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Review
. 2015 Feb 4;4(1):1-12.
doi: 10.5492/wjccm.v4.i1.1.

Modeling cardiac arrest and resuscitation in the domestic pig

Affiliations
Review

Modeling cardiac arrest and resuscitation in the domestic pig

Brandon H Cherry et al. World J Crit Care Med. .

Abstract

Cardiac arrest remains a leading cause of death and permanent disability worldwide. Although many victims are initially resuscitated, they often succumb to the extensive ischemia-reperfusion injury inflicted on the internal organs, especially the brain. Cardiac arrest initiates a complex cellular injury cascade encompassing reactive oxygen and nitrogen species, Ca(2+) overload, ATP depletion, pro- and anti-apoptotic proteins, mitochondrial dysfunction, and neuronal glutamate excitotoxity, which injures and kills cells, compromises function of internal organs and ignites a destructive systemic inflammatory response. The sheer complexity and scope of this cascade challenges the development of experimental models of and effective treatments for cardiac arrest. Many experimental animal preparations have been developed to decipher the mechanisms of damage to vital internal organs following cardiac arrest and cardiopulmonary resuscitation (CPR), and to develop treatments to interrupt the lethal injury cascades. Porcine models of cardiac arrest and resuscitation offer several important advantages over other species, and outcomes in this large animal are readily translated to the clinical setting. This review summarizes porcine cardiac arrest-CPR models reported in the literature, describes clinically relevant phenomena observed during cardiac arrest and resuscitation in pigs, and discusses numerous methodological considerations in modeling cardiac arrest/CPR. Collectively, published reports show the domestic pig to be a suitable large animal model of cardiac arrest which is responsive to CPR, defibrillatory countershocks and medications, and yields extensive information to foster advances in clinical treatment of cardiac arrest.

Keywords: Acidemia; Asphyxia; Cardiopulmonary resuscitation; Countershocks; Hyperoxia; Vasopressin; Ventricular fibrillation.

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Figures

Figure 1
Figure 1
Porcine preparation for cardiac arrest-cardiopulmonary resuscitation studies. The pig is placed in supine recumbency and mechanically ventilated via an endotracheal tube, through which isoflurane anesthesia is administered. Hemodynamic function is monitored by a femoral arterial catheter connected to a pressure transducer, and electrocardiographic activity is monitored by standard limb lead II electrocardiogram. Cardiac arrest is induced by a train of electrical impulses conducted by an intrajugular pacing wire from an electrical stimulator to the right ventricular endocardium. Body temperature is measured with a rectal probe, and end-tidal pCO2 by a sensor placed in the endotracheal tube. Defibrillatory countershocks (200-300 J) are administered with external paddles. Intravenous treatments include normal saline (N/S), phenylephrine (PE), sodium bicarbonate and experimental resuscitative fluids. spO2: Percentage oxyhemoglobin saturation.
Figure 2
Figure 2
Aortic pressures and lead IIelectrocardiogram during cardiac arrest, cardiopulmonary resuscitation and recovery of spontaneous circulation. A: Phasic aortic pressure tracing during the period from pre-arrest baseline to 20 min ROSC. Lettered arrows indicate times at which the electrocardiograms shown in panels B-F were obtained. Vertical lines indicate: (1) induction of ventricular fibrillation cardiac arrest; (2) commencement of precordial compressions (CPR); (3) injection of vasopressin (AVP); (4) defibrillation (Defib) by 200 J countershock; and (5) initiation of intravenous phenylephrine (PE; c. 2 μg/kg per minute) to stabilize systemic arterial pressure during ROSC. Mechanical ventilation was suspended during cardiac arrest and CPR. Panels B-F show 5 s electrocardiographic recordings. CPR: Cardiopulmonary resuscitation; ROSC: Recovery of spontaneous circulation; AVP: Vasopressin; PE: Phenylephrine.

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