THAM administration reduces pulmonary carbon dioxide elimination in hypercapnia - an experimental porcine study

In 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.

In 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.

THAM 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.

In 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.