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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



pulmonic valve ring yieldina; \alvular insufficiency. 

 This causes a semilunar diastolic murmur, the so- 

 called Graham Steell murmur (96). Although it is 

 clear that theoretical acoustic criteria can be set up 

 to differentiate these two, in actual practice the as- 

 sociated nonacoustic phenomena must be used. In the 

 presence of clear-cut hemodynamic evidence for aortic 

 insufficiency one need not invoke the Graham Steell 

 murmur. The difficulty ensues when there is no 

 definite hemodynamic e\'idence for aortic insufficiency. 

 One must also look for circumstances that would 

 produce dilatation of the pulmonic valve ring, namely, 

 the degree of pulmonary hypertension must be severe 

 to e.xpect this to occur. Lacking this evidence, it is 

 much more likely that the murmur is due to aortic 

 valvulitis. Indeed, thus far in our small series, despite 

 the clinical suggestion of Graham Steell murmur, we 

 have not been able to localize the murmur to the 

 right heart, but rather have heard it in the left 

 heart. Our findings, in this respect, are in agreement 

 with the conclusions reached by Brest et al. (13) from 

 their operative series. 



Conversely, consider the patient with known "or- 

 ganic" aortic insufficiency with its attendant semi- 

 lunar diastolic murmur. There may be associated 

 with this a mitral diastolic murmur due to either of 

 two reasons. It may be due to "organic" mitral 

 stenosis. On the other hand it may be due to "func- 

 tional" mitral stenosis, the so-called Austin Flint 

 murmur (32). This murmur is not the semilunar 

 diastolic murmur heard on that part of the thorax 

 where one usually hears murmurs originating at the 

 mitral valve. The Austin Flint murmur is truly a 

 mitral murmur and, as such, has the characteristics 

 of an "organic" murmur. Again there appear to be 

 no rigorous acoustic criteria which will confidently 

 separate these two types, and recourse must be had to 

 the accompanying hemodynamic circumstances. In 

 order to understand the mechanism of production of 

 the Austin Flint murmur and any possible means of 

 providing accurate diagnosis, one must reconsider 

 the function of the mitral vaKe. The anterior or 

 septal leaflet of the mitral valve moves between the 

 inflow and outflow tracts of the left ventricle. In 

 systole this leaflet moves into the inflow tract and 

 shuts off the entrance from the atrium. In diastole 

 the leaflet moves downward (into the ventricle) and 

 anteriorly toward the septum into the outflow tract. 

 In normal diastole the leaflet is free to move into the 

 outflow tract as the ventricle fills only through the 

 inflow tract. However, in the presence of aortic in- 



sufficiency the v^entricle fills from both the inflow 

 tract and the outflow tract with the result that the 

 leaflet is caught between two streams. If the regurgi- 

 tant flow from the aorta is large and forceful enough 

 it will cause the leaflet to impinge in part on the 

 inflow tract. And just as a stenosed valve reduces the 

 inflow orifice and produces a mitral diastolic murmur, 

 so will the normal leaflet held in the stream. The 

 result is a mitral diastolic murmur. If this explanation 

 of the mechanism is a valid one then one associated 

 hemodynamic factor can be deduced. One cannot 

 expect the leaflet to be held in the inflow stream if 

 the amount of regurgitation is small. Therefore, one 

 cannot expect an Austin Flint murmur with minor 

 degrees of aortic insufficiency. The other important 

 factor involves the sounds. If the opening snap is 

 produced as was previously described, then one would 

 not expect this in the presence of a "functional" 

 mitral stenosis, nor would one expect delay in the 

 appearance or a snapping quality to the mitral com- 

 ponent of the first heart sound. 



MURMURS OF NONVALVULAR ORIGIN. When an ab- 

 normal communication, either congenital or ac- 

 quired, exists between two cardiac chambers or 

 vessels, there exists the possibility of flow through 

 this defect with the resultant production of a murmur. 

 This type of approach to the problem is essential, since 

 the mere presence of an anatomical lesion does not 

 assure that a murmur will be generated. There must 

 be flow through it. It is also important to remember 

 that e\'en with flow through an abnormal commimi- 

 cation a murmur, if produced, must reach a certain 

 intensity to be detected on the thorax. 



Consider first communications at the three levels, 

 namely, at the level of the great vessels, at the level 

 of the ventricles, and at the level of the atria. Com- 

 munications at the level of the great vessels (aorta to 

 pulmonary artery) may be congenital, as in patent 

 ductus arteriosus, aortic septal defect (aortico-pulmo- 

 nary window), and ruptured sinus of \'alsalva 

 aneurysm into the pulmonary artery. They may also 

 be acquired as in the Blalock (6) or Potts (78) type of 

 anatomosis designed to increase pulmonary blood 

 flow. In the normal, the pressure in the aorta fluctu- 

 ates between approximately 80 and 120 mm Hg, 

 whereas in the pulmonary artery the pressures vary 

 in the cycle between approximately 10 and 30 mm 

 Hg. If an existing communication docs not signifi- 

 cantly disturb this relationship, then, since the pres- 

 sure in the aorta exceeds the pressure in the pulmo- 



