Carbon dioxide kinetics and capnography during critical care

C T Anderson, P H Breen, C T Anderson, P H Breen

Abstract

Greater understanding of the pathophysiology of carbon dioxide kinetics during steady and nonsteady state should improve, we believe, clinical care during intensive care treatment. Capnography and the measurement of end-tidal partial pressure of carbon dioxide (PETCO2) will gradually be augmented by relatively new measurement methodology, including the volume of carbon dioxide exhaled per breath (VCO2,br) and average alveolar expired PCO2. Future directions include the study of oxygen kinetics.

Figures

Figure 1
Figure 1
(a) Scheme of carbon dioxide stores and transport. PaCO2, arterial PCO2; PACO2, alveolar PCO2; PETCO2, end-tidal PCO2; V̇A, alveolar ventilation; V̇CO2,ti, tissue carbon dioxide production; V̇D, dead space ventilation; V̇E, expired ventilation; V̇I, inspired ventilation. (b) Normal capnogram (tidal PCO2 versus time). Phase I, inspiratory baseline; Phase II, expiratory upstroke; Phase III, alveolar plateau; and Phase IV, inspiratory downstroke. Adapted from Breen [61].
Figure 2
Figure 2
Effect of alveolar dead space (VDalv). The right lung compartment receives no perfusion and contains no carbon dioxide (ignoring interlung unit ventilation). By mass balance for carbon dioxide, VDalv/VTalv = (PaCO2 - PETCO2)/PaCO2. For the sample condition shown, VDalv/VTalv = (40-20)/40= 50%. PaCO2, arterial PCO2; PACO2, alveolar PCO2; PETCO2, end-tidal PCO2; P CO2, mixed venous PCO2;VTalv, alveolar tidal volume.Adapted from Breen [61].
Figure 3
Figure 3
Hydraulic model of carbon dioxide kinetics in the body. Large peripheral tissue carbon dioxide compartment (left) drains through cardiac output ( T) into the smaller central pulmonary carbon dioxide compartment (right). FCO2, fractional carbon dioxide; FRC, functional residual capacity; PaCO2 arterial PCO2; P CO2, mixed venous PCO2; V̇A/ , ventilation : perfusion ratio; VCO2,ti, tissue carbon dioxide production; VDana, anatomical dead space; V̇E, exhaled ventilation (see text). Adapted from Breen and Mazumdar [3].
Figure 4
Figure 4
Initial breath-by-breath effects of adding 11 cmH2O PEEP in mechanically ventilated anesthetized dogs on carbon dioxide volume exhaled per breath (VCO2,br), end-tidal PCO2 (PETCO2), exhaled tidal volume (VT), and cardiac output (QT, aorta flow probe). PaCO2, arterial PCO2; P CO2, mixed venous PCO2. Adapted from Breen and Mazumdar [3].
Figure 5
Figure 5
In five mechanically ventilated dogs, effect of 70 min of RPA occlusion on the following: (a) carbon dioxide volume exhaled per breath (VCO2,br); (b) PCO2; (c) dead space (VD); (d) ascending aortic cardiac output ( T); and (e) mean pulmonary artery pressure (Ppa). RPA occlusion began after time 0 (baseline). Solid symbol denotes significant difference (P < 0.05) from baseline measurement. *All stages during RPA occlusion were significantly different from baseline. PaCO2, arterial PCO2; PETCO2, end-tidal PCO2; P CO2, mixed venous PCO2; VDalv/VTalv, alveolar dead space : tidal volume fraction; VDphy, physiologic dead space. From Breen et al [55].

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