Porth's Essentials of Pathophysiology, 4e

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Nervous System

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central venous pressure that is reflected back into the internal jugular veins and then to the dural sinuses. This briefly raises the ICP. Regulation of Cerebral Blood Flow The blood flow to the brain is maintained at approxi- mately 750 to 900 mL/minute or 15% of the resting car- diac output. 2 The regulation of blood flow to the brain is controlled largely by autoregulatory or local mechanisms that respond to the metabolic needs of the brain. Cerebral autoregulation has been classically defined as the ability of the brain to maintain constant cerebral blood flow despite changes in systemic arterial pressure. This allows the cerebral cortex to adjust cerebral blood flow locally to satisfy its metabolic needs. The autoregulation of cerebral blood flow is efficient within an MABP range of approxi- mately 60 to 140 mm Hg. 2 Although total cerebral blood flow remains relatively stable throughout marked changes in cardiac output and arterial blood pressure, regional blood flow may vary markedly in response to local changes in metabolism. If blood pressure falls below 60 mm Hg, cerebral blood flow becomes severely com- promised, and if it rises above the upper limit of auto- regulation, blood flow increases rapidly and overstretches the cerebral vessels. In persons with hypertension, this autoregulatory range shifts to higher MABP levels. Metabolic factors affecting cerebral blood flow include an increase in carbon dioxide and hydrogen ion concentrations. Increased carbon dioxide provides a potent stimulus for vasodilation—a doubling of the PCO 2 in the blood results in a doubling of cerebral blood flow. Carbon dioxide is thought to increase cere- bral blood flow by first combining with water to form carbonic acid, with subsequent dissociation into hydro- gen ions, which then causes vasodilation of the cere- bral vessels. Other substances, such as lactic acid and pyruvic acid, which increase the acidity of brain tissues, will produce a similar increase in cerebral blood flow. Oxygen deficiency also influences cerebral blood flow. Except during periods of intense brain activity, the rate of oxygen utilization by the brain remains within a nar- row range. If blood flow to the brain becomes insuf- ficient to supply this needed amount of oxygen, the oxygen deficiency causes the cerebral vessels to dilate, returning cerebral blood flow to near normal. The sympathetic nervous system also contributes to the control of blood flow in the large cerebral arteries and the arteries that penetrate into the brain substance. 2 Under normal physiologic conditions, local regulatory and autoregulatory mechanisms override the effects of sympathetic stimulation. However, when local mecha- nisms fail, sympathetic control of cerebral blood pres- sure becomes important. For example, when the arterial pressure rises to very high levels during strenuous exer- cise or in other conditions, the sympathetic nervous system constricts the large and intermediate-sized super- ficial blood vessels as a means of protecting the smaller, more easily damaged vessels. Sympathetic reflexes are also thought to cause vasospasm in the intermediate and large arteries in some types of brain damage, such as that caused by rupture of a cerebral aneurysm.

Stroke (Brain Attack) Stroke is the syndrome of acute focal neurologic deficit resulting from a vascular induced disorder that injures brain tissue. Stroke remains one of the leading causes of morbidity and mortality in the United States. 18,19 The term brain attack has been promoted to raise aware- ness that time-dependent tissue damage occurs and that rapid emergency treatment is necessary, similar to that with heart attack. There are two main types of strokes: ischemic and hemorrhagic. Ischemic strokes reflect infarctions caused by an interruption of blood flow in a cerebral vessel and are the most common type of stroke, accounting for about 87% of all strokes. 7 The less common hemor- rhagic strokes, which have a much higher fatality rate than ischemic strokes, are caused by spontaneous bleed- ing into brain tissue. Intracerebral hemorrhage can also result from ruptured cerebral aneurysms and bleeding from arteriovenous malformations. Additionally, the latest classifications define silent CNS infarction as isch- emic lesions found incidentally on imaging, and tran- sient ischemic attack (TIA) reflecting transient symptoms without infarction on imaging. 20 Ischemic Stroke Ischemic strokes result from a diverse set of causes of cerebrovascular obstruction by thrombosis or emboli (Fig. 37-14). Among the major risk factors for ischemic

Intracranial atherosclerosis

Carotid plaque with arteriogenic emboli

Cardiogenic emboli

Atrial fibrillation Mitral valve disease Left ventricular thrombi

FIGURE 37-14. The most frequent sites of arterial and cardiac abnormalities causing ischemic stroke.