Cardiac Arrest in Pigs With 48 hours of Post‐Resuscitation Care Induced by 2 Methods of Myocardial Infarction: A Methodological Description

Author:

Vammen Lauge12ORCID,Munch Johannsen Cecilie12,Magnussen Andreas2,Povlsen Amalie23ORCID,Riis Petersen Søren2ORCID,Azizi Arezo2,Løfgren Bo245ORCID,Andersen Lars W.1246ORCID,Granfeldt Asger12ORCID

Affiliation:

1. Department of Anesthesiology and Intensive Care Aarhus University Hospital Aarhus Denmark

2. Department of Clinical Medicine Aarhus University Aarhus Denmark

3. Department of Cardiothoracic Anesthesia Copenhagen University HospitalRigshospitalet Denmark Copenhagen Denmark

4. Research Center for Emergency Medicine Aarhus University Hospital Aarhus Denmark

5. Department of Internal Medicine Randers Regional Hospital Randers Denmark

6. Prehospital Emergency Medical Services Central Denmark Region Aarhus Denmark

Abstract

Background Systematic reviews have disclosed a lack of clinically relevant cardiac arrest animal models. The aim of this study was to develop a cardiac arrest model in pigs encompassing relevant cardiac arrest characteristics and clinically relevant post‐resuscitation care. Methods and Results We used 2 methods of myocardial infarction in conjunction with cardiac arrest. One group (n=7) had a continuous coronary occlusion, while another group (n=11) underwent balloon‐deflation during arrest and resuscitation with re‐inflation after return of spontaneous circulation. A sham group was included (n=6). All groups underwent 48 hours of intensive care including 24 hours of targeted temperature management. Pigs underwent invasive hemodynamic monitoring. Left ventricular function was assessed by pressure‐volume measurements. The proportion of pigs with return of spontaneous circulation was 43% in the continuous infarction group and 64% in the deflation‐reinflation group. In the continuous infarction group 29% survived the entire protocol while 55% survived in the deflation‐reinflation group. Both cardiac arrest groups needed vasopressor and inotropic support and pressure‐volume measurements showed cardiac dysfunction. During rewarming, systemic vascular resistance decreased in both cardiac arrest groups. Median [25%;75%] troponin‐I 48 hours after return of spontaneous circulation, was 88 973 ng/L [53 124;99 740] in the continuous infarction group, 19 661 ng/L [10 871;23 209] in the deflation‐reinflation group, and 1973 ng/L [1117;1995] in the sham group. Conclusions This article describes a cardiac arrest pig model with myocardial infarction, targeted temperature management, and clinically relevant post‐cardiac arrest care. We demonstrate 2 methods of inducing myocardial ischemia with cardiac arrest resulting in post‐cardiac arrest organ injury including cardiac dysfunction and cerebral injury.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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