• S Höstman, R Kawati, G Perchiazzi, and A Larsson.
• Hedenstierna Laboratory, Uppsala University, Uppsala, Sweden.
• Acta Anaesthesiol Scand. 2018 Jul 1; 62 (6): 820-828.

BackgroundIn a previous study, we found a rebound of arterial carbon dioxide tension (PaCO2 ) after stopping THAM buffer administration. We hypothesized that this was due to reduced pulmonary CO2 elimination during THAM administration. The aim of this study was to investigate this hypothesis in an experimental porcine hypercapnic model.MethodsIn seven, initially normoventilated, anesthetized pigs (22-27 kg) minute ventilation was reduced by 66% for 7 h. Two hours after commencing hypoventilation, THAM was infused IV for 3 h in a dose targeting a pH of 7.35 followed by a 2 h observation period. Acid-base status, blood-gas content and exhaled CO2 were measured.ResultsTHAM raised pH (7.07 ± 0.04 to 7.41 ± 0.04, P < 0.05) and lowered PaCO2 (15.2 ± 1.4 to 12.2 ± 1.1 kPa, P < 0.05). After the infusion, pH decreased and PaCO2 increased again. At the end of the observation period, pH and PaCO2 were 7.24 ± 0.03 and 16.6 ± 1.2 kPa, respectively (P < 0.05). Pulmonary CO2 excretion decreased from 109 ± 12 to 74 ± 12 ml/min (P < 0.05) during the THAM infusion but returned at the end of the observation period to 111 ± 15 ml/min (P < 0.05). The estimated reduction of pulmonary CO2 elimination during the infusion was 5800 ml.ConclusionsIn this respiratory acidosis model, THAM reduced PaCO2 , but seemed not to increase the total CO2 elimination due to decreased pulmonary CO2 excretion, suggesting only cautious use of THAM in hypercapnic acidosis.© 2018 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

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