O2 Deficit: Non-invasive Sensitive Measure of Impaired Gas Exchange
The concept of determining the oxygen deficit using a non-invasive method was pioneered by John B. West, a globally known physiologist (medical text book author of Respiratory Physiology The Essentials), and a team of respiratory physicians at UC San Diego (UCSD) Medical School.
O2 Deficit is a single measure that indicates the degree of impaired gas exchange. It is obtained non-invasively from a patient’s normal breath at rest. O2 Deficit is the difference between end-tidal O2 in lungs (PAO2) and a calculated partial pressure of arterial oxygen (gPaO2TM). In essence, it reports the degree of inefficiency of the lung to transfer oxygen into the capillary blood. The O2 Deficit is calculated as follows: O2Deficit = PETO2(PAO2) – gPaO2. The value is calculated by a gas exchange monitor (GEM) using samples taken during normal breathing and is expressed in mmHg. Normal patients have single digit to zero values, respiratory patients have a larger gap (e.g., 30 to 50 mmHg, or even higher).
In patients with worsening gas exchange, oxygen deficit typically changes more than oxygen saturation. For example, a patient’s arterial oxygen saturation (SpO2) may fall by only 2% or 3% but their oxygen deficit tends to increase by a much wider margin (e.g., 10 mm Hg) than SpO2, providing a more sensitive indicator of gas exchange impairment. This wider margin allows for medical professionals to recognize deteriorating conditions and response to therapy more readily.