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Abstract: Poster Presentations |

DECLINES IN MIXED VENOUS O2 SATURATION AFTER EXTUBATION ARE RELATED TO INCREASES IN O2 CONSUMPTION FREE TO VIEW

Hazem Ubaissi, MD*; Vinayak Jha, MD; Guillermo Gutierrez, MD
Author and Funding Information

George Washington University, Washington, DC


Chest


Chest. 2008;134(4_MeetingAbstracts):p164001. doi:10.1378/chest.134.4_MeetingAbstracts.p164001
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Abstract

PURPOSE: Decreases in central and mixed venous O2 (ScvO2 and SvO2, respectively) saturations are accepted markers of deficient oxygen delivery. During weaning from mechanical ventilation others have noted decreases in SvO2 in patients who failed weaning (Jubran et al. AJRCCM 1998; 158:1763). Our aim was to determine the relationship of SvO2 to O2 delivery (DO2) and to consumption (VO2) during the immediate post extubation period in cardiac post-operative patients.

METHODS: We monitored continuously arterial O2 saturation (SaO2), SvO2, cardiac output, and mean arterial pressure (MAP) in eight cardiac post-op patients during the time of weaning from mechanical ventilation. Signals were obtained with a computerized data acquisition system developed in house. All patients had an oximetry, continuous cardiac output pulmonary artery catheter ((7.5F CCOmbo and PreSep catheters, Edwards Lifescienses, Irvine, CA, USA). Measurements were taken four minutes prior to extubation, at the time of extubation, and at two and twelve minutes post extubation. Data were analyzed with One-Way ANOVA and Tukey HSD test. The total number of patients was eight(N=8).

RESULTS: SvO2 declined 2 minutes post extubation (p< 0.01; See Table). There were no changes in MAP or DO2. On the other hand, VO2 increased significantly (p<0.01).

CONCLUSION: Decreases in SvO2 in the immediate post extubation period in this patient population are related mainly to a rise in VO2, likely produced by the O2 cost of respiratory muscle work, not to declines in O2 delivery.

CLINICAL IMPLICATIONS: Decreases in SvO2 not always signify tissue hypoxia or a deficient O2 delivery system.Faculty Research Grant from the Richard B. and Lynne V. Cheney Cardiovascular Institute.

DISCLOSURE: Hazem Ubaissi, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 29, 2008

1:00 PM - 2:15 PM


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