DYNAMICS OF PULMONARY CIRCULATION 



1727 



dilation, especially in pulmonary hypertensive sub- 

 jects (4, 369, 386). Granting that these agents are 

 often capable of relieving pulmonarv arterial hvper- 

 tension, it has yet to be shown that their hypotensive 

 effect represents pulmonary vasodilation. 



CARDIOPULMONARY DISORDERS 



Pulmonary Arterial Hypertension 



According to the range of normal values described 

 earlier in this chapter, pulmonary arterial hyper- 

 tension exists when pulmonary arterial pressures 

 exceed approximately 30/18 mm Hg. Even such 

 mildly hypertensive levels have been found to strain 

 the heart if continued for a lifetime (363). Moreover, 

 subjects with "high-normal" pulmonary arterial 

 pressures at rest often become pulmonary hyper- 

 tensive when blood flow is increased acutely, as by 

 occlusion of a pulmonary artery (68) or by exercise 

 (132); the latter observations suggest that pulmonary 

 arterial hypertension occurs frequently in the course 

 of daily activities once pulmonary arterial pressures 

 reach "high-normal" levels at rest. 



The causes of pulmonary arterial hypertension 

 may be conveniently sorted into four categories. 

 Three of these are mechanical (passive) : reduction 

 in the extent and distensibility of the pulmonary 

 vascular bed, increase in pulmonary blood flow, and 

 increase in pulmonary venous pressure; the fourth 

 is vasoconstriction (active). Before considering these 

 mechanisms separately, it should be noted that 

 pulmonary hypertension is more often the conse- 

 quence of a complex interplay of mechanisms than 

 of any single influence operating independently. 

 Moreover, in patients with cardiopulmonary dis- 

 orders, it is generally easier to single out the pre- 

 potent mechanism than to try to quantify the relative 

 contributions of all the mechanisms that could con- 

 ceivably be involved (88). 



restricted vascular bed. In normal animal and 

 man, almost two-thirds of the lungs have to be re- 

 moved before pulmonary arterial pressures reach hy- 

 pertensive levels (89, 252). By way of contrast, there 

 are many pulmonary diseases which surreptitiously 

 reduce the number and caliber of small pulmonary 

 vessels and modify the distensibility of the remaining 

 vessels, so that even a normal pulmonary blood flow 

 is associated with marked pulmonary hypertension. 

 Examples of such diseases are pulmonary emboli, 



pulmonary arteritis, interstitial fibrosis and granu- 

 loma, bullous emphysema, and "primary pulmonary 

 hypertension" (341). The architecture of the thorax 

 may also limit the capacity and expansibility of the 

 pulmonary vascular bed : thus, in subjects with severe 

 kyphoscoliosis, the combination of a dwarfed pulmo- 

 nary vascular bed and an adult cardiac output 

 predisposes to pulmonary hypertension (25). 



increase in pulmonary blood flow. It has been 

 indicated previously, that in the normal pulmonary 

 circulation, the cardiac output has to be tripled 

 before pulmonary hypertensive levels are reached 

 (8g). In patients with congenital cardiac defects and 

 left-to-right shunts, pulmonary hypertension may 

 occur even at lower blood flows because of anatomical, 

 and possibly functional, changes in the vessels. An 

 especially interesting situation obtains in patients in 

 whom both the pulmonarv and systemic circulations 

 communicate, as in the reptilian heart, with the left 

 ventricle. In this case, the partition of the left ven- 

 tricular output between the two circulations is a 

 function of their relative resistances: in time, if 

 pulmonary vascular resistance to perfusion increases, 

 the pulmonary blood flow will diminish even though 

 the level of pulmonary hypertension remains un- 

 changed (440). 



INCREASE IN PULMONARY VENOUS PRESSURE. The tWO 



previous causes of pulmonary arterial hypertension 

 are unrelated to the level of the pulmonary venous 

 pressure. But, in the 1 30 years since James Hope, it 

 has become common knowledge that pulmonary 

 venous hypertension leads to pulmonary arterial 

 hypertension (213). Etiologically, pulmonary arterial 

 hypertension of this type generally originates either 

 in mitral valvular disease or left heart failure. In 

 dogs with acute or subacute (up to ten months) 

 mitral stenosis, the increment in pulmonary arterial 

 pressure appears to be a direct consequence of back 

 pressure: as pulmonary venous pressure and pulmo- 

 nary blood volume increase, the pulmonary capillary 

 and arterial pressures also rise, but not to the same 

 degree as the pulmonary venous pressure; since the 

 decrease in the pressure gradient is associated with an 

 unchanged cardiac output, the calculated pulmonary 

 vascular resistance decreases (176). Clinical counter- 

 parts of this experimental situation are rare but do 

 occur; they are characterized by complete restoration 

 of the pulmonary arterial blood pressure to normal 

 as the pulmonary venous hypertension is relieved. 

 The more common clinical situation is one in 



