DYNAMICS OF PULMONARY CIRCULATION 



1693 



tion similar to that of Newman, but rejected the idea 

 that the volume term in that equation could stand 

 for a significant physiological volume because, in the 

 physiological circuit, there is neither instantaneous 

 nor complete mixing of dye with all of the blood in 

 either heart or lungs. It now seems that the 1932 view 

 is correct (1 1 1, 283, 417). 



bradley: equilibration curves. The method origi- 

 nally devised by Bradley et al. for the estimation of 

 splanchnic blood volume (41) has been applied by 

 others to the estimation of the pulmonary blood vol- 

 ume (326). The method entails the determination of 

 the amount of tracer substance contained in the sys- 

 tem at equilibrium (cardiac output X arteriovenous 

 difference X equilibration time) divided by the 

 equilibration concentration of tracer. From the point 

 of view of application to the lungs, the most vul- 

 nerable part of the equation is the arteriovenous 

 difference. Experiments with models have shown that, 

 in contrast to the splanchnic circulation, the pul- 

 monary circulation is not suited for this type of 

 equilibration method (46). Consequently, it is difficult 

 to place much confidence in the measurements in man 

 which find that all three methods — the Stewart- 

 Hamilton, Bradley, and Newman — provide com- 

 parable values for the pulmonary blood volume 

 (326), particularly when there are other theoretical 

 and practical reasons to expect discrepancies ( 1 1 1 ) . 



Changes in Pulmonary Blood Volume 



Many different approaches have been used to detect 

 a change in pulmonary blood volume. They include: 

 a) lung volumes, b) mechanics of breathing, c) radio- 

 active tracers, d) teeter board. 



lung volumes. In normal subjects the vital capacity 

 is less in the supine than in the upright position. Al- 

 though part of this decrease may reflect a change in 

 the position and tone of the diaphragm (296, 388), 

 an increase in the pulmonary blood volume also seems 

 to be involved since measures which interfere with 

 systemic venous return to the lungs minimize, or 

 prevent, the decrease in vital capacity (188). 

 Clinically, a low vital capacity is found in pulmonary 

 congestion (406). However, in such patients, par- 

 ticularly if pulmonary venous hypertension has been 

 prolonged and severe, the lung volumes may be more 

 encroached upon by pulmonary edema and fibrosis 

 than by an expanded pulmonary blood volume (238, 

 378). 



mechanics of breathing. Pathologists have long been 

 aware that the chronically congested lung is a stiff 

 lung (415). In 1934, Christie and Meakins showed by 

 measurements of pleural pressure in vivo that the 

 chronically congested lung requires a greater dis- 

 tending force than the normal lung (287). Since then, 

 more elaborate ways of measuring and expressing 

 pulmonary distensibility, such as "compliance" 

 (change in lung volume per unit change in pleural 

 pressure) have come into general use for the study of 

 both acute and chronic pulmonary congestion; for 

 the sake of safety and expediency, and at some sacrifice 

 of accuracy, esophageal pressures have been substi- 

 tuted for pleural pressures (fig. 26) (287). 



The effects of acute pulmonary engorgement on 

 pulmonary distensibility have been examined in ani- 

 mals (35, 146) and in man (33, 406). Such studies 

 have shown that pulmonary venous hypertension has 

 a considerably greater effect in reducing pulmonary 

 compliance than does either pulmonary arterial 

 hypertension or an increase in pulmonary blood flow 

 (35); moreover, a decrease in vital capacity parallels 

 a decrease in pulmonary compliance (406). But these 

 studies have also clarified some of the uncertainties 

 which attend the use of a change in compliance as a 



TIDAL 



VOLUME 



ml 



ESOPHAGEAL PRESSURE 

 cm H 2 



200 



60 



25 



20 



03 



COMPLIANCE 



2U 



cm H 2 



WORK AGAINST 



NON -ELASTIC 



RESISTANCE 



(%) 



WORK OF 



BREATHING 



Kq m 



lit V E 



fig. 26. Comparison of the pulmonary pressure-volume dia- 

 gram of a normal subject with that of a patient with severe 

 pulmonary congestion due to mitral stenosis. In the congested 

 lung, the compliance (AV/AP) is approximately a third of 

 normal and the resistance to air flow is normal. If pulmonary 

 congestion is accompanied by edema of the airways ("cardiac 

 asthma"), both the increased resistance to air flow and the 

 stiffer lungs contribute to the inordinate work of breathing. 

 [After Turino & Fishman (406).] 



