciences
119. The P50 of sickle cell hemoglobin is A. 19 mm Hg B. 26 mm Hg C. 31 mm Hg D. 35 mm Hg
119. (C) A P50 less than 26 mm Hg defines a leftward shift of the oxyhemoglobin dissociation curve. This means that at any given Pao2, hemoglobin has a higher affinity for O2. A P50 greater than 26 mm Hg describes a rightward shift of the oxyhemoglobin dissociation curve. This means that at any given Pao2, hemoglobin has a lower affinity for O2. Conditions that cause a rightward shift of the oxyhemoglobin dissociation curve are metabolic and include respiratory acidosis, hyperthermia, increased erythrocyte 2,3-diphosphoglycerate (2,3-DPG) content, pregnancy, and abnormal hemoglobins, such as sickle cell hemoglobin or thalassemia. Alkalosis, hypothermia, fetal hemoglobin, abnormal hemoglobin species, such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin, and decreased erythrocyte 2,3-DPG content will cause a leftward shift of the oxyhemoglobin dissociation curve. Also see explanation to Question 109 (Miller: Miller’s Anesthesia, ed 8, p 1843; West: Respiratory Physiology, ed 9, pp 79–82).
120. Data from the ARDS network trial (ARDSNet) showed increased mortality from A. Atelectrauma B. Volutrauma C. Barotrauma D. Inhaled nitric oxide 32 Part 1 Basic Sciences
120. (B) Adult respiratory distress disorder (ARDS) was first reported in adults in 1967 and is associated with decreased lung compliance. Initial therapies for ARDS included mechanical ventilation with tidal volumes of 10 to 15 mL/kg with rates to achieve a normal pH and Paco2. In 2000, the National Institutes of Health (NIH) ARDS Network (ARDSNet) trial noted a reduction in mortality for patients with ARDS who were ventilated with low tidal volumes (6 mL/kg predicted body weight [PBW]—mortality rate of 31%) compared to traditional tidal volumes (12 mL/kg PBW—mortality rate of 40%). It was felt that the larger tidal volumes caused overdistention of the alveoli (i.e., produced volume trauma or volutrauma). This increased alveolar volume resulted in mechanical injury and a systemic inflammatory response. It was felt that the stretch and not the pressure (barotrauma) caused the release of the inflammatory cytokinins into the circulation. Because the lower tidal volumes used were associated with an elevation of arterial CO2 and lower arterial oxygen levels, the term “permissive hypercapnia and hypoxemia” was used. Patients with ARDS also develop atelectasis. Recruitment maneuvers (sustained breaths of increased airway pressures) were used to re-expand atelectatic alveoli to avoid atelectrauma. However, results with the recruitment breaths showed only a transient increase in oxygenation and no change in mortality. Another respiratory technique proposed included the use of inhaled nitrous oxide (iNO) that can improve ventilation-perfusion mismatch and improve oxygenation. Randomized controlled studies have shown only limited effectiveness with no overall improvement in mortality or duration of ventilation. Further studies are looking at iNO for specific conditions (e.g., severe pulmonary hypertension, right ventricular failure refractory hypoxemia) (Miller: Basics of Anesthesia, ed 6, p 669; Miller: Miller’s Anesthesia, ed 8, pp 3040–3044, 3078–3079).
121. Which of the following is the correct mathematical expression of Fick’s law of diffusion of a gas through a lipid membrane ( ˙V = rate of diffusion, D = diffusion coefficient of the gas, A = area of the membrane, P1 − P2 = transmembrane partial pressure gradient of the gas, T = thickness of the membrane)? A. V D A T P1 P2 ˙ = × × − B. V = A T D (P1 − P2 ) ˙ × C. V = D A(P P ) T ˙ × 1 2 − D. V = D T(P P ) A ˙ × 1 2 −
121. (C) The rate at which a gas diffuses through a lipid membrane is directly proportional to the area of the membrane, the transmembrane partial pressure gradient of the gas, and the diffusion coefficient of the gas, and it is inversely proportional to the thickness of the membrane. The diffusion coefficient of the gas is directly proportional to the square root of gas solubility and is inversely proportional to the square root of the molecular weight of the gas. This is known as Fick’s law of diffusion (Barash: Clinical Anesthesia, ed 7, p 1147).
122. Each of the following is decreased in elderly patients compared with their younger counterparts EXCEPT A. Closing volume B. FEV1 C. Ventilatory response to hypercarbia D. Vital capacity
122. (A) Aging is associated with reduced ventilatory volumes and capacities, and decreased efficiency of pulmonary gas exchange. These changes are caused by progressive stiffening of cartilage and replacement of elastic tissue in the intercostal and intervertebral areas, which decreases compliance of the thoracic cage. In addition, progressive kyphosis or scoliosis produces upward and anterior rotation of the ribs and sternum, which further restricts chest wall expansion during inspiration. With aging, the FRC, residual volume, and closing volume are increased, whereas the vital capacity, total lung capacity, maximum breathing capacity, FEV1, and ventilatory response to hypercarbia and hypoxemia are reduced. In addition, age-related changes in lung parenchyma, alveolar surface area, and diminished pulmonary capillary bed density cause ventilation/perfusion mismatch, which decreases resting Pao2 (Miller: Basics of Anesthesia, ed 6, pp 571–572; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 644).
123. Calculate the Vd/Vt ratio (physiologic dead space ventilation) based on the following data: Paco2 45 mm Hg, mixed expired CO2 tension (Peco2) 30 mm Hg. A. 0.1 B. 0.2 C. 0.3 D. 0.4
123. (C) Physiologic dead space ventilation can be estimated using the Bohr equation (described in the explanation to Question 103): mm Hg mm Hg mm Hg mm Hg mm Hg VD/VT = 45 − 30 = 45 15 45 = 0.33 (Barash: Clinical Anesthesia, ed 7, pp 276–277; West: Respiratory Physiology, ed 9, pp 19–21; Miller: Miller’s Anesthesia, ed 8, pp 446–447). Respiratory Physiology and Critical Care Medicine 43
124. Which of the following statements concerning the distribution of O2 and CO2 in the upright lungs is TRUE? A. Pao2 is greater at the apex than at the base B. Paco2 is greater at the apex than at the base C. Both Pao2 and Paco2 are greater at the apex than at the base D. Both Pao2 and Paco2 are greater at the base than at the apex
124. (A) The ventilation/perfusion ratio is greater at the apex of the lungs than at the base of the lungs. Thus, dependent regions of the lungs are hypoxic and hypercarbic compared to the nondependent regions. Also see explanation to Question 132 (Miller: Miller’s Anesthesia, ed 8, pp 451–454; West: Respiratory Physiology, ed 9, pp 21–22, 44–46).
125. Which of the following acid-base disturbances is the least well-compensated? A. Metabolic alkalosis B. Respiratory alkalosis C. Increased anion gap metabolic acidosis D. Normal anion gap metabolic acidosis
125. (A) The degree to which a person can hypoventilate to compensate for metabolic alkalosis is limited; hence, this is the least well-compensated acid-base disturbance. Respiratory compensation for metabolic alkalosis is rarely more than 75% complete. Hypoventilation to a Paco2 greater than 55 mm Hg is the maximum respiratory compensation for metabolic alkalosis. A Paco2 greater than 55 mm Hg most likely reflects concomitant respiratory acidosis (Miller: Basics of Anesthesia, ed 6, p 342).
126. What is the (calculated) Pao2 of a patient on room air in Denver, Colorado? (Assume a barometric pressure of 630 mm Hg, respiratory quotient of 0.8, and Paco2 of 34 mm Hg.) A. 80 mm Hg B. 90 mm Hg C. 100 mm Hg D. 110 mm Hg
126. (A) Pao2 can be estimated using the alveolar gas equation, which is given as follows: PaO (PB )F Pa R IO CO2 2 = − 47 2 − where Pb is the barometric pressure (mm Hg), Fio2 is the fraction of inspired O2, Paco2 is the arterial CO2 tension (mm Hg), and R is the respiratory quotient (Barash: Clinical Anesthesia, ed 7, p 277; West: Respiratory Physiology, ed 9, p 59).
127. A venous blood sample from which of the following sites would correlate most reliably with Pao2 and Paco2? A. Jugular vein B. Subclavian vein C. Antecubital vein D. Vein on posterior surface of a warmed hand
127. (D) When arterial sampling is not possible, “arterialized” venous blood can be used to estimate ABG tensions. Because blood in the veins on the back of the hands has very little O2 extracted, the O2 content in this blood best approximates the O2 content in a sample of blood obtained from an artery (Stoelting: Basics of Anesthesia, ed 5, p 324).
128. Which of the following pulmonary function tests is LEAST dependent on patient effort? A. Forced expiratory volume in 1 second (FEV1) B. Forced vital capacity (FVC) C. FEF 800 to 1200 D. FEF 25% to 75%
128. (D) Pulmonary function tests can be divided into those that assess ventilatory capacity and those that assess pulmonary gas exchange. The simplest test to assess ventilatory capacity is the FEV1/FVC ratio. Other tests to assess ventilatory capacity include the maximum midexpiratory flow (FEF 25%-75%), MVV, and flow-volume curves. The most significant disadvantage of these tests is that they are dependent on patient effort. However, because the FEF 25% to 75% is obtained from the midexpiratory portion of the flow-volume loop, it is least dependent on patient effort. Also see explanation to Question 97 (Barash: Clinical Anesthesia, ed 7, p 279).
129. A 33-year-old woman with 20% carboxyhemoglobin is brought to the ER for treatment of smoke inhalation. Which of the following is LEAST consistent with a diagnosis of carbon monoxide poisoning? A. Cyanosis B. Pao2 105 mm Hg, oxygen saturation 80% on initial room air arterial blood gases (ABGs) C. 98% oxygen saturation on dual-wavelength pulse oximeter D. Oxyhemoglobin dissociation curve shifted far to the left
129. (A) Carbon monoxide binds to hemoglobin with an affinity greater than 200 times that of oxygen. This stabilizes the oxygen–hemoglobin complex and hinders release of oxygen to the tissues, leading to a leftward shift of the oxyhemoglobin dissociation curve. The diagnosis is suggested when there is a low oxygen hemoglobin saturation in the face of a normal Pao2. The two-wave pulse oximeter cannot distinguish oxyhemoglobin from carboxyhemoglobin so that a normal oxyhemoglobin saturation would be observed in the presence of high concentrations of carboxyhemoglobin. Carbon monoxide poisoning is not associated with cyanosis. See also explanations for Questions 113 and 140 (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 554–555; Miller: Miller’s Anesthesia, ed 8, pp 2679–2680).
130. The Pao2 − Pao2 of a patient breathing 100% O2 is 240 mm Hg. The estimated fraction of the cardiac output shunted past the lungs without exposure to ventilated alveoli (i.e., transpulmonary shunt) is A. 5% B. 12% C. 17% D. 20%
130. (B) The fraction of total cardiac output that traverses the pulmonary circulation without participating in gas exchange is called the transpulmonary shunt. It can be calculated exactly by the equation: ˙ ˙Q s/QT = CaO Cc� CvO O O 2 2 Cc� − − 2 2 where Cc′, Ca, and CvO2 stand for the content of oxygen in the alveolar capillary, artery, and mixed venous samples, respectively. This information is not provided in the question; however, the alveolar-toarterial partial pressure of oxygen difference is using high inspired oxygen concentrations. The alveolar to arterial oxygen difference can be used to estimate venous admixture, most commonly transpulmonary shunt. For every increase in alveolar-arterial O2 of 20 mm Hg, there is an increase in shunt fraction of 1% of the cardiac output. In the example, 240/20 = 12 and the transpulmonary shunt can be estimated at 12% (Miller: Miller’s Anesthesia, ed 44 Part 1 Basic Sciences
131. Each of the following will alter the position or slope of the CO2-ventilatory response curve EXCEPT A. Hypoxemia B. Fentanyl C. N2O D. Ketamine
131. (D) Measuring the ventilatory response to increased Paco2 is a sensitive method for quantifying the effects of drugs on ventilation. In general, all volatile anesthetics (including N2O), narcotics, benzodiazepines, and barbiturates depress the ventilatory response to increased Paco2 in a dose-dependent manner. The magnitude of ventilatory depression by volatile anesthetics is greater in patients with COPD than in healthy patients. Arterial blood gases (ABGs) may need to be monitored during recovery from general anesthesia in patients with COPD. Ketamine causes minimal respiratory depression. Typically, respiratory rate is decreased only 2 to 3 breaths/min and the ventilatory response to changes in Paco2 is maintained during ketamine anesthesia. Also see explanation to Question 105 (Miller: Basics of Anesthesia, ed 6, pp 63–64, 93–94, 110; Miller: Miller’s Anesthesia, ed 8, pp 691–693).
132. Which of the following statements concerning the distribution of alveolar ventilation (˙V A) in the upright lungs is TRUE? A. The distribution of ˙V A is not affected by body posture B. Alveoli at the apex of the lungs (nondependent alveoli) are better ventilated than those at the base C. All areas of the lungs are ventilated equally D. Alveoli at the base of the lungs (dependent alveoli) are better ventilated than those at the apex Respiratory Physiology and Critical Care Medicine 33
132. (D) (See also explantation to Question 124.) The orientation of the lungs relative to gravity has a profound effect on efficiency of pulmonary gas exchange. Because alveoli in dependent regions of the lungs expand more per unit change in transpulmonary pressure (i.e., are more compliant) than alveoli in nondependent regions of the lungs, ˙V A increases from the top to the bottom of the lungs. Because pulmonary blood flow increases more from the top to the bottom of the lungs than does ˙V A, the ventilation/ perfusion ratio is high in nondependent regions of the lungs and is low in dependent regions of the lungs. Therefore, in the upright lungs, the Pao2 and pH are greater at the apex, whereas the Paco2 is greater at the base (Miller: Miller’s Anesthesia, ed 8, pp 451–454; West: Respiratory Physiology, ed 9, pp 21–22, 44–46).
133. In the resting adult, what percentage of total body O2 consumption is due to the work of breathing? A. 2% B. 5% C. 10% D. 20%
133. (A) The work required to overcome the elastic recoil of the lungs and thorax, along with airflow or frictional resistances of the airways, contributes to the work of breathing. When the respiratory rate or airway resistance is high or pulmonary or chest wall compliance is reduced, a large amount of energy is spent overcoming the work of breathing. In the healthy resting adult, only 1% to 3% of total O2 consumption is used for the work of breathing at rest, but up to 50% may be needed in patients with pulmonary disease. Also see explanation to question 110 (Miller: Miller’s Anesthesia, ed 8, p 1563).
134. The anatomic dead space in a 70-kg man is A. 50 mL B. 150 mL C. 250 mL D. 500 mL
134. (B) The conducting airways (trachea, right and left mainstem bronchi, and lobar and segmental bronchi) do not contain alveoli and, therefore, do not take part in pulmonary gas exchange. These structures constitute the anatomic dead space. In the adult, the anatomic dead space is approximately 2 mL/kg. The anatomic dead space increases during inspiration because of the traction exerted on the conducting airways by the surrounding lung parenchyma. In addition, the anatomic dead space depends on the size and posture of the subject. Also see explanation to Question 103 (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 778; Barash: Clinical Anesthesia, ed 7, p 276).
135. The most important buffering system in the body is A. Hemoglobin B. Plasma proteins C. Phosphate D. [HCO3 −]
135. (D) There are three main mechanisms that the body has to prevent changes in pH. The buffer systems (immediate), the ventilatory response (takes minutes), and the renal response (takes hours to days). The buffer systems represent the first line of defense against adverse changes in pH. The [HCO3 −] buffer system is the most important system and represents greater than 50% of the total buffering capacity of the body. Other important buffer systems include hemoglobin, which is responsible for approximately 35% of the buffering capacity of blood, phosphates, plasma proteins, and bone (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 794–799; Miller: Basics of Anesthesia, ed 6. pp 335–336).
136. A decrease in pH of 0.1 unit will result in A. A decrease in serum potassium concentration [K+] of 0.6 mEq/L B. A decrease in [K+] of 1.2 mEq/L C. An increase in [K+] of 0.6 mEq/L D. An increase in [K+] of 1.2 mEq/L
136. (C) Cardiac dysrhythmias are a common complication associated with acid-base abnormalities. The etiology of these dysrhythmias is related partly to the effects of pH on myocardial potassium homeostasis. As a general rule, plasma K+ increases approximately 0.6 for each 0.1 decrease in pH (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, p 1149).
137. An increase in [HCO3 −] of 10 mEq/L will result in an increase in pH of A. 0.10 pH unit B. 0.15 pH unit C. 0.20 pH unit D. 0.25 pH unit
137. (B) Several guidelines can be used in the initial interpretation of ABGs that will permit rapid recognition of the type of acid-base disturbance. These guidelines are as follows: (1) a 1 mm Hg change in Paco2 above or below 40 mm Hg results in a 0.008 unit change in the pH in the opposite direction; (2) the Paco2 will decrease by about 1 mm Hg for every 1 mEq/L reduction in [HCO3 −] below 24 mEq/L; (3) a change in [HCO3 −] of 10 mEq/L from 24 mEq/L will result in a change in pH of approximately 0.15 pH unit in the same direction (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 1146, 1156–1157; Miller: Basics of Anesthesia, ed 6, pp 342–343). Respiratory Physiology and Critical Care Medicine 45
138. A 28-year-old, 70-kg woman with ulcerative colitis is receiving a general anesthetic for a colon resection and ileostomy. The patient’s lungs are mechanically ventilated with the following parameters: ˙V E 5000 mL and respiratory rate 10 breaths/min. Assuming no change in ˙V E, how would ˙V A change if the respiratory rate were increased from 10 to 20 breaths/min? A. Increase by 500 mL B. Increase by 1000 mL C. Decrease by 750 mL D. Decrease by 1500 mL
138. (D) A patient with a Vd of 150 mL and a Va of 350 mL (assuming a normal Vt of 500 mL) will have a Vd minute ventilation ( ˙V D) of 1500 mL and a Va minute ventilation (˙V A) of 3500 mL ( ˙V E of 5000 mL) at a respiratory rate of 10 breaths/min. If the respiratory rate is doubled but ˙V E remains unchanged, then the ˙V D would double to 3000 mL and there would be an increase in ˙V D of 1500 mL and a decrease in ˙V A of 1500 mL. Also see explanation to Questions 103 and 134 (Barash: Clinical Anesthesia, ed 7, pp 275–277; West: Respiratory Physiology, ed 9, pp 16–17; Miller: Miller’s Anesthesia, ed 8, pp 446–447).
139. Each of the following will shift the oxyhemoglobin dissociation curve to the right EXCEPT A. Volatile anesthetics B. Decreased Pao2 C. Decreased pH D. Increased temperature
139. (B) In addition to the items listed in this question, other factors that shift the oxyhemoglobin dissociation curve to the right include pregnancy and all abnormal hemoglobins such as hemoglobin S (sickle cell hemoglobin). For reasons unknown, volatile anesthetics increase the P50 of adult hemoglobin by 2 to 3.5 mm Hg. A rightward shift of the oxyhemoglobin dissociation curve will decrease the transfer of O2 from alveoli to hemoglobin and improve release of O2 from hemoglobin to peripheral tissues. Also see explanation to Question 109 (Miller: Basics of Anesthesia, ed 6, p 56; West: Respiratory Physiology, ed 9, pp 79–82).
140. The half-life of carboxyhemoglobin in a patient breathing 100% O2 is A. 5 minutes B. 1 hour C. 2 hours D. 4 hours
140. (B) The most frequent immediate cause of death from fires is carbon monoxide toxicity. Carbon monoxide is a colorless, odorless gas that exerts its adverse effects by decreasing O2 delivery to peripheral tissues. This is accomplished by two mechanisms. First, because the affinity of carbon monoxide for the O2 binding sites on hemoglobin is more than 200 times that of O2, O2 is readily displaced from hemoglobin. Thus, O2 content is reduced. Second, carbon monoxide causes a leftward shift of the oxyhemoglobin dissociation curve, which increases the affinity of hemoglobin for O2 at peripheral tissues. Treatment of carbon monoxide toxicity is administration of 100% O2. Supplemental oxygen decreases the half-time of carboxyhemoglobin from 4 to 6 hours with room air to about 1 hour with 100% oxygen. Breathing 100% oxygen at 3 atm in a hyperbaric chamber reduces the half-time even more to 15 to 30 minutes. See also explanations for Questions 113 and 129 (Barash: Clinical Anesthesia, ed 7, pp 1515–1516; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 554–555; Miller: Miller’s Anesthesia, ed 8, pp 2679–2680).
141. A disadvantage of using propofol for prolonged sedation (days) of intubated patients in the ICU is potential A. Acidosis B. Tachyphylaxis C. Hyperglycemia D. Bradycardia
141. (A) Propofol infusion syndrome is a rare condition associated with prolonged (greater than 48 hour) administration of propofol at a dose of 5 mg/kg/hr (83 μg/kg/min) or higher. This syndrome was first described in children but later observed in critically ill adults as well. It is manifested by cardiomyopathy with acute cardiac failure, metabolic acidosis, skeletal muscle myopathy, hepatomegaly, hyperkalemia, and lipidemia. It is thought to be related to a failure of free fatty acid transport into the mitochondria and failure of the mitochondrial respiratory chain. Bradycardia can be a late sign with this syndrome and heralds a poor prognosis (Miller: Miller’s Anesthesia, ed 8, p 831).
142. A 17-year-old type 1 diabetic with history of renal failure is in the preoperative holding area awaiting an operation for acute appendicitis. Arterial blood gases are obtained with the following results: Pao2 88 mm Hg, Paco2 32 mm Hg, pH 7.2, [HCO3 −] 12, [Cl−] 115 mEq/L, [Na+] 138 mEq/L, and glucose 251 mg/dL. The most likely cause of this patient’s acidosis is A. Renal tubular acidosis B. Lactic acidosis C. Diabetic ketoacidosis D. Aspirin overdose
142. (A) Calculating the anion gap (i.e., the unmeasured anions in the plasma) is helpful in determining the cause of a metabolic acidosis. Anion gap = [Na+] − ([Cl−] + [HCO3 −]) and is normally 10 to 12 nmol/L. In this case the anion gap = 138 − (115 + 12) = 11, a normal anion gap. Causes of a high anion gap metabolic acidosis include lactic acidosis, ketoacidosis, acute and chronic renal failure, and toxins (e.g., salicylates, ethylene glycol, methanol). Nonanion gap metabolic acidosis include renal tubular acidosis, expansion acidosis (e.g., rapid saline infusion), gastrointestinal (GI) bicarbonate loss (e.g., diarrhea, small bowel drainage), drug-induced hyperkalemia, and acid loads (e.g., ammonium chloride, hyperalimentation). Vomiting and nasogastric drainage are some of the many causes of metabolic alkalosis (Longo: Harrison’s Principles of Internal Medicine, ed 18, pp 365–369; Miller: Basics of Anesthesia, ed 6, pp 340–342).
143. Methods to decrease the incidence of central venous catheter infections include all of the following EXCEPT A. Changing the central catheter every 3 to 4 days over a guidewire B. Using minocycline/rifampin impregnated catheters over chlorhexidine/silver sulfadiazine impregnated catheters for suspected long-term use C. Using the subclavian over the internal jugular route for access D. Using a single lumen over a multilumen catheter
143. (A) Bloodstream infectious complications with central venous catheters are the most common late complication seen with central catheters (>5%). Current Centers for Disease Control and Prevention (CDC) guidelines do not recommend replacing central venous catheters. All the other statements are true. In addition, evidence is suggesting that the use of ultrasound may decrease the time needed to place catheters and the number of skin punctures needed for central vein access and may also decrease infections (Miller: Miller’s Anesthesia, ed 8, p 1367; O’Grady et al: Guidelines for the prevention of intravascular catheter-related infections. Clin Infect Dis 52(9): e164–e166, 2011). 46 Part 1 Basic Sciences
144. Signs of Sarin nerve gas poisoning include all of the following EXCEPT A. Diarrhea B. Urination C. Mydriasis D. Lacrimation
144. (C) Sarin (also called GB), like GA (Tabun), GD (Soman), GF, VR, and VX, is a clear liquid organophosphate that vaporizes at room temperatures. These chemical nerve gases mainly bind with acetylcholinesterase and produce clinical signs of excessive parasympathetic activity. The term DUMBELS—Diarrhea, Urination, Miosis, Bronchorrhea and bronchoconstriction, Emesis, Lacrimation, and Salivation—can help you remember several of the signs. Note the eye signs are pupillary constriction (miosis) and not pupillary dilation (mydriasis). Other signs relate to the cardiovascular system and include bradycardia, prolonged QT interval, and ventricular dysrhythmias. These chemicals also affect the GABA and NMDA receptors and may also cause central nervous system (CNS) excitation (i.e., convulsions) (Barash: Clinical Anesthesia, ed 7, pp 1540–1541; Miller: Miller’s Anesthesia, ed 8, p 2496).
145. Which of the following conditions would be associated with the LEAST risk of venous air embolism during removal of a central line? A. Spontaneous breathing, head up B. Spontaneous breathing, flat C. Spontaneous breathing, Trendelenburg D. Mechanical ventilation, Trendelenburg
145. (D) Venous air embolism occurs when air enters the venous system through an incised or cannulated vein. When cannulating or decannulating central veins, it is important to keep a positive venous-to-atmospheric pressure gradient. This is usually accomplished by placing the site below the level of the heart (i.e., Trendelenburg position). In addition, under mechanical ventilation or when the spontaneously breathing patient exhales or performs a Valsalva maneuver, the venous-to-atmospheric pressure is greater than if a spontaneously breathing patient inhales, a time when the venous pressure may be less than atmospheric pressure (Lobato: Complications in Anesthesiology, pp 198–200; Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, p 101; Marino’s The ICU Book, ed 4, pp 32–33).
146. Which of the following adverse effects is NOT attributable to respiratory or metabolic acidosis? A. Increased intracranial pressure B. Vasoconstriction C. Increased pulmonary vascular resistance D. Increased serum potassium concentration 34 Part 1 Basic Sciences
146. (B) Adverse physiologic effects of respiratory or metabolic acidosis include CNS depression and increased intracranial pressure (ICP), cardiovascular system depression (partially offset by increased secretion of catecholamines and elevated [Ca++]), cardiac dysrhythmias, vasodilation, hypovolemia (which is a result of decreased precapillary and increased postcapillary sphincter tone), pulmonary hypertension, and hyperkalemia (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 1148–1149; Miller: Basics of Anesthesia, ed 6, p 339).
147. Which of the following maneuvers is LEAST likely to raise arterial saturation in a patient in whom the endotracheal tube (ETT) is seated in the right mainstem bronchus? The patient has normal lung function. A. Inflating the pulmonary artery catheter balloon (in the left pulmonary artery) B. Raising hemoglobin from 8 to 12 mg/dL C. Raising Fio2 from 0.8 to 1.0 D. Increasing cardiac output from 2 to 5 L/min
147. (C) Withdrawing the tube into the trachea obviously would improve arterial saturation and is the treatment of choice for inadvertent mainstem intubation. Short of pulling the ETT back, all other successful options address ways of improving arterial oxygenation during one-lung ventilation. In essence, any maneuver that improves the saturation of the venous blood will also improve the saturation of arterial blood (in this question). Normal pulmonary circulation is in series with the systemic circulation. Blood exiting the lungs is nearly 100% oxygenated regardless of the saturation of the venous blood when it exits the right ventricle and enters the lungs via the pulmonary artery. In one-lung ventilation, deliberate or accidental, blood exiting the ventilated side of the lungs (the right side in this question) is also essentially fully saturated, but it mixes with nonoxygenated blood. The nonoxygenated blood has effectively bypassed the lungs by passing through an area that is perfused but not ventilated, that is, a shunt. When the blood from the ventilated lung (nearly 100% oxygenated) mixes with the shunted blood, a mixture will be formed that has saturation less than 100%, but higher than the mixed venous O2 saturation. SvO2 = SaO2 − ˙V O2/ ˙Q × Hgb where Svo2 = mixed venous hemoglobin saturation and Sao2 = arterial oxygen saturation O2 content = 1.39 × [Hgb] × SaO2 + (0.003 × PaO2) The exact saturation of the arterial blood in this question depends on the ratio of blood exiting the right lung versus that exiting the left lung. Fortunately, during one-lung ventilation, the nonventilated lung collapses and in so doing raises its resistance to blood flow. This results in preferentially directing blood to the right ventilated lung. A second factor to consider is how well-saturated the shunted blood is. “Red” blood from the right lung mixes with “blue” blood from the left lung to give a mixture of partially saturated blood. The saturation of the shunted “blue” blood depends on the hemoglobin concentration and cardiac output. From the first equation above you can see that raising either of these would improve the mixed venous oxygen saturation and ultimately the arterial saturation during one-lung ventilation. Inflating the pulmonary artery catheter balloon located in the nonventilated (left) lung would also improve arterial saturation by limiting blood flow to the left lung. Raising the Fio2 from 80% to 100% will do little if anything to improve arterial saturation because the blood exiting the “working” lung is already fully saturated. The small rise in Pao2 that would result from an increase in Fio2, once multiplied by 0.003 (see the second equation above), would be a very small and insignificant number. In other words, raising Fio2 does not improve arterial saturation in the presence of a shunt (Miller: Miller’s Anesthesia, ed 8, p 1386; Miller: Basics of Anesthesia, ed 6, pp 444–445, 636). Respiratory Physiology and Critical Care Medicine 47
148. A 100-kg man is 24 hours status post four-vessel coronary artery bypass graft. Which of the following pulmonary parameters would be compatible with successful extubation in this patient? A. Vital capacity 2.5 L B. Paco2 44 mm Hg C. Maximum inspiratory pressure –38 cm H2O D. All of the above
148. (D) The decision to stop mechanical support of the lungs is based on a variety of factors that can be measured. Guidelines suggesting that cessation of mechanical inflation of the lungs is likely to be successful include a vital capacity greater than 15 mL/kg, arterial Pao2 greater than 60 mm Hg (Fio2 < 0.5), alveolar-arterial (A–a) gradient less than 350 mm Hg (Fio2 = 1.0), arterial pH greater than 7.3, Paco2 less than 50 mm Hg, dead space/tidal volume ratio less than 0.6, and maximum inspiratory pressure of at least −20 cm H2O. In addition to these guidelines, the patient should be hemodynamically stable, conscious, oriented, and in good nutritional status (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 1288, 1297; Miller: Basics of Anesthesia, ed 6, p 667).
149. Which of the following can cause a rightward shift of the oxyhemoglobin dissociation curve? A. Methemoglobinemia B. Carboxyhemoglobinemia C. Hypothermia D. Pregnancy
149. (D) A shift to the left in the oxyhemoglobin dissociation curve occurs with fetal hemoglobin, alkalosis, hypothermia, carboxyhemoglobin, methemoglobin, and decreased levels of 2,3-DPG. Storage of blood lowers 2,3-DPG levels in acid-citrate-dextrose stored blood, but minimal changes are seen in 2,3-DPG with citrate-dextrose-stored blood. A shift to the right occurs with acidosis, hyperthermia, increased levels of 2,3-DPG, inhaled anesthetics, and pregnancy (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 516–517; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 415).
150. A 24-year-old man is brought to the operating room 1 hour after a motor vehicle accident. He has C7 spinal cord transection and ruptured spleen. Regarding his neurologic injury, anesthetic concerns include A. Risk of hyperkalemia with succinylcholine administration B. Risk of autonomic hyper-reflexia with urinary catheter insertion C. Increased risk of hypothermia D. All of the above
150. (C) With acute spinal cord injuries the major anesthetic concerns are airway management and management of hemodynamic perturbations associated with interruption of the sympathetic nervous system below the level of the transection. Hyperkalemia in response to succinylcholine does not occur until at least 24 hours after the injury. Autonomic hyper-reflexia is not a concern in the acute management of patients with spinal cord injuries. There is no evidence that awake intubation (fiberoptic) is superior to direct laryngoscopy as long as in-line traction is held in both cases. These patients are more susceptible to hypothermia compared with patients without spinal cord injuries because they lack thermoregulation below the level of the cord injury (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 255–258).
151. After sustaining traumatic brain injury, a 37-year-old patient in the ICU develops polyuria and a plasma sodium concentration of 159 mEq/L. What pathologic condition is associated with these clinical findings? A. Syndrome of inappropriate antidiuretic hormone (SIADH) B. Diabetes mellitus C. Diabetes insipidus D. Cerebral salt wasting syndrome
151. (C) Polyuria of neurogenic (rather than nephrogenic) diabetes insipidus is caused by diminished or absent antidiuretic hormone (ADH) synthesis or release following injury to the hypothalamus, pituitary stalk, or posterior pituitary gland. Hemoconcentration resulting in hypernatremia often results. In contrast, SIADH is associated with excessive amounts of ADH, which in turn causes hyponatremia. Cerebral salt wasting syndrome results from release of brain natriuretic peptide in subarachnoid hemorrhage patients. The resulting natriuresis-mediated electrolyte perturbation is hyponatremia. Diabetes mellitus and spinal shock do not cause hypernatremia (Longo: Harrison’s Principles of Internal Medicine, ed 18, pp 349–351; Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, p 1115).
152. Which of the following drugs is the best choice for treating hypotension in the setting of severe acidemia? A. Norepinephrine B. Epinephrine C. Phenylephrine D. Vasopressin
152. (D) Vasopressin, also known as antidiuretic hormone, is a naturally occurring peptide synthesized in the hypothalamus and stored in the posterior pituitary. It is used clinically to treat diabetes insipidus, and in the ICU it is used to treat hypotension. Patients with severe sepsis and septic shock have a relative deficiency of vasopressin, and these patients may be sensitive to vasopressin. Vasopressin interacts with a different receptor and, unlike the catecholamines, it is effective even in the presence of acidemia (Miller: Basics of Anesthesia, ed 6, p 676).
153. The end-tidal CO2 measured by an infrared spectrometer is 35 mm Hg. An arterial blood gas sample drawn at exactly the same moment is 45 mm Hg. Which of the following is the LEAST plausible explanation for this? A. Morbid obesity B. Pulmonary embolism C. Intrapulmonary shunt D. Chronic obstructive pulmonary disease (COPD)
153. (C) Confusion may exist between the concepts of shunt versus dead space. Both of these are forms of ˙ V/ ˙Q mismatch. With shunts, there is a gradient between the alveolar and the arterial oxygen partial pressures. Alveolar partial pressure (PA) is calculated from the alveolar gas equation. The Paco2 with shunt is compensated and is usually normal even in the presence of a significant ˙ V/ ˙Q mismatch. Dead space refers to the portion of a breath that does not reach perfused alveoli. In pathologic conditions, such as COPD, morbid obesity, and pulmonary embolism, dead space is increased because air passes into alveoli that are ventilated but not perfused. This air does not participate in gas exchange and simply exits these unperfused alveoli and “dilutes” the carbon dioxide exiting the lungs from the perfused alveoli. Under these circumstances the mixed expired CO2 measured with capnometry will be less than the actual arterial CO2 (Miller: Miller’s Anesthesia, ed 8, pp 444–445; Miller: Basics of Anesthesia, ed 6, pp 58–61).
154. A transfusion-related acute lung injury (TRALI) reaction is suspected in a 48-year-old man in the ICU after a 10-hour operation for scoliosis during which multiple units of blood and factors were administered. Which of the following items is inconsistent with the diagnosis of a TRALI reaction? A. Fever B. Alveolar-to-arterial (A–a) oxygen gradient of 25 mm Hg C. Acute rise in neutrophil count after onset of symptoms D. Bilateral pulmonary infiltrates
154. (C) TRALI reactions are a serious complication of transfusing any product containing plasma, that is, fresh frozen plasma, whole blood, packed red blood cells, platelets, or factor concretes derived from human blood. The clinical diagnosis is made 1 to 2 hours after transfusion (but may occur up to 6 hours later in the ICU). The key features include wide A–a gradient, noncardiogenic pulmonary edema, and leukopenia (not leukocytosis) secondary to sequestration in the lungs. TRALI reactions are one of the leading causes of transfusion-related mortality (Miller: Basics of Anesthesia, ed 6, p 637). 48 Part 1 Basic Sciences
155. If a central line located in the superior vena cava (SVC) is withdrawn such that the tip of the catheter is just proximal to the SVC, it would be located in which vessel? A. Subclavian vein B. Brachiocephalic vein C. Cephalic vein D. Internal jugular vein
155. (B) The right internal jugular vein and the right subclavian vein form the right brachiocephalic vein; similarly, the left internal jugular vein and the left subclavian vein form the left brachiocephalic vein. These two brachiocephalic veins form the SVC (Netter: Atlas of Human Anatomy, ed 5, plates 70, 192, 200, 205).
156. The time course of anticoagulation therapy is variable after different percutaneous coronary interventions (PCIs). Arrange the interventions in order starting with the one requiring the shortest course of aspirin and clopidogrel (Plavix) therapy to the one requiring the longest course. A. Bare-metal stent, percutaneous transluminal coronary angioplasty (PTCA), drug-eluting stent B. Drug-eluting stent, bare-metal stent, PTCA C. PTCA, drug-eluting stent, bare-metal stent D. PTCA, bare-metal stent, drug-eluting stent
156. (D) Patients who have undergone a PCI are placed on a course of a thienopyridine (ticlopidine or clopidogrel) and aspirin. The thienopyridine is used for at least 2 weeks after PTCA, 1 month after a bare-metal stent is placed, and 1 year after a drug-eluting stent is placed. Aspirin is continued for a longer period of time. This is to decrease the chance of thrombosis of the treated coronary artery (ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: Executive Summary. Anesth Analg 106:698–701, 2008).
157. Basic Life Support Working Group’s single rescuer cardiac compression-ventilation ratio for infant, child, and adult victims (excluding newborns) is A. 10:1 B. 15:2 C. 30:2 D. 60:2
157. (C) The universal compression-ventilation ratio for infant, child, and adult victims (excluding newborns) is 30 chest compressions to two breath cycles (5 cycles in 2 minutes). Once an advanced airway is in place, two rescuers no longer deliver “cycles,” but rather compressions at a rate of 100/min and ventilation is 8 to 10/min. For newborns the ratio is 3:1 (90 compressions and 30 breaths/min) (2010 AHA Guidelines for CPR and Emergency Cardiovascular Care: Circulation 122 (Suppl 3) S688, S692–S693, S913).
158. Which of the features below is suggestive of weaponized anthrax exposure as opposed to a common flulike viral illness? A. Widened mediastinum B. Fever, chills, myalgia C. Severe cough D. Pharyngitis Respiratory Physiology and Critical Care Medicine 35
158. (A) After an incubation period (commonly within 2 weeks), inhalational anthrax symptoms initially look like viral flu (fever, chills, myalgia, and a nonproductive cough). Although leukocytosis is common with anthrax and rare with viral flu, white blood cell (WBC) counts initially may be normal at the time the patient presents. After a short while, the patient suddenly appears critically ill, and without treatment, death can occur within a few days. Substernal chest pain, hypoxemia, cyanosis, dyspnea, abdominal pain, and sepsis syndrome are common with inhaled anthrax but rare with viral flu. After the anthrax spores are inhaled, macrophages phagocytize the spores and transport them to mediastinal lymph nodes where the spores germinate, producing enlarged nodes and a widened mediastinum on the chest x-ray film. A widened mediastinum is not seen with viral flu. Pharyngitis is common with viral flu and occasionally is seen with anthrax (Miller: Basics of Anesthesia, ed 6, pp 691–693; Longo: Harrison’s Principles of Internal Medicine, ed 18, pp 1769–1771).
159. Which of the following factors could not explain a Pao2 of 48 mm Hg in a patient breathing a mixture of nitrous oxide and oxygen? A. Hypoxic gas mixture B. Eisenmenger syndrome C. Profound anemia D. Hypercarbia
159. (C) To answer this question it is helpful to review the alveolar gas equation: PAO2 = FIO2 (Pb − PH2O) − PaCO2/R Pao2 = partial pressure of oxygen in the alveolar gas; Fio2 = fraction of inhaled oxygen; Pb = barometric pressure; Ph2o = vapor pressure at 100% saturation (47 mm Hg at 37° C); Paco2 = partial pressure of CO2 in the alveolar gas; R = respiratory quotient. Any factor that lowers Pao2 (below 100 mm Hg or so) will also lower Pao2. Hypoxic gas mixture lowers Fio2, hence Pao2. Hypercarbia makes the term Paco2/R larger and, therefore, reduces Pao2. Eisenmenger syndrome results in a larger shunt fraction and lower Pao2 on that basis (see explanation to Question 147). In normally functioning lungs, anemia has a minimal impact on Pao2 because physiologic shunt is normally only 2% to 5% of cardiac output (Barash: Clinical Anesthesia, ed 6, pp 277–278).
160. During a left hepatectomy under general isoflurane anesthesia, arterial blood gases are: O2 138, CO2 39, pH 7.38, saturation 99%. At the same time, CO2 on infrared spectrometer is 26 mm Hg. The most plausible explanation for the difference between CO2 measured with infrared spectrometer versus arterial blood gas gradient is A. Mainstem intubation B. Atelectasis C. Shunting through thebesian veins D. Hypovolemia
160. (D) The difference between the Paco2 and the CO2 value measured by the infrared spectrometer is a function of the patient’s physiologic dead space. Physiologic dead space is equal to anatomic dead space plus alveolar dead space. Anatomic dead space is roughly 1 mL/lb of body weight. Because anatomic dead space is relatively “fixed,” changes in physiologic dead space are mainly attributable to changes in alveolar dead space. Alveoli that are ventilated, but not perfused, add to alveolar dead space. In essence, air goes into these alveoli but does not participate in gas exchanges and merely exits the alveoli upon exhalation. Ventilation of dead space serves no useful purpose but does result in “dilution” of the exhaled CO2, thus explaining why the CO2 seen on the infrared spectrometer can be substantially lower than that obtained from arterial blood gas analysis. Several factors increase dead space, including lung diseases such as COPD, cystic fibrosis, and pulmonary emboli. In addition, decreased alveolar perfusion from low cardiac output or hypovolemia may also contribute to increased dead space. Mainstem intubation, atelectasis, shunting through thebesian veins, and ablation of hypoxic pulmonary vasoconstriction by isoflurane are various causes of shunting. Shunting is also a mismatch between ventilation and perfusion, but, in contrast to ˙ V/ ˙Q mismatch from dead space ventilation, shunting results in a normal or nearly normal Paco2 but a larger-than-expected A–a O2 gradient. The only choice in this question that would explain an increase in dead space ventilation is hypovolemia (Barash: Clinical Anesthesia, ed 7, pp 276–277; Miller: Basics of Anesthesia, ed 6, pp 328–329). Respiratory Physiology and Critical Care Medicine 49
161. Under which set of circumstances would energy expenditure per day be the greatest? A. Sepsis with fever B. 60% burn C. Multiple fractures D. 1 hour status post liver transplantation
161. (B) The normal human’s resting energy expenditure as well as the postoperative state is about 1800 kcal/24 hr. With starvation (20 days), energy expenditure decreases to about 1080 kcal/day (60% of normal). Patients who have sustained multiple fractures (2160 kcal/day or 120% of normal), major sepsis (2520 kcal/day or 140% of normal), and burns have increased energy expenditures. The energy expenditure in a patient with a major burn also depends on the temperature of the room. The highest energy expenditure is at a room temperature of 25° C (3819 kcal/day or 212% of normal) and is lower at 33° C (3342 kcal/day or 185% of normal) and at 21° C (3600 kcal/day or 200% of normal) (Miller: Miller’s Anesthesia, ed 8, pp 3136–3138).
162. Select the FALSE statement regarding amiodarone (Cordarone). A. It is shown to decrease mortality after myocardial infarction B. It is indicated for ventricular tachycardia and fibrillation refractory to electrical defibrillation C. Adverse effects include pulmonary fibrosis and thyroid dysfunction D. It is useful in treatment of torsades de pointes
162. (D) Amiodarone is useful in the treatment of a variety of supraventricular and ventricular cardiac arrhythmias. For the treatment of ventricular tachycardia or fibrillation that is refractory to electrical defibrillation, the recommended dose is 300 mg IV. Similar to β-blockers, amiodarone decreases mortality after myocardial infarctions. About 5% to 15% of treated patients develop pulmonary toxicity (especially when doses are >400 mg/day, or underlying lung disease is present) and 2% to 4% develop thyroid dysfunction (amiodarone is a structural analog of thyroid hormone). It has a prolonged elimination halftime of 29 hours and a large volume of distribution. Because it prolongs the QTc interval, it may lead to the production of ventricular tachydysrhythmias and thus is not useful in treating torsades de pointes (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 834, 837).
163. A 58-year-old woman is awaiting orthotopic liver transplantation for primary biliary cirrhosis in the ICU. An oximetric pulmonary artery catheter is placed and an Svo2 of 90% is measured. Which of the following blood pressure interventions is the LEAST appropriate for treatment of hypotension in this patient? A. Milrinone B. Norepinephrine C. Vasopressin D. Phenylephrine
163. (A) Patients with cirrhosis have hyperdynamic circulations as noted here with the elevated Svo2 of 90%. The cardiac output is usually increased, peripheral vascular resistance is low, intravascular volume is increased, and arteriovenous shunts are present. Hypotension is common. Milrinone is a positive inotrope with vasodilating properties, something this patient does not need. If a treatment for hypotension is needed, drugs with α-agonist properties may be helpful. In addition, vasopressin is also a good choice because it increases systemic vascular resistance (SVR) but does not increase the already high cardiac output (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, p 714; Miller: Basics of Anesthesia, ed 6, p 457).
164. Each of the following measures is part of the Surgical Care Improvement Project (SCIP) with the goal of preventing perioperative infection EXCEPT A. Normothermia B. Oxygen saturation above 95% in the OR C. Appropriate hair removal preoperatively D. Removal of urinary catheter by postoperative day 2
164. (B) For many years hand hygiene, wearing surgical masks, and sterile techniques have been used to decrease surgical site infections (SSIs). The CDC has also recommended that patients undergo preoperative showering using antiseptic skin wash products to reduce skin bacteria despite no clear studies showing a direct independent relationship decreasing SSIs. In 2004, the National Surgical Infection Prevention Project gave guidelines for antibiotic prophylaxis, whenever there is more than minimal risk of infection. Prophylactic antibiotics should be administered within 1 hour before surgical incision in appropriately selected patients and discontinued within 24 hours after the surgical end time or 48 hours for cardiac patients. More recently, using evidence-based research, the SCIP has suggested several additional measures to decrease the incidence of surgical site infections, including appropriate hair removal at the surgical site (e.g., using depilatory cream or hair clippers rather than razors), glycemic control in cardiac surgical patients (e.g., serum glucose <200 mg/dL the morning after surgery), removal of urinary catheters (e.g., removal on postoperative day 1 or 2 and reassessment of the need every day thereafter), and maintenance of perioperative normothermia (e.g., core temperature should be 36° C on arrival in the PACU). Interestingly, surgical time was not mentioned (Barash: Clinical Anesthesia, ed 7, pp 304–314; Miller: Basics of Anesthesia, ed 6, pp 746–752; Miller: Miller’s Anesthesia, ed 8, pp 100–101, 1104 ).
165. A 55-year-old man with polycystic liver disease undergoes an 8-hour right hepatectomy. The patient receives 5 units of packed red cells, 1000 mL albumin, and 6 L normal saline. The patient is extubated and taken to a postanesthesia care unit (PACU) where ABGs are: Pao2 135, Paco2 44, pH 7.17, base deficit −11, [HCO3 −], 12, 97% saturation, [Cl−] 119, [Na+] 145, and [K+] 5.6. The most likely cause for this acidosis is A. Lactic acid B. Use of normal saline C. Diabetic ketoacidosis D. Polyethylene glycol from bowel prep
165. (B) This patient has a metabolic acidosis. Recall that anion gap = [Na+] − ([Cl−] + [HCO3 −]) and is normally 10 to 12 nmol/L. In this case the anion gap = 145 − (119 + 12) = 14, which is slightly above the normal anion gap range. In looking at this case, the acidosis is quite profound and would most likely be related to the rapid infusion of normal saline. Lactic acid, ketoacidosis, and ethylene glycol produce a high anion gap metabolic acidosis. Narcotics may produce respiratory but not metabolic acidosis. See also Question 142 (Longo: Harrison’s Principles of Internal Medicine, ed 18, pp 365–369; Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, p 1165).
166. Which of the following is the LEAST appropriate use of noninvasive positive-pressure ventilation (NIPPV)? A. Acute respiratory distress syndrome (ARDS) B. COPD exacerbation C. Obstructive sleep apnea D. Multiple sclerosis exacerbation
166. (A) Noninvasive positive-pressure ventilation (NIPPV) refers to delivering positive-pressure ventilation to patients by way of a nasal mask, or full face mask, without the placement of an endotracheal or tracheostomy tube. This mode of therapy requires conscious and cooperative patients and does not protect the airway. NIPPV has been very useful in COPD patients and in immunosuppressed patients in acute respiratory failure. It most likely will fail (i.e., intubation would be needed) in patients with pneumonia and ARDS (Miller: Miller’s Anesthesia, ed 8, p 3068). 50 Part 1 Basic Sciences
167. A 68-year-old asthmatic drunk driver comes into the ER after being in a motor vehicle accident. After a difficult intubation, you fail to observe end-tidal CO2 on the monitor. Reasons for this include all of the following EXCEPT A. You intubated the esophagus by mistake B. You forgot to ventilate the patient C. The connection between the circuit and monitor has become disconnected D. The patient also has a pneumothorax, and high airway pressures are needed to adequately ventilate the patient
167. (D) Capnography has been a valuable monitor for the cardiac and pulmonary systems as well as checking the anesthetic equipment. Forgetting to ventilate the patient, intubating the esophagus, and having the sensing tube become disconnected from the monitor quickly will show no CO2 detected. Any significant reduction in lung perfusion (i.e., air embolism, decreased cardiac output, or decreased blood pressure) increases alveolar dead space and leads to a lowering of the detected CO2. A cardiac arrest where there is no blood flow to the lungs and hence no carbon dioxide going to the lungs would also result in no detectable CO2. As CPR is started, detectable CO2 would be a sign of lung perfusion and ventilation. A patient with a pneumothorax and high airway pressures would still give you CO2 readings (Butterworth: Morgan & Mikhail’s Clinical Anesthesia, ed 5, pp 125–127).
168. A 30-year-old woman has undergone a 2-hour abdominal surgical procedure and is sent to the ICU intubated for postoperative monitoring due to suspected sepsis. Three hours later, the ventilator malfunctions and the resident disconnects the patient from the ventilator and hand ventilates the patient with 100% oxygen. The patient has good bilateral breath sounds, the chest rises nicely, and moisture is seen in the ETT. Shortly thereafter, the patient’s heart rate slows to 30 beats/min and the blood pressure is 50 mm Hg systolic. The next intervention that should be done, in addition to chest compressions, is A. Administer atropine B. Start epinephrine C. Confirm ETT position D. Apply external pacemaker 36 Respiratory Physiology and Critical Care Medicine Answers, References, and Explanations
168. (C) Always confirm an adequate Airway and Breathing before treating a Cardiac rhythm (A, B before C). Having the ETT in proper position for several hours does not ensure that it remains in proper position. In this case, the ETT slipped out of the trachea and went into the esophagus. The only way you know the ETT is in the trachea is to see the tube passing between the vocal cords directly with a conventional laryngoscope or by putting a fiberoptic bronchoscope through the tube and seeing carina. Other forms of confirmation such as bilateral breath sounds, adequate chest rise, and moisture in the tube are helpful but could also be seen with an esophageal intubation. Getting a consistent and adequate end tidal CO2 on a monitor confirms some gas exchange, but in cases where blood does not get to the lungs, as in a cardiac arrest, CO2 cannot be removed from the lungs. The first part in the treatment of bradycardia is adequate ventilation with oxygen. After that the other choices may be indicated (Miller: Miller’s Anesthesia, ed 8, p 1654). 51
169. Which of the following muscle relaxants is eliminated the most by renal excretion? A. Pancuronium B. Vecuronium C. Atracurium D. Rocuronium
169. (A) The duration of action of neuromuscular blocking drugs is related to the dose administered, as well as how the drug is metabolized or handled in the body. Succinylcholine normally is rapidly metabolized by plasma cholinesterase and has an ultrashort duration of action. The intermediate-duration neuromuscular blockers atracurium and cisatracurium undergo chemical breakdown in the plasma (Hofmann elimination), as well as ester hydrolysis. Vecuronium and rocuronium also have intermediate duration of actions and undergo primarily hepatic metabolism and biliary excretion with limited renal excretion (10%-25%). Only the long-duration neuromuscular blocker pancuronium is primarily excreted in the urine (80%). In patients with renal failure, the duration of action of neuromuscular blockers is not prolonged with atracurium or cisatracurium; is slightly prolonged with vecuronium and rocuronium; and is markedly prolonged with d-tubocurarine, pancuronium, doxacurium, and pipecuronium. Of the long-duration drugs, 80% of pancuronium, 70% of doxacurium, and 70% of pipecuronium are renally excreted unchanged in the urine. d-tubocurarine has a little more liver excretion and a little less renal elimination compared with pancuronium (Miller: Miller’s Anesthesia, ed 8, pp 975–977). COMPARATIVE PHARMACOLOGY OF NONDEPOLARIZING NEUROMUSCULAR BLOCKING DRUGS Drug ED95 (mg/ kg) Onset to Maximum Twitch Depression (min) Duration to Return to ≥25%* Intubating Dose (mg/kg) Continuous Infusion (mg/kg/ min) Renal Excretion (% Unchanged) Hepatic Degradation (%) Biliary Excretion (% Unchanged) Hydrolysis in Plasma Pancuronium 0.07 3-5 60-90 0.1 80 10 5-10 No Vecuronium 0.05 3-5 20-35 0.08-0.1 1 15-25 20-30 40-75 No Rocuronium 0.3 1-2 20-35 0.6-1.2 10-25 10-20 50-70 No Atracurium 0.2 3-5 20-35 0.4-0.5 6-8 NS NS NA Enzymatic, spontaneous Cisatracurium 0.05 3-5 20-35 0.1 1-1.5 NS NS NS Spontaneous Mivacurium 0.08 2-3 12-20 0.25 5-6 NS NS NS Enzymatic NA, not applicable; NS, not significant. *Control twitch height (minutes). From Miller RD: Basics of Anesthesia, ed 6, Philadelphia, Saunders, 2011, p 151, Table 12-6.
170. All of the following conditions may develop when using propofol for prolonged sedation in the intensive care unit (ICU) EXCEPT A. Pancreatitis B. Hyperlipidemia C. Metabolic acidosis D. Adrenal suppression
170. (D) Pancreatitis has been reported in patients on long-term propofol infusions. Because of the high fat content of propofol solutions (propofol is insoluble in aqueous solutions and is marketed as an emulsion containing 10% soybean oil, 2.25% glycerol, and 1.2% purified egg phosphatide), patients on long-term infusion should be checked for hyperlipidemia and patients receiving TPN should have the Intralipid portion of the TPN reduced. Propofol infusion syndrome is commonly defined as an acute onset of metabolic acidosis associated with cardiac dysfunction (e.g., bradycardia or right bundle branch block), and one of the following: rhabdomyolysis, hypertriglyceridemia, enlarged liver, or renal failure. Propofol decreases myocardial contractility and reduces systemic vascular resistance but does not cause adrenal suppression. The latter is a feature of etomidate administration (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 536–537; Miller: Basics of Anesthesia, ed 6, p 671).
171. Which of the following β-adrenergic antagonists is a nonselective β1 and β2 blocker? A. Atenolol B. Nadolol C. Esmolol D. Metoprolol
171. (B) β-Adrenergic receptor antagonists are of three generations. First-generation antagonists are nonselective β1 and β2 receptor blockers and include nadolol (Corgard), propranolol (Inderal), sotalol (Betapace), and timolol (Blocadren, Timoptic). Second-generation antagonists are cardioselective β1 receptor blockPharmacology and Pharmacokinetics of Intravenous Drugs 63 ers and include acebutolol (Sectral), atenolol (Tenormin), bisoprolol (Zebeta), esmolol (Brevibloc), and metoprolol (Lopressor). Third-generation β-adrenergic antagonists (mixed antagonists) have nonselective β1 and β2 receptor blocking actions and have additional cardiovascular effects (α1-adrenergic antagonist) and include labetalol (Normodyne, Trandate) and carvedilol (Coreg). Carvedilol also has some antioxidant and anti-inflammatory effects as well. Many of these drugs have additional trade names (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 320–330; Hemmings; Pharmacology and Physiology for Anesthesia, pp 228–229; Miller: Miller’s Anesthesia, ed 8, pp 370–371).
172. A 78-year-old patient with Parkinson disease undergoes a cataract operation under general anesthesia. In the recovery room, the patient has two episodes of emesis and complains of severe nausea. Which of the following antiemetics would be the best choice for treatment of nausea in this patient? A. Droperidol B. Promethazine C. Ondansetron D. Metoclopramide
172. (C) Parkinson disease (paralysis agitans or shaking palsy) is a degenerative CNS disease. It is caused by greater than 80% destruction of dopaminergic neurons in the substantia nigra of the basal ganglia. Dopamine acts as a neurotransmitter to inhibit the rate of firing of neurons that control the extrapyramidal motor system. The imbalance of neurotransmitters that results leads to the extrapyramidal symptoms of this disease. Symptoms include bradykinesia (slowness of movement), muscular rigidity, resting tremor (that lessens with voluntary movement), and impaired balance. Drugs that can produce extrapyramidal effects, such as the dopamine antagonists droperidol, promethazine, and thiethylperazine, as well as the dopamine and serotonin antagonist metoclopramide, are contraindicated. Ondansetron, a 5-hydroxytryptamine type 3 (5-HT3) receptor antagonist, is the preferred drug to treat nausea and vomiting for this patient (Barash: Clinical Anesthesia, ed 7 , p 621; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 646–647).
173. Which of the following diseases is associated with increased resistance to neuromuscular blockade with succinylcholine? A. Myasthenia gravis B. Myasthenic syndrome C. Huntington chorea D. Polymyositis
173. (A) In order for depolarizing muscle relaxants such as succinylcholine to work, the drug must interact with the receptor at the myoneural junction. Patients with myasthenia gravis have fewer acetylcholine receptors on the muscle and are more resistant to succinylcholine but are much more sensitive to nondepolarizing muscle relaxants. Patients with myasthenic syndrome (Eaton-Lambert syndrome) have a decreased release of acetylcholine at the myoneural junction; however, the number of receptors is normal. Patients with myasthenic syndrome are more sensitive to both depolarizing and nondepolarizing muscle relaxants. Huntington chorea is a degenerative CNS disease that is associated with decreased plasma cholinesterase activity, and prolonged responses to succinylcholine use have been seen. The response to depolarizing and nondepolarizing muscle relaxants appears to be unchanged in patients with polymyositis. Succinylcholine is contraindicated in patients with Duchenne muscular dystrophy because of the risks of rhabdomyolysis, hyperkalemia, and cardiac arrest. Nondepolarizing muscle relaxants have a normal response in patients with Duchenne muscular dystrophy, although some patients have prominent coexisting skeletal muscle weakness (Fleisher: Anesthesia and Uncommon Diseases, ed 6, pp 264–265, 313–316, 574; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 247, 444, 448–452).
174. Sedation with which of the following drugs is most likely to resemble normal sleep? A. Propofol B. Midazolam C. Dexmedetomidine D. Ketamine
174. (C) Sedation is commonly used in the ICU to prevent patient injury, decrease anxiety, reduce pain, reduce sympathetic stimulation, and help with ventilator dyssynchrony. Many different drugs have been used, including barbiturates, narcotics (e.g., fentanyl, morphine), benzodiazepines (e.g., midazolam, lorazepam), etomidate, ketamine, antipsychotics (e.g., haloperidol), propofol, and α2-adrenergic agonists (e.g., dexmedetomidine). Although deep sedation was commonly used, more recent evidence has suggested that patients tend to have fewer complications with light sedation and daily awakening (e.g., shorter duration of mechanical ventilation, less cardiovascular depression, and shorter ICU stays). The choice of drugs depends on the particular indications. Dexmedetomidine has several desirable effects, especially in the neurosurgical ICU, including sedation, analgesia, and little effect on respiratory drive. Its sedative properties resemble normal sleep in that the sedated patient can be easily aroused with stimulation and then rapidly fall back to sleep after stimulation ends. Dexmedetomidine does have some disadvantages, such as cost and U.S. Food and Drug Administration (FDA)-approved use for only 24 hours (Barash: Clinical Anesthesia, ed 7, pp 1584, 1599–1600; Miller: Basics of Anesthesia, ed 6, p 672).
175. Which of the following intravenous anesthetics is converted from a water-soluble to a lipid-soluble drug after exposure to the bloodstream? A. Propofol B. Midazolam C. Ketamine D. None of the above
175. (B) Diazepam (Valium) and lorazepam are water-insoluble benzodiazepines and are usually mixed with propylene glycol to become soluble solutions. These propylene glycol solutions are painful when injected. Midazolam has an imidazole ring that allows the drug to be water soluble in an acid pH (pH 3.5). When injected into the bloodstream, midazolam is exposed to the higher physiologic pH and the ring changes shape and the drug becomes lipid soluble. The lipid-soluble form readily crosses the blood-brain barrier to exert its pharmacologic effects. None of the other drugs change form with different pH (Hemmings: Pharmacology and Physiology for Anesthesia, pp 144–145). 64 Part 1 Basic Sciences
176. A 33-year-old, 70-kg patient is brought to the operating room for resection of an anterior pituitary prolactin-secreting tumor. Anesthesia is induced with sevoflurane, nitrous oxide, and oxygen. The patient is intubated and nitrous oxide is discontinued. Anesthesia is maintained with 1.2 minimum alveolar concentration (MAC) sevoflurane in oxygen. The surgeon plans to inject epinephrine into the nasal mucosa to minimize bleeding. What is the maximum volume of a 1:100,000 epinephrine solution that can be administered safely to this patient without producing ventricular arrhythmias? A. 55 mL B. 45 mL C. 35 mL D. 25 mL
176. (C) The amount of submucosally injected epinephrine required to produce ventricular cardiac dysrhythmias (i.e., three or more premature ventricular contractions during or after injection) varies with the volatile anesthetic administered. Patients under halothane anesthesia are particularly sensitive to ventricular arrhythmias, whereas patients with isoflurane, desflurane, and sevoflurane are less sensitive to epinephrine. Fifty percent of patients have ventricular arrhythmias when a dose of 2.1 μg/kg of epinephrine is administered submucosally into patients under halothane anesthesia. Ventricular arrhythmias do not seem to occur when a dose of up to 5 μg/kg of epinephrine is injected submucosally into patients under 1.2 MAC of sevoflurane or isoflurane in oxygen anesthesia. However, when the dose of epinephrine is increased to between 5 and 15 μg/kg, then about one third of patients will exhibit ventricular ectopy under sevoflurane or isoflurane anesthesia. Thus, using the 5 μg/kg maximum dose, a 70-kg patient could receive up to 350 μg of epinephrine (70 kg × 5 μg/kg) or 35 mL of this 1:100,000 solution (10 μg/mL) without ventricular arrhythmias (Johnston: A comparative interaction of epinephrine with enflurane, isoflurane and halothane in man. Anesth Analg 55:709–712, 1976; Navarro: Humans anesthetized with sevoflurane or isoflurane have similar arrhythmic response to epinephrine. Anesthesiology 80:545–549, 1994; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 54–56; Miller: Miller’s Anesthesia, ed 8, p 713).
177. Patients receiving antihypertensive therapy with propranolol are at increased risk for each of the following EXCEPT A. Blunted response to hypoglycemia B. Bronchoconstriction C. Rebound tachycardia after discontinuation D. Orthostatic hypotension
177. (D) β-Adrenergic receptor antagonists are effective in the treatment of essential hypertension and angina pectoris. They can be used to decrease mortality in patients suffering myocardial infarctions; to treat hyperthyroidism or hypertrophic obstructive cardiomyopathy; and to prevent migraine headaches. Although they are useful drugs, their use is limited by many side effects, which include bronchoconstriction, suppression of insulin secretion, blunting of the catecholamine response to hypoglycemia, excessive myocardial depression, atrioventricular heart block, accentuated increases in plasma concentrations of potassium with intravenous infusion of potassium chloride, fatigue, and rebound tachycardia associated with abrupt drug discontinuation. An important advantage of β-adrenergic receptor antagonists used in treating hypertension is the lack of orthostatic hypotension (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 320–324; Miller: Basics of Anesthesia, ed 6, pp 745–775; Miller: Miller’s Anesthesia, ed 8, pp 1217–1218).
178. Atropine causes each of the following EXCEPT A. Decreased gastric acid secretion B. Inhibition of salivary secretion C. Increased lower esophageal sphincter tone D. Mydriasis
178. (C) Anticholinergics are rarely given with premedication today unless a specific effect is needed (e.g., drying of the mouth before fiberoptic intubation, prevention of bradycardia, and, rarely, as a mild sedative). Side effects are many and include relaxation or a decrease of the lower esophageal sphincter tone that may make patients more likely to regurgitate gastric contents. Although these drugs can decrease gastric acid secretion and increase gastric pH, the pH effects are small and the dose needed to accomplish this is much higher than clinically used. The following table compares the effects of various anticholinergics (Hemmings, Pharmacology and Physiology for Anesthesia, pp 229–232; Miller: Basics of Anesthesia, ed 6, pp 75–76; Miller: Miller’s Anesthesia, ed 8, pp 377-378). COMPARATIVE EFFECTS OF ANTICHOLINERGICS ADMINISTERED INTRAMUSCULARLY AS PHARMACOLOGIC PREMEDICATION Effect Atropine Scopolamine Glycopyrrolate Antisialagogue effect + +++ ++ Sedative and amnesic effects + +++ 0 Increased gastric fluid pH 0 0 0/+ Central nervous system toxicity + ++ 0 Relaxation of lower esophageal sphincter ++ ++ ++ Mydriasis and cycloplegia + +++ 0 Heart rate ++ 0/+ + From Miller RD: Basics of Anesthesia, ed 6, Philadelphia, Saunders, 2011, p 76, Table 7-3.
179. Which of the following drugs is capable of crossing the blood-brain barrier? A. Neostigmine B. Pyridostigmine C. Edrophonium D. Physostigmine
179. (D) Neostigmine, pyridostigmine, edrophonium, and physostigmine are anticholinesterase drugs. Neostigmine, pyridostigmine, and edrophonium are quaternary ammonium compounds and do not pass the blood-brain barrier. However, physostigmine is a tertiary amine and does cross the blood-brain barrier. This property makes physostigmine useful in the treatment for central anticholinergic syndrome (also called postoperative delirium or atropine toxicity) (Barash: Clinical Anesthesia, ed 7, pp 382–383). Pharmacology and Pharmacokinetics of Intravenous Drugs 65
180. Which drug exerts its main central nervous system (CNS) action by inhibiting the N-methyl-d-aspartate (NMDA) receptors? A. Propofol B. Midazolam C. Etomidate D. Ketamine
180. (D) Whereas propofol, barbiturates, etomidate, and benzodiazepines exert much, if not all, of their pharmacologic effects via the GABA receptors, ketamine has only weak activity on the GABA receptors. Ketamine’s mechanism of action is complex, with most of the effects due to interaction with NMDA receptors. Ketamine also interacts with monoaminergic, muscarinic, and opioid receptors, as well as voltage-sensitive calcium ion channels (Miller: Basics of Anesthesia, ed 6, pp 109–110).
181. Which of the following opioid-receptor agonists has anticholinergic properties? A. Morphine B. Hydromorphone C. Sufentanil D. Meperidine
181. (D) All of the drugs listed are opioids. Meperidine is structurally similar to atropine and possesses mild anticholinergic properties. In contrast to other opioid-receptor agonists, meperidine rarely causes bradycardia but can increase heart rate. Normeperidine, a metabolite of meperidine with some CNS-stimulating properties, may cause delirium and seizures if the level is high enough. This is more likely in patients who have renal impairment and are receiving meperidine over several days (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 102–104).
182. Which of the following statements about ketamine is FALSE? A. In the United States, it is a racemic mixture of two isomers B. It is a potent cerebral vasodilator and can increase intracranial pressure (ICP) C. Respiratory depression rarely occurs with induction doses D. Its metabolite norketamine is more potent than the parent compound
182. (D) In the United States, ketamine is prepared as a mixture of the two isomers S(+) and R(−). In some countries, the S(+) isomer, which is more potent and has fewer side effects, is available. All of the statements are true except for answer D. Norketamine (ketamine’s primary active metabolite) is one fifth to one third as potent as ketamine and can contribute to prolonged effects (Barash: Clinical Anesthesia, ed 7, pp 743–747; Miller: Basics of Anesthesia, ed 6, pp 109–111).
183. Which of the following vasopressor agents increases systemic blood pressure (BP) indirectly by stimulating the release of norepinephrine from sympathetic nerve fibers and directly by binding to adrenergic receptors? A. Vasopressin B. Ephedrine C. Epinephrine D. Phenylephrine
183. (B) Direct-acting sympathomimetic drugs work directly on the receptors. Indirect-acting sympathomimetic drugs have their effects primarily by entering the neurons and then displacing norepinephrine and causing the release of norepinephrine from the postganglionic sympathetic nerve fibers. Ephedrine, mephentermine, and metaraminol are primarily indirect-acting sympathomimetic agents that also may have some direct-acting properties. The following table summarizes the sympathomimetic agents and their effects on the adrenergic receptors (Miller: Basics of Anesthesia, ed 6, pp 72–73). CLASSIFICATION AND COMPARATIVE PHARMACOLOGY OF SYMPATHOMIMETICS Sympathomimetic α β1 β2 Mechanism of Action Amphetamine ++ + + Indirect Dobutamine 0 +++ 0 Direct Dopamine ++ ++ + Direct Ephedrine ++ + + Indirect and some direct Epinephrine + ++ ++ Direct Isoproterenol 0 +++ +++ Direct Mephentermine ++ + + Indirect Metaraminol ++ + + Indirect and some direct Methoxamine +++ 0 0 Direct Norepinephrine +++ ++ 0 Direct Phenylephrine +++ 0 0 Direct From Stoelting RK: Pharmacology and Physiology in Anesthetic Practice, ed 4, Philadelphia, Lippincott Williams & Wilkins, 2006, p 293.
184. Methadone-induced constipation could be reversed without loss of analgesic effect with which of the following opioid antagonists? A. Naloxone B. Nalmefene C. Naltrexone D. Methylnaltrexone
184. (D) Naloxone, naltrexone, and nalmefene are opioid receptor antagonists that can reverse the central and peripheral effects of opioids (e.g., methadone). Methylnaltrexone is a quaternary ammonium opioid receptor antagonist that does not penetrate the CNS (i.e., does not reverse analgesia) but does antagonize peripheral opioid receptors (i.e., blocks the GI tract’s opioid receptors and can treat opioid-induced constipation). Because of its structure it is not absorbed after oral administration, so it is administered by injection (Hemmings: Pharmacology and Physiology for Anesthesia, pp 265–267; Miller: Miller’s Anesthesia, ed 8, pp 904–906).
185. The treatment of patients with human immunodeficiency virus (HIV) may include indinavir, nelfinavir, or ritonavir. What anesthetic consideration is significant with these drugs? A. Decreased platelet function B. Increased sensitivity to midazolam C. Hypoglycemia D. Hyperkalemia
185. (B) Patients with HIV take at least three drugs simultaneously during their treatment. A variety of antiretroviral drugs such as nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse 66 Part 1 Basic Sciences transcriptase inhibitors (NNRTIs), entry inhibitors, integrase inhibitors, and/or protease inhibitors are used. Indinavir, nelfinavir, and ritonavir are three of many protease inhibitors currently available. All protease enzyme inhibitors have metabolic drug interactions. Most (especially ritonavir in clinical doses) irreversibly inhibits CYP3A4 and this inhibition could last for 2 to 3 days after the drug is stopped. CYP3A4 is involved in the metabolism of benzodiazepines (e.g., midazolam) and many opioids (e.g., fentanyl), and these drugs will have higher concentrations and prolonged elimination times when protease inhibitors are used. Protease inhibitors can also induce the production of the CYP enzymes allowing some drugs (e.g., estrogens) to be metabolized more quickly. In addition, protease inhibitors may cause glucose intolerance, disorders in lipid metabolism, premature atherosclerosis, and diastolic dysfunction leading to heart failure, as well as acute tubular necrosis and nephrolithiasis (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 1623–1660; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 484–491).
186. Neurokinin-1 (NK1) antagonists such as aprepitant have all the following properties EXCEPT A. Anxiolytic B. Antidepressant C. Analgesic D. Antiemetic
186. (C) Aprepitant is an NK1 antagonist (substance P antagonist) with a long half-life of 9 to 13 hours. It is orally administered for the prevention and treatment of PONV, although it seems better in preventing vomiting. NK1 antagonists may act synergistically with 5-HT3 antagonists and/or dexamethasone. Aprepitant is not associated with QTc prolongation. Although marketed for its antiemetic effects, it has some anxiolytic and mild antidepressant effects as well (Hemmings: Pharmacology and Physiology for Anesthesia, p 512; Miller: Miller’s Anesthesia, ed 8, pp 2637, 2967–2968).
187. Which of the following drugs should be administered with caution to patients receiving echothiophate for the treatment of glaucoma? A. Atropine B. Succinylcholine C. Ketamine D. Remifentanil
187. (B) Echothiophate is an organophosphate that inhibits acetylcholinesterase as well as pseudocholinesterase, which is responsible for the metabolism of succinylcholine and ester-type local anesthetics. It does this by forming a phosphorylated complex with acetylcholinesterase. The topical solution is instilled in the eye for treatment of refractory open-angle glaucoma. The amount of drug absorbed may be sufficient to inhibit acetylcholinesterase and cause prolongation in the duration of action of succinylcholine or mivacurium. Because of this, it is “recommended” to wait at least 3 weeks after the stoppage of echothiophate before the administration of these two muscle relaxants. One must wonder about these “recommendations” because clinical cases have shown that when cholinesterase activity is decreased (from echothiophate) to no activity, the increase in duration of neuromuscular block from succinylcholine was less than 25 minutes (Miller: Miller’s Anesthesia, ed 8, p 379).
188. When one of four thumb twitches in the train-of-four (TOF) stimulation of the ulnar nerve can be elicited, how much suppression would there be if you were measuring a single twitch? A. 20 to 25 B. 45 to 55 C. 75 to 80 D. 90 to 95
188. (D) Monitoring neuromuscular blockade for nondepolarizing muscle relaxants can be done in a variety of ways. The simplest way is to measure the reduction or suppression of a single twitch height. This is commonly performed by observing the twitch response of the thumb’s adductor pollicis muscle, after ulnar nerve stimulation. At 90% to 95% reduction of twitch height (i.e., ED90 to ED95) there is good muscle relaxation for intubation and intra-abdominal surgery. However, measuring the reduction of twitch height is not practical. Because there is good correlation between reduction of twitch height and the number of thumb twitches that can be elicited by TOF stimulation, TOF stimulation is more commonly used where four twitches are administered over 2 seconds. If only one twitch of a TOF is demonstrated, single twitch height is depressed at least 85%; with two to four thumb twitches, 70% to 85% depression is seen. Note that the presence of four twitches does not mean that neuromuscular function has completely recovered; in fact, a significant number of receptors may still be occupied by the muscle relaxant (Barash: Clinical Anesthesia, ed 7, p 544).
189. Which of the following muscle relaxants causes slight histamine release at two to three times the ED95 (effective dose in 95% of subjects) dose? A. Rocuronium B. Pancuronium C. Atracurium D. Cisatracurium
189. (C) There are two major chemical classes of nondepolarizing muscle relaxants: the aminosteroids (-onium drugs) and the benzylisoquinolinium (-urium) drugs. In general, the aminosteroids cause no significant histamine release (at the clinical doses of 2 to 3 × ED95), whereas some of the benzylisoquinolinium drugs can. The histamine release primarily occurs with rapid administration of atracurium but does not occur with cisatracurium or doxacurium. The amount of histamine released is rarely of clinical significance. The cardiovascular effects of neuromuscular blocking drugs occur by three main mechanisms: (1) drug-induced histamine release; (2) effects at cardiac muscarinic receptors; or (3) effects on nicotinic receptors at autonomic ganglia. The following table summarizes the mechanisms for the cardiovascular effects of muscle relaxants (Miller: Miller’s Anesthesia, ed 7, p 882). Pharmacology and Pharmacokinetics of Intravenous Drugs 67 CLINICAL AUTONOMIC EFFECTS OF NEUROMUSCULAR BLOCKING DRUGS Drug Autonomic Ganglia Cardiac Muscarinic Receptors Histamine Release Depolarizing Substance Succinylcholine Stimulates Stimulates Slight Benzylisoquinolinium Compounds Mivacurium None None Slight Atracurium None None Slight Cisatracurium None None None d-tubocurarine Blocks None Moderate Steroidal Compounds Vecuronium None None None Rocuronium None Blocks weakly None Pancuronium None Blocks moderately None From Miller RD: Miller’s Anesthesia, ed 7, Philadelphia, Saunders, 2011, p 882, Table 29-11.
190. Termination of action of the neurotransmitter norepinephrine is achieved predominately by which mechanism? A. Reuptake into postganglionic sympathetic nerve endings (uptake 1) B. Dilution by diffusion away from receptors C. Metabolism by catechol-O-methyltransferase (COMT) D. Metabolism by monoamine oxidase (MAO)
190. (A) Postganglionic sympathetic nerve fibers release norepinephrine from the synaptic vesicles in the nerve terminals. Eighty percent of the released norepinephrine rapidly undergoes reuptake into the sympathetic nerve terminals (uptake 1) and reenters storage vesicles for future release. Only a small amount of the norepinephrine that is reabsorbed is metabolized in the cytoplasm by MAO. Twenty percent of the norepinephrine is diluted by diffusion away from the receptors and can gain access to the circulation. COMT, which is located primarily in the liver, metabolizes this norepinephrine (Miller: Miller’s Anesthesia, ed 8, pp 357–358; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 700–701).
191. The incidence of unpleasant dreams associated with emergence from ketamine anesthesia can be reduced by the administration of A. Caffeine B. Droperidol C. Physostigmine D. Midazolam Pharmacology and Pharmacokinetics of Intravenous Drugs 53
191. (D) Administration of ketamine may be associated with visual, auditory, and proprioceptive hallucinations. These unpleasant side effects of ketamine occur on emergence and may progress to delirium. The incidence of emergence delirium from ketamine is dose dependent and occurs in approximately 5% to 30% of patients. Emergence delirium is less frequent after repeated administrations of ketamine. The most effective prevention for emergence delirium is administration of a benzodiazepine (midazolam being more effective than diazepam) about 5 minutes before induction of anesthesia with ketamine. Atropine and droperidol given perioperatively may increase the incidence of emergence delirium (Miller: Basics of Anesthesia, ed 6, pp 110–111; Miller: Miller’s Anesthesia, ed 8, pp 827–828).
192. Which of the following premedications is associated with extrapyramidal side effects? A. Metoclopramide B. Diazepam C. Scopolamine D. Glycopyrrolate
192. (A) Extrapyramidal side effects are seen most often with antipsychotic drugs (e.g., phenothiazines, thioxanthenes, and butyrophenones), but they also can be seen with administration of metoclopramide. Metoclopramide, a dopamine antagonist, increases lower esophageal sphincter tone and stimulates gastric and upper intestinal tract motility. Side effects associated with metoclopramide use include mild sedation, dysphoria, agitation, dry mouth, and, in rare instances, dystonic extrapyramidal reactions (oculogyric crises, trismus, torticollis). Akathisia, or the feeling of unease and motor restlessness, has occurred following IV metoclopramide, which may result in cancellation of elective surgery (Miller: Miller’s Anesthesia, ed 8, p 2963; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 499–502).
193. Succinylcholine, when administered to patients with renal failure, will increase serum [K+] by approximately A. No increase in [K+] B. 0.5 mEq/L C. 1.5 mEq/L D. 2.5 mEq/L
193. (B) Succinylcholine is a depolarizing muscle relaxant that chemically resembles acetylcholine and attaches to the postjunctional membrane ion channel receptors. Sustained opening of ion channels produced by succinylcholine (as opposed to a transient opening with acetylcholine) is associated with leakage of potassium from the interior of cells sufficient to increase plasma concentrations of potassium by about 0.5 mEq/L in normal patients. This slight increase of potassium levels in patients with renal failure is similar to patients with normal renal function (Miller: Miller’s Anesthesia, ed 8, p 963; Miller: Basics of Anesthesia, ed 6, p 148; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 220).
194. Each of the following drugs can enhance the neuromuscular blockade produced by nondepolarizing muscle relaxants EXCEPT A. Calcium B. Aminoglycoside antibiotics C. Magnesium D. Intravenous lidocaine
194. (A) Many drugs can enhance the neuromuscular block produced by nondepolarizing muscle relaxants. These include volatile anesthetics, aminoglycoside antibiotics, magnesium, intravenous local anesthetics, furosemide, dantrolene, calcium channel blockers, and lithium. Calcium does not enhance 68 Part 1 Basic Sciences neuromuscular blockade and, in fact, actually antagonizes the effects of magnesium. In patients with hyperparathyroidism and hypercalcemia there is a decreased sensitivity to nondepolarizing muscle relaxants and shorter durations of action (Miller: Miller’s Anesthesia, ed 8, pp 980–983).
195. Discontinuation of which of the following medications is strongly recommended before elective surgery? A. Clonidine B. Metoprolol C. Monoamine oxidase inhibitors (MAOIs) D. None of the above
195. (D) None of these drugs should be abruptly stopped. Clonidine is a centrally active α-adrenergic agonist that is used in the treatment of hypertension. Severe rebound hypertension can be seen between 8 and 36 hours after the last dose, especially in patients receiving more than 1.2 mg/day. Rebound hypertension, as well as cardiac ischemia, can be seen after discontinuation of β-blocker therapy (e.g., atenolol or metoprolol). In the past, it was recommended to stop MAOIs 2 to 3 weeks before elective surgery because of the possibility of developing hypertensive crisis during surgery. More recently, it has become acceptable to use these drugs up to the time of surgery, because their discontinuance could place the patient at risk for suicide. Certain drug interactions may occur with MAOI use, including skeletal muscle rigidity or hyperpyrexia with meperidine, as well as an exaggerated hypertensive response with the indirect-acting vasopressor ephedrine. Abrupt withdrawal of chronic high-dose tricyclic antidepressant therapy can be associated with withdrawal symptoms (i.e., malaise, chills, coryza, skeletal muscle aching) and is not recommended (Miller: Basics of Anesthesia, ed 6, pp 179–182; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 401–407).
196. Circulating BNP (B-type natriuretic peptide) is a powerful biomarker predicting outcomes of which of the following? A. Heart B. CNS C. Kidneys D. Organ rejection
196. (A) About 40 years ago it was noted that kidney response varies with the type of shock. In canines, hypovolemic shock reduced renal blood flow to 10% of controls, whereas cardiogenic shock reduced renal blood flow to only 75% of controls. The main difference seemed to be related to the atrial pressures (decreased in hypovolemic shock but increased in cardiogenic shock). About 10 years later, a peptide was isolated from the atrium of rats named atrial or A-type natriuretic peptide (ANP). Later a natriuretic peptide was isolated from porcine brains and was named brain or B-type natriuretic peptide (BNP). In humans, BNP is mainly produced in the cardiac ventricles. Natriuretic peptides are primarily released from the atria (ANP) and ventricles (BNP) when the chambers are overdistended. Thus, in the failing heart, BNP is released. Natriuretic peptides have a main effect on the kidneys to excrete sodium and water. They have vasodilating properties and inhibit the release of renin. Blood levels of BNP are used as a marker for the severity of cardiovascular disease and may have a role in preoperative cardiac risk assessment. Nesiritide is a recombinant BNP and is being studied for the treatment of acute heart failure (Barash: Clinical Anesthesia, ed 7, p 141; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 123–125, 131; Miller: Miller’s Anesthesia, ed 8, p 3).
197. Hyperkalemia is NOT a risk for patients receiving succinylcholine with which of the following? A. Multiple sclerosis B. Myasthenia gravis C. Guillain-Barré syndrome D. Becker muscular dystrophy
197. (B) Multiple sclerosis (MS) is an acquired inflammatory autoimmune disease in which there is demyelination of nerve fibers within the CNS. In patients with MS and profound neurologic deficits, succinylcholine may cause hyperkalemia and should be avoided, and nondepolarizing muscle relaxants appear safe. Guillain-Barré syndrome is an inflammatory polyneuritis affecting the peripheral nervous system and associated with muscle weakness. In patients with Guillain-Barré, succinylcholine may cause hyperkalemia and should be avoided, whereas nondepolarizing muscle relaxants are not contraindicated but are avoided because of increased sensitivity and possible prolonged muscle weakness in the postoperative period. Duchenne muscular dystrophy and the less common Becker muscular dystrophy are both X-linked recessive diseases. They are characterized by progressive muscle weakness. In 1992 the U.S. Food and Drug Administration issued a warning with regard to the use of succinylcholine in children and adolescents because succinylcholine has been associated with several deaths when administered to patients with unsuspected muscular dystrophy (many developed hyperkalemia and were later diagnosed as having muscular dystrophy). Nondepolarizing muscle relaxants appear safe, but a slower onset may exist. Myasthenia gravis patients have fewer postsynaptic receptors at the myoneural junction, and, if succinylcholine is administered, they appear to be resistant. Larger doses appear needed (1.5-2 mg/ kg) for intubation, and there is no associated hyperkalemic response. The duration of action of succinylcholine, on the other hand, will be prolonged because these patients receive anticholinesterase therapy (pyridostigmine). They are, however, very sensitive to nondepolarizing muscle relaxants, and a greatly reduced dose of a nondepolarizer should be administered, if at all (Fleisher: Anesthesia and Uncommon Diseases, ed 6, pp 267–273, 297-302, 314–315; Miller: Miller’s Anesthesia, ed 8, pp 1266–1284). Pharmacology and Pharmacokinetics of Intravenous Drugs 69
198. Which of the antibiotics below does NOT augment neuromuscular blockade? A. Clindamycin B. Neomycin C. Streptomycin D. Erythromycin
198. (D) Several antibiotics potentiate neuromuscular blockade. The aminoglycosides (neomycin, streptomycin, gentamicin, and tobramycin) and the lincosamides (clindamycin and lincomycin) can augment neuromuscular blockade. The only drug in question that does not affect neuromuscular blockade is erythromycin (of the macrolide antibiotic group). In addition, tetracyclines, penicillins, and cephalosporins do not affect neuromuscular blockade (Barash: Clinical Anesthesia, ed 7, p 541; Miller: Miller’s Anesthesia, ed 8, pp 981–982).
199. A 43-year-old woman with ascites, hepatopulmonary syndrome, and bleeding esophageal varices is admitted to the ICU. Which of the therapies below is LEAST likely to improve symptoms associated with hepatic encephalopathy (HE)? A. Amino acid–rich total parenteral nutrition (TPN) B. Neomycin C. Lactulose D. Flumazenil
199. (A) With liver failure, the liver cannot adequately detoxify noxious chemicals. Among patients with endstage liver disease, 50% to 70% develop hepatic HE. Symptoms vary from mild confusion, drowsiness, and stupor to coma. The etiology of HE is complex. Because an elevation in blood ammonia levels (easily measured) is strongly associated with HE, treatment is aimed at lowering the ammonia level. Other toxins also contribute to HE. To lower the ammonia level, lactulose (which decreases the absorption of ammonia) and neomycin (which reduces the production of ammonia by reducing the ammonia-producing intestinal flora) are commonly administered. Protein restriction is commonly done to decrease ammonia production, so amino acid–rich TPN is not helpful. Flumazenil (a GABA receptor antagonist) has been shown to produce short-duration reversal of the symptoms of HE in some patients and thus suggests that GABA receptors are somehow activated during HE. GABA receptors are responsible for inhibitory neurotransmission in the CNS (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 280; Miller: Basics of Anesthesia, ed 6, p 457; Miller: Miller’s Anesthesia, ed 8, p 541).
200. 100 mg succinylcholine is administered to a 70-kg anesthetized man before intubation. The patient remains paralyzed for 20 minutes. Which of the parameters below is NOT consistent with this finding? A. Dibucaine number 70 B. Heterozygous for atypical cholinesterase C. Incidence of 1/480 D. Presence of fasciculations with this dose
200. (A) In most patients, an intravenous intubating dose of succinylcholine (1 mg/kg = 2 × the ED95) will show neuromuscular blockade that lasts 5 to 10 minutes. The reason for the short duration of action relates to succinylcholine’s very rapid metabolism by typical plasma cholinesterase (also called pseudocholinesterase or butyrylcholinesterase). Some patients, however, have a prolonged effect, which could be due to either a decrease in the quantity or a genetic qualitative change in the enzyme. Quantitative decreases can be seen in patients with malnutrition, liver disease, pregnancy, burns, or advanced age. Cholinesterase activity can also be decreased by the coadministration of various medications including anticholinesterase drugs (e.g., neostigmine), metoclopramide, and esmolol. A marked quantitative reduction (e.g., severe liver disease) can prolong succinylcholine activity about three times the normal duration of block. A marked prolongation of effect is due to the genetic production of atypical pseudocholinesterase (an inactive form). To investigate the genetic or qualitative change, a dibucaine inhibition test is done. The local anesthetic dibucaine can inhibit a normal enzyme more so than an abnormal enzyme. People with a normal dibucaine number of 70 to 80 are homozygous for the normal typical plasma cholinesterase and have the normal 5- to 10-minute neuromuscular blockade. People who are heterozygous (incidence of 1/480) for the atypical plasma cholinesterase have a dibucaine number of 50 to 60 and a block duration of 20 minutes. Patients who are homozygous for the atypical plasma cholinesterase (incidence 1/3200) have a dibucaine number of 20 to 30 and a block duration from 1 to 3 hours. This genetic variation of plasma cholinesterase is the most common abnormality; however, there are also other, less frequent genetic changes in the plasma cholinesterase. See also Question 260 (Miller: Basics of Anesthesia, ed 6, pp 148–149. Miller: Miller’s Anesthesia, ed 8, pp 960–962, 1135–1136).
201. In which of the following situations is succinylcholine most likely to cause severe hyperkalemia? A. 24 hours after a right hemisphere stroke B. 14 days after a severe burn injury C. 24 hours after a midthoracic spinal cord transection D. 2 days with a severe abdominal infection
201. (B) In normal patients, potassium levels increase about 0.5 mEq/L after the administration of succinylcholine. However, in some acquired conditions the potassium level may increase 5 to 7 mEq/L above the baseline potassium level after administration of succinylcholine. This marked elevation of potassium may lead to cardiac arrest. These acquired conditions include the following: (1) denervation injury as caused by spinal cord injury leading to skeletal muscle atrophy; (2) skeletal muscle injury resulting from third-degree burns (until scarring occurs); (3) acute upper motor neuron injury such as stroke; (4) severe skeletal muscle trauma; and (5) severe abdominal infections. In these acquired conditions the potential to increase potassium levels after succinylcholine usually takes a few days to develop, peaks 10 to 50 days after the initial injury, and may persist for 6 months or more. All factors considered, it might be prudent to avoid administration of succinylcholine to any patient more than 24 hours after the conditions listed here. This vulnerability to hyperkalemia may reflect a proliferation of extrajunctional cholinergic receptors, which provide more sites for potassium to leak outward across the cell membrane during depolarization. Some have suggested that the number of receptors is unchanged but that the receptors themselves have altered affinity to acetylcholine or drugs. Similar marked elevations of potassium may develop in cases of undiagnosed myopathy (Miller: Basics of Anesthesia, ed 6, p 149–150). 70 Part 1 Basic Sciences
202. The most common minor side effect reported after flumazenil administration in anesthesia is A. Nausea and/or vomiting B. Dizziness C. Tremors D. Hypertension
202. (A) Although flumazenil (a specific benzodiazepine antagonist) inhibits the activity at the GABA receptor, it works only at the benzodiazepine recognition site and has no effect in reversing other drugs that work on the GABA site (e.g., barbiturates, etomidate, propofol). It has a fast onset (within minutes), with peak brain levels occurring within 6 to 10 minutes, and a relatively short duration of action. Flumazenil can reverse all benzodiazepine CNS effects, including sedative, amnestic, muscle relaxant, and anticonvulsant effects. Side effects are rare, the most common being nausea, vomiting, or both (about 10%). Nausea occurs more commonly when flumazenil is given to patients after general anesthesia than after conscious sedation. Due to its short clinical duration of action, patients receiving flumazenil should be monitored for possible resedation and respiratory depression (Miller: Miller’s Anesthesia, ed 8, pp 843–844; Physicians Desk Reference, ed 63, 2009, pp 2646–2649; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 290).
203. Ketorolac A. Is a selective cyclooxygenase-2 (COX-2) inhibitor B. Does not inhibit thromboxane A2 (TXA2) C. Does not inhibit prostaglandin I2 D. Exhibits a dose ceiling effect with regard to analgesia
203. (D) Nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., aspirin, acetaminophen, indomethacin, ibuprofen, diclofenac, and ketorolac) inhibit COX enzymes that are involved in the conversion of arachidonic acid to prostaglandin, thromboxane, and prostacyclin. COX-1 is involved with platelet aggregation and gastric mucosal protection; COX-2 is involved with pain, inflammation, and fever. TXA2 has prothrombotic and vasoconstricting properties. Prostacyclin I2 has antithrombotic and vasodilating properties. Ketorolac is a nonselective inhibitor of both COX-1 and COX-2 enzymes. Selective COX-2 drugs (e.g., only celecoxib, currently available in the United States) can be used, but in general these have been shown to cause a small increase in thrombotic issues (but fewer effects on gastric mucosa and platelet activity). Because of a ceiling effect with regard to analgesia, ketorolac has only mild-to-moderate analgesic effects (Hemmings: Pharmacology and Physiology for Anesthesia, pp 272–278; Miller: Basics of Anesthesia, ed 6, pp 703–704; Miller: Miller’s Anesthesia, ed 8, pp 2978–2982).
204. A 37-year-old patient with a history of acute intermittent porphyria is scheduled for knee arthroscopy under general anesthesia. Which of the following drugs is contraindicated in this patient? A. Fentanyl B. Isoflurane C. Propofol D. Etomidate
204. (D) Acute intermittent porphyria is the most serious form of porphyria. This disease affects both the central and peripheral nervous systems. An acute intermittent porphyria attack can be triggered by a variety of conditions, including starvation, dehydration, stress, sepsis, and some drugs, such as etomidate and barbiturates. Drugs that are safe or probably safe include local anesthetics, inhaled anesthetics, neuromuscular blocking drugs, some intravenous anesthetics (propofol and ketamine), some analgesics (acetaminophen, aspirin, morphine, fentanyl, sufentanil), antiemetics (droperidol, H2 blockers, metoclopramide, ondansetron), and neostigmine and naloxone. Drugs that are contraindicated include some intravenous anesthetics (barbiturates), some analgesics (ketorolac, pentazocine), and hydantoin anticonvulsants (Barash: Clinical Anesthesia, ed 7, pp 624–625; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 308).
205. A 57-year-old male is discharged after tooth extraction of two molars. His only medication is paroxetine (Paxil), which he takes for depression. Codeine is a poor analgesic choice for this patient because A. It is likely to be ineffective B. It is likely to cause extreme sedation C. He is at increased risk for nausea D. He is at increased risk for serotonin syndrome 54 Part 1 Basic Sciences
205. (A) Cytochrome P450 (CYP) enzymes are involved in the metabolism of many medications. There are many such isoforms and these are further characterized into families with an Arabic number and further characterized into subfamilies (capital letter). The clinical activity of these enzymes can be increased (induced) or decreased (inhibited) by age, genetics, medications, and some foods. CYP2D6 is needed to convert the inactive codeine to the active morphine. Similarly, CYP2D6 also metabolizes oxycodone into active oxymorphone, and inactive hydrocodone into active hydromorphone. CYP2D6 is inhibited by selective serotonin reuptake inhibitors (SSRIs) as well as with quinidine. SSRIs include fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine (Luvox), citalopram (Celexa), and escitalopram (Lexapro). Thus, patients taking SSRIs or quinidine will get a poor analgesic effect with codeine, oxycodone, and hydrocodone (Hemmings; Pharmacology and Physiology for Anesthesia, pp 64–65, 183–186; Miller: Basics of Anesthesia, ed 6, p 37).
206. If etomidate were accidentally injected into a left-sided radial arterial line, the most appropriate step to take would be A. Left stellate ganglion block B. Administer intra-arterial clonidine C. Slowly inject dilute (0.1 mEq/L) [HCO3 –] D. Observe
206. (D) Although etomidate causes pain on intravenous injection in up to 80% of patients, the unintentional administration of etomidate into an artery does not result in detrimental effects to the artery (Miller: Miller’s Anesthesia, ed 8, p 852).
207. The most important reason for the more rapid onset and shorter duration of action of fentanyl with single dose compared with morphine is the difference in A. Volume of distribution B. Hepatic clearance C. Protein binding D. Lipid solubility
207. (D) Fentanyl is more lipid soluble than morphine, so it passes through the blood-brain barrier more easily and has a faster onset of action. Fentanyl also has a larger volume of distribution, slower plasma clearance, and longer elimination half-life than morphine. However, the duration of action of fentanyl (when given in small doses) is much shorter than that of morphine because fentanyl is rapidly redistributed from the brain to inactive tissue sites (e.g., lipid sites). In larger doses, these tissue sites can Pharmacology and Pharmacokinetics of Intravenous Drugs 71 become saturated, and the pharmacologic action of fentanyl becomes considerably prolonged (Miller: Basics of Anesthesia, ed 7, p 115–119; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 104–105).
208. A narcotic infusion is initiated in a patient without a bolus (loading dose). Of the following drugs, which would reach steady state after 2 hours or less of continuous infusion (fentanyl, remifentanil, alfentanil, and morphine)? A. All of these B. Remifentanil and alfentanil C. Alfentanil only D. Remifentanil only
208. (D) This question illustrates the concept of infusion front-end kinetics. This concept is useful for comparing the kinetics of various intravenous agents used in anesthesia. Remifentanil reaches the steady state in less than 1 hour of continuous infusion. Approximately 8 hours are required to reach the steady state with alfentanil and sufentanil, whereas fentanyl and morphine have not achieved the steady state concentration even after 10 hours of continuous infusion. Another important concept is the time after bolus to reach peak effect: bolus front-end kinetics. This concept is more intuitive to most anesthesia providers. Comparing the same narcotics used in this question, alfentanil and remifentanil reach peak concentration at nearly the same time and fentanyl only slightly later (Miller: Basics of Anesthesia, ed 6, p 119). 100 80 60 40 20 0 0 100 200 Infusion begins at time zero 300 400 500 600 Proportion of steady-state Ce (%) Fentanyl Alfentanil Morphine Sufentanil Infusion duration (min) Remifentanil Infusion: Front-end
209. The period of vulnerability after three courses of bleomycin for testicular cancer is A. 1 month B. 1 year C. Lifelong D. No vulnerability with just three courses
209. (C) Bleomycin is used primarily in the treatment of Hodgkin lymphoma and testicular tumors. Bleomycin causes oxidative damage to nucleotides, which leads to breaks in DNA. Although the more common side effects of bleomycin use are mucocutaneous, dose-related pulmonary toxicity is the most serious side effect. Early signs and symptoms of pulmonary toxicity include dry cough, fine rales, and diffuse infiltrates on x-ray. Approximately 5% to 10% of patients will develop pulmonary toxicity, and about 1% will die from this complication. Most believe that the risk of pulmonary toxicity increases with dose (especially total dose >250 mg), in patients older than 40 years of age, in patients with a creatinine clearance (CrCl) of less than 80 mL/min, and in patients with prior chest radiation or preexisting pulmonary disease. Although a relationship appears to exist between the use of bleomycin and the use of high concentrations of oxygen, the details are unclear. Currently, it has been suggested to use the lowest concentration of oxygen consistent with patient safety with a careful evaluation of oxygen saturation with pulse oximetry in any patient who has received bleomycin (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 1716–1718; Miller: Miller’s Anesthesia, ed 8, p 1951; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 555–565).
210. The unique advantage of rocuronium over other muscle relaxants is its A. Short duration of action B. Metabolism by pseudocholinesterase C. Onset of action D. Lack of need for reversal
210. (C) The first two letters of the word “rocuronium” stand for “rapid onset.” Of the nondepolarizing muscle relaxants currently available, rocuronium has the most rapid onset of action at clinically useful dosages. Rocuronium is a nondepolarizing neuromuscular relaxant with an intermediate duration of action similar to vecuronium, atracurium, and cisatracurium. At an ED95 dose (0.3 mg/kg), the onset time is 1.5 to 3 minutes, whereas with the other intermediate nondepolarizing muscle relaxants, the onset time is 3 to 7 minutes. At larger doses (i.e., 2 × ED95 or 0.6 mg/kg), onset time can be reduced to 1 to 1.5 minutes (Barash: Clinical Anesthesia, ed 7, p 538).
211. Which of the following statements regarding the efficacy of neuromuscular blockade in the setting of acute hypokalemia is correct? A. There is no effect with depolarizing or nondepolarizing muscle relaxants B. There is resistance to effects of both depolarizing and nondepolarizing muscle relaxants C. There is increased sensitivity to effects of both depolarizing and nondepolarizing muscle relaxants D. There is resistance to depolarizing muscle relaxants and increased sensitivity to nondepolarizing muscle relaxants
211. (D) An acute decrease in serum potassium causes hyperpolarization of cell membranes. This causes resistance to depolarizing neuromuscular blockers and an increased sensitivity to nondepolarizing neuromuscular blockers (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 226–227). 72 Part 1 Basic Sciences
212. A patient undergoing which of the following operations would be at highest risk for operative recall? A. Laparoscopic cholecystectomy with total intravenous anesthesia (no volatile) B. Cervical spine fusion with MEP (motor evoked potentials) monitoring C. Pneumonectomy with one-lung ventilation D. Emergency splenectomy after falling from a ladder
212. (D) Awareness during general anesthesia is the postoperative recall of events that happened during the anesthetic. Overall incidence has decreased from about 1% 50 years ago to about 0.1% today (with some variations from study to study). Patients at increased risk include patients undergoing cardiac surgery, endoscopic airway surgery, cesarean sections, and trauma surgery (Miller: Miller’s Anesthesia, ed 8, p 1528).
213. A 58-year-old patient is brought to the emergency room with the following symptoms: miosis, abdominal cramping, salivation, loss of bowel and bladder control, bradycardia, ataxia, and skeletal muscle weakness. The most likely diagnosis is A. Central anticholinergic syndrome B. Malignant neuroleptic syndrome C. Anticholinesterase poisoning D. Serotonin syndrome
213. (C) The symptoms described in this patient are consistent with cholinergic stimulation or increased levels of acetylcholine that occur with anticholinesterase poisoning. Stimulation of the parasympathetic nervous system produces miosis, abdominal cramping, excess salivation, loss of bowel and bladder control, bradycardia, and bronchoconstriction. These symptoms are treated with atropine. The acetylcholinesterase reactivator pralidoxime sometimes is added to treat the nicotinic effects of elevation of acetylcholine at the neuromuscular junction of skeletal muscle (i.e., skeletal muscle weakness, apnea). CNS effects of elevated acetylcholine levels can include confusion, ataxia, and coma. In addition, supportive therapy (the ABCs of resuscitation [Airway, Breathing, Circulation, etc.]) is provided as needed (Miller: Miller’s Anesthesia, ed 8, p 2495).
214. Flumazenil A. Is contraindicated in narcotic addicts B. Can be given orally as well as intravenously C. Can produce seizures in chronic benzodiazepine users D. Has a longer elimination half-life compared to midazolam
214. (C) Flumazenil is a benzodiazepine antagonist used to antagonize the benzodiazepine effects on the CNS. It does not reverse the effects of barbiturates, opiates, or alcohol. Seizures can be precipitated in patients who have been on benzodiazepines for long-term sedation or patients showing signs of serious cyclic antidepressant overdosage (e.g., twitching, rigidity, widened QRS complex, hypotension). Flumazenil has a shorter elimination half-life (0.7-1.3 hours) compared with midazolam (2-2.5 hours). Flumazenil is poorly absorbed orally (Miller: Miller’s Anesthesia, 8, p 843; Physicians’ Desk Reference, ed 63, 2009, pp 2646–2649).
215. What percentage of neuromuscular receptors could be blocked and still allow patients to carry out a 5-second head lift? A. 5% B. 15% C. 25% D. 50%
215. (D) Adequate recovery from neuromuscular blockade is believed to occur when 50% or less of receptors are occupied with muscle relaxants. This can be measured with sustained tetanus at 100 Hz, but this test is very painful. Another method requires patient cooperation and consists of a sustained head lift for 5 seconds in the supine position. The “head lift” test is the standard test to determine adequate muscular function (Miller: Basics of Anesthesia, ed 6, p 158).
216. A 25-year-old woman undergoes thyroidectomy under general anesthesia. Ondansetron 4 mg IV is administered as nausea prophylaxis. She complains of nausea in the recovery room. Which of the follow agents is LEAST likely to be of benefit to her for treatment (rescue) of postoperative nausea and vomiting (PONV)? A. Aprepitant B. Granisetron C. Promethazine D. Droperidol
216. (B) PONV is the second-most common complaint reported in the perioperative period (pain is the number one complaint). Many drugs have been used to both prevent (prophylaxis) and to treat (rescue) PONV. Antiemetics were often administered alone, but now combination therapy of two or more drugs such as dopamine antagonists (e.g., droperidol, metoclopramide), histamine antagonists (e.g., diphenhydramine, promazine), anticholinergics (e.g., scopolamine), steroids (e.g., dexamethasone), neurokinin antagonists (e.g., aprepitant), and serotonin antagonist (e.g., ondansetron, dolasetron, granisetron, and palonosetron) are commonly used. Once a serotonin antagonist is given for prophylaxis, adding more of a serotonin antagonist in the PACU does not seem to help. It is better to use an antiemetic from another class of drugs (Hemmings: Pharmacology and Physiology for Anesthesia, pp 503–551; Miller: Miller’s Anesthesia, ed 8, pp 2947, 2969–2970).
217. Which of the following drugs can prevent tachyarrhythmias in patients with Wolff-Parkinson-White (WPW) syndrome? A. Droperidol B. Pancuronium C. Ketamine D. Verapamil
217. (A) Patients with WPW syndrome are predisposed to develop supraventricular arrhythmias. Sympathetic stimulation (e.g., anxiety, hypovolemia), as well as many drugs (e.g., pancuronium, meperidine, ketamine, ephedrine, digoxin, verapamil), can induce tachyarrhythmias, often by enhancing conduction through accessory atrial pathways. Although verapamil is used to treat supraventricular tachyarrhythmias because of its depressant effects on alveolar nodal conduction, it actually may increase the heart rate in patients with WPW syndrome because it can increase conduction of the accessory pathways. Droperidol, in addition to its antidopaminergic properties, has antidysrhythmic properties that protect against epinephrine-induced dysrhythmias. Proposed mechanisms include α-adrenergic receptor blockade and mild local anesthetic effects. Large doses of droperidol (0.2-0.6 mg/kg) can reduce impulse transmission via the accessory pathways responsible for the tachyarrhythmias that occur in patients with WPW syndrome (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 413–415, 766).
218. The half-life of pseudocholinesterase is A. 1 hour B. 12 hours C. 1 week D. 2 weeks Pharmacology and Pharmacokinetics of Intravenous Drugs 55
218. (B) Pseudocholinesterase (also called plasma cholinesterase) is an enzyme found in plasma and most other tissues (except erythrocytes). Pseudocholinesterase metabolizes the acetylcholine released at the neuromuscular junction, as well as certain drugs such as succinylcholine, mivacurium, and ester-type local anesthetics. It is produced in the liver and has a half-life of approximately 8 to 16 hours. Pseudocholinesterase levels may be reduced in patients with advanced liver disease. The decrease must be greater than 75% before significant prolongation of neuromuscular blockade occurs with succinylcholine (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 218). Pharmacology and Pharmacokinetics of Intravenous Drugs 73
219. Some COX-2 inhibitors (e.g., rofecoxib [Vioxx]) have been withdrawn from the U.S. pharmaceutical market because of serious complications involving A. Platelet inhibition and gastrointestinal (GI) hemorrhage B. Renal failure C. Hypertension D. Promotion of thrombotic state
219. (D) COX inhibitors are useful analgesics for mild-to-moderate pain. There are three types of COX inhibitors: cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and cyclooxygenase-3 (COX-3). COX-3 is a variant of COX-1, and there is some controversy as to its existence in humans. COX inhibitors block prostaglandin synthesis in the periphery and in the CNS. COX-1 has GI mucosal protecting properties and stimulates platelet aggregation. Drugs with COX-1 inhibiting properties can cause gastric and duodenal ulcers and can interfere with platelet aggregation. COX-2 is involved in inflammation. NSAIDs are nonspecific COX-1 and COX-2 inhibitors. Selective COX-2 inhibitors such as celecoxib, valdecoxib, and rofecoxib are effective analgesics with anti-inflammatory effects. They have a lower risk of GI complications and antiplatelet properties than the nonspecific COX-1 and COX-2 inhibitors. Because of an increase in serious thromboembolic events (i.e., strokes and myocardial infarctions), both valdecoxib and rofecoxib have been withdrawn from the market. Currently, celecoxib is the only selective COX-2 inhibitor available in the United States. In addition, both the NSAIDs and selective COX-2 inhibitors can transiently decrease renal function, especially in patients with preexisting renal disease and in patients who are hypovolemic. These renal effects can lead to hypertension, edema, and acute renal failure (Hemmings: Pharmacology and Physiology for Anesthesia, pp 272–277; Miller: Basics of Anesthesia, ed 6, pp 703–704; Barash: Clinical Anesthesia, ed 7, p 437).
220. Which of the following equals the anti-inflammatory activity of 50 mg of prednisone (Deltasone)? A. 100 mg cortisol (Solu-Cortef) B. 80 mg methylprednisolone (Solu-Medrol) C. 7.5 mg dexamethasone (Decadron) D. 4 mg betamethasone (Celestone)
220. (C) The adrenal cortex secretes two classes of steroids, the corticosteroids (glucocorticoids and mineralocorticoids) and the androgens. The main glucocorticoid is hydrocortisone, also called cortisol. The glucocorticoids are used primarily for their anti-inflammatory and immunosuppressive effects, but they also have mineralocorticoid activity (i.e., sodium-retaining effects). These drugs differ in potency, amount of mineralocorticoid effect, and duration of action. The normal amount of cortisol produced daily is about 10 mg, but under stress, the level can increase tenfold. The main mineralocorticoid is aldosterone. The normal amount of aldosterone produced daily is about 0.125 mg. Because fludrocortisone has such significant mineralocorticoid activity, it is used only for this. The following table compares several corticosteroids. In this case, 50 mg of prednisone is equivalent in glucocorticoid activity to 7.5 mg of dexamethasone and 200 mg of hydrocortisone (Hardman: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 10, pp 1655–1666; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 461–464). COMPARATIVE PHARMACOLOGY OF CORTICOSTEROIDS Agent Anti-inflammatory Potency Equivalent Glucocorticoid Dose (mg) Sodium-Retaining Potency Duration of Action (hr) Hydrocortisone or cortisol (Cortef) 1 20 1 8-12 Cortisone (Cortone) 0.8 25 0.8 8-36 Prednisolone (Hydeltrasol) 4 5 0.8 12-36 Prednisone (Deltasone) 4 5 0.8 18-36 Methylprednisolone (Solu-Medrol) 5 4 0.5 12-36 Triamcinolone (Kenalog) 5 4 0 12-36 Betamethasone (Celestone) 25 0.75 0 36-54 Dexamethasone (Decadron) 25 0.75 0 36-54 Fludrocortisone (Florinef) 10 2 250 24 Aldosterone 0 NA 3000 NA, not applicable. From Stoelting RK: Pharmacology and Physiology in Anesthetic Practice, ed 4, Philadelphia, Lippincott Williams & Wilkins, 2006, p 462. 74 Part 1 Basic Sciences
221. The recovery index (RI) of which of the following nondepolarizing muscle relaxants is NOT altered by aging? A. Atracurium B. Vecuronium C. Rocuronium D. Pancuronium
221. (A) The RI of neuromuscular blocking drugs is the time needed for spontaneous recovery of a twitch height from 25% to 75% of the baseline height. The elderly, who tend to have reduced renal and hepatic function, have a prolonged RI for nondepolarizing muscle relaxants that are dependent upon renal or hepatic elimination (e.g., vecuronium, d-tubocurarine, pancuronium, rocuronium). The RI for atracurium and cisatracurium, which are broken down in the plasma, are not prolonged in the elderly (Miller: Miller’s Anesthesia, ed 8, pp 975–976).
222. Side effects associated with cyclosporine therapy include each of the following EXCEPT A. Nephrotoxicity B. Pulmonary toxicity C. Seizures D. Limb paresthesias
222. (B) Cyclosporine is a drug that selectively inhibits helper T-lymphocyte-mediated but not B-lymphocyte– mediated immune responses. It is mainly used alone or in combination with corticosteroids to prevent or treat organ rejection. Other uses include the treatment of Crohn disease, uveitis, psoriasis, and rheumatoid arthritis. Side effects that may accompany the administration of cyclosporine include nephrotoxicity (25%-38%), hypertension, limb paresthesias (50%), headaches, confusion, somnolence, seizures, elevation of liver enzymes, allergic reactions, gum hyperplasia, hirsutism, and hyperglycemia. There appears to be no pulmonary toxicity associated with cyclosporine therapy (Miller: Miller’s Anesthesia, ed 8, p 580).
223. What is the predominant mechanism for succinylcholine- induced tachycardia in adults? A. Direct sympathomimetic effect at postjunctional muscarinic receptors B. Stimulation of nicotinic receptors at autonomic ganglia C. Blockade of nicotinic receptors at autonomic ganglia D. Direct vagolytic effect at postjunctional muscarinic receptors
223. (B) Succinylcholine is basically two acetylcholine molecules hooked together. Succinylcholine may exert cardiovascular effects by: (1) inducing histamine release from mast cells; (2) stimulating autonomic ganglia, which increases neurotransmission at both the sympathetic and parasympathetic nervous systems; and (3) directly stimulating postjunctional cardiac muscarinic receptors. The effect of succinylcholine on heart rate is variable, with both bradycardia and tachycardia possible. The final heart rate depends upon many factors, including the amount of nicotinic stimulation of the sympathetic and parasympathetic ganglia, which is greater for the nondominant autonomic nervous system. For example, when sympathetic nervous system tone is high (as in children), bradycardia is more likely to develop when succinylcholine is administered. When parasympathetic nervous system tone is high (as in many adults), tachycardia, although not common, is more likely to occur when succinylcholine is administered. Bradycardia is more likely to occur when a second intravenous dose of succinylcholine is administered 4 to 5 minutes after the first dose, especially when difficult laryngoscopy (e.g., intense vagal stimulation) is being performed (Miller: Basics of Anesthesia, ed 6, p 150).
224. Bradycardia observed after administration of succinylcholine to children is attributable to which mechanism? A. Nicotinic stimulation at the autonomic ganglia B. Stimulation of the vagus nerve centrally C. Muscarinic stimulation at the sinus node D. Muscarinic blockade at the sinus node
224. (C) Chemically, succinylcholine is two acetylcholine molecules hooked together and has many effects similar to acetylcholine. In addition to causing neuromuscular blockade, succinylcholine stimulates all cholinergic autonomic receptors, including the nicotinic receptors of the sympathetic and parasympathetic ganglia, as well as the muscarinic receptors in the sinus node of the heart. It is this muscarinic effect that causes the bradycardia that can be seen after the administration of succinylcholine in children. Also see explanation to Question 223 (Miller: Miller’s Anesthesia, ed 8, p 962).
225. Which of commonly used drugs below is NOT metabolized by nonspecific esterases? A. Propofol B. Esmolol C. Atracurium D. Remifentanil
225. (A) Propofol’s chemical structure is 2,6-diisopropylphenol (i.e., is not an ester) and thus is not metabolized by esterases. Propofol is rapidly metabolized by the liver to more water-soluble compounds that are then renally excreted. Esmolol is an ester compound and is rapidly metabolized by RBC esterases (short halflife of 9-10 minutes). Atracurium and cisatracurium primarily undergo Hofmann elimination, which is a chemical reaction. Atracurium has a second metabolic route: metabolism by nonspecific plasma esterases. Interestingly, cisatracurium, which is an isolated form of atracurium (1 of the 10 stereoisomers), does not undergo metabolism by nonspecific plasma esterases. The short duration of action of remifentanil is due to its ester structure, which is metabolized by blood and tissue nonspecific esterases. Because of the nonspecific metabolism, its duration of action is not prolonged in patients with pseudocholinesterase deficiency (Miller: Basics of Anesthesia, ed 6, pp 75, 100–101, 125, 154; Miller: Miller’s Anesthesia. ed 8, pp 371, 824, 888–889, 977).
226. Succinylcholine is contraindicated for routine tracheal intubation in children because of an increased incidence of which of the following side effects? A. Hyperkalemia B. Malignant hyperthermia C. Masseter spasm D. Sinus bradycardia
226. (A) Hyperkalemia, malignant hyperthermia, masseter spasm, sinus bradycardia, nodal rhythms, and myalgias are side effects that can be seen after the administration of succinylcholine. In recent years, there have been several case reports of intractable cardiac arrest in apparently healthy children after the administration of succinylcholine. In these cases, hyperkalemia, rhabdomyolysis, and acidosis were documented. Later, muscle biopsy samples demonstrated that many of these cases were subclinical cases of Duchenne muscular dystrophy. For this reason of occasional severe hyperkalemia, succinylcholine is contraindicated for routine tracheal intubation in children (Barash: Clinical Anesthesia, ed 7, p 1227; Miller: Miller’s Anesthesia, ed 8, p 983). Pharmacology and Pharmacokinetics of Intravenous Drugs 75
227. From MOST to LEAST rapid, select the correct temporal sequence of neuromuscular blockade in the adductor of the thumb, the orbicularis oculi, and the diaphragm after administration of an intubating dose of vecuronium to an otherwise healthy patient. A. Diaphragm, orbicularis oculi, thumb B. Orbicularis oculi, diaphragm, thumb C. Orbicularis oculi, thumb, diaphragm D. Orbicularis oculi same as diaphragm, thumb
227. (D) To make intubation easier, it is important to know when the muscles of the airway are maximally relaxed after administration of a neuromuscular relaxant. This often is done with neuromuscular monitoring. However, which muscles one monitors is important because neuromuscular blockade develops faster, lasts a shorter time, and recovers more quickly in the central muscles of the airway (i.e., the larynx, jaw, and diaphragm) than in the more peripheral abductor muscles of the thumb (e.g., ulnar nerve monitoring). Also important is the observation that the pattern of blockade in the orbicularis oculi (e.g., facial nerve monitoring) is similar to that of the laryngeal muscles and the diaphragm. Therefore, when the orbicular oculi muscles are maximally relaxed, intubation would be optimal. When adductor function of the thumb returns to normal, the diaphragm and laryngeal muscles will have recovered (Barash: Clinical Anesthesia, ed 7, p 545).
228. Select the TRUE statement regarding interaction of nondepolarizing neuromuscular blocking drugs when durations of action are dissimilar. A. If a long-acting drug is administered after an intermediate-acting drug, the duration of the long-acting drug will be longer than normal B. If a long-acting drug is administered after an intermediate- acting drug, the duration of the longacting drug will be about the same as expected C. If an intermediate-acting drug is administered after a long-acting drug, the duration of the intermediate-acting drug will be about the same as expected D. If an intermediate-acting drug is administered after a long-acting drug, the duration of action of the intermediate-acting drug will be longer than expected
228. (D) Rarely, it is necessary to change from one nondepolarizing drug to another. A general rule to determine the duration of action of a drug given after another drug of different duration is a matter of simple kinetics. Three half-lives will be required for a clinical changeover so that 95% of the first drug will have cleared for the block duration to begin to take on the characteristics of the second drug. For example, if an intermediate-acting muscle relaxant such as vecuronium is given after a long-acting agent such as pancuronium, the duration of action of vecuronium is prolonged after the first two maintenance doses of vecuronium. After the third maintenance dose the duration of vecuronium is not prolonged (Miller: Miller’s Anesthesia, ed 8, pp 980–981).
229. Select the correct statement regarding the effects of volatile anesthetics on nondepolarizing neuromuscular blocking drugs and the reversal agents. A. Volatile anesthetics potentiate neuromuscular blockade but retard reversal agents B. Volatile anesthetics potentiate both neuromuscular blocking drugs and reversal agents C. Volatile anesthetics retard both neuromuscular blocking drugs and reversal agents D. Volatile anesthetics retard neuromuscular blocking drugs but potentiate reversal agents
229. (A) Volatile anesthetics enhance neuromuscular blockade in a dose-dependent fashion. Recent studies have suggested that antagonism of neuromuscular block is slowed by volatile anesthetics; thus, volatile anesthetic vapor concentrations should be reduced as much as possible at the end of the case to help ensure that reversal will take place as promptly as possible (Miller: Miller’s Anesthesia, ed 8, p 981).
230. Meperidine is contraindicated in patients taking which of the following drugs for Parkinson disease? A. Bromocriptine B. Trihexyphenidyl (Artane) C. Selegiline (Eldepryl) D. Amantadine (Symmetrel) 56 Part 1 Basic Sciences
230. (C) Selegiline is an MAOI that is sometimes used in the treatment of Parkinson disease. Meperidine is the original phenylpiperidine from which a number of other congeners are derived (e.g., fentanyl, sufentanil, alfentanil, remifentanil). Meperidine is rarely used as an analgesic but rather as an anti-shivering drug. Meperidine (as well as methadone and tramadol) is contraindicated in patients taking MAOIs because of the possibility of serotonin syndrome (e.g., agitation, skeletal muscle rigidity, hyperpyrexia) or depression (e.g., hypotension, depressed ventilation, coma) that may result (Miller: Miller’s Anesthesia, ed 8, pp 894–896, 909–910).
231. Emergence delirium occurs most often with A. Sevoflurane B. Desflurane C. Ketamine D. Propofol
231. (A) Some children awaken from general anesthesia and appear restless and inconsolable during the early recovery period from general anesthesia. This is called emergence “excitement” delirium (ED), and more intensive nursing will be needed to prevent such children from hurting themselves as well as prevent them from pulling out intravenous lines or surgical drains. This usually resolves quickly when the child awakens more fully. Although untreated pain is often considered an instigating factor, many children can be pain free and still develop ED. Risk factors include age younger than 5 years (peak incidence, 2-4 years of age), the use of volatile anesthetics (sevoflurane has the highest frequency of ED), otolaryngologic and ophthalmologic surgeries, and anxious parents. Prophylactic treatment with a single IV dose of fentanyl (2.5 μg/kg), clonidine (2 μg/kg), ketamine (0.25 mg/kg), nalbuphine (0.1 mg/kg), or dexmedetomidine (0.15 μg/kg) can decrease the incidence. Some have used IV propofol (1 mg/kg) after turning off sevoflurane at the conclusion of surgery to decrease the incidence of ED. Intranasal fentanyl (1 μg/kg) may be useful when the IV route is unavailable (Davis: Smith’s Anesthesia for Infants and Children, ed 8, p 391; Miller: Basics of Anesthesia, ed 6, p 558; Miller: Miller’s Anesthesia, ed 8, pp 2941–2942).
232. The most common reason for patients to rate anesthesia with etomidate as unsatisfactory is A. PONV B. Pain on injection C. Recall of intubation D. Postoperative hiccups
232. (A) Etomidate, an imidazole derivative, is used most often for induction of general anesthesia, but it also can be used for maintenance of general anesthesia. Etomidate has a relatively short duration of action and provides very stable hemodynamics, even in patients with limited cardiovascular reserve. However, it is associated with several adverse effects. These adverse effects include a high incidence of nausea and vomiting (greater than after thiopental), pain on injection, thrombophlebitis, myoclonic movements, and, sometimes, hiccups. Nausea and vomiting constitute the most common reason patients rate anesthesia with etomidate as unsatisfactory. The addition of fentanyl to etomidate to decrease the pain of injection also increases the incidence of nausea and vomiting (Miller: Miller’s Anesthesia, ed 8, p 852).
233. Which of the following muscle relaxants inhibits the reuptake of norepinephrine by the adrenergic nerves? A. Pancuronium B. Vecuronium C. Rocuronium D. Atracurium
233. (A) Pancuronium tends to increase the heart rate, mean arterial BP, and cardiac output. This may be related to several mechanisms, including a moderate vagolytic effect, norepinephrine release, and decreased reuptake of norepinephrine by adrenergic nerves. The other listed drugs rarely cause direct adrener76 Part 1 Basic Sciences gic stimulation and do not inhibit the uptake of norepinephrine by adrenergic nerves (Miller: Miller’s Anesthesia, ed 8, p 978).
234. The most common side effect of oral dantrolene used to prevent malignant hyperthermia is A. Nausea and vomiting B. Muscle weakness C. Blurred vision D. Tachycardia
234. (B) Dantrolene is a muscle relaxant used orally to help control skeletal muscle spasticity in patients with upper motor neuron lesions, and it can be used acutely in the prevention of malignant hyperthermia in patients undergoing anesthesia. It is given intravenously in the treatment of malignant hyperthermia. Dantrolene has little or no effect on smooth or cardiac muscle at clinical doses. Dantrolene works directly on skeletal muscle by decreasing the amount of calcium released from the sarcoplasmic reticulum. This decreases the excitation–contraction coupling needed for the muscle to contract. The most common side effect of dantrolene administration is skeletal muscle weakness. Other acute side effects include nausea, diarrhea, and blurred vision. When the drug is given intravenously, a brisk diuresis occurs and is related to the mannitol added to make the intravenous solution isotonic. With chronic oral use, patients may rarely develop hepatitis and pleural effusions (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 596–597).
235. A 65-year-old patient is admitted for right upper quadrant pain. Acute cholecystitis is diagnosed and laparoscopic cholecystectomy planned. The patient has no major medical problems other than type 2 diabetes, for which she takes metformin, and depression, for which she takes paroxetine (SSRI inhibitor). Which of the following best describes the rationale for discontinuation of metformin 48 hours before surgery? A. Risk of metabolic acidosis B. Risk of hypoglycemia C. Risk of serotonin syndrome D. None of the above
235. (D) (Please also see explanation to Question 435.) Diabetes mellitus is a disease characterized by altered metabolism of carbohydrates (usually manifested by hyperglycemia), lipids, and proteins. Ninety percent of diabetic patients in the United States have non–insulin-dependent diabetes mellitus (NIDDM) or type 2 diabetes and a relative deficiency in circulating insulin. Diabetic patients also can have a decreased tissue response to circulating insulin (insulin resistance). Oral hypoglycemic agents, most commonly of the sulfonylurea chemical class, can be used in patients with NIDDM. These sulfonylurea drugs have many metabolic effects, including the initial stimulation of the pancreas to release insulin (chronically, insulin secretion is not increased but the hypoglycemic effects are maintained). Tolbutamide (Orinase) and chlorpropamide (Diabinese) are first-generation analogs. The biguanides metformin (Glucophage) and phenformin work by increasing the action of circulating insulin on peripheral tissues and are called antihyperglycemic, not hypoglycemic, agents. There is no risk of hypoglycemia with metformin even with overnight fasting. Phenformin was withdrawn from the market because of an association with lactic acidosis. Metformin, long thought to cause metabolic acidosis, is now understood to do so only in patients who have abnormal kidney or liver function. SSRIs are drugs commonly used for depression. SSRIs have serious side effects, including hyperpyrexia. There have been reports of serotonin syndrome with SSRI and methylene blue, but not with metformin (Miller: Miller’s Anesthesia, ed 8, pp 1219–1220; Miller: Basics of Anesthesia, ed 6, pp 182–183).
236. A 37-year-old man is brought to the operating room for repair of a broken mandible sustained in a motor vehicle accident. No other injuries are significant. The patient has been in treatment for alcohol abuse and takes disulfiram and naltrexone. Which of the following would be the best technique for management of this patient’s postoperative pain? A. Continue naltrexone with round-the-clock low-dose methadone B. Continue naltrexone with small doses of morphine every 4 hours as needed C. Continue naltrexone with small doses of nalbuphine every 4 hours as needed D. Discontinue naltrexone and treat pain with morphine as needed
236. (D) Disulfiram and naltrexone occasionally are administered orally in alcoholic rehabilitation programs. Disulfiram alters the metabolism of alcohol by irreversibly inactivating the enzyme aldehyde dehydrogenase. If the patient drinks alcohol, there is a buildup of acetaldehyde in the blood. This produces the unpleasant effects of flushing, headache, nausea, vomiting, chest pain, tachycardia, hypotension, and confusion. The alcohol sensitivity with disulfiram use may last up to 2 weeks after the drug is stopped. Naltrexone is used with disulfiram in the treatment of alcohol addiction. It appears to block some of the reinforcing properties of alcohol. Patients taking naltrexone with disulfiram have a lower rate of relapse for alcohol. Naltrexone is a pure opioid antagonist. Patients taking naltrexone at the time of surgery will have markedly elevated opioid requirements if opioids are chosen for pain relief. The duration of action of naltrexone is 24 hours, and the drug should be stopped during the hospitalization to allow better pain control with narcotics, as would be desirable in this major surgical procedure (Hardman: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 10, pp 602–604; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 5, p 542; Miller: Miller’s Anesthesia, ed 8, pp 866–868).
237. Which of the following muscle relaxants is most suitable for rapid intubation in a patient in whom succinylcholine is contraindicated? A. Atracurium B. Rocuronium C. Vecuronium D. Cisatracurium
237. (B) Rapid-sequence inductions are performed in cases where rapid control of the airway is needed. Usually this is performed to secure the airway in a patient who should be easily intubated and has a “full stomach.” In these cases, after adequate preoxygenation and suctioning of the airway can be readily performed, an intravenous induction of general anesthesia is performed with cricoid pressure, and a muscle relaxant with a short-onset time is administered. Succinylcholine has the fastest onset time of all neuromuscular relaxants and is the drug of choice. However, in some cases, succinylcholine is contraindicated and another neuromuscular blocker is chosen. Of the drugs listed, rocuronium is the best Pharmacology and Pharmacokinetics of Intravenous Drugs 77 choice because of its rapid onset. Although the onset time of other nondepolarizing neuromuscular relaxants can be sped up with priming (a technique in which 10% of the intubating dose is followed 2 to 4 minutes later with an intravenous induction of general anesthesia and the remaining 90% of the relaxant), rocuronium is fast enough without priming and much simpler to use. In patients who may be difficult to intubate, even with adequate muscle relaxation, an awake intubation should be strongly considered. d-Tubocurare should never have an intubating dose bolused because it causes significant histamine release, and it should be given incrementally over several minutes if used to intubate (Miller: Miller’s Anesthesia, ed 8, p 875).
238. The neuromuscular effects of an intubation dose of vecuronium are terminated by A. Diffusion from the neuromuscular junction back into the plasma B. Nonspecific plasma cholinesterases C. The kidneys D. The liver
238. (A) The effects of nondepolarizing neuromuscular drugs are based on the drug being at the receptor. After intravenous injection of a muscle relaxant, plasma drug concentration immediately starts to decrease. To produce paralysis, the drug must diffuse from the plasma to the neuromuscular junction after injection and bind to the receptors. The drug effect is later terminated by diffusion of drug back into the plasma. Recovery of neuromuscular function occurs when the muscle relaxant diffuses from the neuromuscular junction back into the plasma to be metabolized and/or eliminated from the body (Miller: Miller’s Anesthesia, ed 8, p 871).
239. Respiratory depression produced by which of the following analgesics is not readily reversed by administration of naloxone? A. Meperidine B. Methadone C. Hydromorphone D. Buprenorphine
239. (D) Buprenorphine (Buprenex) is a mixed agonist-antagonist opioid with a very strong affinity for μ receptors. Because of its strong affinity (33 times greater than morphine) and slow dissociation from the receptors, it has a prolonged duration of effect (>8 hours) and shows resistance to reversal from naloxone. In rare cases of respiratory depression, reversal may not be achieved with high doses of naloxone (Miller: Miller’s Anesthesia, ed 8, p 904; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 119).
240. Which of the following intravenous anesthetic agents is associated with the highest incidence of nausea and vomiting? A. Midazolam B. Etomidate C. Ketamine D. Propofol
240. (B) Nausea and vomiting may be associated with any of the drugs listed. Propofol, and perhaps midazolam, may actually be protective in some patients. Of the listed drugs in this question, etomidate has the highest incidence of nausea and vomiting with some reporting an incidence as high as 40% (Barash: Clinical Anesthesia, ed 7, p 489; Miller: Basics of Anesthesia, ed 6, pp 108–112).
241. If naloxone were administered to a patient who is receiving ketorolac for postoperative pain, the most likely result would be A. Bradycardia B. Hypotension C. Pain D. None of the above
241. (D) Naloxone is a pure opioid antagonist (affinity but no intrinsic activity) at all opioid receptors. It mainly is used to reverse narcotic-induced toxicity. In large doses, naloxone may reverse the effects of endogenous opioids that are elevated in conditions of stress (e.g., shock or stroke). Naloxone has no effect on NSAIDs (e.g., ketorolac) (Miller: Miller’s Anesthesia ed 8, pp 905–906).
242. Which drug produces strong pulmonary arterial dilation with the least amount of systemic artery dilation? A. Nitroprusside B. Prostaglandin E1 C. Phentolamine D. Nitric oxide
242. (D) Nitric oxide, nitroglycerin, nitroprusside, phentolamine, amrinone, milrinone, and prostaglandin E all have a vasodilatory effect on the pulmonary arterial tree. However, only nitric oxide has basically no effect on the systemic circulation. The following table compares the relative efficacy of various intravenous vasodilators (Miller: Miller’s Anesthesia, ed 8, pp 3084–3088). RELATIVE EFFICACY OF INTRAVENOUS VASODILATORS ON HEMODYNAMIC VARIABLES Dilation Venous Pulmonary Arterial Systemic Arterial Cardiac Output Nitric oxide 0 +++ 0 ± Nitroglycerin IV +++ + + I, D* Nitroprusside +++ +++ +++ I, D* Phentolamine + + +++ I Hydralazine 0 ? +++ I Nicardipine 0 ? +++ I Amrinone† + + + I Milrinone† + + + I Prostaglandin E1‡ + +++ +++ I, D* 0, none; ±, small and variable; +, mild; +++, strongest effect of that particular drug; D, decrease; I, increase. *Effect on cardiac output depends on net balance of effects on preload, afterload, and myocardial oxygenation. †Amrinone and milrinone are inodilators (they have inotropic plus vasodilating effects). ‡Prostaglandin E1 almost always requires left atrial infusion of norepinephrine to sustain adequate systemic blood pressure. From Stoelting RK, Miller RD: Basics of Anesthesia, ed 5, Philadelphia, Churchill Livingstone, 2006, p 1794. 78 Part 1 Basic Sciences
243. The action of succinylcholine at the neuromuscular junction is terminated by which mechanism? A. Hydrolysis by pseudocholinesterase B. Diffusion into extracellular fluid C. Reuptake into nerve tissue D. Reuptake into muscle tissue Pharmacology and Pharmacokinetics of Intravenous Drugs 57
243. (B) Succinylcholine is rapidly metabolized in the blood by pseudocholinesterase (plasma cholinesterase). This accounts for the large dose required to facilitate intubation. Because pseudocholinesterase is not present at the neuromuscular junction, succinylcholine’s action is terminated after it diffuses into the extracellular fluid (Miller: Miller’s Anesthesia, ed 8, p 961).
244. The LEAST likely side effect of dexmedetomidine in a healthy patient is A. Respiratory arrest B. Bradycardia C. Sinus arrest D. Hypotension
244. (A) Dexmedetomidine is a highly selective α2-adrenergic agonist that is mainly used for sedation. It has a rapid onset of action (<5 minutes) and a peak effect in about 15 minutes. In normovolemic healthy patients, the cardiovascular effects include a decrease in heart rate and cardiac output. The heart-rate changes can be profound, and occasionally sinus arrest may develop. After an IV injection, the BP initially increases (due to peripheral α stimulation), then within 15 minutes returns to normal and is followed by an approximately 15% decrease in BP within an hour. This is related to its CNS α-adrenergic stimulation overriding the peripheral effects. Respiratory changes are minimal, provided that excessive sedation does not produce obstructive apnea. At clinical doses of 1 to 2 μg/kg/min only a mild decrease in tidal volume (Vt) is seen, with no change in respiratory rate. With high doses, the Paco2 may increase about 20% due to a decrease in Vt as the respiratory rate increases (Miller: Miller’s Anesthesia, ed 8, pp 834–838).
245. The advantage of fospropofol (Lusedra) over propofol is the absence of A. Pain on injection B. Risk of hypertriglyceridemia C. Risk of infection, sepsis, or both D. All of the above
245. (D) Fospropofol (Lusedra), approved in December 2008 for monitored anesthesia care, is a prodrug of propofol that, after IV infusion, is rapidly converted into propofol. Because it is water soluble, the problems associated with a lipid vehicle (pain on injection, risk of hypertriglyceridemia, risk of pulmonary embolism, risk of sepsis) are absent (Eisai Corporation product information; Miller: Miller’s Anesthesia, ed 8, pp 822–823).
246. Which of the following features of chronic morphine therapy is NOT subject to tolerance? A. Analgesia B. Respiratory depression C. Constipation D. All are subject to tolerance
246. (C) In addition to analgesia, respiratory depression, nausea, and euphoria, tolerance to sedation with chronic analgesic therapy with morphine will develop after 2 to 3 weeks of treatment. Miosis and constipation occur with narcotic administration regardless of length of therapy. The concept of tolerance is not applicable to these two side effects (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 195).
247. A 78-year-old woman with a history of reactive airways disease takes cimetidine (Tagamet) 400 mg at night. An additional dose is given IV 30 minutes before induction of anesthesia for an exploratory laparotomy. Possible side effects associated with this drug include all of the following EXCEPT A. Bradycardia B. Delayed awakening C. Confusion D. Increased metabolism of diazepam
247. (D) H2-receptor antagonists (e.g., cimetidine, ranitidine, famotidine, nizatidine) can be used preoperatively to increase gastric fluid pH before induction of anesthesia. Elevation of gastric fluid pH (above 2.5) is desirable to decrease the incidence and severity of lung damage if aspiration of gastric contents occurs. H2-receptor antagonists are not uncommonly used as a premedication for parturients, patients with symptomatic gastroesophageal reflux, and obese patients (who tend to have very acidic gastric fluid compared to nonobese patients). H2-receptor antagonists, in contrast to metoclopramide, have no effect on lower esophageal sphincter tone, intestinal motility, or gastric emptying. Although the incidence of side effects is low, side effects occasionally may develop in patients, especially when the drug is administered intravenously and when the drugs are administered to the elderly or to patients with hepatic or renal dysfunction. Bradycardia may develop and may be related to the effects on cardiac H2 receptors. Reversible elevation of plasma aminotransaminase enzymes may occur. H2-receptor antagonists cross the blood-brain barrier and may lead to mental confusion or delayed awakening. Cimetidine impairs the metabolism of drugs such as lidocaine, propranolol, and diazepam. This impairment may be related to the binding of cimetidine to the cytochrome P-450 enzymes (Barash: Clinical Anesthesia, ed 7, p 602).
248. Intraoperative allergic reactions are LEAST common after patient exposure to A. Ketamine B. Latex C. Muscle relaxants D. Hydroxyethyl starch
248. (A) Drug sensitivity has been reported in about 3% to 4% of anesthetic-related deaths. Allergic drug reactions have been reported to occur with most drugs administered during anesthesia, with the exception of ketamine and the benzodiazepines. Although most drug-induced allergic reactions occur within 5 to 10 minutes of exposure, reactions to latex products may take longer than 30 minutes to develop (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 525–529).
249. Which of the following medications would be useful in the definitive treatment of sarin nerve gas poisoning? A. Sodium nitroprusside B. Methylene blue C. Atropine D. All the above are useful
249. (C) Atropine is administered in doses of 2 to 6 mg and is repeated every 5 to 10 minutes until secretions begin to decrease. In most cases, 2 mg every 8 hours is needed. However, doses of 15 to 20 mg are not uncommon and occasionally doses over 1000 mg have been needed. Pralidoxime 600 mg removes the organophosphate compounds from acetylcholinesterase and is often used in conjunction with atropine. Benzodiazepines are often administered to counter the effects of the nerve gases on the GABA system (Barash: Clinical Anesthesiology, ed 7, p 1541). Pharmacology and Pharmacokinetics of Intravenous Drugs 79
250. Alfentanil A. Has a more rapid onset of action compared to fentanyl B. Has a longer duration of action compared with fentanyl C. Is 250 times more potent than fentanyl D. Is excreted unchanged in the urine
250. (A) Alfentanil (a fentanyl analog) is less potent (1/5 to 1/10), has a more rapid onset (within 1.5 minutes), and has a shorter duration of action than fentanyl. The brief duration of action of alfentanil is a result of redistribution to inactive tissue sites and its rapid hepatic metabolism (96% cleared within 1 hour). Renal failure does not alter the clearance of alfentanil (Miller: Basics of Anesthesia, ed 6, p 119, Figure 10-3; Miller: Miller’s Anesthesia, ed 8, p 887; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 196).
251. Which of the following medications is NOT useful in the immediate management of status asthmaticus? A. Terbutaline B. Subcutaneous (SQ) epinephrine C. Magnesium sulfate D. Cromolyn
251. (D) Asthma is an inflammatory illness associated with bronchial hyper-reactivity and bronchospasm. Medications effective in the management of acute exacerbations of bronchial asthma include the rapid-onset inhaled β2-adrenergic receptor agonists (e.g., albuterol, pirbuterol, terbutaline), anticholinergic drugs (e.g., inhaled ipratropium), and IV corticosteroids. In an acute attack, ipratropium (slower in onset than β2-adrenergic receptor agonists) can be effective when used in combination with the rapid-onset β2 agonists. When unresolving bronchospasm occurs and is considered life threatening, the diagnosis of status asthmaticus is made. Although treatment often starts with β2 agonists (two to four puffs every 15-20 minutes), when alveolar ventilation is reduced, inhaled agents may not be successful. In this case, SQ epinephrine (adult dose of 0.2 to 1 mg or 0.2 to 1 mL of 1:1000 solution) can be given. Corticosteroids enhance and prolong the response to β2 agonists, and, in status asthmaticus, IV corticosteroids such as cortisol (Solu-Cortef) 2 mg/kg IV bolus followed by 0.5 mg/ kg/hr, or methylprednisolone (Solu-Medrol) 60 to 125 mg every 6 hours, are administered early in the treatment (but may take several hours to work). Supplemental oxygen is given to keep the oxygen saturation greater than 90%. Because Heliox (70% helium and 30% oxygen) is one third the density of oxygen, it can be tried. IV terbutaline starting at a rate of 0.1 μg/kg/min and increased until improvement is seen or significant tachycardia develops may be useful. Magnesium sulfate at a dose of 25 to 40 mg/kg (maximum of 2 g) administered over 20 minutes has been used. Broad-spectrum antibiotics are also started. In severe cases where fatigue sets in and the Paco2 is rising (e.g., >70-80 mm Hg), general anesthesia with mechanical ventilation may be needed. The volatile anesthetics such as isoflurane, halothane, or sevoflurane can be used not only to sedate but also to relax the smooth muscle in the constricted airways. Cromolyn, however, does not relieve bronchospasm. Cromolyn is used prophylactically because it inhibits antigen-induced release of histamine and other autacoids, such as leukotrienes, from mast cells. Aminophylline once was widely used to treat acute asthma but is rarely used today because it adds little to β2-agonist activity and has significant side effects (Hardman: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 10, pp 733–749; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 185–186).
252. Clonidine A. Is an α2 blocker B. Increases CNS sympathetic response to painful stimuli C. Can be given orally as well as intravenously, but not epidurally or intrathecally D. Decreases postanesthetic shivering
252. (D) Clonidine is an α2-adrenergic agonist. Unlike many peripherally acting antihypertensive drugs (e.g., guanethidine, propranolol, captopril), clonidine primarily stimulates central adrenergic receptors and decreases the sympathetic response. As with other drugs that affect the central release of catecholamines, clonidine not only reduces anesthetic requirements (as represented by a decrease in MAC) but also decreases extremes in arterial BP during anesthesia. Clonidine has analgesic properties and reduces the requirements for opioids. Clonidine has been given orally, intravenously, epidurally, intrathecally, and in peripheral nerve blocks and potentiates the analgesic effect of local anesthetics. α2-Adrenergic agonists can reduce the muscle rigidity seen with the administration of narcotics and can be used to decrease postanesthetic shivering. Patients chronically taking clonidine should not have it discontinued before surgery and should keep taking clonidine to prevent clonidine withdrawal and hypertensive crisis (Miller: Miller’s Anesthesia, ed 8, pp 368, 1218, 1632).
253. The plasma half-time of which of the following drugs is prolonged in patients with end-stage cirrhotic liver disease? A. Diazepam B. Pancuronium C. Alfentanil D. All are prolonged
253. (D) Chronic liver disease may interfere with the metabolism of drugs because of the decreased number of enzyme- containing hepatocytes, decreased hepatic blood flow, or both. Prolonged elimination half-times for morphine, alfentanil, diazepam, lidocaine, pancuronium, and, to a lesser extent, vecuronium have been demonstrated in patients with cirrhosis of the liver. In addition, severe liver disease may decrease the production of cholinesterase (pseudocholinesterase) enzyme, which is necessary for the hydrolysis of ester linkages in drugs such as succinylcholine, and the ester local anesthetics such as procaine (Miller: Basics of Anesthesia, ed 6, p 456).
254. A 24-year-old, 100-kg patient is brought to the emergency room by the fire department after suffering smoke inhalation and third-degree burns on the abdomen, chest, and thighs 30 minutes earlier. The best muscle relaxant choice for the most rapid intubation would be A. 2 mg vecuronium followed by succinylcholine B. 1 mg of vecuronium, then 2 to 4 minutes later, 9 mg vecuronium C. Rocuronium D. Succinylcholine
254. (D) Succinylcholine is the drug of choice (unless contraindicated) when rapid-sequence tracheal intubation is needed. Although hyperkalemic cardiac arrest is a complication of succinylcholine administrations to patients who have sustained burns (as well as crush injuries, spinal cord trauma, or other denervation 80 Part 1 Basic Sciences injuries, chronic illness polyneuropathy, and chronic illness myopathy), the susceptibility for hyperkalemia after a burn injury peaks at 7 to 10 days but may begin as early as 2 days after sustaining a thermal injury. The first 24 hours after the injury are considered safe. Adding a defasciculating dose of a nondepolarizing neuromuscular blocking drug before succinylcholine use to the regimen would slow down achievement of paralysis. Although the “priming” technique of giving 10% of the intubating dose followed 2 to 4 minutes later by the rest of the intubating dose has been used to speed conditions for intubation, it is still slower than succinylcholine, and this technique is rarely used because rocuronium (which provides the most rapid intubating conditions among the nondepolarizing neuromuscular blocking drugs and is a close second behind succinylcholine) is available. An intubating dose of d-tubocurarine should never be given as a bolus because of its moderate histamine release (Miller: Basics of Anesthesia, ed 6, pp 148–149).
255. Clonidine is useful in each of the following applications EXCEPT A. Reducing BP with pheochromocytoma B. Treatment of postoperative shivering C. Protection against perioperative myocardial ischemia D. As an agent for prolonging a bupivacaine spinal
255. (A) Clonidine, a centrally acting α-agonist, decreases sympathetic nervous system outflow and decreases plasma catecholamine concentrations in normal patients, but it has no effect in patients with pheochromocytomas. It is used as an antihypertensive agent for treating essential hypertension, an analgesic when injected epidurally or into the subarachnoid space alone, a drug that prolongs the effect of regional local anesthetics, a drug that can be used to stop shivering (75 μg IV), a drug that can help protect against perioperative myocardial ischemia (when given preoperatively and typically for 4 days after surgery), and a drug that can help decrease the symptoms of narcotic and alcohol withdrawal (Barash: Clinical Anesthesia, ed 7, p 392; Miller: Miller’s Anesthesia, ed 8, p 473; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 394).
256. A 79-year-old man is brought to the operating room for elective repair of bilateral inguinal hernias. The patient has a history of awareness during general anesthesia and refuses regional anesthesia. The patient is preoxygenated before induction of general anesthesia; 5 mg of midazolam and 250 mg of fentanyl are administered. One minute later the patient loses consciousness and chest wall stiffness develops to the extent that positive-pressure ventilation is very difficult. The most appropriate therapy for reversal of chest wall stiffness at this point could include A. Flumazenil B. Naloxone C. Succinylcholine D. Albuterol 58 Part 1 Basic Sciences
256. (C) Skeletal muscle spasm, particularly of the thoracoabdominal muscles (“stiff chest” syndrome), may occur when large doses of opioids are given rapidly. This may be significant enough to prevent adequate ventilation. Although the administration of a muscle relaxant or an opioid antagonist such as naloxone will terminate the skeletal muscle rigidity, reversing the narcotic effect may not be desirable if surgery is needed (Miller: Basics of Anesthesia, ed 6, p 121).
257. Respiratory depression is LEAST after the induction dose of which of the following drugs? A. Etomidate B. Ketamine C. Fentanyl D. Propofol
257. (B) One of the advantages of ketamine is the minimal effect on respirations. After the intravenous induction dose of 2 mg/kg, general anesthesia is induced within 30 to 60 seconds with, at most, a transient decrease in respirations (Paco2 rarely increases more than 3 mm Hg). With unusually high doses, or if opioids are also administered, apnea can occur (Miller: Basics of Anesthesia, ed 6, p 108).
258. A 64-year-old man with colon cancer is anesthetized for hepatic resection of liver metastases. Medical history is significant for ileal conduit surgery for bladder cancer, diabetes treated with glyburide, 50 packs per year smoking history, and family history of malignant hyperthermia. Anesthesia is provided with morphine, midazolam, oxygen, and a propofol infusion. After a 3-unit packed red blood cell (RBC) transfusion and 8 hours of surgery, the following blood gas values are recorded: pH 7.2, CO2 34, [HCO3 –] 14, base deficit −13, [Na+] 135, [K+] 5, [Cl–] 95, glucose 240 mg/dL. The most likely cause of this patient’s acidosis is A. Excessive infusion of normal saline B. Renal tubular acidosis C. Propofol infusion syndrome D. Diabetic ketoacidosis
258. (C) This patient has a partially compensated metabolic acidosis. Metabolic acidosis is commonly divided into those with a normal ion gap, also called hyperchloremic metabolic acidosis (bicarbonate loss is counterbalanced by an increase in chloride levels), and those with a high anion gap. The anion gap can be calculated by determining the difference between the sodium concentration and the sum of the chloride and bicarbonate concentrations (i.e., [Na+] − [Cl–] + [HCO3 –]) and is normally 8 to 14 mEq/L. In this case, the anion gap is 135 − [95 + 14] = 26. This patient, therefore, has a high anion gap acidosis. This question has two forms of acidosis that have a high anion gap: diabetic ketoacidosis (DKA) and propofol infusion syndrome, which causes a lactic acidosis. Because this patient is a type 2 (non–insulin-dependent) diabetic, DKA does not occur and the cause must be propofol infusion syndrome (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 372–373; Miller: Miller’s Anesthesia, ed 8, p 832).
259. Treatment of neuroleptic malignant syndrome may be carried out with administration of the following drugs EXCEPT A. Amantadine B. Dantrolene C. Bromocriptine D. Physostigmine
259. (D) Neuroleptic malignant syndrome (NMS) can be seen in up to 1% of patients treated with antipsychotic drugs. The syndrome has many features that resemble the condition malignant hyperthermia, including increased metabolism, tachycardia, muscle rigidity, rhabdomyolysis, fever, and acidosis. The mortality rate may be 20% to 30%. There are many differences between NMS and malignant hyperthermia. NMS is not inherited and usually takes 24 to 72 hours to develop after the use of neuroleptic drugs (e.g., phenothiazines, haloperidol), whereas malignant hyperthermia presents more acutely. Stopping the antipsychotic medication is obviously necessary. Because dopamine depletion appears to play a role in causing NMS, the dopamine agonists bromocriptine and amantadine appear useful in the treatment. Abrupt withdrawal of levodopa may also cause this syndrome. Succinylcholine and volatile anesthetics, which are known triggers for malignant hyperthermia, are not triggers for NMS. Dantrolene has been used to treat this condition (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 412–413). Pharmacology and Pharmacokinetics of Intravenous Drugs 81
260. A patient with a normal quantity of pseudocholinesterase (plasma cholinesterase) has a dibucaine number of 57. A 1 mg/kg dose of intravenous succinylcholine would likely result in A. Hyperkalemic cardiac arrest B. Paralysis lasting 5 to 10 minutes C. Paralysis lasting 20 to 30 minutes D. Paralysis lasting more than 1 to 3 hours
260. (C) Normal pseudocholinesterase is inhibited 80% by dibucaine (dibucaine number of 80), whereas patients with atypical cholinesterase show only 20% inhibition (dibucaine number of 20). Patients who are heterozygous for atypical pseudocholinesterase (as in this case) have intermediate dibucaine numbers ranging from 50% to 60%. Succinylcholine paralysis after an intubating dose of 1 mg/kg lasts up to 10 minutes with normal pseudocholinesterase, up to 30 minutes in patients with the atypical heterozygous pseudocholinesterase, and may persist for 3 hours or longer in patients who have atypical cholinesterase paralysis. See also Question 200 (Miller: Basics of Anesthesia, ed 6, pp 148–149).
261. Cyanide toxicity may be treated with all of the following drugs EXCEPT A. Sodium nitrite B. Hydroxocobalamin C. Sodium thiosulfate D. Methylene blue
261. (D) Cyanide (hydrocyanic acid [HCN], prussic acid) is a rapidly acting poison. Cyanide is commercially used as a pesticide, but it can be released as a gas from burning nitrogen-containing plastics. Sodium nitroprusside (SNP) is metabolized to cyanide and nitric oxide. The cyanide produced from SNP usually is rapidly metabolized to relatively nontoxic thiocyanate (SCN−), which is excreted into the urine. Although rare, cyanide and/or thiocyanate toxicity can develop in patients receiving prolonged high-dose infusions of nitroprusside. Cyanide binds to iron in the ferric state and inhibits cellular respiration. This produces severe lactic acidosis and cytotoxic hypoxia. Because oxygen is not used well, the venous blood is well oxygenated (elevated central venous oxygen levels and patients are not cyanotic). Treatment (adult doses in parenthesis) can include sodium nitrite (NaNO2—300 mg IV over 10 minutes), amyl nitrite (inhalation), sodium thiosulfate (12.5 g IV over 10 minutes), and hydroxocobalamin (5-10 g IV over 20 minutes). Nitrite converts hemoglobin to methemoglobin, which competes with cytochrome oxidase for the cyanide ion forming cyanmethemoglobin. Nitrite can be administered IV as sodium nitrite or by inhalation with amyl nitrite. Sodium thiosulfate (Na2S2O3), the preferred drug, is a sulfur donor that converts cyanide to thiocyanate. Hydroxocobalamin combines with cyanide to form cyanocobalamin or vitamin B12. Methylene blue is not an antidote for cyanide toxicity and can complicate therapy by converting methemoglobin back to hemoglobin and releasing free cyanide. Although oxygen alone (even under hyperbaric conditions) has little benefit, it should be used because it dramatically potentiates the activity of thiosulfate and nitrites (Barash: Clinical Anesthesia, ed 7, pp 403–404; Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 782–783, 793–796; Miller: Miller’s Anesthesia, ed 8, pp 2501–2503).
262. A prolonged neuromuscular block with succinylcholine can be seen in all of the following patients EXCEPT those A. Chronically exposed to malathion B. Treated with echothiophate for glaucoma C. Treated with cyclophosphamide for metastatic cancer D. Having a C5 isoenzyme variant
262. (D) The duration of neuromuscular block by succinylcholine can be markedly prolonged when the total amount of plasma cholinesterase is very low, the amount is normal but of an abnormal type (i.e., atypical plasma cholinesterase), or an anticholinesterase drug (e.g., neostigmine, echothiophate, or the organophosphate insecticide malathion) is administered. To evaluate a prolonged response to succinylcholine, one needs to evaluate both the total amount of cholinesterase (i.e., quantitative test) and the type of cholinesterase (i.e., qualitative test). Atypical plasma cholinesterase is an inherited disorder that occurs in approximately 1 of every 480 patients with heterozygous genome and in approximately 1 of 3200 patients with homozygous genome. The local anesthetic dibucaine can inhibit normal plasma cholinesterase enzyme better than an abnormal enzyme. In patients with normal plasma cholinesterase, the dibucaine inhibition test reports a number around 80 or produces 80% inhibition. Heterozygotes have a dibucaine number of around 50, and patients who are homozygous for the atypical plasma cholinesterase have a number around 20. Total plasma cholinesterase levels can be reduced with decreased production, as occurs with severe chronic liver disease or with the use of some chemotherapeutic drugs (e.g., cyclophosphamide). The dibucaine number is normal when the total plasma cholinesterase levels are reduced, as well as after the use of anticholinesterase drugs. Patients with a C5 isoenzyme variant have increased plasma cholinesterase activity, a more rapid breakdown of succinylcholine, and a shorter duration of action (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, p 243; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 205–207; Miller: Basics of Anesthesia, ed 6, pp 76, 148–149; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 216–220).
263. Which of the following statements concerning midazolam is FALSE? A. Midazolam has greater amnestic than sedative properties B. Its breakdown is inhibited by cimetidine C. It produces retrograde amnesia D. It facilitates the actions of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the CNS
263. (C) Benzodiazepines are drugs that have the chemical structure of a benzene ring attached to a seven-member diazepine ring. Midazolam, lorazepam, oxazepam, and diazepam are benzodiazepine agonists and flumazenil is an antagonist. Benzodiazepine agonists are all sedatives and possess a number of favorable pharmacologic characteristics, including production of sedation, anxiolysis, anterograde amnesia (acquisition of new information), and anticonvulsant activity. The amnestic properties are greater than the sedative properties, which 82 Part 1 Basic Sciences is why patients sometimes forget what you tell them after the benzodiazepine is given, despite their having what appears to be a lucid discussion with you. They do not produce retrograde amnesia (stored information). They rarely cause significant respiratory or cardiovascular depression and rarely are associated with the development of significant tolerance or physical dependence. The agonist actions of benzodiazepines most likely reflect the ability of these drugs to facilitate the inhibitory neurotransmitter GABA actions in the CNS. Midazolam and diazepam undergo oxidative metabolism, and their metabolites are conjugated with glucuronide before renal excretion. Cimetidine inhibits oxidative metabolism and may prolong the duration of these drugs. Lorazepam and oxazepam primarily undergo conjugation with glucuronic acid, which is not influenced by cimetidine usage or alterations in hepatic function (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 458–467; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 179–181; Miller: Basics of Anesthesia, ed 6, pp 106–109; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 140–153).
264. After a 2-hour vertical gastric banding procedure under desflurane, oxygen, and remifentanil anesthesia, the trocar is removed and the wound is closed. Upon emergence, the most likely scenario is A. Adequate analgesia for 2 hours B. Delayed emergence from narcotic C. Pain D. Respiratory depression in postanesthesia care unit (PACU)
264. (C) Remifentanil is an ultrashort-acting opioid most commonly administered by an IV infusion. Its short duration of action is due to its ester linkage, which allows for rapid breakdown by nonspecific plasma and tissue esterases (primarily within erythrocytes). Its metabolism is not significantly influenced by renal failure, hepatic failure, or pseudocholinesterase levels (because it is not metabolized to any significant extent by plasma pseudocholinesterase). The clinical elimination half-time is less than 6 minutes. For monitored anesthesia care sedation after 2 mg of midazolam, an infusion rate of 0.05 to 0.1 μg/kg/min is used in healthy adults. For analgesia during general anesthesia with controlled respirations, a rate of 0.1 to 1.0 μg/ kg/min is commonly used. A loading dose of 1 μg/kg of remifentanil (or 0.5 μg/kg, if a benzodiazepine was also given) can be given IV over 60 to 90 seconds before starting the infusion. Although it effectively suppresses autonomic and hemodynamic responses to painful stimuli and decreases respirations as well, its rapid dissipation of opioid effect produces rapid onset of postoperative pain (in painful surgical operations), unless other analgesics are administered for postoperative pain before stopping the infusion (Barash: Clinical Anesthesia, ed 7, pp 514–515, 832–834; Miller: Miller’s Anesthesia, ed 8, pp 888–897).
265. An oral surgeon is about to perform a full mouth extraction on a 70-kg, 63-year-old man under conscious sedation. What is the maximum dose of lidocaine with epinephrine that he can safely infiltrate? A. 200 mg B. 300 mg C. 400 mg D. 500 mg
265. (D) The maximum recommended single dose of lidocaine given by infiltration is 300 mg of lidocaine without epinephrine and 500 mg of lidocaine with epinephrine. Careful injection in the mouth is recommended due to the vascular nature of that area (Barash: Clinical Anesthesia, ed 7, p 572; Miller: Miller’s Anesthesia, ed 8, p 1041).
266. Postanesthetic shivering can be treated with all of the following EXCEPT A. Naloxone B. Physostigmine C. Magnesium sulfate D. Dexmedetomidine
266. (A) Postoperative shivering can be caused by many factors, including hypothermia, transfusion reactions, and pain, as well as anesthetics. It is uncomfortable for patients and can make monitoring more difficult, but it also can lead to significant increases in oxygen consumption (up to 200%). The exact etiology in many cases is unclear, but, after routine skin surface warming, pharmacologic treatment may be needed. Clonidine, dexmedetomidine, propofol, ketanserin, tramadol, physostigmine, magnesium sulfate, and narcotics (especially meperidine) have been used. Naloxone use may increase pain and does not help decrease shivering (Barash: Clinical Anesthesia, ed 7, p 1574; Miller: Miller’s Anesthesia, ed 8, pp 1636–1638).
267. The main disadvantage of Sugammadex (ORG 25969) compared with neostigmine is A. Recurarization B. Contraindicated with renal failure C. Not effective with benzylisoquinolinium relaxants D. High incidence of allergic reactions
267. (C) Sugammadex is a cyclodextrin (cyclic oligosaccharide) compound that encapsulates nondepolarizing steroidal muscle relaxants (rocuronium > vecuronium >> pancuronium) and produces rapid reversal of profound block (e.g., reversal of 0.6 mg/kg rocuronium in 3 minutes). Because it has no effect on acetylcholinesterase, there is no need to combine it with the anticholinergics atropine or glycopyrrolate. It works only with steroidal muscle relaxants and has no effect on reversing the benzylisoquinolinium relaxants (e.g., atracurium, cisatracurium, doxacurium, d-tubocurarine). There appear to be no cardiovascular effects with sugammadex. It is available only outside the United States at present (Miller: Basics of Anesthesia, ed 6, p 159; Miller: Miller’s Anesthesia, ed 8, p 965).
268. Which of the biologic substances listed below is by itself the greatest determinant of serum osmolality? A. AVP (arginine vasopressin) B. Angiotensin I C. Aldosterone D. Renal prostaglandins (PGE2)
268. (A) Arginine vasopressin (AVP), also called antidiuretic hormone (ADH), has many actions, but its primary role involves controlling serum osmolality by regulating diuresis. AVP is released by the hypothalamus and directly causes the collecting tubules in the kidney to increase water permeability and reabsorption. This increases blood volume and lowers serum osmolality. Below a serum osmolality of 280 mOsm/kg, AVP is barely detectable; however, when the osmolality is greater than 290 mOsm/kg, AVP is maximally secreted. AVP is also secreted when the intravascular volume is detected to be low (e.g., hemorrhage, heart failure, hepatic cirrhosis, and adrenal insufficiency). Angiotensin I is converted to angiotensin II, Pharmacology and Pharmacokinetics of Intravenous Drugs 83 which is a potent vasoconstrictor and increases aldosterone secretion from the adrenal cortex. Aldosterone is a mineralocorticoid and is involved in sodium reabsorption and potassium excretion in the renal tubules. Aldosterone secretion is stimulated by hypovolemic states. Renal prostaglandins are released from the kidney by sympathetic stimulation or by angiotensin II and help modulate the effects of AVP (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 738; Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 671–704, 721–730; Miller: Basics of Anesthesia, ed 6, pp 449–450).
269. Above which infusion rate does cyanide toxicity become a concern in a healthy adult receiving sodium nitroprusside? A. 0.5 μg/kg/min B. 2 μg/kg/min C. 10 μg/kg/min D. 20 μg/kg/min Pharmacology and Pharmacokinetics of Intravenous Drugs 59
269. (B) Sodium nitroprusside (SNP) is a rapid-acting, direct-acting peripheral vasodilator that is composed of five cyanide moieties for every NO (nitric oxide) moiety. Sodium nitroprusside undergoes rapid metabolism to release NO as the active ingredient. Healthy adults can easily eliminate the cyanide produced during SNP rates of less than 2 μg/kg/min. Above 2 μg/kg/min and especially if the infusion rate is greater than 10 μg/kg/min for 10 minutes, one should be concerned about cyanide toxicity. An early sign of cyanide toxicity is resistance to the hypotensive effects of SNP infusion, especially when the rate is less than 2 μg/kg/min. Other signs include metabolic acidosis and an elevation of mixed venous Po2 values (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 258).
270. Important interactions involving chlorpromazine include all of the following EXCEPT A. Potentiation of the depressant effects of narcotics B. Lowering of the seizure threshold C. Prolongation of the QT interval D. Potentiation of neuromuscular blockade
270. (D) Phenothiazines, such as chlorpromazine (Thorazine), are effective antipsychotic (neuroleptic) drugs that block D2 dopaminergic receptors in the brain. Extrapyramidal effects are not uncommon with these drugs. They also possess antiemetic effects. Phenothiazines with low potency, such as chlorpromazine, have prominent sedative effects, which gradually decrease with treatment. The effects of CNS depressants (e.g., narcotics and barbiturates) are enhanced by concomitant administration of phenothiazines. Lowering the seizure threshold is more common with aliphatic phenothiazines with low potency (e.g., chlorpromazine) compared with piperazine phenothiazines. These drugs are associated with cholestatic jaundice, impotence, dystonia, and photosensitivity. Electrocardiographic abnormalities, such as prolongation of the QT or PR intervals, blunting of T waves, depression of the ST segment, and, on rare occasions, premature ventricular contractions and torsades de pointes, are seen. The antihypertensive effects of guanethidine and guanadrel are blocked by phenothiazines. These drugs have no effect on neuromuscular blockade (Miller: Miller’s Anesthesia, ed 8, p 1219; Hemmings: Pharmacology and Physiology for Anesthesia, pp 189–192).
271. Amrinone A. Is a positive inotropic drug B. Is antagonized by esmolol C. Is a vasoconstrictor D. All the above
271. (A) Amrinone is a noncatecholamine, nonglycoside cardiac inotropic drug that works as a selective phosphodiesterase III (PDE III) inhibitor. Amrinone increases cyclic adenosine monophosphate (cAMP) levels by decreasing cAMP breakdown in the myocardium and vascular smooth muscle. Because the actions of PDE III inhibitors work by a different mechanism than catecholamines (cAMP levels are increased by β-adrenergic receptor stimulation), amrinone can work in the presence of β-blockade and in cases where patients become refractory to catecholamine use. The catecholamine actions can be enhanced with PDE III inhibitors. Amrinone produces both positive inotropic and vasodilatory effects but has no antidysrhythmic effects (Hensley: A Practical Approach to Cardiac Anesthesia, ed 5, p 277).
272. Which statement concerning tricyclic antidepressants in patients receiving general anesthesia is TRUE? A. They should be discontinued 2 weeks before elective operations B. They may decrease the requirement for volatile anesthetics (decrease MAC) C. Meperidine may produce hyperpyrexia in patients taking tricyclic antidepressants D. They may exaggerate the response to ephedrine
272. (D) Tricyclic antidepressants often are administered as the initial treatment of mental depression; however, the more recently developed SSRIs are more frequently used because of fewer side effects. Tricyclic antidepressants work by inhibiting the reuptake of released norepinephrine (and serotonin) into the nerve endings. Although at one time it was recommended to stop tricyclic antidepressants before elective surgery, this has not been shown to be necessary. However, alterations in patient responses to some drugs should be anticipated. The increased availability of neurotransmitters in the CNS can result in increased anesthetic requirements (i.e., increased MAC). In addition, the increased availability of norepinephrine at postsynaptic receptors in the peripheral sympathetic nervous system can be responsible for an exaggerated BP response after administration of an indirect-acting vasopressor such as ephedrine. If a vasopressor is required, a direct-acting drug such as phenylephrine may be preferred. If hypertension occurs and requires treatment, deepening the anesthetic or adding a peripheral vasodilator such as nitroprusside may be needed. The potential for an exaggerated BP response (i.e., hypertensive crisis) is greatest during the acute treatment phase (the first 14-21 days). Chronic treatment is associated with down-regulation receptors and a decreased likelihood of an exaggerated BP response after administration of a sympathomimetic. Tricyclics have significant anticholinergic side effects (e.g., dry mouth, blurred vision, increased heart rate, urinary retention) and caution is especially important in elderly patients who may develop anticholinergic delirium despite the therapeutic doses administered. Caution 84 Part 1 Basic Sciences is advised with the use of meperidine in patients taking MAOIs (not tricyclic antidepressants) because of the possibility of inducing seizure, hyperpyrexia, or coma (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 535–536).
273. Which of the following types of insulin preparations has the fastest onset of action if administered subcutaneously? A. Glargine (Lantus) B. Lispro (Humalog) C. Regular (Humulin-R) D. NPH (Humulin-N)
273. (B) In normal nondiabetic patients, about 40 units of insulin are secreted every day. There are many SQ insulin preparations available. After SQ administration the onset of action is very rapid with Lispro and Aspart (15 minutes); rapid with Regular (30 minutes); intermediate with NPH or Lente (1-2 hours); and slow with Glargine (1.5 hours) and Ultralente (4-6 hours) (Hines: Stoelting’s Anesthesia and Co- Existing Disease, ed 6, pp 380–381). INSULIN PREPARATIONS Insulin Preparation Hours after Subcutaneous Administration Onset Peak Duration Very rapid acting Lispro (Humalog) 0.25 1-2 3-6 Aspart (NovoLog) 0.25 1-2 3-6 Rapid acting Regular (Humulin-R, Novolin-R) 0.5 2-4 5-8 Intermediate acting NPH (Humulin-N) 1-2 6-10 10-20 Lente 1-2 6-10 10-20 Long acting Glargine (Lantus) 1-2 Peakless About 24 Ultralente 4-6 8-20 24-48 From Hines RL: Stoelting’s Anesthesia and Co-Existing Disease, ed 5, Philadelphia, Saunders, 2008, p 371.
274. Which of the following mechanisms best explains the anticoagulative properties of tirofiban? A. Cyclooxygenase (COX) inhibition B. Interaction with von Willebrand factor (vWF) C. Interaction with antithrombin III D. Enhanced anti-Xa activity
274. (B) The GPIIb/IIIa receptor is specific for platelets. Platelet activation changes the shape of the receptor and increases its affinity for fibrinogen and vWF. GPIIb/IIIa receptor antagonists (e.g., tirofiban, abciximab, and eptifibatide) reversibly bind to the platelet GPIIb/IIIa receptor and block the binding of fibrinogen to platelets. They do not prolong the prothrombin time or the activated partial thromboplastin time. These drugs are administered intravenously as a bolus and then as a continuous infusion. The plasma half-life after a bolus intravenous injection is 2 hours for tirofiban, 2.5 hours for eptifibatide, and only 30 minutes for abciximab. The biologic half-life of these drugs is 4 to 8 hours for tirofiban, 4 to 6 hours for eptifibatide, and 12 to 24 hours for abciximab. The longer duration of action for abciximab is primarily due to clearance by the reticuloendothelial system (tirofiban and eptifibatide are cleared by the kidney) and its stronger affinity to the receptor (Hemmings: Pharmacology and Physiology for Anesthesia, pp 662–664; Miller: Basics of Anesthesia, ed 6, p 359; Miller: Miller’s Anesthesia, ed 8, p 1873).
275. The duration of action of remifentanil is attributable to which mode of metabolism? A. Spontaneous degradation in blood (Hofmann elimination) B. Hydrolysis by nonspecific plasma esterases C. Hydrolysis by pseudocholinesterase D. Rapid metabolism in the large intestine
275. (B) Remifentanil is rapidly hydrolyzed by nonspecific plasma and tissue esterases, making it ideal for an infusion where precise control is sought. The onset and offset of remifentanil is rapid (clinical half-time of <6 minutes). Because the activity of these nonspecific esterases is not usually affected by liver and renal failure, remifentanil is well suited for such patients (Miller: Basics of Anesthesia, ed 6, p 125).
276. Pain at the intravenous site is LEAST with which IV drug? A. Diazepam B. Etomidate C. Ketamine D. Propofol
276. (C) Pain with the intravenous injection is common with diazepam, etomidate, methohexital, and propofol. It is very rare after thiopental and ketamine (Miller: Basics of Anesthesia, ed 6, pp 102,109,112).
277. A 35-year-old patient with a history of grand mal seizures is anesthetized for thyroid biopsy under general anesthesia consisting of 4 mg midazolam with infusion of propofol (150 μg/kg/min) and remifentanil (1 μg/ kg/min). The patient takes phenytoin for control of seizures. After 30 minutes, the infusion is stopped and the patient is transported intubated to the recovery room where he is arousable, but not breathing. The most reasonable course of action would be A. Administer naloxone B. Administer flumazenil C. Administer naloxone and flumazenil D. Ventilate by hand
277. (D) Patients anesthetized with total intravenous anesthesia (TIVA), in this case consisting of midazolam, remifentanil, and propofol, sometimes require a few minutes to resume breathing after the infusions are stopped. Although it may seem appropriate to reverse this patient and avoid the need for hand ventilation, reversing benzodiazepines (midazolam) with flumazenil may precipitate seizures in epileptic patients, and, because remifentanil has such a short elimination half-life (<6 minutes), reversal with naloxone is not necessary. The patient needs a brief period to allow the propofol to wear off, during which hand or mechanical ventilation will be necessary (until the patient breathes spontaneously). Also, muscle weakness must be ruled out if a muscle relaxant has been used, and normocapnia should be assured given that hyperventilation may reduce the arterial CO2 below the apneic threshold (Miller: Miller’s Anesthesia, ed 8, p 897). Pharmacology and Pharmacokinetics of Intravenous Drugs 85
278. Which of the following α-antagonists produces an irreversible blockade? A. Phentolamine B. Prazosin C. Phenoxybenzamine D. Labetalol
278. (C) Phentolamine, prazosin, yohimbine, tolazoline, and terazosin are competitive and reversible α-adrenergic antagonists. Phenoxybenzamine produces an irreversible α-adrenergic blockade. Once phenoxybenzamine’s α-blockade develops, even massive doses of sympathomimetics are ineffective until phenoxybenzamine’s action is terminated by metabolism. Phentolamine and phenoxybenzamine are nonselective α1 and α2 antagonists, prazosin is a selective α1 antagonist, and yohimbine is a selective α2 antagonist (Hemmings: Pharmacology and Physiology for Anesthesia, pp 227–229).
279. Metoprolol is relatively contraindicated for treatment of tachycardia in the setting of A. Hypertrophic obstructive cardiomyopathy (HOCM) B. WPW syndrome (with narrow QRS) C. Prolonged QT syndrome D. Cardiac tamponade
279. (C) Symptomatic bradycardia as a result of excessive β-adrenergic receptor blockade can be treated with a variety of drugs, as well as with a pacemaker. Treatment depends upon severity of symptoms. Atropine can block any parasympathetic nervous system contribution to the bradycardia. If atropine is not effective, then a pure β-adrenergic receptor agonist can be tried. For excessive cardioselective β1 blockade, dobutamine can be used; for a noncardiac selective β1 and β2 blockade, isoproterenol can be chosen. Dopamine is not recommended because the high doses needed to overcome β-adrenergic receptor blockade will cause significant α-adrenergic receptor–induced vasoconstriction. Glucagon at an initial dose of 1 to 10 mg intravenously followed by an infusion of 5 mg/hr often is believed to be the drug of choice for β-adrenergic blockade overdosage. Glucagon increases myocardial contractility and heart rate, primarily by increasing cAMP formation (not via β-adrenergic receptor stimulation) and, to a lesser extent, by stimulating the release of catecholamines. Other drugs that have been used include aminophylline and calcium chloride. Aminophylline inhibits phosphodiesterase, resulting in an increase in cAMP. Thus, like glucagon, aminophylline increases cardiac output and heart rate via a non–β-adrenergic receptor–mediated mechanism. Calcium chloride may prove useful to counteract any decrease in myocardial contractility induced by the β-blockade; however, this effect may be transient (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 331–332).
280. A dose of 150 mg of IV dantrolene is administered to a 24-year-old, 75-kg man in whom incipient malignant hyperthermia is suspected. An expected consequence of this therapy would be A. Muscle spasticity in the postoperative period B. Hypothermia C. Cardiac dysrhythmias D. Diuresis
280. (D) Dantrolene is a skeletal muscle relaxant that is effective in the treatment of malignant hyperthermia. Dantrolene is formulated with mannitol (300 mg mannitol/20 mg dantrolene) so that diuresis is promoted during dantrolene therapy. Myoglobinuria from malignant hyperthermia–associated muscle breakdown accumulates in the renal tubules and can cause kidney failure if urine output is not maintained. Dantrolene works within the muscle cell to reduce intracellular levels of calcium. In the usual clinical doses, dantrolene has little effect on cardiac muscle contractility. In fulminant malignant hyperthermia, cardiac dysrhythmias may occur, but this is related to perturbations in pH and electrolytes. (Verapamil should not be used, because it interacts with dantrolene and may produce hyperkalemia and myocardial depression. Lidocaine appears safe.) Some side effects of short-term administration include muscle weakness (which may persist for 24 hours after dantrolene therapy is discontinued), nausea and vomiting, diarrhea, blurred vision, and phlebitis. Hypothermia may also occur with malignant hyperthermia treatment but is related to ice packing, not to dantrolene administration per se. When decreasing the fever, cooling should be stopped when core temperature reaches 38° C to avoid hypothermia. Hepatotoxicity has been demonstrated only with long-term use of oral dantrolene (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 638).
281. Atracurium differs from cisatracurium in which way? A. Molecular weight B. Formation of laudanosine C. Histamine release D. No renal metabolism
281. (C) Cisatracurium is a stereoisomer of atracurium and as such has the same molecular weight. Both drugs undergo Hofmann elimination and form laudanosine. Atracurium is also estimated to undergo two thirds of its metabolism via ester hydrolysis catalyzed by nonspecific plasma esterases (not pseudocholinesterase). Neither drug requires renal or hepatic input for its degradation; hence, both can be used with renal or hepatic failure. Atracurium causes histamine release, whereas cisatracurium does not (Miller: Basics of Anesthesia, ed 6, p 154).
282. Signs and symptoms of opioid withdrawal include all of the following EXCEPT A. Increased BP and heart rate B. Seizures C. Abdominal cramps D. Jerking of the legs 60 Part 1 Basic Sciences Group 283-287
282. (B) Withdrawal from opioids is rarely life-threatening but may complicate postoperative care. Opioid withdrawal may spontaneously start within 6 to 12 hours after the last dose of a short-acting opioid and as long as 72 to 84 hours after a long-acting opioid in addicted patients. The duration of withdrawal symptoms also depends on the opioid; for heroin, withdrawal symptoms last 5 to 10 days, and for methadone, even longer. Opioid withdrawal can be precipitated within seconds if naloxone is administered intravenously to an addict. (Naloxone is contraindicated in opioid addicts for this reason.) Signs and symptoms of withdrawal include craving for opioids, restlessness, anxiety, irritability, nausea, vomiting, abdominal cramps, muscle aches, insomnia, sympathetic stimulation (increased heart rate, increased BP, mydriasis, diaphoresis) as well as tremors, jerking of the legs (origin of the term “kicking the habit”), and hyperthermia. Seizures, however, are very rare and if seizures occur, one should consider that withdrawal 86 Part 1 Basic Sciences from other drugs may also be occurring (e.g., from barbiturates) or that an underlying seizure disorder may also exist (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 546). For Questions 283-287: Side effects of each of the intravenous induction agents (thiopental, diazepam, etomidate, propofol, and ketamine) occur. Some are unique for each drug.
283. Adrenal suppression A. Ketamine B. Diazepam C. Etomidate D. Propofo
283. (C) Etomidate is unique among the intravenous induction agents because it can cause adrenocortical suppression by inhibiting the conversion of cholesterol to cortisol. This can occur after a single induction dose and may persist for 4 to 8 hours. The clinical significance of this temporary adrenocortical suppression is unclear. However, in the ICU with prolonged sedation, clinical adrenal insufficiency may develop (i.e., hypotension, hyponatremia, and hyperkalemia). Here corticosteroids should be administered in stress doses (e.g., cortisol 100 mg/day) (Miller: Basics of Anesthesia, ed 6, pp 111–112).
284. Thrombosis, phlebitis, specific antagonist available A. Ketamine B. Diazepam C. Etomidate D. Propofo
284. (B) Diazepam is a benzodiazepine drug and was widely used intravenously for anesthesia until midazolam was developed. Although it is an effective sedative and amnestic drug, diazepam causes significant pain on injection and at times venous irritation and thrombophlebitis. This does not seem to occur with midazolam. Benzodiazepines do not suppress the adrenal gland. The most significant problem with benzodiazepines is respiratory depression. Benzodiazepines are unique among the intravenous sedatives because a specific benzodiazepine receptor antagonist is available (flumazenil). One problem with flumazenil is its relatively short duration of action (half-life about 1 hour), which is shorter than that of diazepam (21-37 hours) and midazolam (1-4 hours) (Miller: Basics of Anesthesia, ed 6, p 109).
285. Pain on injection, severe hypotension in elderly A. Ketamine B. Diazepam C. Etomidate D. Propofo
285. (D) Pain on injection is common with diazepam, etomidate, and propofol but rare with thiopental and ketamine. However, hemodynamic stability is common with etomidate and diazepam, whereas hypotension is common after propofol and thiopental, especially in patients who are volume-depleted or elderly. Hypertension may develop with ketamine use due to its sympathetic nervous system stimulation (Miller: Basics of Anesthesia, ed 6, pp 99–102).
286. Increases ICP A. Ketamine B. Diazepam C. Etomidate D. Propofo
286. (A) ICP tends to fall after the administration of thiopental, etomidate, and propofol and can either fall or remain unchanged with benzodiazepines. Ketamine, however, can increase ICP and should be avoided in patients with intracranial mass lesions and elevated ICP because it can further increase the ICP (Miller: Basics of Anesthesia, ed 6, pp 109–111).
287. Lactic acidosis may develop with prolonged use A. Ketamine B. Diazepam C. Etomidate D. Propofol
287. (D) Propofol infusion syndrome (lactic acidosis) may develop when high-dose infusions (i.e., >75 μg/kg/ min) are infused for longer than 24 hours. Early signs include tachycardia; later on, severe metabolic acidosis, bradyarrhythmias, and myocardial failure may develop. The cause appears to be related to impaired fatty acid oxidation in the mitochondria (Miller: Basics of Anesthesia, ed 6, pp 99–102). For Questions 288-292: Antihypertensive agents are used primarily in the treatment of essential hypertension to reduce BP toward normal. These agents include direct-acting smooth muscle relaxants or vasodilators (e.g., hydralazine), centrally acting α2-sympathetic receptor agonists (e.g., clonidine), peripheral adrenergic receptor antagonists (e.g., labetalol), calcium channel blockers, diuretics, angiotensin-converting enzyme (ACE) inhibitors (e.g., captopril, lisinopril), and angiotensin receptor blockers (ARBs) (Barash: Clinical Anesthesiology, ed 7, pp 392, 399, 403–404).
288. Reduces MAC A. Clonidine B. Hydralazine C. Losartan D. Labetalol
288. (A) Central-acting sympathomimetic agents such as clonidine produce some sedative effects and can reduce the anesthetic requirement or MAC.
289. Blockade of angiotensin receptor A. Clonidine B. Hydralazine C. Losartan D. Labetalol
289. (C) Losartan (Cozaar) blocks the hormone angiotensin at the receptor. It is pharmacologically similar to ACE inhibitors, but with fewer side effects. It is useful for treatment of diabetic patients and those with cardiovascular disease. Hyperkalemia is a potential side effect of therapy with this drug.
290. With high doses may cause a systemic lupus erythematosus–like syndrome A. Clonidine B. Hydralazine C. Losartan D. Labetalol
290. (B) Approximately 10% to 20% of patients who are chronically taking hydralazine (i.e., >6 months) develop a systemic lupus erythematosus–like syndrome, especially if the daily dose is high (e.g., >200 mg). The systemic lupus erythematosus–like syndrome will resolve once hydralazine therapy is discontinued.
291. Produces α-adrenergic receptor and β-adrenergic receptor blockade A. Clonidine B. Hydralazine C. Losartan D. Labetalol
291. (D) Labetalol is an α1-adrenergic receptor and nonselective β-adrenergic receptor antagonist. Pharmacology and Pharmacokinetics of Intravenous Drugs 87
292. May result in severe rebound hypertension when abruptly discontinued A. Clonidine B. Hydralazine C. Losartan D. Labetalol
292. (A) Abrupt discontinuation of chronically administered clonidine (especially if the dose is >1.2 mg/day) may result in severe rebound hypertension within 8 to 36 hours after the last dose. For Question 293: Some drugs inhibit coagulation and do so through a myriad of different pathways. An understanding of these drugs and their mechanisms is helpful to the anesthesia provider.
293. Alternative to heparin for cardiopulmonary bypass A. Argatroban B. Clopidogrel C. Abciximab D. Fondaparinux
293. (A) Patients susceptible to HIT-2 (heparin-induced thrombocytopenia) should wait 3 months for a clinically significant decrease in the antibody titer before receiving heparin. If waiting is not possible and surgery involving cardiopulmonary bypass cannot be delayed, direct thrombin inhibitors like hirudin, bivalirudin, or argatroban can be used as anticoagulants for bypass surgery (Miller: Basics of Anesthesia, ed 6, pp 358–359).
294. Glycoprotein (GP)IIb/IIIa inhibition A. Argatroban B. Clopidogrel C. Abciximab D. Fondaparinux
294. (C) Abciximab (ReoPro, plasma half-life 30 minutes), tirofiban (Aggrastat, plasma half-life 2 hours), and eptifibatide (Integrilin, plasma half-life 2.5 hours) are potent inhibitors of platelet activity. They block the binding of vWF and fibrinogen to the GPIIb/IIIa receptors on platelets. These drugs are used in the treatment of acute coronary syndrome. If surgery is required, therapy with eptifibatide and tirofiban should be stopped for 24 hours. Abciximab should be stopped for 72 hours before an operation. All three of these drugs produce thrombocytopenia and are metabolized by the kidney, but dialysis as reversal is only effective with tirofiban (Barash: Clinical Anesthesia, ed 7, pp 437–438, Miller: Miller’s Anesthesia, ed 8, p 1873; Miller: Basics of Anesthesia, ed 6, pp 357–359).
295. Direct thrombin inhibition A. Argatroban B. Clopidogrel C. Abciximab D. Fondaparinux
295. (A) Argatroban is a direct thrombin inhibitor. Please see explanation and reference for Question 293.
296. Used after angioplasty often for a year or more to prevent restenosis A. Argatroban B. Clopidogrel C. Abciximab D. Fondaparinux
296. (B) The thienopyridine compounds, ticlopidine and clopidogrel, are P2Y12 adenosine diphosphate (ADP) receptor antagonists. Binding to this ADP receptor suppresses expression of GPIIb/IIIa and prevents fibrinogen from binding to platelets. Although platelet function studies, per se, are not a reliable way to test the effects of clopidogrel, there is a test to measure the inhibition of the GPIIb/ IIIa receptor. Clopidogrel is an inactive prodrug that must be metabolized into the active form by liver oxidases. A genetic polymorphism exists whereby patients are unable to oxidize clopidogrel into the active compound, thus making it therapeutically ineffective (Barash: Clinical Anesthesia, ed 7, p 437; Miller: Basics of Anesthesia, ed 6, pp 357–359).
297. Anti-Xa activity mechanism of action A. Argatroban B. Clopidogrel C. Abciximab D. Fondaparinux
297. (D) Fondaparinux is an antagonist of factor Xa. It also binds with antithrombin III. Its principal use is deep vein thrombosis prophylaxis, and there is no antidote for it other than stopping therapy and letting it wear off. Because it is renally eliminated, dose must be reduced in patients with renal failure. It is not approved for patients with history of heparin-induced thrombocytopenia (Barash: Clinical Anesthesia, ed 7, p 439).
298. Of the list, most likely to be associated with opioid induced hyperalgesia A. Methadone B. Remifentanil C. Tapentadol (Nucynta) D. Butorphanol
298. (B) Both acute tolerance to opioids and opioid-induced hyperalgesia (OIH) require more analgesics to treat pain. With tolerance the pharmacologic response is less over time; thus, more opioids are needed to relieve the same amount of pain (e.g., chronic back pain). With OIH there is an exaggerated response to painful stimuli. This can occur under certain situations such as an exaggerated response to pain when a remifentanil infusion is stopped (rapid offset of analgesia). To prevent this when using remifentanil-based anesthesia, it is wise to add a longer duration opioid (e.g., morphine) and/or to add nonopioid analgesics before stopping a remifentanil infusion (if pain is expected in the postoperative period). Although the etiology of OIH is unknown, it may involve both central and peripheral nervous system adaptations involving the NMDA receptor (Barash: Clinical Anesthesia, ed 7, p 506; Hemmings: Pharmacology and Physiology for Anesthesia, pp 267–268).
299. Demonstrates ceiling effect with regard to respiratory depression A. Methadone B. Remifentanil C. Tapentadol (Nucynta) D. Butorphanol
299. (D) Mixed agonist-antagonist drugs, such as butorphanol, nalbuphine, and pentazocine, are partial agonists at the κ receptor and complete competitive antagonists at the μ receptor. Both the analgesia and respiratory depressant effects of these drugs approach a ceiling effect. They are used as analgesics for mild-to-moderate pain. They are also used to reverse excessive opioid-induced respiratory depression due to their μ antagonism, while maintaining some analgesia at the κ receptor (Miller: Miller’s Anesthesia, ed 8, pp 903–904; Hemmings: Pharmacology and Physiology for Anesthesia, pp 265–266). 88 Part 1 Basic Sciences
300. Antagonism of NMDA receptors A. Methadone B. Remifentanil C. Tapentadol (Nucynta) D. Butorphanol
300. (A) Although opioids are mainly thought to work on opioid receptors, methadone is also a most potent NMDA receptor antagonist (6-18 times that of morphine). This property appears to be useful in reducing the effects of opioid tolerance and withdrawal syndrome (Barash: Clinical Anesthesia, ed 7, p 505; Hemmings: Pharmacology and Physiology for Anesthesia, p 264).
301. Norepinephrine reuptake inhibitor (NRI) A. Methadone B. Remifentanil C. Tapentadol (Nucynta) D. Butorphanol
301. (C) Tapentadol (Nucynta) is a new opioid marketed for fewer GI and CNS side effects. It has a dual mechanism of action: as an agonist for the μ receptor site and as a norepinephrine reuptake inhibitor (NRI). It should not be used in patients taking MAOIs, because an adrenergic crisis may develop. It is also contraindicated with SSRIs, because it may lead to serotonin syndrome. It is only available orally (Barash: Clinical Anesthesia, ed 7, p 505; Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, p 508). For Questions 302-305: Depolarizing neuromuscular blockade usually is described as having two phases. Phase I blockade occurs with depolarization of the postjunctional membrane. Phase II blockade occurs when the postjunctional membrane has become repolarized but does not respond normally to acetylcholine (i.e., often termed desensitized, but other factors are involved). This can occur when the dose of succinylcholine is greater than 2 to 4 mg/kg. The response of a muscle to electrical nerve stimulation for a phase II block is similar to that for a nondepolarizing block. Nondepolarizing neuromuscular blockade is only of one type (Miller: Basics of Anesthesia, ed 6, pp 148–149).
302. Block is antagonized with anticholinesterase drugs A. True of nondepolarizing blockade only B. True of phase I depolarizing blockade only C. True of phase II depolarizing blockade only D. True of nondepolarizing and phase II depolarizing blockade
302. (D) Although the mechanisms of a nondepolarizing and a phase II depolarizing block likely are different, they both can be antagonized with anticholinesterase drugs.
303. Block is enhanced with anticholinesterase drugs A. True of nondepolarizing blockade only B. True of phase I depolarizing blockade only C. True of phase II depolarizing blockade only D. True of nondepolarizing and phase II depolarizing blockade
303. (B) Only a phase I depolarizing block is enhanced with the use of anticholinesterase drugs.
304. Post-tetanic facilitation occurs A. True of nondepolarizing blockade only B. True of phase I depolarizing blockade only C. True of phase II depolarizing blockade only D. True of nondepolarizing and phase II depolarizing blockade
304. (D) Post-tetanic facilitation occurs when a single twitch that is induced a short period of time after tetanic stimulation is larger than the amplitude of the tetanus. This occurs with a phase II depolarizing blockade as well as with a nondepolarizing blockade.
305. Sustained response to tetanic stimulus is seen A. True of nondepolarizing blockade only B. True of phase I depolarizing blockade only C. True of phase II depolarizing blockade only D. True of nondepolarizing and phase II depolarizing blockade
305. (B) The amplitude of the muscle response to sustained tetanic stimulation remains the same with phase I depolarizing blockade, but it shows a marked fade with a phase II depolarizing blockade or a nondepolarizing blockade. SUMMARY OF MUSCULAR RESPONSES TO NERVE STIMULATION WITH DIFFERENT TYPES OF BLOCKADE Stimulation Phase I Depolarizing Phase II Depolarizing Nondepolarizing Single twitch Decreased Decreased Decreased Tetanic stimulation Decreased height but no fade Fade Fade Post-tetanic facilitation None Yes Yes Train of four All twitches same, decrease in height Marked fade Marked fade Train-of-four ratio >0.7 <0.4 <0.7 Anticholinesterase Enhances Antagonizes Antagonizes For Questions 306-315: A simple way to measure the potency of inhaled drugs is to measure their MAC values. MAC is the minimum alveolar concentration of an inhaled drug at 1 atmosphere (atm) (1 atm = 760 mm Hg) where 50% of patients do not move in response to a painful stimulus. It is commonly measured as the end-expired drug concentration. Various physiologic or pharmacologic factors can increase or decrease MAC. In general, factors that increase metabolic function of the brain (e.g., hyperthermia) or elevate brain catecholamines (e.g., MAOIs, tricyclic antidepressants, cocaine, acute amphetamine use) increase MAC, and factors that depress function (e.g., intravenous anesthetics, acute ethanol use, narcotics, hypothermia) decrease MAC. Recently, it has been suggested that there might be a genetic component to MAC, because redheaded females have about a 20% increase in MAC compared with dark-haired females (Barash: Clinical Anesthesia, ed 7, pp 458–459). Pharmacology and Pharmacokinetics of Intravenous Drugs 89
306. Amphetamines A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
306. (D) Acute amphetamine use increases MAC, whereas chronic amphetamine use decreases MAC.
307. α2 Agonists (clonidine, dexmedetomidine) A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
307. (C) α2 Agonists decrease MAC.
308. Hyperthyroidism A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
308. (A) Changes in thyroid function (e.g., hyperthyroidism, hypothyroidism) do not seem to affect MAC. However, the cardiovascular response to volatile drugs is altered with thyroid function.
309. Acute ethanol ingestion A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
309. (C) With acute administration, ethanol is a CNS depressant and decreases MAC. Chronic ethanol administration increases MAC.
310. Lidocaine A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
310. (C) Lidocaine use decreases MAC.
311. Lithium A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
311. (C) Patients on lithium therapy have lower MAC values. This may be related to the lower catecholamine levels in the brain.
312. Opioids A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
312. (C) Opioids produce a dose-dependent decrease in MAC (up to about 50%).
313. Duration of anesthesia A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
313. (A) The duration of anesthesia, as well as the gender of the patient, does not affect MAC.
314. Pregnancy A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
314. (C) Pregnancy lowers MAC. This may be related to the sedative effects of progesterone. Pregnant patients also are very sensitive to local anesthetics.
315. Pao2 35 mm Hg A. No change in MAC B. Increases MAC C. Decreases MAC D. Acute administration increases MAC; chronic administration decreases MAC
315. (C) Severe hypoxia (Pao2 of 38 mm Hg), as well as severe anemia (<4.3 mL/oxygen/dL of blood), decreases MAC. For Questions 316-320: The goals of pharmacologic premedication must be individualized to meet each patient’s requirements. Some of these goals include amnesia, relief of anxiety, sedation, analgesia, reduction of gastric fluid volume, elevation of gastric fluid pH, prophylaxis against allergic reactions, and reduction of oral and respiratory secretions. The drugs most commonly used to achieve these goals include benzodiazepines, barbiturates, opioids, H2-receptor antagonists, nonparticulate antacids, antihistamines, and anticholinergic agents. The anticholinergics atropine, scopolamine, and glycopyrrolate are rarely given with premedication today unless a specific effect is needed (e.g., drying of the mouth before fiberoptic intubation, prevention of bradycardia, and, rarely, as a mild sedative). Atropine and scopolamine are tertiary compounds that can readily cross lipid membranes such as the blood-brain barrier. These tertiary amines can produce sedation, amnesia, CNS toxicity (central anticholinergic syndrome manifested as delirium or prolonged somnolence after anesthesia), mydriasis, and cycloplegia (whereas glycopyrrolate, a quaternary compound, does not cross lipid membranes well). All three anticholinergics can cause drying of airway secretions by inhibiting salivation, can cause tachycardia (although bradycardia can be seen in some patients), can decrease the lower esophageal sphincter tone, and can increase body temperature by inhibiting sweating. The main differences are listed in the table following the explanation to Question 178 (Miller: Basics of Anesthesia, ed 6, p 76).
316. Least effective antisialagogue A. Atropine B. Glycopyrrolate C. Scopolamine D. Atropine and scopolamine
316. (A) All three anticholinergics can cause drying of airway secretions by inhibiting salivation, but atropine is the least effective of these drugs.
317. Produces best sedation A. Atropine B. Glycopyrrolate C. Scopolamine D. Atropine and scopolamine
317. (C) To produce sedation, the drug must pass the blood-brain barrier. This is much more prominent with scopolamine and much less so with atropine. Glycopyrrolate does not cause any sedation.
318. Causes greatest increase in heart rate A. Atropine B. Glycopyrrolate C. Scopolamine D. Atropine and scopolamine
318. (A) Atropine has the best blocking effect on muscarinic receptors of the heart.
319. Does not produce central anticholinergic syndrome A. Atropine B. Glycopyrrolate C. Scopolamine D. Atropine and scopolamine
319. (B) The toxic state known as central anticholinergic syndrome requires passage of the drug across the blood-brain barrier and, therefore, precludes glycopyrrolate from causation.
320. May produce mydriasis and cycloplegia when placed topically in the eye A. Atropine B. Glycopyrrolate C. Scopolamine D. Atropine and scopolamine
320. (D) Both atropine and scopolamine can cause ocular effects (scopolamine more so than atropine), including mydriasis and cycloplegia when applied topically to the eye. Caution is suggested when scopolamine is given intramuscularly to patients with glaucoma. IV administration of atropine to prevent or treat bradycardia appears to have little effect on the eye. If a scopolamine patch is placed to help prevent PONV, one needs to carefully wash one’s hands after application, because rubbing an eye with any scopolamine on the fingers may lead to unilateral mydriasis. 90
321. The minimum alveolar concentration (MAC) is highest in neonates (0-30 days old) versus other age groups with which of the following? A. Isoflurane B. Sevoflurane C. Desflurane D. N2O
321. (B) The MAC for inhalation agents varies with age. For most volatile anesthetics, the highest MAC values are for infants 1 to 6 months old. In infants younger than 1 month or older than 6 months, the MAC is lower for isoflurane, halothane, and desflurane. Sevoflurane is different. For sevoflurane, the MAC for neonates 0 to 30 days old is 3.3%, for infants 1 to 6 months old it is 3.2%, and for infants 6 to 12 months old it is 2.5% (Miller: Miller’s Anesthesia, ed 8, p 2764).
322. The rate of increase in the alveolar concentration of a volatile anesthetic relative to the inspired concentration (Fa/Fi) plotted against time is steep during the first moments of inhalation with all volatile anesthetics. The reason for this observation is that A. Volatile anesthetics reduce alveolar ventilation (Va) B. There is minimal anesthetic uptake from the alveoli into pulmonary venous blood C. Volatile anesthetics increase cardiac output initially D. The volume of the anesthetic breathing circuit is small
322. (B) The alveolar partial pressure of a volatile anesthetic, which ultimately determines the depth of general anesthesia, is determined by the relative rates of input to removal of the anesthetic gases to and from the alveoli. Removal of anesthetic gases from the alveoli is accomplished by uptake into the pulmonary venous blood, which is most dependent on an alveolar partial pressure difference. During the initial moments of inhalation of an anesthetic gas, there is no volatile anesthetic in the alveoli to create this partial pressure gradient. Therefore, the uptake for all volatile anesthetic gases will be minimal until the resultant rapid increase in alveolar partial pressure establishes a sufficient alveolar-to-venous partial pressure gradient to promote uptake of the anesthetic gas into the pulmonary venous blood. This will occur in spite of other factors, which are discussed in the explanation to Question 333 (Miller: Miller’s Anesthesia, ed 8, pp 648–649).
323. During spontaneous breathing, volatile anesthetics A. Increase tidal volume (Vt) and decrease respiratory rate B. Increase Vt and increase respiratory rate C. Decrease Vt and decrease respiratory rate D. Decrease Vt and increase respiratory rate
323. (D) At concentrations of 1 MAC or less, volatile anesthetics, as well as the inhaled anesthetic N2O, will produce dose-dependent increases in the respiratory rate in spontaneously breathing patients. This trend continues at concentrations greater than 1 MAC for all of the inhaled anesthetics except isoflurane. With the exception of N2O, the evidence suggests that this effect is caused by direct activation of the respiratory center in the CNS rather than by stimulation of pulmonary stretch receptors. Additionally, volatile anesthetics decrease Vt and significantly alter the breathing pattern from the normal awake pattern of intermittent deep breaths separated by varying time intervals to one of rapid, shallow, regular, and rhythmic breathing (Miller: Miller’s Anesthesia, ed 8, pp 691–692).
324. Which of the following can NOT be considered an advantage of low-flow anesthesia? A. Conservation of fossil fuel B. Less ozone depletion C. Reduced room pollution D. Conservation of absorbent
324. (D) Barium-containing absorbents that interact with volatile anesthetics and produce carbon monoxide and compound A are no longer used in clinical practice. They have been replaced with calcium-containing products such as Amsorb Plus. Consequently, absorbent granules are “consumed” by CO2 produced by the patient, not by the total flow of anesthetic gases. On the contrary, with low flow techniques, recirculation (rebreathing) of expired gases results in more rapid depletion of the CO2 absorbent. Volatile anesthetics are organic compounds, specifically alkanes (halothane) and substituted methylethyl ethers (desflurane, isoflurane) or substituted isopropyl methyl ether (sevoflurane). They are ultimately derived from petroleum sources and are then halogenated to become substituted organic compounds. They join a myriad of other organic halides such as hairspray, propellants, refrigerants, and solvents that collectively contribute to the depletion of the ozone layer in the earth’s atmosphere. The main greenhouse gases are CO2, methane, and N2O. N2O constitutes roughly 5% of the greenhouse gases. Another rationale for the use of low-flow anesthesia is the introduction of less waste into the OR. The disadvantage of low-flow anesthesia is that the Fio2 will continually drop during the administration of anesthesia (unless 100% oxygen is administered), and vigilance is required because this drop may approach or even reach the level of a hypoxic mixture (Miller: Miller’s Anesthesia, ed 8, pp 664–665).
325. The main reason desflurane is not used for inhalation induction in clinical practice is because of A. Its low blood/gas partition coefficient B. Its propensity to produce hypertension in high concentrations C. Its propensity to produce airway irritability D. Its propensity to produce tachyarrhythmias
325. (C) Although desflurane has a low blood/gas partition coefficient (0.42) and should produce rapid induction of anesthesia, its marked pungency and airway irritation make inhalation inductions very difficult. Not only do patients dislike the scent, but the airway irritation often leads to coughing, increased salivation, breath holding, and sometimes laryngospasm (especially if the concentration is rapidly increased). In addition, with abrupt increases in concentration, patients often experience tachycardia and hypertension, thought to be due to increased sympathetic discharge (Miller: Basics of Anesthesia, ed 6, p 95). Pharmacology and Pharmacokinetics of Volatile Anesthetics 97
326. A medical group planning a trip to South America has a large supply of old enflurane vaporizers (vapor pressure = 170 mm Hg). Which volatile agent could be delivered through an enflurane vaporizer in such a manner that the dialed setting equals the vaporizer’s output? A. Desflurane B. Sevoflurane C. Isoflurane D. None; all other volatile agents will be at least 30% off
326. (B) A vaporizer’s specificity is based on the vapor pressure of the anesthetic agent for which it is made. Filling a vaporizer with an agent whose vapor pressure is higher results in a higher concentration in the vaporizer’s output. Similarly, a volatile agent with a lower vapor pressure produces an output with a lower concentration than that seen on the dial. The vapor pressure of enflurane, 172 mm Hg (20° C), most closely approximates the vapor pressure of sevoflurane, which is 160 mm Hg (Miller: Basics of Anesthesia, ed 6, p 81).
327. Select the TRUE statement regarding blood pressure when 1.5 MAC N2O-isoflurane is substituted for 1.5 MAC isoflurane-oxygen. A. Blood pressure is less than awake value but greater than that seen with isoflurane-O2 B. Blood pressure is equal to awake value C. Blood pressure is greater than awake value D. Blood pressure is less than isoflurane-O2 pressure
327. (A) When N2O is substituted for an equal MAC value of isoflurane, the resulting blood pressure is greater than that seen with the same MAC value achieved with isoflurane as the sole anesthetic agent. When administered alone, N2O does not alter arterial blood pressure, stroke volume, systemic vascular resistance, or baroreceptor reflexes. The administration of N2O increases heart rate slightly, which may result in a mild increase in cardiac output. In vitro, N2O has a dose-dependent direct depressant effect on myocardial contractility, which is probably overcome in vivo by sympathetic activation (Miller: Basics of Anesthesia, ed 6, p 93).
328. Which of the following volatile anesthetics decreases systemic vascular resistance? A. Sevoflurane B. Isoflurane C. Desflurane D. All of the above
328. (D) All of the present-day volatile anesthetics reduce blood pressure in a dose-dependent fashion. Desflurane, sevoflurane, and isoflurane cause this primarily through reductions in systemic vascular resistance. The obsolete agents, halothane and enflurane, produce hypotension via direct myocardial depression (Miller: Basics of Anesthesia, ed 6, pp 90–91).
329. With which of the following inhalational agents is cardiac output moderately increased? A. N2O B. Sevoflurane C. Desflurane D. Isoflurane
329. (A) The older agent halothane tended to decrease the cardiac output, whereas sevoflurane, desflurane, and isoflurane tend to maintain cardiac output. N2O tends to increase cardiac output primarily because of the mild increase in sympathetic tone (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 53).
330. Select the FALSE statement about isoflurane (≤1 MAC). A. May attenuate bronchospasm B. Increases right atrial pressure C. Decreases mean arterial pressure D. Decreases cardiac output
330. (D) At concentrations of 1 MAC, isoflurane may attenuate antigen-induced bronchospasm, presumably by decreasing vagal tone. At similar concentrations, isoflurane will not reduce cardiac output in patients with normal left ventricular function. Additionally, isoflurane will decrease stroke volume, mean arterial pressure, and systemic vascular resistance in a dose-dependent manner. Cardiac output remains unchanged because decreases in systemic vascular resistance result in a reflex increase in heart rate that is sufficient to offset the decrease in stroke volume. However, dose-dependent decreases in both stroke volume and cardiac index can be seen when isoflurane is administered in concentrations greater than 1 MAC (Miller: Basics of Anesthesia, ed 6, pp 90–95).
331. Abrupt and large increases in the delivered concentration of which of the following inhalational anesthetics may produce transient increases in systemic blood pressure and heart rate? A. Desflurane B. Isoflurane C. Sevoflurane D. N2O
331. (A) Desflurane can (but does not always) produce increased blood pressure and heart rate when the concentrations are rapidly increased. This may be related to airway irritation and a sympathetic response. This has also occurred with isoflurane, but to a much less frequent and usually lower extent. The other agents listed do not cause this sympathetic response with a rapid increase in concentration. If desflurane is increased slowly or a prior dose of narcotic is given, this increase in blood pressure and heart rate may not occur (Miller: Basics of Anesthesia, ed 6, pp 90–92).
332. Discontinuation of 1 MAC of which volatile anesthetic followed by immediate introduction of 1 MAC of which second volatile anesthetic would temporarily result in the greatest combined anesthetic potency? A. Isoflurane followed by desflurane B. Sevoflurane followed by desflurane C. Desflurane followed by isoflurane D. Desflurane followed by sevoflurane
332. (A) Of all the options listed, desflurane has the lowest solubility constant, which results in a very rapid rise in Fa/Fi. The rate of rise is very similar to that seen with N2O and results in the most rapid attainment of 1 MAC concentration once the new volatile anesthetic has been initiated. Isoflurane has the highest blood/gas solubility coefficient of all the options, reflecting the largest quantity of gas stored in the blood. This reservoir will result in the slowest decline in the alveolar concentration of this volatile agent upon discontinuation. The combination of these different solubilities will ultimately result in the highest combined MAC when 1 MAC of isoflurane is discontinued and 1 MAC of desflurane is introduced (Miller: Basics of Anesthesia, ed 6, p 88; Morgan & Mikhail: Clinical Anesthesiology, ed 4, pp 156–157, 159).
333. Cardiogenic shock has the greatest impact on the rate of increase in Fa/Fi for which of the following volatile anesthetics? A. Isoflurane B. Desflurane C. Sevoflurane D. N2O
333. (A) The alveolar partial pressure of an anesthetic is determined by the rate of input relative to removal of the anesthetic from the alveoli, as explained in Question 322. During induction, the anesthetic gas is removed from the alveoli by uptake into the pulmonary venous blood. The rate of uptake is influenced by cardiac output, the blood/gas solubility coefficient, and the alveolar-to-venous partial pressure difference of the anesthetic. At a lower cardiac output, a slower rate of uptake of volatile anesthetic from the alveoli into the pulmonary venous blood results in a faster rate of increase in the alveolar concentration. This will result in an increased Fa/Fi. Uptake of poorly soluble anesthetic gases from the alveoli is minimal, and the rate of rise of Fa/Fi is rapid and virtually independent of cardiac output. Uptake of the more soluble anesthetics, such as isoflurane, from the alveoli into the pulmonary venous blood can be considerable and will be reflected by a slower rate of rise of the Fa/Fi ratio. Cardiogenic shock will have the 98 Part 1 Basic Sciences smallest impact on the most insoluble agents, such as desflurane, sevoflurane, and N2O, whereas the impact on the rate of rise of Fa/Fi of the relatively soluble anesthetic gases, such as isoflurane, will be more profound (Miller: Miller’s Anesthesia, ed 8, pp 645–646).
334. The vessel-rich group receives what percent of the cardiac output? A. 45% B. 60% C. 75% D. 90%
334. (C) The vessel-rich group that receives approximately 75% of the cardiac output is composed of the brain, heart, spleen, liver, splenic bed, kidneys, and endocrine glands. This group, however, constitutes only 10% of the total body weight. Because of this large blood flow relative to tissue mass, these organs take up a large volume of volatile anesthetic and equilibrate with the partial pressure of the volatile anesthetic in the blood and alveoli during the earliest moments of induction (Miller: Basics of Anesthesia, ed 6, p 87; Miller: Miller’s Anesthesia, ed 8, pp 647–648).
335. What percent desflurane is present in the vaporizing chamber of a desflurane vaporizer (pressurized to 1500 mm Hg and heated to 23° C)? A. Nearly 100% B. 85% C. 65% D. 45%
335. (D) Desflurane is unique among the current commonly used volatile anesthetics because of its high vapor pressure of 664 mm Hg. Because of this, the vaporizer is pressurized to 1500 mm Hg and is electrically heated to 23° C to give more predicable concentrations: 664/1500 = about 44%. If the desflurane is used at 1 atm the concentration will be about 88% (Barash: Clinical Anesthesia, ed 7, pp 666–668; Miller: Basics of Anesthesia, ed 6, pp 202–203; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 60–64).
336. A 25-year-old man is undergoing lymph node dissection for testicular cancer under general anesthesia. He has received four courses of bleomycin. The sevoflurane vaporizer is set at 1.8%, the oxygen at 100 mL/ min, and air at 900/mL/min. The Fio2 of the fresh gas flow is A. 26% B. 29% C. 34% D. 41%
336. (B) Fresh gas flow = 1 L per minute (1000 mL/min). Fio2 = [(100 mL/min) + (900 × 0.21 mL/min)]/1000 mL/min = (100 + 180)/1000 = 289/1000 = 29% Anesthetic flow meters are designed to deliver gases very accurately (Miller: Miller’s Anesthesia, ed 8, pp 760–761).
337. How would a right mainstem intubation affect the rate of increase in arterial partial pressure of volatile anesthetics? A. It would be reduced to the same degree for all volatile anesthetics B. It would be accelerated to the same degree for all volatile anesthetics C. It would be reduced the most for highly soluble agents D. It would be reduced the most for poorly soluble agents
337. (D) The situation described here is a transpulmonary shunt. In patients with transpulmonary shunting, blood emerging from unventilated alveoli contains no anesthetic gas. This anesthetic-deficient blood mixes with blood from adequately ventilated, anesthetic-containing alveoli, producing an arterial anesthetic partial pressure considerably less than expected. Because uptake of anesthetic gas from the alveoli into pulmonary venous blood will be less than normal, transpulmonary shunting accelerates the rate of rise in the Fa/Fi ratio but reduces the rate of increase in the arterial partial pressure of all volatile anesthetics. The degree to which these changes occur depends on the solubility of the given volatile anesthetic. For poorly soluble anesthetics, such as N2O, transpulmonary shunting only slightly accelerates the rate of rise in the Fa/Fi ratio, but it significantly reduces the rate of increase in arterial anesthetic partial pressure. The opposite occurs with highly soluble volatile anesthetics, such as halothane and isoflurane (Miller: Miller’s Anesthesia, ed 8, pp 646–647).
338. During a breast biopsy with the patient under general anesthesia, the end-tidal carbon dioxide (CO2) is 25 mm Hg on infrared spectrometer. Which of the following could NOT account for these findings? A. Mainstem intubation B. Enormous dead space C. Incipient cardiac arrest D. Overventilation
338. (A) CO2 is a very soluble gas. making the end-tidal CO2 (ETCO2) at the level of the alveoli virtually identical to arterial CO2 (Paco2). Because we measure ETCO2 on the total exhaled gas, the alveolar CO2 is diluted with the gas in the dead space (e.g., alveoli are ventilated but are not perfused as well as the Pharmacology and Pharmacokinetics of Volatile Anesthetics 99 respiratory passageways). A gradient of 2 to 5 mm Hg between Paco2 and ETCO2 is seen in normal healthy patients. Any condition that increases dead space or reduces lung perfusion (i.e., increases V/Q) such as pulmonary embolism, severe hypotension, low cardiac output, and cardiac arrest will decrease ETCO2. ETCO2 can also decrease with an increase in minute ventilation (increased removal of CO2) and can decrease with hypothermia (decreased production of CO2). Of course, ETCO2 can rapidly decrease to zero with any failure to ventilate (e.g., esophageal intubation, circuit disconnection, failure to turn the ventilator on after manual ventilation is stopped) as well as with disruption of the sampling lines. Because CO2 rapidly equilibrates between the bloodstream and the alveolar gas, an endotracheal tube that slips into a mainstem gives the same minute ventilation as an endotracheal tube in the trachea (airway pressure, however, would increase). Increased ETCO2 can have many causes, including hypoventilation, rebreathing of exhaled gas, increased absorption of CO2 from the abdomen distended with CO2 during laparoscopy, malignant hyperthermia, sepsis, and administration of bicarbonate used to treat metabolic acidosis (Barash: Clinical Anesthesia, ed 7, pp 704–705; Miller: Basics of Anesthesia, ed 6, pp 328–329; Butterworth: Morgan and Mikhail’s Clinical Anesthesiology, ed 5, pp 123–127).
339. Isoflurane, when administered to healthy patients in concentrations less than 1.0 MAC, will decrease all of the following EXCEPT A. Cardiac output B. Myocardial contractility C. Stroke volume D. Systemic vascular resistance
339. (A) Isoflurane is unique among the volatile agents in that it does not reduce cardiac output (cardiac index) at concentrations of 1 MAC or less in healthy volunteers (Miller: Basics of Anesthesia, ed 6, pp 90–92).
340. Increased Va will accelerate the rate of rise of the Fa/Fi ratio the MOST for A. Desflurane B. Sevoflurane C. Isoflurane D. N2O
340. (C) The rate of input of volatile anesthetics from the anesthesia machine to the alveoli is influenced by three factors: Va, the inspired anesthetic partial pressure, and the characteristics of the anesthetic breathing system. Increased Va will accelerate the rate of increase in Fa/Fi for all volatile anesthetics. However, the magnitude of this effect is dependent on the solubility of the inhaled anesthetic. The rate of increase in Fa/Fi depends very little on Va for poorly soluble anesthetics because the uptake of these is minimal. In contrast, the rate of increase in Fa/Fi for highly soluble anesthetics depends significantly on Va. Isoflurane is the most soluble inhaled anesthetic listed in this question (blood/gas solubility coefficient 1.46). Therefore, an increase in Va will accelerate the rate of increase in Fa/Fi the most for isoflurane. Blood/ gas solubility coefficients for the other volatile anesthetics are as follows: halothane 2.54, enflurane 1.90, sevoflurane 0.69, desflurane 0.42, and N2O 0.46 (Miller: Miller’s Anesthesia, ed 8, pp 647–650).
341. Select the correct order from greatest to least for anesthetic requirement. A. Adults > infants > neonates B. Adults > neonates > infants C. Infants > neonates > adults D. Neonates > adults > infants
341. (C) Anesthetic requirement increases from birth until approximately age 3 to 6 months. Then, with the exception of a slight increase at puberty, anesthetic requirement progressively declines with aging. For example, the MAC for halothane in neonates is approximately 0.87%, in infants it is approximately 1.2%, and in young adults it is approximately 0.75%. A notable exception to this pattern is seen with sevoflurane, for which MAC is the highest with neonates. If the question pertained only to sevoflurane, the correct response would have been C. Please review the answer to Question 321 (Miller: Miller’s Anesthesia, ed 8, p 2764).
342. Which of the following MOST closely determines anesthetic effect? A. Volume percent administered to patient B. Partial pressure at the level of the central nervous system (CNS) C. Solubility in blood D. End-tidal concentration 92 Part 1 Basic Sciences
342. (B) The exact mechanism in which volatile anesthetics exert their effects is not fully understood and remains a topic of considerable research. The most obvious effect of general anesthesia, unconsciousness (hypnosis), is produced at the level of the brain. The end-tidal concentration of the volatile in question reflects the level of anesthesia “seen” by the brain, but only once equilibrium has been reached. At equilibrium, Palveolar = Parterial = PCNS. After three (95% equilibrium) to four (99% equilibrium) time constants, the end-tidal concentration and the partial pressure of the anesthetic at the brain (and blood for that matter) would be the same, provided delivery has remained constant. A time constant is defined as capacity (of the brain) divided by flow (of anesthetic-laden blood) and is expressed by the following equation: τ = V λ ÷ Q The time constant, τ, is about 3 to 4 minutes for modern volatile anesthetics. Accordingly, 10 to 15 minutes must elapse before assuming that the partial pressure of the anesthetic has reached equilibrium in the brain. For this reason, choice D is an incorrect response for this question, because no mention is made of time (Barash: Clinical Anesthesia, ed 7, pp 447–454; Miller: Basics of Anesthesia, ed 6, p 86; Hemmings: Pharmacology and Physiology for Anesthesia, ed 1, pp 50–51).
343. A 31-year-old moderately obese woman is receiving a general anesthetic for cervical spinal fusion. After induction and intubation, the patient is mechanically ventilated with isoflurane at a vaporizer setting of 2.4%. The N2O flow is set at 500 mL/min, and the oxygen flowmeter is set at 250 mL/min. The infrared spectrometer displays an inspired isoflurane concentration of 1.7% and an expired isoflurane concentration of 0.6%. Approximately how many MAC of anesthesia would be represented by the alveolar concentration of anesthetic gases? A. 0.85 MAC B. 1.1 MAC C. 1.8 MAC D. 2.1 MAC
343. (B) Two principles of MAC must be considered in this situation. First, MAC is additive, so the fraction of MAC of each individual gas must be added to arrive at total MAC. The second is that alveolar concentrations of soluble agents are reflected more accurately by end-expiratory concentrations rather than by either inspiratory concentrations or gradients between inspiratory and expiratory concentrations. 100 Part 1 Basic Sciences Because N2O is very insoluble, it is reasonable to assume that equilibrium will be established early. The inspiratory concentration of N2O, approximately 0.6 MAC, should approximate the alveolar concentration. However, the expiratory concentrations of the more soluble volatile anesthetics should be used to estimate the alveolar concentration. The end-expiratory isoflurane concentration of 0.6 reflects approximately 0.5 MAC, which in addition to the 0.6 MAC of N2O would be closest to answer C: 1.1 MAC (Miller: Basics of Anesthesia, ed 6, pp 83–84).
344. The graph in the figure depicts A. The second gas effect B. The concentration effect C. The concentrating effect D. The effect of solubility on the rate of rise of Fa/Fi
344. (B) The figure shown in this question depicts the concentration effect. Note that the inspired anesthetic concentration influences not only the maximum attainable alveolar concentration but also the rate at which the maximum alveolar concentration can be attained. The greater the inhaled anesthetic concentration, the faster the increase in Fa/Fi (Miller: Basics of Anesthesia, ed 6, pp 84–85).
345. The rate of induction of anesthesia with isoflurane would be slower than expected in patients A. With anemia B. With chronic renal failure C. In shock D. With a right-to-left intracardiac shunt
345. (D) The depth of general anesthesia is directly proportional to the alveolar anesthetic partial pressure. The faster the rate of increase in Fa/Fi, the faster the induction of anesthesia. With the exception of a rightto- left intracardiac shunt (see explanation to Question 337 on effect of shunt on the rate of increase in Fa/Fi and explanation to Question 346 on the effect of shunt on arterial anesthetic partial pressure and rate of induction of anesthesia), all of the conditions listed in this question will accelerate the rate of increase in Fa/Fi and thus the rate of induction of anesthesia (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 30).
346. A right-to-left intracardiac shunt would have the GREATEST impact on the rate of inhalation induction with which of the following inhalation anesthetics? A. Desflurane B. Isoflurane C. It would speed up induction for all agents equally D. It would slow down induction for all agents equally
346. (A) In general, a right-to-left intracardiac shunt or transpulmonary shunt will slow the rate of induction of anesthesia. This occurs because of a dilutional effect of shunted blood, which contains no volatile anesthetic, on the arterial anesthetic partial pressure coming from ventilated alveoli. The impact of a rightto- left shunt on the rate of increase in pulmonary arterial anesthetic partial pressure, and ultimately the rate of induction of anesthesia, is greatest for poorly soluble volatile anesthetics. This occurs because the uptake of poorly soluble volatile anesthetics into pulmonary venous blood is minimal; thus, the dilutional effect of the shunt on pulmonary venous anesthetic partial pressure is essentially unopposed. In contrast, the uptake of highly soluble volatile anesthetics is sufficient to partially offset the dilutional effect. Of the anesthetics listed in the question, desflurane is the least soluble (Miller: Miller’s Anesthesia, ed 8, p 645).
347. A left-to-right tissue shunt, such as arteriovenous fistula, physiologically most resembles which of the following? A. A left-to-right intracardiac shunt B. A right-to-left intracardiac shunt C. Ventilation of unperfused alveoli D. A pulmonary embolism
347. (A) Both a left-to-right intracardiac shunt and a left-to-right tissue shunt, such as an arteriovenous fistula, will result in a higher partial pressure of anesthetic gas in the blood returning to the lungs, ultimately resulting in a more rapid rise in Fa/Fi. However, this effect is minimal and in most cases is clinically insignificant (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 30).
348. A fresh gas flow rate of 2 L/min or greater is recommended for administration of sevoflurane because A. The vaporizer cannot accurately deliver the volatile at lesser flow rates B. It prevents the formation of fluoride ions C. It prevents the formation of compound A D. It diminishes rebreathing
348. (D) Sevoflurane is a highly insoluble volatile anesthetic that combines with CO2 absorbents to form a vinyl ether known as compound A. The blood/gas partition coefficient for sevoflurane is 0.69. The vaporizer manufactured by Ohmeda is capable of delivering concentrations ranging from 0.2% to 8% at fresh-gas flow rates of 0.2 to 15 L/min. Its vapor pressure is 160 mm Hg at 20° C, which is similar to the vapor pressure for the other volatile anesthetics except desflurane (664 mm Hg at 20° C). Gas flows greater than 2 L/min prevent the rebreathing of compound A (not the formation of it), thus reducing the possibility of renal toxicity associated with it (Miller: Miller’s Anesthesia, ed 8, p 662).
349. A left-to-right shunt in a neonate with a patent ductus arteriosus (PDA) has what effect on inhalation induction? A. Speeds it up B. Slows down with insoluble volatile agents C. Slows with soluble volatile agents D. No effect with any volatile agent
349. (D) Left-to-right shunts (e.g., PDA, atrial septal defect, ventricular septal defect) are associated with an increase in blood flow through the lungs. With inhalation induction there is no real effect on induction rate. Remember also that a decrease in systemic vascular resistance seen with inhalation agents (e.g., sevoflurane) and positive-pressure ventilation tend to decrease the magnitude of the left-to-right shunt. However, with right-to-left shunts (e.g., tetralogy of Fallot) there is decreased blood flow through the lungs and a slower inhalation induction. With a right-to-left shunt, the decrease in systemic vascular resistance can increase the shunt and lead to a decrease in oxygenation. Intravenous drugs work more rapidly in right-toleft shunts. Halothane may be preferred (to sevoflurane) in right-to-left shunts because halothane decreases contractility and better maintains systemic vascular resistance (Miller: Basics of Anesthesia, ed 6, p 551).
350. Smokers are MOST likely to show a mild but transient increase in airway resistance after intubation and general anesthesia with which of the following? A. Isoflurane B. Sevoflurane C. Halothane D. Desflurane
350. (D) Volatile anesthetics produce minimal bronchodilation unless airway resistance is increased (bronchospasm). This is explained by the fact that airway smooth muscle tone is ordinarily low, and additional bronchodilation is difficult to demonstrate. The irritating effects of desflurane can be reduced by prior administration of fentanyl or morphine (Miller: Basics of Anesthesia, ed 6, p 95). Pharmacology and Pharmacokinetics of Volatile Anesthetics 101
351. If a patient is anesthetized with 6% desflurane in a hyperbaric chamber at 1 atm and the pressure is increased to 2 atm, the desflurane dial should be set to which setting if the anesthesia provider wishes to maintain the anesthetic at the same level? A. 3% B. 6% C. 12% D. Cannot be determined without knowledge of Fio2
351. (A) Please see also Question 342 and its answer. The determinant of anesthetic effect is partial pressure, ultimately at the CNS. If a patient is in a hyperbaric chamber under 2 atm (1520 torr), the effective partial pressure from a desflurane vaporizer would be doubled for any given dial setting in comparison with sea level. A 6% setting at sea level would be 760 × 0.06, or 45.6 mm Hg desflurane. The desflurane vaporizer is unique in that it is more akin to a dual gas blender. To achieve a partial pressure of 45.6 mm Hg (at 2 atm), the dial should be set at 3% (Miller: Miller’s Anesthesia, ed 8, pp 771–772).
352. 0.5 1 0 60 80 70 50 0 5 10 PaO2 (mm Hg) N2O output (L/min) Minutes from end of N2O anesthesia Mean, SE N2O PaO2 The graph above depicts which of the following? A. Diffusion hypoxia B. Second gas effect C. Context sensitive half-time of desflurane D. Concentration effect
352. (A) This classic graph depicts the effect of switching from 21% oxygen and 79% N2O to 21% oxygen and 79% nitrogen—that is, air. When this occurs, large volumes of N2O are released into the lungs and dilute all gases, including oxygen and CO2. The reduction in O2 results in hypoxia, and the resulting fall in CO2 reduces the drive to breathe. This combination occurs at a time when most patients have narcotics and other respiratory depressants in the body. For this reason, it is wise to administer 100% oxygen to patients for several minutes after they emerge from general anesthesia (Miller: Miller’s Anesthesia, ed 8, pp 656–657).
353. Which of the following organs is NOT considered a member of the vessel-rich group? A. Lungs B. Brain C. Heart D. Kidney
353. (A) The vessel-rich group receives 75% of the cardiac output and represents 10% of the weight of a lean adult. In a sense, the lungs receive virtually 100% of the cardiac output, but this is the right-sided CO (the supply side for oxygen) and therefore does not “count” in the classic definition. Lung parenchyma, ironically, uses a very small quantity of oxygen compared with the brain, liver, kidney, and myocardium (Miller: Miller’s Anesthesia, ed 8, p 648).
354. In isovolumic normal human subjects, 1 MAC of isoflurane anesthesia depresses mean arterial pressure by approximately 25%. The single BEST explanation for this is A. Reduction in heart rate B. Venous pooling C. Myocardial depression D. Decreased systemic vascular resistance
354. (D) At 1 MAC concentrations, isoflurane depresses mean arterial pressures primarily by decreasing systemic vascular resistance. The decrease in mean arterial pressure may be greater than that seen with the administration of halothane. However, heart rate will be increased, and stroke volume will decrease to a lesser extent than is seen with the administration of 1 MAC halothane (Miller: Miller’s Anesthesia, ed 8, p 713).
355. If cardiac output and Va are doubled, the effect on the rate of rise of Fa/Fi for isoflurane compared with that which existed immediately before these interventions will be A. Doubled B. Somewhat increased C. Unchanged D. Somewhat decreased
355. (B) Changes in both cardiac output and Va will affect the rates of rise of Fa/Fi, but in opposite directions. An increase in cardiac output will decrease the rate of Fa/Fi, whereas an increase in Va will increase the rate of Fa/Fi. However, these two opposing options do not completely offset each other because the increased cardiac output also accelerates the equilibrium of the anesthetic between the blood and the tissues. This equilibrium results in a narrowing of the alveolar-to-venous partial pressure difference and attenuates the impact of the increased cardiac output on uptake. The net result will be a slight increase in the rate of rise of Fa/Fi (Miller: Miller’s Anesthesia, ed 8, p 646). Doubled Normal Doubled Normal Doubled Normal Nitrous oxide Halothane Methoxyflurane
356. Which of the following characteristics of inhaled anesthetics most closely correlates with recovery from inhaled anesthesia? A. Blood/gas partition coefficient B. Brain/blood partition coefficient C. Fat/blood partition coefficient D. MAC
356. (A) Blood/gas partition coefficient is the option listed that most closely correlates with recovery from inhaled anesthesia. A higher blood/gas partition coefficient reflects a larger quantity of gas dissolved in the blood for a given alveolar concentration. Other factors that affect emergence from anesthesia include Va, cardiac output, tissue concentrations, and metabolism (Miller: Miller’s Anesthesia, ed 8, p 654).
357. After a 12-hour 60% N2O-desflurane anesthetic, evidence of N2O can be best detected by histologic examination of A. Bone marrow B. Renal tubules C. Hepatocytes D. None of the above
357. (A) N2O interferes with the enzyme methionine synthetase, which catalyzes the conversion of homocysteine to methionine. Chronic exposure to N2O leads to a disease state similar to vitamin B12 deficiency, but with one important difference: it is not alleviated with vitamin B12 supplementation. In healthy patients, megaloblastic changes can be seen in the bone marrow after just 12 hours of exposure to 50% N2O (or higher). In patients who are seriously ill, these changes can be seen even earlier. The other disease caused by vitamin B12 deficiency, subacute combined degeneration of the spinal cord, appears only after months of exposure, as is seen in long-term N2O abusers (Miller: Miller’s Anesthesia, ed 8, p 664).
358. An unconscious, spontaneously breathing patient is brought to the operating room (OR) from the intensive care unit for wound débridement. Which of the following maneuvers would serve to slow induction of inhalational anesthesia through the tracheostomy? A. Using isoflurane instead of sevoflurane (using MAC-equivalent inspired concentrations) B. Increasing fresh gas flow from 2 to 6 L/min C. Esmolol 30 mg intravenously D. None of the above
358. (A) Four main factors affect the total or rate of rise of the alveolar concentration of anesthetic (Fa) and hence the inhalation induction of anesthetics. These factors are the inspired concentration of anesthetic (Fi), the solubility of the anesthetic, the Va, and the cardiac output. The rate of rise in Fa/Fi is faster with the less soluble anesthetics, as noted by the blood/gas partition coefficients. The blood/gas partition coefficient measured at 37° C is the least with desflurane (0.45), followed closely by N2O (0.47), then sevoflurane (0.65), isoflurane (1.4), enflurane (1.8), and halothane (2.5); it is the highest with ether (12). Thus, replacing sevoflurane with isoflurane would slow down induction. Increasing the minute ventilation as well as increasing the fresh gas flow rate allows more of the anesthetic to get into the lungs and offset the uptake of anesthetic by the blood, thus speeding the induction of inhalational anesthesia. Decreasing the cardiac output also accelerates the rise of Fa/Fi, resulting in faster inhalation induction (decreases the amount of blood exposed to the lung and decreases the uptake of anesthesia) (Miller: Miller’s Anesthesia, ed 8, pp 647–650; Miller: Basics of Anesthesia, ed 6, pp 84–87).
359. Which of the settings below would give the highest arterial oxygen concentration during inhalation induction of general anesthesia with sevoflurane? Oxygen Air N2O A. L/min 1 2 0 B. L/min 2 0 2 C. L/min 2 2 2 D. L/min 2 3.5 0
359. (B) The table below contains a fifth column, Fio2. Choices B and D appear to be tied at 50%. The question asks for arterial oxygen concentration (not Fio2). During induction of general anesthesia, N2O is rapidly taken up into the blood, resulting in the so-called second gas effect and a concentrating effect. Concentration of oxygen in this manner is termed “alveolar hyperoxygenation” and results in a transient increase in Pao2 of approximately 10% (Miller: Basics of Anesthesia, ed 6, p 85). Oxygen Air N2O Fio2 A. L/min 1 2 0 0.47 B. L/min 2 0 2 0.50 C. L/min 2 2 2 0.40 D. L/min 2 3.5 0 0.50
360. If a patient were anesthetized 90 minutes with 1.25 MAC isoflurane followed by 30 minutes of 1.25 MAC sevoflurane anesthesia, wake-up would be A. The same as 2 hours of isoflurane anesthesia B. The same as 2 hours of sevoflurane anesthesia C. Less than 2 hours of isoflurane anesthesia, but greater than 2 hours of sevoflurane D. Greater than 2 hours of isoflurane anesthesia
360. (A) The insoluble volatile agent desflurane has the advantage of rapid washout and therefore rapid recovery. The downside is the higher cost of desflurane compared with isoflurane. A study was devised to test wake-up after volunteers were anesthetized with isoflurane for the first 75% of the anesthetic and switched to sevoflurane for the last 25%. The results showed that the “hybrid” lasted as long as an anesthetic that consisted of isoflurane alone and proved the futility of this strategy (Miller: Miller’s Anesthesia, ed 8, pp 656–657).
361. An anesthesia circuit is primed in preparation for an inhalation induction (with open adjustable pressure-limiting valve). The anesthesia hose is occluded with a flow of 6 L/min. The anesthesia circuit (canisters, hoses, mask, anesthesia bag) contains 6 L. A machine malfunction allows administration of 100% N2O. Approximately how much N2O would there be in the circuit when the malfunction is discovered at the 1-minute mark? A. 32% B. 48% C. 63% D. 86%
361. (C) Calculation of the washin of N2O requires use of the concept of time constant. Given a volume of 6 L for the circle system, the time constant is 6 L/(6 L/min) or 1 minute. The numbers to remember for time constants are 63%, 84%, and 95% for 1, 2 and 3 time constants, respectively. A properly functioning anesthesia machine would never allow the administration of 100% N2O, but this nightmare scenario is given purely for illustrative purposes (Barash: Clinical Anesthesia, ed 7, p 451).
362. Which of the following factors lowers MAC for volatile anesthetics? A. Serum sodium 151 mEq/L B. Red hair C. Body temperature 38° C D. Acute ethanol ingestion 94 Part 1 Basic Sciences
362. (D) Acute ethanol ingestion is the only factor listed that will reduce MAC. Acute amphetamine ingestion raises MAC, as do hypernatremia, hyperthermia, and naturally occurring red hair. Gender, thyroid function, and Paco2 between 15 and 95 mm Hg and Pao2 greater than 38 mm Hg have no effect on MAC (Miller: Basics of Anesthesia, ed 6, p 82). Pharmacology and Pharmacokinetics of Volatile Anesthetics 103
363. Each of the following factors can influence the partial pressure gradient necessary for the achievement of anesthesia EXCEPT A. Inspired anesthetic concentration B. Cardiac output C. Va D. Ventilation of nonperfused alveoli (dead space)
363. (D) This table summarizes the factors that influence the partial pressure gradients. A right-to-left intrapulmonary shunt affects the delivery of inhaled anesthetics, but lung dead space does not, because the latter does not produce a dilutional effect on the arterial partial pressure of the anesthetic in question (Miller: Basics of Anesthesia, ed 6, pp 84–87). FACTORS DETERMINING PARTIAL PRESSURE GRADIENTS NECESSARY FOR ESTABLISHMENT OF ANESTHESIA Input from Anesthesia Machine to Alveoli Uptake from Alveoli to Pulmonary Blood Uptake from Arterial Blood to Brain Inspired anesthetic concentration Blood gas partition coefficient Brain/blood partition coefficient Alveolar ventilation Cardiac output Cerebral blood flow Characteristics of the anesthesia breathing system Alveolar-to-venous partial pressure difference Arterial-to-venous partial pressure difference From Stoelting RK, Miller RD: Basics of Anesthesia, ed 4, New York, Churchill Livingstone, 2000, p 26.
364. Which of the following volatile anesthetics is unique in containing preservative? A. Sevoflurane B. Desflurane C. Isoflurane D. None of the above
364. (D) Halothane was the only “modern” volatile anesthetic (methoxyflurane also contained a preservative) that contains a preservative, thymol. Because halothane was at risk for degradation into chloride, hydrochloric acid, bromide, hydrobromic acid, and phosgene, it was stored in amber-colored bottles, and thymol was added to prevent spontaneous oxidation. None of the currently used volatile agents contains a preservative (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 44).
365. If the alveolar-to-venous partial pressure difference of a volatile anesthetic (Pa − Pv) is positive (i.e., Pa > Pv) and the arterial-to-venous partial pressure difference (Pa − Pv) is negative (i.e., Pv > Pa), which of the following scenarios is MOST likely to be true? A. The vaporizer has been shut off at the end of the case B. Induction has just started C. Steady state has been achieved D. The vaporizer was shut off during emergence, then turned back on
365. (D) The delivery of anesthetic gases to a patient is a complex series of events that starts with the anesthesia machine and culminates with achievement of an anesthetic partial pressure in the brain (PBr). The partial pressure measured in the blood for any volatile agent is either rising (at first rapidly, then more slowly) or falling (rapidly at first, then more slowly). The vessel-rich group reaches steady state in about 12 minutes (for any dialed level of volatile agent). The rest of the body, however, approaches, but virtually never reaches, equilibrium (e.g., the equilibrium half-time for the fat group is 30 hours for sevoflurane). Hence, a true zero gradient is never achieved in the steady state. When the anesthetic is discontinued or reduced, there is a fall in the arterial partial pressure such that it is less than the venous partial pressure. In fact, when the venous partial pressure exceeds the arterial partial pressure, it means that the volatile agent has been reduced (or shut off) because the lungs are “cleansing” the blood as the volatile-filled blood passes through them. The newly “cleansed” blood then finds its way to the left ventricle with a very low Pa for the volatile agent in question (Barash: Anesthesiology, ed 7, pp 450–453).
366. Anesthetic loss to the plastic and rubber components of the anesthetic circuit, hindering achievement of an adequate inspired concentration, is a factor with which of the following anesthetics? A. Desflurane B. Isoflurane C. Sevoflurane D. N2O
366. (B) Anesthetic agents are soluble in the rubber and plastic components found in the anesthesia machine. This fact can impede the development of anesthetic concentrations of these drugs. The worst offender is the obsolete volatile agent methoxyflurane. However, both isoflurane and halothane are soluble in rubber and plastic, but to a lesser degree. Sevoflurane, desflurane, and N2O have little or no solubility in rubber or plastic. A different but important issue should be borne in mind regarding the loss of sevoflurane. This agent can be destroyed in appreciable quantities by Baralyme (no longer available) and soda lime, but not calcium hydroxide lime (Amsorb) (Miller: Miller’s Anesthesia, ed 8, pp 660–661).
367. Factors predisposing to formation and/or rebreathing of compound A include each of the following EXCEPT A. Low fresh gas flow B. Use of calcium hydroxide lime rather than soda lime C. High absorbent temperatures D. Fresh absorbent
367. (B) Compound A is an ether that forms when sevoflurane interacts with absorbent granules. In rats, compound A is a nephrotoxin that causes damage to the proximal renal tubule. It is believed that compound A is not nephrotoxic in humans, at least not at the concentrations that are achieved clinically (even with fresh gas flows as low as 1 L/min). The factors that lead to increased concentrations of compound A are use of fresh absorbent, use of Baralyme instead of soda lime, high absorbent temperatures, higher concentrations of sevoflurane in the anesthesia system, and closed-circuit or low-flow anesthesia. Calcium hydroxide lime (Amsorb) does not contain KOH or NaOH and does not interact with sevoflurane to produce compound A or other volatile agents to produce carbon monoxide (Miller: Miller’s Anesthesia, ed 8, p 790).
368. The effects of a left-to-right shunt such as an arteriovenous fistula on inhalation induction of anesthesia is to A. Speed up induction B. Slow down induction C. Slow down inhalation induction only if an intracardiac (right-to-left) shunt also exists D. Speed up inhalation induction only if an intracardiac (right-to-left) shunt also exists
368. (D) A left-to-right peripheral shunt such as an arteriovenous fistula delivers volatile-containing venous blood to the lungs. This action offsets the dilutional effect of a right-to-left intracardiac or pulmonary shunt and speeds up induction. The increase in the anesthetic partial pressure from an arteriovenous fistula is detectable only in the setting of a concomitant right-to-left shunt (Miller: Basics of Anesthesia, ed 6, p 87). 104 Part 1 Basic Sciences
369. The following volatile agents are correctly matched with their degree of metabolism (determined by metabolite recovery): A. Sevoflurane 2% B. Isoflurane 0.2% C. Desflurane 0.02% D. All are correctly matched
369. (D) Each of the volatile agents is correctly paired with its percentage of recovered metabolites. Sevoflurane is metabolized 2% to 5% through oxidative pathways using the cytochrome P-450 enzyme pathway. Likewise, the other volatile agents are all oxidatively metabolized in varying degrees. The obsolete anesthetic methoxyflurane underwent 50% metabolism, resulting in high concentrations of fluoride ions and resultant renal failure in some patients. Halothane is unique among the volatile agents in that it can undergo reductive metabolism in the face of low oxygen availability in the liver (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 77–80).
370. Which of the components below is NOT considered in the process of “washin” of the anesthesia circuit at the onset of administration? A. Infrared spectrometer tubing and reservoir B. Expiratory limb C. Anesthesia bag D. CO2 absorber
370. (A) By definition, the washin of the anesthesia circuit refers to the filling of the components of the circuit with anesthetic gases. The total washin volumes are around 7 L and break down as follows: anesthesia bag 3 L, anesthesia hoses 2 L, and anesthesia absorbent compartment 2 L. All of the components listed are part of the anesthesia circuit except the infrared spectrometer tubing. The infrared spectrometer and mass spectrometer take away (sample) from incoming gases through aspiration but do not dilute them (Miller: Miller’s Anesthesia, ed 8, pp 660–661).
371. Which of the following maneuvers would NOT increase the rate of an inhalation induction? A. Giving the patient an inotropic infusion B. Substituting sevoflurane for isoflurane C. Overpressurizing D. Carrying out the induction in San Diego instead of Denver
371. (A) Increasing minute ventilation is one of two methods for manipulating ventilation to increase the rate of establishing anesthesia. Another method is increasing inspired concentration, which can be achieved by turning up the dial above the desired steady state concentration (overpressurizing) to reach steady state more quickly, or increasing fresh gas flow to reduce or eliminate rebreathing (dilution). Substituting a less soluble anesthetic, such as sevoflurane for isoflurane, also establishes anesthesia more rapidly. Carrying out the induction in San Diego instead of Denver constitutes administering the anesthetic at higher atmospheric (barometric) pressure, which decreases the uptake and hence increases the rate of rise of Fa/Fi—that is, accelerates the establishment of anesthesia. The administration of an inotropic agent increases cardiac output, which also increases uptake and slows the rate of induction (Barash: Clinical Anesthesia, ed 7, pp 451–454; Miller: Basics of Anesthesia, ed 6, pp 84–88).
372. Which of the following anesthetics would undergo 90% elimination the most rapidly after a 6-hour Whipple procedure under 1 MAC for the duration of the operation? A. Isoflurane B. Sevoflurane C. Desflurane D. Sevoflurane and desflurane are tied
372. (C) In a comparison of the pharmacokinetics of elimination for volatile anesthetics, desflurane is the fastest. The time for a 50% reduction (decrement) in the alveolar partial pressure of the “modern” anesthetics is roughly the same: about 5 minutes, regardless of anesthetic duration. For longer anesthetics, however, the 80% and 90% decrement times become markedly different. In the present example, the 90% decrement time for desflurane after a 6-hour anesthetic is 14 minutes. This is in stark contrast to sevoflurane (65 minutes) and isoflurane (86 minutes). Please see Question 376 and its explanation (Miller: Basics of Anesthesia, ed 6, pp 88–90; Miller: Miller’s Anesthesia, ed 8, pp 654–655).
373. After induction and intubation of a healthy patient and institution of a ventilator, the sevoflurane vaporizer is set at 2%, and fresh gas flow is 1 L/min (50% N2O and 50% O2). The inspired concentration on the infrared spectrometer 1 minute later is 1.4%. The MAIN reason for the difference between the dial setting and the concentration shown on the infrared spectrometer is A. Rapid uptake of sevoflurane B. Insufficient fresh gas flow for correct vaporizer function C. Second gas effect D. Dilution
373. (D) A properly functioning vaporizer will produce the concentration set on the dial (plus or minus a small tolerance) provided the fresh gas flow rate is greater than 250 mL/min and less than 15 L/min. The 1 L/min rate in this question is well within the limits of the vaporizer. The fact that rebreathing occurs with a circular anesthesia system causes a significant dilutional effect. It is true that uptake would enhance dilution, but it (uptake), per se, is not the main reason for this discrepancy. Uptake is considered in the discussion of the Fa/Fi ratio. This question addresses the characteristics of the anesthesia machine and the relationship between dial setting and delivered concentration. To achieve a desired concentration (e.g., 2%), you must either raise the fresh gas flow to convert the system to a nonrebreathing system or set the vaporizer to a higher level than is actually desired: the concept of overpressurization. In this era of cost containment, the latter is more economical (Miller: Basics of Anesthesia, ed 6, p 207).
374. After cessation of general anesthesia that consisted of air, oxygen, and a volatile agent only, the patient is given 100% oxygen. Each of the following serves as a reservoir for volatile anesthesia and may delay emergence EXCEPT A. Rebreathed exhaled gases B. The absorbent C. The patient D. Gases emerging from the common gas outlet Pharmacology and Pharmacokinetics of Volatile Anesthetics 95
374. (D) The anesthesia circuit can delay emergence significantly if the patient is not disconnected (functionally) from it. Anesthetic gases become dissolved in the rubber and plastic components of the breathing circuit. Likewise, the soda lime can serve as a depository for anesthetics as well as the patient’s own exhaled gases. To reduce these effects to nearly zero, the fresh gas flow should be raised to at least 5 L/min. Fresh gases emerge via the common gas outlet and do not contain volatile agents or N2O because they (volatile agents and N2O) are shut off during emergence (Miller: Miller’s Anesthesia, ed 8, pp 660–661).
375. Which of the following characteristics of volatile anesthetics is necessary for calculation of the time constant? A. Blood/gas partition coefficient B. Brain/blood partition coefficient C. Oil/gas partition coefficient D. All of the above
375. (B) The time constant is defined as capacity divided by flow. The time constant for a volatile anesthetic is determined by the capacity of a tissue to hold the anesthetic relative to the tissue blood flow. The capacity of a tissue to hold a volatile anesthetic depends both on the size of the tissue and on the affinity of the tissue for the anesthetic. The brain time constant of a volatile anesthetic can be estimated by doubling the brain/blood partition coefficient for the volatile anesthetic. For example, the time constant of halothane Pharmacology and Pharmacokinetics of Volatile Anesthetics 105 (brain/blood partition coefficient of 2.6) for the brain (mass of approximately 1500 g, blood flow of 750 mL/min) is approximately 5.2 minutes (Eger: Anesthetic Uptake and Action, ed 1, pp 85–87; Miller: Basics of Anesthesia, ed 6, p 86).
376. The concept of “context sensitive half-time” emphasizes the importance of the relationship between half time and A. Va B. Blood solubility C. Concentration D. Duration
376. (D) This concept highlights the fact that the difference in half-time values among the volatile anesthetics is similar for all volatiles if the anesthetic duration is very brief. With the administration of volatile anesthetics for longer times, the differences in recovery time become more profound. For example, after a 1-hour anesthetic with desflurane (blood/gas tissue coefficient 0.45), a 95% reduction in the alveolar concentration can be reached in 5 minutes. With an hour-long sevoflurane anesthetic (blood/gas tissue coefficient 0.65), a 95% reduction requires 18 minutes, and an hour-long isoflurane anesthetic (blood/gas tissue coefficient 1.4) requires more than 30 minutes to reach a 95% reduction in the alveolar concentration (Miller: Basics of Anesthesia, ed 6, pp 89–90; Miller: Miller’s Anesthesia, ed 8, pp 654–655).
377. Select the FALSE statement regarding pharmacokinetics for volatile anesthetics. After three time constants A. 6 to 12 minutes have elapsed for “modern anesthetics” B. The arterial-to-venous partial pressure difference (for the volatile) for the brain is very small C. The expired volatile concentration will rise much less slowly than in the preceding 12 minutes D. The venous blood will contain 95% of volatile content of arterial blood
377. (D) After a period of time equal to three time constants, the venous blood exiting the vessel-rich group will be at the 95% level, but the blood as a whole will have a level of less than 95%. The venous blood contains a mixture of blood from the vessel-rich group, the muscle group, the fat group, and the vessel-poor group, and at the three time constant mark will be less than 95% (Miller: Basics of Anesthesia, ed 6, pp 86–88).
378. Halothane (1 MAC) A No change No change Decreased B Decreased Decreased Decreased C Increased Decreased No change or slight increase D Increased Decreased Decreased
378. (A)The information for these questions is summarized in the graphs below. Halothane is unique among the volatile agents listed in that it does not affect the heart rate or systemic vascular resistance in the MAC ranges studied. Sevoflurane reduces heart rate until about 1 MAC, at which time it produces a dose-dependent increase in heart rate (Miller: Basics of Anesthesia, ed 6, pp 90–92).
379. Isoflurane (1 MAC) A No change No change Decreased B Decreased Decreased Decreased C Increased Decreased No change or slight increase D Increased Decreased Decreased
379. (C)The information for these questions is summarized in the graphs below. Halothane is unique among the volatile agents listed in that it does not affect the heart rate or systemic vascular resistance in the MAC ranges studied. Sevoflurane reduces heart rate until about 1 MAC, at which time it produces a dose-dependent increase in heart rate (Miller: Basics of Anesthesia, ed 6, pp 90–92).
380. Desflurane (1 MAC) A No change No change Decreased B Decreased Decreased Decreased C Increased Decreased No change or slight increase D Increased Decreased Decreased
380. (D) The information for these questions is summarized in the graphs below. Halothane is unique among the volatile agents listed in that it does not affect the heart rate or systemic vascular resistance in the MAC ranges studied. Sevoflurane reduces heart rate until about 1 MAC, at which time it produces a dose-dependent increase in heart rate (Miller: Basics of Anesthesia, ed 6, pp 90–92).
381. Sevoflurane (1 MAC) Heart Rate Systemic Vascular Resistance Cardiac Index A No change No change Decreased B Decreased Decreased Decreased C Increased Decreased No change or slight increase D Increased Decreased Decreased
381. (B) The information for these questions is summarized in the graphs below. Halothane is unique among the volatile agents listed in that it does not affect the heart rate or systemic vascular resistance in the MAC ranges studied. Sevoflurane reduces heart rate until about 1 MAC, at which time it produces a dose-dependent increase in heart rate (Miller: Basics of Anesthesia, ed 6, pp 90–92).
382. Each of the following treatments might be useful in restoring a prolonged prothrombin time (PT) to the normal range EXCEPT A. Recombinant factor VIII B. Vitamin K C. Fresh frozen plasma (FFP) D. Cryoprecipitate
382. (A) PT and aPTT are common tests used to evaluate coagulation factors. The PT primarily tests for factor VII in the extrinsic pathway, as well as factors I, II, V, and X of the common pathway. The aPTT primarily tests for factors VIII and IX of the intrinsic pathway, as well as factors I, II, V, and X of the common pathway. Although the PT is prolonged with deficient function of factors I, II, V, VII, or X, it is more sensitive to deficiencies of factor VII and less so with deficiencies of factor I or II. In fact, the PT is not prolonged until the level of fibrinogen (factor I) is less than 100 mg/dL and may be prolonged for only 2 seconds when the level of factor II (prothrombin) is 10% of normal. Factors II, VII, IX, and X are vitamin K–dependent factors, and their formation is blocked with Coumadin therapy. Administering factor VIII will not help a prolonged PT (Miller: Miller’s Anesthesia, ed 8, pp 1872–1874; Barash: Clinical Anesthesia, ed 7, pp 415–416).
383. Proper processing of platelet concentrates (to avoid future hemolytic transfusion reactions) before administration involves A. Type and crossmatching B. ABO and Rh matching C. Rh matching only D. ABO matching only
383. (C) Platelet concentrates contain a fair amount of plasma and white blood cells (WBCs) but relatively few red blood cells (RBCs). Although ABO-compatible platelet transfusions are preferred (platelets survive better, and crossmatching for subsequent RBCs is easier), in emergencies it has been noted that platelets often give adequate hemostasis without regard to ABO compatibility. Even though there are only small quantities of RBCs in platelets, the RBCs present can cause Rh immunization if Rh-positive platelet concentrates are injected into Rh-negative patients. Thus, until childbirth is no longer possible, Rh-negative women should receive only Rh-negative platelets (Miller: Miller’s Anesthesia, ed 8, p 1860; Hoffman: Hematology, ed 6, p 1655).
384. The most common inherited coagulopathy is A. Hemophilia A B. Hemophilia B C. von Willebrand disease (vWD) D. Factor V deficiency
384. (C) Coagulopathies can be inherited or acquired. Of the inherited coagulopathies, vWD is the most common, affecting 1 in 100 to 500 people. Both hemophilia A (factor VIII) deficiency and hemophilia B (factor IX or Christmas disease) are X-linked recessive disorders. Hemophilia A occurs in 1 to 2 per 10,000 male individuals, and hemophilia B occurs in 1 per 100,000 male individuals. Factor V, factor VII, factor X, and prothrombin (factor II) deficiencies are exceedingly rare autosomal recessive disorders (Miller: Miller’s Anesthesia, ed 8, p 1872; Barash: Clinical Anesthesia, ed 7, p 432).
385. In a 70-kg patient, 1 unit of platelet concentrate should increase the platelet count by A. 2000 to 5000/mm3 B. 5000 to 10,000/mm3 C. 15,000 to 20,000/mm3 D. 20,000 to 25,000/mm3
385. (B) Platelet count is increased about 5000 to 10,000/mm3 per unit of platelet concentrate in the typical 70- kg patient. Each unit contains greater than 5.5 × 1010 platelets (Miller: Miller’s Anesthesia, ed 8, pp 1840, 1860; Barash: Clinical Anesthesia, ed 7, p 421).
386. A 68-year-old patient receives a 1-unit transfusion of packed red blood cells (RBCs) in the recovery room after a laparoscopic prostatectomy. As the blood is slowly dripping into his peripheral intravenous line, the patient complains of itching on his chest and arms, but his vital signs remain stable. The antibody most likely responsible for this is directed against A. Rh B. ABO C. MN, P, and Lewis D. None of the above
386. (D) This is an example of a typical allergic reaction. All of the other choices in this question may be involved in hemolytic reactions. Allergic reactions are a form of nonhemolytic transfusion reactions, which are thought to be caused by foreign proteins in the transfused blood. The reactions occur in about 3% of all transfusions, and they present with urticaria, erythema, pruritus, fever, and sometimes respiratory symptoms. When such a reaction occurs, the transfusion is stopped and supportive therapy, including antihistamines, is administered. If the symptoms resolve and there are no signs of a hemolytic reaction (no free hemoglobin in the plasma or urine) or a severe anaphylactic reaction, the transfusion can be resumed (Miller: Miller’s Anesthesia, ed 8, p 1853; Barash: Clinical Anesthesia, ed 7, p 425).
387. The likelihood of a clinically significant hemolytic transfusion reaction resulting from administration of type-specific blood is less than A. 1 in 250 B. 1 in 500 C. 1 in 1000 D. 1 in 10,000
387. (C) Hemolytic transfusion reactions are often the result of clerical error. Three main blood compatibility tests can be performed to reduce the chance of a hemolytic reaction: ABO Rh typing, antibody screening, and crossmatching. With correct ABO and Rh typing, the possibility of an incompatible transfusion is less than 1 per 1000. If you add a type and screen, the possibility of an incompatible transfusion is less than 1 per 10,000. Optimal safety occurs when crossmatching is performed (Miller: Miller’s Anesthesia, ed 8, p 1840).
388. Frozen erythrocytes can be stored for A. 1 year B. 3 years C. 5 years D. 10 years
388. (D) Blood is most often stored as a liquid at about 4° C but can also be frozen for prolonged storage. Because of the added expense of frozen blood, it is used primarily for rare blood types and for autologous use. Blood that has already been collected has a cryoprotective agent (e.g., glycerol) added and is then frozen and stored at a temperature of −65° C (when 40% glycerol is used) or −120° C (when 20% glycerol is used). Currently, the U.S. Food and Drug Administration (FDA) allows frozen blood to be used up to 10 years from the time of collection (Barash: Clinical Anesthesia, ed 7, p 416). 112 Part 2 Clinical Sciences
389. Which of the following clotting factors has the shortest half-life? A. Factor II B. Factor V C. Factor VII D. Factor IX
389. (C) Factor VII is one of the four vitamin K–dependent clotting factors (factors II, VII, IX, and X). It also has the shortest half-life of all the clotting factors (4-6 hours) and is the first factor to become deficient in patients with severe hepatic failure, warfarin (Coumadin) anticoagulation therapy, and vitamin K deficiency. The PT is most sensitive to decreases in factor VII (Barash: Clinical Anesthesia, ed 7, pp 411–412).
390. Which of the measures below does NOT reduce the incidence of transfusion-related acute lung injury (TRALI)? A. Exclusion of female donors B. Use of autologous blood C. Leukocyte reduction D. Use of blood less than 14 days old
390. (C) TRALI occurs within 6 hours of blood component administration. Patients experience noncardiogenic pulmonary edema with acute bilateral pulmonary infiltrates and hypoxemia (PaO2/Fi O2 ≤300 mm Hg or oxygen saturation ≤90% on room air with no evidence of left atrial hypertension). The pathologic changes associated with TRALI are complex and may involve low-pressure pulmonary edema secondary to neutrophil activation and sequestration in the lungs. Older transfusion products (>14 days), female donors (especially multiparous patients), and pooled platelets compared with apheresis platelets are associated with a higher frequency of this condition. Interestingly, although leukocytes may be part of the activation process, leukocyte reduction does not seem to significantly decrease the incidence of TRALI but does decrease the incidence of febrile reactions and the risk of CMV, and it may decrease leukocyteinduced immunomodulation. Treatment for TRALI reactions is supportive (Barash: Clinical Anesthesia, ed 7, pp 417–428; Miller: Basics of Anesthesia, ed 6, p 376; Miller: Miller’s Anesthesia, ed 8, p 1859).
391. A 42-year-old woman is anesthetized for resection of a large (22-kg), highly vascular sarcoma in the abdomen. During the resection, 20 units of RBCs, 6 units of platelets, 10 units of cryoprecipitate, 5 units of FFP, and 1 L of albumin are administered. At the conclusion of the operation, the patient’s vital signs are stable, and she is transported to the intensive care unit. Three and a half hours later, a diagnosis of sepsis is made, and antibiotic therapy is started. Which of the items below would be the most likely cause of sepsis in this patient? A. Packed RBCs B. Cryoprecipitate C. Platelets D. FFP
391. (C) Of the five blood products listed in this question, platelets are the most likely to cause bacterial sepsis. Platelet-related sepsis is estimated to occur in 1 case per 12,000. The source of bacteria can be donor blood or contamination during the collection, processing, and storage of the blood. If platelets are cooled, then rewarmed, the platelets tend not to function very effectively. Because platelets are stored at room temperature of 20 to 24° C, bacteria tend to survive and multiply. All other listed blood products are cooled. Whole blood and packed RBCs are cooled to 4° C (unless they are frozen, which would be colder). FFP and cryoprecipitate are frozen to below −70° C. Albumin is heat sterilized, making it a sterile preparation that then can be safely stored at room temperatures (Miller: Miller’s Anesthesia, ed 8, pp 1859–1860; Barash: Clinical Anesthesia, ed 7, pp 423–425).
392. Blood is routinely screened (serologically) for A. Hepatitis A B. Severe acute respiratory syndrome (SARS) C. West Nile virus D. Bovine spongiform encephalitis (BSE, or mad cow disease)
392. (C) Hepatitis A transmission is very rare and is screened for by history alone (not serologically) because there is no carrier state for the virus and the disease is relatively mild. A decrease in the transmission for various other infectious agents has been attributed to the recent addition of nucleic acid testing (see table). At present, there are no screening tests available for malaria, Chagas, SARS, variant Creutzfeldt-Jakob disease, or BSE (Miller: Miller’s Anesthesia, ed 8, pp 1856–1858; Barash: Clinical Anesthesia, ed 7, pp 415–416). TESTS USED FOR DETECTING INFECTIOUS AGENTS IN ALL UNITS OF BLOOD, 2008 Virus RNA Minipool Antibody To Human immunodeficiency virus (HIV) Nucleic acid technology HIV-1, HIV-2 Hepatitis C virus (HCV) Nucleic acid technology HCV Hepatitis B virus (HBV) HBV Human T-cell lymphotropic virus (HTLV) HTLV-1, HTLV-2 West Nile virus Nucleic acid technology
393. The blood volume of a 10-kg, 1-year-old infant is A. 600 mL B. 800 mL C. 1000 mL D. 1300 mL
393. (B) Blood volume decreases with age. A preterm newborn has a blood volume of 100 to 120 mL/kg, a term newborn has a blood volume of about 90 mL/kg, an infant (3-12 months) has a blood volume of 80 mL/kg, a child older than 1 year has a blood volume of 70 mL/kg, and an adult has a blood volume of 65 mL/kg. This 10-kg, 1-year-old infant would have an estimated blood volume (EBV) of 800 mL (Barash: Clinical Anesthesia, ed 7, p 1246).
394. Which of the infections below is the most common transfusion-related infection? A. Human T-cell lymphotropic virus (HTLV)-II B. Hepatitis B C. Hepatitis C D. Human immunodeficiency virus (HIV)
394. (B) The risk of transfusion-transmitted infection with a unit of screened blood in the United States varies from study to study, but it is very infrequent with CMV because of leukocyte-reduced blood: 1 in 205,000 for hepatitis B, 1 in 1,935,000 for hepatitis C, 1 in 2,135,000 for HIV, 1 in 2,993,000 for HTLV-II, and 1 in more than 1,100,000 for West Nile virus. Thus, the most common transfusionassociated infection in the United States is now hepatitis B. The infective agent for syphilis does not survive at 4° C, making transmission unlikely for whole blood, packed RBCs, FFP, or cryoprecipitate. It is possible for platelets (stored at room temperature) to transmit syphilis (Miller: Miller’s Anesthesia, ed 8, pp 1856–1858). Blood Products, Transfusion, and Fluid Therapy 113
395. A 40-year-old, 78-kg patient with hemophilia A is scheduled for a right total knee arthroplasty. His laboratory test results show a hematocrit of 40, a factor VIII level of 0%, and no inhibitors to factor VIII. How much factor VIII concentrate do you need to give him to bring his factor VIII level to 100%? A. 3000 units B. 2500 units C. 2000 units D. 1500 units
395. (A) The most common type of hemophilia is hemophilia A, an X-linked recessive disease causing a reduction in factor VIII activity. The disease occurs with a frequency of 1 in 5000 male individuals. This disease can be severe (<1% factor VIII), moderate (1%-4% factor VIII), or mild (5%-30% factor VIII). Patients with mild hemophilia rarely have spontaneous bleeding. Laboratory studies show a normal platelet count and normal PT but a prolonged aPTT. The primary goal of preoperative preparation of patients with hemophilia A is to increase plasma factor VIII activity to a level that will ensure adequate hemostasis (i.e., 50%-100%), then maintain a level (>40% factor VIII levels) for 7 to 10 days. One unit of factor VIII is equal to 1 mL of 100% activity of normal plasma. Thus, to calculate the initial dose, first calculate the patient’s blood and then the plasma volume. Then calculate the amount of activity needed to increase the factor VIII level. In this case, the blood volume is 78 kg × 65 mL/kg, or about 5000 mL. Knowing that the RBC volume is 40% (i.e., hematocrit is 40) makes the plasma volume 60%. Thus, the plasma volume is 5000 mL × 0.6, or about 3000 mL. Because the patient is starting at 0% activity and you wish to raise it to 100% activity, you will need 3000 units. (If you wish to raise the activity by 40%, then 3000 mL of plasma × 0.4 for 40% activity = 1200 units.) In addition, because the half-life of factor VIII is about 12 hours, about 1500 units will remain after 12 hours. An infusion of 1500 units in 12 hours, or 125 units per hour, will be a good starting maintenance infusion rate. Factor VIII can be administered as factor VIII concentrate or cryoprecipitate (about 10 units/mL). Patients with factor VIII inhibitors (10%-20% of patients with hemophilia) require more factor VIII. Hematology consultation should be considered for all patients with hemophilia, and routine checking of factor VIII levels should be performed (Marx: Rosen’s Emergency Medicine, ed 8, p 1614).
396. A 38-year-old man is undergoing a total colectomy under general anesthesia. Urine output has been 20 mL/hr for the last 2 hours. Volume replacement has been adequate. The rationale for administering 5 to 10 mg of furosemide to this patient is to A. Offset the effects of increased antidiuretic hormone (ADH) B. Improve renal blood flow C. Convert oliguric renal failure to nonoliguric renal failure D. Offset the effects of increased renin
396. (A) Serum ADH levels increase during painful stimulation associated with surgery, as well as during positivepressure mechanical ventilation. Small doses of furosemide (i.e., 0.1 mg/kg) will counteract this effect during surgery (Miller: Miller’s Anesthesia, ed 8, p 1773; Barash: Clinical Anesthesia, ed 7, pp 344–345).
397. A 65-year-old man involved in a motor vehicle accident (MVA) is brought to the emergency room with a blood pressure of 60 mm Hg systolic. He is transfused with 4 units of type O, Rh-negative whole blood and 4 L of normal saline solution. After the patient is brought to the operating room, his blood type is determined to be A positive. Which of the following is the most appropriate blood type for further intraoperative transfusions? A. Type A, Rh-positive whole blood B. Type O, Rh-negative RBCs C. Type A, Rh-positive RBCs D. Type O, Rh-negative whole blood
397. (B) Type O, Rh-negative blood is also called universal donor blood because the transfused RBCs lack the antigens needed to be hemolyzed. Because the plasma of O-negative blood contains anti-A and anti-B antibodies, it is preferable to administer packed RBCs (with little plasma) over whole blood (lots of plasma) in an emergency. However, if two or more units of type O-negative, uncrossmatched whole blood are administered to a patient and subsequent blood typing reveals the patient’s blood type to be A, B, or AB, then switching back to the patient’s own blood type could lead to major intravascular hemolysis of the transfused RBCs and, therefore, is not advised. The use of type O-negative universal donor whole blood, or preferably RBCs, is recommended. In the male patient or the older female patient who will not have more children, type O-positive whole blood can be administered if few type O, Rh-negative units are available and massive transfusion is anticipated. Only after it is determined that the patient has low enough levels of transfused anti-A and anti-B antibodies should the correct type of blood be administered (Miller: Miller’s Anesthesia, ed 8, p 1840).
398. The criterion used to determine how long blood can be stored before transfusion is A. 90% of transfused erythrocytes must remain in circulation for 24 hours B. 70% of transfused erythrocytes must remain in circulation for 24 hours C. 70% of transfused erythrocytes must remain in circulation for 72 hours D. 75% of transfused erythrocytes must remain in circulation for 7 days
398. (B) The requirement for blood storage states that at least 70% of the erythrocytes must remain in circulation for 24 hours after a transfusion for the transfusion to be successful. Erythrocytes that survive longer than 24 hours after transfusion appear to have a normal life span (Miller: Miller’s Anesthesia, ed 8, p 1841).
399. The rationale for storage of platelets at room temperature (22° C) is A. There is less splenic sequestration B. It optimizes platelet function C. It reduces the chance for infection D. It decreases the incidence of allergic reactions Blood Products, Transfusion, and Fluid Therapy 109
399. (B) At a pH below 6.0 or in cold temperatures such as 4° C (the temperature used for blood storage), platelets undergo irreversible shape changes. The optimal temperature for platelet storage is 22° C ± 2° C, or room temperature. There are two major problems with platelet storage at this recommended temperature. First, the pH falls because of platelet metabolism. Second, bacterial growth is possible, which could potentially lead to sepsis and death. To minimize these problems, platelet storage is limited to 5 days at 22° C (Miller: Miller’s Anesthesia, ed 8, pp 1859–1861; Barash: Clinical Anesthesia, ed 7, pp 417–418).
400. An 18-year-old woman involved in an MVA is brought to the emergency room in shock. She is transfused with 10 units of type O, Rh-negative whole blood over 30 minutes. After infusion of the first 5 units, bleeding is controlled, and her blood pressure rises to 85/51 mm Hg. During the next 15 minutes, as the remaining 5 units are infused, her blood pressure slowly falls to 60 mm Hg systolic. The patient remains in sinus tachycardia at 120 beats/min, but the QT interval is noted to increase from 310 to 470 msec, and the central venous pressure increases from 9 to 20 mm Hg. Her breathing is rapid and shallow. The most likely cause of this scenario is A. Citrate toxicity B. Hyperkalemia C. Hemolytic transfusion reaction D. Tension pneumothorax
400. (A) Whole blood is rarely used today except in emergency cases when the rapid infusion of blood and volume is needed. Stored blood contains citrate, an anticoagulant that binds ionized calcium. When whole blood is rapidly transfused (i.e., >50 mL/70 kg/min) the citrate binds with calcium, producing transient decreases in ionized calcium. The abrupt decrease in ionized calcium can lead to prolonged QT intervals, an increase in left ventricular end-diastolic pressure, and arterial hypotension. Within 5 minutes of stopping the transfusion, ionized calcium levels return to normal. The volume of an average unit of whole blood is 500 mL. This patient received 10 units of whole blood, or 5000 mL, over 30 minutes, then another 5 units in 15 minutes. This averages to a rate greater than 160 mL/min (Miller: Miller’s Anesthesia, ed 8, pp 1840–1841). 114 Part 2 Clinical Sciences
401. A 20-kg, 5-year-old child with a hematocrit of 40% could lose how much blood and still maintain a hematocrit of 30%? A. 140 mL B. 250 mL C. 350 mL D. 450 mL
401. (C) A 20-kg, 5-year-old child has an EBV of 70 mL/kg = 1400 mL. The acceptable blood loss can be determined by use of the following formula: maximum allowable blood loss (in mL) = EBV × (Hcts − Hct1)/ Hcts where EBV is the estimated blood volume (in mL), Hcts is the starting hematocrit, and Hct1 is the lowest acceptable hematocrit. For this patient, the maximal allowable blood loss = 1400 × (40 − 30/40) = 1400 × (10/40) = 350 mL. This assumes that the patient is getting volume expansion with crystalloid (3 mL per mL of blood loss). Also see explanation to Question 393 (Barash: Clinical Anesthesia, ed 7, p 1246).
402. A 100-kg male patient has a measured serum sodium concentration of 105 mEq/L. How much sodium would be needed to bring the serum sodium to 120 mEq/L? A. 600 mEq B. 900 mEq C. 1200 mEq D. 1500 mEq
402. (B) The normal serum sodium concentration is 135 to 145 mEq/L. Hyponatremia occurs when the serum level is less than 135 mEq/L. Clinical symptoms correspond not only to the level of hyponatremia but also to how rapidly sodium levels are falling. Hyponatremia is most commonly not a deficiency in total body sodium but rather is an excess of total body water (e.g., absorption of irrigating fluids as seen in transurethral resection of the prostate syndrome, and syndrome of inappropriate antidiuretic hormone secretion). It can also be caused by an excessive loss of sodium, as is seen in severe sweating, vomiting, diarrhea, burns, and the use of diuretics. With acute falls in serum sodium, neurologic symptoms (confusion, restlessness, drowsiness, seizures, coma) resulting from cerebral edema can be seen at serum levels below 120 mEq/L. Cardiac symptoms (ventricular tachycardia, ventricular fibrillation) can be seen at levels below 100 mEq/L. Therapy for severe hyponatremia includes water restriction, loop diuretics, and at times the administration of hypertonic saline (3% NaCl). The dose of sodium needed for correction can be calculated by multiplying the total body water (TBW = body weight × 0.6) times the increase in sodium desired; that is, Dose of Na+ = Body weight × 0.6 × (desired Na+ level − current Na+ level in mEq/L) In this patient, the calculated dose of sodium would be 100 (weight in kg) × 0.6 × (120 mEq/L-105 mEq/L) = 900 mEq. Three percent NaCl is infused no faster than 100 mL/hr. Too rapid a correction may lead to central pontine myelinolysis. Once the level reaches 120 mEq/L, further treatment usually consists of water restriction and diuretics (Miller: Miller’s Anesthesia, ed 8, p 1773).
403. Paramedics respond to an MVA site and immediately stabilize the neck, secure the airway, and place an intravenous line into a 19-year-old 70-kg man lying in a pool of blood. Before the infusion is started, 3 milliliters of blood are withdrawn for hemoglobin and drug screening. The first responders estimate that the patient has lost one half of his entire blood volume. Given a starting value of 18 g/dL, the new value would likely be A. 9 g/dL B. 11 g/dL C. 14 g/dL D. 17 g/dL
403. (D) The intravascular half-life of crystalloid solution is 20 to 30 minutes, whereas the intravascular halflife of colloid is 3 to 6 hours. To restore intravascular volume, for each mL of blood lost, 3 to 4 mL of crystalloid or 1 mL of colloid is administered. In this case, though, the blood sample is drawn before the infusion is started, so the hemoglobin drawn should be similar to his hemoglobin concentration immediately before the MVA (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 1161–1164).
404. A 23-year-old woman who has been receiving total parenteral nutrition (TPN) (15% dextrose, 5% amino acids, and intralipids) for 3 weeks is scheduled for surgery for severe Crohn disease. Induction of anesthesia and tracheal intubation are uneventful. After peripheral intravenous access is established, the old central line is removed and a new central line is placed at a different site. At the end of the operation, a large volume of fluid is discovered in the chest cavity on chest x-ray film. Arterial blood pressure is 105/70 mm Hg, heart rate is 150 beats/min, and Sao2 is 96% (pulse oximeter). The most appropriate initial step is to A. Place a chest tube B. Change the single-lumen to a double-lumen endotracheal tube C. Start a dopamine infusion D. Check the blood glucose level
404. (D) Abrupt discontinuation of TPN that contains 10% to 20% dextrose may result in profound rebound hypoglycemia. Tachycardia in this patient may signify hypoglycemia. Prompt diagnosis and treatment of severe hypoglycemia are essential if neurologic damage is to be avoided. Whenever a central line is placed for TPN, it should be properly checked before the hypertonic infusion is started (Miller: Miller’s Anesthesia, ed 8, p 1782).
405. In an emergency when there is a limited supply of type O-negative RBCs, type O-positive RBCs are reasonable for transfusion for each of the following patients EXCEPT A. A 60-year-old woman with diabetes who was involved in an MVA B. A 23-year-old man who sustained a gunshot wound to the upper abdomen C. An 84-year-old man with a ruptured abdominal aortic aneurysm D. A 21-year-old, gravida 2, para 1 woman with placenta previa who is bleeding profusely
405. (D) In an emergency when massive amounts of blood are immediately required and the supply of O-negative RBCs in the blood bank is low, it is acceptable to transfuse O-positive RBCs into male patients or into female patients past the age of childbirth before the patient’s blood type is known. This is because delaying blood transfusion for blood typing may be more hazardous to the patient than the risk of a significant transfusion reaction based on Rh type for these patients. However, for the female patient who has the potential for pregnancy, administration of Rh-positive RBCs is not recommended (unless no Rh-negative RBCs are available). This is because an Rh-negative patient who receives Rh-positive RBCs would experience isoimmunization. For these women, future pregnancies with Rh-positive fetuses could be associated with erythroblastosis fetalis. Note: RBCs are preferred over whole blood because Rh-negative whole blood contains a large quantity of anti-A and anti-B antibodies in the plasma (Turgeon: Clinical Hematology, ed 1, pp 50–51).
406. Hetastarch exerts an anticoagulative effect through interference with the function of A. Antithrombin III B. Factor VIII C. Fibrinogen D. Prostacyclin
406. (B) Hetastarch (hydroxyethyl starch) and dextran 70 (glucose polymers with mean molecular weights of 70,000) are colloid solutions that are used for intravascular fluid volume expansion. Both hetastarch and dextran have been associated with allergic reactions, can interfere with coagulation, and can cause hypervolemia. Hetastarch, unlike dextran, does not interfere with crossmatching of blood at the recommended maximal daily dose of 20 mL/kg. Neither compound needs to be administered through a filter. Hetastarch also reduces levels of vWF significantly as well as availability of glycoprotein IIb/IIIa, and it can become directly incorporated into the fibrin clot (Miller: Miller’s Anesthesia, ed 8, p 1783). Blood Products, Transfusion, and Fluid Therapy 115
407. All of the following characterize packed RBCs that have been stored for 35 days at 4° C in citrate phosphate dextrose adenine-1 (CPDA-1) anticoagulant preservative EXCEPT A. Serum potassium greater than 70 mEq/L B. pH less than 7.0 C. Blood glucose less than 100 mg/dL D. P50 of 28
407. (D) RBCs are cooled to about 4° C to decrease cellular metabolism. CPDA-1 is a preservative anticoagulant solution often added to blood. It contains citrate, phosphate, dextrose, and adenine. The citrate is used to bind calcium and acts as an anticoagulant. Phosphate acts as a buffer. Dextrose is added as an energy source for cellular metabolism on the day of donation to raise the blood sugar to greater than 400 mg/dL. At 35 days, the glucose level drops below 100 mg/dL. Adenine is added as a substrate source so that the cells can produce adenosine triphosphate. Other biochemical changes include a fall in pH to about 6.7 and a rise in plasma potassium from around 4 mEq/L on the day of donation to 76 mEq/L at 35 days. Concentrations of 2,3-diphosphoglycerate fall below 1 μM/mL, which causes a leftward shift in the oxyhemoglobin dissociation curve that allows for an increased oxygen affinity for the hemoglobin. This leftward shift produces a P50 value less (not greater) than the normal 26 mm Hg (Miller: Miller’s Anesthesia, ed 8, pp 1841–1842).
408. What is the storage life of whole blood stored with citrate phosphate dextrose (CPD)? A. 14 days B. 21 days C. 35 days D. 42 days 110 Part 2 Clinical Sciences
408. (B) Many preservation solutions are used for whole blood and RBCs. Acid citrate dextrose, CPD, and citrate phosphate double dextrose (CP2D) each allows blood to have a shelf life of 21 days. In 1978, the FDA approved the additive adenine to CPD. This extended the shelf life of blood by 2 weeks. CPDA-1 has a shelf life of 35 days. These solutions were used mainly for whole blood. However, when component therapy became more widespread, it was noted that packing the RBCs by removing the plasma also removed a significant amount of adenine and glucose. By use of an additive solution (which contains primarily adenine, glucose, and saline) to the CPD or CP2D whole blood that has the plasma removed, the packed RBCs can now be stored for 42 days. The three different additive solutions currently used in the United States are Adsol (AS-1), Nutricel (AS-3), and Optisol (AS-5) (Miller: Miller’s Anesthesia, ed 8, p 1841).
409. In the adult, the liver is the primary organ for A. Hemoglobin synthesis B. Hemoglobin degradation C. Factor VIII synthesis D. Antithrombin III synthesis
409. (D) The liver produces most of the coagulation factors except for factor III (tissue thromboplastin), factor IV (calcium), and factor VIII (von Willebrand factor). The liver also produces the coagulation regulatory protein C, protein S, and antithrombin III. Fetal RBCs are produced exclusively by the liver; in the adult, 80% of RBCs are produced by the bone marrow and only 20% are produced in the liver. The degradation of blood is primarily by the reticuloendothelial system (Hemmings: Pharmacology and Physiology for Anesthesia, ed 1, p 477; Miller: Basics of Anesthesia, ed 6, p 456).
410. Anticoagulation with low-molecular-weight heparin (LMWH) can be best monitored through which of the following laboratory tests? A. Activated partial thromboplastin time (aPTT) B. Anti-Xa assay C. Thrombin time D. Reptilase test
410. (B) LMWH is produced by the fractionation or cleaving of “unfractionated heparin (UFH)” into shorter fragments. The anticoagulant properties of UFH and LMWH are complex and somewhat different. UFH binds to and activates antithrombin (more effectively than LMWH) and can be monitored easily with the aPTT. At the usual clinical doses of LMWH, aPTT is not prolonged. LMWH, on the other hand, is more effective in inactivating factor Xa and can be monitored by anti-Xa levels (although commonly this is not performed because of the more predictable action of prophylactic dosing of LMWH). At high doses of LMWH, antifactor Xa values are more commonly measured. Thrombin time is a measure of the ability of thrombin to convert fibrinogen to fibrin. It is prolonged with low amounts of fibrinogen, heparin, and fibrin degradation products (FDPs). A reptilase test is done by adding reptilase to plasma and waiting for a clot to form and is prolonged in the presence of lupus anticoagulant, FDPs, fibrinogen deficiency, or abnormal fibrinogen. It is not prolonged in the presence of heparin (Miller: Miller’s Anesthesia, ed 8, pp 1872–1874; Barash: Clinical Anesthesia, ed 7, p 439).
411. Heparin resistance is likely in patients with which of the following heritable conditions? A. Factor V Leiden mutation B. Prothrombin G20210A gene mutation C. Protein S deficiency D. Antithrombin or antithrombin III (AT3) deficiency
411. (D) The four selections to this question are four of the five major hereditary conditions associated with hypercoagulation. They cause an increased likelihood of clot formation by either increasing prothrombotic proteins (e.g., factor V Leiden mutation, prothrombin G20210A gene mutation) or decreasing endogenous antithrombotic proteins (e.g., antithrombin deficiency, protein C deficiency, protein S deficiency). Clot may also develop if heparin resistance occurs (usual doses produce less than the expected prolongation of the partial thromboplastin time or the activated clotting time) and is not recognized, as during cardiopulmonary bypass. It may occur as a result of excessive binding of heparin to plasma proteins or an insufficient amount of antithrombin. Because heparin binds to and potentiates antithrombin’s activity, conditions with low amounts of antithrombin show resistance. Treatment of AT3 deficiency is replacement of AT3 with either specific AT III concentrate (Thrombate III) or FFP. Replacement of antithrombin to 100% activity is recommended before cardiac surgery in patients with congenital AT3 deficiency (Miller: Miller’s Anesthesia ed 8, pp 1871–1872, 1876–1877; Young: Clinical Hematology, ed 1, pp 1116–1118). 116 Part 2 Clinical Sciences
412. Von Willebrand disease (vWD) could be treated by any of the following EXCEPT A. Cryoprecipitate B. Desmopressin (DDAVP) C. FFP D. Recombinant factor VIII
412. (D) vWD is the most common inherited abnormality affecting platelet function and is caused by a quantitative or qualitative deficiency of a protein called von Willebrand factor (vWF). vWF is produced by endothelial cells and platelets and appears to have two main functions: it acts as an adhesion protein that diverts platelets to sites of vascular injury, and it helps protect factor VIII from inactivation and clearance. Patients with vWD have prolonged bleeding times and a reduced amount of factor VIII. Patients with hemophilia A also have a decrease in factor VIII but normal bleeding times. Type 1 vWD is the most common type (60%-80%) and is associated with a quantitative decrease in circulating plasma vWF caused by a decrease in release of available vWF. Type 2 vWD (20%-30%) has several subtypes and is associated with qualitative deficiency of vWF. Type 3 vWD is the least frequent (1%-5%) and the most severe form, wherein there is almost no vWF and very low factor VIII levels (3%-10% of normal). Treatment of vWD includes DDAVP, which increases the release of available vWF, or blood products that contain vWF and factor III (e.g., cryoprecipitate, FFP, or factor III concentrates). Recombinant factor VIII is not used because it does not contain vWF (Miller: Miller’s Anesthesia, ed 8, pp 1123, 1872; Barash: Clinical Anesthesia, ed 7, p 433).
413. The significance of immunoglobulin A (IgA) antibodies in transfusion medicine is related to A. Allergic reaction B. Febrile reaction C. Delayed hemolytic reaction (immune extravascular reaction) D. Diagnosis of TRALI reaction
413. (A) Although allergic reactions after blood transfusions are common (up to 3%), true nonhemolytic anaphylactic reactions are rare. When anaphylactic reactions develop (often with only a few milliliters of blood or plasma transfused), the signs and symptoms may include dyspnea, bronchospasm, laryngeal edema, chest pain, hypotension, and shock. These reactions are caused by the transfusion of “foreign” IgA protein to patients who have hereditary IgA deficiency and have formed anti-IgA as a result of previous transfusions or from earlier pregnancies. Treatment includes stopping the transfusion and administering epinephrine and steroids. If further transfusion is needed, washed RBCs or RBCs from IgA-deficient donors should be used (Miller: Miller’s Anesthesia, ed 8, p 1853; Barash: Clinical Anesthesia, ed 7, p 426).
414. The most common cause of mortality associated with administration of blood is A. TRALI B. Non-ABO hemolytic transfusion reaction C. Microbial infection D. Anaphylactic reaction
414. (A) For the years 2005 to 2006, 125 confirmed transfusion-related fatalities were listed by the FDA in the United States. The most common cause was TRALI (51%), followed by non-ABO hemolytic transfusion reaction (20%), microbial infection (12%), ABO hemolytic transfusion reaction (7%), death from transfusion-associated circulatory overload (TACO) (7%), and other (2%). Since March 2004, when voluntary bacterial detection testing was implemented for platelet transfusions, there has been a decrease in fatalities associated with transfusion of bacterially contaminated apheresis platelets. Considering about 29 million components are transfused each year (2004 calendar year) in the United States, the reported incidence of death is quite small (www.fda.gov/cber/blood/fatal/0506.htm; Miller: Miller’s Anesthesia, ed 8, pp 1855–1860; Barash: Clinical Anesthesia, ed 7, pp 425–427). TRANSFUSION-RELATED FATALITIES IN THE UNITED STATES, 2004 TO 2006 Cause of Fatality 2004-2006 Average per Year TRALI 86 29 Other reactions (non-ABO hemolytic therapy; anaphylaxis) 67 22 Bacterial contamination 20 7 ABO hemolytic transfusion therapy 15 5 Transfusion not ruled out 31 10 TRALI, transfusion-related acute lung injury. From Miller RD: Miller’s Anesthesia, ed 7, Philadelphia, Saunders, 2011, Table 55-6.
415. Fluid resuscitation during major abdominal surgery with which of the following agents is associated with the BEST survival data? A. 5% Albumin B. 6% Hydroxyethyl starch C. Dextran 70 D. None of the above
415. (D) There is controversy not only as to which intravenous fluid is the best but also how much to give. Most would suggest that isotonic crystalloids should be the initial resuscitative fluids to any trauma patients, and they are certainly less expensive than 5% albumin, 6% hydroxyethyl starch, and dextran 70. Clear advantages of one fluid over another are hard to find (Miller: Miller’s Anesthesia, ed 8, p 1800; Barash: Clinical Anesthesia, ed 7, pp 338–339). Blood Products, Transfusion, and Fluid Therapy 117
416. Which of the following processes reduces the possibility of transmission of cytomegalovirus (CMV) to a susceptible recipient via transfusion of RBCs?
416. (B) Transmission of CMV to patients who have normal immune mechanisms is benign and self-limiting, but in patients who are immunocompromised (e.g., premature newborns, solid organ and bone marrow transplant patients, acquired immunodeficiency syndrome patients), CMV infection can be serious and life threatening. Leukocyte reduction can reduce CMV transmission, but restriction of blood products from seronegative donors is preferred (Miller: Miller’s Anesthesia, ed 8, pp 1857–1858; Barash: Clinical Anesthesia, ed 7, p 424).
417. What is the process aimed at reducing graft-versushost disease (GVHD) in transfusion recipients? A. Washing erythrocytes B. Reduction of leukocytes C. Irradiation D. Storage in Adsol 111 Blood Products, Transfusion, and Fluid Therapy Answers, References, and Explanations
417. (C) GVHD is an often fatal condition that occurs in patients who are immunocompromised. It occurs when donor lymphocytes (graft) establish an immune response against the recipient (host). Blood products that have a significant amount of lymphocytes include RBCs and platelets. FFP and cryoprecipitate appear to be safe. Although directed donor units from first-degree relatives and leukoreduction may reduce the incidence of GVHD, only irradiated products (which inactivates donor lymphocytes) can prevent GVHD (Miller: Miller’s Anesthesia, ed 8, p 1858; Barash: Clinical Anesthesia, ed 7, p 428). 118
418. A 78-year-old patient with a history of hypertension and adult-onset diabetes for which she takes chlorpropamide (Diabinese) is admitted for elective cholecystectomy. On the day of admission, blood glucose is noted to be 270 mg/dL, and the patient is treated with 15 units of regular insulin subcutaneously (SQ) in addition to her regular dose of chlorpropamide. Twenty-four hours later after overnight fasting, the patient is brought to the operating room (OR) without her daily dose of chlorpropamide and is anesthetized. A serum glucose is measured and found to be 35 mg/dL. The MOST likely explanation for this is A. Insulin B. Chlorpropamide C. Hypovolemia D. Effect of general anesthesia
418. (B) Patients with insulin-dependent diabetes and non–insulin-dependent diabetes require special consideration when presenting for surgery. Geriatric age patients come to the OR in the fasting state and without having taken their morning dose of their oral diabetic agent. Chlorpropamide is the longest-acting sulfonylurea and has a duration of action up to 72 hours. Accordingly, it is prudent to measure serum glucose before inducing anesthesia and periodically during the course of the anesthetic and surgery. Regular insulin has a peak effect 2 to 3 hours after SQ administration and a duration of action approximately 6 to 8 hours and would therefore not cause a serum glucose of 35 mg/dL 24 hours after it was administered (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 479, 483–484).
419. Select the TRUE statement. A. Dibucaine is an ester-type local anesthetic B. A dibucaine number of 20 is normal C. The dibucaine number represents the quantity of normal pseudocholinesterase D. None of the above
419. (D) Dibucaine is an amide-type local anesthetic that inhibits normal pseudocholinesterase by approximately 80%. In patients who are heterozygous for atypical pseudocholinesterase, enzyme activity is inhibited by 40% to 60%. In patients who are homozygous for atypical pseudocholinesterase, enzyme activity is inhibited by only 20%. The dibucaine number is a qualitative assessment of pseudocholinesterase. Quantitative as well as qualitative determination of enzyme activity should be carried out in any patient who is suspected of having a pseudocholinesterase abnormality (Miller: Basics of Anesthesia, ed 6, p 149).
420. A 56-year-old patient with a history of liver disease and osteomyelitis is anesthetized for tibial débridement. After induction and intubation, the wound is inspected and débrided with a total blood loss of 300 mL. The patient is transported intubated to the recovery room, at which time the systolic blood pressure falls to 50 mm Hg. Heart rate is 120 beats/min, arterial blood gases (ABGs) are Pao2 103, Paco2 45, pH 7.3, with 97% O2 saturation with 100% Fio2. Mixed venous blood gases are Pvo2 60 mm Hg, Pvco2 50, and pH 7.25. Which of the following diagnoses is MOST consistent with this clinical picture? A. Hypovolemia B. Congestive heart failure (CHF) C. Cardiac tamponade D. Sepsis with acute respiratory distress syndrome
420. (D) All hypotension can be broadly broken down into two main categories: decreased cardiac output and decreased systemic vascular resistance. Flow or cardiac output can be further subdivided into problems related to decreased heart rate (i.e., bradycardia versus problems related to decreases in stroke volume). Normal Po2 in mixed venous blood is 40 mm Hg. Increased mixed venous arterial oxygen levels can be due to many conditions including high cardiac output, sepsis, left-to-right cardiac shunts, impaired peripheral uptake (e.g., cyanide), and decreased oxygen consumption (e.g., hypothermia), as well as sampling error. The other choices in this question all represent conditions whereby cardiac output is diminished and consequently would not be consistent with the data given in the question (Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 360–361).
421. Normal tracheal capillary pressure is A. 10 to 15 mm Hg B. 15 to 20 mm Hg C. 25 to 30 mm Hg D. 35 to 40 mm Hg
421. (C) Tracheal capillary arteriolar pressure (25-35 mm Hg) is important to keep in mind in patients who are intubated with cuffed endotracheal tubes. If the endotracheal tube cuff exerts a pressure greater than capillary arteriolar pressure, tissue ischemia may result. Persistent ischemia may lead to destruction of tracheal rings and tracheomalacia. Endotracheal tubes with low-pressure cuffs are recommended in patients who are to be intubated for periods longer than 48 hours because this will minimize the chances for development of tissue ischemia (Miller: Miller’s Anesthesia, ed 8, pp 1665–1667).
422. How many hours should elapse before performing a single-shot spinal anesthetic in a patient who is receiving 1 mg/kg enoxaparin (Lovenox) twice a day for the treatment of a deep vein thrombosis? A. 6 hours B. 12 hours C. 24 hours D. 48 hours
422. (C) Enoxaparin, dalteparin, and ardeparin are low-molecular-weight heparins (LMWHs). Because of the possibility of spinal and epidural hematoma in the anticoagulated patient with neuraxial blockade, caution is advised. The plasma half-life of LMWH is two to four times longer than standard heparin. These drugs are commonly used for prophylaxis for deep vein thrombosis. These drugs are also used at high doses for treatment of deep vein thrombosis and (off label) as “bridge therapy” for patients chronically anticoagulated with warfarin (Coumadin). In these patients who are being prepared for surgery, Coumadin is discontinued and LMWH started. With high-dose enoxaparin administration (1 mg/kg twice daily), it is recommended to wait at least 24 hours before administration of a single-shot spinal anesthetic (Miller: Miller’s Anesthesia, ed 8, p 1691; Barash: Clinical Anesthesia, ed 7, p 929; Third Consensus Conference on Neuraxial Anesthesia and Anticoagulation, Jan-Feb 2010; http://www.asra.com/publications-anticoagulation-3rd-edition-2010.php).
423. Which of the following peripheral nerves is MOST likely to become injured in patients who are under general anesthesia? A. Ulnar nerve B. Median nerve C. Radial nerve D. Common peroneal nerve
423. (A) The principal mechanism of peripheral nerve injury is ischemia caused by stretching or compression of the nerves. Anesthetized patients are at increased risk for peripheral nerve injuries because they are unconscious and unable to complain about uncomfortable positions that an awake patient would not tolerate and because of reduced muscle tone that facilitates placement of patients into awkward positions. The ulnar nerve in particular is vulnerable because it passes around the posterior aspect of the medial epicondyle of the humerus. The ulnar nerve may become compressed between the medial epicondyle and the sharp edge of the operating table, leading to ischemia and possible nerve injury, which may be transient or permanent (Miller: Basics of Anesthesia, ed 6, pp 310–312). 132 Part 2 Clinical Sciences
424. Which of the following is the most plausible explanation for the lack of analgesia with codeine administration? A. Lack of CYP2D6 enzyme B. VKORC1 polymorphism C. CYP3A4 polymorphism D. Lack of μ receptors
424. (A) The orally administered prodrug codeine (methylmorphine) must be metabolized to morphine in order to work. About 7% to 10% of white patients have an inactive variant of the enzyme CYP2D6, which is the enzyme needed to metabolize codeine. In these patients, as well as in patients who have the normal enzyme but the enzyme is inhibited (e.g., coadministration of quinidine), codeine does not produce analgesia but morphine will produce the expected analgesia. The CYP2D6 enzyme is also needed to metabolize oxycodone into oxymorphone and hydrocodone into hydromorphone. In addition, some patients have a polymorphism form of CYP2D6 that results in very rapid metabolism of codeine and can result in morphine toxicity (Miller: Miller’s Anesthesia, ed 8, pp 574–575).
425. A 62-year-old patient with a bare-metal stent in the mid portion of the left anterior descending artery is scheduled for rotator cuff repair under general anesthesia. The stent was placed 6 weeks before surgery and the patient is on dual therapy (aspirin and clopidogrel). Which of the paradigms below would be best for managing his anticoagulation before surgery? A. Continue both up to the day of surgery B. Stop both 7 to 10 days before surgery C. Stop aspirin and continue clopidogrel D. Stop clopidogrel and continue aspirin
425. (D) Patients who have undergone percutaneous coronary intervention (PCI) with and without stents require dual antiplatelet therapy (usually aspirin and clopidogrel) to prevent restenosis or acute thrombosis at the site of the stent, often for the patient’s lifetime. Cessation of these drugs should be reviewed with the patient’s cardiologist. In general, if the elective surgical procedure may involve bleeding, the elective procedure is delayed for at least 2 weeks after balloon angioplasty without a stent, 6 weeks after a baremetal stent, and 12 months after a drug-eluting stent has been placed. Then the clopidogrel is stopped and restarted as soon as possible after the surgery (aspirin is usually continued). In an emergency situation and when the patient is taking clopidogrel, platelet transfusion may be needed (effectiveness of platelets depends on the last dose of clopidogrel—platelets are effective after 4 hours but much better 24 hours after the last dose of clopidogrel) (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 13-–14; Miller: Basics of Anesthesia, ed 6, pp 168–170).
426. A patient with which of the following eye diseases would be at greatest risk for retinal damage from hypotension during surgery? A. Strabismus B. Open eye injury C. Glaucoma D. Severe myopia
426. (C) Blood flow to the retina can be decreased by either a decrease in mean arterial pressure or an increase in intraocular pressure. Decreased blood flow and stasis are more likely in patients with glaucoma because of their elevated intraocular pressure. During periods of prolonged hypotension, the incidence of retinal artery thrombosis increases in these patients (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 253-–254; Miller: Basics of Anesthesia, ed 6, p 487).
427. Naltrexone is A. A narcotic with local anesthetic properties B. An opioid agonist-antagonist similar to nalbuphine C. A pure opioid antagonist with a shorter duration of action than naloxone D. An opioid antagonist used for treatment of previously detoxified heroin addicts
427. (D) Naloxone (Narcan) is a competitive inhibitor at all opioid receptors but has the greatest affinity for μ receptors. Its duration of action is relatively short (elimination half-life of about 1 hour). For this reason, one must be vigilant for the possibility of renarcotization when reversing long-acting narcotics. Naltrexone (ReVia) is the N-cyclopropylmethyl derivative of oxymorphone with a long elimination half-life of 8 to 12 hours. It is currently available only as an oral preparation and is used to block the euphoric effects of injected heroin in addicts who have been previously detoxified. Nalmefene (Revex) is another opioid antagonist that can be administered orally or parenterally and has an extremely long duration of action (elimination terminal half-life of 8.5 hours) (Miller: Miller’s Anesthesia, ed 8, pp 906–907; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, p 290).
428. Which of the following mechanisms is most frequently responsible for hypoxia in the recovery room? A. Ventilation/perfusion mismatch B. Hypoventilation C. Hypoxic gas mixture D. Intracardiac shunt
428. (A) In the recovery room, the most common cause of postoperative hypoxemia is an uneven ventilation/ perfusion distribution caused by loss of lung volume resulting from small airway collapse and atelectasis. Risk factors for ventilation/perfusion mismatch in the postoperative period include old age, obstructive lung disease, obesity, increased intra-abdominal pressure, and immobility. Supplemental oxygen should be administered to keep the Pao2 in the 80 to 100 mm Hg range, which is associated with a 95% saturation of hemoglobin. Other measures can be taken to restore lung volume, which include recovering obese patients in the sitting position, coughing, and deep breathing (Barash: Clinical Anesthesia, ed 7, pp 1566–1567).
429. Hypoparathyroidism secondary to the inadvertent surgical resection of the parathyroid glands during total thyroidectomy typically results in symptoms of hypocalcemia how many hours postoperatively? A. 1 to 2 hours B. 3 to 12 hours C. 12 to 24 hours D. 24 to 72 hours
429. (D) Airway obstruction after total thyroidectomy may be caused by a postoperative hematoma, compression of the trachea, tracheomalacia, bilateral recurrent laryngeal nerve damage, or hypocalcemia resulting from inadvertent removal of the parathyroid glands. Although the airway symptoms of hypocalcemia can develop as early as 1 to 3 hours after surgery, they typically do not develop until 24 to 72 hours postoperatively. Because the laryngeal muscles are particularly sensitive to hypocalcemia, early symptoms may include inspiratory stridor, labored breathing, and eventual laryngospasm. Therapy consists of IV administration of calcium gluconate or calcium chloride (Miller: Basics of Anesthesia, ed 6, p 634; Barash: Clinical Anesthesiology, ed 7, p 1330).
430. Damage to which nerve may lead to wrist drop? A. Radial B. Axillary C. Median D. Ulnar
430. (A) Damage to the radial nerve is manifested by weakness in abduction of the thumb, inability to extend the metacarpophalangeal joints, wrist drop, and numbness in the webbed space between the thumb and General Anesthesia 133 index fingers. The radial nerve passes around the humerus between the middle and lower portions in the spiral groove posteriorly. As it wraps around the bone, the radial nerve can become compressed between it and the OR table, resulting in nerve injury (Barash: Clinical Anesthesia, ed 7, pp 808, 949).
431. The most common cause of bronchiectasis is A. Cigarette smoking B. Air pollution C. α1-Antitrypsin deficiency D. Recurrent bronchial infections
431. (D) Bronchiectasis is one of several obstructive lung diseases characterized by a diminished FEV1 when pulmonary function is evaluated. It is characterized by permanently dilated bronchi that frequently contain purulent secretions. The affected bronchi are often highly vascularized, giving rise to the possibility of hemoptysis. Collateral circulation through the intercostal and bronchial arteries is also possible in these patients. If these vessels connect with the pulmonary circulation, pulmonary hypertension and eventual cor pulmonale are possible sequelae. Any patient with chronic bronchial infections may develop bronchiectasis (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 195–196).
432. A 6-year-old child is transported to the recovery room after a tonsillectomy. The patient was anesthetized with isoflurane, fentanyl, and N2O. Twenty minutes before emergence and tracheal extubation, droperidol was administered. The anesthesiologist is called to the recovery room because the patient is “making strange eye movements.” The patient’s eyes are rolled back into his head, and his neck is twisted and rigid. The most appropriate drug for treatment of these symptoms is A. Dantrolene B. Diazepam C. Glycopyrrolate D. Diphenhydramine
432. (D) Drugs that block dopamine receptors may cause acute dystonic reactions in some patients. The incidence with droperidol is about 1%. Treatment is the administration of a drug that crosses the blood-brain barrier with anticholinergic properties such as diphenhydramine or benzatropine. Although glycopyrrolate is an anticholinergic drug, it would not be useful in this setting because it does not cross the blood-brain barrier (Miller: Miller’s Anesthesia, ed 8, p 2963; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 414).
433. A 32-year-old army officer is unable to oppose the left thumb and left little finger after an 8-hour exploratory laparotomy under general anesthesia. He had an IV induction through a peripheral IV and had a second IV placed in the antecubital fossa after he was asleep. Damage to which of the following nerves would MOST likely account for this deficit? A. Radial B. Ulnar C. Median D. Musculocutaneous
433. (C) The median nerve is most frequently injured at the antecubital fossa by extravasation of IV drugs that are toxic to neural tissue, or by direct injury caused by the needle during attempts to cannulate the medial cubital or basilic veins. The median nerve provides sensory innervation to the palmar surface of the lateral three and one-half fingers and adjacent palm, and motor function to the abductor pollicis brevis, flexor pollicis brevis, and opponens pollicis muscles (Miller: Basics of Anesthesia, ed 6, p 313).
434. Pheochromocytoma would be MOST likely to coexist with which of the following? A. Insulinoma B. Pituitary adenoma C. Primary hyperaldosteronism (Conn syndrome) D. Medullary carcinoma of the thyroid
434. (D) Pheochromocytoma is an endocrine tumor (with release of catecholamines) in which 90% of patients are hypertensive, 90% of the tumors originate in one adrenal medulla, and 90% of all pheochromocytomas are benign. This disease is rare (<0.1% of hypertension in adults), but when it occurs, it is often seen with a triad of diaphoresis, tachycardia, and headache in patients with hypertension. Other symptoms include palpitations, tremulousness, weight loss, hyperglycemia, hypovolemia, and in some cases dilated cardiomyopathy and CHF. Death as a result of pheochromocytoma is due to cardiac conditions (e.g., myocardial infarction, CHF) or an intracranial bleed. In about 5% of cases, pheochromocytomas show an autosomal dominant pattern and may coexist with other endocrine diseases such as medullary carcinoma of the thyroid and hyperparathyroidism. This combination is called multiple endocrine neoplasia (MEN) type II or IIA (Sipple syndrome). MEN type IIB consists of pheochromocytoma, medullary carcinoma of the thyroid, and neuromas of the oral mucosa. The von Hippel-Lindau disease consists of hemangiomas of the nervous system (i.e., retina or cerebellum), and 10% to 25% of these patients also have a pheochromocytoma. The average-sized pheochromocytoma contains 100 to 800 mg of norepinephrine (Barash: Clinical Anesthesia, ed 7, pp 1339–1340; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 392–395).
435. Which of the following oral antidiabetic drugs is unique in that it does NOT produce hypoglycemia when administered to a fasting patient? A. Glyburide (Micronase) B. Glipizide (Glucotrol) C. Tolbutamide (Orinase) D. Metformin (Glucophage)
435. (D) Oral agents that are used to help control hyperglycemia in type 2 diabetic patients (relative β-cell insufficiency and insulin resistance) include four major drug classes: 1. Drugs that stimulate insulin secretion (hypoglycemia is a risk) a. sulfonylureas i. first-generation (chlorpropamide, tolazamide, tolbutamide) ii. second-generation (glimepiride, glipizide, glyburide) b. meglitinides (repaglinide, nateglinide) 2. Drugs that decrease hepatic gluconeogenesis (hypoglycemia not a risk) a. biguanides (metformin) 3. Drugs that improve insulin sensitivity (hypoglycemia not a risk) a. thiazolidinediones (rosiglitazone, pioglitazone) b. glitazones 4. Drugs that delay carbohydrate absorption (hypoglycemia not a risk) a. α-glucosidase inhibitors (acarbose, miglitol) 134 Part 2 Clinical Sciences Only drugs that stimulate insulin secretion are a risk for producing hypoglycemia. Initial therapy is usually with second-generation sulfonylureas (more potent and fewer side effects than first-generation sulfonylureas) or with a biguanide (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 1255–1270; Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 376–380; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 481–485).
436. The onset of delirium tremens (DTs) after abstinence from alcohol usually occurs in A. 8 to 24 hours B. 24 to 48 hours C. 2 to 4 days D. 4 to 7 days
436. (C) Although early mild symptoms of alcohol withdrawal can be seen within 6 to 8 hours after a substantial drop in the serum alcohol levels, DTs, which is seen in about 5% of patients, is a life-threatening medical emergency that develops 2 to 4 days after the cessation of alcohol in alcoholics. Symptoms of DTs include hallucinations, combativeness, hyperthermia, tachycardia, hypertension or hypotension, and grand mal seizures. Treatment of severe alcohol withdrawal consists of fluid replacement, electrolyte replacement, and IV vitamin administration with particular attention paid to thiamine. Aggressive administration of benzodiazepines is indicated to prevent seizures (5-10 mg of diazepam every 5 minutes until the patient becomes sedated but not unconscious). β-Blockers are used to suppress overactivity of the sympathetic nervous system, and lidocaine may be effective in the treatment of cardiac dysrhythmias (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 544).
437. A 78-year-old retired coal miner with an intraluminal tracheal tumor is scheduled for tracheal resection. Which of the following is a relative contraindication for tracheal resection? A. Need for postoperative mechanical ventilation for underlying lung disease B. Tumor located at the carina C. Documented liver metastases D. Ischemic heart disease with a history of CHF
437. (A) Operations on the trachea may be indicated in patients who have tracheal tumors or patients who had a previous trauma to the trachea resulting in tracheal stenosis or tracheomalacia. Eighty percent of the operations on the trachea involve segmental resection with primary anastomosis, 10% involve resection with prosthetic reconstruction, and another 10% involve insertion of a T-tube stent. These operations frequently are very complicated and require constant communication between the surgeon and the anesthesiologist. Preoperative pulmonary function tests are indicated in all patients who are to undergo elective tracheal resection. Severe lung disease necessitating postoperative mechanical ventilation is a relative contraindication for tracheal resection because positive airway pressure may cause wound dehiscence (Miller: Miller’s Anesthesia, ed 8, pp 1987–1988).
438. A 78-year-old patient with multiple myeloma is admitted to the intensive care unit (ICU) for treatment of hypercalcemia. The primary risk associated with anesthetizing patients with hypercalcemia (levels of 14-16 mg/dL) is A. Coagulopathy B. Cardiac dysrhythmias C. Hypotension D. Laryngospasm 120 Part 2 Clinical Sciences
438. (B) Hypercalcemia is associated with a number of signs and symptoms, including hypertension, dysrhythmias, shortening of QT interval, kidney stones, seizure, nausea and vomiting, weakness, depression, personality changes, psychosis, and even coma. Generally, patients with total serum calcium levels of 12 mg/dL or less do not require any intervention, with the possible exception of rehydration with saline. Higher calcium levels may be associated with clinical symptoms and should be treated before anesthetizing the patient. Caution should be taken with digitalis administration to any patient who is hypercalcemic because some patients may exhibit extreme digitalis sensitivity (Miller: Miller’s Anesthesia, ed 8, p 1794; Barash: Clinical Anesthesia, ed 7, pp 354–355). NORMAL CALCIUM LEVELS Serum Calcium Serum Ionized Calcium Conventional units (mEq/L) 4.5-5.5 mEq/L 2.1-2.6 mEq/L Conventional units (mg/dL) 9.0-11.0 mg/dL 4.25-5.25 mg/dL SI units (mmol/L) 2.25-2.75 mmol/L 1.05-1.30 mmol/L
439. Just before induction of general anesthesia for an 85-year-old demented man with an ischemic bowel, he mentions to you that he forgot to take his greencapped eye drops. He states that not taking it daily will result in blindness. The green-capped eye drops are A. NaCl drops used to prevent his eye from drying out B. Antibiotic drops C. Steroids D. Used to produce miosis
439. (D) Red-top eye drops cause mydriasis and should be used with caution in patients with closed-angle glaucoma. Green-top eye drops cause miosis, and the pupillary constriction helps keep the drainage route open in patients with glaucoma and helps prevent an acute attack of glaucoma. Clear or white-top eye drops do not change pupillary size.
440. A normal, healthy 3-year-old child was involved in a motor vehicle accident. He is coming emergently to the OR. Drug doses need to be calculated, but his weight is not known. What value should be used to estimate the 3-year-old child’s weight? A. 8 kg B. 10 kg C. 12 kg D. 14 kg
440. (D) When reviewing growth curves, the normal 40-week term newborn weighs about 3.5 kg. Infants then double their birth weight by 5 months and triple their weight by 1 year. Therefore, the average 1-year-old weighs 10 kg (22 lb). From the age of 1 to 6 years, children gain about 2 kg per year. Thus, an average 2-year-old weighs 12 kg, 3-year-old weighs 14 kg, 4-year-old weighs 16 kg, 5-year-old weighs 18 kg, and 6-year-old weighs 20 kg. From age 6 to 10 years, children gain about 3 kg per year (Davis: Smith’s Anesthesia for Infants and Children, ed 8, pp A6-A13). General Anesthesia 135
441. A 62-year-old man undergoes an emergency craniotomy for subdural hematoma. Two years earlier, a VVI pacemaker was placed for third-degree heart block. The patient received vancomycin 1 g IV before arriving in the OR. General anesthesia is induced with propofol 160 mg IV and the lungs are hyperventilated to a Paco2 of 25 mm Hg by mask. Just before tracheal intubation, the patient’s heart rate decreases from 70 to 40 beats/min and the pacemaker spikes that were previously present in lead II of the electrocardiogram disappear. The MOST likely cause of bradycardia in this patient is A. Hypocarbia B. Vancomycin allergy C. A side effect of propofol D. Pacemaker battery failure
441. (A) Causes for acute pacemaker malfunction in the OR are numerous and include threshold changes, inhibition, generator failure, and lead or electrode dislodgement or breakage. A VVI pacemaker may be inhibited by myopotentials. In this regard, administration of succinylcholine could actually inhibit a VVI pacemaker. Similarly, electrocautery can inhibit a VVI pacemaker through electromagnetic interference. Should this occur (in most cases, depending on manufacturer), a magnet should be placed over the pacemaker to convert it into a VOO pacemaker, eliminating the possibility of further inhibition. Pacemakers should be evaluated preoperatively to eliminate the possibility of generator failure. Lead breakage or dislodgement is an unlikely cause of pacemaker failure unless the surgeon is working in the vicinity of the electrodes. Acute threshold changes are almost always associated with changes in the serum potassium concentration. In this particular patient, hyperventilation causes a respiratory alkalosis that results in the intracellular shifting of serum potassium. The net result is that the electrical threshold for the pacemaker is raised, preventing ventricular capture (Miller: Miller’s Anesthesia, ed 8, p 1476; Thomas: Manual of Cardiac Anesthesia, ed 2, pp 382–383).
442. A 28-year-old obese patient has diminished breath sounds bilaterally at the lung bases 18 hours after an emergency appendectomy under general anesthesia. Which of the following maneuvers would be LEAST effective in preventing postoperative pulmonary complications in this patient? A. Coughing B. Voluntary deep breathing C. Performing a forced vital capacity (FVC) D. Use of incentive spirometry
442. (C) Therapies aimed at increasing functional residual capacity (FRC) of the lungs are useful in reducing the incidence of postoperative pulmonary complications. Forced expiratory maneuvers may lead to airway closure, which would be of no benefit for this patient (Miller: Miller’s Anesthesia, ed 8, pp 447, 2932–2934).
443. Below what value of cerebral blood flow (CBF) will signs of cerebral ischemia first begin to appear on the electroencephalogram (EEG)? A. 6 mL/100 g/min B. 15 mL/100 g/min C. 22 mL/100 g/min D. 31 mL/100 g/min
443. (C) The human brain is able to maintain neuronal function in the face of decreasing CBF below the normal level of 50 mL/100 g/min. Because O2 delivery is directly related to CBF, EEG evidence of cerebral ischemia will appear if CBF is diminished sufficiently. The CBF reserve, however, is substantial, and the first signs of cerebral ischemia do not appear on EEG until CBF has fallen to approximately 22 mL/100 g/min. When CBF has fallen to 15 mL/100 g/min, the EEG becomes isoelectric. Irreversible membrane damage and cellular death do not occur, however, until CBF falls to 6 mL/100 g/min. Areas of the brain in which CBF falls in the 6 to 15 mL/100 g/min range are referred to as zones of ischemic penumbra. Several hours may elapse in these areas of the brain before irreversible membrane damage occurs (Miller: Miller’s Anesthesia, ed 8, p 410).
444. A 67-year-old patient is mechanically ventilated in the ICU 2 days after repair of a ruptured abdominal aortic aneurysm. To maintain Pao2 in the 60 to 65 range, 10 cm H2O positive end-expiratory pressure (PEEP) is added to the ventilator cycle. The patient’s blood pressure has averaged 110/65 before addition of PEEP. After addition of PEEP, the blood pressure is noted to slowly fall to an average of approximately 95/50. The best explanation for this decrease in blood pressure is A. Tension pneumothorax B. Decreased venous return to the heart C. Increased afterload on the right side of the heart D. Increased afterload on the left side of the heart
444. (B) Positive end-expiratory pressure (PEEP) is the maintenance of positive airway pressure during the entire ventilator cycle. The addition of PEEP to the ventilator cycle is often recommended when Pao2 is not maintained above 60 mm Hg, when breathing an Fio2 of 0.50 or greater. Although not completely understood, PEEP is thought to increase arterial oxygenation, pulmonary compliance, and FRC by expanding previously collapsed but perfused alveoli, thereby decreasing shunt and improving ventilation/ perfusion matching. An important adverse effect of PEEP is a decrease in arterial blood pressure caused by a decrease in venous return, left ventricular filling and stroke volume, and cardiac output. These effects are exaggerated in patients with decreased intravascular fluid volume. Other potential adverse effects of PEEP include pneumothorax, pneumomediastinum, and subcutaneous emphysema (Miller: Miller’s Anesthesia, ed 8, pp 3077–3078; Miller: Basics of Anesthesia, ed 6, p 667).
445. The mechanism of action of clopidogrel is A. Adenosine diphosphate (ADP) receptor blockade (P2Y12) B. Platelet glycoprotein IIB/IIIa antagonism C. Cyclooxygenase COX-1 and COX-2 inhibition D. Direct thrombin inhibition
445. (A) Platelets contain two purinergic receptors (P2Y1 and P2Y12). Clopidogrel (Plavix) is a prodrug and an irreversible inhibitor of platelet P2Y12 receptors, which blocks the ADP receptors and inhibits platelet activation, aggregation, and degranulation. There is wide interindividual variability for clopidogrel to inhibit ADP-induced platelet aggregation, and some patients are resistant to its effects. Glycoprotein IIb/IIIa inhibitors block fibrinogen binding to platelet glycoprotein IIb/IIIa receptors, which is the final common pathway of platelet aggregation and includes the intravenous drugs abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Aspirin, naproxen, and ibuprofen inhibit platelet COX-1 and inhibit the release of ADP by platelets and platelet aggregation. Selective COX-2 inhibitors such as celecoxib, parecoxib, and valdecoxib have no effect on platelet function because only COX-1 inhibitors affect platelet function. Direct thrombin inhibitors suppress platelet function and include the parenteral drugs hirudin, argatroban, lepirudin (Refludan), desirudin (Iprivask), bivalirudin (Angiomax), and drotrecogin α (Xigris), as well as the oral drug dabigatran (Pradaxa, Pradax) and ximelagatran (Brunton: Goodman & Gilman’s The Pharmacological Basis of Therapeutics, ed 12, pp 859-871; Miller: Basics of Anesthesia, ed 6, pp 358-359; Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, pp 277–281, 516–518). 136 Part 2 Clinical Sciences
446. Which of the following is most closely associated with minimum alveolar concentration (MAC)? A. Blood/gas partition coefficient B. Oil/gas partition coefficient C. Vapor pressure D. Brain/blood partition coefficient
446. (B) As a rough approximation, if one divides 150 by the MAC for any given volatile anesthetic, the quotient will be approximately equal to the oil/gas partition coefficient. For example, if one were to divide the MAC of halothane (0.75) into 150, the quotient would be 200, which is very close to the actual oil/gas partition coefficient for halothane (224). Similarly, if one were to divide the MAC of enflurane (1.68) into 150, the quotient would be 89, which is very similar to the oil/gas partition coefficient for enflurane (98). The fact that anesthetics with a high oil/gas partition coefficient (i.e., lipid-soluble agents) have lower MACs supports the Meyer-Overton theory (critical volume hypothesis) (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 29).
447. A 15-year-old, 65-kg patient with Cushing disease is to undergo a transsphenoidal hypophysectomy to remove a pituitary adenoma. General anesthesia is induced with propofol IV, and tracheal intubation is facilitated with vecuronium 0.20 mg/kg IV. Anesthesia is maintained with isoflurane, N2O, and O2. Mannitol 1 g/kg is administered IV to reduce intracranial pressure. At the end of the operation, the patient is extubated and taken to the ICU. Over the next 6 hours the patient has a total urine output of 8.3 L. Serum sodium concentration is 154 mEq/L, serum potassium concentration is 4.8 mEq/L, and serum glucose concentration is 160 mg/dL. Urine specific gravity is 1.002 and urine osmolality is 125 mOsm/L. The most likely cause of the large urine output is A. Osmotic diuresis from mannitol B. Excess mineralocorticoid activity C. Hyperglycemia D. Central diabetes insipidus
447. (D) Diabetes insipidus is characterized by hypernatremia, serum hyperosmolality, polyuria, and urine hypo-osmolality. Diabetes insipidus may occur after any intracranial procedure, but it is particularly common in surgery involving the pituitary gland. It may develop intraoperatively, but it commonly develops 4 to 12 hours postoperatively. Intravenous half-normal saline and dextrose 5% in water are started as replacement fluids. The pharmacologic treatment for diabetes insipidus is desmopressin acetate (synthetic 1-desamino-8-darginine vasopressin [DDAVP]) commonly started when the urine output is greater than 350 to 400 mL/ hr. In a conscious patient, it is not essential to administer DDAVP because the patient may increase his oral intake to compensate for polyuria. In the unconscious patient, however, administration of DDAVP is necessary. Desmopressin (DDAVP) may be administered SQ, IV, or intranasally. Fortunately, diabetes insipidus related to surgery and head trauma usually is transient (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, pp 404–405; Barash: Clinical Anesthesia, ed 7, p 1013).
448. Scopolamine should not be given as a premedication in patients with which of the following neurologic diseases? A. Parkinson disease B. Alzheimer disease C. Multiple sclerosis D. Narcolepsy General Anesthesia 121
448. (B) The principal feature of Alzheimer disease is progressive dementia. The onset typically occurs after age 60 years and may affect as many as 20% of patients older than age 80 years. In addition to age, other risk factors include history of serious head trauma (e.g., boxing), Down syndrome, and presence of the disease in a parent or sibling. One biochemical feature of this disease is a decrease in the enzyme choline acetyltransferase in the brain. There is a strong correlation between reduced enzyme activity and decreased cognitive function. Interestingly, administration of the anticholinergic drugs scopolamine or atropine (but not glycopyrrolate, which does not cross the blood-brain barrier) causes confusion similar to that seen in the early stages of Alzheimer disease. Conversely, administration of anticholinesterase drugs capable of penetrating the blood-brain barrier, such as donepezil (Aricept), galantamine, rivastigmine (Exelon), and tacrine are used to treat patients with Alzheimer disease. Physostigmine may have beneficial effects in some patients as well. Scopolamine is therefore a poor choice for premedication in patients with Alzheimer disease (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 6, p 245; Butterworth: Morgan & Mikhail’s Clinical Anesthesiology, ed 5, pp 619–620).
449. A 63-year-old man is scheduled to undergo a right hemicolectomy under general anesthesia. Anesthesia is induced with propofol 2 mg/kg IV and fentanyl 100 μg IV. Succinylcholine 1.5 mg/kg IV is administered to facilitate tracheal intubation. Anesthesia is maintained with isoflurane and N2O. After all four twitches of the train-of-four stimulus return to baseline values, vecuronium 10 mg IV is administered. Gentamicin 80 mg and cefazolin 1 g are administered IV as a prophylactic treatment. At the end of surgery, two of four thumb twitches can be elicited to trainof- four stimulation of the ulnar nerve, and neuromuscular blockade is antagonized with neostigmine 0.05 mg/kg IV and atropine 0.015 mg/kg IV. The patient, however, begins to move before the incision is completely closed, and succinylcholine 40 mg IV is given. Fifteen minutes later, all anesthetics are discontinued and the patient is ventilated with 100% O2, but the patient remains apneic. The most likely cause of apnea is A. Fentanyl B. Recurarization C. Succinylcholine D. Gentamicin
449. (C) At the end of any general anesthetic, spontaneous ventilation must be restored before the patient can be extubated. The differential diagnosis for persistent apnea includes muscle relaxants (inadequate reversal or pseudocholinesterase deficiency), volatile anesthetics, narcotics, hypocarbia, damage to the phrenic nerves bilaterally, and the possibility of a central nervous system (CNS) event. Succinylcholine is hydrolyzed by pseudocholinesterase to succinylmonocholine and choline. This is further hydrolyzed by plasma cholinesterase to succinic acid and choline. All of the anticholinesterase agents used to reverse nondepolarizing neuromuscular blockade also inhibit pseudocholinesterase. Administration of succinylcholine to any patient who has already received an anticholinesterase will result in a prolonged block from the succinylcholine because it can no longer be easily hydrolyzed. In this patient, therefore, succinylcholine would be by far the most likely cause of apnea at the end of the operation (Stoelting: Pharmacology and Physiology in Anesthetic Practice, ed 4, p 218).
450. A 53-year-old woman with endometrial cancer is undergoing an abdominal hysterectomy under general anesthesia with desflurane. During the first hour of anesthesia, urine output is 100 mL. Blood loss is minimal. When the patient is placed in the Trendelenburg position, the urine output declines to virtually zero. The most likely explanation for this sudden decrease in urine output in this patient is A. Pooling of urine in the dome of the bladder B. Increased central venous pressure C. Increased antidiuretic hormone (ADH) production from surgical stimulation D. Hypovolemia
450. (A) Complete or almost complete cessation of urine flow suggests a postrenal obstruction. However, at times pooling of the urine in the dome of the bladder should be considered as a possible cause of oliguria in this patient in the absence of significant bleeding (Miller: Miller’s Anesthesia, ed 8, pp 556–557).
451. Which of the following diseases is NOT associated with a decrease in Dlco? A. Emphysema B. Obesity C. Pulmonary emboli D. Anemia
451. (B) DL is defined as the diffusing capacity of the lung. When a nontoxic, low concentration of carbon monoxide is used for the measurement, it is called Dlco. The normal value of Dlco is 20 to 30 mL/min/mm Hg and is influenced by the volume of blood (hemoglobin) within the pulmonary circulation. Thus, diseases associated with a decrease in pulmonary blood volume (i.e., anemia, emphysema, hypovolemia, General Anesthesia 137 pulmonary hypertension) will be reflected by a decrease in the Dlco. Dlco is also decreased with oxygen toxicity as well as pulmonary edema. Conditions associated with an increased Dlco include the supine position, exercise, obesity, and left-to-right cardiac shunts (Barash: Clinical Anesthesia, ed 7, pp 369–370, 373–374; Miller: Miller’s Anesthesia, ed 8, p 365).
452. Each of the following postoperative complications of thyroid surgery can result in upper airway obstruction EXCEPT A. Cervical hematoma B. Tetany C. Bilateral superior laryngeal nerve injury D. Bilateral recurrent laryngeal nerve injury
452. (C) Patients undergoing thyroid surgery are at risk for airway obstruction from a number of causes. Postoperative hemorrhage sufficient to cause a large hematoma could compress the trachea and cause airway obstruction because of the close proximity of the thyroid gland to the trachea. Permanent hypoparathyroidism is a rare complication that may cause hypocalcemia leading to progressive stridor followed by laryngospasm. The most common nerve injury after thyroid surgery is damage to the abductor fibers of the recurrent laryngeal nerve. Unilaterally, this is manifested as hoarseness. Bilateral recurrent laryngeal nerve damage, however, may lead to airway obstruction during inspiration. Selective injury of the adductor fibers of the recurrent laryngeal nerve is a possible complication of thyroid surgery. This injury would leave the vocal cords open because the abductor fibers would be unopposed, placing the patient at great risk for aspiration. The superior laryngeal nerve has an extrinsic branch that innervates the cricothyroid muscle (which tenses the vocal cords) and an internal branch that provides sensory innervation to the pharynx above the vocal cords. Bilateral damage to this nerve would result in hoarseness and would predispose the patient to aspiration but would not lead to airway obstruction per se (Miller: Basics of Anesthesia, ed 6, p 469).
453. The MOST sensitive early sign of malignant hyperthermia (MH) during general anesthesia is A. Tachycardia B. Hypertension C. Fever D. Increased end-expiratory CO2 tension (Peco2)
453. (D) MH is a clinical syndrome that may develop rapidly or take hours to manifest, sometimes not occurring until the patient is in the recovery room. Clinical signs include hypertension, tachycardia, respiratory acidosis, metabolic acidosis, muscle rigidity, myoglobinuria, and fever. The diagnosis of MH is unlikely, however, if only one of these signs is manifested. Because MH is a metabolic disorder, one of the first sensitive signs is an increase in the production of CO2 and concomitant respiratory acidosis. This is the most reliable early sign of the syndrome (Barash: Clinical Anesthesia, ed 7, pp 612, 622–624).
454. A 78-year-old woman is anesthetized for a right hemicolectomy for 3 hours. At the end of the operation the patient’s blood pressure is 130/85 mm Hg, heart rate is 84 beats/min, core body temperature is 35.4° C, and Peco2 on infrared spectrometer is 38 mm Hg. Which of the following would be the LEAST plausible reason for prolonged apnea in this patient? A. Residual neuromuscular blockade B. Narcotic overdose C. Unrecognized obstructive pulmonary disease and high baseline Paco2 D. Persistent intraoperative hyperventilation
454. (D) Hyperventilation to Paco2 of 20 mm Hg or higher for more than 2 hours will result in active transport of HCO3 – out of the CNS. This results in spontaneous breathing at a lower (not higher) Paco2. The other choices should be included in the differential diagnosis of apnea (Hines: Stoelting’s Anesthesia and Co-Existing Disease, ed 5, pp 359–361; Miller: Basics of Anesthesia, ed 6, pp 62–64, 340; Barash: Clinical Anesthesia, ed 7, pp 271–273).
455. A 68-year-old woman with severe rheumatoid arthritis undergoes pulmonary function evaluation before an elective abdominal surgery. Forced expiratory volume in 1 second (FEV1) and FVC are within normal limits; however, the maximum voluntary ventilation (MVV) is only 40% of predicted. The next step in the pulmonary function evaluation of this patient should be to A. Obtain ABGs on room air B. Obtain a flow-volume loop C. Obtain a measurement of peak flow D. Obtain a ventilation/perfusion scan
455. (B) Maximum voluntary ventilation (MVV) is a nonspecific pulmonary function test that measures the endurance of the ventilatory muscles and indirectly reflects the compliance of the lung and thorax as well as airway resistance. A decreased MVV may be caused by impairment to inspiration or expiration. In this patient, FEV1 is normal, which strongly suggests that the ventilatory impairment is during inspiration. A flow-volume loop would be a very useful confirmatory test (Barash: Clinical Anesthesia, ed 7, pp 1033–1034).
456. Which of the following is NOT a component of the postanesthetic discharge scoring system (PADSS) used to evaluate the suitability of a patient to be discharged from an ambulatory surgical facility? A. Drinking B. Ambulation C. Absence of nausea and vomiting D. Pain control
456. (A) Guidelines for safe discharge of patients from ambulatory surgical centers include stable vital signs, ability to walk without dizziness, controlled pain, absence of nausea and vomiting, and minimal surgical bleeding. The PADSS is a tool for objectively assessing a patient’s readiness for discharge from the surgical center and includes these five criteria. Requirements to drink fluids and to void before home discharge are controversial and are not parameters included in the PADSS (Barash: Clinical Anesthesia, ed 7, pp 1560–1561).
457. During emergency repair of a mandibular jaw fracture in an otherwise healthy 19-year-old man, the patient’s temperature is noted to rise from 37° C on induction to 38° C after 2 hours of surgery. Which of the following informational items would be LEAST useful in ruling out MH in this patient? A. Normal heart rate and blood pressure B. History of negative caffeine-halothane contracture test carried out 6 months earlier C. History of an uncomplicated general anesthetic at age 16 years with halothane and succinylcholine D. Normal ABGs drawn when the patient’s temperature reached 38° C 122 Part 2 Clinical Sciences
457. (C) Malignant hyperthermia (MH) is a difficult diagnosis to make on clinical grounds alone. Signs of MH may be fulminant or very subtle. They may occur immediately after induction or may not be manifested until the patient has reached the recovery room or even later. MH is a disorder of metabolism and is associated with hypertension, tachycardia, dysrhythmias, respiratory acidosis, metabolic acidosis, muscular rigidity, rhabdomyolysis, and fever. Contrary to what one might believe based on the name of this disease, fever is typically a late finding. Other diseases that may mimic MH include alcohol withdrawal, acute cocaine toxicity, bacteremia, pheochromocytoma, hyperthyroidism, and neuroleptic malignant syndrome. An elevation in temperature alone with normal blood gases, heart rate, and blood