Abstract
Purpose of study: In the event of sudden cardiac arrest, the 2010 American Heart Association (AHA) guidelines recommend defined cardiopulmonary resuscitation (CPR) compression depths and defibrillation energies for both paediatric (<8 yrs) and adult patients for patient recovery. However there is limited information regarding the damaging effects of resuscitation on the tissues of the heart at a structural and genomic level. This study investigated the extent of gross and microscopic structural cardiac damage associated with implementing the 2010 AHA guidelines in a porcine model of cardiac arrest.Materials and methods: Ventricular fibrillation (VF) was induced in paediatric and adult porcine models. Following defibrillation and CPR as per the recommended guidelines, tissue samples were collected. Structural changes in the myocardial tissue were assessed using standard histological staining and ultrastructural damage to the tissues assessed using electron microscopy (EM). RNA was extracted from tissue samples and quantitative real time-PCR was performed to assess the mRNA expression of key genes associated with early markers of cardiovascular damage (troponin-1, DES, IL6, FABP3, Cx43). Clinical biomarker expression levels of Troponin I were also quantified pre and post treatment via the Vet iStat (Abaxis, USA).Results: All animals sustained gross structural damage including broken ribs, 3 animals had perforated atria and considerable damage to the ventricles was evident in the histological specimens. EM analysis revealed minor modifications in the ultrastructural appearance of the myocardial tissues. An increase in cardiac troponin-1 was observed in both adult and paediatric models post-resuscitation.Conclusions: This study highlights the extent of myocardial damage at a structural and genomic level, associated with implementing current resuscitation guidelines. It is evident that more research is needed to review the specificity and sensitivity of resuscitation to assist in determining the best method of post arrest treatment that increases the chance of resuscitation with minimal consequential damage.
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