The brain is highly vulnerable to the effects of hypotension and untreated hypertension, both of which are important risk factors for continued cerebral ischemia, intracranial hemorrhage (ICH), and to a lesser extent, subarachnoid hemorrhage (SAH).

The brain plays an important role in the modulation and control of blood pressure (BP) through the baroreceptor reflex, the brain stem pressor and depressor center, and the interaction between the bulbospinal pressor and depressor center. Further, activation and/or dysfunction of these structures may occur during acute neurologic insults triggered by direct injury or, more commonly, by neurohumoral stimulation as a protective response to further neurologic damage.

BLOOD PRESSURE THERAPEUTICS

After a neurologic emergency, it is often desirable to maintain mean arterial pressure (MAP) or cerebral perfusion pressure (CPP) within a relatively narrow range because a patient's autoregulation at the site of injury may not be intact. Excessive hypertension can compromise the brain's ability to autoregulate cerebral blood flow (CBF) and may aggravate elevated intracranial pressure (ICP) and cerebral edema. In contrast, hypotension may worsen ischemic damage in marginally perfused tissue and can trigger cerebral vasodilation and ICP plateau waves.

Initial interventions for elevated blood pressure should begin with antihypertensive medication injections, such as labetalol, hydralazine, or enalaprilat. However, once these medications have been maximized, a short-acting continuous IV infusion with a predictable dose-response relationship and favorable safety profie should be initiated.