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Experimental subarachnoid hemorrhage (SAH) in dogs was produced by introducing blood into the subarachnoid space through a catheter connected to an artery of the animal. The intact animals and those with preserved vagi and heart sympathetic innervation, developed arrhythmias with short latencies which correlated with the sudden increase in the intracranial pressure. The animals with sections of both vagi and heart sympathetic innervation, but with an intact spinal cord, developed arrhythmias that were delayed and did not correlate with the changes in intracranial pressure. These arrhythmias were preceded by changes in the QT interval, T wave and ST segment. It was concluded that the arrhythmias could be produced either by direct autonomic discharges to the heart or by increased circulating and tissue catecholamines. The clinical implications of these findings are discussed.
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