The Cause of Arterial Hypoxemia at Rest in Patients With “Alveolar-Capillary Block Syndrome”*

Abstract

Hypoxemia in patients with "alveolar-capillary block syndrome" is believed to be due to a barrier to the diffusion of oxygen caused by thickened alveolar and capillary membranes (1, 2). Theoretical considerations indicate that thickened membranes should not result in a Po2 difference between alveolar gas and pulmonary capillary blood when patients with impaired diffusion breathe 100 per cent 02. Inhalation of 02, therefore, should always correct hypoxemia in patients in whom a barrier to diffusion is the only defect. The reasoning is as follows: inhalation of 02 at sea level raises alveolar Po2 to about 670 mm Hg, and the large initial Po2 difference between alveolar gas and blood entering the pulmonary capillaries (600 to 630 mm Hg) causes a rapid diffusion of 02 across even thickened alveolarcapillary membranes and prompt saturation of the hemoglobin (3, 4). After hemoglobin is saturated with 02, the 02 behaves like an inert gas and enters the blood only in physical solution and almost instantaneously, so that blood leaving the pulmonary capillaries is in equilibrium with the Po2 in the alveolar gas.Our original plan was to test this theory by measuring directly the arterial Po2 of patients with "pure" alveolar-capillary block syndrome while they were breathing pure 02. If the theory is correct (and if pulmonary artery-to-vein shunts are not increased in these patients) the arterial Po2 should equal that of healthy subjects breathing pure 02 (620 to 650 mm Hg). On analysis of our data we realized that the arterial hypoxemia in patients with alveolar-capillary block syndrome

Venous Admixture to the Pulmonary Circulation in Human Subjects Breathing 100 Per Cent Oxygen*

“…It is apparent from this plot that as diffusing capacity worsens, so does venous admixture, suggesting that both effects are related to one mechanism that alters alveolar units in such a way that they cease to function as diffusing units and act instead as shunting units. This could result from obliteration of alveolar spaces, or marked thickening of the alveolar-capillary membrane (10,24). In this respect, there is a striking resemblance between the relationship plotted in Figure 2 and that calculated by Finley, Swenson, and Comroe (10) for the change in diffusing capacity with increased thickness of the alveolar-capillary membrane.…”

“…These patients have also been shown to have grossly uneven distribution of ventilation in relation to blood flow (10). Since these two mechanisms contribute more importantly to the altered gas exchange than the reduction in pulmonary diffusing capacity itself, one might question the applicability of the term "alveolar-capillary block" (46) in these cases.…”

“…The role of diffusion impairment in the causation of arterial hypoxemia has been recently reevaluated ( 10), and a number of newer approaches have permitted a more precise definition of the distribution of ventilation-perfusion ratios and of its importance in gas exchange (11)(12)(13)(14)(15) incidence and magnitude of increased "direct" venous admixture in pulmonary disease (10,(16)(17)(18)(19). The paucity of such reports has probably been due to the lack of practical techniques for the accurate measurement of blood oxygen tension at high levels.…”

Effect of Slow Expiration With Glottis Opened in Lateral Posture (ELTGOL) on Mucus Clearance in Stable Patients With Chronic Bronchitis

“…In the most advanced stage, impaired gas exchange is inevitable. 31 This impairment can reduce the activity and social participation of individuals with hypoxemic COPD. In the future, the long-term effects of ELT-GOL, such as exacerbation frequency and intensity, hospitalizations, and quality of life, can be investigated to develop a full understanding of this technique.…”

Small Airways in Idiopathic Pulmonary Fibrosis

“…These patients usually have exertional breathlessness, a diffuse interstitial infiltrate on chest X ray, decreased lung volumes, decreased diffusing capacity, and hypoxemia which worsens with exercise. Although the hypoxemia in IPF was initially thought to result from a diffusion barrier to oxygen (17), current data suggest that it mostly results from a ventilation-perfusion imbalance (18,19).…”