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Using pulmonary gas exchange to estimate shunt and deadspace in lung disease: theoretical approach and practical basis.
Wagner, Peter D; Malhotra, Atul; Prisk, G Kim.
  • Wagner PD; Division of Pulmonary, Critical Care, Sleep Medicine and Physiology, University of California, San Diego, California.
  • Malhotra A; Division of Pulmonary, Critical Care, Sleep Medicine and Physiology, University of California, San Diego, California.
  • Prisk GK; Division of Pulmonary, Critical Care, Sleep Medicine and Physiology, University of California, San Diego, California.
J Appl Physiol (1985) ; 132(4): 1104-1113, 2022 04 01.
Article in English | MEDLINE | ID: covidwho-1759485
ABSTRACT
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 O2 more than CO2, whereas poorly (or non) perfused regions, as seen in PVO, affect CO2 more than O2. Exhaled O2 and CO2 concentrations at the mouth are measured over several ambient-air breaths, to determine mean alveolar Po2 and Pco2. A single arterial blood sample is taken over several of these breaths for arterial Po2 and Pco2. The resulting alveolar-arterial Po2 and Pco2 differences (AaPo2, aAPco2) 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 AaPO2 of almost 50 torr, but an aAPco2 of only 3 torr. In contrast, a 30% alveolar deadspace (from PVO) without shunt leads to an AaPO2 of only 12 torr, but an aAPco2 of 9 torr. This approach can identify and quantify physiological shunt and deadspace when present singly or in combination.NEW & NOTEWORTHY 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 Po2 and Pco2 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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: COVID-19 / Lung Diseases Limits: Humans Language: English Journal: J Appl Physiol (1985) Journal subject: Physiology Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: COVID-19 / Lung Diseases Limits: Humans Language: English Journal: J Appl Physiol (1985) Journal subject: Physiology Year: 2022 Document Type: Article