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JAMA Revisited
November 19, 2014

Gaskell and the Physiology of the Heart

JAMA. 2014;312(19):2048. doi:10.1001/jama.2013.279846

The stirring events of recent weeks, when men’s minds have been turned from the paths of intellectual life into other fields of human activity, should not make us oblivious of the names which deserve honor because of what they represent in science. For this reason we shall not forego the opportunity to refer to the death of Dr. Walter Holbrook Gaskell at his home in England, Sept. 4, 1914, at the age of 67 years. To this talented physiologist, stimulated by the environment of the Cambridge school under the influence of Michael Foster and trained in Ludwig’s laboratory at Leipsic, we owe some of the fundamental observations regarding the mechanism of the phenomenon known as heart-block—a condition to-day recognized clinically and studied experimentally wherever the medical sciences flourish. It was Gaskell who invented the term “heart-block” and produced it experimentally by clamping the auriculoventricular and sino-auricular grooves, which he calls “the two natural blocking points” of the muscular contraction wave. One of his biographers, Dr. Fielding H. Garrison of the Army Medical Museum in Washington, has summarized the importance of Gaskell’s endeavors in this field as follows: In his view, the original Stannius experiments become simple cases of temporary block. This view has been brilliantly confirmed by the discovery of the vestigial muscular structures known as the auriculoventricular bundle of His and the sino-auricular node of Keith and Flack; also by the clinical and pathologic findings in the disease described by Morgagni in 1761 and now known as heart-block or the Stokes-Adams syndrome. Gaskell even produced the two-, three- and four-time gallops of modern clinicians, in which the ventricle drops one or more of its beats. Schiffs observation that the ventricle of a dying heart beats slower than the auricle is interpreted as the effect of a gradually increasing block. Gaskell also produced the clinical condition known as “fibrillation of the heart” in an isolated strip of cardiac muscle, interpreting the phenomenon as due to blocking of the connections between individual muscle cells. In recent medicine, the various rhythmic disorders of the heart are regarded, not as cases of nervous unbalance, but as the effects of blocking of the peristaltic wave which passes from sinus venosus to bulbus arteriosus, and from muscle fiber to muscle fiber.1

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