SNA

Question 1

1. What are the two principal branches of the autonomic nervous system (ANS)?

Answer 1

1. The two principal branches of the autonomic nervous system (ANS) are the sympathetic and parasympathetic nervous systems. (70)

Question 2

2. What is the primary function of the sympathetic nervous system (SNS)?

Answer 2

2. The sympathetic nervous system (SNS) is responsible for increasing cardiac output and shunting blood to the skeletal muscles to enable the “fight or flight” response necessary when an organism is threatened. (70)

Question 3

3. What is the primary function of the parasympathetic nervous system (PNS)?

Answer 3

3. The parasympathetic nervous system (PNS) is responsible for the body’s maintenance functions such as digestion and genitourinary function. (70)

Question 4

4. The heart, the vasculature, the bronchial tree, the uterus, the gastrointestinal tract, and the pancreas all have dual innervation from the SNS and PNS. Which response, sympathetic or parasympathetic, predominates in each of these organs?

Answer 4

4. Most organs receive dual innervation from the SNS and PNS. When an organ receives these dual inputs one or the other normally predominates. In the heart, the rate and force of the contraction are mainly determined by the cholinergic (PNS) response. Vascular tone is determined solely by adrenergic (SNS) inputs. The tone of the smooth muscle of the bronchial tree is predominantly controlled by PNS inputs. Uterine tone is primarily controlled by SNS inputs. The gastrointestinal tract’s primary inputs are from the PNS. The pancreas’s insulin release is controlled exclusively by the SNS. (70)

Question 5

5. Where do the preganglionic fibers of the SNS originate?

Answer 5

5. The preganglionic fibers of the SNS originate from the thoracolumbar (T1-L2/L3) neurons of the spinal cord. (70)

Question 6

6. Where are the ganglia of the SNS located?

Answer 6

6. Most of the ganglia of the SNS are distributed in paired ganglia, creating the sympathetic chains that are immediately lateral to the left and right borders of the vertebral column. Other sympathetic fibers extend to ganglia along the midline in the celiac or mesenteric plexuses. (70)

Question 7

7. How are sympathetic signals amplified to create a broad and diffuse response?

Answer 7

7. The initial sympathetic signal is amplified as the preganglionic fibers not only synapse at the ganglion of the level of their origin but also course up and down the sympathetic chain, activating ganglia of the adjacent spinal levels as well, thereby widening the body’s response to the sympathetic signal. (70)

Question 8

8. What neurotransmitter and receptor are involved in the autonomic ganglia?

Answer 8

8. The neurotransmitter released at both sympathetic and parasympathetic ganglia is acetylcholine (ACh), and the postganglionic receptors that bind the ACh in both the SNS and the PNS are nicotinic receptors. (72)

Question 9

9. What is the most common neurotransmitter released by the postganglionic sympathetic neurons when they synapse with their target organs?

Answer 9

9. The neurotransmitter released at the terminal end of the postganglionic sympathetic fibers at the synapse with its target organ is usually norepinephrine. (72)

Question 10

10. What are the other classic neurotransmitters of the SNS?

Answer 10

10. Besides norepinephrine, the other classic neurotransmitters of the SNS are epinephrine and dopamine. (72)

Question 11

11. What are some of the common cotransmitters released at the terminal of the postganglionic sympathetic fibers, and what do they do?

Answer 11

11. Identified sympathetic cotransmitters include adenosine triphosphate (ATP) and neuropeptide Y. These molecules are released into the sympathetic synapse at the target organ and modulate the sympathetic activity. (72)

Question 12

12. What receptor types do the various classic sympathetic neurotransmitters bind to at the target organ?

Answer 12

12. Norepinephrine and epinephrine bind to postsynaptic adrenergic receptors located on the target organ. These receptors include α1-, β1-, β2-, and β3-receptors. (72)

Question 13

13. Where are α2-receptors located, and what happens when they are stimulated?

Answer 13

13. α2-Receptors are located presynaptically on the terminal end of the postganglionic nerve fiber. When norepinephrine binds to the α2-receptor, subsequent norepinephrine release is decreased, creating a negative feedback loop. (72)

Question 14

14. What postsynaptic receptors does dopamine bind to?

Answer 14

14. Dopamine binds postsynaptically to dopamine-1 (D1) receptors, α-receptors, and β-receptors. (72)

Question 15

15. What are the chemical intermediates in the synthesis of norepinephrine from tyrosine substrate, and where does this process occur?

Answer 15

15. Tyrosine is converted to dihydroxyphenylalanine (DOPA), DOPA is converted to dopamine, and dopamine is converted to norepinephrine. These transformations occur in the postganglionic sympathetic nerve ending. (72)

Question 16

16. What is the rate-limiting step in the synthesis of norepinephrine, and what enzyme catalyzes this step?

Answer 16

16. The rate-limiting step in the synthesis of norepinephrine is the conversion of tyrosine to DOPA. The enzyme that catalyzes this reaction is tyrosine hydroxylase. (72)

Question 17

17. Where is epinephrine synthesized?

Answer 17

17. Norepinephrine is converted to epinephrine in the adrenal medulla. The enzyme that catalyzes the methylation of norepinephrine to epinephrine is phenylethanolamine N-methyltransferase. (72)

Question 18

18. What percent of the norepinephrine reserve stored in vesicles at the sympathetic nerve terminal is released with each depolarization of the postganglionic nerve?

Answer 18

18. Approximately 1% of the stored norepinephrine is released with each depolarization, so there is a tremendous functional reserve of norepinephrine at the sympathetic nerve terminal. (72)

Question 19

19. How is the action of norepinephrine at the synapse terminated?

Answer 19

19. After being released from the adrenergic receptor(s), most of the norepinephrine in the synaptic cleft is actively taken up at the presynaptic nerve terminal and transported to vesicles for reuse. Norepinephrine that escapes reuptake and makes its way into the bloodstream is metabolized by either the monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT) enzyme in the blood, liver, or kidney. (72)

Question 20

20. Where do the preganglionic fibers of the PNS originate?

Answer 20

20. The preganglionic fibers of the PNS arise from cranial nerves III, VII, IX, and X and from sacral nerve roots (S1-S4). (72)

Question 21

21. Where are the ganglia of the PNS located?

Answer 21

21. Unlike the ganglia of the SNS that are located in ganglionic chains on either side of the vertebral column, the ganglia of the PNS are located close to or within their target organs. (72)

Question 22

22. What is the primary neurotransmitter of the PNS?

Answer 22

22. ACh is released from both the presynaptic and postsynaptic receptors, making it the primary neurotransmitter of the PNS. (73)

Question 23

23. How are the postganglionic neurons of the PNS different from the postganglionic neurons of the SNS?

Answer 23

23. The postganglionic neurons of the PNS are short (because the PNS ganglia are close to or within the target organs), and they release ACh from their terminal end when the postganglionic neuron depolarizes. (73)

Question 24

24. What happens to acetylcholine (ACh) after it is released into the synaptic cleft?

Answer 24

24. ACh released from the parasympathetic neuron binds to postsynaptic muscarinic receptors on the target cell. Upon release from these receptors, ACh is rapidly metabolized within the synapse by the cholinesterase enzyme. (73)

Question 25

25. Which adrenergic effect of norepinephrine predominates, the α or the β? What are the usual clinical responses seen with the administration of norepinephrine?

Answer 25

25. Norepinephrine’s stimulatory effects on α1-adrenergic receptors predominate. This leads to an increase in systemic vascular resistance and a resultant increase in diastolic, systolic, and mean arterial pressure. The increase in systemic vascular resistance can also lead to a reflex bradycardia. (73)

Question 26

26. What risks are associated with the administration of norepinephrine?

Answer 26

26. Besides the acute risks associated with severe hypertension that can occur with the administration of norepinephrine, the vasoconstriction caused by norepinephrine can decrease the blood flow to the pulmonary, renal, and mesenteric circulations so infusions must be carefully monitored to decrease the risk of injury to these vital organs. Additionally, prolonged norepinephrine infusions can cause ischemia of the fingers because of the marked peripheral vasoconstriction. (73)

Question 27

27. What receptors does epinephrine stimulate?

Answer 27

27. Epinephrine binds to and stimulates α- and β-adrenergic receptors. (73)

Question 28

28. What life-threatening events are treated with epinephrine?

Answer 28

28. Exogenous epinephrine is given intravenously to treat cardiac arrest, circulatory collapse, and anaphylaxis. (73)

Question 29

29. Name two ways that the local vasoconstrictive effects of epinephrine are used clinically.

Answer 29

29. Epinephrine is commonly added to local anesthetics to decrease the spread of the local anesthetic. It can also be injected locally to decrease surgical blood loss from the soft tissue (as in tumescent anesthesia for liposuction). (73)

Question 30

30. What are the therapeutic effects of intravenous epinephrine?

Answer 30

30. Among the therapeutic effects of intravenous epinephrine are positive inotropy, chronotropy, and enhanced conduction through the heart (β1-mediated); smooth muscle relaxation in the vasculature and bronchial tree (β2-mediated); and vasoconstriction (α1-mediated). The predominant effect depends on the dose of epinephrine administered. (73)

Question 31

31. What are the primary endocrine and metabolic effects of epinephrine administration?

Answer 31

31. Epinephrine’s primary endocrine and metabolic effects are increased blood glucose (via decreased insulin release), increased lactate, and increased free fatty acids. (73)

Question 32

32. What are the usual infusion rates for the catecholamines dopamine, norepinephrine, epinephrine, and dobutamine?

Answer 32

32. All the exogenous catecholamines have short half-lives, so they are administered as continuous infusions. The usual dose for dopamine is 2 to 20 µg/kg/min. The usual dose of norepinephrine is 0.01 to 0.1 µg/kg/min. The usual dose of epinephrine is 0.03 to 0.15 µg/kg/min. The usual dose of dobutamine is 2 to 20 µg/kg/min. (73)

Question 33

33. In what circumstances is an intravenous dose of 1.0 mg of epinephrine appropriate?

Answer 33

33. An intravenous dose of 1.0 mg epinephrine is given for cardiovascular collapse, asystole, ventricular fibrillation, electromechanical dissociation, or anaphylactic shock. This dose of epinephrine is chosen because it constricts the peripheral vasculature while maintaining myocardial and cerebral perfusion. (73)

Question 34

34. What are epinephrine’s primary effects at low, medium, and high infusion rates?

Answer 34

34. At low infusion rates (1 to 2 µg/min), epinephrine’s primary action is a β2-mediated decrease in airway resistance and vascular tone. At medium doses (2 to 10 µg/min) of epinephrine one usually sees an increase in heart rate, an increase in myocardial contractility, and increased conduction through the AV node. At high doses (>10 µg/min), the α1-effects predominate and there is a generalized vasoconstriction with a reflex bradycardic response. (73)

Question 35

35. What are the mechanisms of action of epinephrine for the treatment of bronchospasm? How is the epinephrine administered? What is the dosing?

Answer 35

35. Epinephrine is effective therapy for bronchospasm both because of its direct effect as a bronchodilator (via relaxation of the bronchial smooth muscle) and because it decreases antigen-induced release of bronchospastic substances (as may occur during anaphylaxis) by stabilizing the mast cells that release these substances. When using epinephrine to treat bronchospasm, it can be given subcutaneously. The usual subcutaneous dose is 300 µg every 20 minutes, with a maximum of three doses. (74)

Question 36

36. What is the concern when giving epinephrine to a patient during a halothane-based anesthetic?

Answer 36

36. Epinephrine decreases the myocardial refractory period, so giving epinephrine during a halothane-based anesthetic increases the risk of cardiac arrhythmias associated with the administration of halothane. This risk seems to be lower in pediatric cases (the population in which halothane is still used), and the arrhythmic risk increases with hypocapnia. (74)

Question 37

37. What receptors bind dopamine?

Answer 37

37. Dopamine is bound by α-, β-, and dopaminergic receptors. (75)

Question 38

38. In what two ways does dopamine exert its sympathomimetic effects?

Answer 38

38. Dopamine binds to the adrenergic receptors on target cells to cause a direct adrenergic effect. Dopamine also causes the release of endogenous norepinephrine from storage vesicles. This is referred to as dopamine’s indirect sympathomimetic effect. (75)

Question 39

39. How is dopamine metabolized?

Answer 39

39. Dopamine, like the other endogenous catecholamines, is rapidly metabolized by MAO and COMT. The rapid metabolism by these enzymes results in dopamine’s half-life of 1 minute. (75)

Question 40

40. How does the dose of dopamine administered affect the receptors it binds and its clinical effect?

Answer 40

40. At doses between 0.5 and 2 µg/kg/min the dopamine-1 receptors are stimulated, resulting in renal and mesenteric vascular dilation. At doses between 2 and 10 µg/kg/min, the β1-adrenergic effects predominate with increases in cardiac contractility and cardiac output. At doses greater than 10 µg/kg/min, the α1-adrenergic effects predominate, and there is generalized vasoconstriction negating any benefit to renal perfusion. (75)

Question 41

41. Does dopamine provide a clinical benefit to patients in shock?

Answer 41

41. Whereas previous literature suggested that low-dose dopamine infusions protected the kidneys and aided in diuresis, more recent studies have shown that dopamine does not provide a beneficial effect on renal function. Its use for patients in shock has been called into question as it may increase mortality risk and can be associated with arrhythmic events. (75)

Question 42

42. What receptors are stimulated by isoproterenol?

Answer 42

42. Isoproterenol is bound by the β1- and β2-adrenergic receptors, with its β1-adrenergic effects predominating. Because it is not taken up into the adrenergic nerve ending like the endogenous catecholamines, its half-life is longer than that of the endogenous catecholamines. (75)

Question 43

43. What are two clinical uses for isoproterenol?

Answer 43

43. Isoproterenol can be used as a chronotropic agent after heart transplantation as well as to initiate atrial fibrillation during cardiac electrophysiology ablation procedures. (75)

Question 44

44. Which adrenergic receptors are stimulated by dobutamine?

Answer 44

44. Dobutamine stimulates β1-adrenergic receptors without significant effects on β2-, α-, or dopaminergic receptors. (75)

Question 45

45. What patients are most likely to benefit from treatment with dobutamine?

Answer 45

45. Dobutamine is particularly useful in patients with congestive heart failure (CHF) or myocardial infarction complicated by low cardiac output. Doses lower than 20 µg/kg/min usually do not cause tachycardia. Because dobutamine has no indirect adrenergic action, it is effective even in catecholamine-depleted states such as chronic CHF. (76)

Question 46

46. What is the problem with prolonged administration of dobutamine?

Answer 46

46. Prolonged treatment with dobutamine causes downregulation of β-receptors, and tolerance to its hemodynamic effects is significant after 3 days. To avoid this problem of tachyphylaxis, intermittent infusions of dobutamine have been used in the long-term treatment of heart failure. (76)

Question 47

47. Which receptors are stimulated by fenoldopam?

Answer 47

47. Fenoldopam is a selective dopamine-1 agonist. (77)

Question 48

48. What are the pharmacologic effects of fenoldopam?

Answer 48

48. Fenoldopam is a potent vasodilator that increases renal blood flow and diuresis. It is usually administered as a continuous infusion at 0.1 to 0.8 µg/kg/min. (77)

Question 49

49. What are the clinical uses for fenoldopam?

Answer 49

49. Because of unconvincing data from clinical trials, fenoldopam is no longer used to treat CHF or chronic hypertension. It is still used as an alternative to sodium nitroprusside to treat severe acute hypertension because it has fewer side effects and improved renal function. Its peak effects occur in 15 minutes. (77)

Question 50

50. Through what two mechanisms do most noncatecholamine sympathomimetic amines exert their effects?

Answer 50

50. Noncatecholamine sympathomimetic amines exert their effects on the α- and β-receptors via both direct and indirect actions. The direct effects result from the binding of these compounds to the adrenergic receptors like other sympathomimetic agents. The indirect effects result from the release of endogenous norepinephrine stores that these compounds induce. (77)

Question 51

51. Name three noncatecholamine sympathomimetic amines.

Answer 51

51. Mephentermine, metaraminol, and ephedrine are all noncatecholamine sympathomimetic amines. The only one widely used today is ephedrine. (77)

Question 52

52. What are the advantages and disadvantages of using ephedrine to treat hypotension in pregnancy?

Answer 52

52. Animal models suggest that ephedrine does not decrease uterine blood flow significantly, and as a result, it has been the drug of choice for treating hypotension in the parturient for many years. Recent studies, however, suggest that phenylephrine causes less fetal acidosis than ephedrine, and so the use of phenylephrine to treat hypotension in pregnant patients is on the rise. (77)

Question 53

53. What is the cause of tachyphylaxis after repeat doses of ephedrine?

Answer 53

53. The response to the indirect sympathomimetic effects of ephedrine wanes as the body’s stores of norepinephrine available for release become depleted. (77)

Question 54

54. Should ephedrine be used to treat life-threatening events?

Answer 54

54. Although ephedrine is widely used as a first-line drug to treat intraoperative hypotension, data from the closed claims database suggest that relying on ephedrine in situations in which there is life-threatening hypotension rather than switching earlier to epinephrine may contribute to an increase in morbidity from these events. (77)

Question 55

55. What is the primary effect of phenylephrine, and when is its use common?

Answer 55

55. The primary effect of the α1-agonists such as phenylephrine is to cause vasoconstriction. The rise in blood pressure that results leads to a reflex slowing of the heart rate. These agents are used when blood pressure is low and cardiac output is adequate (e.g., to treat the hypotension that can accompany the delivery of a spinal anesthetic). Phenylephrine is also used when a decrease in afterload compromises coronary perfusion in the context of aortic stenosis. (77)

Question 56

56. What is the usual dosing for intravenous phenylephrine?

Answer 56

56. Phenylephrine has a rapid onset of action and a short duration of action (5 to 10 minutes). It can be given as a bolus of 40 to 100 µg or as an infusion starting at 10 to 20 µg/min. (77)

Question 57

57. Besides its effects on the cardiovascular system, what other pharmacologic actions does phenylephrine have?

Answer 57

57. Phenylephrine is also a mydriatic and nasal decongestant. It can be applied topically to the nostril to prepare the nose for nasotracheal intubation. (77)

Question 58

58. What is the mechanism of action of the α2-adrenergic agonists?

Answer 58

58. The α2-agonists bind the presynaptic α2-receptor on the postganglionic sympathetic neuron and decrease the release of norepinephrine. This results in a decrease in the overall sympathetic tone of the patient. (77)

Question 59

59. What are the clinical effects of administering α2-agonists?

Answer 59

59. Besides the decrease in blood pressure, the α2-agonists have sedative, anxiolytic, and analgesic effects. (77)

Question 60

60. What is “clonidine withdrawal”?

Answer 60

60. Acute stoppage of chronic clonidine therapy can lead to a rebound hypertensive crisis, so clonidine should be continued throughout the perioperative period. If a patient is unable to take clonidine orally, administration can be topical via a transdermal patch. (78)

Question 61

61. What drug is commonly used to treat clonidine withdrawal?

Answer 61

61. Labetalol is commonly used to treat clonidine withdrawal syndrome. (78)

Question 62

62. How does the administration of an α2-agonist affect a patient’s anesthetic requirements?

Answer 62

62. α2-Agonists reduce the requirements for other intravenous or inhaled anesthetics as part of a general or regional anesthetic technique. (78)

Question 63

63. What effect do the α2-agonists have on perioperative mortality risk?

Answer 63

63. The α2-agonists have been shown to decrease the incidence of myocardial infarction and reduce the perioperative mortality risk in patients undergoing vascular surgeries. (78)

Question 64

64. What is the indication for epidural clonidine?

Answer 64

64. Epidural clonidine is indicated for the treatment of intractable pain. (78)

Question 65

65. How is clonidine used in the treatment of chronic pain?

Answer 65

65. Clonidine is used to treat chronic pain in patients with reflex sympathetic dystrophy and other neuropathic pain syndromes. (78)

Question 66

66. What is the distribution half-life of dexmedetomidine?

Answer 66

66. The distribution half-life of dexmedetomidine is less than 5 minutes, making its clinical effect quite short. (78)

Question 67

67. What is the dosing for a dexmedetomidine infusion?

Answer 67

67. Because of its short clinical effect, dexmedetomidine is run as a continuous infusion of 0.3 to 0.7 µg/kg/h either with or without a 1-µg/kg loading dose given over 10 minutes. (78)

Question 68

68. What makes dexmedetomidine an attractive agent for use in awake fiberoptic endotracheal intubations?

Answer 68

68. Dexmedetomidine increases sedation, analgesia, and amnesia when used in conjunction with agents that produce those effects. The relatively minor impact of α2-induced sedation on respiratory function combined with its short duration of action has made dexmedetomidine a popular sedative agent for awake fiberoptic endotracheal intubations. (78)

Question 69

69. What makes dexmedetomidine an attractive agent for use in patients with obstructive sleep apnea?

Answer 69

69. Infusions of dexmedetomidine in the perioperative period in obese patients with obstructive sleep apnea minimize the need for narcotics while providing adequate analgesia. (78)

Question 70

70. What are two common uses for β2-adrenergic agonist drugs?

Answer 70

70. β2-Adrenergic agonists (metaproterenol and albuterol) are used to treat reactive airway disease. Ritodrine (another β2-agonist) is used to interrupt premature labor. All these agents lose their β2-selectivity when given at higher doses, which leads to β1-associated adverse effects. (78)

Question 71

71. What side effects are commonly associated with the use of α1-antagonists as antihypertensive therapies?

Answer 71

71. The common side effects of α1-blockers used for antihypertensive therapy are orthostatic hypotension, fluid retention, and nasal stuffiness. (78)

Question 72

72. What must happen before there is complete recovery from α1-blockade with phenoxybenzamine?

Answer 72

72. Because phenoxybenzamine irreversibly binds α1-receptors, new receptors must be synthesized before complete recovery can occur. (78)

Question 73

73. What are the primary clinical effects of treatment with phenoxybenzamine?

Answer 73

73. The primary clinical effects of treatment with phenoxybenzamine are decreased blood pressure and increased cardiac output (both are the result of decreased peripheral vascular resistance). Its primary adverse effect is orthostatic hypotension that can lead to syncope. (78)

Question 74

74. Phenoxybenzamine is most often used to treat what disease?

Answer 74

74. Phenoxybenzamine is most often used to create a “chemical sympathectomy” ahead of resection of a pheochromocytoma (a catecholamine-secreting tumor). Effective α-adrenergic blockade in these patients makes arterial blood pressure less labile intraoperatively and has decreased the surgical mortality rate dramatically. (78)

Question 75

75. What is the treatment for phenoxybenzamine overdose?

Answer 75

75. When exogenous sympathomimetic drugs are given following α-blockade, their effects are inhibited. Nevertheless, a phenoxybenzamine overdose is treated with an infusion of norepinephrine. Presumably, this is effective because some of the α-receptors remain free of the phenoxybenzamine. Vasopressin can also be used to overcome the effects of phenoxybenzamine. (78)

Question 76

76. What effect does prazosin have on serum lipid levels?

Answer 76

76. Prazosin lowers low-density lipid levels and raises high-density lipid levels. (78-79)

Question 77

77. Why are episodes of intraoperative hypertension more common in patients receiving prazosin as compared to phenoxybenzamine during pheochromocytoma resection?

Answer 77

77. Prazosin provides competitive antagonism to α-receptors, as compared to the irreversible binding that occurs with phenoxybenzamine. Therefore, intraoperative hypertension can be seen in patients who received prazosin when an increase in circulating catecholamines occurs, such as during direct surgical manipulation of the pheochromocytoma. (79)

Question 78

78. What are some of the clinical indications for β-blocker therapy?

Answer 78

78. β-Blocker therapy is used in ischemic heart disease, postinfarction management, arrhythmias, hypertrophic cardiomyopathy, hypertension, heart failure, migraine prophylaxis, thyrotoxicosis, and glaucoma. (79)

Question 79

79. What are the current recommendations for initiating β-blockade perioperatively according to the American College of Cardiology/American Heart Association?

Answer 79

79. According to the American College of Cardiology/American Heart Association (ACC/AHA), the continuation of perioperative β-blockade started 1 day or less before noncardiac surgery in high-risk patients prevents nonfatal myocardial infarction, but it increases the rate of death, hypotension, bradycardia, and stroke. Additionally, there are insufficient data regarding the continuation of β-blockers started 2 days or more before noncardiac surgery. The current ACC/AHA guideline for perioperative noncardiac surgery management is that chronic β-blocker therapy continue in the perioperative period, but β-blocker therapy should not be started on the day of surgery. (79)

Question 80

80. What is the effect of β-blocker therapy in patients who have heart failure with reduced ejection fraction?

Answer 80

80. In patients with heart failure and reduced ejection fraction, β-blocker therapy has been shown to reverse ventricular remodeling and reduce mortality risk. (79)

Question 81

81. What are the significant characteristics that differentiate the intravenous β-blockers commonly used in anesthetic practice?

Answer 81

81. The β-blockers commonly used during anesthesia are propranolol, metoprolol, labetalol, and esmolol. These intravenous agents are differentiated based on their duration of action and cardioselectivity. (79)

Question 82

82. What are the primary effects of the cardioselective (β1-selective) β-blockers?

Answer 82

82. With β1-selective blockade, velocity of atrioventricular conduction, heart rate, and cardiac contractility all decrease. Renin release and lipolysis also decrease with β1-blockade. At higher doses, the cardioselectivity of the β1-blockers is lost and β2-receptors are also blocked, which can lead to bronchoconstriction, vasoconstriction, and decreased glycogenolysis. (79)

Question 83

83. What are the cardiac side effects of β-blockade?

Answer 83

83. Life-threatening bradycardia or asystole may occur with β-blockade. In addition, β-blockade can precipitate heart failure in patients with compromised cardiac contractility. (79)

Question 84

84. What are the risks of treating diabetics with β-blockers?

Answer 84

84. Diabetes mellitus is a relative contraindication to the long-term use of β-blockers because warning signs of hypoglycemia (tachycardia and tremor) can be masked and because compensatory glycogenolysis is inhibited. (79)

Question 85

85. What is the role of β-blockers in patients who have pheochromocytomas?

Answer 85

85. To avoid worsening the hypertension in patients with pheochromocytomas, β-blockers should only be given after the patient is fully α-blocked. (79)

Question 86

86. How should a β-blocker overdose be treated?

Answer 86

86. A β-blocker overdose may be treated with atropine. Isoproterenol, dobutamine, glucagon, or cardiac pacing may also be necessary depending on the patient’s symptoms and response to initial therapy. (79)

Question 87

87. Which drug-drug interactions are particularly concerning when a patient is on β-blockers?

Answer 87

87. The combination of a β-blocker with either verapamil or digoxin can lead to life-threatening effects on heart rate (verapamil or digoxin) and contractility (verapamil) or conduction (digoxin). (79)

Question 88

88. How is propranolol metabolized?

Answer 88

88. Propranolol is highly lipid soluble and extensively metabolized in the liver, so changes in liver function or hepatic blood flow can profoundly affect propranolol’s clinical response and duration of action. (80)

Question 89

89. What effect does propranolol have on the oxyhemoglobin dissociation curve?

Answer 89

89. Propranolol shifts the oxyhemoglobin dissociation curve to the right. (80)

Question 90

90. What is the intravenous dosing for the cardioselective β-blocker metoprolol?

Answer 90

90. Intravenous dosing for metoprolol is 2.5 to 5 mg every 2 to 5 minutes up to a total dose of 15 mg. The doses are titrated to the patient’s heart rate and blood pressure. (80)

Question 91

91. What adrenergic receptors are antagonized by labetalol?

Answer 91

91. Labetalol is a competitive antagonist of the α1- and β-adrenergic receptors. (80)

Question 92

92. What is the dosing for labetalol?

Answer 92

92. Five to 10 mg of labetalol can be given intravenously every 5 minutes. Because, like propranolol, it is metabolized in the liver, changes in hepatic blood flow affect its clearance. (80)

Question 93

93. Why is labetalol used to treat hypertension during pregnancy?

Answer 93

93. Labetalol is used acutely and chronically to treat hypertension during pregnancy because uterine blood flow is not affected by labetalol therapy, even with significant reductions in blood pressure. (80)

Question 94

94. What accounts for the short half-life of esmolol?

Answer 94

94. Esmolol is hydrolyzed by plasma esterases, resulting in a half-life for the drug of only 9 to 10 minutes. (80)

Question 95

95. When is cardioselective esmolol an especially good choice for β-blockade?

Answer 95

95. Because of its short half-life, esmolol is particularly useful when the duration of β-blockade desired is short or in critically ill patients in whom the adverse effects of bradycardia, heart failure, or hypotension may require rapid discontinuation of the drug. (80)

Question 96

96. What are the pharmacologic effects of the muscarinic antagonists?

Answer 96

96. The muscarinic antagonists cause an increase in heart rate, sedation, and dry mouth. (80)

Question 97

97. How does the tertiary structure of atropine affect its clinical actions?

Answer 97

97. The tertiary structure of atropine and scopolamine (as opposed to the quaternary structure of glycopyrrolate) makes it possible for them to cross the blood-brain barrier. As a result, atropine and scopolamine have more central nervous system (CNS) effects than glycopyrrolate. (80)

Question 98

98. In what kinds of cases are muscarinic antagonists still commonly given as premedications?

Answer 98

98. Preoperative use of muscarinic antagonists continues in some pediatric and otorhinolaryngologic cases or when planning fiberoptic endotracheal intubation to dry the oral secretions. (80)

Question 99

99. Why is glycopyrrolate given when neuromuscular blockade is reversed with the anticholinesterase drugs?

Answer 99

99. Glycopyrrolate is given along with the reversal agent to block the adverse effects (bradycardia) of the anticholinesterase. Glycopyrrolate is used because it has a longer duration of action than atropine and because, unlike atropine or scopolamine, it does not cross the blood-brain barrier, so there are fewer CNS side effects (sedation or delirium). (80)

Question 100

100. What are the common uses and side effects of a scopolamine patch?

Answer 100

100. A scopolamine patch is used prophylactically to protect against postoperative nausea and vomiting. It can be associated with adverse eye, bladder, skin, and psychological effects. (81)

Question 101

101. What is the central anticholinergic syndrome, and how is it treated?

Answer 101

101. The distortion of mentation (delusions and/or delirium) that can result from atropine or scopolamine’s effects on the CNS has been labeled the “central anticholinergic syndrome.” It is treated with physostigmine, a cholinesterase inhibitor that has a tertiary structure that allows it to cross the blood-brain barrier. (81)

Question 102

102. What is the mechanism of action of the cholinesterase inhibitors (anticholinesterases)?

Answer 102

102. The cholinesterase inhibitors inhibit the cholinesterase enzyme that normally catalyzes the inactivation of ACh at the nicotinic and muscarinic receptors. As a result, these drugs sustain cholinergic agonism at the cholinergic receptors. (81)

Question 103

103. What is the clinical use for the cholinesterase inhibitors in the perioperative period?

Answer 103

103. The cholinesterase inhibitors are used clinically in the perioperative period to reverse muscle relaxation produced by nondepolarizing neuromuscular blocking drugs. The accumulation of ACh that results from the administration of the anticholinesterases allows ACh to more effectively compete with nondepolarizing neuromuscular blocking drugs for sites on the nicotinic receptor, thereby overcoming the effects of the paralytic agents. They are also used for the treatment of myasthenia gravis. (81)

Question 104

104. What is the anesthetic risk for patients who use echothiophate eye drops?

Answer 104

104. Echothiophate iodine irreversibly binds the cholinesterase enzyme and can interfere with the metabolism of succinylcholine (as the anticholinesterases impair the function of the pseudocholinesterase enzyme as well), leading to a marked prolongation of succinylcholine’s paralytic effects. (81)