ECMO improves survival following cardiogenic shock due to carbon monoxide poisoning - an experimental porcine model

Abstract

BackgroundSevere intoxication with carbon monoxide (CO) is extremely lethal and causes numerous deaths due to cardiac or respiratory failure. Conventional intensive treatment may not be sufficient. The aim of this study was to investigate the treatment effect of extracorporeal veno-arterial extracorporeal membrane oxygenation (ECMO) following severe CO poisoning in an experimental porcine model.MethodsA total of twelve pigs were anaesthetized, routinely monitored and intoxicated by inhalation of CO until the beginning of cardiac failure and randomized to a treatment (ventilator using an FiO2 of 100% or ECMO). In the case of cardiac arrest, advanced resuscitation using standard guidelines was performed for at least 10 min. ECMO was also initiated in the ventilation group if the return of spontaneous circulation did not occur within 10 min. Lung tissue biopsies were obtained before and after CO intoxication.ResultsAll animals in the ECMO group survived; however, one had to be resuscitated due to cardiac arrest. A single animal survived in the ventilator group, but five animals suffered from cardiac arrest at an average of 11.8 min after initiation of treatment. Conventional resuscitation failed in these animals, but four animals were successfully resuscitated after the establishment of ECMO.A significant decrease was noticed in PO2 with increasing HbCO, but there was no increase in pulmonary vascular resistance. No differences in H&E-stained lung tissue biopsies were observed.ConclusionsThe use of ECMO following severe CO poisoning greatly improved survival compared with conventional resuscitation in an experimental porcine model. This study forms the basis for further research among patients.

An innovative ovine model of severe cardiopulmonary failure supported by veno-arterial extracorporeal membrane oxygenation

“…Ventricular brillation is the most frequent side-effect of previous experimental cardiogenic shock models, leading to death in up to 50% of animals [16,17,21,27]. To reduce the loss of animals, antiarrhythmics were administered before ethanol injection, and this resulted in ventricular brillation in only one animal.…”

“…In particular, reproducing a stable cardiogenic shock model by ligating major coronary arteries often resulted in refractory and lifethreatening ventricular arrhythmias [16][17][18][19]. Other methods, such as carbon monoxide poisoning or druginduced CS (beta-blockers), have resulted in heterogeneous outcomes and cause a global decrease in ventricular contractility, different to regional wall motion abnormalities usually seen in myocardial infarction [20,21].…”

A total closed chest sheep model of cardiogenic shock by percutaneous intracoronary ethanol injection

“…First, systemic or selective coronary hypoxemia 5 is responsible for a generalized diminished cardiac function due to the hibernating myocardial condition: in this setting, cellular mechanisms of adaptation are not the same than in distinct infarcted myocardium. Similar concerns should be taken into account in the case of global toxicity, induced by carbon monoxide 6 . The use of microspheres could overcome this difficulty 7 , but the injection in the left main coronary artery has a generalized effect on the left ventricle and is associated with a jeopardized cellular death in the whole myocardial wall thickness.…”

“…The use of microspheres could overcome this difficulty 7 , but the injection in the left main coronary artery has a generalized effect on the left ventricle and is associated with a jeopardized cellular death in the whole myocardial wall thickness. Furthermore, the set-up of several studies requires STMCS activation soon after 6 , 7 or even before 8 CS induction in order to avoid premature death of animals, or an open-chest procedure for coronary ligatures 9 , which completely modifies the heart-pericardium and heart–lung interactions. In recent studies suggesting that early mechanical percutaneous support prior to revascularization might reduce the size of myocardial necrosis 10 , a condition of mild systemic hypo-perfusion is obtained rather than an effective hemodynamic CS.…”

Cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme

“…However, due to the lack of efficacy basis, the application of hyperbaric oxygen to ACOP patients still lacks relevant evidence (7). In recent years, due to the development of extracorporeal circulation technology, extracorporeal membrane oxygenation (ECMO) technology has been gradually applied to the treatment of ACOP, and Simonsen et al (8) reported that ECMO treatment can improve the survival rate of ACOP patients with cardiogenic shock, but its exact efficacy is currently less studied.…”