Non-invasive Measurement of Pulmonary Gas Exchange Efficiency: The Oxygen Deficit

Abstract

The efficiency of pulmonary gas exchange has long been assessed using the alveolar-arterial difference in PO2, the A-aDO2, a construct developed by Richard Riley ~70years ago. However, this measurement is invasive (requiring an arterial blood sample), time consuming, expensive, uncomfortable for the patients, and as such not ideal for serial measurements. Recent advances in the technology now provide for portable and rapidly responding measurement of the PO2 and PCO2 in expired gas, which combined with the well-established measurement of arterial oxygen saturation via pulse oximetry (SpO2) make practical a non-invasive surrogate measurement of the A-aDO2, the oxygen deficit. The oxygen deficit is the difference between the end-tidal PO2 and the calculated arterial PO2 derived from the SpO2 and taking into account the PCO2, also measured from end-tidal gas. The oxygen deficit shares the underlying basis of the measurement of gas exchange efficiency that the A-aDO2 uses, and thus the two measurements are well-correlated (r2~0.72). Studies have shown that the new approach is sensitive and can detect the age-related decline in gas exchange efficiency associated with healthy aging. In patients with lung disease the oxygen deficit is greatly elevated compared to normal subjects. The portable and non-invasive nature of the approach suggests potential uses in first responders, in military applications, and in underserved areas. Further, the completely non-invasive and rapid nature of the measurement makes it ideally suited to serial measurements of acutely ill patients including those with COVID-19, allowing patients to be closely monitored if required.

Validation of Noninvasive Assessment of Pulmonary Gas Exchange in Patients with Chronic Obstructive Pulmonary Disease during Initial Exposure to High Altitude

“…Q mismatch [11]. This O 2 deficit has been shown indeed to strongly correlate with the conventional A-aDO 2 in hypoxemic patients [12] and in healthy volunteers exercising in a hypoxic environment [13].…”

“…In particular, we identified that the inaccuracy (i.e., the increase in cPaO 2 -mPaO 2 difference) of the measurement was independently associated with the difference between PaCO 2 and PETCO 2 . This statistical relationship may partially explain some errors in the estimated PaO 2 , as the algorithm of the AGM100, considering the Bohr effect, corrects the cPaO 2 using the PETCO 2 [10,11]. Measurement of PETCO 2 in healthy people breathing a hypoxic mixture has been shown to be highly reproducible and can be considered as a reliable surrogate of PaCO 2 [27].…”

“…The O 2 deficit, promptly computed by the AGM100 from the measured PETO 2 and cPaO 2 may represent another important clinical parameter similar to A-aDO 2 to investigate the underlying mechanisms of hypoxemia [11]. Such alternative may also be a paradigm shift compared to the A-aDO 2 , since PaO 2 and PAO 2 are inversely calculated or measured among the two methods [9,11]. This allows the O 2 deficit option to better considers lung units with high .…”

“…-Non-invasive AGM100 measurement was first performed: participants were asked to breathe through a mouthpiece (with a nose clip) to record PETO 2 and PETCO 2 , while SpO 2 was continuously measured with a finger pulse oximeter, connected to the device. After automatic detection of a breathing steady-state, the measurement was automatically stopped and values for SpO 2 , PETO 2 , and PETCO 2 were recorded, and the cPaO 2 and O 2 deficit were calculated [10,11]. -Immediately after the AGM100 measurement, an arterial blood sample was collected by radial artery puncture while participants were breathing ambient air.…”

“…This new and non-invasive pulmonary gas exchange measurement may thus represent a promising method for the assessment of gas exchange impairment [8,11]. One small validation study (n = 23) reported a mean bias of −4 mmHg between cPaO 2 and mPaO 2 in a heterogeneous group of patients [12].…”