• O Yamanaka, Y Fujiwara, T Nakamura, K Miyakawa, G Kamishima, M Endoh, and F Ichikawa.
• Department of Cardiology, International Goodwill Hospital.
• Kokyu To Junkan. 1992 Jul 1;40(7):715-9.

AbstractA 35-year-old man was hospitalized after a sudden onset of transient syncopal attack without accompanying complaints of headache or nausea. He was slightly disorientated but neurologically normal. He had a blood pressure of 150/90mmHg and a pulse rate of 40/min. An ECG showed marked sinus brady-cardia with ventricular escaped rhythm followed by advanced atrioventricular (AV) block. Some components of conducted ventricular beats showed aberration. There was no significant ST or T wave abnormality in normally captured QRS components except for prominent T in leads II, III and aVF. At first, we thought that he might require temporary pacing because of Adams-Stokes attack. However, after administration of atropine sulfate, the ECG returned to normal sinus rhythm with heart rate of 88/min. Then he began to complain of headache followed by a convulsive seizure. A CT scan and angiogram revealed a ruptured aneurysm at the top of the basilar artery, which was successfully clipped. A wide spectrum of ECG changes can be demonstrated in practically all patients with subarachnoid hemorrhage (SAH). Prolonged QT interval, ST-T changes, U wave, sinus tachycardia, or ventricular premature complex are the common abnormalities probably caused by increased circulating catecholamine. As bradyarrhythmia in patients with SAH is an uncommon finding, its mechanism has not yet been defined. Transient sinus bradycardia with advanced AV block in this patient might have been caused not by elevated intracranial pressure (Cushing phenomenon) but by drastic discharge of the parasympathetic nerve. This case serves to illustrate the vigilance required in determining whether abnormalities of cardiac rhythm are instrumental in causing neurological symptoms and signs or a disorder of cerebral function.

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