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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



hypertension which followed the induced (transient) 

 imbalance between the outputs of the two ventricles 

 (411). 



Since then, many other experimental procedures 

 have been used to produce pulmonary edema: 

 vagotomy, vagal stimulation, intravenous infusion of 

 fluid, left heart failure, increase in intracranial 

 pressure, exhibition of epinephrine, and exhibition of 

 ammonium chloride (411)- These share a common 

 denominator: an excessively high pulmonary venous 

 and capillary pressure. Accordingly, they are con- 

 sistent with Welch's hypothesis; and, the origin of 

 the pulmonary edema which these procedures effect 

 is to be regarded in the light of Starling's law of 

 transcapillary exchange (1 74). 



It would be misleading to imply that an inordinate 

 filtration pressure in the pulmonary capillaries 

 underlies all types of experimental and clinical 

 pulmonary edema. For example, the pulmonary 

 edema caused by a-naphthylthiourea does seem to 

 depend on an increase in capillary permeability 

 (114); an increase in capillary permeability has also 

 been postulated to account for the bilateral pulmonary 

 edema which follows the injection of a starch sus- 

 pension into a lobar pulmonary artery (227). How- 

 ever, continued emphasis on hemodynamic balances 

 promises to be rewarding for several reasons: a) the 

 usual forms of pulmonary edema do seem explicable 

 in terms of the usual determinants of transcapillary 

 exchange of water, solutes, and colloids, i.e., in terms 

 of Starling's law (174, 385, 411); b) many earlier 

 types of so-called "'neurogenic" pulmonary edema 

 disappeared when subjected to analysis in terms of 

 conventional hemodynamic parameters (64, 372); 

 < ) uncertainties as to the precise mechanisms involved 

 in special types of pulmonary edema are bound to 

 prevail until elusive parameters, such as capillary 

 pressure, volume, and permeability on the one hand, 

 and the role of the lymphatics on the other, can be 

 precisely measured and defined in quantitative terms 

 (325); and d) mysterious influences should only be 

 given credence when the local hemodynamic and 

 physicochemical mechanisms operating across capil- 

 lary walls have been taken into full account, and found 

 wanting (217). 



Pulmonary Hypotension 



During bleeding to the point of systemic arterial 

 hvpotension as well as during traumatic and his- 

 tamine shock, the circulating blood volume, the 

 cardiac output, and the central venous pressures 



decrease (100, 289, 391). However, despite the pro- 

 gressive decline in systemic arterial and left atrial 

 blood pressures, the pulmonary arterial pressure 

 tends to stabilize at approximately two-thirds of its 

 initial value. This stability presumably involves the 

 gradual closure of portions of the pulmonary vascular 

 tree as intraluminal pressures in these areas fall. As a 

 result of the preferential closure of certain portions of 

 the pulmonary vascular tree during systemic hypo- 

 tension, the affected portions of the lungs become 

 excessively ventilated for their perfusion, leading to 

 an appreciable arterial-alveolar difference in carbon 

 dioxide tension (of the order of 8 mm Hg) and to the 

 creation of an "alveolar dead space." Restoration of 

 the circulating blood volume raises the pulmonary 

 arterial pressure to supracontrol values even though 

 slight systemic arterial hypotension persists (160). 



Pulmonarx Arteriovenous Fistula 



The surgical production of a pulmonary arterio- 

 venous anastomosis is associated with a decrease in 

 systemic arterial oxygenation and in pulmonary 

 arterial (mean) pressure. The subsequent course of 

 the experimental animal, as well as the natural 

 history of the human subject with a pulmonary 

 arteriovenous fistula (155), is determined by the size 

 of the shunt and the degree of systemic arterial 

 hypoxemia which it effects. If systemic hypoxemia is 

 sufficiently marked, a considerable polycythemia will 

 ensue leading, in turn, to an increase in the viscosity 

 of the blood, an increase in the resistance to blood 

 flow through the usual resistance vessels and the 

 diversion of more and more of the right ventricular 

 output through the low-resistance shunt (fig. 49). 



Pulmonic Stenosis 



A hindrance to the exit of blood from the right 

 ventricle occurs commonly as a congenital cardiac 

 malformation; either the valve or the infundibulum 

 or the main pulmonary artery may be the seat of the 

 stenosis. Experimentally, stenosis of the pulmonary 

 artery has been produced in different ways (12). In 

 all, severe narrowing of the lesion is necessary before 

 the right ventricle becomes strained. 



In the absence of an abnormally large blood flow 

 across the pulmonary valve, the physiologic hallmark 

 of pulmonic stenosis is right ventricular hypertension 

 coupled with a systolic blood pressure gradient 

 between the right ventricle and pulmonary artery 

 (fig. 50). In acute animal experiments, a constriction 



