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In Response: Concerns With Rate of Rise of Carbon Dioxide During Apnea With Buccal Oxygenation

Toner, Andrew J. FRCA; Heard, Andrew FRCA

doi: 10.1213/ANE.0000000000002390
Letters to the Editor: Letter to the Editor

Department of Anaesthesia, Royal Perth Hospital, Perth, Western Australia, Australia,

The issue of the rate of carbon dioxide rise is an important one for readers of the apneic oxygenation literature. This can only be measured with any meaningful accuracy using serial arterial blood gas analysis or continuous transcutaneous monitoring.1 The original description of the Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE) technique by Patel and Nouraei2 based estimates of carbon dioxide rise predominantly on end-tidal values obtained with mechanical ventilation after apnea (20/24 patients), with only 4 having arterial blood gas data—an approach that has since been proven to underestimate the true rate of carbon dioxide accumulation by half. Indeed, a subsequent randomized trial of the THRIVE approach failed to show a difference in carbon dioxide accumulation compared to controls in children,3 and no equivalent randomized trials in adults have been published to date. We did not anticipate the buccal oxygenation approach to influence carbon dioxide clearance and therefore did not design our study to rigorously assess this. Peak end-tidal measurements were taken with the delivery of vital capacity breaths after intubation to ensure carbon dioxide levels were not encroaching dangerous levels for our patient cohort. In our current practice, we use continuous transcutaneous carbon dioxide monitoring during prolonged apnea, with predefined thresholds for instigating a period of ventilation.

The authors do correctly point out that the apnea times reported within our study are a marginal overestimate of the true apnea period.4 The study stopwatch was started when both propofol (Schneider effect site 7 µg/mL) and remifentanil (Minto effect site 4 ng/mL) target-controlled infusions were running, and apnea followed shortly afterward. The rationale for this design was to use an objective start point rather than rely on each investigator’s subjective assessment of apnea onset—is perception of absent chest wall movements or loss of capnography trace reliable between individuals? Notably, we originally described the apnea time more accurately as the “study time,” but in the course of the peer-review process the 2 terms were considered equivalent enough to interchange.

Overall, we welcome and encourage a critical interpretation of all apneic oxygenation studies—a key part of the quest to translate a physiological phenomenon first described in 19595 into sustainable clinical gains.

Andrew J. Toner, FRCAAndrew Heard, FRCADepartment of AnaesthesiaRoyal Perth HospitalPerth, Western Australia,

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1. Gustafsson IM, Lodenius Å, Tunelli J, Ullman J, Jonsson Fagerlund M. Apnoeic oxygenation in adults under general anaesthesia using Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE)—a physiological study. Br J Anaesth. 2017;118:610–617.
2. Patel A, Nouraei SA. Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE): a physiological method of increasing apnoea time in patients with difficult airways. Anaesthesia. 2015;70:323–329.
3. Humphreys S, Lee-Archer P, Reyne G, Long D, Williams T, Schibler A. Transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) in children: a randomized controlled trial. Br J Anaesth. 2017;118:232–238.
4. Makkar JK, Singh NP, Singh PM. Prolongation of apnea time in obese patients—concerns with rate of rise of CO2. Anesth Analg. 2017;125:1422–1423.
5. Frumin MJ, Epstein RM, Cohen G. Apneic oxygenation in man. Anesthesiology. 1959;20:789–798.
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