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HANDBOOK OF PIIVSIOLOGY 



CIRCULATION I 



after pericardiectomy support, in part, the expla- 

 nation offered, but the problem is complicated by the 

 frequent accompaniment of underlying myocardial 

 disease. When a precise identification of the part 

 played by each process (pericardial and myocardial) 

 is available, differences in the acoustic manifestations 

 may be used to identify the relative role played by 

 each process. 



OPENING SNAP OF .ATRIOVENTRICULAR VALVE. As men- 

 tioned in the analysis of the normal sounds, the 

 opening of the atrioventricular valve is rarely if ever 

 accompanied by an audible sound. On occasion it 

 has been reported that such an event has been seen in 

 the chest phonocardiogram. In states in which there 

 is a marked increase in flow across the valve, and 

 most especially with disease of the atrioventricular 

 valve, an audible acoustic event may be present. In 

 the former situation the event, not associated with 

 valvular pathology, represents an opening sound. For 

 example, in patients with atrial septal defect with a 

 large left-to-right shunt the greatly increased flow 

 across the tricuspid valve may be associated with a 

 sound occurring at the time of the opening of that 

 valve (53). The abnormal sound, usually called a 

 snap because of its quality, occurs in the presence of 

 stenosis of the atrioventricular valve. In order to 

 understand this phenomenon more fully it is necessary 

 to consider first the dynamics of the atrioventricular 

 valve in the normal and in the presence of stenosis 

 (2, 14). Since in most human clinical situations the 

 event is a direct consequence of mitral valve pa- 

 thology, the following discussion will concern itself 

 with this valve. 



The human mitral valve consists of two leaflets, a 

 larger anterior or septal leaflet and a smaller posterior 

 or mural leaflet. The line of appro.ximation viewed 

 from the left atrium is not a straight line but a 

 crescent with the concavity directed anteriorly. The 

 point at which the line of approximation meets the 

 valve ring is the commissure and one is located 

 anteriorly and laterally, the other posteriorly and 

 medially. Beneath these commissures on the ven- 

 tricular side are located the respective papillary 

 muscles which connect to the leaflets, mainly at the 

 commissures, by the chordae tendineae. A frequent 

 natural misconception is to regard the anterior 

 papillary muscles as connecting to the anterior leaflet 

 and the posterior papillary muscle to the posterior 

 leaflet. In actual fact the major attachments of the 

 anterior papillary muscle go to each leaflet primarily 

 at the anterolateral commissure, and those of the 



posterior papillary muscle to the posteromedial com- 

 missure. Since the papillary muscles depolarize first 

 and repolarize last it may be considered that their 

 function, during systole, is to guard the commissures. 

 This is, in effect, an extension of a concept of papillary 

 muscle function originally proposed by Lepeschkin 

 (56). During diastole the papillary muscles are relaxed 

 and allow the leaflets to move freely down into the 

 ventricle under the force of atrial flow. When the 

 commissure is viewed from the side it can be seen 

 that the major attachments of the chordae form a V 

 or a }' from the papillary muscle to the leaflet. With 

 rheumatic inflammation there is, because of the in- 

 volvement of the chordae tendineae as well as the 

 leaflets, a filling in of the I' or the }' and a fusion of 

 the chordae which is thereby associated with a fusion 

 of the line of approximation of the leaflets at the 

 commissures. There results a stenosis of the orifice in 

 which the leaflets proper are unaffected, but they are 

 now held not only at the valve ring but also at the 

 commissures and, for a variable distance, in toward 

 the center of the line of approximation. In this circum- 

 stance, when ventricular pressure falls below atrial 

 pressure, the bodies of the leaflets proper are free to 

 move toward the ventricle, but this movement is 

 soon checked by the fusion at the commissures. It is 

 this checking of the downward movement of the 

 leaflet, much like a sail filling with wind, that appears 

 to be responsible for the opeiting snap of the valve. 

 The most direct evidence for this explanation comes 

 from the observations of Sellers (91) at the time of 

 operation. With a finger in the ventricle and a stetho- 

 scope on the heart he was able to note obliteration of 

 the opening snap when he prevented the leaflets from 

 bellying downward. Since the presence of the opening 

 snap depends not only on the presence of stenosis but 

 also on the mobility of the leaflet, it is not surprising 

 that when the pathology extends into the leaflet proper 

 and renders it immobile an opening snap is not ob- 

 served. 



The presence of an opening snap, denoting as it 

 does the time of opening of the atrioventricular valve, 

 allows for a measurement of the duration of isometric 

 relaxation of the ventricle by acoustic means. This 

 time interval is that from the closing of the semilunar 

 valve, at which time the second sound component 

 occurs, to the opening of the atrioventricular valve, 

 at which time the opening snap occurs. It must be 

 remembered that so far as the second sound is con- 

 cerned this must refer to the component of the sound 

 due to closure of the semilunar vahe on that side of 

 the heart from which the opening snap occurs. The 



