Normobaric oxygen paradox and the microcirculation in the critically ill patient: a prospective observational study

Introduction

The normobaric oxygen paradox (NOP) is a recent concept that postulates the use of intermittent hyperoxia to stimulate erythropoietin (EPO) production [1]. Hyperoxia increases oxygen free radicals and may lead to endothelial damage and vasoconstriction [2]. We evaluated the microvascular response to transient hyperoxia and its effects on EPO production.

Methods

Six patients with hemodynamic stability and mechanically ventilated with FiO₂ <50% were included in this prospective observational study. Patients underwent a 2-hour period of hyperoxia (FiO₂ 100%). The sublingual microcirculation (sidestream dark-field imaging (SDF)) was evaluated at baseline (t0), 2 hours after hyperoxia (t1), and 2 hours after return to basal FiO₂ (t2). SDF monitoring was continuously performed also during the variation of FiO₂ for 2 minutes. EPO levels were assayed at baseline and for 2 days.

Results

An early vasoconstriction and a trend towards total vessel density (TVD) reduction were observed at t1 (Figure 1). The TVD tended to increase without returning to baseline levels at t2. EPO increased in four patients out of 6 (P = NS). A negative correlation was found between the change in TVD after hyperoxia (t1 - t0) and the change in EPO (r = -0.88, P = 0.03).

Figure 1

TVD and NOP.

Conclusion

Hyperoxia leads to vasoconstriction that seems to be reversible at hyperoxia cessation. Further data are needed to verify the efficacy of the NOP in stimulating erythropoiesis in the critically ill. There might be a relation between hyperoxia-induced reduction in vessel density and the EPO increase.