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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



have seen this in two cases in which the right ven- 

 tricular systohc pressure was artificially raised by 

 partially occluding; the pulmonary tree. The form of 

 the murmur remained the same, though there was 

 diminution in intensity with eventual disappearance 

 when the two systolic pressures JDCcame equal. In tiie 

 usual clinical circumstance, intensity is dependent 

 upon an additional factor, namely, defect size. Ordi- 

 narily, an increased level of right ventricular systolic 

 pressure is found in tiie congenital type of lesion in 

 patients with large defects. 



With identity of systolic pressures as found clinically 

 there may be a left-to-right shunt, no shunt, or a 

 right-to-left shunt. Here, as in great vessel defects, 

 the exact hemodynamic circumstance determines the 

 intracardiac location of miu'mur production or the 

 absence of a murmur. 



A number of interesting problems remain con- 

 cerning the murmur produced l)y a ventricular septal 

 defect. One has already l^een alluded to, namely, the 

 exact relationship between pressures and the question 

 of flow through the shunt in diastole. For example, 

 despite the fact that presumably left ventricular dia- 

 stolic pressure is greater than right we have not ob- 

 served a diastolic component to this murmur even 

 when listening just at the defect within the heart. 

 Clearly, more detailed studies (;f dynamics, shunt 

 flows, and position of the leaflets of the atrioventricular 

 valves is needed to tell whether there is a communi- 

 cation in diastole and, if so, the nature of any possible 

 flow. In addition, studies are needed on the differ- 

 ences, if any, between defects of the membranous 

 and muscular portions of the .septum. It has been 

 suggested that contraction of the septum during 

 systole changes the size of the latter type of defect 

 and thereby alters the acoustics. This highly likely 

 phenomenon deserves more careful investigation. We 

 have also seen, particularly in cases with elevated 

 right heart pressures, minor deviations in murmur 

 form, such as a short silent period after the first 

 heart sound. The precise meaning of such obser- 

 vations and their \aluc remain to be in\'estigated. 



Defects in the atrial septum present an extremely 

 fascinating situation acoustically. To understand this, 

 an understanding of the altered hemodynamics pro- 

 duced by this lesion is necessary. In the usual clinical 

 situation such a defect produces a left-to-right shunt. 

 This is due not only to the greater distensibility of the 

 right atrium than of the left but also to the greater 

 diastolic distensil)ility of the rigiit \cntricle than of 

 the left. The result is an increase in inflow into the 



right ventricle in diastole with a necessary increase in 

 stroke output in systole. This increased volume of 

 blood then flows through the lungs to be returned to 

 the left atrium and made available for reshunting 

 through the lesser circulation. The amount of blood 

 that passes through the mitral \al\e and is thereby 

 available for left \entricular ejection and circulation 

 through the body is either normal or reduced. The 

 time-course of flow through the defect itself appears 

 to be tliroughout the cycle with the major shunt in 

 ventricular diastole, though the details of this and the 

 time at which the small right-to-left shunt occurs 

 remains to be elucidated completely. Recordings from 

 the site of the lesion indicates that many patients 

 have a murmur in \entricular diastole (31, 59, 63). 

 It appears, however, that the intensity of this murmur 

 rarely if ever is sufficient to allow it to be heard on 

 the thorax. There is, though, an increased flow 

 across both the tricuspid valve (in diastole) and the 

 pulmonic valve (in systole). Both of these ha\e the 

 potential for producing murmurs becau.se often the 

 flow is torrential. It is most usual in patients with 

 atrial septal defect to hear a systolic murmur. Since 

 this min-mur is ejection in type it appears to be of 

 semilunar valve in origin. Comparison of this murmur 

 on the thorax with recordings from within the lieart 

 reveals the virtual identity with the miumur tiiat 

 can be localized to the pulmonary arter\". In like 

 manner, the increased flow across the tricuspid \alve 

 may, if the flow is great enough, produce a diastolic 

 murmur that has the characteristics of a murmur 

 originating from an atrioventricular valve. It must 

 be remembered that neither one of these murmurs is 

 produced by the flow through the defect itself but 

 rather by the increased flow through the riglit heart. 

 When one compares the acoustic events that arise 

 out of shunts at the three levels an interesting point 

 arises. In the usual circumstance, the murmurs from 

 great vessel communications and from ventricular 

 septal defects arise out of flow through the lesion 

 itself. It is in this way that they, as well as the murmurs 

 from organic \al\ular lesions, come to have certain 

 recognizaljle ciiaracteristics. Howe\er, for atrial septal 

 defect the murmurs that reach sufllcient intensity to 

 Ije heard on tlie thorax come not from flow through 

 the defect Ijut from increased flow across usually 

 normal valves. It is for this reason that these murmurs 

 are not necessarily characteristic of the lesion and a 

 precise correlation must depend upon associated 

 hemodynamic and acoustic data. 



Occasionalh , communications mav exist between 



