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Chronic heart failure (CHF) increases the resistance to gas transfer across the alveolar-capillary interface. Recent reports highlight the pathophysiologic relevance of changes in the lung leading to impaired fluid and gas exchange in the distal airway spaces. Under experimental conditions, an acute pressure or volume overload can injure the alveolar blood-gas barrier. This may disrupt its anatomic configuration, cause the loss of regulation of fluid-flux, and thereby affect alveolar gas conductance properties. These ultrastructural changes have been identified under the term of stress failure of the alveolar-capillary membrane. In the short term, these alterations are reversible due to the reparative properties of the alveolar surface. However, when the alveolarcapillary membrane is chronically challenged, for instance in patients with CHF, by noxious stimuli, such as humoral, cytotoxic, and genetic factors other than by mechanical trauma, remodeling of pathophvsiologic and clinical importance may take place. These changes in some respects resemble the remodeling process in the heart. Emerging findings support the view that, in patients with CHF, alveolar-capillary membrane dysfunction may contribute to symptom exacerbation and exercise intolerance, and may be an independent progiiosticator of clinical course. Angiotensin-converting enzyme inhibitors ameliorate the alveolar membrane gas conductance abnormality, reflecting improvement in the remodeling process. This article reviews the putative mechanisms involved in the impairment in gas diffusion in CHF patients and provides a link between physiologic changes and clinical findings. (CHEST 2003; 124:1090-1102)
Key words: alveolar gas diffusion: exercise; heart failure
Abbreviations: ACE = angiotensin-converting enzyme; AQP = aquaporin; CHF = chronic heart failure; CO = carbon monoxide; DLCO = lung diffusing capacity for carbon monoxide; DM = alveolar-capillary membrane conductance; DMCO = pulmonary membrane diffusing capacity for carbon monoxide; Q(dot above) = perfusion; [theta]CO = rate of carbon monoxide uptake by whole blood; SaO^sub 2^ = arterial oxygen saturation; Vc = pulmonary capillary blood volume available for gas exchange; V(dot above)CO^sub 2^ = carbon dioxide output; V(dot above)E = minute ventilation; V(dot above)O^sub 2^ = oxygen uptake
It has become increasingly apparent that, in patients with chronic heart failure (CHF), the involvement of the respiratory system and the occurrence of gas exchange inefficiency have important clinical and prognostic implications.1-6 When left ventricular dysfunction develops, the lung circulation and distal airway spaces become susceptible to the untoward...