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HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



that with the severest lesion there is no valve closure. 

 In such circumstances, despite the very forceful \'en- 

 tricular contraction, the e\idence is that there is no 

 first heart sound component produced. Witli lesser 

 degrees than this the sound component is less than 

 normal in amplitude but still present. The strict 

 dependence of the acoustic manifestations upon dy- 

 namics can be seen in the cases of mitral valve in- 

 sufficiency produced by mitral commissurotomy. We 

 have observed an occasional patient with mitral 

 stenosis in whom mitral commissurotomy unfortu- 

 nately, either by splitting of a valve leafletor by cutting 

 a chorda tendinea, was followed by mitral insuf- 

 ficiency. In such a circumstance the regurgitation is 

 not produced by failure of the valve to close, but 

 rather by a failure of the valve to hold closed during 

 ventricular systole. These patients retained their loud 

 sound. Similarly, patients with a congenitally cleft 

 mitral valve have had a loud first heart sound. In 

 such a circumstance the valve that is present closes 

 normally but part of the valve is missing. Such obser- 

 vations strengthen the belief that the closure of the 

 atrioventricular valve is the integral feature leading 

 to the acoustic event. 



With stenosis of the semilunar valve there are two 

 main changes in the component of the second sound 

 due to closure of the involved valve, a delay in 

 appearance time and a diminution in intensity. It has 

 also been suggested that under certain circumstances 

 there are significant changes in quality (71). In this 

 situation, as with atrioventricular valve, the significant 

 hemodynamic alteration is the increase in resistance 

 to flow across the stenotic valve. There is compen- 

 sation on the part of the ventricle, such that flow is 

 maintained by increasing the energy expended with 

 each contraction. By increasing stroke work, that is, 

 raising a normal stroke volume to a higher pressure 

 level, the resistance can be overcome and a reasonably 

 normal flow maintained. This is, of course, dependent 

 upon the ability of the ventricle to meet the increased 

 load and upon the severity of the stenosis. From the 

 acoustic standpoint the important hemodynamic cor- 

 relate is that as stroke work increases the duration of 

 mechanical systole increases. It is this increase that is 

 responsible for the delay in the time of appearance of 

 the second sound. It has been pointed out that for 

 situations where ventricular compensation is adequate 

 there appears to be a generally linear relationship 

 between the severity of the stenosis and the degree 

 of the splitting of the second sound (55). The phe- 

 nomenon of increased splitting of the second sound 

 here is due to the fact that, except in unusual circimi- 



stances, only one .semilunar valve is invohed, so that 

 the duration of mechanical systole and the appearance 

 time of the second sound on the uninvolved side can 

 be presumed to be normal. The decrease in the in- 

 tensity of the sound is due apparently to the vahular 

 pathology and the fact that there is impaired motion 

 of the leaflets. 



With insufficiency of the semilunar valve there are 

 variable alterations in the second sound component 

 depending upon the mechanism of production of the 

 regurgitation. In some situations the \al\e leaflets are 

 normal or only slightly damaged. Here insufficiency 

 may be due to dilatation of the valve ring making it 

 impossible for the cusps to meet all along their line 

 of closure. If the circulatory dynamics are normal 

 there will be little or no change in the second sound. 

 If the insufliciency is hemodynamically significant, 

 calling forth an increased ventricular stroke output 

 with a low diastolic pressure, then the second .sound 

 may well be increased in intensity. On the other 

 hand if the pathology involves primarily the valve 

 leaflets themselves, so that they cannot meet at all, 

 then there will be disappearance of the second sound. 



Alterations in the third and fourth heart sounds 

 in the presence of heart disease will be discussed below 

 in the section on gallop sounds. 



For a discussion of the nature of the alterations in 

 the normal heart sounds produced by various other 

 diseases, reference should be made to the monographs 

 on acoustics noted earlier. 



Ahnormal Heart Sounds 



In addition to the alterations in the nature of the 

 normal sounds, disease states may also be associated 

 with the production of abnormal sounds. Some of these 

 appear to be new phenomena, that is, they have no 

 counterpart in the normal. Others perhaps represent 

 normally occurring e\ents with merely changes in 

 intensity and/or quality. This point deserves further 

 investigation. The so-called abnormal sounds, like 

 the normal acoustic events, are dependent for their 

 genesis upon certain hemodynamic events. Here again 

 the correlate is with a dynamic event and not neces- 

 sarily with a specific disease process. 



GALLOP SOUND. The most celebrated of all the ab- 

 normal sounds is the gallop sound, so called because 

 it converts the normal double rhythm of each cycle 

 into a triple rhvthm and is thereby reminiscent of the 

 sounds made bv a galloping horse. Two types of 

 gallop rluthni are recognized. One is the proto- 



