The Wenckebach type of auriculo-ventricular block is characterized by a progressive lengthening of the A-V conduction time, ending in a completely blocked auricular complexthe Wenckebach period. These periodically recurring dropped beats were first recognized clinically by Wenckebach in 1899 from a careful analysis of radial arteriograms; Engelmann (1896) had noted the same phenomenon in the frog's heart a few years earlier. Changing conduction times, due to varying degrees of recovery of the A-V junction, were postulated by them to account for the dropped beats. A typical feature of the progressive prolongation of the P-R interval is that the most marked increase in the conduction time is seen in the second complex of the group. Later ones show only slightly greater prolongation. The shortest A-V conduction time is seen in the first complex after the dropped beat; i.e. following the longest pause or the longest R-P interval.Clinically, the Wenckebach type of A-V block is seen especially in digitalis poisoning, in infective myocarditis, due particularly to rheumatic fever and diphtheria, in myocardial fibrosis or infarction due to coronary artery disease, and occasionally in other lesions of the conduction system. It occurs at low auricular rates, most often under the influence of digitalis, or at the high auricular rates of paroxysmal tachycardia (Wenckebach and Winterberg, 1927;Decherd, et al., 1943). A-V block, often of the Wenckebach type, has been produced experimentally by increasing the auricular rate

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Starling (1915) showed that the normal heart dilates only when increased work is thrown upon it. In disease the heart dilates without any increase in work imposed upon it. It is obviously of importance to know in what particulars the failing heart differs from the normal. The experiments recorded here amplify the results of Starling and Visscher (1927) in elucidating this problem. In their experiments it was found that the energy liberation in the normal heart is fixed by the size of the heart at the beginning of contraction; i.e., at the end of diastole. The size of the heart is a measure of the length of the muscle fibers; consequently their results may be expressed by saying that the quantity of energy liberated in contraction is determined by the length of the fiber at the time of contraction.As a matter of fact, we are more fundamentally interested in the amount of work the heart can do than we are in the total energy it can liberate. Therefore the proportion of the total energy which can be put to useful work, which is the efficiency, becomes a matter of first importance. In cardiac decompensation in man, as well as under certain conditions in experiments on hearts of lower animals, the heart dilates progressively in spite of a uniform or even decreasing load. One ordinarily speaks of such a heart as having poor tone. The heart of a decompensated patient does little work in spite of its enormous size and its apparent effort. The question as to whether the heart under these circumstances is defective in liberating less energy than a normal heart would, or is defective in being unable to use the energy for work in ejecting blood, was investigated by Starling and Visscher (1927). They found that when the mammalian heart lost its normal tonus, and dilated enormously in order to do amounts of work that when fresh it could do at small volume, the total energy

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