• Graciela Tuhay, María Carolina Pein, Fabio Daniel Masevicius, Daniela Olmos Kutscherauer, and Arnaldo Dubin.
• Servicio de Terapia Intensiva, Sanatorio Otamendi y Miroli, Buenos Aires, Argentina.
• Crit Care. 2008 Jan 1; 12 (3): R66R66.

IntroductionCritically ill patients might present complex acid-base disorders, even when the pH, PCO2, [HCO3-], and base excess ([BE]) levels are normal. Our hypothesis was that the acidifying effect of severe hyperlactatemia is frequently masked by alkalinizing processes that normalize the [BE]. The goal of the present study was therefore to quantify these disorders using both Stewart and conventional approaches.MethodsA total of 1,592 consecutive patients were prospectively evaluated on intensive care unit admission. Patients with severe hyperlactatemia (lactate level > or = 4.0 mmol/l) were grouped according to low or normal [BE] values (<-3 mmol/l or >-3 mmol/l).ResultsSevere hyperlactatemia was present in 168 of the patients (11%). One hundred and thirty-four (80%) patients had low [BE] levels while 34 (20%) patients did not. Shock was more frequently present in the low [BE] group (46% versus 24%, P = 0.02) and chronic obstructive pulmonary disease in the normal [BE] group (38% versus 4%, P < 0.0001). Levels of lactate were slightly higher in patients with low [BE] (6.4 +/- 2.4 mmol/l versus 5.6 +/- 2.1 mmol/l, P = 0.08). According to our study design, the pH, [HCO3-], and strong-ion difference values were lower in patients with low [BE]. Patients with normal [BE] had lower plasma [Cl-] (100 +/- 6 mmol/l versus 107 +/- 5 mmol/l, P < 0.0001) and higher differences between the changes in anion gap and [HCO3-] (5 +/- 6 mmol/l versus 1 +/- 4 mmol/l, P < 0.0001).ConclusionCritically ill patients may present severe hyperlactatemia with normal values of pH, [HCO3-], and [BE] as a result of associated hypochloremic alkalosis.

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