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Clinical Investigations in Critical Care |

Hyperlactatemia and Pulmonary Lactate Production in Patients With Fulminant Hepatic Failure*

Timothy S. Walsh, MBChB; Stuart McLellan, MBChB; Simon J. Mackenzie, MBChB; Alistair Lee, MBChB
Author and Funding Information

*From the Department of Anaesthetics, Intensive Care Unit and Scottish Liver Transplant Unit, Royal Infirmary, Edinburgh, Scotland.

Correspondence to: Dr Timothy S Walsh, Department of Anaesthetics, Royal Infirmary of Edinburgh, Lauriston Place, Edinburgh, Scotland EH3 9YW



Chest. 1999;116(2):471-476. doi:10.1378/chest.116.2.471
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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.

Design: 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.

Interventions: None.

Measurement and 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.

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