666 HANDBOOK OF PHVSIOLOGY — > CIRCULATION I 



S.W L V 

 Gm M 



40 



30 



20 



10 - 



Ao, P 

 mm Hg 



S V 

 cc 



H R 





 15 

 10 



5 





 200 



150 



S M R 



C M R 



M R F = 2 1-24 L /MIN 



e u 



J_ 



_L 



10 15 



L A "Z" Cm H2O 



20 



25 



FIG. 6. Effect on left ventricular curve of mitral regurgitant 

 flow (MRF). sM.R., vvfithout; cM.R., with mitral regurgitation: 

 SWLV, left \entricular stroke work in gram meters; Ao.P., 

 mean aortic pressure; SV, stroke volume; HR, heart rate/min; 

 LA ''Z'\ left atrial Z point pressure. Dog weight, 25.4 kg. 

 [From Braunwald el al. (29).] 



Braunwald et al. (27) in three experiments on 

 dogs, induced mitral regurgitant flows of 2 to 4 

 liter per min while forward cardiac output was held 

 constant. This did not influence the duration of 

 ventricular ejection into the aorta. In contrast, in 

 three other dogs of similar weight, aortic regurgitant 

 flows of 2.2 to 3.5 liters per min were accompanied 

 by substantial increases in the duration of systolic 

 ejection, comparable to those observed when total 

 ventricular stroke volume was increased by similar 

 amounts in the absence of regurgitation. 



STUDIES IN M.AN. From clinical and patho-anatomical 

 observations Edwards & Burchell (54) point out two 

 striking phenomena occurring in mitral incompetence 

 in man. First, mitral insufficiency may be present 

 for years and may be well tolerated up to a certain 

 point. Beyond that point clinical evidence for gross 

 mitral incompetence may become apparent and the 

 disease may continue in a severe, unrelenting, and 

 possibly fulminating manner. Second, in some pa- 

 tients with dilated left ventricles, signs of mitral in- 



competence may be demonstrated during life; but at 

 necropsN' no anatomic basis for the incompetence may 

 be demonstrated either in the nature of the chordae 

 or leaflets. 



These observations may serve to explain many of 

 the different results obtained by different researchers, 

 since it has not been possible, in the intact individual, 

 to separate the myocardial factor from the vahular 

 damage — at least no attempt has been made to 

 analyze these factors in clinical cases. This should be 

 possible now with the aid of the angiocardiographic 

 technique. 



McDonald et al. (149) studied patients with severe 

 symptoms due to mitral valve disease and .separated 

 a larger group with stenosis, as the prominent feature, 

 from a small group with incompetence based on the 

 findings at surgical correction. The size of the mitral 

 orifice was calculated by the Gorlin formula. The 

 statement that a severe degree of mitral stenosis and 

 of incompetence cannot coexist .seems self-evident. 

 McDonald and liis group found in cases with domi- 

 nant incompetence and without significant stenosis 

 that the left ventricular diastolic pressure surprisingly 

 was seldom raised in the presence of marked ele\a- 

 tion of left atrial mean pressure. The elevation of 

 left atrial mean pressiux found was, on the other 

 hand, greater tiian could be caused by a regurgitant 

 jet. Thus a considerable increase of left atrial mean 

 pressure appears to be necessary for sutiicient diastolic 

 blood flow through the mitral valve to maintain the 

 large total left ventricular output (composed of a 

 huge regurgitant flow and a reduced aortic flow). 

 Tills mechanism was, more often than left ventricular 

 failure, the cause of elevated pulmonary pressure in 

 this series of patients with mitral incompetence. 



Davila (43), w-ho studied 58 patients with mitral 

 incompetence during operation, also found a small 

 atrioventricular pressure gradient during diastole 

 in some of tlie cases with pure and pronounced mitral 

 regurgitation. He al.so emphasized the ventricular- 

 atrial svstolic gradient that occurs across the leaking 

 valve (fig. 7) and at least partly determined the 

 amount of regurgitation. This gradient increases after 

 surgical correction of the lesion, due either to a de- 

 crease in atrial pressure or to an increase in left 

 ventricular and aortic systolic pressures. In Davila's 

 series the atrial pressure decreased in most cases. 



Davila also attempted to analyze the dynamics of 

 the left ventricle. The total ejection time of the left 

 ventricle in the aorta shortened slightly with less 

 than normal difference in pressure between the left 

 ventricle and the aorta during the rapid ejection 



