Affiliation:
1. From the Section of Experimental Medicine, University of Kansas School of Medicine, Kansas City, Kansas
Abstract
The work performance of the hypothermic heart muscle and its possible relationship to ventricular fibrillation was studied in 42 canine heart-lung preparations. With lowering of temperature the work capacity of the heart declined proportional to the decline in heart rate. The maximum stroke volume remained uniformly high over a wide range of hypothermia, until arrhythmia interfered at temperatures around 22°C. Although the work capacity gradually decreased with lower temperature, it was found to be considerably higher than the work load the heart has to cope with in an intact animal at the same temperature. Spontaneous ventricular fibrillation occurred at the same temperature range in denervated heart-lung preparations as in intact hypothermic animals. No relationship was found between the onset of fibrillation and the work load of the heart prior to its onset. Myocardial mechanical failure is therefore not considered to be the cause of ventricular fibrillation in hypothermia. The increased blood viscosity at lower temperatures did not account for the marked prolongation of the ejection phase. Variations in stroke volume likewise did not effect significantly its duration. Epinephrine markedly shortened both ejection and relaxation phase of the hypothermic heart. Epinephrine had a marked inotropic effect upon the hypothermic heart, while the accelerator effect decreased with lowering of temperature. At 22°C or below, where sinus rhythm was no longer present, epinephrine induced ectopic impulse formation in multiple foci which led to ventricular fibrillation.
Publisher
American Physiological Society
Cited by
38 articles.
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