STENOSIS AND INSUFFICIENCY 



673 



normal or almost normal pulmonary and systemic 

 hemodynamics (and who usually were free of symp- 

 toms except during strenuous exercise). In patients 

 with more marked alteration of pulmonary hemo- 

 dynamics and already with symptoms during; slight 

 activity, the renal blood flow was lower but the 

 glomerular filtration rate was still within normal 

 limits. In still more disabled patients — i.e., with more 

 tight mitral stenosis — these functions were also more 

 depressed, with a decrease of glomerular filtration 

 rate as well. In a fairly small group with clinically 

 overt symptoms of right heart failure the findings 

 were qualitatively the same, although those in failure 

 had lower total blood flow, higher pulmonary ar- 

 terial pressure, higher pulmonary vascular resistance, 

 elevated renal venous (or right atrial) pressure, and 

 slightly lower renal blood flow. Studies conducted 

 during exercise showed that these patients reacted 

 with more pronounced decrease in renal blood flow 

 during a slight e.xercise test than normal individuals, 

 with a concomitant decrease in sodium excretion. 



It was also found that the alterations in renal blood 

 flow and renal function had no patho-anatomical 

 basis but seemed to be due to some regulatory mecha- 

 nism. Hydralazine, fever, pregnancy, or the infusion 

 of 3 per cent glucose in water thus increased the renal 

 blood flow to or toward normal figures. The possible 

 pathway for this regulatory mechanism could not be 

 defined. There was no good correlation between the 

 renal changes, on the one hand, and cardiac output, 

 arteriovenous oxygen difTerence, pulmonary wedge, 

 or pulmonary arterial pressure, on the other. The 

 stroke output seemed to be fairly well correlated with 

 the renal findings. 



Similar results were obtained by Barger and asso- 

 ciates (10-12) who studied the influence of graded 

 destruction of the right heart valves on the renal 

 function in the dog. They demonstrated that the 

 renal response to exercise was altered earlier than 

 general hemodynamic changes could be found. In 

 further studies they showed that creation of minimal 

 heart lesions (pulmonary insufficiency) changed the 

 renal response to aldosterone or norepinephrine 

 from the normal toward what was found in the dog 

 with congestive failure. 



The renal changes seemed to be more marked with 

 mitral valvular disease than with aortic or congenital 

 heart disease, which is of interest in view of what was 

 found by Huckabee (106) regarding the anaerobic 

 capacity of the heart in these valvular lesions. 



Donald and his group studied the behavior of the 

 blood flow in several regions, notably splanchnic. 



muscular, and cerebral flow in patients with mitral 

 stenosis. They found that the blood flow to the exer- 

 cising muscles (50) was about 8 per cent of that found 

 in normal subjects with a normal cardiac output re- 

 sponse to effort. As the cardiac output in the patients 

 with mitral stenosis was low and fixed, the increase 

 in blood flow to the exercising muscles was achieved 

 by a considerable reduction of blood flow to the whole 

 skin, to muscles not involved in the exercise, to the 

 splanchnic area, and the kidneys. Only the cerebral 

 flow was exempt and continued at the resting level, 

 whereas the coronary flow was presumed to be suffi- 

 cient, since the patients did not complain of any 

 anginal symptoms. Donald suggests that both humoral 

 and neural mechanisms were responsible for the 

 integrated circulatory response in patients with 

 cardiac disease during mild exercise. 



Huckabee & Judson (107) have developed a 

 method to evaluate the anaerobic metabolic rate in 

 man, in order to study the adequacy of peripheral 

 flow. By determining total body water, arterial and 

 venous oxygen concentration, oxygen con.sumption, 

 cardiac output, and the levels of blood pyruvate and 

 lactate, they were able to calculate the "excess" 

 lactate production, which is defined as the amount of 

 lactate produced above that secondary to nonh\poxic 

 causes. This serves as an estimate of the energy derived 

 from the anaerobic lactate dehydrogenase system. 

 In normal subjects 5 per cent of the energy required 

 during mild exercise was supplied through anaerobic 

 metabolism, whereas in patients in heart failure 20 

 to 50 per cent of the energy needed for mild exercise 

 was supplied by anaerobic metabolism [see also (i 76)]. 



Huckabee (106) also studied several patients not in 

 failure. These consisted of 1 1 patients with mitral 

 valvular disease (7 patients with mitral incompetence 

 and 2 with both stenosis and regurgitation), 6 pa- 

 tients with aortic valvular deformity (2 stenosis and 

 4 regurgitation, or both stenosis and regurgitation), 

 2 with tricuspid regurgitation and two with pulmonic 

 valvular stenosis. All cases were studied at rest and 

 during exercise, and the excess lactate concentration 

 and anaerobic metabolic rate were calculated to 

 judge the efficiency of cardiac performance. Although 

 all patients considered themselves to be completely 

 well and were engaged in full-time work, Huckabee 

 demonstrated a definite abnormality of cardiac output 

 response in patients with atrioventricular valve de- 

 formity, whereas those with semilunar valve deformity 

 showed a normal response to exercise. Huckabee 

 thought that the decreased response to slight physical 

 activity in the patients with mitral or tricuspid disease 



