MECHANISMS UNDERLYING ELECTROCARDIOGRAPHIC CHANGES OBSERVED IN ANOXIA

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Abstract
Expts. were designed to seek the cause of the reduction of voltage and distortion of QRS in all leads, and of T and S-T changes observed in anoxia; special attention was paid to the QRS changes. Multiple direct leads from the ventricles of dogs with open chests and simultaneously recorded Ecgs show no lengthening of interpunctal intervals, or of P-R, or of the duration of QRS at any level of anoxia to somewhat below 8% in inspired air. At 7% and below, with cardiac dilatation and failure, the intervals do lengthen. But with moderate levels which, in closed chest animals, cause the QRS and T changes under analysis no impairment of conduction is evident. Furthermore, there is no reduction of voltage of local spikes or of QRS is open chest animals until the failure levels of 7% and below are reached. Therefore the cause of the changes seen in moderate anoxia in closed chest animals are not due to changes in the condition of the heart itself. In further anoxia expts. with unopened chests and natural respiration, the chest girth was measured at frequent intervals. As the O2% is reduced the expiratory girth of the chest increases, and in proportion as the chest increases in size, QRS is reduced in voltage, and develops the distortion. The anoxic change in QRS can be produced without anoxia by inflating the chest with air. The T change is really cardiac, but as yet is no index to tolerance to anoxia.

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