Subarachnoid hemorrhage and the heart.
Electrocardiographic abnormalities, both morphological and rhythmic, are frequently seen in association with spontaneous subarachnoid hemorrhage. These changes, which often reflect subendocardial damage, seem to be caused by hypothalamic stimulation leading to an acute increase in sympathetic tone. As a result, potentially life-threatening ventricular arrhythmias may develop in subarachnoid hemorrhage patients. These arrhythmias have responded to sympathetic blocking agents, which may also have a protective effect on subendocardial tissue in this setting. There is no evidence that the prophylactic administration of propranolol or other autonomic blockers significantly alters outcome in these patients. Ultimate morbidity and mortality are clearly related to the degree of intracerebral-intraventricular hemorrhage and vasospasm. This article reviews experimental and clinical evidence regarding the causes of cardiac abnormalities after subarachnoid hemorrhage, the types of abnormalities most frequently seen, their relationship with subendocardial lesions, and the role of autonomic blockers.
D000328:Adult; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000209:etiology*; D001634:Bibliographies as Topic; D002395:Catecholamines / Q000097:blood; D003327:Coronary Disease / Q000209:etiology; D004562:Electrocardiography; D004699:Endocardium / Q000473:pathology; D005260:Female; D006352:Heart Ventricles / Q000473:pathology; D006470:Hemorrhage / Q000209:etiology; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology; D010646:Phentolamine / Q000627:therapeutic use; D011433:Propranolol / Q000627:therapeutic use; D013345:Subarachnoid Hemorrhage / Q000150:complications*
D002395:Catecholamines; D011433:Propranolol; D010646:Phentolamine