Abstract Title

Structural impact of cardiac arrest and resuscitation on right vs. left ventricular myocardium

Presenter Name

Shehzad Y. Batliwala

Abstract

BACKGROUND: Cardiac arrest imposes ischemia on the entire body including the heart itself. Although cardio-cerebral resuscitation and defibrillation are essential to save the cardiac arrest victim, these interventions can damage the heart by initiating reperfusion injury culminating in oxidative stress, inflammation and edema. However, the literature contains a paucity of information on the effects of cardiac arrest, precordial compressions and trans-thoracic countershocks on myocardium structure and the degree of acute inflammation that occurs following cardiac arrest-resuscitation-induced ischemia-reperfusion. Moreover, the specific post-resuscitation structural differences in left vs. right ventricular myocardium have never been reported. The right ventricle is positioned directly beneath the anterior chest wall and receives the initial impact of the forceful precordial chest compressions; furthermore, the right ventricular wall is thinner and less robust than the left ventricular free wall and interventricular septum. Therefore, structural damage resulting from resuscitation efforts may differ in the right vs. left ventricles. Accordingly, this study tested the hypothesis that cardiac arrest, closed-chest cardio-cerebral resuscitation and transthoracic countershocks produce structural injury that is more severe in the right than left ventricular myocardium.

METHODS: Isoflurane-anesthetized Yorkshire swine, 25-40 kg of both genders were studied. The heart was arrested by a rapid train of impulses administered with an intravascular pacing wire. After 6 minutes of arrest, precordial compressions were applied at a rate of 100/min for 4 minutes. Transthoracic countershocks (200-300 J) were administered until spontaneous cardiac rhythm was restored. At 72 hours recovery, the heart was excised, and 1 x 1 cm, transmural biopsies of left and right ventricular free wall were collected, formalin-fixed and paraffin-embedded. Non-arrested sham experiments were also performed for comparison with cardiac arrest-resuscitation. Sections were cut, stained with hematoxylin and eosin, and 20 random high power (125 x) fields were examined and scored by an investigator blinded to the protocol. Specific structural endpoints included extracellular expansion, neutrophil invasion and hypercontracted tissue.

RESULTS: Sections of left and right ventricular myocardium are currently being analyzed in 6 cardiac arrest and 6 sham experiments for neutrophillic damage and infiltration. It is anticipated that tissue injury will be evident in both ventricles.

CONCLUSIONS: The finding of greater extracellular volume, neutrophil count and cardiomyocyte hypercontracture in right vs. left ventricular myocardium will be taken as evidence supporting the hypothesis. Such an outcome would argue for development of interventions to promote post-resuscitation myocardial structural recovery.

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Structural impact of cardiac arrest and resuscitation on right vs. left ventricular myocardium

BACKGROUND: Cardiac arrest imposes ischemia on the entire body including the heart itself. Although cardio-cerebral resuscitation and defibrillation are essential to save the cardiac arrest victim, these interventions can damage the heart by initiating reperfusion injury culminating in oxidative stress, inflammation and edema. However, the literature contains a paucity of information on the effects of cardiac arrest, precordial compressions and trans-thoracic countershocks on myocardium structure and the degree of acute inflammation that occurs following cardiac arrest-resuscitation-induced ischemia-reperfusion. Moreover, the specific post-resuscitation structural differences in left vs. right ventricular myocardium have never been reported. The right ventricle is positioned directly beneath the anterior chest wall and receives the initial impact of the forceful precordial chest compressions; furthermore, the right ventricular wall is thinner and less robust than the left ventricular free wall and interventricular septum. Therefore, structural damage resulting from resuscitation efforts may differ in the right vs. left ventricles. Accordingly, this study tested the hypothesis that cardiac arrest, closed-chest cardio-cerebral resuscitation and transthoracic countershocks produce structural injury that is more severe in the right than left ventricular myocardium.

METHODS: Isoflurane-anesthetized Yorkshire swine, 25-40 kg of both genders were studied. The heart was arrested by a rapid train of impulses administered with an intravascular pacing wire. After 6 minutes of arrest, precordial compressions were applied at a rate of 100/min for 4 minutes. Transthoracic countershocks (200-300 J) were administered until spontaneous cardiac rhythm was restored. At 72 hours recovery, the heart was excised, and 1 x 1 cm, transmural biopsies of left and right ventricular free wall were collected, formalin-fixed and paraffin-embedded. Non-arrested sham experiments were also performed for comparison with cardiac arrest-resuscitation. Sections were cut, stained with hematoxylin and eosin, and 20 random high power (125 x) fields were examined and scored by an investigator blinded to the protocol. Specific structural endpoints included extracellular expansion, neutrophil invasion and hypercontracted tissue.

RESULTS: Sections of left and right ventricular myocardium are currently being analyzed in 6 cardiac arrest and 6 sham experiments for neutrophillic damage and infiltration. It is anticipated that tissue injury will be evident in both ventricles.

CONCLUSIONS: The finding of greater extracellular volume, neutrophil count and cardiomyocyte hypercontracture in right vs. left ventricular myocardium will be taken as evidence supporting the hypothesis. Such an outcome would argue for development of interventions to promote post-resuscitation myocardial structural recovery.