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HANDBOOK OF PHYSIOLOGY 



CIRCULATION 1 



curring semilunar valve opening sound or whethei it 

 occurs after this event and represents an additional 

 sound. Our experience is in agreement with the latter 

 suggestion. 



The systolic ejection sound may be mistaken for the 

 second component of a split first heart sound. More 

 often it is the other way around. Whereas there do 

 appear to be circumstances in which a true splitting 

 of the first heart sound does occur, much more 

 frequently when two separate acoustic events are 

 heard in close appro.\imation, it is the addition of an 

 ejection sound which causes the doubling. At the 

 present time there appear to be no completely satis- 

 factory acoustic criteria for deciding the precise site 

 of origin of an ejection sound and recourse must be 

 had to the accompanying clinical picture. However, 

 several differentiating features have been described 

 (52, 54, 73). Ejection sounds that arise from the 

 pulmonary artery are said to bequite sharp in quality 

 and of maximal intensity at the pulmonary area on 

 the thorax, and to become louder in expiration. One 

 might expect intensification with inspiration as is 

 noted with other right heart sounds. It is possible that 

 if the audibility of the sound is due to closer approxi- 

 mation of the dilated pulmonary artery to the chest, 

 changes in intensity with respiration are due to alter- 

 ations in the amount of interposed lung. This is 

 merely a conjecture. The mechanism of the respira- 

 tory variation deserves further investigation. In 

 contradistinction to right-sided ejection sounds, those 

 that arise in the aorta are said to be less sharp in 

 quality, audible at i^oth the aortic and mitral areas 

 on the thorax, and less augmented by expiration. 



Third, the term systolic click, which has been 

 applied to a number of systolic acoustic events, refers 

 to the sharp clicking sound heard often in midsystole 

 or late systole, though it may occur at any time in 

 systole. Systolic clicks may be single or multiple and, 

 when multiple, may be mistaken for a systolic murmur. 

 There is no certain explanation as to their site of ori- 

 gin. The current opinion of interested observers sug- 

 gests that they are most likely extracardiac in origin, 

 coming possibly either from the pericardium or from 

 the pleuropericardial junction. The fact that these 

 events occur at varying times in systole, either spon- 

 taneously or with respiration, lends credence to the 

 suggestion that they are not related to or produced 

 by an intracardiac hemodynamic event. These 

 acoustic phenomena in them.selves appear to carry no 

 clinical significance, though they have often been 

 heard following episodes of pericarditis or in the 

 presence of extensive pleural in\'olvement from tu- 



berculosis (68). Their clinical importance lies mainly 

 in the fact that they may be mistaken for other less 

 benign events. 



It is suggested that the term systolic click be re- 

 served for this type of acoustic event, and that the 

 term ejection sound be used to refer to the early 

 sound described above. The term ejection click or 

 early systolic click, although descriptive of the event, 

 may lead to a confusion of terms. 



PERICARDIAL FRICTION RUB. In situations in which the 

 normal lubricating function of the apposed layers of 

 pericardium is lost, the movement of the heart within 

 these diseased membranes may cause them to produce 

 audible acoustic events. In most circumstances the 

 sounds produced have a to-and-fro quality with one 

 component during ventricular systole and the other 

 in diastole, more commonly presystole but at times 

 protodiastole. Occasionally all three components are 

 audible. The sounds are usually described as leathery 

 or scratchy and traditionally are said to sound as 

 though they are close to the ear. Due undoubtedly to 

 the nature of the pathology, which always is transient 

 and often varying in degree, there are character- 

 istically marked changes in the intensity and location 

 of the sounds and often of the presence or absence of 

 the several components with time. Localization on 

 the chest for the same reason is also x'ariable. The most 

 frequent clinical problem is that of certain differenti- 

 ation between these pericardial sounds and murmurs 

 of intracardiac origin. The problem if not solved by 

 one observation may often be resolved by serial obser- 

 vations. 



Aiiirmtirs 



In the discussion on the physical basis of murmur 

 production it was pointed out that these acoustic 

 events arise out of disturbances in the pattern of 

 blood flow. The location within the circulation at 

 which the disturbance arises and its time-course in 

 the cardiac cycle are dependent upon both the ana- 

 tomical structure involved and the physiological cir- 

 cumstances at the time of its production. Certain 

 anatomical lesions cause changes in the pattern of 

 blood flow at the lesion and at specific times in the 

 cardiac cycle, and thereby produce characteristic 

 acoustic information. In this circumstance, the re- 

 lationship between the lesion and the murmur is 

 close, and the murmur may be virtually diagnostic or 

 even pathognomonic. Wlien the hemodynamic conse- 

 quences of any given lesion are atypical or when two 



