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209 Evaluation of acute cardiac damage in a porcine model of defibrillation
  1. Fiona Rogan1,
  2. Rebecca Funston2,
  3. Brian Meenan1,
  4. George Burke1
  1. 1Ulster University
  2. 2HeartSine Technologies

Abstract

Introduction Transthoracic defibrillation is performed to correct life threatening cardiac arrhythmias of the heart, i.e. ventricular fibrillation (VF) and ventricular tachycardia (VT). These are due to chaotic electrical excitation of the heart chambers and loss of coordinated contraction of myocytes that could induce cardiac arrest. Resuscitation guidelines recommend defined defibrillation energies for patient recovery, research indicates that these techniques may cause myocardial damage. However, there is limited information regarding the defibrillation potentially damaging effects on the tissues of the heart at structural and genomic levels. This study investigates the extent of myocardial injury associated with the use of increasing energies (75J, 150J, 200J and 360J) of defibrillation in a porcine model of cardiac arrest using genomic, histological and ultrastructural analysis techniques.

Methodology General anaesthesia was induced in swine models (≈10–40 kg) in accordance with The Home Office guidelines. VF was induced and defibrillation administered, each animal receiving 20 shocks at the defibrillation energy protocol at 3 min intervals followed by 6 hour recovery period. Upon completion, animals were humanely euthanised. Cardiac tissues were excised and processed for genomic, histological and ultrastructural analyses and examination.Results:Haemodynamic results demonstrated ROSC occurred in all pigs. Troponin I levels were elevated 3–4 hours after the completion of defibrillation protocol. Gross pathological examination demonstrated no unusual changes. Histological and SEM analysis indicate defibrillation causes changes to the porcine cardiac tissue as evidenced by instances of hypereosinophilia, increased collagen-I deposition and areas of multifocal acute subendocardial, epicardial and myocardial necrosis. qPCR analysis indicates defibrillation induces genomic changes, there was an upregulation in the mRNA expression of structural and inflammation related genes such as Collagen-I, IL-6/18 and MCP1. Hydroxyproline analysis and SEM imaging also illustrated minor changes in collagen content and structural appearance of the tissue, further supported with Image J colour hue analysis.

Discussion The current paradox is cardiac defibrillation depends on the successful selection of energy to generate sufficient current flow through the heart to achieve defibrillation, whilst causing minimal injury to the heart. At this acute timeframe (post protocol), the animal models illustrated biological effects from repeated defibrillation upon cardiac tissues at a structural and genomic level and suggests there is a cardioprotective measure taken by the cardiomyocytes due to electrical overstimulation. In conclusion, these results show repeated defibrillation at increasing energies produces immediate changes to the functional myocardium at a genomic, microscopic and ultrastructural level.

  • Defibrillation
  • Cardiac
  • Damage

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