PHONOCARDIOGRAPHY 



709 



delays the appearance of the pulmonic component 

 and makes the aortic component appear earlier. 

 Consequently, with inspiration there is a loss of the 

 splitting (fig. 4). This phenomenon, as mentioned 

 above, has been called paradoxical splitting of the 

 second sound. It seems preferable to state that there 

 is reversed splitting of the second sound with a normal 

 respiratory response. 



There is a paradox here, however, if subsequent 

 investigations confirm the suggestion that in left 

 bundle branch block, and in some cases of right 

 bundle branch block, ventricular activity is not 

 different from that in the normal. It becomes then a 

 problem to explain the obvious delay in the second 

 sound component. A possible explanation, capable of 

 investigation and proof, or denial, resides in the clin- 

 ical experience that whereas right bundle branch block 

 may or may not be associated with myocardial disease, 

 it is decidedly unusual to have left bundle branch 

 block without disease of the left ventricle. One might 

 then suggest, as Braunwald and Morrow have, that 

 the problem is not purely an electrical phenomenon, 

 but also a mechanical one, in which the abnormality 

 is the duration of mechanical systole. For, if the onset 

 of ventricular activity of the involved ventricle is not 

 delayed, but the duration of mechanical s\stole is pro- 

 longed, then there will be delay in rela.xation and in 

 the appearance of the second sound component. The 

 question is deserving of further investigation, since 

 such an explanation off'ers the possibility of diff"er- 

 entiating bundle branch block associated with myo- 

 cardial disea.se from that not associated with myo- 

 cardial disease. 



Effect of Disease Slates on Heart Sounds 



In addition to the production of abnormal heart 

 sounds and murmurs, to be described below, various 

 disease states will alter the normal heart sounds. Again, 

 no attempt will be made to provide a complete listing 

 of these, but rather to cite the ways in which disease 

 alters cardiac dynamics and thereby the ac- 

 companying acoustic representation. 



The most clear-cut correlation between dynamics 

 and acoustics is seen when disease invoh'es the heart 

 vahes. Furthermore, since the acoustic representation 

 of valve action is best seen with valve closure, the 

 direct effect of disease of the atrioventricular \al\e is 

 seen in alterations in the first heart sound. Similarly, 

 the direct eff'ect of disease of the semilunar valve is 

 seen best in alterations in the .second sound, but these 

 are not the onlv chans;es seen. Alterations in the other 



sounds may be difficult to verify. They can be second- 

 ary changes, clue not primarily to the valve lesion but 

 to the alterations in the circulation or compensations 

 for the abnormal load placed on it by the primary 

 lesion. For example, hemodynamically significant 

 lesions of the mitral valve change the first heart sound 

 by a direct action on the cardiac events at the time 

 of the onset of ventricular activity. Oftentimes there 

 are changes in the second sound, particularly the 

 pulmonic component, due to the secondary circula- 

 tory alterations, such as pulmonary hypertension. 



With stenosis of the atrioventricular valve, es- 

 pecially that produced by rheumatic fever, there is 

 an increase in the intensity of the component of the 

 first sound associated with valve closure, a change in 

 the quality, best described as a snapping quality, and 

 a delay in the appearance of the sound. Two factors 

 seem to be important in the genesis of this change. 

 First is the alteration in dynamics at the time of valve 

 closure. In the normal, the resistance to flow offered 

 by the valve is so low that with present recording 

 techniques little or no difference between atrial and 

 ventricular pressures can be noted during the filling 

 phases of ventricular diastole. Since the pressures are 

 virtually identical the increase in ventricular pressure 

 at the onset of ventricular systole carries ventricular 

 pressure quicklv above atrial pressure. In this circum- 

 stance there is said to be partial (or even perhaps 

 complete) flotation of the valve leaflets towards a 

 closed position, with valve closure (and/or valve 

 closure sound) soon after the onset of mechanical 

 ventricular activity. In the presence of stenosis, the 

 resistance to flow offered by the valve is increa.sed and 

 a recognizable difference between atrial and ven- 

 tricular pressures is observed. Consequently, at the 

 onset of \entricular activity, ventricular pressure must 

 rise to a higher le\el than in the normal to exceed 

 atrial pressure. The result is that the intersal between 

 the onset of \entricular activity and the sound associ- 

 ated with \al\e closure is increased. In addition to 

 this, inspection of the ventricular pressure curve 

 indicates that at this later time the rate of rise of the 

 pressure is greater, suggesting a more rapid rate of 

 vahe motion which might well contribute to the 

 increased intensity. It has been suggested that the 

 change in the quality of the sound to a snapping one 

 is related to the second important factor, that of the 

 change in the valve structure as a result of the rheu- 

 matic inflammation and subsequent scarring. 



With insufficiency of the atrioventricular valve, the 

 resultant of rheumatic fever, the pathology involves a 

 retraction and bindins; down of the valve leaflets so 



