ANOXIA AND VENTRICULAR FIBRILLATION; WITH A SUMMARY OF EVIDENCE ON THE CAUSE OF FIBRILLATION

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Abstract
Experiments are described showing that ventricular fibrillation is more readily produced in isolated rabbit hearts by electrical stimulation when the oxygen supply to the heart is reduced. This evidence completes investigations which have been made into factors affecting the production of fibrillation. These investigations have shown that factors which shorten the duration of the action potential, particularly those which cause the “plateau” to disappear, facilitate fibrillation, and those which lengthen the duration of the action potential prevent fibrillation. The reason for the length of the cardiac action potential may therefore be to prevent fibrillation. When the action potential is of normal length the fact that two adjacent fibres are out of phase does not matter; the one which is first to contract is not re-excited by the one which is second to contract, because at that moment the first is inexcitable. If the action potential is short, then the first may be already repolarized and may be excited by spread of excitation from the second. Factors which inhibit metabolism shorten the action potential.