FURTHER OBSERVATIONS ON EXPERIMENTAL AORTIC INSUFFICIENCY

Abstract

To evaluate the pressure changes produced by the operation of purely physical laws and by simultaneous alterations in the physiological responses of the heart, and to harmonize seeming discrepancies in results obtained by pressure and volumetric studies of aortic regurgitation, the effects of experimental aortic leaks on the pressure changes in the aorta and left ventricle were reinvestigated. Optical pressure curves were recorded from dogs whose heart rate was slow, constant and under control. Leaks of different sizes were produced in some cases by an instrument previously described and in others by a newly designed valve spreader which enabled the production of maximum leaks uncomplicated by stenosis.[long dash]Analysis of the systolic portions of the pressure curves elucidated two points: a, the cause,s of the greater steepness, larger amplitude and high systolic pressure following leaks, and b, the steep decline of pressure late in systole, i.e., the true "systolic collapse." The former characteristic phenomena were found to be due mostly to the lower arterial resistance against which ejection begins in aortic insufficiency, but the increased systolic discharge which promptly occurs as a result of an increased initial tension contributes materially to these changes and is solely responsible for the restoration of systolic pressure to or above normal levels. The redistribution of the percentile discharge so that the increment of ejection is expelled largely during the early phase of ejection fully accounts for the steeper systolic decline following the pressure summit. The increased diastolic decline of pressure often referred to as the "diastolic collapse" was carefully studied as regards the magnitude and steepness of the pressure drop which precedes and follows ventricular filling from the left auricle. It was found that with even moderate leaks 40 to 50% of the pressure fall may occur during isometric relaxation, while with maximum leaks this may equal 80% of the total decline of pressure during diastole. In all but maximum sized leaks this early diastolic decline of aortic pressure occurs in two stages designated as incisural and post-incisural which are clearly separated by a halt and change of pressure gradient. With full sized leaks a continuous abrupt decline of pressure takes place. The evidence is conclusive that whatever the actual volume of back-flow (which must be established by other types of ex-periments) a considerable per cent, increasing with the size of leak, flows back previous to the opening of the a-v valves. It was established that the size of the leak is the chief factor which determines both the actual and percentile decline of pressure during isometric relaxation and hence, contrary to previous opinion, is the chief factor which modifies the degree of regurgitation. On the other hand, it was found that such changes in heart rate as are likely to occur in patients affect the pressure drop relatively little in case of small leaks and not at all when the leaks are large. Finally, it was demonstrated that although the actual volume of regurgitation is definitely increased by augmenting the peripheral resistance the percentile regurgitation is not altered as long as the ventricle is capable of responding with an increased stroke through a further rise of initial tension. Thus while the external work is increased by a concomitant high resistance the net discharge remains unaffected.