The alveolar‐arterial PO2 difference (A—aDO2) was determined at various levels of alveolar ventilation in anesthetized, tracheotomized dogs, ventilated with room air by means of a volume cycled respirator; the ventilation being changed by varying the tidal volume, keeping the respiratory rate constant.—A decrease in ventilation was accompanied by a marked decrese in A—aDO2, and vice versa: At PaCO2≤30 mm Hg (mean 25.5 mm Hg) A—aDO2 was 28.3 mm Hg (range 18—42 mm Hg), at PaCO2 31–50 mm Hg (mean 41.5 mm Hg) A—aDO2 was 19.3 mm Hg (range 13—30 mm Hg); at PaCO2≥51 mm Hg (mean 60.5 mm Hg).A—aDO2 was 9.7 mm Hg (range 5—14 mm Hg).—Assuming an arterio‐venous difference in hemoglobin O2 saturation of 20% and 40%, respectively, the A—aDO2 for the 3 PCO2 intervals were calculated as venous admixture, being 7.1, 10.4 and 23.0%, and 3.7, 5.5 and 13.0%, respectively.—This indicates that reduction of the alveolar ventilation is accompanied by increasing disturbances of the alveolar‐arterial gas exchange,—of the nature uneven distribution of ventilation and perfusion, and/or venous admixture.The inverse relationship between the extent of the disturbances of alveolar‐arterial gas exchange and A—aDO2 in these studies show that A—aDO2 should only be used for the evaluation of changes in the alveolar‐arterial gas exchange when the alveolar ventilation remains unchanged.
No takes yet. Share an insight, caveat, or question.
Kim et al. (1968) studied this question.