OBJECTIVES: Coronary perfusion pressure (CPP) during resuscitation from cardiac arrest has been shown to correlate with return of spontaneous circulation. Adrenergic blockade of beta-1 and alpha-1 receptors is common in the long-term management of ischemic heart disease and congestive heart failure. We sought to compare the CPP response to vasopressin vs. epinephrine in a swine model of cardiac arrest following pre-arrest adrenergic blockade. METHODS: Eight anesthetized and instrumented swine were administered 0.1mg epinephrine and arterial pressure and heart rate response were measured. An infusion of labetalol was then initiated and animals periodically challenged with epinephrine until adrenergic blockade was confirmed. The left anterior descending coronary artery was occluded to produce ventricular fibrillation (VF). After 7min of untreated VF, mechanical chest compressions were initiated. After 1min of compressions, 1mg epinephrine was given while CPP was recorded. When CPP values had returned to pre-epinephrine levels, 40U of bolus vasopressin was given. Differences in CPP (post-vasopressor-pre-vasopressor) were compared within animals for the epinephrine and vasopressin response and with eight, non-adrenergically blocked, historical controls using Bayesian statistics with a non-informative prior. RESULTS: The CPP response following epinephrine was 15.1mmHg lower in adrenergically blocked animals compared to non-adrenergically blocked animals (95% Highest Posterior Density [HPD] 2.9-27.2mmHg lower). CPP went up 18.4mmHg more following vasopressin when compared to epinephrine (95% HPD 8.2-29.1mmHg). The posterior probability of a higher CPP response from vasopressin (vs. epinephrine) in these animals was 0.999. CONCLUSIONS: Pre-arrest adrenergic blockade blunts the CPP response to epinephrine. Superior augmentation of CPP is attained with vasopressin under these conditions. Copyright Â
OBJECTIVES: Coronary perfusion pressure (CPP) during resuscitation from cardiac arrest has been shown to correlate with return of spontaneous circulation. Adrenergic blockade of beta-1 and alpha-1 receptors is common in the long-term management of ischemic heart disease and congestive heart failure. We sought to compare the CPP response to vasopressin vs. epinephrine in a swine model of cardiac arrest following pre-arrest adrenergic blockade. METHODS: Eight anesthetized and instrumented swine were administered 0.1mg epinephrine and arterial pressure and heart rate response were measured. An infusion of labetalol was then initiated and animals periodically challenged with epinephrine until adrenergic blockade was confirmed. The left anterior descending coronary artery was occluded to produce ventricular fibrillation (VF). After 7min of untreated VF, mechanical chest compressions were initiated. After 1min of compressions, 1mg epinephrine was given while CPP was recorded. When CPP values had returned to pre-epinephrine levels, 40U of bolus vasopressin was given. Differences in CPP (post-vasopressor-pre-vasopressor) were compared within animals for the epinephrine and vasopressin response and with eight, non-adrenergically blocked, historical controls using Bayesian statistics with a non-informative prior. RESULTS: The CPP response following epinephrine was 15.1mmHg lower in adrenergically blocked animals compared to non-adrenergically blocked animals (95% Highest Posterior Density [HPD] 2.9-27.2mmHg lower). CPP went up 18.4mmHg more following vasopressin when compared to epinephrine (95% HPD 8.2-29.1mmHg). The posterior probability of a higher CPP response from vasopressin (vs. epinephrine) in these animals was 0.999. CONCLUSIONS: Pre-arrest adrenergic blockade blunts the CPP response to epinephrine. Superior augmentation of CPP is attained with vasopressin under these conditions. Copyright Â