Which antihypertensive agents would be preferred in a patient with known elevated intracranial pressure?
Should we even be trying to lower blood pressure in this setting in the first place?
When tight blood pressure control is directly tied to neurological and cardiovascular outcomes, the ideal approach should be intensive-care monitoring and a continuous infusion. We are quick to make such a recommendation for hypotensive patients requiring vasopressors but often are reluctant to make similar recommendations of patients on the other end of the blood pressure spectrum.
In the setting of increased in ICP due to neurological emergencies, the agents of choice all have two things in common: short half-life and neutral effect on ICP. Continuous infusions of labetalol and nicardipine are effective antihypertensive agents which do not increase ICP in this setting and are easily titratable. Agents such as hydralazine, nitroglycerin, and sodium nitroprusside all act as cerebral vasodilators and thus increase ICP despite lowering blood pressure. Reviewing the current medication regimen, hydralazine may be a poor choice of antihypertensive agent while clonidine and carvedilol seem to have a neutral effect on ICP.
Should we even attempt to lower blood pressure in this setting? Cerebral perfusion pressure (CPP) is related to mean arterial pressure (MAP) and intracranial pressure (ICP) as follows:
CPP = MAP - ICP
*Note that ICP is often measured in cm H2O (or CSF) but in this equation must be mmHg. The conversion is 1 mmHg = 1.36 cm H2O.
Per the above equation, acute drops in MAP may result in decrease in CPP. The Cushing reflex is the constellation of hypertension (predominantly systolic with a wide pulse pressure) and bradycardia as a response to marked increase in ICP as an effort to maintain CPP (late stages of this reflex also include apnea which completes the Cushing's triad). Per UpToDate recommendation, CPP should remain greater than 60 mmHg and hypertension should only be treated when CPP is greater than 120 mmHg.
A hypothetical patient with a BP of 200/90 has a MAP of approximately 127 mmHg. If the ICP is >7 mmHg (~9.5 cm H20), the CPP is still less than 120 mmHg. One could argue not acutely lowering BP in this patient.
Furthermore, the presence of longstanding hypertension may alter the autoregulation set-point. Accustomed to mitigating elevated MAP by vasoconstriction, cerebral vasculature may not be able to accommodate a rapid decrease in MAP, thus increasing risk of ischemic injury. However, traumatic brain injury and stroke can also damage the cerebral vasculature's ability to autoregulate potentially raising ICP further in setting of uncontrolled hypertension.
In summary, management of hypertension in setting of elevated ICP is controversial and partially dependent upon the reason for elevated ICP. The choice of antihypertensive in this setting should be one that does not cause an increase in ICP and ideally should have rapid onset of action, short half-life, and no active metabolites. Before treating HTN in setting of elevated ICP, keep in mind the goal CPP of 60-120 mmHg.
Daniel Edmonston, Nephrology Fellow, Duke University