Background We sought to evaluate the efficacy of lipid emulsion in reversing bupivacaine-induced cardiovascular collapse when added to a resuscitation protocol that included the use of epinephrine and vasopressin. Methods Following induction of general anesthesia and instrumentation, 19 mixed-breed domestic swine had cardiovascular collapse induced by an intravenous bolus of 10 mg/kg bupivacaine. After 5 minutes of resuscitation including chest compressions, epinephrine (100 μg/kg) and vasopressin (1.5 u/kg), animals were randomized to receive either a bolus of 20% lipid emulsion (4 mL/kg) followed by a continuous infusion (0.5 mL· kg−1 ·min−1) or an equal volume of saline. Investigators were blinded to the treatment assignment. The primary end-point was return of spontaneous circulation (mean arterial pressure of ≥ 60 mmHg for ≥ 1 minute). Results Treatment groups were similar with respect to baseline measurements of weight, sex, hemodynamic and metabolic variables. The rates of return of spontaneous circulation were similar between groups, 3 of 10, in the lipid group, and 4 of 9, in the saline group (P = 0.65). Total serum bupivacaine concentrations were higher in the lipid group at the 10-minute time point, (mean ± SEM: 23.13 ± 5.37 ng/mL versus 15.33 ± 4.04 ng/mL, P = 0.004). More norepinephrine was required in the lipid group compared to the saline group to maintain a mean arterial pressure > 60 mmHg during the 60 minute survival period (mean ± SEM: 738.6 ± 94.4 vs. 487.3 ± 171.0 μg). Conclusions In this swine model, lipid emulsion did not improve rates of return of spontaneous circulation after bupivacaine-induced cardiovascular collapse.

These data suggest that altering the inflammatory response after cardiac arrest is not necessary for the beneficial effects of hypothermia. These data do not support a specific role of circulating cytokines in the neurologic injury after cardiac arrest.

Background— The scaling exponent (ScE) of the ventricular fibrillation (VF) waveform correlates with duration of VF and predicts defibrillation outcome. We compared 4 therapeutic approaches to the treatment of VF of various durations. Methods and Results— Seventy-two swine (19.5 to 25.7 kg) were randomly assigned to 1 of 9 groups (n=8 each). VF was induced and left untreated until the ScE reached 1.10, 1.20, 1.30, or 1.40. Animals were treated with either immediate countershock (IC); 3 minutes of CPR before the first countershock (CPR); CPR for 2 minutes, then drugs given with 3 more minutes of CPR before the first shock (CPR-D); or drugs given at the start of CPR with 3 minutes of CPR before the first shock (Drugs+CPR). Return of spontaneous circulation (ROSC) and 1-hour survival were analyzed with χ 2 and Kaplan-Meier survival curves. IC was effective when the ScE was low but had decreasing success as the ScE increased. No animals in the 1.30 or 1.40 groups had ROSC from IC (0 of 16). CPR did not improve first shock outcome in the 1.20 CPR group (3 of 8 ROSC). Kaplan-Meier survival analyses indicated that IC significantly delayed time to ROSC in both the 1.3 ( P =0.0006) and the 1.4 ( P =0.005) groups. Conclusions— VF of brief to moderate duration is effectively treated by IC. When VF is prolonged, as indicated by an ScE of 1.3 or greater, IC was not effective and delayed time to ROSC. The ScE can help in choosing the first intervention in the treatment of VF.

Background-Hypothermia has been shown to improve survival and neurological outcomes for ventricular fibrillation (VF) cardiac arrest. The electrophysiological mechanisms of hypothermia are not well-understood, nor are the effects of beginning cooling during the resuscitation.