Dissociation of mixed venous oxygen saturation and cardiac index during opioid induction

To evaluate the independent effects of opioid induction and paralysis on changes in mixed venous oxygen saturation (SvO2).

Prospective, with each patient serving as his or her own control.

Cardiac operating rooms of a major U.S. teaching hospital.

15 elective patients for aortocoronary bypass graft surgery.

Prior to induction with sufentanil 2 to 3 micrograms/kg (t1), after recovery from succinylcholine 1 to 1.5 mg/kg (t2), and after subsequent paralysis with vecuronium (t3), we recorded cardiac index (VO2), arterial oxygen saturation (SaO2), and SvO2, then calculated oxygen consumption (VO2) and arterial oxygen content (CaO2).

SvO2 increased from 75% at t1 to 82% at t2 (p = 0.03) and to 83% at t3 (p = 0.006). CI decreased from 3.1 L/min/m2 at t1 to 2.5 L/min/m2 at t2 (p = 0.023) and to 2.1 L/min/m2 at t3 (t1 vs. t3, p = 0.019; t2 vs. t3, p = NS). Calculated VO2 decreased from 2.88 ml O2/min/kg at t1 to 2.09 ml O2/min/kg at t2 (p = 0.03) and to 1.87 ml O2/min/kg at t3 (t1 vs. t3, p = 0.002; t2 vs. t3, p = 0.027). CaO2 remained unchanged.

Opioid anesthesia, not paralysis, increases SvO2. Most of the decrease in VO2 occurs from anesthesia, not paralysis. The direct relationship between CI and SvO2 no longer holds upon induction of anesthesia. Parallel changes in CI cannot be inferred based on SvO2 alone.