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Published on: April 7, 2021
Electrolyte redistribution during acute respiratory acid-base changes: an in vivo study using apnoea testing
Micah L A Heldeweg1, Martin Krbec2, Martin Vancura3
1Department of Anaesthesiology, Amsterdam University Medical Centres, Amsterdam, The Netherlands; Department of Intensive Care, Amsterdam University Medical Centres, Amsterdam, The Netherlands; Department of Anaesthesia and Intensive Care Medicine, The Third Faculty of Medicine, Charles University and FNKV University Hospital, Prague, Czech Republic.
Background:
Acute respiratory acid-base changes induce pH-dependent electrolyte redistribution. Although this response has been characterised in vitro, the in vivo changes depend on multicompartment buffering and remain poorly defined.
Methods:
We conducted a multicentre retrospective study of patients undergoing apnoea testing for organ donation after determination of brain death, a clinical model allowing in vivo study of acute ventilatory changes. The primary outcome was the pH-dependent change in strong ion difference (SID). Secondary analyses examined individual electrolytes, pH-SID effect modification by physiological variables, and how well the derived model agreed with observed SID changes compared with a simple bedside pH-correction method (ΔSID=-15×ΔpH).
Results:
In 263 participants, pH decreased from 7.40 (0.07) to 7.23 (0.07) and returned to 7.40 (0.08). Per pH unit increase, SID changed by -11.7 meq L-1 (95% CI -13.1 to -10.3; P<0.001), driven primarily by sodium ion (Na) (52% of change -7.2 mM; P<0.001) and chloride ion (Cl) (36% of change +3.7 mM; P<0.001). Higher haemoglobin concentration was associated with a higher pH-dependent SID change, together explaining 53% of within-patient variability. Agreement between predicted and observed SID changes was only modestly improved by using the derived model vs a simplified pH-correction model (sd of differences 1.74 vs 1.92 meq L-1).
Conclusions:
Acute respiratory acid-base disturbances produce in vivo Na and Cl redistribution associated with pH change that are modulated by haemoglobin concentration. The observed pH-dependent electrolyte redistribution is consistent with physiological buffering and can be reasonably approximated using a simple bedside pH-correction model.
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