CHAPTER 37 Intracranial and Cerebrovascular Disease
1 What is cerebrovascular insufficiency?
Cerebrovascular insufficiency results from an inadequate supply of blood flow, oxygen, and/or glucose to the brain. Cerebral ischemia develops, and neurologic damage will ensue if the underlying process is not corrected within 3 to 8 minutes.
2 Compare global ischemia with focal ischemia
Global ischemia refers to global hypoxia (respiratory failure, asphyxia) or circulatory arrest wherein the brain is not perfused. Focal ischemia can result from vasospasm, traumatic, hemorrhagic, embolic, or atherosclerotic events. If the underlying cause is reversed rapidly and perfusion and oxygenation are restored, neurologic damage can be avoided.
3 How does cerebrovascular insufficiency manifest itself?
Manifestations include transient ischemic attacks (TIAs) and cerebrovascular accidents (CVAs).
TIAs are acute in onset, involve neurologic dysfunction for minutes to hours (<24 hours), resolve spontaneously, and are associated with a normal computed tomography (CT) scan.
CVAs may develop acutely or chronically progress over time (minutes to days). Strokes can be classified as minor, with an eventual full recovery, or major, with severe and permanent disability or death. In addition to cerebrovascular abnormalities, CVAs are associated with other comorbidities, including hypertension, diabetes, coagulopathies, atrial fibrillation, mitral valve disease, endocarditis, and substance abuse.
4 What is the etiology of cerebrovascular accidents and transient ischemic attacks?
Atherosclerosis at the bifurcation of the common carotid artery is the source of most cerebral ischemic events. The thrombus itself or more likely embolic plaques and debris can dislodge to the brain, resulting in neurologic injury. Resolution of TIAs within 24 hours is the result of the inherent mechanisms of the body for breaking down such emboli. Ischemia of the brainstem and the temporal and occipital lobes is thought to be caused by a transient decrease in blood flow or blood pressure in the vertebrobasilar system. Hypoperfusion to the brain secondary to the atherosclerotic stenosis itself accounts for less than 10% of ischemic events.
5 Are other factors involved in neurologic outcome following an episode of cerebrovascular insufficiency?
The type and size of plaque or embolus, the site of ischemia, the extent of collateral circulation, the duration of inadequate perfusion, and the inherent response of the brain to the insult all contribute to the neurologic sequelae.
6 List the risk factors for cerebral ischemic events
Hypertension and cigarette smoking are the strongest risk factors. Cardiac diseases (e.g., left ventricular hypertrophy, atrial fibrillation, cardiomyopathy, endocarditis, valvular disease, coronary artery disease) are major risk factors. Other risk factors include age, diabetes, hyperlipidemia, coagulopathies, vascular disease elsewhere, and a maternal history of stroke. The 5-year risk of stroke in a patient who has had a TIA is nearly 35%.
7 Who is a candidate for carotid endarterectomy?
Asymptomatic bruits are heard in 5% to 10% of the adult population. A 1989 prospective study of 566 patients with asymptomatic carotid bruits revealed a 1-year stroke or TIA rate of 2.5% compared with a rate of 0.7% in patients without carotid bruits. The European Carotid Surgery Trial (ECST) demonstrated that carotid endarterectomy (CEA) is not indicated for most patients with moderate (30% to 69%) stenoses, even if they are symptomatic. However, the rate of stroke or TIA increases dramatically with increasing stenosis, reaching a 1-year stroke or TIA rate of 46% for stenoses greater than 80%. It is well accepted that symptomatic patients and asymptomatic patients with a stenosis >70% are candidates for CEA.
Carotid stenting is now available for patients who fit these criteria but are high-risk surgical candidates. Stenting is an alternative to CEA in this select patient population and involves only local anesthesia and a small femoral incision.
8 Define cerebral autoregulation. How is it affected in cerebrovascular disease and what are the anesthetic implications?
Cerebral autoregulation is the ability of the brain to maintain cerebral blood flow relatively constant (40 to 60 ml/100 g/min) over a wide range (50 to 150 mm Hg) of arterial pressures. Stenosis or obstruction in the internal carotid artery causes a pressure drop beyond the obstruction. In an effort to maintain cerebral blood flow, the cerebral vasculature dilates. As the degree of carotid obstruction progresses, the cerebral vasculature distal to the obstruction maximally dilates. At this point the cerebral vasculature loses its autoregulatory ability. Cerebral blood flow becomes passive and depends on systemic blood pressure. It thus becomes critically important to maintain the blood pressure of patients with carotid stenosis because they have minimal or no autoregulatory reserve to counter anesthetic-induced reductions in blood pressure.
9 How are the cerebral responses to hypercapnia and hypocapnia altered in cerebrovascular disease? What are the anesthetic implications?
Normal cerebral vessels are highly sensitive to arterial carbon dioxide partial pressure (PaCO2), dilating in response to hypercapnia and constricting in response to hypocapnia. However, in ischemic and already maximally vasodilated areas of the brain, this relationship breaks down, and responses to hypercapnia and hypocapnia may be paradoxical. Because cerebral vessels in an area of ischemia are already maximally dilated, hypercapnia may result in dilation of only normally responsive vessels outside the area of ischemia. This phenomenon, termed steal, may divert blood flow away from the ischemic area, further compromising perfusion. On the other hand, hypocapnia may cause vessels in normal areas to undergo constriction, diverting blood to marginally perfused areas. This phenomenon is termed the Robin Hood or inverse steal effect. Therefore it is generally recommended that normocapnia be maintained in patients undergoing endarterectomy.
10 What is normal cerebral blood flow? At what level is cerebral blood flow considered ischemic?
Normal cerebral blood flow in humans is 40 to 60 ml/100 g/min (15% of cardiac output). The cerebral metabolic rate for oxygen in adults is 3 to 4 ml/100 g/min (20% of whole-body oxygen consumption). The cerebral blood flow at which ischemia becomes apparent on electroencephalogram (EEG), termed the critical regional cerebral blood flow, is 18 to 20 ml/100 g/min.
11 How do inhalational anesthetics affect cerebral perfusion and cerebral metabolic rate?
In the normal brain cerebral blood flow varies directly with the cerebral metabolic rate for oxygen. Inhalational agents are said to uncouple this relationship. They decrease the cerebral metabolic rate for oxygen but concurrently cause dilation of cerebral blood vessels, thus increasing cerebral blood flow.
12 How should patients having carotid endarterectomy be monitored?
In addition to standard monitoring, intra-arterial blood pressure monitoring is indicated to continuously monitor blood pressure. Carotid surgery does not involve large fluid shifts, and monitoring central venous or pulmonary artery pressures is rarely necessary. Since the potential for uncontrolled carotid arterial bleeding always exists, large-bore intravenous access is recommended. Additional intravenous lines dedicated for the use of vasoactive and anesthetic agents is also recommended.
13 Is regional or general anesthesia preferred for the endarterectomy patient?
No controlled, randomized, prospective study exists that demonstrates a long-term benefit of one technique over the other. Ultimately the choice between regional and general anesthesia is based on patient suitability and preference, surgeon and anesthesiologist experience and expertise, and the availability of cerebral perfusion monitoring.
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