Chapter 27 Central Nervous System Disease
Neurophysiology
5. Name some factors that influence cerebral blood flow.
6. What is normal cerebral blood flow?
7. What is the relationship between cerebral metabolic rate and cerebral blood flow?
8. For every 1° C decrease in temperature below normal body temperature, what is the corresponding decrease in cerebral blood flow?
9. Define cerebral perfusion pressure.
10. Within what range of mean arterial pressures will cerebral blood flow remain relatively constant?
11. What is the time course within which cerebral vasculature changes in response to alterations in mean arterial pressure? What is the clinical implication of this?
12. What are factors that impair the autoregulation of cerebral blood flow?
13. Describe the relationship between PaCO2 and cerebral blood flow.
14. How much does cerebral blood flow change for every 1 mm Hg increase or decrease in PaCO2 from 40 mm Hg?
15. What is a potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than 30 mm Hg?
16. Below what PaO2 will cerebral blood flow increase?
17. What are the effects of volatile anesthetics on cerebral blood flow and intracranial pressure?
18. What are the effects of nitrous oxide on cerebral blood flow and intracranial pressure?
19. What are the effects of ketamine on cerebral blood flow and intracranial pressure?
20. What are the effects of thiopental on cerebral blood flow and intracranial pressure?
21. What are the effects of propofol on cerebral blood flow and intracranial pressure?
22. What are the effects of etomidate on cerebral blood flow and intracranial pressure?
23. What are the effects of dexmedetomidine and clonidine on cerebral blood flow and intracranial pressure?
24. What are the effects of benzodiazepines on cerebral blood flow and intracranial pressure?
25. What are the effects of opioids on cerebral blood flow and intracranial pressure?
26. What are the effects of neuromuscular blocking drugs on cerebral blood flow and intracranial pressure?
Intracranial pressure
27. What is a normal intracranial pressure?
28. How does the body compensate for increasing intracranial pressure? What implications does this have clinically?
29. How do drug-induced increases in cerebral blood flow affect the intracranial pressures of normal patients and of patients with intracranial tumors?
30. Name some methods used to decrease elevated intracranial pressure.
31. Name some signs and symptoms that may be noted preoperatively that provide evidence that a patient may have an increased intracranial pressure.
Anesthesia for neurosurgery
34. What monitors are typically used for intracranial neurosurgery?
35. What two devices can be used to measure the intracranial pressure?
36. What measures can an anesthesiologist undertake to attenuate increases in arterial blood pressure and intracranial pressure during direct laryngoscopy?
37. How is maintenance anesthesia usually achieved in patients undergoing intracranial neurosurgery?
38. What minimum alveolar concentration (MAC) of volatile anesthetic should be administered when used for maintenance anesthesia in patients undergoing intracranial neurosurgery?
39. What is the desired range of PaCO2 to optimize cerebral blood flow intraoperatively?
40. What is a potential problem of the administration of positive end-expiratory pressure (PEEP) during mechanical ventilation of the lungs in patients undergoing intracranial neurosurgery?
41. How do peripheral vasodilators affect cerebral blood flow? What is the recommendation regarding the use of these drugs intraoperatively in patients undergoing intracranial neurosurgery?
42. Why might neuromuscular blockade be maintained throughout intracranial surgical procedures?
43. How can cerebral swelling be treated intraoperatively?
44. What are some potential problems that can occur with the administration of mannitol?
45. How should intravenous fluid administration be managed intraoperatively in patients undergoing intracranial neurosurgery?
46. Why should glucose-containing intravenous solutions be avoided in neurosurgical patients?
47. Why should coughing and straining by patients awakening from anesthesia be avoided after intracranial surgery? What are some methods by which these responses by the patient can be avoided?
48. Why is rapid awakening desirable in neurosurgical procedures?
49. How should delayed recovery after intracranial surgery be evaluated? When should tension pneumocephalus be considered as a possible cause of postoperative delayed recovery?
50. What drug is commonly used to treat hypertension on emergence from anesthesia for intracranial neurosurgery?
51. Why are patients undergoing neurosurgical procedures at an increased risk for venous air embolism?
52. Describe the pathophysiology of a venous air embolism. What percent of adult patients have a probe patent foramen ovale?
53. What are methods by which a venous air embolism can be detected? Which of these is the most sensitive?
54. What are some signs of a clinically significant venous air embolism?
55. What is the treatment for a venous air embolism?
56. Why should nitrous oxide administration be discontinued in the presence of a venous air embolism?
57. What are the advantages of a pulmonary artery catheter in the presence of a venous air embolism?
58. How efficacious is the use of PEEP in the prevention of a venous air embolism?
59. What typically causes death in a fatal venous air embolism?
Intracranial mass lesions
60. What are some of the presenting signs and symptoms of patients with an intracranial tumor?
61. What are the anesthetic goals for patients undergoing surgical resection of an intracranial tumor?
62. Why is it important to limit drug-induced depression of ventilation with preoperative medicines in patients who are scheduled to undergo surgical resection of an intracranial tumor?
63. How is the induction of general anesthesia in patients undergoing surgical resection of an intracranial tumor achieved?
64. What are the advantages and disadvantages of the sitting position for the resection of intracranial tumors?
65. Name some anesthetic considerations that are unique to posterior fossa tumors.
Intracranial aneurysms and arteriovenous malformations
66. How do patients with ruptured intracranial aneurysms usually present?
67. What is the goal of the anesthetic management of a patient undergoing resection of an intracranial aneurysm or arteriovenous malformation?
68. What are the major complications of intracranial aneurysm rupture?
69. How might the electrocardiogram of patients with a ruptured intracranial aneurysm appear?
70. When is vasospasm after cerebral aneurysm rupture most likely to occur? How is it diagnosed?
71. What is the treatment for vasospasm after cerebral aneurysm rupture?
72. What are the different treatment options for intracranial aneurysms?
73. What are the different treatment options for intracranial arteriovenous malformations?
74. What are special considerations during temporary clip placement during resection of intracranial aneurysms?
Carotid disease
75. What are the indications for carotid endarterectomy?
76. How should patients scheduled for a carotid endarterectomy be evaluated preoperatively?
77. What are the anesthetic goals for patients undergoing a carotid endarterectomy? What is the critical period during this surgery?
78. How should the arterial blood pressure be managed during a carotid endarterectomy?
79. How should the PaCO2 be managed during a carotid endarterectomy?
80. What is the purpose of intraoperative neurologic monitoring during a carotid endarterectomy? What are some methods of intraoperative neurologic monitoring?
81. Does local or general anesthesia have better outcomes for carotid endarterectomy?
82. How is local anesthesia for a carotid endarterectomy achieved? What is an advantage of local anesthesia for this procedure?
83. How is general anesthesia for a carotid endarterectomy usually achieved? What is an advantage of general anesthesia for this procedure?
84. What are some potential postoperative complications after carotid endarterectomy?
85. What are the consequences of postoperative hypertension after carotid endarterectomy?
Answers*
Neuroanatomy
1. The arterial blood supply to the brain is from three blood vessels, including the right and left internal carotids and the vertebrobasilar artery. Anastomoses between these vessels form the circle of Willis, and provide for a collateral blood supply for cerebral protection against ischemia. (476)
2. The classic depiction of the circle of Willis is found in less than half of human brains and collateralization may not be complete in all individuals. (476-477, Figure 30-1)
3. The blood-brain barrier is composed of capillary endothelial cells with tight junctions. This barrier allows the passage of lipid-soluble substances such as carbon dioxide, oxygen, and some anesthetic agents but prevents the passage of large macromolecules such as proteins. (476)
4. The blood-brain barrier may be disrupted in conditions such as acute systemic hypertension, head trauma, infection, arterial hypoxemia, severe hypercapnia, intracranial tumors, and sustained seizure activity. (476)
Neurophysiology
5. Factors that influence cerebral blood flow include the cerebral metabolic rate, cerebral perfusion pressure and autoregulation, the PaO2, the PaCO2, and anesthetic drugs. (477)
6. Normal cerebral blood flow is 50 mL per 100 g of brain tissue per minute and represents approximately 15% of cardiac output. Although the brain is a very small percent of body weight, its high metabolic rate and inability to store energy account for the high percent of cardiac output it receives. (477)
7. The cerebral metabolic rate directly affects cerebral blood flow through cerebral flow-metabolism coupling. Increases or decreases in metabolic rate result in a proportional increase or decrease in cerebral blood flow. (477)
8. For every 1° C decrease in temperature below normal body temperature there is a corresponding decrease in cerebral blood flow by about 7%. This effect is due to the decrease in the cerebral metabolic rate caused by the decrease in temperature. (477)
9. Cerebral perfusion pressure is defined as the difference between mean arterial pressure and central venous pressure or intracranial pressure, whichever is greater. (478)
10. In healthy, normotensive individuals cerebral blood flow remains relatively constant between cerebral perfusion pressures of 50 to 150 mm Hg. Within this range the cerebral vasculature is able to vasodilate or vasoconstrict in response to changes in mean arterial blood pressure to maintain a constant cerebral blood flow. Below a cerebral perfusion pressure of 50 mm Hg (mean arterial pressure of about 65 mm Hg assuming an intracranial pressure of 15 mm Hg) cerebral blood flow decreases proportionally to mean arterial pressure. Above a cerebral perfusion pressure of about 150 mm Hg, cerebral blood flow increases proportionally to the mean arterial pressure. This response of the cerebral vasculature to alterations in the mean arterial pressure to maintain a constant cerebral blood flow is termed “autoregulation.” (478)
11. The time course within which cerebral vasculature changes in response to alterations in mean arterial pressure is 1 to 3 minutes. That is, within 1 to 3 minutes of an alteration in the mean arterial pressure, the cerebral vasculature is able to respond appropriately to maintain a constant cerebral blood flow. In the interim, with drastic increases or decreases in mean arterial pressure, there may be a brief period of respective cerebral hyperperfusion or hypoperfusion. (478)
12. Autoregulation of cerebral blood flow may be impaired in the presence of intracranial mass lesions, head trauma, intracranial surgery, subarachnoid hemorrhage, severe hypothermia, or volatile anesthetics. Chronic arterial hypertension or sympathetic nervous system stimulation results in a shift of the autoregulatory curve to the right, such that cerebral blood flow is maintained between pressures higher than 60 to 150 mm Hg. This effect is believed to occur after 1 to 2 months of hypertension. (478)
13. Cerebral blood flow is linearly related to the PaCO2, such that increases in the PaCO2 result in increases in cerebral blood flow and vice versa. This effect of the PaCO2 occurs as a result of the effect of the arterial carbon dioxide tension on the pH of the cerebrospinal fluid. An increase in PaCO2
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