Review ArticleAlveolar Gas Diffusion Abnormalities in Heart Failure
Section snippets
Alveolar-Capillary Membrane
To guarantee an optimal gas exchange, the alveolar-capillary unit needs to be thin, resistant, and “fluid-free.” Several important mechanisms preserve these physiologic properties. Figure 1 depicts the 3-layer configuration (epithelium, interstitial space, and endothelium) of the alveolar-capillary unit with cellular pathways involved in water and Na+ transport.
Acute LV failure promotes an increase in capillary pressure or volume that disrupts the anatomic configuration of the membrane and
Clinical Relevance of Gas Diffusion Abnormalities in Chronic Heart Failure
Measurement of lung diffusion capacity for carbon monoxide (DLCO) or nitric oxide (DLNO) is generally used in clinical practice to evaluate the effectiveness of diffusive O2 transport.27 As originally suggested by Roughton and Forster,28 for a given alveolar volume (VA) and hemoglobin concentration, gas diffusion depends on 2 resistances arranged in series according to the following equation:
1/DLCO = 1/DM + 1/θCO × Vc, where DM is the alveolar-capillary membrane conductance, θCO is the rate of CO
Interventions Improving Gas Diffusion in Chronic Heart Failure
In patients with HF who undergo heart transplantation, diffusion abnormalities may persist despite an improvement in hemodynamic status.53 A relationship has also been established between the time course of the disease and extent of gas transfer alterations.54 Thus, impaired DLCO in chronic disease may not fully depend on a reduction of the global perfusion of the lung but may be related to the persistence of structural changes of the membrane. The clinical significance of this may even be
Conclusions
The resistance to gas diffusion across the alveolar-capillary membrane is increased in HF. Disruption of the alveolar anatomic configuration and impairment of cellular pathways involved in the fluid–flux regulation and gas exchange efficiency (ie, “stress failure” of the alveolar-capillary membrane) are well characterized in different experimental models of lung capillary injury. Similar changes may distinguish acute HF in humans and may be reversible. In the chronic phase of HF, a reduced
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2018, Heart Failure ClinicsCitation Excerpt :The cellular pathways involved in the transition to a fibrotic LA chamber may have a common background with pathways involved in the microvasculature lung remodeling process (see later in this article) and have been identified in angiotensin II and transforming growth factor beta-1 as actually the most potent stimulators of collagen synthesis. When LAP is abnormally increased, 2 major vascular modifications occur39: the first is a stress failure of the capillaries and alveolar membrane, showing as a typical acute phenomenon induced by barotrauma injury of lung microvessels, which disrupts endothelial function and permeability and impairs the biological and functional properties of the alveolar unit (gas exchange and fluid filtration and reabsorption). Overt pulmonary edema is the significant clinical correlate of capillary stress failure.
This report was supported by the Monzino Foundation, Milano, Italy.
No conflict of interest exists.