The Science Journal of the American Association for Respiratory Care

2012 OPEN FORUM Abstracts


Lara Brewer, Kyle M. Burk, Simón A. Rodriguez, Joseph Orr; University of Utah Health Sciences Center, Salt Lake City, UT

Introduction: One cause of the observed difference between arterial and end-tidal CO2 is dilution of the end-tidal gas by gas from the alveolar dead space. Alveolar dead space ratio (VDalv/VTalv) is the fraction of the alveolar tidal volume (total volume minus airway dead space) that ventilates non-perfused alveoli. High dead space ratio (Vd/Vt) has been identified as a pulmonary-specific predictor of mortality for patients with early ARDS. As the percentage of unperfused alveoli increases, the magnitude of the PetCO2-PaCO2 gradient is expected to increase since the inspired air remains in the dead space without equilibrating with the blood. In an animal study, we evaluated the linearity and strength of the relationship between alveolar dead space ratio and PetCO2-PaCO2 gradient. Methods: Five male swine (27-30 kg) were ventilated with FiO2 of > 0.4, Vt of 12 mL/kg, and I:E time ratio of 1:2; An arterial cannula provided continuous BP and periodic ABG samples. The NM3 volumetric capnometry monitor (Philips Respironics, Wallingford, CT) recorded PetCO2, Vdalv and Vtalv. An acute lung injury was induced by intravenous injection of 0.8 mL/kg oleic acid. Two Vt and two RR settings were used to create four ventilation levels during which ABG was sampled. ABG was sampled at 5, 15, and 30 minutes after each ventilator settings change. At the time of each ABG measurement, the corresponding PetCO2 was recorded. The PaCO2 values, along with the corresponding volumetric capnography data were used to calculate the alveolar dead space ratio. We plotted the PetCO2-PaCO2 gradient versus the alveolar dead space ratio. Results: Figure 1 shows the mean and standard deviation of the PetCO2-PaCO2 gradient for each range of alveolar dead space ratio. The figure also shows the individual arterial and end-tidal PCO2 measurements from which the gradients were calculated. Linear regression analysis of the data shows a linear relationship between alveolar dead space ratio and arterial end-tidal gradient (r2 = 0.925). The gradient increases by approximately 6.8 mm Hg for each 0.1 increase in the alveolar dead space ratio (VDalv/VTalv). Conclusion: The relationship between alveolar dead space ratio and PetCO2-PaCO2 gradient is linear and strong based on our data. Since airway dead space has little effect on PetCO2 measurement, we expect the relationship is less direct for the total dead space ratio (Vd/Vt) than it is for the alveolar dead space ratio (VDalv/VTalv). Sponsored Research - Philips Medical