Metabolic acid-base adaptation triggered by acute persistent hypercapnia in mechanically ventilated patients with acute respiratory distress syndrome.
OBJECTIVE
Hypercapnia 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.


METHODS
The 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.


RESULTS
The 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.


CONCLUSIONS
In 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.
Departamento de Nefrologia, Faculdade de Medicina do ABC, Santo André, SP, Brazil.
Thiago Gomes
TG
Romano
Unidade de Terapia Intensiva, Disciplina de Emergências Clínicas, Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.
Mario Diego Teles
MD
Correia
Unidade de Terapia Intensiva, Hospital Sírio Libanês, São Paulo, SP, Brazil.
Pedro Vitale
PV
Mendes
Unidade de Terapia Intensiva, Disciplina de Emergências Clínicas, Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.
Fernando Godinho
FG
Zampieri
Unidade de Terapia Intensiva, Hospital Sírio Libanês, São Paulo, SP, Brazil.
Alexandre Toledo
AT
Maciel
Unidade de Terapia Intensiva, Disciplina de Emergências Clínicas, Hospital das Clinicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brazil.
Marcelo
M
Park
D000136:Acid-Base Equilibrium / Q000502:physiology*; D000328:Adult; D002118:Calcium / Q000097:blood; D016208:Databases, Factual; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000150:complications* / Q000209:etiology; D019344:Lactic Acid / Q000097:blood; D008274:Magnesium / Q000097:blood; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D012121:Respiration, Artificial / Q000009:adverse effects / Q000379:methods*; D012128:Respiratory Distress Syndrome / Q000628:therapy*; D012189:Retrospective Studies; D012964:Sodium / Q000097:blood
D019344:Lactic Acid; D012964:Sodium; D008274:Magnesium; D011188:Potassium; D002118:Calcium