Control data were assigned a value of 100 in order to compensate for individual differences between animals with respect to the size and shape of the chest and body, elastic factors, and thoracic transmission characteristics.
Previous studies in this laboratory having demonstrated that AV valve closure is not directly responsible for the rapid vibrations of the first heart sound, the mechanism of production of this "sound" was studied further in 30 experiments in dogs. The experiments were performed with multiple pressure catheterization, and intracardiac phonocatheterization, and were compared with external phonocardiograms and electrocardiograms. In 10 experiments, the first derivatives of the left and right ventricular pressures were also recorded. In four experiments, direct epicardial and arterial sound tracings were obtained.
These experiments revealed that three groups of vibrations, or components, were often visible in the external phonocardiogram, and in intracardiac and epicardial tracings. The first component follows the onset of left ventricular pressure rise and closure of the mitral valve but coincides with the rapid rise of the first derivative of LV pressure. The second component has no relationship with right heart events, occurs before aortic valve opening, and coincides with the sudden change of course of the first derivative of LV pressure. The third component occurs slightly after aortic valve opening, and seems related to sudden increase of aortic wall tension. It is probably the physiological equivalent of the aortic "ejection sound." Thus, the first two components are both left ventricular in origin while the third is of aortic origin.
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