ECG Changes in Subarachnoid Haemorrhage: A Synopsis

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Abstract

Subarachnoid haemorrhage (SAH) is a neurological emergency with high mortality rates. It is mainly caused by rupture of an aneurysm (congenital/infectious/traumatic) or rupture of an arteriovenous malformation. Electrocardiograms (ECGs) done in patients with SAH have shown morphological changes as well as arrhythmias. Subarachnoid haemorrhage (SAH) patients have often been misdiagnosed to have cardiac abnormalities based on their ECGs when in many of those instances the ECG change had been the result of the SAH itself. They have led to unnecessary and wasteful investigations and therapies in many occasions. Hence the current article is an effort at consolidating the information available in an attempt to avoid possible errors in diagnosis by house staff and internists. There are two mechanisms that might mediate ECG changes in patients with SAH, i.e. autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamine. Hypothalamic stimulation may cause ECG changes without associated myocardial damage whereas elevated catecholamine levels have been correlated with QT-interval prolongation and myocardial damage.

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Most cited references 21

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Medical complications of aneurysmal subarachnoid hemorrhage

Gail L Kongable, Nina J Solenski, E. Clarke Jr Haley … (1995)

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Serial electrocardiographic recording in aneurysmal subarachnoid hemorrhage.

P Brouwers, E F Wijdicks, D Hasan … (1989)

We prospectively studied serial electrocardiograms in 61 patients with aneurysmal subarachnoid hemorrhage. Electrocardiographic changes were related to the initial level of consciousness, to subsequent events, and to outcome after 3 months. All 61 patients had at least one abnormal electrocardiogram, but cardiac disease did not contribute directly to morbidity or mortality. Fast rhythm disturbances, ischemic changes, or both on the electrocardiograms were significantly correlated with poor outcome but not with specific outcome events, particularly not with rebleeding or cerebral ischemia. The Glasgow Coma Scale score on admission and the amount of cisternal and (to a lesser extent) intraventricular blood on the initial computed tomogram were also significantly correlated with poor outcome, but these factors only partially confounded the relation between electrocardiographic abnormalities and poor outcome. We conclude that in patients with aneurysmal subarachnoid hemorrhage, electrocardiographic abnormalities do not herald impending cardiac disease but indirectly reflect adverse intracranial factors. Electrocardiographic abnormalities may therefore have some independent value in predicting poor outcome.

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Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage.

Giuseppe Di Pasquale, Giuseppe Pinelli, Alvaro Andreoli … (1987)

To determine the frequency and severity of cardiac arrhythmias in intracranial subarachnoid hemorrhage, 120 nonselected patients were prospectively studied by 24-hour Holter monitoring. Arrhythmias were found in 96 of 107 patients (90%) with adequate Holter recording: ventricular premature complexes in 49, nonsustained ventricular tachycardia in 5, supraventricular premature complexes in 29, paroxysmal supraventricular tachycardia or atrial fibrillation in 9, sinoatrial block and arrest in 29, second-degree atrioventricular block in 1, atrioventricular dissociation in 4 and idioventricular rhythm in 2. Life-threatening ventricular arrhythmias (torsades de pointes-type ventricular tachycardia) occurred in 4 patients, degenerating into either ventricular flutter or fibrillation in 2. ST-segment changes suggestive of acute transitory myocardial ischemia were found in 8 patients (1.5 mm or more of ST depression in 7 patients and 1.5 mm or more of ST elevation in 1 patient). The frequency and severity of arrhythmias were significantly higher in patients studied within 48 hours of subarachnoid hemorrhage; serious ventricular arrhythmias were associated with QTc prolongation more than 550 ms and with hypokalemia less than 3.5 mEq/liter. No correlation was found between age, clinical condition, site and extent of subarachnoid hemorrhage and either the occurrence or severity of arrhythmias. The results of our study indicate an extremely high incidence of arrhythmias, sometimes serious, in subarachnoid hemorrhage, especially in the first 48 hours after hemorrhage. Continuous electrocardiographic monitoring is therefore mandatory.