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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



Meaning of Pulmonary Vascular Resistance 



Generally speaking, the pulmonary circulation — 

 which receives the same blood flow as the systemic 

 circulation at one-fifth the blood pressure — is a low- 

 resistance circuit. In the normal pulmonary circula- 

 tion, the pulmonary vascular resistance is ordinarily 

 of the order of o. i to 0.3 R units (table 1). But in 

 evaluating data for resistance, at least three separate 

 problems are involved: /) the precise measurement 

 of the parameters invoked in the equation for re- 

 sistance, i.e., pressure drop across the pulmonary 

 vascular bed divided by the rate of pulmonary blood 

 flow; 2) the decision as to whether a change in calcu- 

 lated resistance means a change in pulmonary vascu- 

 lar caliber; and 3) the interpretation of a change in 

 caliber in terms of the mechanism which effected it, 

 i.e., vasomotor or passive (61, 132). 



With respect to the values substituted in the equa- 

 tion for resistance, it is self-evident that calculations 

 of pulmonary vascular resistance, which are to be 

 meaningful in vasomotor terms or even in terms of 

 vascular caliber, presuppose accurate measurements 

 of blood flow and pressures. Under certain stressful 

 conditions, such as exercise, acute hypoxia, and acute 

 hypercapnia, heightened respiratory excursions com- 

 plicate the precise measurement of pressures, and pul- 

 monary blood flow is easily miscalculated. Moreover, 

 Permutt and co-workers have recently likened the 

 pulmonary vessels to a series of Starling valves and 

 warned against blind faith in the left atrial (or pul- 

 monary venous) pressure as a measure of pulmonary 

 outflow pressure. In particular, they have stressed 

 that any situation in which alveolar pressure exceeds 

 pulmonary venous pressure, by creating a discon- 

 tinuity in pressure between the capillaries and the 

 pulmonary veins, invalidates the use of the pulmonary 

 venous pressure for the calculation of total pulmonary 

 vascular resistance (315, 354). Accordingly, just as the 

 studies of West et al. (427) suggest a spectrum of 

 ventilation-perfusion relationships in the lung of up- 

 right man, the model of Permutt et al. (unpublished 

 observations) suggests a distribution of the de- 

 terminants of resistance to perfusion, depending on 

 the relationships of pulmonary arterial, left atrial, and 

 alveolar pressures in the different parts of the upright 

 lung. The precise relationships between the normal 

 imbalances between ventilation and perfusion on the 

 one hand, and the interplay of alveolar and pul- 

 monary vascular pressure on the other, remain to be 

 elucidated. 



With respect to the second problem, i.e., the equa- 



tion of a change in calculated pulmonary vascular 

 resistance to a change in pulmonary vascular calibers, 

 there are at least two different types of enigmas. One is 

 the possibility that a change in "anomalous viscosity," 

 which is customarily disregarded, may masquerade 

 as a change in caliber (197, 260, 430); since this 

 source of confusion is most apt to become appreciable 

 when pulmonary blood flow drops to exceedingly low 

 levels, the practice of ignoring it seems reasonable as 

 long as levels of pulmonary blood flow are of the same 

 order of magnitude as that ordinarily encountered 

 in vivo. The other is the equivocal anatomical mean- 

 ing of a change in caliber, since a change in geometry 

 may arise not only from a change in the diameters of 

 patent vessels but also a change in the number of 

 parallel paths which are being perfused (267). 



Finally, before pulmonary vasomotricity can be 

 invoked, it is axiomatic that all conceivable passive 

 mechanisms for affecting vascular calibers (table 2) 

 be taken into full account. One such passive mecha- 

 nism, particularly likely during artificial ventilation, 

 is the mechanical distortion of the vessels by adjacent 

 lung tissue at abnormal lung volumes (397)- Another, 

 more universal, source of confusion is an undetected 

 change in transmural pressure operating subtly to 



table 2. Factors Conceivably Involved in a Change 

 in Pulmonary Vascular Resistance 



MECHANICAL (PASSIVE) 



Passive cardiocirculatory effects 



1 . Back pressure from left atrium or pulmonary veins 



2. Change in pulmonary blood flow 



3. Change in pulmonary blood volume 



4. Bronchial collateral circulation 



a) Nutrition of nerves, ganglia, and smooth muscle 



b) Patency of collateral circulation 

 Passive respiratory effects 



1 . Change in alveolar pressures 



a) Tone of bronchial smooth muscles 

 bl Secretions of bronchial glands 



c) Alveolar surface tensions 



2. Change in intrathoracic pressures 



3. Tone of interstitial smooth muscle 



4. Pericapillary edema 



VASOMOTOR (ACTIVE) 



Originating from without the lungs 



1. Autonomic nervous system (including systemic chemo- 



receptors) 



2. Catecholamines 

 Originating within the lungs 



1. "Critical" closure of small muscular vessels 



2. Intravascular chemoreceptors 



3. Chemical stimuli (directly on vascular muscle) 



4. Deranged vascular metabolism 



5. Local reflexes 



