Neurogenic cardiac injury after subarachnoid hemorrhage

Electrocardiographic abnormalities and myocardial enzyme release occur frequently after subarachnoid hemorrhage, but are often regarded as neurocardiac epiphenomena of little practical significance. In contrast to this view, echocardiographic studies have shown that a reversible and presumably neurogenic form of left ventricular dysfunction occurs in nearly 10% of patients with acute subarachnoid hemorrhage. Angiographic studies have convincingly shown that this form of myocardial injury does not result from coronary artery disease, and electrocardiographic studies have shown a close association with symmetric T-wave inversion and severe QT-segment prolongation. Catecholamine-induced contraction band necrosis, the likely cause of 'neurogenic-stunned myocardium', has been associated with desensitization and uncoupling of myocardial β-receptors from secondary messenger systems. Echocardiography is critical for diagnosing neurogenic cardiac injury in patients with subarachnoid hemorrhage, and invasive hemodynamic monitoring is the key intervention for optimizing cerebral perfusion and limiting complications from hypertensive hypervolemic therapy in the operating room and intensive care unit.