5i6 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



distensible. The net results of these altered atrial 

 dynamics are shown in figure 21 (upper). During 

 efferent vagal nerve stimulation the atrial '"a" waves 

 are diminished, the mean atrial pressure is increased, 

 and ventricular end diastolic pressure decreased in 

 spite of a longer diastole. 



Whereas the relation between ventricular end 

 diastolic pressure and stroke work is determined only 

 by the performance characteristics of the ventricle, 

 the relation between mean atrial pressure and stroke 

 work is determined by the performance charac- 

 teristics of the atrium as well as the ventricle. The 

 importance of these considerations is exemplified by 

 the plot of mean left atrial pressure against cardiac 

 output in figure 20 (lower, panel C), an experiment in 

 which it was demonstrated that efferent vagal nerve 

 stimulation had no effect on the performance charac- 

 teristics of the ventricle (fig. 20, lower, C). When 

 the transport function of the atrium was inhibited by 

 vagal stimulation, mean left atrial pressure had to be 

 2 cm H2O higher in order to maintain a cardiac out- 

 put of I liter per min. At 2 liters per min it had to be 

 5 cm H2O higher and at 3 liters per min it had to be 

 1 1 cm H2O higher. Since such data indicate the im- 

 portance of a normally functioning atrium, it invites 

 consideration of the possibility that when an elevated 

 venous pressure is observed, failure of the atrium as 

 well as the ventricle mav be a contributing factor 

 (67a). 



F. Effect of Autonomic Xerve Stimulation on 

 Closure of the Mitral Valve 



The mechanisin of closure of atrioventricular 

 valves has not been one which can be descriised with 

 certainty. One authoritative view (64) summarizes 

 the present status with the statement "undoubtedly 

 the most important factor in all valve closure is a 

 change in polarity of the pressure differential across 

 the valve orifice. In the case of the atrioventricular 

 valves the rise in ventricular pressure (through con- 

 traction of the ventricle) above that in the atrium is 

 the most important factor in closure."" There is little 

 basis for disputing McKusick"s first sentence; the 

 second one, as will be shown below, may be open to 

 question. 



Henderson & Johnson (47) in 1912, after studying 

 excised heart valves, postulated that a ventricular 

 systole not preceded by an atrial systole would pro- 

 duce regurgitation because the valve leaflets had not 

 been apposed by the jet effect through the valve. 

 .'\lihout;ii we agree witii the end result of their 



analysis we nevertheless concur with Wiggers" objec- 

 tion to their explanation (127). Evidence that the 

 activity of the atrium is relevant to AV valve closure 

 is to be found in the experiments of Prinzmetal et at. 

 (76), who observed the atrium to enlarge after experi- 

 mentally inducing atrial fibrillation. After inducing 

 atrial fibrillation, Daley et al. (33) were able to 

 recover from the atrium more of the dye which had 

 been injected into the ventricle than during normal 

 rhythm. The frequency of tricuspid regurgitation in 

 patients with atrial fibrillation (69) also indicates the 

 importance of atrial systole for A\' valve closure. 

 Although it may be objected that the hearts of such 

 patients are diseased, this objection loses some of its 

 weight when the regurgitation appears with the 

 on.set of fibrillation and disappears when normal 

 sinus rhythm is re-established in the same patient (69). 



From the point of view of both demonstrable evi- 

 dence and the conceptual analysis of the problem. 

 Little (59, 107) has contributed more to the under- 

 standing of tricuspid valve closure than any other 

 single investigator. He observed that, subsequent to 

 atrial systole, when pressure in the right atrium is 

 falling, the pressure in the right ventricle is, after a 

 brief decline, well maintained. Further, he appre- 

 ciated the significance of his observations. However, 

 even Little entertains a certain dichotomy in regard 

 to this question for, although he does mention that 

 "the reversal of the normal atrioventricular pressure 

 gradient as a result of atrial relaxation results in at 

 least a momentary backflow of blood into the atrium," 

 he nevertheless concludes that ''the increase in 

 ventricular pressure resulting from atrial systole is 

 sufficient to reverse the atrioventricular pressure 

 gradient before the onset of ventricular contraction.'" 



The tracings from the left atrium and ventricle 

 shown in figures 10, 23, and 28 are relevant to this 

 problem and afford the basis for a certain degree of 

 conceptual simplification. In figure 10, which shows 

 tracings from a ventricle on the low or sensitive part of 

 its pressure-length curve, attention is drawn to the 

 stepwise and plateau-like elevation of ventricular 

 pressure after each atrial beat. Further, the sustained 

 increase in ventricular segment length subsequent to 

 each atrial systole is noteworthy. In figure 23.4 the 

 upward arrow indicates the tracing of left atrial pres- 

 sure, and the downward arrow indicates a super- 

 imposed tracing of left ventricular diastolic pressure. 

 An unequivocal ventriculo-atrial pressure gradient, 

 at times amounting to more than 8 cm H.;0, is estab- 

 lished as a consequence of atrial systole and what 

 must certainlv ha\e been mitral \al\e closure. As 



A 



