Strong ion acid–base abnormality and lactate:pyruvate ratio in children following cardiopulmonary bypass

Objectives

To describe post-cardiopulmonary bypass (post-CPB) acid–base derangement in terms of the Fencl–Stewart strong ion approach and the lactate:pyruvate ratio (LPR).

Methods

A prospective observational study set in the PICU of a university hospital. Arterial blood gas, serum lactate, pyruvate, and electrolytes were measured on admission to the PICU following cardiac surgery with CPB. LPR, corrected chloride (cCl = 140 × Cl/Na), and unmeasured anions or cations (strong ion gap) were calculated using modified Fencl–Stewart equations. CPB time, percent predicted mortality (PIM I), PICU mortality, and duration of: ventilation; inotropic support; and PICU stay were recorded. Data are reported as the median (range), or n (%), and are analysed by Mann–Whitney and Fisher's Exact tests. Ninety-four children, median age 51 months (0.03–166), median weight 14 kg (2.1–50), were enrolled.

Results

Surgery was performed for cyanotic heart disease in 41 children (44%) and acyanotic heart disease in 53 children (56%). Median CPB time was 80 min (17–232). One child died (PICU mortality 1%). Predicted mortality was 2% (SMR 0.50). The median pH was 7.38 (7.17–7.61). Of 69 children with standard bicarbonate < 22 mmol/l, the primary factor causing metabolic acidosis was elevated cCl in 32 patients (46%), lactate in three patients (4%), unmeasured anions in two patients (4%), and mixed in 32 patients (46%). The median base excess (BE) was -5.0 meq/l (-12.9 to -2.5), with chloride effect of -10.8 meq/l (-24 to +1.2), free water effect of -0.6 meq/l (-3.3 to +1.8), albumin effect of +3.5 meq/l (-0.6 to +6.8), and unmeasured cation effect of +3.7 meq/l (-10.7 to +17). The median cCl was 113 mmol/l (101–126). Hyperchloraemia (cCl >110 mmol/l) occurred in 66 children (70%) and was negatively associated with use of adrenaline by infusion (P = 0.005). Median lactate was 1.9 mmol/l (0.7–9.1) and hyperlactataemia (> 2 mmol/l) occurred in 41 children (44%). The median LPR was 18.8 (5.4–35) and LPR was raised (> 20) in 42 children (45%). Hyperlactataemia plus raised LPR was associated with use of adrenaline by infusion (P = 0.0009), CPB time (P = 0.04), percent predicted mortality (P = 0.05) and PICU stay (P = 0.03). Median albumin was 30 g/l (16–44) and hypoalbuminaemia (< 35 g/l) occurred in 81 children (86%). The median calculated strong ion gap was -3.8 mmol/l (-18.4 to +9.1) (i.e. unmeasured cation predominance).

Conclusion

In this group of children with low mortality post-CPB, hyperchloraemia was primarily responsible for metabolic acidosis, although both hyperlactataemia and raised LPR were common. Both hypoalbuminaemia and unmeasured cations limited the magnitude of the base deficit.