Research
The concentration of oxygen, lactate and glucose in the central veins, right heart, and pulmonary artery: a study in patients with pulmonary hypertension
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* Corresponding author: Guillermo Gutierrez ggutierrez@mfa.gwu.edu
1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, The George Washington University Medical Center, Pennsylvania Avenue, NW Washington, District of Columbia, 20037, USA
2 Department of Radiology, The George Washington University Medical Center, Pennsylvania Avenue, NW Washington, District of Columbia, 20037, USA
3 Division of Cardiology, Department of Medicine, The George Washington University Medical Center, Pennsylvania Avenue, NW Washington, District of Columbia, 20037, USA
4 Department of Anesthesiology and Critical Care Medicine, The George Washington University Medical Center, Pennsylvania Avenue, NW Washington, District of Columbia, 20037, USA
Critical Care 2007, 11:R44 doi:10.1186/cc5739
Published: 11 April 2007Abstract
Introduction
Decreases in oxygen saturation (SO2) and lactate concentration [Lac] from superior vena cava (SVC) to pulmonary artery have been reported. These gradients (ΔSO2 and Δ[Lac]) are probably created by diluting SVC blood with blood of lower SO2 and [Lac]. We tested the hypothesis that ΔSO2 and Δ[Lac] result from mixing SVC and inferior vena cava (IVC) blood streams.
Methods
This was a prospective, sequential, observational study of hemodynamically stable individuals with pulmonary artery hypertension (n = 9) who were about to undergo right heart catheterization. Catheters were advanced under fluoroscopic guidance into the IVC, SVC, right atrium, right ventricle, and pulmonary artery. Samples were obtained at each site and analyzed for SO2, [Lac], and glucose concentration ([Glu]). Analysis of variance with Tukey HSD test was used to compare metabolite concentrations at each site.
Results
There were no differences in SO2 or [Lac] between IVC and SVC, both being greater than their respective pulmonary artery measurements (P < 0.01 for SO2 and P < 0.05 for [Lac]). SO2 and [Lac] in right atrium, right ventricle, and pulmonary artery were similar. ΔSO2 was 4.4 ± 1.4% (mean ± standard deviation) and Δ[Lac] was 0.16 ± 0.11 mmol/l (both > 0; P < 0.001). Δ[Glu] was -0.19 ± 0.31 mmol/l, which was not significantly different from zero, with SVC [Glu] being less than IVC [Glu].
Conclusion
Mixing of SVC with IVC blood does not account for the development of ΔSO2 and Δ[Lac] in hemodynamically stable individuals with pulmonary artery hypertension. An alternate mechanism is mixing with coronary sinus blood, implying that ΔSO2 and Δ[Lac] may reflect changes in coronary sinus SO2 and [Lac] in this patient population.