Stoelting Study 3

Front 1

2. In general, how similar are the properties and clinical effects of the two newer volatile anesthetic agents desflurane and sevoflurane when compared with the properties of the older volatile anesthetic agents isoflurane and halothane?

Back 1

2. The two newer volatile anesthetic agents, desflurane and sevoflurane, have lower blood and tissue solubilities than the older volatile anesthetic agents isoflurane and halothane. This property of desflurane and sevoflurane allows for greater control with its administration and potentially less time to recovery from anesthesia with its discontinuation. Other properties of these two agents, inc1uding their effects on circulation and ventilation, closely resemble the effects of the older volatile anesthetic agents

Front 2

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

Back 2

3. The volatile anesthetics all produce a dose-dependent decrease in mean arterial blood pressure, although the mechanism by which they exert their effects varies. Halothane primarily acts to decrease blood pressure by decreasing myocardial contractility and cardiac output. Isofiurane, desfiurane, and sevofiurane primarily act to decrease blood pressure through their effects of peripheral vasodilation and an associated decrease in systemic vascular resistanc~. Nitrous oxide, when administered alone, does not alter blood pressure.

Front 3

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

Back 3

4. Nitrous oxide, when administered alone, does not alter blood pressure. The substitution of nitrous oxide for an equipotent dose of a volatile anesthetic therefore results in less of a decrease in arterial blood pressure than would have otherwIse occurred if the volatile anesbetic were administered alone. This is in part the basis for the administration of nitrous oxide in combination with a volatile anesthetic. The combination of nitrous oxide with a volatile anesthetic allows for an increase in the minimum alveolar concentration (MAC) of anesthesia delivered without the cardiovascular effects of the volatile anesthetic administered alone at the same MAC.

Front 4

5. What are the cardiovascular effects of surgical stimulation? How do volatile anestheI tics modify this response?

Back 4

5. Surgid. stimulation results in sympathetic nervous system stimulation. This may manifest as an increase in heart rate and blood pressure, even while under general anesthesia. Volatile anesthetics attenuate the sympathetic nervous system response m a dose-dependent manner. For example, 1.47 MAC halothane prevents the rise in blood pressure and heart rate in response to surgical incision in 50% of patients. Conversely, the sympathetic nervous system stimulation associated with surgical stimulation may attenuate the decrease in arterial blood pressure that is associated with a given dose of volatile anesthetic

Front 5

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

Back 5

6. The effect of the inhaled anesthetics on heart rate varies, but in general increases in heart rate are seen with the administration of all the volatile anesthetic agents except halothane. The administration of halothane does not result in any change in heart rate. The heart rate is unchanged by the administration of desflurane at doses up to 1 MAC. When higher levels of desflurane concentrations are achieved, desfiurane increases heart rate in a dose-dependent manner. The administration of isofturane increases heart rate, especially at doses less than 1 MAC. This effect of isoflurane on heart rate is more likely to occur in young :~~tsl·:::r:C~l~~:l~~U:::ts~n s!~::::elSin~:::S:~~: ~~~:~::~~~! administered at doses greater than 1.5 MAC. Heart rate is unchanged or minimally increased with the administration of nitrous oxide. The increase in heart rate that accompanies the administration of desfiurane, isofiurane, and sevoflurane is thought to be mediated reflexively by the carotid sinus baroreceptors when decreases in arterial bOOd pressure are sensed. This reflex remains intact when these agents induce a decrease in blood pressure with their administration, although the resultant increase in heart rate varies. Halothane, however, inhibits the baroreceptor reflex response. The administration of halothane and the associated decrease in blood pressure are therefore not accompanied by an increase in heart rate.

Front 6

7. How can the effect of inhaled anesthetics on heart rate during the induction of anesthesia be attenuated?

Back 6

7. Opioids are useful in the attenuation of the volatile anesthetic-induced changes in heart rate during the induction of anesthesia.

Front 7

8. How do inhaled anesthetics affect cardiac output?

Back 7

8. Halothane produces a dose-dependent decrease in cardiac output that parallels the decrease in blood pressure that is seen with the administration of these agents. It is believed that the reason for the decrease in cardiac output that is associated with halothane is the lack of a compensatory increase in heart rate. Neither desfiurane, isofiurane, nor sevoflurane produces a dose-dependent decrease in cardiac output. This may be due in part to the increase in heart rate that accompanies the decrease in blood pressure when these agents are administered. Nitrous oxide is associated with a mild increase in cardiac output, possibly reflecting weak: sympathomimetic effects of this drug.

Front 8

9. How is the cardiac stroke volume calculated? How do inhaled anesthetics affect the calculated cardiac stroke volume? What is the mechanism by which this occurs?

Back 8

9. Cardiac stroke volume is cardiac output divided by heart rate. Alterations in the cardiac stroke voillme caused by the administration of volatile anesthetics can be calculated from the cardiac output and heart rate that results from the administration of each anesthetic. Because desflurane, isoflurane, and sevoflurane produce little change in cardiac output but increase heart rate, it follows that the stroke volume associated with the administration of each of these agents is decreased.

Front 9

10. How do inhaled anesthetics affect myocardial contractility? What is the mechanism by which this occurs? Which patients may be at particular risk of the effects of inhaled anesthetics on myocardial contractility?

Back 9

10. The effects of inhaled anesthetics on myocardial contractility have been studied in vitro using isolated pap.liary muscle preparations. These studies have shown that the volatile anesthetics directly produce a dose-dependent decrease in lity. This effect ::>f myocardial depres8ion Jlas found to be greatest with the administration of halothane, and less with isoflurane. sevofluraile, and desflurane

Front 10

11. How do inhaled anesthetics affect right atrial pressure?

Back 10

11. Right atrial pressure, or central venous pressure, is increased with the administration of halothane, isoflurane, desflurane, and nitrous oxide. These volatile agents probably produce an increase in right atrial pressure through direct · negative inotropic effects on the myocardium. The increase in right atrial pressure associated with the administration of nitrous oxide is likely due to mild mcreases In pulmonary vascular resistance. The administration of sevoflurane does not appear to remit in an increase in right atrial pressure

Front 11

12. How is systemic vascular resistance calculated? How do inhaled anesthetics affect the calculated systemic vascular resistance?

Back 11

12. Systemic vascular resistance is calculated by the mean arterial pressure minus right atrial pressure divided by cardiac output. Alterations in systemic vascular resistance caused by the administration of volatile anesthetics can be calculated from the mean arterial pressure, right atrial pressure, and cardiac output that I results from the administration of each anesthetic. Isofiurane, sevofiurane, and desflurane administration lead to dose-dependent decreases in systemic vascular resistance.

Front 12

l3. How do inhaled anesthetics affect cerebral blood flow?

Back 12

13. All the volatile anesthetics increase cerebral blood flow through vasodilation of the cerebral vasculature, although the anesthetics each affect the vasculature to varying degrees. The administration of halothane appears to increase cerebral blood flow the most, whereas the administration of isoflurane results in the least increase in cerebral blood flow

Front 13

14. How do inhaled anesthetics affect skeletal muscle blood flow?

Back 13

14. The administration of isoflurane produces a twofold to threefold increase in skeletal muscle blood flow. The increase in skeletal muscle blood flow by isoflurane contributes to the associated decrease in systemic vascular resistance. No other volatile anesthetics increase skeletal muscle blood flow with their administration. Nitrous oxide does not result in any change in skeletal muscle blood flow, whereas the adninistration of halothane results in an indirect decrease in skeletal muscle blood flow through its effects of decreasing the perfusion pressure.

Front 14

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

Back 14

15. Halothane, sevoflurane, and desflurane have been shown to cause mild coronary artery vasodilation. Isofturane has been shown to selectively dilate small coronary arterioles in animal models. Coronary artery steal syndrome can occur when coronary arterioles undergo vasodilation and blood flow is diverted from narrowed arterioles that are already maximally dilated to healthy arterioles with less resistance. This theoretically could result in ischemia in the areas supplied

Front 15

16. How do inhaled anesthetics affect pulmonary vascular resistance?

Back 15

16. Volatile anesthetics have minimal effect on the pulmonary vasculature in the absence of any underlying pulmonary disease. Nitrous oxide may increase pulmonary vascular resistance secondary to its mild sympathomimetic effects. This appears to be panicularlr true in patients with co-existing pulmonary hypertension. I

Front 16

17. The administration of which inhaled anesthetic can lead to sympathetic nervous system stimulation?

Back 16

17. Sympathetic nervous system stimulation appears to accompany the administration of desflurane when an abrupt and large increase in the concentration of desfiurane is delivered to the patient. This stimulation of the sympathetic nervous system is reflected as a transient increase in heart rate and systemic blood pressure. The plasma concentration of norepinephrine has been shown to I be increased during this time of sympathetic nervous system stimulation. These transient responses to increased desfiurane concentration delivery can be blunted by the prior administration of an opioid or by more gradually increasing the desfturane concentration.

Front 17

18. How do inhaled anesthetics affect cardiac rhythm? What cardiac dysrhythmias are commonly seen? How should cardiac dysrhythmias in the presence of a volatile anesthetic be treated?

Back 17

18. The only inhaled anesthetic that has any effect on cardiac rhythm is halothane. The administration of halothane may be accompanied by a junctional cardiac rhythm and a decrease in blood pressure. The junctional rhythm is likely due to the suppression of the activity of the sinus node by halothane. The administration of halothane also results in decreases in the amount of circulating epinephrine necessary to elicit premature ventricular contractions. Adults are more sensitive to this effect of halothane than children, such that children are able to tolerate higher doses of subcutaneous epinephrine injection during halothane anesthesia

Front 18

.9. How do the circulatory effects of inhaled anesthetics change over time with the administration of the same, continuous dose of an inhaled anesthetic? What is the mechanism by which these changes occur?

Back 18

19. The inhalation of a volatile anesthetic for longer than 5 hours is associated with an increase in heart rate, cardiac output, and right atrial pressure when compared with the values of these after about 1 hour of anesthesia. The effects of increased cardiac output and decreased systemic vascular resistance together result in no change in blood pressure, or rather a recovery from the effects of the volatile anesthetic. The degree to which these changes occur vary with the inhaled anesthetic. The administration of halothane appears to have the greatest timerelated changes in cardiovascular measurements after 5 hours of inhalation, whereas minimal changes occur over time with the administration of isoflurane and desflurane. Thus, the continued administration of halothane results in the greatest degree of recovery from its cardiovascular effects among the volatile anesthetics. The cardiovascular changes that are noted after 5 hours of volatile mesthetic inhalation are attenuated or completely prevented by the prior administration of propranolol.

Front 19

20. How are the circulatory effects of volatile anesthetics altered during spontaneous ventilation versus mechanical ventilation?

Back 19

20. Circulatory effects of volatile anesthetics are altered during spontaneous ventilation versus mechanical stimulation mainly through associated differences in the PaC020 Carbon dioxide often accumulates when patients are spontaneously ventilating while an inhaled anesthetic is being administered. The accumulation of carbon dioxide may stimulate the sympathetic nervous system, leading to an increase in heart rate, an increase in myocardial contractility, an increase in cardiac output, peripheral vasodilation, and a decrease in systemic vascular resistance. A patient who is being administered a volatile anesthetic does not exhibit any significant alterations in blood pressure when switched from controlled ventilation to spontaneous ventilation. This may be due to the increase in venous return that also accompanies spontaneous ventilation, thereby opposing the effects th~t may otherwise have been noted by the accumulation of carbon dioxide.

Front 20

21. What are some variables that may influence the cardiovascular effects produced intraoperatively by inhaled anesthetics?

Back 20

21. There are several variables that may influence the cardiovascular effects produced intraoperatively by inhaled anesthetics. First, the patient's co-existing diseases ffily contribute to the cardiovascular response to inhaled anesthetics, particularly if the disease is cardiac in nature. Some cardiac disease states that may influence the patient's cardiovascular response include congestive heart failure, ischemic heart disease, and stenotic valvular lesions. Second, a patient's regularly prescribed drug therapy may influence the cardiovascular effects of inhaled anesthetics.

Front 21

25. How much influence does the choice of inhaled anesthetic have on the incidence of postoperative pulmonary complications?

Back 21

25. The choice of inhaled anesthetics administered to maintain anesthesia has not been shown to influence the incidence of postoperative pulmonary complications. (53)

Front 22

26. How is the ventilatory drive affected by inhaled volatile anesthetics? What is the mechanism by which inhaled anesthetics are thought to affect the ventilatory drive?

Back 22

26. Inhaled volatile anesthetics produce a dose-dependent depression of the ventilatory drive. The mechanism by which this occurs is thought to be primarily through the direct depression of the medullary ventilatory centers, with some contribution from depressant effects on intercostal muscle function. Each inhaled anesthetic depresses ventilation to a different degree.

Front 23

27. How is the rate of breathing affected by inhaled volatile anesthetics? How does isoflurane differ from the other inhaled anesthetics with respect to how it influences the rate of breathing?

Back 23

27. Inhaled volatile anesthetics produce a dose-dependent increase in the rate of breathing. Although the exact mechanism for this effect of inhaled anesthetics is unclear, it is believed to result from central nervous system stimulation by the anesthetic. Isofiurane differs from the other anesthetics with regard to its effects on the rate of breathing in that it only increases the rate of breathing when administered at doses of up to 1 MAC.

Front 24

28. How is the tidal volume affected by inhaled volatile anesthetics!

Back 24

28. Inhaled volatile anesthetics decrease the tidal volume of individuals breathing the inhaled anesthetic. The mechanism by which this occurs is unclear.

Front 25

29. How is the minute ventilation affected by inhaled volatile anesthetics?

Back 25

29. Overall, the breathing pattern of patients who are being administered an inhaled volatile anesthetic is regular, rhythmic, rapid, and shallow. The decrease in tidal volume is not sufficiently compensated by the incJease in respiratory rate, however. This results in a decrease in the minute ventilation of individuals breathing an inhaled anesthetic. The resting Paco2 of these patients is increased as a result. The resting Paco2 is used as an index to evaluate the degree of iratory depression that is pIOduced by inhaled anesthetics. '

Front 26

31. What is the ventilatory response of an awake, healthy, spontaneously ventilating individual for every 1 mm Hg increase in the PaC02?

Back 26

31. The minute ventilation increases by 1 to 3 L/min in an awake, healthy, spontaneously ventilating individual for every 1 mm Hg increase in the Paco2

Front 27

32. How do inhaled anesthetics affect the carbon dioxide response curve?

Back 27

32. The carbon dioxide response curve gives useful information about the effects of drugs on ventilation. Inhaled anesthetics, including nitrous oxide, produce both a dose-dependent depression of the slope and a rightward shift of the carbon dioxide response curve. The decreased slope of the carbon dioxide response curve represents a decreased sensitivity to the ventilatory stimulant effects of carbon dioxide.

Front 28

33. How does the presence of chronic obstructive pulmonary disease influence the PaC02 of an individual being administered a volatile anesthetic?

Back 28

33. Patients with chronic obstructive pulmonary disease appear to have an obtunded ventilatory response to an increased Pac~ that is proportional to the degree of )bstruction of the airways. These patients may therefore have an accentuated increase in Paeth whenaWninistered a volatile anesthetic.

Front 29

35. How does surgical stimulation affect the ventilation of an anesthetized, spontaneously ventilating patient inhaling a volatile anesthetic?

Back 29

35. Surgical stimulation leads to an increase in both a patient's respiratory rate and tidal volume. The rrunute ventilation may increase by as much as 40% with I surgical stimulation, and the Paco2 subsequently decreases. The decrease in PaC02 is partially offset secondary to an increase in the production of carbon ide during surgical stimulation, such that the decrease in the Paco2 is only )y 4 to 6 mm Hg.

Front 30

37. How do inhaled anesthetics affect respiratory muscle function?

Back 30

37. Normal breathing relies on proper functioning of the intercostal muscles and the diaphragm. Expansion of the rib cage is produced by contraction of the intercostal muscles, which is coupled with descent of the diaphragm for optimal respiratory function. The administration of inhaled anesthetics, and in particular halothane, suppresses intercostal muscle function while sparing the diaphragm.

Front 31

38. Define the apneic threshold. What is the approximate difference between the apneic threshold Pac02 and the resting Paco2?

Back 31

38. The apneic threshold is defined as the maximum Paco2 level that a patient can have that will not initiate spontaneous ventilation. The difference between the apneic threshold Paco2 and the resting Paco2 is about 5 mm Hg. This appears to be true regardless of the resting Paco2 of a patient.

Front 32

39. What is the roost reliable method by which to decrease the Paco2 of a spontaneously ventilating patient being administered a volatile anesthetic?

Back 32

39. The most reliable method by which to decrease the Paco2 of a spontaneously ventilating patient being administered a volatile anesthetic is through the initiation of mechanical ventilation of the lungs. Assisted ventilation of the lungs is not reliable, given that a spontaneously ventilating individual will become apneic when the Paco2 has decreased by about 5 nun Hg below the resting Paco2

Front 33

40. What is the ventilatory response to arterial hypoxemia in an awake, healthy, spontaneously ventilating individual?

Back 33

40. In an awake, ~althy, spontaneously ventilating individual there is an increase in the minute ventilation In response to a decrease of Pao2 below 60 mm Hg. This response is mediated by the carotid bodies.

Front 34

41. How does the inhalation of an anesthetic at 0.1 minimun alveolar concentration (MAC) and at 1 MAC affect the ventilatory response to arterial hypoxemia?

Back 34

41. The inhalation of a volatile anesthetic at 0.1 MAC significantly obtunds the ventilatory response to arterial hypoxemia, whereas the inhalation of a volatile anesthetic at 1 MAC obliterates the ventilatory response to arterial hypoxenua.

Front 35

42. How do subanesthetic doses of inhaled anesthetics affect the usual synergistic ventilatory response to arterial hypoxemia and hypercapnia? What is the clinical relevance of this?

Back 35

42. Sub anesthetic doses of inhaled anesthetics have a greater effect on the ventilatory response to hypoxemia than on the ventilatory response to hypercapnia. The synergistic effect to stimulate ventilation that occurs when arterial hypoxemia and hypercapnia are both present in healthy, awake individuals is also attenuated by inhaled anesthetics. Clinically, this effect of subanesthetic doses of inhaled anesthetics becomes relevant in patients recovering from anesthesia.

Front 36

43. How do volatile anesthetics afect bronchial tone'! What is the mechanism by which this is thought to occur?

Back 36

43. Volatile anesthetics have all been shown to be bronchodilators and exert some attenuation of bronchospasm with their administration. The exact mechanism by which these bronchodilating effects occur is not known. They may exert this effect primarily by decreasing efferent vagal tone from the central nervous system. The additive effects of halothane and a beta-2 agonist on bronchial tone lends further evidence that this may be the case. It is believed that they also directly relax bronchial smooth muscle.

Front 37

14. How beneficial is the administration of bronchodilating volatile anesthetics for the treatment of bronchospasm?

Back 37

44. There may be some benefit to the administration of the volatile anesthetics for the treatment of bronchospasm because the bronchodilating effects of halothane in combination with albuterol have been shown to be additive. There is, however, no evidence to show that the bronchodilating effects of volatile anesthetics are an effective method for treating status asthmaticus. I

Front 38

45. Which two volatile anesthetics are thought to be airway irritants? How is this manifest clinically? How does this limit their clinical utility?

Back 38

45. Isoflurane and desfiurane are both considered to be modestly irritating to the airways when administered to awake patients. Clinically, the administration of these volatile anesthetics to awake patients may result in coughing, breath holding, and the production of secretions. This effect of isofiurane and desfiurane is not attenuated by the prior administration of nitrous oxide or an opioid. Isofturane and desfturane are thus limited in their clinical utility for an inhalation induction of anesthesia.

Front 39

46. How do inhaled anesthetics affect the hypoxic pulmonary vasoconstriction reflex?

Back 39

46. Hypoxic pulmonary vasoconstriction is a reflex response of pulmonary arterioles to vasoconstrict in areas of low alveolar Pao2 in an attempt to decrease perfusion the hypoxic pulmonary vasoconstriction reflex in models studied to evaluate the hypoxic pulmonary vasoconstriction reflex in models studied to evaluate this effect. The mechanism for the effect is unknown, but it is believed to be multifactorial.