Unless cardiac output is reduced, alveolar ventilation can be monitored without arterial blood gas analysis by estimating arterial carbon dioxide tension (PaO2) from rebreathing measurement of mixed venous carbon dioxide tension (PvCO2) (PaCO2 = 0.8 PvCO2). If cardiac output is reduced, the PvCO2 - PaCO2 difference increases, reflecting the increased venoarterial carbon dioxide (CO2) content difference (Fick principle). A reduction in cardiac output can thus be quantified without catheterization of the central circulation by measuring both PaCO2 and PvCO2. The significance of such a reduction in cardiac output for oxygen (O2) delivery to tissues is determined by calculation of mixed venous O2 saturation (SvO2), using the inter-relationship of CO2 production to O2 consumption. With normal arterial oxygenation (SaO2) and hemoglobin concentration, PaCO2 less than 0.8 PvCO2 - 12 implies a reduction in cardiac output such that SvO2 is less than 33 per cent, which indicates inadequate O2 delivery to tissues. Ear oximetry and rebreathing measurement of PvCO2 are simple, noninvasive, bedside techniques.
