Holy Name Hospital Teaneck, NJ
Correspondence to: Randolph P. Cole, MD, Holy Name Hospital, 718 Teaneck Rd, Teaneck, NJ 07666; e-mail: firstname.lastname@example.org
In his editorial on the pitfalls of the routine use of pulse oximetry in the ICU in a recent issue of CHEST (November 2004), Demers1 related an anecdote regarding a young female patient with an acute drug overdose who was receiving mechanical ventilatory support and in whom a delayed arterial blood gas measurement revealed a Pco2 less than half the normal value. We are told that a repeat blood gas measurement 2 h after halving the respiratory rate (and therefore the minute ventilation) was basically unchanged and that only after an additional 7 h was the arterial Pco2 in the mid-40 mm Hg range. The author argued that this reflected the large-body CO2 stores (stated as 28 L) in series with the CO2 present in alveolar gas.
These results seem to be at odds with published information on the kinetics of CO2 clearance. Sullivan et al2hyperventilated sedated, paralyzed, healthy male subjects for 2 h until their Pco2 reached plateau values between 13 and 25 mm Hg, and then decreased minute ventilation to between 25% and 53% of the baseline values for the five subjects. The response in Paco2 was rapid, with an increase to half the final asymptotic value in approximately 10 min. The data fit best a two-component exponential model with a fast-space rate constant of 0.58 min−1 and a slow-space rate constant of 0.034 min−1, corresponding to half-times of 1.5 and 23 min, respectively. The estimate given in the editorial for CO2 storage space seems to have been considerably higher than the estimates in the literature (2.05 to 3.17 mL/kg/mm Hg, or 5.7 to 8.9 L for an individual weighing 70-kg with a Paco2 of 40 mm Hg).4 The observed lack of rise in Paco2 over an extended period of time might represent unappreciated extra ventilatory efforts or some clinical situation in which the metabolic production of CO2 was decreasing over time.
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