[684 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



PULMONARY 

 ARTERY 



SYSTEMIC 

 ARTERY 



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80 



VENOUS ADMIXTURE 



fig. 14. Model of the lungs. Any inhomogencity of ventilation and perfusion is represented as 

 "virtual venous admixture." Pulmonary arteriovenous shunts appear as •'anatomical venous ad- 

 mixture." According to this model, the alveolar-arterial difference in oxygen tension may be sub- 

 divided into three components: diffusion, virtual venous admixture, and anatomical venous ad- 

 mixture. As indicated in the text, this is an oversimplification. [After Briehl & Fishman (51).] 



327, 345): the standard tactic is to express deviations 

 from homogeneity in terms of their effect on the 

 alveolar-arterial differences in oxygen tension ("A-a 

 gradient"). By partitioning the A-a gradient into 

 three components (fig. 14), it is possible not only to 

 identify the venous admixture component, but also 

 to separate it into anatomical and "virtual" portions; 

 the "virtual" venous admixture is then an expression 

 of the inhomogeneity of pulmonary capillary perfusion 

 with respect to other gas-exchanging parameters 



(14. 23, 51). 



The picture which has emerged from this type of 

 approach is illustrated in figure 15: alveoli which 

 are excessively perfused for their ventilation (V A /Q 

 < 0.8) contribute to the virtual venous admixture; 

 those which are perfused but nonventilated (V A /Q. 

 = o) appear as anatomical venous admixture; those 

 which are excessively ventilated for their perfusion 

 (V A /Q. > 0.8) contribute to the "physiological" dead 

 space, the "alveolar" dead space, and to the alveolar- 

 arterial gradient for carbon dioxide (347* 377)- 



While this model is the basis of much of contempo- 

 rary thinking about the distribution of blood flow 

 with respect to gas exchange, it is known to be inade- 

 quate on several practical and theoretical accounts: 

 a) the fractionation of A-a gradient is technically 

 difficult and apt to be imprecise, especially in patients 

 with diffuse pulmonary disease; b) the model does 

 not recognize other inhomogeneities, e.g., between 

 perfusion and diffusing capacity or between stroke 

 output and pulmonary capillary blood volume, which 



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140 



160 



fig. 15. Hypothetical distribution of alveolar ventilation- 

 perfusion ratios (VA/Q) within the normal human lung. Values 

 for VA/Q range from zero at the mixed venous blood point 

 (perfusion but no ventilation) to infinity at the inspired air 

 point (ventilation without perfusion). According to this model, 

 the VA/Q ratio of each alveolus fixes its respiratory exchange 

 ratio (R) as well as its gas tensions (Pa n „, Pa 02 , and Pa co J. 

 [Based on Riley & Cournand (345) and Rahn (327).] 



consequently appear as imbalances between ventila- 

 tion and perfusion (319, 413); and c) basic assump- 

 tions, such as the type of statistical distribution of 

 ventilation-perfusion ratios among the alveoli may 

 be erroneous (128). 



In practice, the mixing formula shown in figure 

 16 is generally applied to data obtained during 

 ambient air breathing to determine the total venous 

 mixture, i.e., the sum of the anatomical and the 

 virtual; by repeating the measurements during 

 high-oxygen breathing, the virtual component is 

 minimized so that the venous admixture consists 

 almost entirely of the anatomical component (23). 



