Hypoxemia in the presence or absence of systemic inflammation does not increase blood lactate levels in healthy volunteers.

Purpose: Elevated lactate levels are a sign of critical illness and may result from insufficient oxygen delivery. We investigated whether hypoxemia and/or systemic inflammation, results in increased lactate levels in healthy volunteers. Materials and

Methods: 30 healthy volunteers were exposed to either 3.5 h of hypoxemia (FiO2 ± 11.5%), normoxemic endotoxemia (FiO2 21%, administration of 2 ng/kg endotoxin), or hypoxemic endotoxemia (n = 10 per group). Blood lactate, hemoglobin, SpO2, PaO2, PaCO2, pH, and hemodynamic parameters were serially measured.

Results: Hypoxemic treatment resulted in lower SpO2 (81.7 ± 2.6 and 81.4 ± 2.4% in the hypoxemia and hypoxemic endotoxemia groups, respectively) and hyperventilation with a PaCO2 decrease of 0.8 ± 0.5 and 1.5 ± 0.6 kPa and an increase in pH. Arterial oxygen content (CaO2) decreased by 20.5 ± 2.9 and 23.5 ± 4.4%, respectively. Lactate levels were slightly, but significantly higher in both hypoxemic groups compared with the normoxemic endotoxemia group over time (p < 0.0001 for both groups), but remained below 2.3 mmol/L in all subjects. Whereas PaO2 and SpO2 did not correlate with lactate levels, PaCO2, pH and CaO2 did.

Conclusions: Hypoxemia, in the absence or presence of inflammation does not result in relevant increases of lactate. The small increases in lactate observed are likely to be due to hyperventilation-related decreases in glycolysis.