PHONOCARDIOGRAPHY 



711 



diastolic gallop, in which the gallop sound occurs in 

 early diastole at the end of the phase of early rapid 

 ventricular filling. The other is the presystolic gallop 

 which occurs late in diastole during the phase of late 

 rapid ventricular filling. The question as to whether 

 or not these sounds represent new phenomena cannot 

 be answered at the present time, since they appear to 

 occur at the same time that one expects the normal 

 third and fourth sounds to occur. There also seem to 

 be no rigorous criteria which, at least on a hemo- 

 dynamic basis, will allow one to differentiate between 

 the normal and the abnormal sound. In view of the 

 fact that this differentiation can be of great clinical 

 importance it is suggested that the problem is de- 

 serving of solution. Furthermore, the traditional expla- 

 nation for the production of gallop sounds has been 

 challenged, and there is no certain evidence at present 

 as to which explanation is the more likely. It is not 

 clear either whether under differing circumstances 

 there may be different mechanisms. This dichotomy 

 has been discussed above in the section on the normal 

 diastolic sounds. Briefly, to recapitulate, the tra- 

 ditional view holds that the sound, either gallop 

 sound, is due to the sudden "checking" of the outward 

 inovement of the ventricular wall, whereas the newer 

 viewpoint suggests that the filling of the ventricle 

 causes a sufficient rise in ventricular pressure to close 

 the atrioventricular valve, transiently. From simul- 

 taneous recordings of atrial and ventricular pressure 

 tracings in patients with gallop sounds we have seen 

 cases where it would appear that ventricular pressure 

 docs rise above atrial pressure at the time of the 

 sound, indicating that atrioventricular valve closure 

 may occur. However, recordings in other patients 

 have not shown this. It may well be that in intact 

 man the manner in which intravascular pressures now 

 have to he taken cannot yield recordings with the 

 fidelity needed to answer the question. Whetiier or 

 not transient atrioventricular valve closure occurs 

 may be better answered with high speed cineangi- 

 ography. One observation on the question of valve 

 motion appears pertinent. We have seen an occa- 

 sional patient with severe mitral insufficiency due to 

 rheiunatic fever in whom there appears to be no 

 mitral closure sound. This is in keeping, as described 

 above, with the nature of the pathology which causes 

 a binding down of the leaflets and the hemodynamic- 

 acoustic correlate which relates this sound to the 

 events associated with closure of the mitral valve. If 

 this reasoning is correct, then the additional presence 

 of a gallop sound, identified by recordings from within 

 the heart as coming from that ventricle, could not be 



explained on the basis of transient atrioventricular 

 valve closure. 



In human clinical situations the presence of a 

 gallop sound correlates best with the presence of 

 ventricular failure. Identification of the ventricle of 

 origin can be carried out by resorting to the effect of 

 respiration on sound intensity. The mode of action is 

 the same as that for the normal diastolic sounds, 

 namely, that inspiration can be expected to increa.se 

 the intensity of a gallop sound from the right ventricle 

 and decrease the intensity of a left ventricular gallop 

 The presystolic gallop, related as it is to mechanical 

 activity of the atrium, disappears, as expected, in the 

 presence of atrial fibrillation. Finally, at sufficiently 

 rapid rates to cause early and late diastolic filling to 

 occur simultaneously, the two gallop sounds may 

 occur simultaneously. The term summation gallop has 

 been applied to this situation. 



Di.ASTOLic KNOCK. Closely related hemodynamically to 

 the protodiastolic gallop sound of ventricular failure 

 is the diastolic knock or diastolic sound of constrictive 

 pericarditis. The term is applied to the sound that 

 occurs at the end of the phase of early rapid ven- 

 tricular filling in this disease, and with the start of the 

 rapid early diastolic pressure rise in the ventricle 

 (74). At times the forcefulness of the outward thrust 

 is sufficient to be palpable, as it may be also with a 

 gallop, and even forceful enough to warrant the term, 

 diastolic heartbeat (105). The phenomenon of the 

 sound and its tactile counterpart seem to arise out of 

 the change in the nature of ventricular filling imposed 

 by the pathological process. In the normal, the inrush 

 of blood into the ventricle at the onset of diastole is 

 met by a distensible ventricular wall which gives way 

 so that volume increases with little or no increase in 

 pressure. In constrictive pericarditis, presumably be- 

 cause of restriction by the diseased pericardium, the 

 ventricle is not allowed to yield and diastolic pressure 

 rises rapidly to plateau with, it is thought, early 

 cessation of ventricular filling. This abrupt transient 

 as blood is suddenly checked on its way into the 

 ventricle appears responsible for the sound and the 

 "diastolic heartbeat." This explanation is, perhaps, 

 somewhat at variance with the observations of 

 Mounsey (74) on the right ventricular pressure. How- 

 ever, it would seem wise to record right and left 

 ventricular pressures before any final conclusion is 

 reached. One of the questions that deserves an answer 

 is the true role that the diseased pericardium plays in 

 the alteration of the hemodynamics and, consequently, 

 the acoustics. Hemodvnamic studies made before and 



