ObjectiveHypercapnia resulting from protective ventilation in acute respiratory
distress syndrome triggers metabolic pH compensation, which is not entirely
characterized. We aimed to describe this metabolic compensation.MethodsThe data were retrieved from a prospective collected database. Variables
from patients' admission and from hypercapnia installation until the third
day after installation were gathered. Forty-one patients with acute
respiratory distress syndrome were analyzed, including twenty-six with
persistent hypercapnia (PaCO2 > 50mmHg > 24 hours) and 15
non-hypercapnic (control group). An acid-base quantitative physicochemical
approach was used for the analysis.ResultsThe mean ages in the hypercapnic and control groups were 48 ± 18
years and 44 ± 14 years, respectively. After the induction of
hypercapnia, pH markedly decreased and gradually improved in the ensuing 72
hours, consistent with increases in the standard base excess. The metabolic
acid-base adaptation occurred because of decreases in the serum lactate and
strong ion gap and increases in the inorganic apparent strong ion
difference. Furthermore, the elevation in the inorganic apparent strong ion
difference occurred due to slight increases in serum sodium, magnesium,
potassium and calcium. Serum chloride did not decrease for up to 72 hours
after the initiation of hypercapnia.ConclusionIn this explanatory study, the results indicate that metabolic acid-base
adaptation, which is triggered by acute persistent hypercapnia in patients
with acute respiratory distress syndrome, is complex. Furthermore, further
rapid increases in the standard base excess of hypercapnic patients involve
decreases in serum lactate and unmeasured anions and increases in the
inorganic apparent strong ion difference by means of slight increases in
serum sodium, magnesium, calcium, and potassium. Serum chloride is not
reduced.