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Abstract: Slide Presentations |

THE SUPERIOR VENA CAVA-TO-PULMONARY ARTERY O2 SATURATION GRADIENT IS RELATED TO MYOCARDIAL VENOUS OYGENATION FREE TO VIEW

Hector Y. Vazquez, MD*; Pablo Comignani, MD; Yanina Arzani, MD; F. Javier Hurtado, MD; Juan Riva, MD; Guillermo Gutierrez, MD, PhD
Author and Funding Information

The George Washington University Medical Center, Washington, DC


Chest


Chest. 2007;132(4_MeetingAbstracts):493b. doi:10.1378/chest.132.4_MeetingAbstracts.493b
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Abstract

PURPOSE: An O2 saturation gradient from superior vena cava (SVC) to pulmonary artery (PA) has been known to occur in critically ill patients. This gradient (ΔSO2), defined as ΔSO2 = (SO2)scv –(SO2)PA, is likely to be the result of mixing SVC blood with blood of lower SO2. Possible sources of lower SO2 blood are the inferior vena cava (IVC) or the coronary veins. We tested the hypothesis that ΔSO2 is the result of mixing SVC with coronary venous outflow in cardiac post-operative patients.

METHODS: Prospective, sequential observational study conducted in persons undergoing cardio-pulmonary bypass surgery (n = 20). Following the induction of anesthesia, patients had a PAC inserted via the right internal jugular vein. A jugular central venous catheter also was advanced into the IVC to a position just above the diaphragm. Catheters postion were verified manually. Before aortic cross clamping and prior to the beginning of cardiopulmonary bypass, simultaneous blood samples were drawn from the IVC catheter and the SVC and PA ports of the PAC A triple lumen catheter was then rapidly passed into the coronary sinus (CS) and a blood sample was drawn. All blood samples were immediately analyzed for O2 saturations.

RESULTS: Sampling site SO2 (mean ± SEM, n=20 ): IVC 85.1 ± 1.1%; SVC 83.4 ± 1.1%; CS 48.0 ± 2.4%; PA 77.5 ± 1.2%; ΔSO2 5.9 ± 0.6.

CONCLUSION: In patients about to undergo coronary artery bypass, the genesis of ΔSO2 cannot be explained by mixing of SVC with IVC blood. Given the low coronary sinus SO2 values in relation to those of the SVC, we conclude that ΔSO2 must be the result of mixing SVC blood with coronary venous blood.

CLINICAL IMPLICATIONS: This finding supports the hypothesis that changes in ΔSO2 reflect alterations in myocardial venous O2 saturation. Further studies are needed to establish the clinical utility of monitoring ΔSO2 as a marker of myocardial oxygenation in cardiac post-op and otehr critically ill patients.

DISCLOSURE: Hector Vazquez, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 24, 2007

10:30 AM - 12:00 PM


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