664 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



The increase in cardiac output during physical 

 effort occurs concomitantly with an increase in left 

 atrial pressure, and presumably in the gradient over 

 the stenosed valve. For more marked increases in 

 output the pressure in the pulmonary veins and capil- 

 laries reaches heights which are close to the oncotic 

 pressure of the blood, and favors the transudation 

 of fluid and the appearance of pulmonary edema. 

 When higher values of pulmonary venous pressure 

 are reached, the pulmonary arterial pressure usually 

 increases out of proportion to the increase in venous 

 pressure. 



In some patients with a tight mitral stenosis the 

 left atrial pressure has been found to be compara- 

 tively low, concomitant with a low cardiac output. 

 This has usually been the case in patients with ex- 

 cessive pulmonary arterial hypertension, right heart 

 failure, or both, or in the presence of atrial fibrillation. 



Studies repeated in the same patients after the 

 stenosed valve has been opened (valvulotomy or 

 commissurotomy) have shown decreased pulmonary 

 vascular pressures and increased cardiac output, 

 both at rest and during exercise. There are, however, 

 a certain number of cases where clinical improvement 

 has occurred with only a slight decrease of pulmonary 

 pressures and unchanged or even decreased cardiac 

 output. 



Attempts have been made to influence the cardiac 

 output in patients with mitral stenosis with the use of 

 ganglionic blocking agents, other drugs like digitalis 

 glucosides, or the rapid infusion of various fluids. 

 Generally the output has been increased when digi- 

 talis was given only if congestive heart failure was the 

 reason for the low output (70). When a rapid infusion 

 of dextran was given to patients with mitral stenosis, 

 augmenting the blood volume, the cardiac output 

 rose less than in a comparable study of healthy in- 

 dividuals (177). When hexamethonium was given 

 to block sympathetic impulses, the pressures in the 

 pulmonary circuit fell considerably without change 

 in cardiac output (214). 



These studies thus seem to indicate that neither 

 mechanical factors (increase in filling pressure with 

 augmented blood volume) nor nervous (sympathetic) 

 block alone are responsible for the low cardiac output 

 seen in some patients with mitral stenosis. 



It has been suggested that high pulmonary arterial 

 pressure per se is a factor tending to keep the output 

 low and fixed. A close examination of the literature 

 reveals, however, that only a few cases with such an 

 excessively high pulmonary arterial pressure have 

 been adequately studied during rest and exercise. 



Only when such pressure was associated with signs 

 of right ventricular failure was the output low and 

 fixed. The presence of right heart failure with or 

 without tricuspid incompetence was, on the other 

 hand, more frequently the most obvious finding in 

 the patients with low and fixed output — usually 

 with a moderate rather than an excessive ele\'ation 

 in pulmonary arterial pressure. 



The balance between the maintenance of an ade- 

 quate blood supply to the periphery and avoidance 

 of pulmonary edema is precarious in pronounced 

 mitral stenosis. The range in variations of pressure 

 and flow under these circumstances must necessarily 

 be limited. It is rather remarkable to what extent 

 many patients can carry on a useful life with marked 

 mitral stenosis. An adequate regulation of total 

 cardiac output, heart rate, diastolic filling time and 

 pulmonary lymph flow, as well as the fact that most 

 activities are carried out in the upright position, with 

 the pulmonary blood volume thus relati%-ely small, 

 seems to be of greatest importance. The supposed 

 protective nature of the pulmonary arterial hyper- 

 tension does not seem to be of any great importance 

 in this connection. 



Mitral Incompetence 



Incompetence has always been easier to produce 

 experimentally than stenosis (181). Thus, experi- 

 mental studies of mitral incompetence were started 

 much earlier and provided better information than 

 those on mitral stenosis. It was found early that in- 

 competence of the mitral vahe gave rise to a systolic 

 pulsatile expansion of the left atrium together with a 

 rise of its pressure. It was also suggested early that 

 this pressure rise increased the filling of the left ven- 

 tricle, with restoration of the forward cardiac output, 

 and was transferred to the pulmonary circulation, 

 leading eventually to pulmonary hypertension (178). 



Acute mitral incompetence was produced in dogs by 

 MacCallum & McClure (144). They found an acute 

 decrease of the systemic blood pressure, with marked 

 fluctuations of the left atrial pressure. The pulmonary 

 arterial and systemic \enous pressures remained 

 unchanged in these short-term experiments, except 

 for some change in the pulmonary arterial pulse 

 contour, probably due to the backward transmission 

 of the regurgitant pressure wave. 



The hydrodynamic factors affecting the degree of 

 mitral regurgitation was studied, by Rodbard & 

 Williams (170), in specially constructed models. They 

 concluded that forward flow into the aorta was en- 



