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Abstract
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.