There have been numerous reports demonstrating electrocardiographical changes secondary to subarachnoid hemorrhage, consisting of atrial and ventricular arrhythmias, alterations in QRS configuration, Q-T interval prolongation, T-wave abnormalities, and S-T segment elevation or depression. Abnormalities of cardiac muscle and subendocardial hemorrhage have been seen in patients dying of subarachnoid hemorrhage. Experimental work has shown that electrical impulses in the sympathetic nervous system and hypothalamus produce most of these changes, and the implication is that these changes can be prevented by sympathetic blockade. Pulmonary edema also has been shown to occur frequently after subarachnoid hemorrhage, and again the sympathetic nervous system is implicated in the pathophysiology. Studies done illustrating these points are discussed and conclusions drawn with reference to therapy.