PMID: 6399208Jun 1, 1984

Experimental studies into mechanisms of cardiac arrest

Archives of Emergency Medicine
D C Russell

Abstract

Experimental studies have revealed that a wide variety of different pathophysiological mechanisms may induce ventricular fibrillation (VF) and cardiac arrest during acute myocardial ischaemia or infarction. Distinct phases of enhanced vulnerability (the amount of current required to stimulate ectopic activity in the heart following application of an extra stimulus) to VF follow coronary occlusion and correspond to 'pre-hospital', 'in-hospital' and 'out-of-hospital' periods of arrhythmogenesis. Electrophysiological evidence suggests very early (phase 1a) VF results from multiple re-entrant excitation within the ischaemic zone. Slowed and fragmented conduction and inhomogeneities in refractoriness rapidly develop which mapping studies show to occur in association with development of spatial inhomogeneities in residual blood flow distribution and metabolism. Onset of VF may be triggered by adrenergic mechanisms or influenced by peripheral metabolic responses. Automatic mechanisms (spontaneous pacemaker activity) may induce later VF or VF on reperfusion or trigger re-entry. Findings indicate no single therapeutic approach to be likely to protect against all forms of cardiac arrest.

References

Sep 1, 1971·The American Journal of Cardiology·B Surawicz
Jan 1, 1972·British Heart Journal·A ArmstrongS L Morrison
Jul 1, 1971·Investigative Radiology·C SnyderK Amplatz
Oct 1, 1968·Annals of Surgery·P A EbertD C Sabiston
Jan 1, 1982·Proceedings of the National Academy of Sciences of the United States of America·J L SwainE W Holmes

Citations

Jan 1, 1985·Molecular Aspects of Medicine·J H BottingM J Walker

Related Concepts

Coronary Heart Disease
Canis familiaris
Electrophysiology (Science)
Heart
Cardiac Arrest
Cardiac Conduction System
Myocardium
Norepinephrine Receptors
Ventricular Fibrillation

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