Milrinone and esmolol decrease cardiac damage after resuscitation from prolonged cardiac arrest

• Published in: Acta anaesthesiologica Scandinavica 2015-04, Vol.59 (4), p.465-474
• Main Authors: ZOERNER, F., LENNMYR, F., WIKLUND, L., MARTIJN, C., SEMENAS, E.
• Format: Article
• Language: English
• Subjects: Acid-Base Equilibrium; Adrenergic beta-Antagonists - therapeutic use; Anaesthesiology and Intensive Care; Anestesiologi och intensivvård; Animals; Cardiac arrest; cardioprotection; Cardiopulmonary Resuscitation; Cardiotonic Agents - therapeutic use; epinephrine; esmolol; Fluid Therapy; Heart Arrest - complications; Heart Arrest - pathology; Heart Diseases - pathology; Heart Diseases - prevention & control; I/R injury; Male; milrinone; Milrinone - therapeutic use; myocardial ischemia; Myocardium - pathology; Propanolamines - therapeutic use; reperfusion injury; resumption of spontaneous circulation; resuscitation; ROSC; Survival Analysis; Swine; Troponin I - blood; Vasoconstrictor Agents - therapeutic use; vasopressin; Vasopressins - therapeutic use
• ISSN: 0001-5172; 1399-6576; 1399-6576
• DOI: 10.1111/aas.12480

Background Long‐term survival after cardiac arrest (CA) due to shock‐refractory ventricular fibrillation (VF) is low. Clearly, there is a need for new pharmacological interventions in the setting of cardiopulmonary resuscitation (CPR) to improve outcome. Here, hemodynamic parameters and cardiac damage are compared between the treatment group (milrinone, esmolol and vasopressin) and controls (vasopressin only) during resuscitation from prolonged CA in piglets. Methods A total of 26 immature male piglets were subjected to 12‐min VF followed by 8‐min CPR. The treatment group (n = 13) received i.v. (intravenous) boluses vasopressin 0.4 U/kg, esmolol 250 μg/kg and milrinone 25 μg/kg after 13 min, followed by i.v. boluses esmolol 375 μg/kg and milrinone 25 μg/kg after 18 min and continuous esmolol 15 μg/kg/h infusion during 180 min reperfusion, whereas controls (n = 13) received equal amounts of vasopressin and saline. A 200 J monophasic counter‐shock was delivered to achieve resumption of spontaneous circulation (ROSC) after 8 min CPR. If ROSC was not achieved, another 200 J defibrillation and bolus vasopressin 0.4 U/kg would be administered in both groups. Direct current shocks at 360 J were applied as one shot per minute over maximally 5 min. Hemodynamic variables and troponin I as a marker of cardiac injury were recorded. Results Troponin I levels after 180 min reperfusion were lower in the treatment group than in controls (P