Abstract

This study determined how three factors interact to limit cardiopulmonary O2 delivery, O2 extraction and maximal aerobic capacity (VO2max): 1) breathing hypoxic gas; 2) impairing pulmonary gas exchange; and 3) reducing circulatory capacitance for O2. Five goats ran on a treadmill at VO2max following oleic‐acid induced acute lung injury (ALI) or with no lung injury (NLI). Goats breathed normoxic or hypoxic inspired gas fractions (FIO2 0.21 or 0.12) with and without small amounts of CO to maintain carboxyhemoglobin fractions (FHbCO) of 0.02 or 0.30. Hypoxia and ALI induced hypoxemia and reduced O2 delivery by different mechanisms: hypoxia reduced alveolar O2 partial pressure (PO2), whereas, ALI increased alveolar‐arterial PO2 difference. Elevated FHbCO lowered O2 delivery by reducing circulatory capacitance for O2 and reduced O2 extraction by increasing hemoglobin (Hb) affinity for O2. All combinations of hypoxia, ALI and elevated FHbCO attenuated the reduction in VO2max compared to the sum of each treatment’s individual effects on VO2max when administered separately. Hypoxia and ALI administered in combination attenuated the reduction in O2 delivery without affecting O2 extraction. Elevated FHbCO and ALI attenuated the decrease in O2 delivery because increased arterial O2 saturation partially compensated for reduced circulatory capacitance. The addition of ALI to the combination of hypoxic gas and elevated FHbCO attenuated the decrease in VO2max because the decrease in O2 delivery was attenuated and O2 extraction synergistically increased. Results from this study are applicable to individuals, e.g., soldiers, rescue workers and miners, that experience traumatic lung injury while breathing hypoxic and CO‐containing gases associated with fires.Grant Funding Source: Supported by U.S. Army Medical Research and Materiel Command with L‐3 Communications/Jaycor.

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