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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



which the pulmonary arterial pressure is inordinately 

 high for the level of the pulmonary venous pressure, 

 the pulmonary blood volume is not abnormally 

 large, and relief of the pulmonary venous hypertension 

 does not completely restore the pulmonary arterial 

 pressure to normal levels. In such patients, the 

 persistence of pulmonary arterial hypertension after 

 relief of the back pressure is attributable to secondary- 

 effects, i.e., to anatomical changes in the lungs and 

 vessels, possibly abetted by constriction of the small 

 pulmonary arteries (238). 



One prevalent notion about chronic pulmonary 

 venous hypertension is that it elicits "protective" 

 vasoconstriction of pulmonary precapillary vessels. 

 Although it is self-evident that pulmonary arterial 

 hypertension must occur if sufficient forward flow is 

 to continue in the face of pulmonary venous hyper- 

 tension, the teleological advantage of pulmonary 

 precapillary vasoconstriction is not entirely clear: 

 heightened "arteriolar" tone would increase the 

 pressure work of the right heart and only reduce 

 capillary blood pressure if it succeeded in reducing 

 the pulmonary capillary blood flow. Teleologically, 

 the prevention of undue filtration pressures in the 

 pulmonary capillaries would be more economically 

 accomplished by quieting the heart rather than by- 

 increasing the right ventricular work. Indeed, the 

 inability to resolve the question of protective vaso- 

 constriction again emphasizes that pulmonary vaso- 

 motor activity is exceedingly difficult to recognize 

 in the abnormal pulmonary circulation, particularly 

 when structural changes have extended beyond the 

 vessels into the surrounding lung. 



PULMONARY ARTERIAL VASOCONSTRICTION. In normal 



dog, cat, and man, pulmonary arterial vasocon- 

 striction rarely evokes more than a mild pulmonary 

 hypertension. On the other hand, in cattle, con- 

 traction of the sphincteric pulmonary arterioles 

 often effects dramatic increases in pulmonary arterial 

 pressure (199). This correlation between vascular 

 structure and the intensity of the pulmonary vascular 

 response raises the prospect that pulmonary vascular 

 disease may, by thickening vascular media, enable 

 the small muscular vessels to contract with unusual 

 vigor. However, this ingenious notion has yet to be 

 critically tested (181). 



Cor Pulmonale 



Pulmonary hypertension attracts clinical attention 

 when it causes the right heart to enlarge (dilate or 



BRONCHITIS 



AND 

 EMPHYSEMA 



/ 



\ 



RESTRICTED 



PU LMONARY 



VASCULAR BED 



ALVEOLAR 

 HYPOVENTILATION 



\ 



/ 



PU LMONARY 

 H Y PERTENSION 



COR 

 PULMONALE 



HEART 

 FAILURE 



fig. 48. The evolution of cor pulmonale and right heart 

 failure in chronic pulmonary emphysema. Alveolar hypo- 

 ventilation contributes to pulmonary hypertension by way of 

 hypoxia and respiratory acidosis: hypoxia elicits pulmonary 

 vasoconstiiction, polycythemia, hypervolemia, increased blood 

 viscosity, and increased cardiac output; acidosis elicits pulmo- 

 nary vasoconstriction. 



hypertrophy) or to fail. The term cor pulmonale is 

 generally reserved for right ventricular enlargement 

 which originates either in diffuse pulmonary disease 

 or in ineffective performance of the chest bellows. As 

 a rule, pulmonary hypertension underlies cor pul- 

 monale; in some types of lung disease, particularly 

 those associated with hypoxemia, the abnormal 

 pressure work of the right heart may be supple- 

 mented by an abnormally high cardiac output, i.e., 

 flow work (89, 339, 341). 



It has become clear that the genesis of cor pul- 

 monale is to be sought in the mechanisms which 

 ordinarily determine the normal pulmonarv arterial 

 pressure; only the combinations and the prepotent 

 influences differ. For example, in diffuse interstitial 

 diseases of the lung (e.g., "alveolar-capillary block") 

 anatomic changes in pulmonary vessels and paren- 

 chvma operate without benefit of increased flow or 

 hypoxia. On the other hand, in the concentric alveolar 

 hypoventilation of extreme obesity, respiratory 

 paralysis or kyphoscoliosis, hypoxia and respiratory 

 acidosis elicit pulmonary hypertension in subjects 

 with normal lungs. Finally, in the most common 



