Chapter 4 Autonomic Nervous System
1. What are the two principal branches of the autonomic nervous system (ANS), and what is the primary function of each?
The sympathetic nervous system
2. Where do the preganglionic fibers of the sympathetic nervous system (SNS) originate?
3. Where are the ganglia of the SNS located?
4. How are sympathetic signals amplified to broaden the sympathetic response?
5. What neurotransmitter and receptor are involved in the autonomic ganglia?
6. What is the most common neurotransmitter released by the postganglionic sympathetic neurons when they synapse with their target organs?
7. What are the other neurotransmitters of the SNS?
8. What are some of the common cotransmitters released at the terminal of the postganglionic sympathetic fibers, and what do they do?
9. What receptor types do the various classic sympathetic neurotransmitters bind to at the target organ?
10. Where are α2 receptors located, and what happens when they are stimulated?
11. What are the chemical intermediates in the synthesis of norepinephrine from tyrosine substrate, and where does this process occur?
12. What is the rate limiting step in the synthesis of norepinephrine, and what enzyme catalyzes this step?
13. Where is epinephrine synthesized?
14. What percent of the norepinephrine reserve stored in vesicles at the sympathetic nerve terminal is released with each depolarization of the postganglionic nerve?
15. How is the action of norepinephrine at the synapse terminated?
The parasympathetic nervous system
16. Where do the preganglionic fibers of the parasympathetic nervous system (PNS) originate?
17. Where are the ganglia of the PNS located?
18. How are the postganglionic neurons of the PNS different from the postganglionic neurons of the SNS?
19. What happens to ACh after it is released into the synaptic cleft?
Adrenergic pharmacology
20. Which adrenergic effect of norepinephrine predominates, the α or the β? What are the usual clinical responses seen to administration of norepinephrine?
21. What risks are associated with the administration of norepinephrine?
22. What receptors does epinephrine stimulate?
23. What life-threatening events are treated with epinephrine?
24. Name two ways that the local vasoconstrictive effects of epinephrine are used clinically.
25. What are the therapeutic effects of intravenous epinephrine?
26. Which response, sympathetic or parasympathetic, predominates in the following organs? The heart, the vasculature, the bronchial tree, the uterus, the gastrointestinal tract, and the pancreas.
27. What are the usual infusion rates for the catecholamines dopamine, norepinephrine, epinephrine, and dobutamine?
28. What are the primary endocrine and metabolic effects of epinephrine administration?
29. In what circumstances is an intravenous bolus of 1.0 mg of epinephrine appropriate?
30. What are epinephrine’s primary effects at low, medium, and high infusion rates?
31. What are the mechanisms of action of epinephrine for the treatment of bronchospasm? How is the epinephrine administered? What is the dosing?
32. What is the concern when giving epinephrine to a patient during a halothane-based anesthetic?
33. What receptors bind dopamine?
34. In what two ways does dopamine exert its sympathomimetic effects?
35. Which vascular beds are uniquely dilated by dopamine?
36. How is dopamine metabolized?
37. How does the dose of dopamine administered affect its clinical response?
38. How does dopamine affect renal function in shocklike states?
Synthetic catecholamines
39. What receptors are stimulated by isoproterenol?
40. Why has isoproterenol fallen into disuse?
41. Which adrenergic receptors are stimulated by dobutamine?
42. What patients are most likely to benefit from treatment with dobutamine?
43. What is the problem with prolonged administration of dobutamine?
44. Which receptors are stimulated by fenoldopam?
Noncatecholamine sympathomimetic amines
47. Through what two mechanisms do most noncatecholamine sympathomimetic amines exert their effects?
48. Name three noncatecholamine sympathomimetic amines.
49. What are the advantages and disadvantages of using ephedrine to treat hypotension in pregnancy?
50. What is the cause of tachyphylaxis after repeat doses of ephedrine?
51. Should ephedrine be used to treat life-threatening events?
α2-Adrenergic agonists
55. What is the mechanism of action of the α2-adrenergic agonists?
56. What are the clinical effects of administering α2 agonists?
57. What is “clonidine withdrawal”?
58. What drug is commonly used to treat clonidine withdrawal?
59. How does the administration of an α2 agonist affect a patient’s anesthetic requirements?
60. What effect do the α2 agonists have on perioperative mortality?
61. How is clonidine used in the treatment of chronic pain syndromes?
62. What is the context-specific half-life of dexmedetomidine?
63. What is the dosing for a dexmedetomidine infusion?
64. What makes dexmedetomidine an attractive agent for use in awake intubations?
65. What makes dexmedetomidine an attractive agent for use in patients with sleep apnea?
α-Adrenergic receptor antagonists
67. What side effects are commonly associated with the use of α1 antagonists as antihypertensive therapies?
68. What must happen before there is complete recovery from α1-blockade with phenoxybenzamine?
69. What are the primary clinical effects of treatment with phenoxybenzamine?
70. Phenoxybenzamine is most often used to treat what disease?
β-Adrenergic antagonists
73. What are some of the clinic indications for β-blocker therapy?
74. What benefit has been demonstrated for the use of perioperative β-blockers in patients at risk for coronary artery disease?
75. What are the risks of giving perioperative β-blockers?
76. What are the current recommendations for initiating β-blockade perioperatively?
77. What are the significant characteristics that differentiate the intravenous β-blockers commonly used in anesthetic practice?
78. What are the primary effects of the cardioselective (β1 selective) β-blockers?
79. What are the cardiac side effects of β-blockade?
80. What are the risks of treating diabetics with β-blockers?
81. Can β-blockers be used in patients who have pheochromocytomas?
82. How should a β-blocker overdose be treated?
83. Which drug-drug interactions are particularly concerning when a patient is on β-blockers?
84. How is propranolol metabolized?
85. What effect does propranolol have on the oxyhemoglobin dissociation curve?
86. What is the intravenous dosing for the cardioselective β-blocker metoprolol?
87. What adrenergic receptors are antagonized by labetalol?
88. What is the dosing for labetalol?
89. Why is labetalol used to treat hypertension during pregnancy?
90. What accounts for the short half-life of esmolol?
91. When is esmolol an especially good choice for β-blockade?
Cholinergic pharmacology
92. What are the pharmacologic effects of the muscarinic antagonists?
93. How does the quaternary structure of glycopyrrolate affect its clinical actions?
94. In what kinds of cases are muscarinic antagonists still commonly given as premedications?
95. Why is glycopyrrolate given when neuromuscular blockade is reversed with the anticholinesterase drugs?
96. What are the common uses and side effects of a scopolamine patch?
97. What is the central anticholinergic syndrome and how is it treated?
98. What is the mechanism of action of the cholinesterase inhibitors (anticholinesterases)?
99. What is the clinical use for the cholinesterase inhibitors in the perioperative period?
100. What is the anesthetic risk for patients who use echothiophate eye drops?
Answers*
1. The two principal branches of the ANS are the sympathetic and parasympathetic nervous systems. 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. The parasympathetic nervous system (PNS), on the other hand, is responsible for the body’s maintenance functions such as digestion and genitourinary function. (66)
