[Alveolar-capillary dysfunction in heart failure].
Heart failure increases the resistance to gas transfer across the alveolar-capillary interface. In different experimental conditions of vascular capillary injury, peculiar anatomical and functional abnormalities of the alveolar unit have been reported and consist of a disruption of its anatomical configuration and of a loss of fluid-flux regulation and gas exchange efficiency (i.e. "stress failure" of the alveolar-capillary membrane). In heart failure, the pathophysiological relevance of these changes has been only recently appreciated. Alveolar-capillary membrane conductance and capillary blood volume are subcomponents of lung diffusion capacity. A reduction of the former with an increase of the latter and consequent impairment of gas exchange are typical of heart failure syndrome. Alveolar-capillary membrane conductance abnormalities have been shown to be a sensitive index of the underlying lung tissue damage, bring an independent prognostic information and play a significant role in the pathogenesis of exercise limitation and ventilatory abnormalities. This review examines the current knowledge on this topic.
De Vita
Stefano
S
Istituto di Cardiologia Università degli Studi Via Parea, 4 20138 Milano.
Guazzi
Marco
M
Oreglia
Jacopo
J
Guazzi
Maurizio D
MD
D000328:Adult; D001798:Blood Proteins / Q000032:analysis; D015824:Blood-Air Barrier / Q000502:physiology*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications; D015444:Exercise; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology*; D006400:Hematocrit; D006439:Hemodynamics; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D011379:Prognosis; D011653:Pulmonary Diffusing Capacity; D011659:Pulmonary Gas Exchange; D012120:Respiration Disorders / Q000209:etiology; D012307:Risk Factors
D001798:Blood Proteins; D006454:Hemoglobins