670 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



and/or failure have occurred, the diastoUc pressure 

 is elevated also. The right atrial systolic pressure and, 

 in advanced cases, the atrial mean pressure also, are 

 increased. 



The production of pulmonary stenosis in the ex- 

 perimental animal may thus lead to right ventricular 

 hypertrophy and ultimately failure, when the stenosis 

 is marked enough — in contrast to pulmonary regur- 

 gitation which seems to be of minor importance 

 even when the regurgitation is completely free. This 

 is in good conformance with the findings of Greene 

 et al. (92), who found that half of their reported pa- 

 tients with pure pulmonary stenosis died in right 

 heart failure. 



Tricuspid Vali'ii/ar Deformities 



Barger and his associates (11, 12) created tricuspid 

 incompetence in dogs by tricuspid avulsion. Resting 

 mean right atrial pressure increased 75 to 1 30 mm 

 of water. With exercise the right atrial pressure in- 

 creased further. Despite the elevation of the mean 

 atrial pressure none of the dogs had any gross reduc- 

 tion in work tolerance. 



The changes in the right atrial pressure pulse varied 

 with the extent of insufficiency of the tricuspid \alve. 

 In mild insufficiency atrial pressure was elevated only 

 during \entricular systole. In complete avulsion of 

 the tricuspid leaflets right atrial pressure was nearly 

 identical with right ventricular pressure. 



When pulmonary stenosis also was produced in 

 these dogs the atrial pressure rose further, work 

 tolerance decreased, and right heart failure developed, 

 characterized by markedly dilated right ventricle, 

 elevated atrial pressure and distended veins, dyspnea 

 on exertion, decreased work tolerance, hepatomegaly, 

 ascites, tachycardia at rest, and a relatively fixed 

 heart rate even during exercise. 



Yu et al. (212) reported hemodynamic studies in 

 five patients with tricuspid stenosis and concomitant 

 rheumatic mitral stenosis. The authors point out the 

 presence of a diastolic gradient between the right 

 atrium and ventricle, most pronounced during early 

 diastole. This gradient was accentuated by exercise 

 and was not dependent upon the presence or absence 

 of sinus rhythm. It is of interest that the end-diastolic 

 pressure of the right ventricle was elevated in three 

 of the cases (artifact?). Resting cardiac index and 

 stroke index were subnormal in four patients with 

 decreased stroke output during exercise. 



McCord and collaborators (146, 148) reported 

 hemodynamic studies in three patients with tricuspid 



stenosis of rheumatic origin and associated with mitral 

 stenosis as well. The cardiac index was low, with only 

 a small rise on exercise, moderately elevated pres- 

 sures in the pulmonary artery, and markedly ele- 

 vated right atrial pressure. The authors stress the 

 inadequacy of analyzing only the right atrial pressure 

 pulse for the diagnosis of tricuspid stenosis, since 

 typical changes with increased a waves may occur in 

 right ventricular hypertrophy : During exercise, with 

 its increased blood transport, the abnormalities of 

 the pulse may increase and be easier to evaluate. For 

 exact assessment of the degree of stenosis, both atrial 

 and ventricular pressures must be registered. 



The importance of demonstrating a pressure gradi- 

 ent across the vahe for the diagnosis of tricuspid 

 stenosis must thus be stressed, since right ventricular 

 hypertrophy alone may modify the right atrial pres- 

 sure curve in a way similar to true stenosis. 



In a study in patients with heart disease of varying 

 etiology Korner & Shillingford (122) demonstrated 

 that the effective cardiac output in patients with 

 tricuspid incompetence did not increase on exercise 

 in a normal fashion. They conclude that the regurgi- 

 tant flow through the tricuspid valve is important in 

 maintaining a low, fixed cardiac output in some cases 

 of congesti\'e cardiac failure. This ma\' have a special 

 significance, since right ventricular dilatation in 

 myocardial failure in itself may cause a fiuictional 

 tricuspid incompetence (139, 150). 



The factor of tricuspid incompetence must also 

 be taken into consideration when discussing the role 

 of pulmonary hvpertension in keeping the cardiac 

 output fixed in mitral stenosis, as most cases with 

 such a low and fixed output ha\e signs of tricuspid 

 incompetence, whether the pulmonary arterial blood 

 pressure is markedly elexated or not. 



PULMONARY BLOOD VESSELS AND PULMONARY 

 V.^SCUL.'XR RESIST.ANCE 



The fact that the most conspicuous symptoms in 

 patients with mitral stenosis and ad\anced chronic 

 left ventricular failure originate in the pulmonary 

 circuit has focused attention on the pulmonary vascu- 

 lar bed. Several groups have demonstrated the occur- 

 rence of various degrees of increased vascular resist- 

 ance in the pulmonary circulation. This increased 

 resistance has been thought to be due to anatomical 

 changes in the distal arterial branches ("arterioles"'), 

 to increased tone of these vessels, or to a combination 

 of both (6, 32, 55, 64, 65, 77, 78, 82, 97, 103, 139). 



