Esmolol reduces myocardial injury induced by resuscitative endovascular balloon occlusion of the aorta (REBOA) in a porcine model of hemorrhagic shock.

PURPOSE

Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes myocardial injury from increased aortic afterload and supraphysiologic cardiac output. However, pharmacologic methods to attenuate high cardiac output and reduce myocardial injury have not been explored. We hypothesized that the use of esmolol during REBOA would reduce myocardial injury.

METHODS

Ten pigs were anesthetized and instrumented. Following 25% total blood volume hemorrhage, animals underwent 45 min of supraceliac (zone 1) REBOA with or without titration of esmolol to maintain heart rate between 80 and 100 beats per minute. Following the REBOA interventions, animals underwent 275 min of standardized critical care.

RESULTS

During REBOA, heart rate was significantly lower in the esmolol group compared to control animals (100 [88 - 112] vs 193 [172 - 203] beats/minute, respectively, p < 0.001) and the average mean arterial pressure (MAP) was lower in the esmolol group (88.0 [80.3-94.9] vs 135.1 [131.7-140.4] mmHg, respectively, p = 0.01). During the critical care phase, there were no differences in heart rate or MAP between groups. Animals in the intervention group received 237.9 [218.7-266.5] µg/kg of esmolol. There was a significant increase from baseline in serum troponins for the control group (p = 0.006) and significantly more subendocardial hemorrhage compared to animals treated with esmolol (3 [3 - 3] and 0 [0 - 0], p = 0.009, respectively).

CONCLUSION

In our porcine model of hemorrhagic shock, zone 1 REBOA was associated with myocardial injury. Pharmacologic heart rate titration with esmolol during occlusion may mitigate the deleterious effects of REBOA on the heart.