Bohr Dead Space Calculation
Randolph H. Hastings, Ron Dueck · Anesthesia & Analgesia · 2012
To the Editor The recent article by Tusman et al.1 uses mass balance equations to apportion ventilation as if it were divided between a single perfused alveolar compartment and a dead space compartment. The model is quantified by the Christian Bohr equation, VD/VT = 1 - PĒCO2/PaCO2 where PCO2 is the mixed expired PCO2 value, and arterial PCO2 (PaCO2) is the CO2 tension in the as if alveolar compartment.2 To our knowledge, Bohr did not explain how to determine PaCO2, and the issue has been a subject for debate.3 Tusman et al. proposed using the midpoint of phase III on the volume capnogram (expired PCO2 versus expired volume) as the estimate. This method will run into problems if alveolar dead space is present, because gas from the perfused alveolar compartment and the alveolar dead space (unperfused alveoli) empty together and mix in expired gas (shown in Tusman et al. Fig. 1). Thus, alveolar dead space dilutes the PCO2 in phase III, potentially underestimating PaCO2 and VD. The end-tidal PCO2 may be diluted as well and does not avoid the issue in estimating PaCO2. Pulmonary embolism is one of the clinical entities with a significant increase in alveolar dead space. If dead space measurements were available, a clinician might consider this information as one piece of evidence in making the diagnosis. However, the capnogram PCO2 values decrease with pulmonary embolism because of dilution by alveolar dead space gas.4 The physician could be steered in the wrong direction, delaying the correct diagnosis and proper therapy. Instead, the correct assessment that dead space volume had increased would be provided by the Enghoff modification to the Bohr equation, which uses PaCO2 to estimate the PCO2 of the perfused alveolar compartment. PaCO2 is not diluted by dead space gas. Thus, it does not exhibit the same decrease as capnographic CO2 measurements but will also increase if ventilation cannot be increased. For example, Breen et al. reported that right pulmonary artery occlusion to model pulmonary embolism in dogs increased PaCO2 by 24 torr with an appropriate increase in Enghoff dead space. In contrast, capnographic PCO2 values decreased slightly. In addition to embolic diseases, the method by Tusman et al. for calculating the dead space may underestimate the dead space in the presence of alveolar regions with low or zero blood flow (West zone 1), say because of hypovolemia or imposition of high positive end-expiratory pressure.5 Interested readers might consult a nice review by Hedenstierna and Sandhagen6 that discusses how parallel versus series arrangement of unperfused respiratory compartments affects dead space estimates. Randolph H. Hastings, MD, PhD Ron Dueck, MD Department of Anesthesiology VA San Diego Healthcare System San Diego, California [email protected]