Our results raised the problem of the mechanism of the impairment in gas exchange. Since the inert gas solution was always infused into a vein of the superior vena caval system, only intrathoracic shunt (iey an intracardiac or intrapulmonary shunt) could be evaluated. An extrathoracic origin of these Va/Q alterations could not be estimated. An atrial right-to-left shunt, by reopening of the foramen ovale, was improbable due to the low pulmonary pressures. The measured percentage of shunt in these patients was thus attributed to perfusion of unventilated areas. Three possibilities could account for this abnormal true shunt.
Ruff et al, using xenon-1 found a raised closing vblume in cirrhotic patients. In eight of the ten patients, the closing volume was above the functional residual capacity, indicating premature airway closure during normal breathing. These authors suggested that the gas trapping was due to mechanical compression of small airways or to interstitial pulmonary edema resulting from low albumin levels, or to sodium retention, increased capillary permeability, hormone-dependent water retention, or reduced pulmonary lymph drainage. This would produce perfused but unventilated units of lung, creating microatelectasis.
A second possibility would be an impairment in hypoxic pulmonary vasoconstriction in cirrhotic patients; however, pharmacologic inhibition of HPV only has a small effect on Pa02 in normal and diseased lungs. In addition, Naeije et al, in a study performed on 24 patients with hepatic cirrhosis breathing hypoxic mixture, distinguished pulmonary vascular “responders” from “nonresponders” to hypoxia. The “responders” and the “nonresponders” could not be discriminated on the basis of their blood gas levels, hepatic function tests, or circulatory state. Daoud et al found a failure of HPV during hypoxia in ten cirrhotic patients with a hyperkinetic circulatory state. Our patients also had a hyperkinetic heart syndrome with low PVR and a long-standing cirrhosis. These abnormalities are indicative of a dilated pulmonary microcirculation and may partly explain the presence of a large true shunt. The right-to-left shunt could be ascribed to direct arteriovenous anastomoses. These have, in fact, been demonstrated by various techniques such as pulmonary angiography, radioisotopic, technetium-labeled macroaggregated albumin injections, or postmortem studies.
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