Decreases in Mixed Venous Blood O2 Saturation in Cardiac Surgery Patients Following Extubation

Author:

Williams Jeffrey1,McLean Anna1,Ahari Jalil1,Jose Arun1,Al-Helou Georges1,Ibi Italo2,Najam, MD Farzad3,Gutierrez Guillermo1

Affiliation:

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

2. Department of Anesthesiology, The George Washington University Medical Center, Washington, DC, USA

3. Department of Surgery, The George Washington University Medical Center, Washington, DC, USA

Abstract

Background: Decreases in mixed venous O2 saturation (SvO2) have been reported to occur in postcardiac surgery patients during weaning from mechanical ventilation. Our aim was to establish whether the physiological mechanism responsible for this phenomenon was a decrease in systemic O2 delivery (DO2) or an increase in global O2 consumption ([Formula: see text] O 2). Methods: We studied 21 mechanically ventilated, postoperative cardiac patients for 30 minutes before and 60 minutes after extubation. We monitored continuously arterial O2 saturation by pulse oximetry (SaO2) and central venous O2 saturation (ScvO2) with an oximetry catheter. Mixed venous O2 saturation (SvO2) and cardiac output were also measured continuously with an oximetry pulmonary artery catheter. Systemic O2 delivery and [Formula: see text] O 2 were calculated according to accepted formulae. Results: Immediately following extubation, ScvO2 and SvO2 decreased rapidly ( P < .01). Systemic O2 consumption increased from 65 (57) mL·min−1 to 194 (66) mL·min−1 ( P < .05) with no changes in DO2. Consequently, systemic O2 extraction rose from 38% (8%) to 45% (9%; P < .01). Preoperative left ventricular ejection fraction correlated with the decline in SvO2 postextubation. All patients weaned successfully. Conclusions: Decreases in SvO2 after discontinuation of ventilatory support in postcardiac surgery patients occur as [Formula: see text] O 2 increases in response to greater energy requirements by muscles of ventilation that are not initially matched by increases in DO2.

Publisher

SAGE Publications

Subject

Critical Care and Intensive Care Medicine

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