PHONOCARDIOGRAPHY 



723 



the greater and lesser circulations not at comparable 

 levels, as described above, but from one lesel to 

 another. For example, the aorta, through a ruptured 

 sinus of Valsalva aneurysm, may communicate with 

 either the right ventricle or the right atrium (30). 

 The form of the acoustic e\ents is determined by the 

 pressure gradient and consequent flow that ensues. If 

 the normal pressure values are retained, the aortic 

 pressure in lioth lesions is always greater than the 

 pressure of the chamber into which the shunt empties, 

 with the result that continuous murmurs are present. 

 It would be virtually impossible for any other situation 

 to obtain with a communication into the right atrium, 

 whereas for a shunt into the ventricle there may be 

 identity of the pressures in systole. In this case the 

 gradient would be present only in diastole, and if 

 flow were present only in diastole then the murmur 

 would l)e present only in diastole. An interesting 

 situation that resembles this, but has peculiarities of 

 its own, is the communication between a coronary 

 artery and the various levels of the lesser circulation. 

 The best described of these (33) is the circumstance 

 in which the shunt enters the right ventricle. Here the 

 pressure gradient would suggest a continuous murmur, 

 which is the observed phenomenon. However, in 

 order to understand the acoustic phenomenon in its 

 entiret\' recourse must be had to the time-course of 

 coronary flow, which one expects to be the prime 

 correlate of murmur production. Due to the nature 

 of coronarv flow, which is greater in diastole than in 

 systole, the murmur has a diastolic accentuation, 

 which gives it an unique and \irtually diagnostic 

 form. Gasul el al. have suggested that flow in systole 

 is reduced due to reduction in the size of the fistula 

 during systole, and ha\e called vipon diastolic .suction 

 of the ventricle to explain the nature of the flow in 

 diastole. A true understanding of the acoustic phe- 

 nomena awaits a more detailed description of the 

 time-course of flow through the shunt. Such inlor- 

 mation would be of value in explaining the absence 

 of diastolic accentuation of the murmur when the 

 shunt from the coronary artery enters either atrium or 

 pulmonary artery. 



At the next level down, there are cases in which 

 the left ventricle communicates with tiie right atrium. 

 This may occur directly through the portion of the 

 membranous septum abox'e the implantation of the 

 septal leaflet of the tricuspid valve or just below this 

 point and the entrance into the right atrium obtained 

 through a defect in the tricuspid valve. In this situ- 

 ation the pres.sures will be different during systole 



from the onset of left ventricular activity until at 

 least the left \entricular pressure reaches its diastolic 

 level. Since during diastole right atrial pressure is 

 identical with right \'entricular pressure, an analogy 

 with \entricular septal defect may be drawn. From 

 this one would expect that the acoustic representation 

 of such a lesion would mimic a ventricular septal 

 defect entering the right ventricle, and such is the 

 case. Again, where the acoustic manifestations of 

 two lesions have reason to be identical, differentiation 

 must be made by as.sociated phenomena. 



The presence of an arteriovenous fistula in the 

 thorax (or for that matter anywhere) is yet another 

 source of acoustic phenomena. A fistula between the 

 pulmonarv artcrv and pulmonary vein is associated 

 with flow through the lesion throughout the cardiac 

 cycle, since there is usually a pressure gradient 

 throughout the cycle, except perhaps at the end of 

 diastole. This fact, coupled with the fact that the 

 gradient is greater in systole than in diastole, suggests 

 the production of a continuous murmur with accentu- 

 ation in systole. Similarly, a systemic arteriovenous 

 fistula, as for example, between the subclavian artery 

 and vein, yields a pressure gradient throughout the 

 cycle, greater in systole, and therefore, too, a con- 

 tinuous murmur with systolic accentuation. It is to 

 be noted that in form, these murmurs resemble those 

 that arise out of communications between the aorta 

 and pulmonary artery. 



Normal arteriovenous communications may pro- 

 duce continuous murmurs in the same way that 

 abnormal arteriovenous connections do. This situ- 

 ation arises when there is increased flow through 

 channels that normally carry small flow loads. Such 

 a circumstance may occur normally when specific 

 physiological demands call for increased flow. For 

 example, during lactation the markedly increased 

 mammary blood flow may produce a continuous 

 murmur (43, go). Also when there is arterial ob- 

 struction, the development of collaterals, if great 

 enough, may increase the flow through these vessels 

 enough to produce murmurs. For example, coarc- 

 tation of the aorta, which impedes flow at the aortic 

 isthmus, calls forth the development of collateral 

 circulation which supplies the lower part of the body. 

 The increased flow through the vessels around the 

 shoulder girdle and intercostal vessels may produce 

 murmurs, as well as the murmur produced by flow 

 through the stenosed isthmus itself. For this lesion 

 Spencer et al. (95) have shown that the murmur 

 produced by the collateral channels is systolic in 



