Increasing importance of release velocity with vasopressor use in a porcine model of cardiac arrest

Abstract

Introduction:Wehave previously reported the benefit of faster release velocity on central blood flows in a porcine model of prolonged CPR without rescue shocks or vasopressor administration. We examined the importance of release velocity with vasopressor administration during the same model of prolonged CPR. Methods: CPR hemodynamics in four domestic swine were studied using standardmonitoring. Flowprobeswere placed on the inferior vena cava (IVC) and the right common carotid. Ventricular fibrillation (VF) was electrically induced. A mechanical chest compression (CC) device was started after ten minutes of untreated VF. CC release was changed so that sternal recoil lasted 100ms (WF1), 200ms (WF2), or 300ms (WF3). CC were delivered at a rate of 100 perminute and a depth of 48mm. Transitions between randomized waveforms occurred every 2min. Vasopressors were given every two minutes using the following pattern: epinephrine (1ml/kg), epinephrine (1ml/kg), vasopressin (40U/kg). Results: Throughout the first 18min of CC, aortic pressure was significantlyhigher and right atrial pressurewas significantly lower with WF1 and WF2 compared to WF3 (p<0.05). Carotid flow was higher with WF1 compared to WF3 (p<0.05). IVC flow was higher with WF1 in the first 8min of CC compared to WF3. Min 8 to 18 showed similar IVC flows for WF1 and WF2 which were higher than WF3 (p<0.05). During the first 18min of CC, IVC and carotid blood flows produced by WF3 with vasopressors were 3-fold less than those produced by WF3 in our no-vasopressor model. Conclusions: The use of vasopressors increased the impact of CC release velocity. The arterial-venous pressure difference, cerebral blood flow, and venous return were highest when the sternal recoil timewas 100ms. However, the use of vasopressors tended to decrease carotid and IVC flow and exacerbated the negative effect of slow release.