Abstract
The experiments reported deal with the mechanisms through which successive intraventricular injections of K and Ca salts abrogate the fibrillary state and restore a coordinated beat. Doses of KCl smaller than those utilized to arrest fibrillary contractions can produce in the normally beating heart a state resembling fibrillation, but not actually identical with it. The changes preceding and leading up to this condition are analyzed in detail and the so-called "fibrillary contractions" are compared with those resulting from faradic stimulation. We conclude that in this instance the incoordination is the result of depressed conduction, first in the bundle branches and internal layers of the ventricle, and subsequently in diverse portions of the myocardium. Incoordination follows when some fractions escape complete depression, but total cessation occurs when they are completely depressed. The so-called "fibrillation" due to use of K salts differs from that following faradic stimulation in the slower, coarser and more regular waves which run over both ventricles. The electrical deflections are larger and more regular while their frequencies (150-270 per min.) are much less than are those which follow after faradic stimulation (660-1200 per min.). The conclusion is reached that the condition produced by K is not a complete incoordination. The production of such a condition is in itself no contra-indication to the employment of KCl solution for arresting existing fibrillation, but emphasizes the importance of employing doses sufficiently large to produce complete depression in all fractions of the heart. The minimal dose that can ordinarily be relied upon to arrest fibrillation is about 50 mgm. per kgm. Evidence is presented that K salts administered intraventricularly produce their action after being distributed through the myocardium. This distribution cannot be accounted for by diffusion, nor by an overflow into the aorta and entry into the coronary system. It is chiefly forced through the Thebesian vessels by low but positive pressures within the ventricular cavities. Subsequent injections of CaCl2 fail to restore coordinate beats unless fluid is massaged into the aorta and thus circulated through the coronary system. This is not due to the fact that Ca is not distributed through the walls by the Thebesian vessels as is K, but rather to the fact that the K is not readily washed out of the tissue unless assisted by massage sufficient to restore a coronary perfusion with the animal''s own blood.

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