668 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



The right-sided lesions of the semikinar valves 

 are basically not much different from the correspond- 

 ing left-sided lesions, except for the fact that the 

 right \entricle has a weaker myocardium to start 

 with, corresponding to the lower pressure in the 

 pulmonary artery as compared to the pressure in the 

 aorta. The right ventricular myocardium has, how- 

 ever, the same ability for hypertrophy as the left. 

 Many of the right-sided lesions observed usually do 

 not develop until the pressure in the pulmonary cir- 

 cuit has been elevated to a considerable degree. 

 This is mostly due to the occurrence of valvular lesions 

 of the left heart and is part of the natural history of 

 rheumatic heart disease. The lesion then develops in 

 a situation where the right ventricular myocardium 

 is more like the left, due to the existing hypertrophy. 



Some diflerence seems to exist between right and 

 left hearts as the consequence of lesions in the atrio- 

 ventricular valve apparatus. Much of the difference 

 in dynamic behavior of the right and the left atria, 

 respectively, is due to differences in the venous pool 

 behind them. The much larger venous pool behind 

 the right atrium permits more flexibility than the 

 smaller venous pool behind the left atrium, where 

 fairly small pressure rises can have great consequences 

 on the pulmonary circulation and pulmonary func- 

 tion. Fatal pulmonary edema may thus be caused 

 by the regulatory mechanism aiming at adequate 

 peripheral blood flow, and may occur before the 

 myocardium has failed completely. 



Some of the studies reported during recent years 

 have been concerned with the production of conges- 

 tive heart failure in animals. Interference with the 

 pulmonary and/or tricuspid valves seems to be the 

 easiest and perhaps the only feasible way to create 

 chronic congestive failure in dogs similar to the state 

 observed in man. 



Pulmonary Incompetence 



Pulmonic regurgitation has been produced in dogs 

 by complete or partial pulmonary valvectomy (60, 

 118). No change in pulmonary arterial pulse pres- 

 sure was seen when less than one valvular cusp was 

 removed; frequently no change was observed after 

 removal of an aortic cusp. Widening of the pulmonary 

 arterial pulse pressure could be produced by removal 

 of more than one cusp, or by inducing pulmonary 

 hypertension after removal of only one cusp. 



Pulmonary hypertension was instituted by mechani- 

 cal constriction of the pulmonary vascular bed or by 

 hypoxia. In these dogs the systolic pulmonary artery 



pressure was 51 to 76 mm Hg in the preoperative 

 and 59 to 92 mm Hg in the postoperative period. No 

 evidence of right ventricular failure was noted up to 

 6 months after the operation. [Several of these dogs 

 remained in good clinical condition for some years 

 after complete valvulectomy. — Ed.] 



Of a total of nine animals in which the cardiac 

 output was determined, six showed evidence of a 

 diminished cardiac output postoperatively. The 

 diminution was small, and the authors are hesitant 

 to conclude that partial pulmonary valvectomy pro- 

 duces permanent lowering of the cardiac output. 



Kay & Thomas (112) also produced pulmonary 

 insufliciency in dogs with a similar technique and 

 observed more marked hemodynamic changes. One 

 dog died in congestive failure and all 1 5 dogs exhibited 

 signs of right ventricular dilatation. Ten of the dogs 

 had systolic pressures in the right ventricle of 50 mm 

 Hg or more, and in three, the systolic pressure was 

 above 90 mm Hg. The diastolic pressure in the pul- 

 monary artery was low. There seemed to be some 

 systolic gradient over the incompetent valve. Although 

 no determination of blood flow was made, this seems 

 to indicate a large stroke volume with marked regur- 

 gitation, in contrast to the milder regurgitation of the 

 dogs of Fowler et al. (79). 



Barger and collaborators (11), during studies aimed 

 at the creation of right heart failure, could not demon- 

 strate any signs of heart failure or increase in right 

 atrial pressure, even during strenuous exercise in 

 dogs in which pulmonary insufficiency had been 

 created through a\ulsion of the \alve leaflets or 

 through widening of the pulmonary ring. 



Pulmonary regurgitation is a lesion that can be 

 recorded rather frequently following long-standing 

 pulmonary hypertension with or without valvular 

 lesions in the left heart. It is rare as a single occur- 

 rence although some studies of such cases have been 

 reported in the literature (133, 156). These reports 

 indicate that in youth an isolated, although dynami- 

 cally significant, pulmonic valvular regurgitation is 

 well tolerated. As long as the blood pressure in the 

 pulmonary artery is within normal limits or only 

 .slightly elevated, the amount of regurgitation and thus 

 load on the right ventricle seem to be small. This 

 finding is in good agreement with most of the experi- 

 mental studies cited above. 



Pulmonary Stenosis 



Fineberg & Wiggers (73) studied tiie right \cntric- 

 ular and aortic pressures during progressive circular 



