Myocardial damage and cardiac arrhythmias after intracranial hemorrhage. A critical review.

I Myocardial Damage and Cardiac Arrhythmias After Intracranial Hemorrhage. A Critical Review • Evidence is presented which supports the theory that intracranial hemorrhage may secondarily cause myocardial damage and cardiac arrhythmias. Fatal intracranial hemorrhage occasionally is accompanied by ECG changes which are consistent with myocardial infarction; histological examination of the heart revealed a variable amount of myocardial damage. After intracranial hemorrhage in animals, myocardial damage was frequent. Similar myocardial damage was produced in animals by intravenous infusion of norepinephrine or acetylcholine and by electrical stimulation of the stellate ganglia, vagus nerve or mesencephalic reticular formation. Atrial and ventricular arrhythmias and various degrees of A-V block were reported in patients suffering from subarachnoid hemorrhage. Similar cardiac arrhythmias were found in animals after intracranial hemorrhage, and with electrical stimulation of the vagus nerve, stellate ganglia or CNS centers. Available data suggest that increased or altered autonomic activity may be the mechanism whereby intracranial hemorrhage produces myocardial damage and cardiac arrhythmias. The efficacy of autonomic blockade in preventing myocardial damage, which was secondary to experimental intracranial hemorrhage in animals, was demonstrated. It is suggested that the initiation of therapy with autonomic blocking drugs, as soon as possible after the onset of intracranial hemorrhage in patients, may be useful in preventing myocardial damage and cardiac arrhythmias. Additional Key Words sympathetic nervous system intracerebral hemorrhage subarachnoid hemorrhage parasympathetic nervous system autonomic blockade • The purpose of this review is to present the evidence for the theory that intracranial hemorrhage secondarily causes myocardial damage and cardiac arrhythmias. It is anticipated that this review will alert the practicing clinician to these two possible complications of intracranial hemorrhage, and suggest an acceptable plan of management to prevent them. Hopefully, this review also will serve to stimulate needed research in a relatively neglected area, when one considers the morbidity and mortality in the large patient population affected. Little information exists about the actual mechanism of death in patients who have suffered a fatal intracranial hemorrhage. 1 In a study of 100 stroke patients, who died within seven days after the onset of symptoms, 14% had no important pathological findings outside of the nervous system at the time of postmortem examination. 1 Subsequent discussion will indicate that cardiac arrhythmias should be considered as a highly probable cause of death in this group of patients, as well as in patients in the same study who had demonstrable myocardial lesions. In a …