Treatment modalities for hypertensive patients with intracranial pathology

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Abstract
To review the cerebrovascular pathophysiology of hypertension, and the risks and benefits of antihypertensive therapies in the patient with intracranial ischemic or space-occupying pathology. Review of English language scientific and clinical literature, using MEDLINE search. Pertinent literature is referenced, including clinical and laboratory investigations, to demonstrate principles of pathophysiology and controversies regarding the treatment of hypertension in patients with intracranial ischemic or space-occupying pathology. The literature was reviewed to summarize the pathophysiology, risks, and benefits of antihypertensive therapies in the patient with intracranial ischemic or space-occupying pathology. Treatment strategies were outlined with a particular emphasis on how antihypertensive agents may affect the brain. Cerebral autoregulation typically occurs over a range of cerebral perfusion pressures between 50 and 150 mm Hg. Chronic hypertension results in adaptive changes that allow cerebral autoregulation to occur over a higher range of pressures. Acute hypertension (rapid increase in perfusion pressure above the autoregulatory limit) may result in cerebral edema, persistent vasodilation, and brain injury. Treatment of a hypertensive emergency must be undertaken conservatively since the chronically hypertensive patient is at risk for ischemic brain injury when perfusion pressure is rapidly decreased beyond autoregulatory limits. In the patient with head injury or primary neurologic injury, acute antihypertensive intervention can result in further brain injury. Selection of appropriate antihypertensive therapy necessitates the careful consideration of agent-specific effects on cerebral blood flow, autoregulation, and intracranial pressure. For example, some vasodilators treat hypertension but also dilate the cerebral vasculature, and increase cerebral blood volume and intracranial pressure while decreasing cerebral perfusion pressure. Pharmacologic blockade of alpha1- or beta1-adrenergic receptors can reduce arterial blood pressure with little or no effect on intracranial pressure within the autoregulatory range. Like the direct peripheral vasodilators, calcium-channel antagonists are limited by cerebral vasodilation and increased intracranial pressure. Angiotensin converting enzyme inhibitors can also be used for mild to moderate hypertension but have the potential to further increase intracranial pressure in patients with intracranial hypertension. Barbiturates offer an alternative antihypertensive therapy since they decrease blood pressure as well as cerebral blood flow and oxygen metabolism. The treatment of acute hypertension in the patient with intracranial ischemic or space-occupying pathology requires an understanding of the pathophysiology of hypertension and determinants of cerebral perfusion pressure. Individual agents should be selected based on their ability to promptly and reliably decrease blood pressure, while considering effects on cerebral blood flow and intracranial pressure.