![]() In contrast, a 30% alveolar deadspace (from PVO) without shunt leads to an AaPO 2 of only 12 torr, but an aAPco 2 of 9 torr. For example, a 30% shunt (from pneumonia) with no alveolar deadspace produces an AaPO 2 of almost 50 torr, but an aAPco 2 of only 3 torr. The resulting alveolar-arterial Po 2 and Pco 2 differences (AaPo 2, aAPco 2) are converted to corresponding physiological shunt and deadspace values using the Riley and Cournand 3-compartment model. A single arterial blood sample is taken over several of these breaths for arterial Po 2 and Pco 2. Exhaled O 2 and CO 2 concentrations at the mouth are measured over several ambient-air breaths, to determine mean alveolar Po 2 and Pco 2. It is based on knowing that poorly (or non) ventilated regions, as occur in pneumonia, affect O 2 more than CO 2, whereas poorly (or non) perfused regions, as seen in PVO, affect CO 2 more than O 2. Although stimulated by COVID-19, we propose a generally applicable bedside gas exchange approach to identifying PVO occurring alone or in combination with pneumonia, addressing both its theoretical and practical aspects. Imaging and hemodynamic approaches to identifying diffuse pulmonary vascular obstruction (PVO) in COVID (or acute lung injury generally) are problematic particularly when pneumonia is widespread throughout the lung and hemodynamic consequences are buffered by pulmonary vascular recruitment and distention. ![]() The common pulmonary consequence of SARS-CoV-2 infection is pneumonia, but vascular clot may also contribute to COVID pathogenesis.
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