Abstract

Introduction: Although mechanical CPR devices provide automated delivery of fixed depth chest compressions, the consistency of hemodynamic support during prolonged resuscitation efforts is unclear, particularly in the absence of concomitant vasopressor treatment. In light of recent concerns regarding potentially harmful effects of epinephrine, we evaluated the hemodynamic support generated by 20 min of mechanical CPR without concurrent vasopressor administration in a porcine model of cardiac arrest (CA). Methods: Swine (n=10) were subjected to 7-8 min of CA following electrical induction of ventricular fibrillation. CPR was subsequently performed for 20 min using a mechanical compression system (LUCAS 3.1, Stryker) programmed to administer 102 compressions/min at a fixed depth of 2.1 inches. Aortic pressure (Ao), coronary perfusion pressure (CPP), and cerebral oxygen saturation (rSO 2 ; near-infrared spectroscopy) were continuously recorded. Results were compared to a separate group of swine (n=11) that received manual CPR with a compression rate of 100/min and depth necessary to achieve peak Ao of 100 mmHg. Results: Initially, mechanical CPR generated significantly higher peak Ao and CPP vs. manual CPR ( Figure ). However, by 4 min CPR, peak Ao and CPP were no longer different between groups. Both parameters continued to decline in the mechanical CPR group but remained stable in animals receiving manual CPR. Cerebral rSO 2 values fell from 57±2 % at baseline to 42±4 % during CA (p<0.01) but were not significantly improved by mechanical or manual CPR. Conclusion: The superior hemodynamic support initially offered by mechanical CPR deteriorates during prolonged CPR when pharmacologic vasopressor support is absent. These results demonstrate that a fixed compression depth does not necessarily produce consistent hemodynamic support and suggest that concomitant vasopressor administration may be necessary to sustain Ao and CPP during prolonged mechanical CPR.

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