STENOSIS AND INSUFFICIENCY 



665 



hanced by increases in atrial pressure, ventricular 

 filling, viscosity of the blood, celerity of ventricular 

 contraction, and by lateral pressure effects on the 

 regurgitant orifice. The tendency to mitral regurgita- 

 tion was, on the other hand, increased by a rise in 

 systemic arterial pressure, enlargement of the regur- 

 gitant orifice, or reduced celerity of ventricular con- 

 traction. 



Rodbard and Williams also discussed the influence 

 of the relative positions of the aortic and mitral orifices 

 to each other. The proximity of the aortic orifice to 

 the mitral opening was found to reduce the tendency 

 to reflux, because of competition of the two valve 

 areas for streamlines of flow. 



Wiggers & Feil (204) produced acute mitral in- 

 competence in dogs and studied the influence of the 

 lesion on atrial, ventricular, and aortic pressure 

 pulses, as well as on atrial and \entricular volumes. 

 Immediately after the induction of the lesion, the 

 volume of blood was reduced in the aorta and in- 

 creased in the left atrium. There was thus an increase 

 in initial pressure of the left ventricle, confirming 

 Straub's earlier observations that there was a definite 

 retention of blood in the left ventricle that increased 

 its diastolic volume. The tidal volume during mitral 

 insufficiency represents the amount of the systolic 

 discharge into the aorta and the volume regurgitated 

 into the left atrium. Experiments conducted by Wig- 

 gers and Feil indicated that within a few beats after 

 the production of a leak the systolic discharge was 

 restored approximately to normal, due to the in- 

 creased ejected volume. 



This compensation may be explained by the follow- 

 ing: The higher left atrial pressure and greater dias- 

 tolic inflow supply a larger volume for systolic ejection. 

 The mechanism whereby the left ventricle can expel 

 this larger volume is the increased initial tension 

 within the ventricle. By increasing the velocity of 

 pressure developed, as well as the force of its stroke, 

 the larger inflow is actually expelled from the ven- 

 tricle during systole. Should this mechanism fail, 

 systolic residues would progressively accumulate, 

 rapidly and fatally dilating the ventricles. The amount 

 of regurgitation in these experiments was not meas- 

 ured, and the conclusions may not be valid except 

 for acute and moderate size leaks. 



The compensation in forward blood flow does not 

 include the restoration of aortic and left atrial pres- 

 sures to normal, for once the arteriovenous balance 

 has been upset the arterial system contains less blood 

 and the left atrium more. In the acute experiments 

 by Wiggers & Feil (204) no peripheral compensa- 



tory mechanisms came into play, which may explain 

 why they did not find any back pressure effects in 

 the pulmonary artery or on the right heart; nor did 

 they find complete restoration of aortic pressure to 

 normal. 



The chief backflow occurred during systolic ejec- 

 tion and during a short interval (0.08 to 0.09 sec) 

 into diastole. Little regurgitation occurred during 

 the early phase of the systolic isometric tension in- 

 crease. 



When arterial resistance was increased in the 

 systemic circuit the regurgitant volume at once in- 

 creased markedly, thereby raising the left atrial pres- 

 sure and causing a damming back of blood into the 

 pulmonary artery and right heart [see also (61)]. 



In the anesthetized open-chest dog, Braunwald 

 et al. (29) studied the effect of varying amounts of 

 mitral regurgitation, using a specially designed prepa- 

 ration which permitted accurate measurement of the 

 regurgitant flow. This regurgitant flow occurred 

 through a separate connection between the ventricle 

 and atrium. 



Mitral regurgitant flows, from nothing to three 

 times resting cardiac output, were tolerated with 

 slight alterations of efi'ective cardiac output, aortic, 

 left atrial, and left ventricular pressures. There was 

 little depression of the efi'ective left ventricular func- 

 tion curves with regurgitant flows of approximately 

 2 liters per min. Any given increase in regurgitant 

 flow required substantially smaller increments in 

 ventricular filling pressure than similar increases in 

 effective cardiac output. With any given regurgitant 

 orifice, regurgitant flow was a function of aortic 

 pressure. 



When left atrial pressures were initially elevated 

 by producing high effective left ventricular work 

 levels and mitral regurgitation then progressively 

 increased, substantial increments in mean left atrial 

 and left ventricular filling pressures were produced. 

 The extent of this rise, resulting from anv given 

 degree of mitral regurgitation, was a function of the 

 mean left atrial pressure prior to the induction of 

 regurgitation. The importance of the relationship 

 between myocardial contractility and the hemody- 

 namic effects of any given mitral regurgitant lesion 

 was stressed (fig. 6). 



The experimental design did not allow the regurgi- 

 tant flow to go through the mitral valve. The com- 

 petition between mitral and aortic orifices, discussed 

 by Rodbard and Williams, therefore did not come 

 into play and the results may not be strictly compar- 

 able to those found in the intact circulation. 



