Hemodynamic Complications After Neurosurgery

Abstract

Postoperative cardiopulmonary complications may present following neurologic surgery and include hyper- or hypotension, bradycardia, myocardial ischemia, and hypoxemia. These physiologic disturbances may result secondary to the effects of surgical stress on preexisting medical comorbidities such as essential hypertension, coronary artery disease, or cardiomyopathy. Emergence hypertension, pain, and agitation can produce tachycardia and increase myocardial oxygen demand resulting in ischemia in susceptible patients. Electrolyte disturbances and intravascular volume shifts secondary to hyperosmotic therapy can precipitate arrhythmias, hypotension, or cardiac failure. Fluid loading and vasopressor administration such as for hypertensive, hypervolemic (triple H) therapy during treatment for cerebral vasospasm can precipitate pulmonary edema and heart failure.

Cardiopulmonary complications may also occur as a result of interactions between the central nervous system and the cardiac and/or autonomic systems. While some of these effects have been recognized for nearly a century, most remain incompletely understood. Neurogenic pulmonary edema (NPE) may complicate traumatic brain injury, subarachnoid hemorrhage (SAH), or herniation syndromes. Electrocardiographic disturbances, myocardial injury, and heart failure may develop following SAH. Cushing’s triad occurs in association with increased intracranial pressure and is comprised of bradycardia, hypertension, and respiratory failure.