Improved Perfusion Through the Aerated Part of the Lung by Prostacyclin Administration

Abstract

Severe ventilation-perfusion mismatching and the development of pulmonary hypertension as a consequence of a diffuse and severe inflammation of the lung are characteristic for the acute respiratory failure (ARF) or acute respiratory distress syndrome (ARDS). The raise in pulmonary vascular resistance (PVR) is triggered by the hypoxic pulmonary vasoconstriction (HPV), a compensatory physiologic response to hypoxia. Additionally, the alteration of the vascular bed with an increase of capillary permeability and altered transcapillary filtration pressures promotes the shift of protein rich fluid to the interstitium and thus the development of high permeability pulmonary edema. An up to twofold increase in lung weight results in progressive atelectasis in the dependent parts of the lung due to increased gravitational forces. This, in combination with flooding of the alveolar space with proteinaceous fluid, decreases alveolar ventilation and promotes shunt perfusion and thereby the reduction in arterial oxygenation. The increase in intrapulmonary right to left shunt is mainly responsible for profound hypoxemia, whereas a reduction of diffusion capacity may play only a minor role.