Inalatório

Question 1

1. According to written documentation, what were the first three drugs used to provide general anesthesia to patients undergoing painful surgical procedures?

Answer 1

1. The first three drugs in recorded history used to facilitate an anesthetic state for surgical procedures were nitrous oxide, diethyl ether, and chloroform. (83)

Question 2

2. Was the first public demonstration of anesthesia considered successful? What property of the anesthetic administered to the patient may have been responsible? How did this compare to the second public demonstration in the same institution with a different anesthetic?

Answer 2

2. The first public demonstration of anesthesia involved administration of nitrous oxide to a patient undergoing dental extraction at the Massachusetts General Hospital. Many attendees at the demonstration were skeptical because the patient vocalized and moved during the procedure. Because nitrous oxide is not potent, its delivered concentration is limited. The second demonstration of anesthesia, performed with diethyl ether, was considered successful because the patient was quiet and still (note that ether is roughly 100 times more potent than nitrous oxide). (84)

Question 3

3. Describe the advantages and disadvantages of each of the three first anesthetics.

Answer 3

3. Advantages of nitrous oxide were its lack of odor, nonflammability, and apparent absence of toxicity. Its principal disadvantage was its low potency. Advantages of diethyl ether were its potency, providing excellent conditions for surgery. Its disadvantages were flammability, unpleasant odor, and association with nausea and vomiting. Chloroform had the advantage of a more rapid induction, lack of flammability, and less risk of postoperative nausea. Its disadvantage was related to adverse outcome in many patients, including hepatotoxicity and death after surgery. (83-85)

Question 4

4. What were the principal disadvantages of anesthetics developed during the early 20th century?

Answer 4

4. Anesthetics developed and promoted during the first half of the 20th century had properties of pleasant odor and faster induction and emergence but had disadvantages of flammability (divinyl ether, ethylene, cyclopropane) and toxicity (chloroform, ethyl chloride, and trichloroethylene, all fully chlorinated). (85)

Question 5

5. Name the six modern potent inhaled anesthetics.

Answer 5

5. The six modern potent inhaled anesthetics, all introduced after 1950, are halothane, methoxyflurane, enflurane, isoflurane, sevoflurane, and desflurane. (85)

Question 6

6. What innovation in synthetic chemistry permitted development of modern inhaled anesthetics? How does the characteristic molecular structure of anesthetics synthesized in this manner confer clinical advantage?

Answer 6

6. Early inhaled anesthetics were halogenated strictly with chlorine. Modern inhaled anesthetics are partly or wholly halogenated with fluorine. Fluorination conferred the more favorable characteristics to the modern inhaled anesthetics of greater stability and lesser toxicity. (85)

Question 7

7. What are some advantages and disadvantages of halothane?

Answer 7

7. At the time it was introduced into clinical practice in 1956, halothane was advantageous because of its nonflammability, pleasant odor, and faster induction and emergence than previous anesthetics. Halothane’s disadvantages are its sensitization of the myocardium to the dysrhythmogenic effects of catecholamines and its potential to cause postoperative liver injury. (85)

Question 8

8. What are some disadvantages of methoxyflurane?

Answer 8

8. A major disadvantage of methoxyflurane is its dose-related nephrotoxicity due to an inorganic fluoride resulting from its metabolism. (86)

Question 9

9. What are some advantages and disadvantages of enflurane?

Answer 9

9. Enflurane, introduced into clinical practice in 1972, was advantageous over halothane in that it did not sensitize the myocardium to catecholamines, nor was it associated with hepatotoxicity. Its major disadvantage was that its metabolism could lead to EEG-confirmed seizure activity, especially when administered in high concentrations and in the presence of hypocapnia. (86)

Question 10

10. What are some advantages and disadvantages of isoflurane?

Answer 10

10. At the time of its introduction into clinical practice in 1980, isoflurane’s advantages included its lack of association with cardiac dysrhythmias, lack of organ toxicity, and rapid induction and emergence properties. There were no clear disadvantages of isoflurane at that time. (86)

Question 11

11. What are some advantages and disadvantages of sevoflurane and desflurane?

Answer 11

11. Sevoflurane and desflurane are both wholly halogenated with fluorine, which accounts for their low blood solubility and their rapid induction and emergence. Although expensive and hard to synthesize, the increase in outpatient anesthesia cases led to demand for their use. (86)

Question 12

12. What characterizes the anesthetic state?

Answer 12

12. No single, accepted definition is used to constitute the anesthetic state. Characteristics of the anesthetic state include immobility, amnesia, analgesia, and skeletal muscle relaxation. (86)

Question 13

13. Which characteristics of the anesthetic state are achieved by the administration of inhaled volatile anesthetics?

Answer 13

13. Characteristics of the anesthetic state that are achieved by inhaled volatile anesthetics include immobility, amnesia, and skeletal muscle relaxation. Analgesia is difficult to define in an amnestic, immobile patient, but surrogate measures of perception of painful stimuli (i.e., increases in heart rate or blood pressure at the time of incision or intubation) suggest that inhaled anesthetics do not possess analgesic characteristics at concentrations typically used in clinical practice. (87)

Question 14

14. Which characteristics of the anesthetic state are achieved by the administration of nitrous oxide?

Answer 14

14. Immobility is a characteristic of the anesthetic state that is achieved by nitrous oxide, but nitrous oxide is not reliable in doing so when administered alone. It has amnestic effects at higher concentrations (although these are difficult to assure) and, in contrast to potent inhaled anesthetics, does not contribute to skeletal muscle relaxation. (87)

Question 15

15. What is the mechanism of action of inhaled anesthetics in the central nervous system?

Answer 15

15. Inhaled anesthetics are thought to produce central nervous system depression by enhancing inhibitory ion channels and blocking excitatory ion channels. Anesthetics may also affect the release of neurotransmitters. (87)

Question 16

16. Why are vaporizers required for the inhaled administration of volatile anesthetics?

Answer 16

16. Volatile anesthetics exist as liquids at room temperature and at atmospheric pressure. The inhaled delivery of these anesthetics requires that the anesthetics be vaporized. Vaporizers allow not only the vaporization of liquid anesthetics, but they also reliably and accurately deliver the specified concentration of anesthetic to the common gas outlet and ultimately to the patient. Nitrous oxide exists as a gas at room temperature and therefore does not require a vaporizer for inhaled delivery to a patient. (87)

Question 17

17. Describe how a vaporizer for volatile anesthetics works.

Answer 17

17. Conventional volatile anesthetic vaporizers are classified as agent-specific, variable-bypass, flow-over, temperature-compensated, and out-of-circuit. Vaporizers are agent-specific, designed and calibrated for a specific gas. The vapor pressure of the anesthetic gas, a physical property that is unique to each anesthetic, determines the quantity of anesthetic in the gas phase. The concentration of anesthetic vaporizer output is controlled by the clinician adjusting the dial on the vaporizer. Fresh gases pass through the flowmeters, mix in the common manifold, and then enter the vaporizers. Once in the vaporizer there are two different streams of flow that the gases can take. The gases may be diverted to the bypass chamber, or they may enter the vaporizing (sump) chamber where it comes into contact with a reservoir of liquid anesthetic. The bypass valve adjusts the amount of gas that enters each of the two chambers, and the concentration of anesthetic is determined by the splitting ratio of the flow stream as controlled by the clinician. The vaporizer compensates for temperature, such that when the temperature of the vapor is warm, more gas is directed to the vaporizer outlet via the bypass chamber than when the temperature is relatively cooler. The opposite occurs when the temperature is relatively cooler. That is, more of the gas is directed toward the vaporizing chamber. This allows the vaporizer to compensate for changes in temperature, so the desired concentration of volatile anesthetic is maintained. Typically, about 20% of the gas flows through the vaporizing chamber. A higher dialed concentration will result in more gas going to the vaporizing chamber than otherwise. In the vaporizing chamber, the gas passes over a series of wicks saturated with liquid anesthetic, becomes saturated, and then mixes with unsaturated gas before being delivered at the set concentration. (87)

Question 18

18. What is the potential effect of tilting or overfilling a vaporizer?

Answer 18

18. The potential effect of tilting or overfilling a vaporizer is the delivery of an overdose of anesthetic. (87)

Question 19

19. What are the characteristics of desflurane that preclude its delivery in the conventional variable-bypass vaporizer?

Answer 19

19. The volatility of desflurane precludes its delivery in a conventional variable-bypass vaporizer. At 20° C, the vapor pressure of desflurane is 700 mm Hg (near boiling state at room temperature), whereas those of isoflurane and sevoflurane are 238 mm Hg and 157 mm Hg, respectively. Because of its volatility, unpredictable and possibly dangerously high concentrations of desflurane would be delivered if a conventional vaporizer were used. The Tec 6 heated vaporizer is specifically designed for desflurane; it heats the desflurane gas to 2 atm pressure to accurately deliver the desired concentration. (88)

Question 20

20. What considerations must be taken into account when administering inhaled anesthetics at high altitude?

Answer 20

20. No adjustment needs to be made for variable-bypass vaporizers when administering sevoflurane or isoflurane at high altitude, but an adjustment is needed when administering desflurane. Although vaporizer output is expressed in volume percent, the clinically relevant measure is anesthetic partial pressure. At high altitude, the decreased ambient pressure results in a lower anesthetic partial pressure despite the same volume percent output, so adjustments are necessary. (88)

Question 21

21. How should the dialed concentration of desflurane be adjusted by the clinician when administering desflurane at high altitude?

Answer 21

21. When administering desflurane at high altitude, the clinician must adjust the vaporizer setting using the following equation: required anesthetic setting = (desired anesthetic setting at sea level in mm Hg) / (local barometric pressure in mm Hg). (88)

Question 22

22. What are the advantages of using low fresh gas flow rates when administering inhaled anesthetics?

Answer 22

22. Use of low fresh gas flow rates (0.5 to 1 L/min) minimizes waste of anesthetic into the environment, decreases cost, and helps conserve body temperature. (88)

Question 23

23. What are nonrebreathing fresh gas flow rates? What are advantages and disadvantages of administering inhaled anesthetics at this rate?

Answer 23

23. Nonrebreathing fresh gas flow rates meet or exceed the patient’s minute ventilation. They allow rapid titration of anesthetic levels but result in greater loss of anesthetic to the environment. (88)

Question 24

24. How do inhaled anesthetics affect the environment?

Answer 24

24. Inhaled anesthetics are greenhouse gases that contribute to climate change by trapping heat in the atmosphere. Most of the anesthetic is vented to the environment, so minimizing fresh gas flow during maintenance reduces environmental impact. (88)

Question 25

25. What characteristics of any given inhaled anesthetic determine its potential environmental impact?

Answer 25

25. The potential environmental impact is determined by both the atmospheric lifetime of the anesthetic and its unique infrared absorption spectrum. (88)

Question 26

26. Which inhaled anesthetic has the most atmospheric longevity?

Answer 26

26. Nitrous oxide has the most atmospheric longevity, with an estimated lifetime of 114 years. (88)

Question 27

27. Which volatile anesthetic has the greatest carbon dioxide equivalent impact on the environment? Which volatile anesthetic has the lowest?

Answer 27

27. Desflurane has the greatest carbon dioxide equivalent impact, while sevoflurane has the lowest. (88)

Question 28

28. What are two potentially toxic compounds that can be produced as a result of the degradation or metabolism of volatile anesthetics?

Answer 28

28. Two potentially toxic compounds produced are compound A and carbon monoxide. (88)

Question 29

29. What is a potentially toxic compound that can be produced as a result of the interaction between sevoflurane and the carbon dioxide absorbent? What factors may increase this risk?

Answer 29

29. Compound A can be produced as a result of the interaction (alkaline degradation) between sevoflurane and the carbon dioxide absorbent (soda lime or Baralyme), with higher risk associated with low fresh gas flows, high sevoflurane concentrations, and higher absorbent temperatures. (88)

Question 30

30. What is the potential risk of human exposure to compound A? How can this risk be minimized?

Answer 30

30. Exposure to compound A is of concern for nephrotoxicity. Although transient renal effects (proteinuria, enzymuria, glycosuria) have been observed with prolonged low-flow sevoflurane administration, no permanent injury has been demonstrated. To minimize risk, manufacturer recommendations advise restricting sevoflurane administration at fresh gas flows below 2 L/min to no more than 2 MAC-hours. (88)

Question 31

31. What is a potentially toxic compound that can be produced as a result of the interaction between desflurane and the carbon dioxide absorbent? What factors may increase this risk?

Answer 31

31. Carbon monoxide can be produced, with higher production associated with the use of Baralyme, higher anesthetic concentrations, increased temperature, and desiccation of the absorbent. (88)

Question 32

32. What is the potential risk of carbon monoxide production from the carbon dioxide absorbent?

Answer 32

32. The risk is undiagnosed carbon monoxide poisoning, as its toxicity may be masked by anesthesia and normal pulse oximetry readings. (88)

Question 33

33. What is the potential risk resulting from the temperature increase in the carbon dioxide absorbent canister? How can this risk be minimized?

Answer 33

33. The exothermic reaction can lead to dangerous temperature rises, potentially causing explosion or fire. This risk is minimized by preventing absorbent desiccation through regular changes, reducing fresh gas flows when the machine is idle, and monitoring absorbent condition. (88)

Question 34

34. How are relative inhaled anesthetic potencies compared?

Answer 34

34. Relative potency is compared by the minimum alveolar concentration (MAC) required to suppress movement in 50% of patients in response to surgical incision. (89)

Question 35

35. What are minimum alveolar concentration (MAC) values for isoflurane, sevoflurane, desflurane, and nitrous oxide in a person whose age is between 30 to 55 years?

Answer 35

35. In persons aged 30 to 55 years, MAC values are approximately: isoflurane 1.15%, sevoflurane 1.85%, desflurane 6%, and nitrous oxide 104%. (89)

Question 36

36. What concentration of anesthetic is sufficient to provide amnesia in volunteers? How does this value relate to surgical patients?

Answer 36

36. The expired concentration preventing recall in 50% of volunteers was 0.20 MAC and 0.40 MAC for 95% prevention. However, caution is needed in extrapolating these values to surgical patients due to differences in painful stimulation and individual variability. (89)

Question 37

37. What factors increase MAC?

Answer 37

37. Factors that increase MAC include younger age (peaking at 6 months), acute amphetamine use, cocaine, ephedrine, hyperthermia, hypernatremia, and red hair color. (89)

Question 38

38. What factors decrease MAC?

Answer 38

38. Factors that decrease MAC include older age, hyponatremia, anemia, hypothermia, hypoxia, pregnancy, acute alcohol ingestion, chronic amphetamine use, and the administration of various drugs (propofol, etomidate, barbiturates, ketamine, opioids, local anesthetics, benzodiazepines, α2-agonists, lithium, verapamil). (89)

Question 39

39. Describe the process by which induction of anesthesia is achieved by an inhaled anesthetic.

Answer 39

39. Induction is achieved by delivering inhaled anesthetic from the alveoli to the brain via the arterial blood. A high inspired partial pressure creates a gradient that, along with high fresh gas flow, allows the alveolar and ultimately brain partial pressures to rise until equilibrium is reached. (89)

Question 40

40. What six factors determine the alveolar partial pressure of anesthetic?

Answer 40

40. The alveolar partial pressure is determined by the inspired partial pressure, alveolar ventilation, the volume of the breathing circuit, fresh gas flow, anesthetic solubility in blood/tissues, cardiac output, and the alveolar-to-venous partial pressure difference. (90)

Question 41

41. Describe a strategy that allows maintenance of stable anesthetic partial pressure in the brain after the induction of anesthesia.

Answer 41

41. Once equilibration is reached, decreasing the dialed concentration of anesthetic (by reducing vaporizer setting and/or fresh gas flow) helps maintain a stable brain partial pressure as tissue uptake diminishes. (90)

Question 42

42. What is the concentration effect?

Answer 42

42. The concentration effect is the phenomenon by which a higher inspired anesthetic partial pressure overcomes blood uptake, thereby accelerating the rise in alveolar (and brain) partial pressure during induction. (90)

Question 43

43. What is the “second gas effect”?

Answer 43

43. The second gas effect describes how the rapid uptake of a high-volume “first” gas (typically nitrous oxide) concentrates a companion gas (oxygen or potent volatile anesthetic) in the alveoli, potentially enhancing its uptake. (90)

Question 44

44. How might hyperventilation lead to inhaled anesthetic overdose?

Answer 44

44. Hyperventilation increases anesthetic input into the alveoli while decreasing uptake (via reduced cardiac output), potentially leading to an excessive rise in brain anesthetic concentration and myocardial depression. (90)

Question 45

45. What are some characteristics of the anesthetic breathing system that influence the rate of increase of the alveolar partial pressure of anesthetic?

Answer 45

45. Factors include the volume of the breathing system, the solubility of the anesthetic in the circuit’s materials, and the gas inflow rate; high fresh gas flows can overcome the buffering effect of circuit components. (91)

Question 46

46. How is anesthetic solubility expressed?

Answer 46

46. Anesthetic solubility is expressed as a partition coefficient (e.g., blood-gas partition coefficient), indicating the ratio of anesthetic concentration between two phases at equilibrium. (91)

Question 47

47. How does anesthetic solubility in blood influence speed of induction?

Answer 47

47. Higher solubility in blood means more anesthetic must be dissolved before equilibrium is reached, slowing induction. (91)

Question 48

48. What is the clinical relevance of the tissue-blood partition coefficient?

Answer 48

48. It determines the time to equilibration between tissue (e.g., brain) and blood; lower tissue-blood solubility leads to faster equilibration and quicker induction. (91)

Question 49

49. What is the clinical relevance of anesthetic transfer by intertissue diffusion?

Answer 49

49. Direct transfer of anesthetic from lean to adipose tissue can affect the overall uptake and distribution, especially in larger patients. (92)

Question 50

50. How does nitrous oxide affect the enzyme methionine synthase? How might this relationship affect patients receiving nitrous oxide?

Answer 50

50. Nitrous oxide inactivates methionine synthase, which can disrupt vitamin B12 and folate metabolism and may lead to neurologic or hematologic sequelae in susceptible patients. (92)

Question 51

51. How does nitrous oxide affect closed air-filled spaces in the body? What is the clinical relevance of this?

Answer 51

51. Nitrous oxide diffuses into closed air-filled spaces faster than nitrogen diffuses out, leading to expansion and/or increased pressure in these spaces, which can be dangerous in conditions like pneumothorax or middle ear surgery. (92)

Question 52

52. How does cardiac output affect the rate of induction of an inhaled anesthetic?

Answer 52

52. Higher cardiac output increases anesthetic uptake from the alveoli, slowing the rise in alveolar partial pressure and delaying induction; lower cardiac output speeds induction. (92)

Question 53

53. How does a shunt affect the rate of induction of an inhaled anesthetic?

Answer 53

53. A right-to-left shunt dilutes the anesthetic concentration by mixing shunted (anesthetic-free) blood with ventilated blood, slowing induction. (92)

Question 54

54. How does wasted ventilation affect the rate of induction of an inhaled anesthetic?

Answer 54

54. Wasted ventilation (ventilation of nonperfused alveoli) does not dilute blood anesthetic partial pressure and therefore does not affect induction rate. (93)

Question 55

55. What does the alveolar-to-venous anesthetic partial pressure difference reflect?

Answer 55

55. It reflects the uptake of anesthetic by tissues; as tissues equilibrate with the alveoli, the difference narrows. (93)

Question 56

56. What are some differences between the induction of inhaled anesthesia and recovery from anesthesia?

Answer 56

56. Recovery is slower due to the absence of a concentration effect, the existence of anesthetic reservoirs in tissues, and minimal metabolism of modern anesthetics, leading to a gradual decline in brain anesthetic concentration. (93-94)

Question 57

57. How are volatile anesthetics metabolized?

Answer 57

57. All volatile anesthetics undergo some degree of hepatic metabolism, with halothane, isoflurane, and desflurane being metabolized to trifluoroacetate and sevoflurane to hexafluoroisopropanol. (94)

Question 58

58. What factors influence the context-sensitive half-time of inhaled anesthetics?

Answer 58

58. Factors include the size and perfusion of tissue reservoirs (blood, vessel-rich tissues, muscle, fat) and the anesthetic’s solubility in these tissues. (94)

Question 59

59. What is the clinical impact of vessel-poor tissue reservoirs of inhaled anesthetic on recovery?

Answer 59

59. They have a longer context-sensitive half-time, meaning residual anesthetic may delay recovery of functions such as swallowing and ventilatory drive. (94)

Question 60

60. What is diffusion hypoxia?

Answer 60

60. Diffusion hypoxia occurs at the end of a nitrous oxide anesthetic when rapid diffusion of nitrous oxide from the blood into the alveoli dilutes alveolar oxygen; this is prevented by administering 100% oxygen. (95)

Question 61

61. Why might an individual patient’s responses vary in the circulatory effects of equipotent doses of a given inhaled volatile anesthetic?

Answer 61

61. Variability may be due to differences in age, surgical stimulation, comorbidities (e.g., myocardial dysfunction, valve lesions), intravascular volume status, and concurrent drug administration. (95)

Question 62

62. How do inhaled volatile anesthetics affect arterial blood pressure? What is the mechanism by which this effect occurs?

Answer 62

62. Inhaled volatile anesthetics produce a dose-dependent decrease in mean arterial pressure. Halothane decreases blood pressure mainly by reducing myocardial contractility and cardiac output, whereas isoflurane, desflurane, and sevoflurane primarily cause peripheral vasodilation and decreased systemic vascular resistance. (95)

Question 63

63. How does the substitution of nitrous oxide for an equipotent portion of volatile anesthetic affect arterial blood pressure at a given anesthetic dose?

Answer 63

63. Substituting nitrous oxide for part of the volatile anesthetic results in a smaller decrease in arterial blood pressure because nitrous oxide has minimal effect on blood pressure. (95)

Question 64

64. How do inhaled volatile anesthetics affect heart rate? What is the mechanism by which this occurs?

Answer 64

64. Halothane has minimal effect on heart rate, whereas isoflurane, sevoflurane, and desflurane tend to increase heart rate, often as a reflex response to decreased blood pressure; desflurane may directly stimulate the sympathetic system at higher concentrations. (96)

Question 65

65. How do inhaled volatile anesthetics affect the cardiac index?

Answer 65

65. Halothane produces a dose-dependent decrease in cardiac index, while isoflurane, sevoflurane, and desflurane minimally affect cardiac index over a range of concentrations in healthy adults. (96-97)

Question 66

66. How does the rapid concentration increase of volatile anesthetics affect hemodynamics?

Answer 66

66. A rapid increase, especially with desflurane above 1 MAC, can cause marked increases in heart rate and blood pressure due to sympathetic stimulation; this effect is attenuated by concomitant use of opioids or β-blockers and adaptation over time. (97)

Question 67

67. How do inhaled volatile anesthetics affect myocardial rhythm?

Answer 67

67. Only halothane significantly affects myocardial rhythm, potentially causing junctional rhythms and sensitizing the heart to ventricular extrasystoles, particularly in the presence of catecholamines and hypercarbia. (97)

Question 68

68. How do inhaled volatile anesthetics affect the QT interval?

Answer 68

68. Inhaled volatile anesthetics, particularly halothane and sevoflurane, prolong the QT interval; however, the clinical significance is uncertain, though sevoflurane is generally avoided in patients with congenital long QT syndrome. (98)

Question 69

69. How do inhaled volatile anesthetics affect coronary artery blood flow? What is coronary artery steal syndrome? What is its clinical relevance?

Answer 69

69. Isoflurane has been shown to dilate small coronary arterioles; theoretically, this could divert blood away from stenotic vessels (coronary steal), but in practice, isoflurane, sevoflurane, and desflurane appear to have cardioprotective effects. (98)

Question 70

70. What is ischemic preconditioning? How does this apply to volatile anesthetics and myocardial protection?

Answer 70

70. Ischemic preconditioning is a phenomenon where brief episodes of ischemia protect the myocardium from subsequent prolonged ischemic injury. Volatile anesthetics appear to mimic this protective effect (anesthetic preconditioning) via similar mechanisms (e.g., KATP channel activation). (99)

Question 71

71. How is the rate of breathing affected by inhaled volatile anesthetics?

Answer 71

71. Inhaled volatile anesthetics cause a dose-dependent increase in the rate of breathing. (99)

Question 72

72. How is the tidal volume affected by inhaled volatile anesthetics?

Answer 72

72. Inhaled volatile anesthetics decrease tidal volume, leading to increased dead space ventilation. (99)

Question 73

73. How is the minute ventilation and overall pattern of ventilation affected by inhaled volatile anesthetics?

Answer 73

73. Inhaled anesthetics increase respiratory rate while decreasing tidal volume, resulting in a regular, rapid, shallow breathing pattern and an overall decrease in minute ventilation, which is reflected by an increased resting PaCO2. (99)

Question 74

74. How is the ventilatory drive affected by inhaled volatile anesthetics?

Answer 74

74. Inhaled anesthetics depress the ventilatory drive in a dose-dependent manner by directly depressing the medullary centers and impairing chest wall mechanics, leading to a blunted CO2 response. (99)

Question 75

75. How does the addition of nitrous oxide to a volatile anesthetic affect the ventilatory drive and the resultant PaCO2?

Answer 75

75. The addition of nitrous oxide does not significantly change PaCO2 compared to volatile anesthetic alone, resulting in less increase in PaCO2 than when a volatile agent is used by itself. (99-100)

Question 76

76. How do inhaled volatile anesthetics affect hypoxic pulmonary vasoconstriction?

Answer 76

76. Inhaled volatile anesthetics have minimal inhibitory effect on hypoxic pulmonary vasoconstriction. (100)

Question 77

77. How do inhaled volatile anesthetics affect bronchial tone?

Answer 77

77. All potent inhaled anesthetics promote bronchodilation and attenuate bronchospasm, partly by reducing vagal activity and directly relaxing bronchial smooth muscle. (100)

Question 78

78. How do inhaled anesthetics differ in their capacity to cause airway irritation? How do these differences affect their use in various clinical situations?

Answer 78

78. Sevoflurane, halothane, and nitrous oxide are nonpungent and cause minimal airway irritation, making them suitable for inhalational induction, whereas isoflurane and desflurane are pungent and more likely to irritate the airway, limiting their use for induction without adjuncts. (100)

Question 79

79. How does nitrous oxide affect cerebral blood flow and intracranial pressure?

Answer 79

79. Nitrous oxide increases cerebral blood flow through vasodilation; its effect is blunted by intravenous anesthetics and is minimized by limiting its inspired concentration to less than 0.7 MAC. (100)

Question 80

80. How do inhaled volatile anesthetics affect cerebral blood flow and intracranial pressure?

Answer 80

80. Potent inhaled anesthetics at concentrations above 0.6 MAC increase cerebral blood flow via vasodilation and raise intracranial pressure; however, they do not abolish the cerebrovascular responsiveness to CO2. (100)

Question 81

81. How do inhaled volatile anesthetics affect cerebral metabolic oxygen requirements?

Answer 81

81. Inhaled volatile anesthetics decrease the cerebral metabolic oxygen requirement while simultaneously increasing cerebral blood flow, effectively uncoupling metabolism from flow at higher concentrations. (100)

Question 82

82. How do inhaled volatile anesthetics affect intracranial pressure?

Answer 82

82. Intracranial pressure increases with all volatile anesthetics when concentrations exceed 1 MAC. (100)

Question 83

83. How do inhaled volatile anesthetics affect cerebral autoregulation?

Answer 83

83. Cerebral autoregulation is impaired by all inhaled volatile anesthetics at concentrations below 1 MAC, reducing the brain’s ability to maintain constant blood flow over a range of systemic pressures. (100-101)

Question 84

84. How do inhaled volatile anesthetics affect evoked potentials?

Answer 84

84. Both volatile anesthetics and nitrous oxide depress the amplitude and increase the latency of somatosensory evoked potentials in a dose-dependent manner, with motor evoked potentials becoming unreliable at low concentrations. (101)

Question 85

85. What electroencephalographic (EEG) changes occur with increasing concentration of inhaled volatile anesthetics?

Answer 85

85. Increasing anesthetic depth with volatile agents is characterized by increased EEG amplitude and synchrony, progressing to burst suppression at higher concentrations (approximately 1.5 to 2.0 MAC). (101)

Question 86

86. How do inhaled volatile anesthetics affect neuromuscular function?

Answer 86

86. They produce mild, dose-related skeletal muscle relaxation and potentiate the effects of neuromuscular blocking drugs, delaying recovery of neuromuscular function postoperatively. (101)

Question 87

87. Which inhaled anesthetics have the potential to trigger malignant hyperthermia?

Answer 87

87. All volatile anesthetics can trigger malignant hyperthermia in susceptible individuals, with halothane having a higher reported risk compared to isoflurane, sevoflurane, or desflurane; nitrous oxide is not a trigger. (101)

Question 88

88. How do inhaled volatile anesthetics affect the liver?

Answer 88

88. All volatile anesthetics have the potential to cause severe hepatic injury (fulminant hepatic failure) via an immunologic mechanism involving trifluoroacetate formation, with halothane being most notable. (101)

Question 89

89. How do inhaled volatile anesthetics affect the kidneys?

Answer 89

89. Methoxyflurane’s extensive metabolism produces high plasma fluoride levels leading to renal toxicity, while other agents have minimal renal effects; however, historical concerns about fluoride-induced renal injury have not been substantiated for modern agents like sevoflurane. (102)