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Cardiac Arrest Prior to Venoarterial Extracorporeal Membrane Oxygenation: Risk Factors for Mortality

Fux, Thomas PhD1,2; Holm, Manne PhD1,2; Corbascio, Matthias PhD2,3; van der Linden, Jan PhD1,2

doi: 10.1097/CCM.0000000000003772
Clinical Investigations
Editor's Choice

Objectives: Mortality after cardiac arrest remains high despite initiation of venoarterial extracorporeal membrane oxygenation. We aimed to identify pre-venoarterial extracorporeal membrane oxygenation risk factors of 90-day mortality in patients with witnessed cardiac arrest and with greater than or equal to 1 minute of cardiopulmonary resuscitation before venoarterial extracorporeal membrane oxygenation. The association between preimplant variables and all-cause mortality at 90 days was analyzed with multivariable logistic regression.

Design: Retrospective observational cohort study.

Setting: Tertiary medical center.

Patients: Seventy-two consecutive patients with cardiac arrest prior to venoarterial extracorporeal membrane oxygenation cannulation.

Interventions: None.

Measurements and Main Results: Median age was 56 years (interquartile range, 43–56 yr), 75% (n = 54) were men. Out-of-hospital cardiac arrest occurred in 12% (n = 9) of the patients. Initial cardiac rhythm was nonshockable in 57% (n = 41) and shockable in 43% (n = 31) of patients. Median cardiopulmonary resuscitation duration was 21 minutes (interquartile range, 10–73 min; range, 1–197 min]. No return of spontaneous circulation was present in 64% (n = 46) and postarrest cardiogenic shock in 36% (n = 26) of the patients at venoarterial extracorporeal membrane oxygenation cannulation. Median duration of venoarterial extracorporeal membrane oxygenation was 5 days (interquartile range, 2–12 d). The 90-day overall mortality and in-hospital mortality were 57% (n = 41), 53% (n = 38) died during venoarterial extracorporeal membrane oxygenation, and 43% (n = 31) were successfully weaned. All survivors had Cerebral Performance Category score 1–2 at discharge to home. Multivariable logistic regression analysis identified initial nonshockable cardiac arrest rhythm (odds ratio, 12.2; 95% CI, 2.83–52.7; p = 0.001), arterial lactate (odds ratio per unit, 1.15; 95% CI, 1.01–1.31; p = 0.041), and ischemic heart disease (7.39; 95% CI, 1.57–34.7; p = 0.011) as independent risk factors of 90-day mortality, whereas low-flow duration, return of spontaneous circulation, and age were not.

Conclusions: In 72 patients with cardiac arrest before venoarterial extracorporeal membrane oxygenation initiation, nonshockable rhythm, arterial lactate, and ischemic heart disease were identified as independent pre-venoarterial extracorporeal membrane oxygenation risk factors of 90-day mortality. The novelty of this study is that the metabolic state, expressed as level of lactate just before venoarterial extracorporeal membrane oxygenation initiation seems more predictive of outcome than cardiopulmonary resuscitation duration or absence of return of spontaneous circulation.

1Division of Perioperative Medicine and Intensive Care, Section Cardiothoracic Surgery and Anesthesiology, Karolinska University Hospital, Stockholm, Sweden.

2Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.

3Heart and Vascular Division, Karolinska University Hospital, Stockholm, Sweden.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (

The authors have disclosed that they do not have any potential conflicts of interest.

This work was performed at the Karolinska University Hospital, SE-17176 Stockholm, Sweden.

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Cardiac arrest (CA) is associated with an in-hospital mortality rate of between 75 and 93% (1–5). Several factors have been associated with outcome after CA including CA location, immediate start of cardiopulmonary resuscitation (CPR), initial CA rhythm, CPR (low-flow) duration, underlying etiology, comorbidity, and post-CA interventions. In patients with return of spontaneous circulation (ROSC), in-hospital mortality still remains between 40% and 90% despite optimization of ventilatory, hemodynamic, and metabolic variables (4, 6–9).Venoarterial extracorporeal membrane oxygenation (VA ECMO) can rapidly be implemented to provide mechanical cardiopulmonary support (extracorporeal CPR [E-CPR]) to reestablish adequate end-organ perfusion and oxygenation as the only remaining life-saving option when all other means of resuscitative or supportive therapies have failed (2, 4, 6, 10–15). Several studies have shown that this technique may improve survival in patients with irreversible postarrest cardiogenic shock (CS) (6, 12) or refractory in- or out-of-hospital CA compared with conventional CPR (2, 5, 10, 16–18). Despite VA ECMO support the overall in-hospital mortality rate still remains greater than 70% (2). However, the mortality rates vary widely (40–100%) related to patient heterogeneity in the cause of CA, CA location, no-flow and CPR duration, proportion non-ROSC versus postarrest CS, and often-limited sample sizes (19–21).

Previous studies of VA ECMO in conjunction with CA have mainly focused on refractory CA where VA ECMO was initiated during continuous cardiac compression. Only limited data have been published describing patients that have achieved sustained ROSC but nonetheless develop postarrest CS necessitating VA ECMO (4, 6, 12). Furthermore, there is limited data available on preimplant risk factors (i.e., before VA ECMO cannulation), which can be rapidly assessed during CPR or refractory postarrest CS to facilitate risk prediction and decision-making in an unselected CA-population. Nonreporting of missing data and absence of correlation analyses on identified outcome factors also often complicates interpretation of earlier findings.

The aim of this study was to identify independent pre-VA ECMO risk factors for 90-day mortality in patients with CA and CPR greater than or equal to 1 minute prior to VA ECMO, independently if VA ECMO was initiated during CPR or if ROSC was achieved but postarrest CS ensued.

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We performed a retrospective study examining the medical records of patients receiving VA ECMO after CA at a single tertiary care center (Karolinska University Hospital, Stockholm, Sweden) between October 2006 and January 2015. The primary endpoint was death from any cause at 90 days after VA ECMO initiation. The Regional Ethics Review Board approved this study (project number 2008/1695-31, 2012/119–32). Inclusion criteria were all patients presenting with in- or out-of-hospital CA, presumed or confirmed to be of cardiac etiology, receiving conventional CPR with a duration of greater than or equal to 1 minute and where CPR either continued until VA ECMO had been employed or resulted in sustained ROSC followed by refractory postarrest CS before VA ECMO. All CA were witnessed by trained medical personnel who immediately initiated conventional CPR, which limited the no-flow time to almost zero and excluded bystander impact on CPR quality. Patients with out-of-hospital CA were transported to our institution for immediate evaluation of suitability as candidates for VA ECMO support (all cannulations were performed in-hospital). Patients were eligible for VA ECMO at the discretion of the VA ECMO response team (cardiothoracic intensivist, interventional cardiologist, and cardiothoracic surgeon) and employed as a bridge to neurologic assessment and diagnostic interventions and therapies, when there was a potential for recovery, in the absence of severe comorbidities associated with short life expectancy. Baseline characteristics and the laboratory data at VA ECMO initiation (i.e., just before cannulation) were together with complications and outcome obtained from the medical records. Location of cannulation, type of cannulation, and complications were presented for descriptive purposes but not included in the statistical analysis as they were not pre-VA ECMO factors. The VA ECMO circuit, implantation technique, and patient management during VA ECMO have been described elsewhere (22–24). Weaning from VA ECMO was attempted when expectation of further cardiac improvement was not expected. Patients with severe neurologic injuries, refractory multiple organ failure, or when final weaning failed without patients being candidates for other destination therapies, were weaned off VA ECMO during withdrawal of life support.

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Refractory CS was defined as CS with evidence of progressive tissue hypoxia and end-organ failure unresponsive to conventional medical therapy including adequate intravascular volume loading and support with high doses of vasopressors. Ischemic heart disease (IHD) was defined as a history of myocardial infarction, angina pectoris, percutaneous coronary intervention/coronary bypass grafting, or where coronary angiography had shown evidence of coronary artery disease. No-flow duration was defined as the time (without chest compressions) from CA to initiation of CPR, and low-flow duration as the time with CPR (i.e., CPR duration) until sustained ROSC was achieved or VA ECMO initiated. Postarrest CS following sustained ROSC was defined as myocardial dysfunction with progressive hypoperfusion and tissue hypoxia refractory to intravascular volume loading and increasing doses of inotropic and vasopressor agents. Favorable neurologic outcome was defined as Cerebral Performance Category (CPC) scores of 1 (good performance) and 2 (moderate disability) on a 5-point scale (25) at the time of hospital discharge to home.

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Statistical Analyses

Categorical variables were presented as numbers and percentages and compared with the chi-square, Likelihood ratio, or Fisher exact tests. Because most continuous variables were nonnormally distributed (all except body mass index, weight, and hemoglobin), all data were expressed as median and interquartile range (IQR) and compared with the Mann-Whitney U test. Logistic regression was used to assess the impact of pre-VA ECMO variables on likelihood for death at 90-days after VA ECMO initiation. Statistical significance was set by p value of less than 0.05. The seven variables identified as being significant in the univariable analysis were subjected to multicollinearity analysis, prior to multivariable logistic regression analysis. Five variables, none with missing data, were included in the multivariable logistic regression model. To assess the impact of nonlinearity on the logistic regression analysis the continuous variables included in the model were transformed by using restricted cubic splines (the restricted cubic spline analysis is presented in Supplemental Digital Content 1 – Document 1, Goodness of fit was verified by the Hosmer-Lemeshow test. Cumulative survival curves for 90 days follow-up was generated utilizing the Kaplan-Meier method and compared using the log-rank test. Statistical analyses were performed with SPSS Version 25 for Windows (IBM SPSS Statistics, Armonk, NY) and Stata Statistical Software: Release 14 (StataCorp LP, College Station, TX).

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We included 72 patients who received VA ECMO following CA during the study period. Baseline characteristics before VA ECMO (i.e., before cannulation) were compared between survivors with nonsurvivors at 90 days after VA ECMO initiation (Table 1). There were significant differences between survivors and nonsurvivors regarding IHD prevalence, initial CA rhythm, low-flow duration, ROSC, mean arterial pressure (MAP), arterial pH, and lactate just before cannulation. All variables compared between survivors and nonsurvivors are presented in Table S1, Supplemental Digital Content 2, The no-flow duration was near to zero as all CA were witnessed by healthcare professionals on site with almost direct upstart of resuscitation. Forty-six patients (64%) received VA ECMO during ongoing CPR (absence of ROSC). The remaining 26 patients (36%) were initially successfully resuscitated to sustained ROSC after a median of 10 minutes (IQR, 2–17 min) but subsequently deteriorated secondary to refractory postarrest CS and VA ECMO was initiated as salvage therapy. Sixty patients (83%) were peripherally cannulated by a femoral venoarterial (96%) or femoral-internal jugular vein access (4%). The primary endpoint all-cause mortality at 90 days was 57% (n = 41). The 90-day mortality in patients with VA ECMO initiation during CA (n = 46) was 74% (34/46) and in patients with postarrest CS (n = 26) was 27% (7/26) (p < 0.001). Thirty-eight patients (53%) died during VA ECMO (Table 2). The in-hospital mortality was 57% (n = 41) and 43% (n = 31) of the 72 patients included in the study were discharged to home, all having a good neurologic outcome (CPC score 1–2). The main causes of death during VA ECMO were anoxic brain injuries and multiple organ failure, 21% (n = 15) respectively, and within 90 days anoxic brain injury 22% (n = 16) (Table 2). In the univariable logistic regression analysis, the following variables were significantly associated with 90-day mortality: IHD, initial nonshockable rhythm, absence of ROSC, low-flow duration, MAP, arterial pH, and lactate (Table 3). Due to high collinearity with lactate, MAP and pH were excluded from the model. We favored the exclusion of pH and not lactate as the latter is a more robust variable being less sensitive to the influence of Paco2 and administration of buffer solutions during CPR. The restricted cubic splines analysis indicated that a nonlinearity did not impact the logistic regression analysis, which supports the use of the model (the restricted cubic spline analysis is presented in Supplemental Digital Content – Document 1, The chi-square for Hosmer-Lemeshow test was 7.619 with a significance level of p value equals to 0.47 thereby supporting our model. The model as a whole correctly classified 83% of the cases. The sensitivity of the model was 85% and its specificity was 81%, giving a positive and negative predictive value of 85% and 81%, respectively. In the multivariable logistic regression analysis, three independent factors made significant contributions to the model (Table 3). All variables subjected to logistic regression analysis are presented in Table S2 (Supplemental Digital Content 3, The most significant risk factor was nonshockable rhythm as initial presenting CA rhythm followed by presence of IHD and arterial lactate level. Figure 1 depicts the Kaplan-Meier survival curves until 90 days after VA ECMO initiation indicating significant worse outcome for (A) lactate level greater than or equal to 17 mmol/L (153 mg/dL) (90% specificity), and (B) nonshockable compared with shockable rhythm. All patients (8/8) with a lactate level greater than 20 mmol (180 mg/dL) died within 6 days. The most frequent complications after initiation of VA ECMO were renal failure necessitating hemodialysis (54%) followed by pneumonia (43%) and anoxic brain injuries (19%) (Fig. 2).







Figure 1.

Figure 1.

Figure 2.

Figure 2.

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The present study identified initial nonshockable rhythm, presence of IHD, and arterial lactate, as independent pre-VA ECMO risk factors for 90-day mortality in patients with CA receiving conventional CPR with a duration of greater than or equal to 1 minute prior to VA ECMO.

This is to our knowledge the first study on specifically pre-VA ECMO factors for prognostication to facilitate swift decision-making in unselected patients with CA of verified or presumed cardiac etiology and with low-flow duration down to 1 minute when VA ECMO is considered, irrespectively if patients were cannulated during E-CPR or with refractory postarrest CS. Our finding that initial nonshockable rhythm was an independent predictor of mortality after VA ECMO initiation (Fig. 1) is in accordance with several other reports (6, 10, 26–30). In contrast, the study by Dennis et al (31) did not find such an association, most probably due to a type II error with only three out of 37 included patients with asystole (i.e., nonshockable rhythm).

Furthermore, our study verified pre-VA ECMO lactate level to be predictive of mortality. In conventional CPR, lactate levels have previously been identified as a survival and neurologic prognostic marker (32). In the setting of CA or refractory postarrest CS, arterial lactate levels indicate the extent of anaerobic metabolism secondary to hypoperfusion and tissue hypoxia (33) and therefore represents a surrogate marker of “no and low-flow duration” with insufficient tissue perfusion resulting in end-organ failure (9, 34). Metabolic acidosis can be treated with IV bicarbonate, which will influence base excess and arterial pH but not arterial lactate. Likewise, arterial lactate will not be influenced by arterial carbon dioxide pressure levels, in contrast to arterial pH. Arterial lactate has in agreement with our study also been found to be an independent pre-VA ECMO predictor of survival in a limited number of previous CA studies (11, 21, 30, 31, 35), which may be explained by missing lactate data in the majority of studies. This study identified arterial lactate with an odds ratio for 90-day mortality of 1.15 per mmol/L, which implies that the 90-day mortality risk increases 12-fold at a lactate level of 10 mmol/L.

Based on our daily practice, we divided the study population into three chosen subgroups of lactate with arbitrary cut off levels of less than 10, 10–20, greater than 20 mmol/L (Table 1) to facilitate clinical interpretation of lactate as a significant risk factor. Furthermore, after receiver operating characteristic (ROC) analysis the cut off level of greater than or equal to 17 was chosen (Fig. 1A) as it corresponded to a specificity of 90% (ROC survival of 10%), implying that at a lactate level of 17 identified greater than 90% of the patients that died in our study population. A cut off level of 20 mmol/L would have identified 100% of nonsurvivors and at the same time raised the question if ECMO out of ethical reasons should be offered to patients with a near to or 100% expected mortality. Using the 20 mmol/L criterion, eight of 72 patients (11%) should not have been cannulated. Similarly, Mégarbane et al (36) in a study including 66 E-CPR patients identified a pre-VA ECMO lactate level greater than or equal to 21 mmol/L to be associated with 100% mortality. Hence, we recommend that lactate concentration should be obtained prior to patient cannulation to be used in patient selection and prognostication. However, in acute cardiotoxic poisoning with acebutolol and flecainide leading to refractory CA, lactate levels can reach extreme values before cannulation and still be associated with survival (37). In addition, IHD was identified as a predictor of mortality, which is supported by previous studies indicating poor outcome in patients with IHD experiencing CA (22) and that sudden cardiac death, being the worldwide leading cause of all deaths, occurs in the majority in patients with atherosclerotic coronary artery disease (65–85%) (38).

Admittedly, we also identified low-flow duration and absence of ROSC as significant risk factors for 90-day mortality in the univariable logistic regression analysis. However, both factors lost their significance in the multivariable analysis (p = 0.398 and p = 0.262, respectively) in contrast to the factors nonshockable rhythm, lactate, and IHD. Low-flow duration has been reported to be an independent predictor of outcome in several studies (3, 10, 26, 27, 39), but in contrast to our study, those studies did not include lactate in the analyses. Thus, this may further support that arterial lactate represents a metabolic marker superior to the precarious factor low-flow duration, the latter being influenced by CPR quality, the often-inexact no and low-flow time estimations, and the possibility of undetected interim periods of ROSC during ongoing CPR. Thus, the metabolic state, expressed as level of lactate just before start of VA ECMO, seems to be more predictive of outcome than low-flow time (i.e., CPR duration) or absence of ROSC. This further strengthens that lactate should be obtained from patients during and after CPR when VA ECMO is considered as salvage therapy.

There are no universal criteria time criteria to define refractory CA. Most previous studies have excluded patients with arbitrary low-flow durations (below 10–30 min). In contrast, to evaluate the influence of the time component low-flow duration on outcome, we included patients with low-flow durations down to 1 minute (median, 21 min; IQR, 10–73 min). This enabled us to analyze the complete range of low-flow durations with other factors, including lactate.

Age has been associated with mortality in previous CA related VA ECMO studies (2, 27, 28). In contrast, in our and other studies, which have included lactate (11, 21, 31, 35), age did not reach statistical significance. This may be a due to a type II error or maybe more presumably that age was neutralized by many other covariates included in the various study models. The primary endpoint mortality within 90-days after initiation of VA ECMO in our study was chosen over 30-day mortality, as 5.6% of the patients (n = 4) had VA ECMO support greater than or equal to 30 days. Likewise, the Kaplan-Meier survival curves flattened out before reaching 90 days (Fig. 1). We preferred logistic regression for categorical vital status at 90 days rather than Cox regression for time-dependent outcomes analyses, given the nonproportional hazards with early high risk. Furthermore, we preferred the outcome variable mortality at 90 days (57%) to the alternative alive at hospital discharge (43%) as the former includes a specific time span.

Advantages of this study despite the modest number of patients included were that all CA were witnessed by healthcare professionals with immediate initiation of CPR, thereby excluding the influence of no-flow duration and the precarious variable of bystander CPR. Together with registered low-flow durations down to 1 minute, irrespective if resuscitation was followed by ROSC or not, facilitates interpretation of low-flow duration’s predictive contribution to outcome. Furthermore, identification of significant risk factors was based on complete data including CPR variables and laboratory values.

This retrospective mono-center study with a heterogeneous patient population did not allow for randomization or include a matched control cohort. However, its heterogeneity reflects the clinical reality in centers providing VA ECMO to unselected patients with CA prior to VA ECMO initiation and thereby provides for external validity (generalizability) of our findings. Even though this study population is relatively small and our findings may not allow definitive recommendations, our analysis is based on variables without missing data, a fact often not addressed in many studies.

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In patients with CA and CPR duration of greater than or equal to 1 minute before VA ECMO, we identified nonshockable rhythm, IHD, and arterial lactate as independent pre-VA ECMO risk factors of 90-day mortality, whereas low-flow duration, ROSC, and age were not significant. These novel findings illustrate that initial CA rhythm and metabolic assessment may be more important than rigid time or age limits when considering use of VA ECMO support during CPR or in postarrest CS.

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1. Goldberger ZD, Chan PS, Berg RA, et al.; American Heart Association Get With The Guidelines—Resuscitation (formerly National Registry of Cardiopulmonary Resuscitation) Investigators: Duration of resuscitation efforts and survival after in-hospital cardiac arrest: An observational study. Lancet 2012; 380:1473–1481
2. Richardson AS, Schmidt M, Bailey M, et al. ECMO Cardio-Pulmonary Resuscitation (ECPR), trends in survival from an international multicentre cohort study over 12-years. Resuscitation 2017; 112:34–40
3. Chen CT, Chiu PC, Tang CY, et al. Prognostic factors for survival outcome after in-hospital cardiac arrest: An observational study of the oriental population in Taiwan. J Chin Med Assoc 2016; 79:11–16
4. Bougouin W, Aissaoui N, Combes A, et al.; SDEC Investigators: Post-cardiac arrest shock treated with veno-arterial extracorporeal membrane oxygenation: An observational study and propensity-score analysis. Resuscitation 2017; 110:126–132
5. Blumenstein J, Leick J, Liebetrau C, et al. Extracorporeal life support in cardiovascular patients with observed refractory in-hospital cardiac arrest is associated with favourable short and long-term outcomes: A propensity-matched analysis. Eur Heart J Acute Cardiovasc Care 2016; 5:13–22
6. Pineton de Chambrun M, Bréchot N, Lebreton G, et al. Venoarterial extracorporeal membrane oxygenation for refractory cardiogenic shock post-cardiac arrest. Intensive Care Med 2016; 42:1999–2007
7. Sandroni C, D’Arrigo S, Nolan JP. Prognostication after cardiac arrest. Crit Care 2018; 22:150
8. Neumar RW, Nolan JP, Adrie C, et al. Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation 2008; 118:2452–2483
9. Jentzer JC, Chonde MD, Dezfulian C. Myocardial dysfunction and shock after cardiac arrest. Biomed Res Int 2015; 2015:314796
10. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: An observational study and propensity analysis. Lancet 2008; 372:554–561
11. Ellouze O, Vuillet M, Perrot J, et al. Comparable outcome of out-of-hospital cardiac arrest and in-hospital cardiac arrest treated with extracorporeal life support. Artif Organs 2018; 42:15–21
12. Chonde M, Sappington P, Kormos R, et al. The use of ECMO for the treatment of refractory cardiac arrest or postarrest cardiogenic shock following in-hospital cardiac arrest: A 10-year experience. J Intensive Care Med 2018; 1:1525–1489
13. Callaway CW, Soar J, Aibiki M, et al.; Advanced Life Support Chapter Collaborators: Part 4: Advanced life support: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Circulation 2015; 132:S84–145
14. Bednarczyk JM, White CW, Ducas RA, et al. Resuscitative extracorporeal membrane oxygenation for in hospital cardiac arrest: A Canadian observational experience. Resuscitation 2014; 85:1713–1719
15. Xie A, Phan K, Tsai YC, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest: A meta-analysis. J Cardiothorac Vasc Anesth 2015; 29:637–645
16. Lin JW, Wang MJ, Yu HY, et al. Comparing the survival between extracorporeal rescue and conventional resuscitation in adult in-hospital cardiac arrests: Propensity analysis of three-year data. Resuscitation 2010; 81:796–803
17. Maekawa K, Tanno K, Hase M, et al. Extracorporeal cardiopulmonary resuscitation for patients with out-of-hospital cardiac arrest of cardiac origin: A propensity-matched study and predictor analysis. Crit Care Med 2013; 41:1186–1196
18. Kim SJ, Kim HJ, Lee HY, et al. Comparing extracorporeal cardiopulmonary resuscitation with conventional cardiopulmonary resuscitation: A meta-analysis. Resuscitation 2016; 103:106–116
19. Fagnoul D, Combes A, De Backer D. Extracorporeal cardiopulmonary resuscitation. Curr Opin Crit Care 2014; 20:259–265
20. Singal RK, Singal D, Bednarczyk J, et al. Current and future status of extracorporeal cardiopulmonary resuscitation for in-hospital cardiac arrest. Can J Cardiol 2017; 33:51–60
21. Zhang Y, Li CS, Yuan XL, et al. Association of serum biomarkers with outcomes of cardiac arrest patients undergoing ECMO. Am J Emerg Med 2018; 36:2020–2028
22. Cesana F, Avalli L, Garatti L, et al. Effects of extracorporeal cardiopulmonary resuscitation on neurological and cardiac outcome after ischaemic refractory cardiac arrest. Eur Heart J Acute Cardiovasc Care 2018; 7:432–441
23. Haneya A, Philipp A, Diez C, et al. A 5-year experience with cardiopulmonary resuscitation using extracorporeal life support in non-postcardiotomy patients with cardiac arrest. Resuscitation 2012; 83:1331–1337
24. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation 2015; 86:88–94
25. Jacobs I, Nadkarni V, Bahr J, et al.; International Liaison Committee on Resuscitation; American Heart Association; European Resuscitation Council; Australian Resuscitation Council; New Zealand Resuscitation Council; Heart and Stroke Foundation of Canada; InterAmerican Heart Foundation; Resuscitation Councils of Southern Africa; ILCOR Task Force on Cardiac Arrest and Cardiopulmonary Resuscitation Outcomes: Cardiac arrest and cardiopulmonary resuscitation outcome reports: Update and simplification of the Utstein templates for resuscitation registries: A statement for healthcare professionals from a task force of the International Liaison Committee on Resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa). Circulation 2004; 110:3385–3397
26. Kagawa E, Inoue I, Kawagoe T, et al. Assessment of outcomes and differences between in- and out-of-hospital cardiac arrest patients treated with cardiopulmonary resuscitation using extracorporeal life support. Resuscitation 2010; 81:968–973
27. Park SB, Yang JH, Park TK, et al. Developing a risk prediction model for survival to discharge in cardiac arrest patients who undergo extracorporeal membrane oxygenation. Int J Cardiol 2014; 177:1031–1035
28. Wang CH, Chou NK, Becker LB, et al. Improved outcome of extracorporeal cardiopulmonary resuscitation for out-of-hospital cardiac arrest–a comparison with that for extracorporeal rescue for in-hospital cardiac arrest. Resuscitation 2014; 85:1219–1224
29. Yukawa T, Kashiura M, Sugiyama K, et al. Neurological outcomes and duration from cardiac arrest to the initiation of extracorporeal membrane oxygenation in patients with out-of-hospital cardiac arrest: A retrospective study. Scand J Trauma Resusc Emerg Med 2017; 25:95
30. Debaty G, Babaz V, Durand M, et al. Prognostic factors for extracorporeal cardiopulmonary resuscitation recipients following out-of-hospital refractory cardiac arrest. A systematic review and meta-analysis. Resuscitation 2017; 112:1–10
31. Dennis M, McCanny P, D’Souza M, et al.; Sydney ECMO Research Interest Group: Extracorporeal cardiopulmonary resuscitation for refractory cardiac arrest: A multicentre experience. Int J Cardiol 2017; 231:131–136
32. Donnino MW, Andersen LW, Giberson T, et al.; National Post-Arrest Research Consortium: Initial lactate and lactate change in post-cardiac arrest: A multicenter validation study. Crit Care Med 2014; 42:1804–1811
33. Wang CH, Huang CH, Chang WT, et al. Monitoring of serum lactate level during cardiopulmonary resuscitation in adult in-hospital cardiac arrest. Crit Care 2015; 19:344
34. Kalogeris T, Baines CP, Krenz M, et al. Ischemia/reperfusion. Compr Physiol 2016; 7:113–170
35. Jung C, Janssen K, Kaluza M, et al. Outcome predictors in cardiopulmonary resuscitation facilitated by extracorporeal membrane oxygenation. Clin Res Cardiol 2016; 105:196–205
36. Mégarbane B, Deye N, Aout M, et al. Usefulness of routine laboratory parameters in the decision to treat refractory cardiac arrest with extracorporeal life support. Resuscitation 2011; 82:1154–1161
37. Mégarbane B, Leprince P, Deye N, et al. Emergency feasibility in medical intensive care unit of extracorporeal life support for refractory cardiac arrest. Intensive Care Med 2007; 33:758–764
38. El-Sherif N, Boutjdir M, Turitto G. Sudden cardiac death in ischemic heart disease: Pathophysiology and risk stratification. Card Electrophysiol Clin 2017; 9:681–691
39. Wengenmayer T, Rombach S, Ramshorn F, et al. Influence of low-flow time on survival after extracorporeal cardiopulmonary resuscitation (eCPR). Crit Care 2017; 21:157

cardiac arrest; cardiopulmonary resuscitation; extracorporeal life support; extracorporeal membrane oxygenation; postarrest cardiogenic shock; prognostication

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