Oxygen consumption modulation: effects of an opioid agonist on tissue oxygenation following lateral positioning in cardiovascular surgical patients with low oxygen delivery
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Nursing procedures, such as routine lateral positioning, that increase sympathetic stimulation and metabolic demand may have adverse physiological consequences for critically ill patients compromised by cardiorespiratory dysfunction and insufficient compensatory mechanisms to increase oxygen delivery (DO2) (Gawlinski & Dracup, 1998). A prospective, single group, quasi-experimental, repeated measures, factorial design was used to evaluate the clinical efficacy of a preprocedural morphine intervention (0.10 mg/kg iv) to attenuate oxygen consumption (VO2) response following lateral positioning in a convenience sample of 30 mechanically ventilated, cardiovascular surgical patients with low DO2 (M = 355, SD = 71). Subjects were randomized to either the left or right 45-degree lateral position. Mixed-venous oxygen saturation (SvO2) and VO2 via indirect calorimetry were measured at baseline and every 1-minute for 10 minutes following turning procedures, with and without the morphine intervention. Without morphine, lateral positioning was associated with a 17.3% peak increase in VO2I from baseline, typically occuring between minutes 4 and 5 after the turn, and a 7.2% decrease in SvO2 from baseline to minute 1 following the turn. When morphine was received before the turn, mean VO2I was no significantly lower at minutes 1 (p = .64) and 5 (p = .41) following the turn; however, mean SvO2 was significantly higher at minutes 1 (p = .000) and 5 (p = .001) following the turn. Furthermore, the probability of SvO2 returning to baseline within 10 minutes following the turn was 73% with morphine and only 50% without morphine (p = .05). Preliminary findings suggested morphine blunted cardiovascular responses and resulted in undesirable reductions in DO2I and cardiac index and increases in oxygen extraction; therefore, the routine use of preprocedural morphine for attenuating oxygen demand-induced VO2 response is not recommended.