Study objectives: To determine whether the lungs of
patients with fulminant hepatic failure release lactate, and if so,
whether this release relates to systemic lactate concentration or acid
base status. Another objective was to examine the accuracy of lactate
flux calculations in critically ill patients.
Prospective observational study.
Setting: The ICU of a
major teaching hospital.
Patients: Twelve patients
with fulminant hepatic failure; 30 other critically ill patients in
whom a pulmonary artery catheter was in place.
results: The precision of whole-blood lactate measurements was
assessed in 30 patients with critical illnesses of variable etiology
who had a wide range of arterial lactate concentrations. The
reliability of lactate measurements decreased with increasing lactate
concentration. In each patient with liver failure, pulmonary lactate
flux was calculated on three occasions using the Fick principle.
Arterial blood lactate concentration was consistently higher than
venous concentrations, indicating lactate release by the lungs (mean
difference, 0.15 mmol/L; 95% confidence interval, 0.09 to 0.21;
p < 0.001). Mean pulmonary lactate production for the 12 patients
was 83 mmol/h (range, 22 to 210 mmol/h). No patient had significant
acute lung injury. Correlations were found among the arterial lactate
concentration and both the arteriovenous (AV) lactate difference
(p < 0.025) and pulmonary lactate production (p < 0.05), but not
with acid-base status or cardiac output. The reliability of individual
AV lactate difference calculations and pulmonary lactate flux
calculations was poor.
Conclusion: The lungs release
lactate in patients with fulminant hepatic failure at a rate
proportional to the degree of systemic hyperlactatemia. However, the
measurement errors associated with pulmonary lactate flux calculations
using the Fick principle are large, so individual measurements should
be interpreted with caution.