Update '96 on pulmonary gas exchange pathophysiology in pneumonia

The major determinant of abnormal pulmonary gas exchange in patients with pneumonia is characterized by marked increases in intrapulmonary shunt combined with mild to moderate ventilation-perfusion (VA/Q) inequalities. Other mechanisms influencing the levels of arterial hypoxemia, such as disequilibrium of alveolar to endcapillary oxygen diffusion or increased intrapulmonary parenchymal oxygen uptake, are trivial in the clinical arena. These pathophysiological findings mostly concur with the structural derangement of pneumonic areas. On breathing oxygen, the dispersion of pulmonary blood flow, an index sensitive to both normal and low VA/Q ratios, increases (worsens), suggesting that hypoxic pulmonary vasoconstriction is abolished, whereas intrapulmonary shunt remains unchanged. This response differs from that developed by patients with acute respiratory distress syndrome (ARDS) in whom shunt increases moderately, thereby suggesting the development of reabsorption atelectasis, but VA/Q abnormalities remain unaltered. The effects of different drugs aimed at blocking the cyclooxygenase pathway to potentially enhance the mitigated hypoxic pulmonary vasoconstriction in the consolidated lung regions have shown to be individually variable and, in general, minimally beneficial; in contrast, the recent introduction of aerosolized vasodilators may benefit patients.