• Jack A Loeppky, Milton V Icenogle, Arvind Caprihan, Marcos F Vidal Melo, and Stephen A Altobelli.
• Lovelace Medical Foundation, New Mexico Resonance, Cardiology Section, VA Medical Center, 1501 San Pedro Dr SE, Albuquerque, NM 87108, USA. Loeppky@unm.edu
• Eur. J. Appl. Physiol. 2006 Nov 1; 98 (5): 450-60.

AbstractRebreathing in a closed system can be used to estimate mixed venous PCO2 (PvCO2) and cardiac output, but these estimates are affected by VA/Q heterogeneity. The purpose of this study was to validate a mathematical model of CO2 exchange during CO2 rebreathing in 29 patients with chronic obstructive pulmonary disease (COPD), with baseline arterial PCO2 (PaCO2) ranging from 28 to 60 mmHg. Rebreathing increased end-tidal PCO2 (PETCO2) by 20 mmHg over 2.2 min. This model employed baseline values for inspired (bag) PCO2, estimated PvCO2, distribution of ventilation and blood flow in one high VA/Q and one low VA/Q compartment, the ventilation increase and conservation of mass equations to simulate time courses of PICO2, PETCO2, PvCO2, and PaCO2. Measured PICO2 and PETCO2 during rebreathing differed by an average (SEM) of 1.4 (0.4) mmHg from simulated values. By end of rebreathing, predicted PvCO2 was lower than measured and predicted PaCO2, indicating gas to blood CO2 flux. Estimates of the ventilatory response to CO2, quantified as the slope (S) of the ventilation increase versus PETCO2, were inversely related to gas-to-blood PCO2 disequilibria due to VA/Q heterogeneity and buffer capacity (BC), but not airflow limitation. S may be corrected for these artifacts to restore S as a more valid noninvasive index of central CO2 responsiveness. We conclude that a rebreathing model incorporating baseline VA/Q heterogeneity and BC can simulate gas and blood PCO2 in patients with COPD, where VA/Q variations are large and variable.

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