Tissue oximetry by near-infrared spectroscopy in a porcine model of out-of-hospital cardiac arrest and resuscitation.

INTRODUCTION: Monitoring during resuscitation remains relatively crude. Near-infrared spectroscopy (NIRS) measures aggregate oxygen saturation in a volume of tissue. We assessed the utility of continuous StO2 measurement in a porcine model of cardiac arrest, and explored the effects of differential vasoconstriction on StO2. We hypothesized that (1) StO2 trends correspond with the onset of loss of pulses, resuscitation, and return of spontaneous circulation (ROSC); (2) epinephrine has a dose-dependent effect on StO2.
METHODS: We anesthetized and instrumented 7 female swine, placing a NIRS probe on the left forelimb to recorded StO2. After 8 min of untreated VF and 2 min of CPR, we randomized animals to 0.015 mgkg(-1) (SDE) or 0.1mgkg(-1) (HDE) epinephrine. After 3 min of CPR, animals were defibrillated. Animals with ROSC were given SDE, then HDE for subsequent hemodynamic deteriorations. Data were analyzed with descriptive statistics and generalized linear model (alpha=0.05) to determine overall slope of pooled StO2 across animals for resuscitation segments.
RESULTS: Four animals received HDE and three SDE. All achieved ROSC. Significant coefficients (ΔStO2 min(-1)) were noted for resuscitation segments. StO2 decreased after loss of pulses (-29.1; 95%CI -33.4, -24.7; p<0.01) but plateaued during CPR (-0.2; 95%CI -1.2, 0.8; p=0.71). There was a graded decline in StO2 between SDE (-1.3; 95%CI -1.5, -1.2; p<0.01) and HDE (-3.1; 95%CI -5.8, -0.4; p=0.03). The slowest change occurred with ROSC (0.4; 95%CI 0.3, 0.5; p<0.01).
CONCLUSIONS: In a porcine model of OHCA, peripheral StO2 rapidly decreased after loss of pulses, but did not improve with CPR or epinephrine. It increased extremely slowly after ROSC.