Using pulmonary gas exchange to estimate shunt and deadspace in lung disease: theoretical approach and practical basis

• Published in: Journal of applied physiology (1985) 2022-04, Vol.132 (4), p.1104-1113
• Main Authors: Wagner, Peter D, Malhotra, Atul, Prisk, G Kim
• Format: Article
• Language: English
• Subjects: Alveoli; Carbon Dioxide; COVID-19; Gas exchange; Hemodynamics; Humans; Innovative Methodology; Lung Diseases; Pathogenesis; Physiology; Pneumonia; Pulmonary Gas Exchange - physiology; SARS-CoV-2; Severe acute respiratory syndrome coronavirus 2; Viral diseases
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00621.2021

The common pulmonary consequence of SARS-CoV-2 infection is pneumonia, but vascular clot may also contribute to COVID pathogenesis. 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. 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. It is based on knowing that poorly (or non) ventilated regions, as occur in pneumonia, affect O more than CO , whereas poorly (or non) perfused regions, as seen in PVO, affect CO more than O . Exhaled O and CO concentrations at the mouth are measured over several ambient-air breaths, to determine mean alveolar Po and Pco . A single arterial blood sample is taken over several of these breaths for arterial Po and Pco . The resulting alveolar-arterial Po and Pco differences (AaPo , aAPco ) are converted to corresponding physiological shunt and deadspace values using the Riley and Cournand 3-compartment model. For example, a 30% shunt (from pneumonia) with no alveolar deadspace produces an AaPO of almost 50 torr, but an aAPco of only 3 torr. In contrast, a 30% alveolar deadspace (from PVO) without shunt leads to an AaPO of only 12 torr, but an aAPco of 9 torr. This approach can identify and quantify physiological shunt and deadspace when present singly or in combination. Identifying pulmonary vascular obstruction in the presence of pneumonia (e.g., in COVID-19) is difficult. We present here conversion of bedside measurements of arterial and alveolar Po and Pco into values for shunt and deadspace-when both coexist-using Riley and Cournand's 3-compartment gas exchange model. Deadspace values higher than expected from shunt alone indicate high ventilation/perfusion ratio areas likely reflecting (micro)vascular obstruction.