Experiments with quinidine on conduction and on the refractory period in the dog's heart

Abstract

These experiments are based on the theory of fibrillation developed by Garrey and Mines on the suggestion of A. G. Mayer and recently elaborated by T. Lewis. The theory, although it illustrates best the condition known as flutter, is directly applicable also to the state of fibrillation. In the normal heart the stimulus for contraction arises at the sinus node and passes in a radial fashion to the rest of the muscle of the auricle. In flutter, and in fibrillation, there is apparently no fixed point at which the stimulus originates. It appears to be dislocated from the node but it is not yet known what activity goes on in this structure when the abnormal rhythm prevails. Instead of the usual arrangement, an excitation wave courses continuously through the muscle of the auricle, usually over a circular path about the openings of the great veins, as Lewis's experiments show. In order that a continuous circuit may be maintained it appears to be necessary (1) that the path shall have a sufficient length; (2) that the rate of passage shall be sufficiently slow, and (3) that when the stimulus returns to its starting point, the muscle is ready to receive it. It is clear, on this plan, that: (1) if the muscle mass involved is too small, a path long enough to permit the development of a circus becomes impossible; (2) if the rate of conduction is too fast, the stimulus returns to its starting point before the muscle at that point is ready for its reception; (3) if the refractory period of the muscle at the starting point is prolonged beyond the time consumed by the stimulus to make its circuit, the muscle cannot be reëUxcited.