Survival and Factors Associated with Survival with Extracorporeal Life Support During Cardiac Arrest

Introduction: In case of no return of spontaneous circulation (ROSC) after conventional cardio-pulmonary resuscitation (CPR), out-of-hospital cardiac arrest (OHCA) patients could be referred for extracorporeal life support (ECLS). Guidelines have been published concerning this specific situation (1). The aim of our study was to describe the prognosis of OHCA patients and verify if referral to ECLS was compliant with these recommendations mainly studying time intervals (no-flow < 5 min, low-flow < 100 min). Methods: A prospective survey on OHCA referred to ECLS was implemented from 03/01/12 until 06/11/15 in an Emergency Medical Service (EMS) located in Paris area (France). This survey included 43 patients referred to hospital for ECLS. Variables were given as means and percentages. Results: Patients referred to ECLS were more often men (77%), with a mean age of 51 years old. Most of 43 OHCA occurred at home (51%), although 26% occurred on public area and 16% at workplace. In 40% of cases, CPR was performed by a witness and in 33% by a health professional. A first Basic Life Support ambulance arrived on scene within 7 min 50 sec, whereas EMS ambulance arrived on scene within 18 min 27 sec after OHCA. At EMS arrival on scene, patients were on asystole (44%), ventricular fibrillation (37%), and on spontaneous circulation (12%). The no-flow time interval was 4 min 10 sec on average (6 patients had a no-flow over 5 min) with 43% of patients with no no-flow. Low-flow time-interval was 44 min. External electric shock was delivered before EMS arrival on 21% of cases, and EMS itself delivered a shock in 40% of cases. Epinephrine was used for all patients, 10.35 mg on average. No patient survived OHCA after referral to ECLS. Discussion: Although this is a small series of 43 patients, no OHCA patient referred to ECLS survived. These results are mainly due to a non-shockable initial condition or too long no-flow time intervals. In order to improve the outcome and bring benefit to the proper expected patients through a cost-effective pathway, we released a reminder of the right recommendations in our EMS. (1) Riou B., Adnet F., Baud F et al. A. Recommandation sur les indications de l’assistance circulatoire dans le traitement des arrêts cardiaques réfractaires. Ann Fr Anesth Réanim 2009 ; 28 : 182-6.

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Extracorporeal resuscitation with carbon monoxide improves renal function by targeting inflammatory pathways in cardiac arrest in pigs

AJP Renal Physiology ◽

10.1152/ajprenal.00241.2019 ◽

2019 ◽

Vol 317 (6) ◽

pp. F1572-F1581 ◽

Cited By ~ 1

Author(s):

Jakob Wollborn ◽

Bjoern Schlueter ◽

Christoph Steiger ◽

Cornelius Hermann ◽

Christian Wunder ◽

...

Keyword(s):

Carbon Monoxide ◽

Renal Function ◽

Cardiac Arrest ◽

Renal Injury ◽

Porcine Model ◽

Life Support ◽

Apoptotic Cell ◽

Extracorporeal Life Support ◽

Successful Resuscitation ◽

Extracorporeal Resuscitation

Deleterious consequences like acute kidney injury frequently occur upon successful resuscitation from cardiac arrest. Extracorporeal life support is increasingly used to overcome high cardiac arrest mortality. Carbon monoxide (CO) is an endogenous gasotransmitter, capable of reducing renal injury. In our study, we hypothesized that addition of CO to extracorporeal resuscitation hampers severity of renal injury in a porcine model of cardiac arrest. Hypoxic cardiac arrest was induced in pigs. Animals were resuscitated using a conventional [cardiopulmonary resuscitation (CPR)], an extracorporeal (E-CPR), or a CO-assisted extracorporeal (CO-E-CPR) protocol. CO was applied using a membrane-controlled releasing system. Markers of renal injury were measured, and histopathological analyses were carried out. We investigated renal pathways involving inflammation as well as apoptotic cell death. No differences in serum neutrophil gelatinase-associated lipocalin (NGAL) were detected after CO treatment compared with Sham animals (Sham 71 ± 7 and CO-E-CPR 95 ± 6 ng/mL), while NGAL was increased in CPR and E-CPR groups (CPR 135 ± 11 and E-CPR 124 ± 5 ng/mL; P < 0.05). Evidence for histopathological damage was abrogated after CO application. CO increased renal heat shock protein 70 expression and reduced inducible cyclooxygenase 2 (CPR: 60 ± 8; E-CPR 56 ± 8; CO-E-CPR 31 ± 3 µg/mL; P < 0.05). Caspase 3 activity was decreased (CPR 1,469 ± 276; E-CPR 1,670 ± 225; CO-E-CPR 755 ± 83 pg/mL; P < 0.05). Furthermore, we found a reduction in renal inflammatory signaling upon CO treatment. Our data demonstrate improved renal function by extracorporeal CO treatment in a porcine model of cardiac arrest. CO reduced proinflammatory and proapoptotic signaling, characterizing beneficial aspects of a novel treatment option to overcome high mortality.

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