![]() ![]() The respiratory drive from the brain is an active system (which can increase minute ventilation up to 10 L/min for every 3 mmHg PaCO 2 increment unless PaCO 2 is exceedingly high) ( 1) whilst the mathematical relationship between alveolar CO 2 tension (or PaCO 2 for simplicity), carbon dioxide production (VCO 2 ~200 mL/min for an average adult that can increase up to 10 folds with vigorous exercise) and minute alveolar ventilation represents a passive system ( Figure 1A) ( 2). In a spontaneously breathing patient, there are two determinants of PaCO 2. In this correspondence, we briefly describe how we can visually interpret the interactions of different pathophysiological mechanisms in determining PaCO 2 in a spontaneously breathing or mechanically ventilated patient. Incorrect interpretation of PaCO 2 level-even when it is within the normal range-can have dangerous consequences in a spontaneously breathing patient ( 1). Although many clinicians are aware of the physiological mechanisms for PaCO 2 homeostasis, they often have difficulty understanding how different compensatory mechanisms interact, and why such interactions are not always successful in achieving normocapnia. Email: 19 January 2021 Accepted: 21 March 2021 Published: 25 July 2021.Ĭhanges in PaCO 2 in hospitalised patients are common and associated with an increased risk of morbidity and mortality. ![]() Department of Intensive Care Medicine, Royal Perth Hospital, Perth, Australia.
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