Therapeutic hypertension: principles and methods

Abstract

In the treatment of neurosurgical patients, elevation of systemic blood pressure is indicated in many clinical situations. An important example is the maintenance of cerebral perfusion pressure in the setting of head injury. With the loss of autoregulation, coupled with high intracranial pressure, cerebral perfusion is often highly dependent on mean arterial pressure. Frequently, hypertension must be induced with vasoactive agents to prevent secondary ischemia. Another example is the treatment of vasospasm following subarachnoid hemorrhage. While control of intravascular volume and maintenance of cardiac output is important, many centers primarily depend on induced hypertension to prevent neurological deficits. While there is clear therapeutic benefit, induced hypertension is associated with significant risks. Sympathetomimetics can disrupt conduction, frequently producing premature ventricular contractions or arrhythmias. Increases in afterload can add stress to the heart, worsening myocardial ischemia or decreasing the ejection fraction. Excessive use of pressors can produce inadequate systemic perfusion and acidosis. Most commonly, pulmonary edema can occur without judicious monitoring of intravascular volume and cardiac output. In this excellent review, a team of experienced neurointensivists details the indications, principles, and guidelines for the use of therapeutic hypertension. In particular, their focus on the proper evaluation and manipulation of the preload, afterload, cardiac output and contractility in addition to the blood pressure is important. Personally, I do not institute prolonged induced hypertension without the use of a Swan–Ganz catheter to monitor both the pulmonary artery wedge pressure and the cardiac output. In addition, their discussion of the possible misreadings from an arterial line is very helpful.