DYNAMICS OF PULMONARY CIRCULATION 



1 73 1 



of the pulmonary arterial lumen of at least 40 per 

 cent is needed to raise systolic pressure appreciablv 

 in the right ventricle; greater degrees of constriction 

 are needed to produce right ventricular failure, i.e., 

 dilatation of the right heart, abnormally high end- 

 diastolic pressures in the right ventricle, and tri- 

 cuspid regurgitation (12). Parenthetically, it may be 

 noted that pulmonic stenosis is an excellent physio- 

 logical tool for stimulating the proliferation of the 

 pulmonary collateral arterial circulation (263, 264). 



Pulmonary I 'alvular Insufficiency 



Pulmonary valvular insufficiency has been 

 produced experimentally in dogs (123) and during 

 remedial cardiac surgery in man (fig. 50). After 

 avulsion of the valve, not only does the pulmonary 

 arterial diastolic pressure fall to right-ventricular 



diastolic levels, but a systolic right ventricular- 

 pulmonary arterial pressure gradient may also appear. 

 This gradient is a consequence of unusually rapid and 

 turbulent flow during systole rather than of pulmonic 

 stenosis (123). 



Pulmonic insufficiency is generally regarded as a 

 benign lesion : in dogs, performance on the treadmill 

 as well as end-diastolic pressures in the right ven- 

 tricle remains normal after months of exercise and 

 despite right ventricular systolic pressures approxi- 

 mating 100 mm Hg (12). However, pulmonic in- 

 sufficiency may bring the heart closer to the brink of 

 its reserve so that an additional lesion, e.g., tricuspid 

 insufficiency may precipitate overt heart failure (12). 

 Whether the cardiac reserve is sufficient to tolerate 

 pulmonary valvular insufficiency for a lifetime, or 

 only for a few years, remains to be established. 



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