Role of the Cardiologist in Management of Subarachnoid Haemorrhage

Patients with aneurysmal subarachnoid haemorrhage (SAH) frequently have cardiovascular complications that include: blood pressure fluctuations, cardiac arrhythmias and ECG changes. ECG abnormalities, haemodynamic instability and pulmonary oedema, frequently associated with this pathologic condition, contribute to the morbidity and mortality of subarachnoid haemorrhage (SAH). Actually ECG changes occur in 50% to 100% of the patients during the acute stage of SAH, with the most common abnormalities involving the ST segment, T wave and QT interval. In most cases, these abnormalities are clinically inconsequential and are attributed to neurally mediated electrophysiological effects. Some SAH patients, however, show evidence of structural cardiac damage. ECG abnormalities which are indistinguishable from those due to acute myocardial infarction (ST segment elevation or depression) have occasionally been reported in SAH. These patients exhibited findings (which are completely reversible) similar to an acute myocardial infarction on ECG examination, as well as elevated cardiac enzymes and findings of left ventricular wall motion abnormalities, mostly anterior wall akynesis, causing the reduction of left ventricular ejection fraction. Occurrence of pulmonary oedema has been described in ten to 25% of SAH patients. Pulmonary oedema may be neurogenic or cardiogenic in origin and both are a consequence of increased adrenergic tone. There is evidence that the most important consequence of cardiovascular effects secondary to subarachnoid haemorrhage is increased susceptibility to sudden death. The increased adrenergic tone, due to high catecholamine levels and sympathetic cranial nerves stimulation can explain the origin of tachyarrhythmias. The mechanism proposed to explain the origin of bradyarrhythmias is an increased vagal tone.