Research

Lactate concentration gradient from right atrium to pulmonary artery

Guillermo Gutierrez^1*, Lakhmir S Chawla², Michael G Seneff³, Nevin M Katz⁴ and Hasan Zia⁵

• * Corresponding author: Guillermo Gutierrez ggutierrez@mfa.gwu.edu

Author Affiliations

¹ Professor of Medicine and Anesthesiology, Pulmonary and Critical Care Medicine Division and Department of Medicine, The George Washington University Medical Center Washington, DC, USA

² Assistant Professor of Anesthesiology and Medicine, Critical Care Medicine Division, Department of Anesthesiology, The George Washington University Medical Center Washington, DC, USA

³ Associate Professor Anesthesiology, Critical Care Medicine Division, Department of Anesthesiology, The George Washington University Medical Center Washington, DC, USA

⁴ Clinical Professor of Surgery, Cardio-Thoracic Critical Care, Department of Surgery, The George Washington University Medical Center Washington, DC, USA

⁵ Senior Resident, Division of General Surgery, Department of Surgery, The George Washington University Medical Center Washington, DC, USA

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Critical Care 2005, 9:R425-R429 doi:10.1186/cc3741

See related commentary http://ccforum.com/content/9/4/337

Published: 10 June 2005

Abstract

Introduction

We compared simultaneous measurements of blood lactate concentration ([Lac]) in the right atrium (RA) and in the pulmonary artery (PA). Our aim was to determine if the mixing of right atrial with coronary venous blood, having substantially lower [Lac], results in detectable decreases in [Lac] from the RA to the PA.

Methods

A prospective, sequential, observational study was conducted in a medical-surgical intensive care unit. We enrolled 45 critically ill adult individuals of either sex requiring pulmonary artery catheters (PACs) to guide fluid therapy. Immediately following the insertion of the PAC, one paired set of blood samples per patient was drawn in random order from the PAC's proximal and distal ports for measurement of hemoglobin concentration, O₂ saturation (SO₂) and [Lac]. We defined Δ[Lac] as ([Lac]_ra - [Lac]_pa), ΔSO₂ as (S_raO₂ - S_paO₂) and the change in O₂ consumption (ΔVO₂) as the difference in systemic VO₂ calculated using Fick's equation with either S_raO₂ or S_paO₂ in place of mixed venous SO₂. Data were compared by paired Student's t-test, Spearman's correlation analysis and by the method of Bland and Altman.

Results

We found S_raO₂ > S_paO₂ (74.2 ± 9.1 versus 69.0 ± 10.4%; p < 0.001) and [Lac]_ra > [Lac]_pa (3.9 ± 3.0 versus 3.7 ± 3.0 mmol.l^-1; p < 0.001). Δ[Lac] correlated with ΔVO₂ (r² = 0.34; p < 0.001).

Conclusion

We found decreases in [Lac] from the RA to PA in this sample of critically ill individuals. We conclude that parallel decreases in SO₂ and [Lac] from the RA to PA support the hypothesis that these gradients are produced by mixing RA with coronary venous blood of lower SO₂ and [Lac]. The present study is a preliminary observation of this phenomenon and further work is needed to define the physiological and clinical significance of Δ[Lac].