Abstract
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 ≥ 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.
Highlights
Ill patients might present complex acid– base disorders, even when the pH, PCO2, [HCO3-], and base excess ([BE]) levels are normal
Protons derived from ATP hydrolysis that cannot be reutilized in oxidative phosphorylation might be the actual explanation for metabolic acidosis [1,2]
The main finding of the present study was that 20% of the patients with severe hyperlactatemia showed normal pH, [HCO3-], [BE], and [SID] levels because of the simultaneous presence of hypochloremic metabolic alkalosis
Summary
Ill patients might present complex acid– base disorders, even when the pH, PCO2, [HCO3-], and base excess ([BE]) levels are normal. Metabolic acidosis of hypoxic states or anaerobic exercise has been traditionally explained by lactate production. There is biochemical evidence that lactate production does not cause acidosis, but retards its development [1,2]. There is some evidence showing that aerobic lactate production (that is, during catecholamine administration) is associated with metabolic acidosis [3,4]. Lactic acidosis is the most frequent cause of metabolic acidosis [6] and one of the most common metabolic abnormalities in critically ill patients [5]. For a correct diagnostic and prognostic evaluation of critically ill patients, severe metabolic acid–base disorders such as lactic acidosis must be identified
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