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HANDBOOK OF PHYSIOLOGY ^^ CIRCULATION I 



atrial hemodynamics and tlie jugular venous pulse, 

 acoustico-mechanical correlates can be made which 

 can be used to reflect hemod\namics. For example, 

 the pulmonic component of the second sound denotes 

 the beginning of the phase of isometric relaxation of 

 the right ventricle. The beginning of the v descent ot 

 the jugular \'enoiis pulse, indicating the opening of the 

 tricuspid \'alve, denotes the end of this phase. There- 

 fore, the interval between these two events is a measure 

 of the duration of right \entricular isometric relaxa- 

 tion. Abnormal increases in this interval have been 

 used to indicate pulmonary hypertension (39). Disease 

 of the tricuspid \'alve, Ijoth stenosis and insufficiency, 

 if it reflects itself in changes in right atrial hemody- 

 namics, can be detected in the jugular pulse. Simi- 

 larly, decrease in right ventricular distensibility with 

 increased force of right atrial contraction, as seen, for 

 example, in severe pulmonic stenosis, primary pul- 

 monary hypertension, and others, will be reflected in 

 an increased amplitude of the a wa\e. 



A thoroughgoing study of the jugular venous pulse 

 and its relationship to the acoustic events of the heart 

 has been published by Altmann (i) and should be 

 consulted bv those interested. 



tends to complicate the usefulness of this phenomenon 

 in identification of the components of the second 

 sound. Using a mean figure for time delay one can 

 often be satisfied as to which component is which. 

 However, this is not always the case. .Since there is no 

 s\nchrony of aortic valve closure with the dicrotic 

 notch (as recorded) it can be seen that should any 

 part of the second sound coincide with this ev'ent, it 

 is therel:)y ruled out as aortic valve closure, as is any 

 event that follows the dicrotic notch. These points are 

 often useful. 



Disease of the aortic valve, both stenosis and insuffi- 

 ciency, if it alters central aortic dynamics, will be re- 

 flected in the carotid artery pulse contour. Since, 

 oftentimes, the degree of \alvular in\ol\ement is re- 

 flected in the change in central aortic pulse contour, 

 one may be permitted to see the same correlation with 

 the carotid pulse (22). 



Pulse tracings of arteries more distally situated (i.e., 

 brachial, radial, femoral) may be recorded. They 

 have a value in assessing certain aspects of the arterial 

 circulation, but the uncertainties of transmission time 

 make them unreliable as correlates of the acoustic 

 events of the heart. 



CAROTID ARTERY PULSE. This surfacc phenomenon re- 

 flects directly the time-course, amplitude, and shape 

 of the pulse of the carotid artery, and, indirectly, of the 

 aorta. Here the time delay is agreed tipon to be 

 appreciable, should be measured by those who are 

 using this parameter to correlate with acoustics, and 

 must always be taken into account when used. Again, 

 no thoroughgoing analysis of the relationship between 

 aortic and carotid pulse times has been undertaken 

 for the variety of disease states. It is known that the 

 dicrotic notch of the wave occurs simultaneously with 

 aortic valve closure and traditionally all measure- 

 ments of time delay are made from this feature. Here 

 again the implication is made that over this short dis- 

 tance of arterial tree all phases of the wave travel with 

 virtually the same velocity, an assumption which 

 needs to be investigated. This has greatest bearing, 

 perhaps, on the attempts to define the duration of left 

 ventricular isometric contraction as the inter\al from 

 mitral valve closure (the first loud part of the first 

 heart sound) to the beginning of the upstroke of the 

 carotid pulse corrected by moving the whole curse 

 forward until the dicrotic notch coincides with the 

 aortic valve closin-e sound. 



The unfortunate feature of the problem of the time 

 delay of the pulse reaching the carotid artery is that it 



LOW FREqUENCY RECORDINGS FROM THE THORAX. In 



much the same way that vibrations in the audible 

 frequency range are transmitted to the chest wall, 

 vibrations of lower than audible frequency are also 

 transmitted. These are due apparently to changes in 

 the size, shape, and position of the heart and great 

 vessels during the cardiac cycle. The most commonly 

 used are those caused by the impingement of a cardiac 

 or vascular structure against the anterior and left 

 lateral thoracic wall. These include, in the main, the 

 two ventricles, the pulmonary artery, and at times the 

 aorta. They are not direct mechanical correlates in 

 the sense that intravascular pres.sures or pulses, or their 

 surface representations are, but they do serve as corre- 

 lates, since they reflect certain definite ex-ents. To say 

 that they represent well-defined events would per- 

 haps be overstating the case, since here too a rigorous 

 appraisal of the detailed etiology of these \ibrations in 

 various disease states is not available. 



The most frequently used in empirical clinical corre- 

 lations are those due to ventricular activity. Since 

 either ventricle may be the responsible agent it must 

 be remembered that before acoustic correlation can be 

 carried out the responsible ventricle must be identified. 

 It has been suggested that this can be done with the 

 precordial electrocardiogram (37). Rivero Carvallo's 



