Warenits, Alexandra Maria;
Müller, Matthias;
Magnet, Ingrid Anna Maria;
Ettl, Florian;
Hamza, Ouafa;
Kottbauer, Felix;
Högler, Sandra;
Podesser, Bruno;
Holzer, Michael;
Weihs, Wolfgang;
Kiss, Attila
Abstract 214: Cardiac Arrest and Extracorporeal Cardiopulmonary Resuscitation Impairs Left Ventricle Hemodynamic Function in a Ventricular Fibrillation Cardiac Arrest Model in Rats
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Media type:
E-Article
Title:
Abstract 214: Cardiac Arrest and Extracorporeal Cardiopulmonary Resuscitation Impairs Left Ventricle Hemodynamic Function in a Ventricular Fibrillation Cardiac Arrest Model in Rats
Contributor:
Warenits, Alexandra Maria;
Müller, Matthias;
Magnet, Ingrid Anna Maria;
Ettl, Florian;
Hamza, Ouafa;
Kottbauer, Felix;
Högler, Sandra;
Podesser, Bruno;
Holzer, Michael;
Weihs, Wolfgang;
Kiss, Attila
Description:
<jats:p>
<jats:bold>Introduction:</jats:bold>
Extracorporeal Cardiopulmonary Resuscitation (ECPR) may achieve ROSC after prolonged CA when conventional cardiopulmonary resuscitation fails. We investigated the impact of ECPR on cardiac hemodynamic recovery and hypothesized, that left ventricular hemodynamic function is impaired in resuscitated hearts.
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<jats:p>
<jats:bold>Methods:</jats:bold>
Adult male Sprague-Dawley rats (500 g, n=36) were subjected to 6 or 8 min of ventricular fibrillation CA, thereafter resuscitated with ECPR (open reservoir, roller pump, membrane oxygenator, draining catheter in the right jugular vein, inflow catheter in the right femoral artery; custom made bypass system), mechanical ventilation and drugs (epinephrine, bicarbonate, heparin). After defibrillation and ROSC, rats survived for 14 days and were compared to 7 sham animals. The hearts were isolated and mounted onto an erythrocyte-perfused, isolated working heart (WH) system. Cardiac output, left ventricular systolic pressure (LVSP), coronary flow and pressure-volume (P-V) relationships (by increasing the afterload in 10 mmHg increments) were measured. Myocardium of all rats was evaluated pathohistological in hematoxylin-eosin staining.
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<jats:p>
<jats:bold>Results:</jats:bold>
ROSC was achieved in 18 animals after 6 min of CA, of which 10 survived 14 d and 7 were investigated in WH, in 8 min CA group 15 achieved ROSC of which 5 survived to 14 d and 2 were investigated in WH and compared to the hearts of 7 sham animals. At defined afterload (60 mm Hg; baseline) there was no difference in cardiac hemodynamics between sham and 6 min CA group. In contrast, 8 min CA rats showed a tendency towards decrease in cardiac output and LVSP compared to sham animals. Notably, both CA groups showed impaired P-V loop relationship and subsequently less tolerance to hemodynamic stress. Histologically all 8 min CA rats showed multiple foci of myocardial scarring.
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<jats:p>
<jats:bold>Conclusions:</jats:bold>
CA led to impaired left ventricular hemodynamics in 8 min CA rats resuscitated with ECPR. In addition, hearts were more vulnerable to hemodynamic stress after successful resuscitation. For investigating the effects of future therapy approaches during and after resuscitation from CA on the heart function, isolated WH might be a promising approach in resuscitation research.
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