Venoarterial Extracorporeal Membrane Oxygenation in Adults With Cardiac Arrest
Journal of Intensive Care Medicine 1-10 ª The Author(s) 2015 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0885066615583651 jic.sagepub.com
Jignesh K. Patel, MD1, Elinor Schoenfeld, PhD2, Sam Parnia, MD1, Adam J. Singer, MD3, and Norman Edelman, MD1
Abstract Cardiac arrest (CA) is a major cause of morbidity and mortality worldwide. Despite the use of conventional cardiopulmonary resuscitation (CPR), rates of return of spontaneous circulation and survival with minimal neurologic impairment remain low. Utilization of venoarterial extracorporeal membrane oxygenation (ECMO) for CA in adults is steadily increasing. Propensitymatched cohort studies have reported outcomes associated with ECMO use to be superior to that of conventional CPR alone in in-hospital patients with CA. In this review, we discuss the mechanism, indications, complications, and evidence for ECMO in CA in adults. Keywords Cardiac Arrest (CA), Extracorporeal Membrane Oxygenation (ECMO), Cardiopulmonary Resuscitation (CPR)
Introduction Cardiac arrest (CA) is a major cause of morbidity and mortality worldwide. Regardless of the advancements over the past 50 years in ventilation administration, cardiostimulant medications, chest compressions, and electrical defibrillation, achievement of return of spontaneous circulation (ROSC) with conventional cardiopulmonary resuscitation (CPR) remains difficult. Furthermore, despite attainment of ROSC, some patients experience rearrest and/or poor neurological outcomes. Extracorporeal membrane oxygenation (ECMO) was introduced in the 1970s as a means of support in patients with respiratory or cardiac failure.1,2 Recent improvements in extracorporeal technology and increasing data supporting favorable clinical outcomes with the use of ECMO in cardiopulmonary disease have generated interest as well as enhanced utilization in critical care medicine.3-5 In this review, we discuss the physiology, indications, and utilization of venoarterial ECMO specifically in adults with CA.
What is Venoarterial ECMO? Venoarterial ECMO provides rapid temporal circulatory assistance to patients with shock or CA.6 It consists of an extracorporeal circuit that directly oxygenates and removes carbon dioxide from the blood via a membrane oxygenator (a gas exchange device that utilizes a semipermeable membrane to separate blood from gas). When blood is drained from a central vein and returned to a central vein, a process known as venovenous ECMO, the device provides gas exchange only. When blood is drained from the venous
system and pumped into an artery, a process known as venoarterial ECMO, the circuit provides both respiratory and circulatory support. ECMO systems. The ECMO system is composed of bypass cannulae, a centrifugal (or roller) pump, a heat exchanger, and a membrane oxygenator.7 The traditional venoarterial ECMO circuit extends from the cannula (inserted from the femoral vein) in the right atrium to the femoral artery (Figure 1). Oxygenation via the membrane oxygenator is needed as pulmonary blood circulation is bypassed. Extracorporeal circuits are efficient at removing carbon dioxide and can do so at blood flow rates much lower than what is needed to achieve adequate oxygenation.8,9 The principal determinants of blood oxygenation for a given device are the fraction of oxygen delivered via the oxygenator, the amount of blood flow through the circuit, and the function of the native lungs while the determinants of 1 Division of Pulmonary and Critical Care, Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA 2 Department of Preventive Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA 3 Department of Emergency Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA
Received January 10, 2015, and in revised form March 12, 2015. Accepted for publication March 13, 2015. Corresponding Author: Jignesh K. Patel, Department of Medicine, Stony Brook University Medical Center, Health Science Center T17-040, Stony Brook, NY, USA. Email: [email protected]
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Journal of Intensive Care Medicine In the setting of CA, chest compressions can often be ceased following achievement of adequate pump flows on venoarterial ECMO. Although circulatory support is in effect, the underlying cause of CA (eg, acute coronary syndrome, electrolyte abnormalities, pulmonary embolism, drug intoxication, etc) should be identified and treated accordingly. While primary percutaneous coronary intervention (PCI) for acute myocardial infarction has been demonstrated to improve clinical outcomes,15 emergent coronary angiography in patients with CA in the absence of acute electrocardiographic changes remains controversial and may vary according to provider preference and institutional algorithms.16-21 Therapeutic hypothermia has been shown to improve clinical outcomes in out-of-hospital patients with CA with and without a shockable rhythm.17,18,22,23 In hemodynamically stable, ECMO-treated, comatose patients, mild hypothermia may be induced by priming the ECMO circuit with cold saline and utilizing the heat exchanger to rapidly achieve target temperatures of 32 C to 34 C.7
Figure 1. Venoarterial extracorporeal membrane oxygenation (ECMO) circuit.
carbon dioxide removal are the sweep gas flow rate (ie, the rate of gas flow through the oxygenator) and the rate of blood flow.10 Although ECMO cannulation has traditionally been performed in the operating room (or at the bedside) by cardiothoracic surgeons performing cutdown procedures for cannulation, percutaneous approaches have become more frequently adopted.3,11 Cannulation is usually performed with arterial cannulae measuring 15 to 17F and venous cannulae measuring 17 to 19F. If the cannulae are not sufficiently large, hemolysis tends to be severe. The venoarterial ECMO circuit traditionally extends from the cannula (inserted from the femoral vein) in the right atrium for drainage coupled with femoral arterial reinfusion. Reinfusion flow travels retrograde up the aorta and may meet resistance from left ventricle (LV)-generated antegrade flow. The location of the interface between antegrade and retrograde flow may vary depending on the severity of native myocardial dysfunction. Oxygen delivery to the coronary and cerebral vasculature can be inadequate in the setting of both impaired native gas exchange and poorly oxygenated blood pumped from the LV. Occasionally, this may necessitate venous drainage combined with both arterial and venous return (ie, venoarterial-venous ECMO). An additional reinfusion cannula with a ‘‘Y’’ connection originating from the femoral arterial reinfusion cannula can be inserted directly into an internal jugular vein to permit oxygenation of the coronary and cerebral circulation via return of oxygenated blood into the native cardiac circulation while concomitantly providing circulatory support. Venoarterial ECMO may result in LV overdistention and worsening pulmonary edema in the setting of severe LV dysfunction.12-14 The LV decompression in these circumstances can be facilitated with percutaneous insertion of a microaxial flow pump.13,14
Indications for ECMO in CA The 2010 American Heart Association guidelines for CPR and emergency cardiovascular care do not recommend the routine use of ECMO for CA.15,24 However, ECMO may be considered when the time without spontaneous circulation is short and resuscitation attempts are adequate (ie, CPR > 10 minutes, appropriate use of guideline-directed medications [eg, epinephrine, vasopressin, etc], and defibrillation for shockable rhythms). The guidelines emphasize that ECMO use should be restricted to centers at which it is readily available and that its initiation and management require highly trained personnel and specialized equipment. The inclusion criteria for ECMO in adults with CA can vary widely among institutions, given the substantial costs and manpower associated with its use (Table 1). Criteria that are often utilized include age cutoffs (usually excluding elderly patients), rhythm at the time of CPR (favorable to ventricular arrhythmias), time interval from the patient’s collapse to initiation of resuscitation (often necessitates 15 minutes or less), presumed etiology of the arrest (ie, cardiac origin, pulmonary embolism, etc), and if ROSC is not achievable despite optimal CPR (eg, within 20 minutes).25,26 Patients with terminal illnesses preceding the arrest, previous severe neurologic damage, current intracranial hemorrhage, arrest of traumatic origin with uncontrolled bleeding, arrest of septic origin, irreversible organ failure leading to CA when no physiological benefit could be expected despite maximal therapy (hepatic failure, late stage of adult respiratory distress syndrome, etc), acute aortic dissection, and significant peripheral vascular disease precluding bypass cannulation would be poor candidates for ECMO.25,27,28
Clinical Outcomes With ECMO Use in CA To date, there are no randomized controlled trials investigating the impact of ECMO for adults with CA. Most data
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Table 1. Inclusion and Exclusion Criteria for Venoarterial ECMO Use in Cardiac Arrest. Inclusion criteria Age cutoffs, usually age 10 min
Shin et al29,30
60
60
Retrospective observational; propensity score matched
Witnessed IHCA Mortality or significant CPR > 10 min neurologic impairment
Maekawa et al31
24
24
Prospective observational; propensity score matched
Witnessed OHCA CPR > 20 min
Mortality or significant neurologic impairment
Time Frame In-hospital: HR 0.51 (95% CI 0.35-0.74) 30 days: HR 0.47 (95% CI 0.28-0.77) 1 year: HR 0.53 (95% CI 0.33-0.83) In-hospital: HR 0.17 (95% CI 0.04-0.71) 6 months: HR 0.48 (95% CI 0.29-0.77) 2 years: 80.0% vs 95.0%, P ¼ .002 3 months: 70.8% ECMO þCPR vs 91.7% CPR, P ¼ .013
Abbreviations: PS, propensity score; IHCA, in-hospital cardiac arrest; OHCA, out-of-hospital cardiac arrest; CPR, cardiopulmonary resuscitation; HR, hazard ratio; CI, confidence interval; ECMO, extracorporeal membrane oxygenation.
retrieved on outcomes have been observational studies and propensity analyses (Tables 2 and 3). In-hospital CA. In a 3-year prospective, observational study of patients with witnessed in-hospital CA undergoing CPR for more than 10 minutes, Chen et al performed a matching process based on propensity score was done to balance potential prognostic factors in both groups and to formulate a balanced 1:1 matched cohort study.28 Propensity analysis matched 46 patients who received conventional CPR with 46 patients who received ECMO with CPR. Unmatched patients who received ECMO with CPR had a higher survival rate to discharge (28.8% vs 12.3%; log-rank P < .0001) and a better 1-year
survival (18.6% vs 9.7%) than those who received conventional CPR (log-rank P ¼ .007). Between the propensity scorematched groups, there was still a significant difference in survival to discharge (hazard ratio [HR] 0.51, 95% confidence interval [CI] 0.35-0.74, P < .0001), 30-day survival (HR 0.47, 95% CI 0.28-0.77, P ¼ .003), and 1-year survival (HR 0.53, 95% CI 0.33-0.83, P ¼ .006) favoring ECMO with CPR over conventional CPR.28 In multivariate analysis, an initial rhythm of ventricular fibrillation/tachycardia and use of ECMO were positively associated with survival to discharge. In a retrospective, single-center, observational study at a tertiary care university hospital in Korea by Shin et al, 406 adult patients with witnessed in-hospital CA receiving CPR for >10
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Table 3. Observational Studies of Patients Receiving ECMO and CPR for Cardiac Arrest. Study
No. Patients ECMO þ CPR
Inclusion Criteria
Clinical Outcome
Chen et al32
135
Witnessed IHCA CPR > 10 min
Avalli et al33
42
IHCA and OHCA
Wang et al34
230
IHCA and OHCA
Sawamoto et al35
26
Accidental hypothermic OHCA
Johnson et al36
26
OHCA
Haneya et al37
85
IHCA and OHCA
Le Guen et al27
51
Witnessed OHCA
Thiagarajan et al38
Leick et al39
295
OHCA
28
OHCA
Time Frame
Miscellaneous
Survival rate with an acceptable neurologic status
At discharge: 34.1% Mortality risk factors: longer CPR duration (probability of survival was 0.5, 0.3, or 0.1 when CPR duration was 30, 60, or 90 min), acute coronary syndrome, and higher organ dysfunction in first 24 hours Survival rate with 6 Months: 38% – good neurological (IHCA) vs 5% outcome (OHCA), P < .05 – Survival At discharge: 31.2% (IHCA) vs 38.7% (OHCA), P ¼ .26 Favorable neurologic At discharge: 25.1% outcome (IHCA) vs 25.8% (OHCA), P ¼ .55 At discharge: 38.5% Factors associated with favorable Survival rate with neurological outcome: absence of favorable asystole, nonasphyxial neurological hypothermia, higher arterial pH, outcome and lower serum lactate Survival rate At discharge: 15% – ECMO-related In-hospital: 69% complication rate (mostly bleeding and ischemic events) Survival rate At discharge: 34% Among survivors, 93% were without ECMO-related In-hospital: 33% severe neurologic deficit. The complication rate survival rate in the IHCA patients receiving ECMO was higher than their OHCA counterparts (42% vs 15%; P < .02). 28 Days: 4% Significant correlation (r ¼ .36, P ¼ Survival rate with a .01) between blood lactate and favorable time delay between CA and neurologic ECMO onset. outcome 90% died within 48 hours of presentation Survival rate At discharge: 27% Factors associated with lower mortality: acute myocarditis compared with noncardiac diagnoses (OR 0.18, 95% CI 0.050.69) and percutaneous cannulation technique (OR 0.42, 95% CI 0.21-0.87). Survival rate 30 Days: 39.3% Door-to-ECMO time was significantly longer in nonsurvivors (42.5 vs 25.0 min, P < .01). Door-to-ECMO time was the only independent predictor of 30-day mortality. KM survival analysis demonstrated a benefit favoring patients with a door-to-ECMO time 6 cm/s were successfully weaned.79 Upon additional administration of heparin, the circuit is usually clamped for approximately 10 minutes during which time, blood pressure, heart rate, pulmonary artery pressures, arterial and mixed venous oxygen saturation, and presence of any arrhythmias are looked for to assess hemodynamic stability. If a patient is deemed to be hemodynamically stable, the patient can be weaned from ECMO and the cannulae can be removed by manual compression or surgically. However, if the patient is deemed unstable, the circuit should be declamped and circulatory support should immediately be resumed.
Conclusion Contemporary advances in extracorporeal technology have led to increasing use of ECMO in the setting of CA. Although the feasibility and efficacy of ECMO for adults with in-hospital CA has been reported (in nonrandomized trials), the safety and efficacy of ECMO for out-of-hospital patients with CA remain unknown. Rates of favorable recovery remain low in refractory patients with CA, despite treatment with ECMO. Delineation of the optimal patient population and optimal timing in relation to the time of CA must still be addressed. Randomized controlled trials of adequate sample size are warranted to evaluate the impact of this technology (compared to conventional resuscitation methods) on adults with CA. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
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shock and cardiac arrest: a meta-analysis of 1,866 adult patients. Ann Thorac Surg. 2014;97(2):610-616. Johnson SM, Itoga N, Garnett GM, Kilcommons M, Puapong DP, Woo RK. Increased risk of cardiovascular perforation during ecmo with a bicaval, wire-reinforced cannula. J Pediatr Surg. 2014;49(1):46-49; discussion 49-50. von Segesser LK. Heparin-bonded surfaces in extracorporeal membrane oxygenation for cardiac support. Ann Thorac Surg. 1996;61(1):330-335; discussion 340-331. Muehrcke DD, McCarthy PM, Stewart RW, et al. Complications of extracorporeal life support systems using heparin-bound surfaces. The risk of intracardiac clot formation. J Thorac Cardiovasc Surg. 1995;110(3):843-851. Lamarche Y, Chow B, Bedard A, et al. Thromboembolic events in patients on extracorporeal membrane oxygenation without anticoagulation. Innovations (Phila). 2010;5(6):424-429. Dunne B, Xiao P, Andrews D. Successful use of factor viia to control life-threatening post-operative haemorrhage in a patient on extra-corporeal membrane oxygenation. Heart Lung Circ. 2012; 21(4):229-230. Repesse X, Au SM, Brechot N, et al. Recombinant factor VIIa for uncontrollable bleeding in patients with extracorporeal membrane oxygenation: report on 15 cases and literature review. Crit Care. 2013;17(2):R55. Swaminathan M, Shaw AD, Greenfield RA, Grichnik KP. Fatal thrombosis after factor vii administration during extracorporeal membrane oxygenation. J Cardiothorac Vasc Anesth. 2008; 22(2):259-260. Subramaniam K, Boisen M, Shah PR, Ramesh V, Pete A. Mechanical circulatory support for cardiogenic shock. Best Pract Res Clin Anaesthesiol. 2012;26(2):131-146. Chen YC, Tsai FC, Chang CH, et al. Prognosis of patients on extracorporeal membrane oxygenation: the impact of acute kidney injury on mortality. Ann Thoracic Surg. 2011;91(1):137-142. Aissaoui N, Luyt CE, Leprince P, et al. Predictors of successful extracorporeal membrane oxygenation (ECMO) weaning after assistance for refractory cardiogenic shock. Intensive Care Med. 2011;37(11):1738-1745.
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Journal of Intensive Care Medicine 1-10 ª The Author(s) 2015 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0885066615583651 jic.sagepub.com
Jignesh K. Patel, MD1, Elinor Schoenfeld, PhD2, Sam Parnia, MD1, Adam J. Singer, MD3, and Norman Edelman, MD1
Abstract Cardiac arrest (CA) is a major cause of morbidity and mortality worldwide. Despite the use of conventional cardiopulmonary resuscitation (CPR), rates of return of spontaneous circulation and survival with minimal neurologic impairment remain low. Utilization of venoarterial extracorporeal membrane oxygenation (ECMO) for CA in adults is steadily increasing. Propensitymatched cohort studies have reported outcomes associated with ECMO use to be superior to that of conventional CPR alone in in-hospital patients with CA. In this review, we discuss the mechanism, indications, complications, and evidence for ECMO in CA in adults. Keywords Cardiac Arrest (CA), Extracorporeal Membrane Oxygenation (ECMO), Cardiopulmonary Resuscitation (CPR)
Introduction Cardiac arrest (CA) is a major cause of morbidity and mortality worldwide. Regardless of the advancements over the past 50 years in ventilation administration, cardiostimulant medications, chest compressions, and electrical defibrillation, achievement of return of spontaneous circulation (ROSC) with conventional cardiopulmonary resuscitation (CPR) remains difficult. Furthermore, despite attainment of ROSC, some patients experience rearrest and/or poor neurological outcomes. Extracorporeal membrane oxygenation (ECMO) was introduced in the 1970s as a means of support in patients with respiratory or cardiac failure.1,2 Recent improvements in extracorporeal technology and increasing data supporting favorable clinical outcomes with the use of ECMO in cardiopulmonary disease have generated interest as well as enhanced utilization in critical care medicine.3-5 In this review, we discuss the physiology, indications, and utilization of venoarterial ECMO specifically in adults with CA.
What is Venoarterial ECMO? Venoarterial ECMO provides rapid temporal circulatory assistance to patients with shock or CA.6 It consists of an extracorporeal circuit that directly oxygenates and removes carbon dioxide from the blood via a membrane oxygenator (a gas exchange device that utilizes a semipermeable membrane to separate blood from gas). When blood is drained from a central vein and returned to a central vein, a process known as venovenous ECMO, the device provides gas exchange only. When blood is drained from the venous
system and pumped into an artery, a process known as venoarterial ECMO, the circuit provides both respiratory and circulatory support. ECMO systems. The ECMO system is composed of bypass cannulae, a centrifugal (or roller) pump, a heat exchanger, and a membrane oxygenator.7 The traditional venoarterial ECMO circuit extends from the cannula (inserted from the femoral vein) in the right atrium to the femoral artery (Figure 1). Oxygenation via the membrane oxygenator is needed as pulmonary blood circulation is bypassed. Extracorporeal circuits are efficient at removing carbon dioxide and can do so at blood flow rates much lower than what is needed to achieve adequate oxygenation.8,9 The principal determinants of blood oxygenation for a given device are the fraction of oxygen delivered via the oxygenator, the amount of blood flow through the circuit, and the function of the native lungs while the determinants of 1 Division of Pulmonary and Critical Care, Department of Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA 2 Department of Preventive Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA 3 Department of Emergency Medicine, Stony Brook University Medical Center, Stony Brook, NY, USA
Received January 10, 2015, and in revised form March 12, 2015. Accepted for publication March 13, 2015. Corresponding Author: Jignesh K. Patel, Department of Medicine, Stony Brook University Medical Center, Health Science Center T17-040, Stony Brook, NY, USA. Email: [email protected]
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Journal of Intensive Care Medicine In the setting of CA, chest compressions can often be ceased following achievement of adequate pump flows on venoarterial ECMO. Although circulatory support is in effect, the underlying cause of CA (eg, acute coronary syndrome, electrolyte abnormalities, pulmonary embolism, drug intoxication, etc) should be identified and treated accordingly. While primary percutaneous coronary intervention (PCI) for acute myocardial infarction has been demonstrated to improve clinical outcomes,15 emergent coronary angiography in patients with CA in the absence of acute electrocardiographic changes remains controversial and may vary according to provider preference and institutional algorithms.16-21 Therapeutic hypothermia has been shown to improve clinical outcomes in out-of-hospital patients with CA with and without a shockable rhythm.17,18,22,23 In hemodynamically stable, ECMO-treated, comatose patients, mild hypothermia may be induced by priming the ECMO circuit with cold saline and utilizing the heat exchanger to rapidly achieve target temperatures of 32 C to 34 C.7
Figure 1. Venoarterial extracorporeal membrane oxygenation (ECMO) circuit.
carbon dioxide removal are the sweep gas flow rate (ie, the rate of gas flow through the oxygenator) and the rate of blood flow.10 Although ECMO cannulation has traditionally been performed in the operating room (or at the bedside) by cardiothoracic surgeons performing cutdown procedures for cannulation, percutaneous approaches have become more frequently adopted.3,11 Cannulation is usually performed with arterial cannulae measuring 15 to 17F and venous cannulae measuring 17 to 19F. If the cannulae are not sufficiently large, hemolysis tends to be severe. The venoarterial ECMO circuit traditionally extends from the cannula (inserted from the femoral vein) in the right atrium for drainage coupled with femoral arterial reinfusion. Reinfusion flow travels retrograde up the aorta and may meet resistance from left ventricle (LV)-generated antegrade flow. The location of the interface between antegrade and retrograde flow may vary depending on the severity of native myocardial dysfunction. Oxygen delivery to the coronary and cerebral vasculature can be inadequate in the setting of both impaired native gas exchange and poorly oxygenated blood pumped from the LV. Occasionally, this may necessitate venous drainage combined with both arterial and venous return (ie, venoarterial-venous ECMO). An additional reinfusion cannula with a ‘‘Y’’ connection originating from the femoral arterial reinfusion cannula can be inserted directly into an internal jugular vein to permit oxygenation of the coronary and cerebral circulation via return of oxygenated blood into the native cardiac circulation while concomitantly providing circulatory support. Venoarterial ECMO may result in LV overdistention and worsening pulmonary edema in the setting of severe LV dysfunction.12-14 The LV decompression in these circumstances can be facilitated with percutaneous insertion of a microaxial flow pump.13,14
Indications for ECMO in CA The 2010 American Heart Association guidelines for CPR and emergency cardiovascular care do not recommend the routine use of ECMO for CA.15,24 However, ECMO may be considered when the time without spontaneous circulation is short and resuscitation attempts are adequate (ie, CPR > 10 minutes, appropriate use of guideline-directed medications [eg, epinephrine, vasopressin, etc], and defibrillation for shockable rhythms). The guidelines emphasize that ECMO use should be restricted to centers at which it is readily available and that its initiation and management require highly trained personnel and specialized equipment. The inclusion criteria for ECMO in adults with CA can vary widely among institutions, given the substantial costs and manpower associated with its use (Table 1). Criteria that are often utilized include age cutoffs (usually excluding elderly patients), rhythm at the time of CPR (favorable to ventricular arrhythmias), time interval from the patient’s collapse to initiation of resuscitation (often necessitates 15 minutes or less), presumed etiology of the arrest (ie, cardiac origin, pulmonary embolism, etc), and if ROSC is not achievable despite optimal CPR (eg, within 20 minutes).25,26 Patients with terminal illnesses preceding the arrest, previous severe neurologic damage, current intracranial hemorrhage, arrest of traumatic origin with uncontrolled bleeding, arrest of septic origin, irreversible organ failure leading to CA when no physiological benefit could be expected despite maximal therapy (hepatic failure, late stage of adult respiratory distress syndrome, etc), acute aortic dissection, and significant peripheral vascular disease precluding bypass cannulation would be poor candidates for ECMO.25,27,28
Clinical Outcomes With ECMO Use in CA To date, there are no randomized controlled trials investigating the impact of ECMO for adults with CA. Most data
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Table 1. Inclusion and Exclusion Criteria for Venoarterial ECMO Use in Cardiac Arrest. Inclusion criteria Age cutoffs, usually age 10 min
Shin et al29,30
60
60
Retrospective observational; propensity score matched
Witnessed IHCA Mortality or significant CPR > 10 min neurologic impairment
Maekawa et al31
24
24
Prospective observational; propensity score matched
Witnessed OHCA CPR > 20 min
Mortality or significant neurologic impairment
Time Frame In-hospital: HR 0.51 (95% CI 0.35-0.74) 30 days: HR 0.47 (95% CI 0.28-0.77) 1 year: HR 0.53 (95% CI 0.33-0.83) In-hospital: HR 0.17 (95% CI 0.04-0.71) 6 months: HR 0.48 (95% CI 0.29-0.77) 2 years: 80.0% vs 95.0%, P ¼ .002 3 months: 70.8% ECMO þCPR vs 91.7% CPR, P ¼ .013
Abbreviations: PS, propensity score; IHCA, in-hospital cardiac arrest; OHCA, out-of-hospital cardiac arrest; CPR, cardiopulmonary resuscitation; HR, hazard ratio; CI, confidence interval; ECMO, extracorporeal membrane oxygenation.
retrieved on outcomes have been observational studies and propensity analyses (Tables 2 and 3). In-hospital CA. In a 3-year prospective, observational study of patients with witnessed in-hospital CA undergoing CPR for more than 10 minutes, Chen et al performed a matching process based on propensity score was done to balance potential prognostic factors in both groups and to formulate a balanced 1:1 matched cohort study.28 Propensity analysis matched 46 patients who received conventional CPR with 46 patients who received ECMO with CPR. Unmatched patients who received ECMO with CPR had a higher survival rate to discharge (28.8% vs 12.3%; log-rank P < .0001) and a better 1-year
survival (18.6% vs 9.7%) than those who received conventional CPR (log-rank P ¼ .007). Between the propensity scorematched groups, there was still a significant difference in survival to discharge (hazard ratio [HR] 0.51, 95% confidence interval [CI] 0.35-0.74, P < .0001), 30-day survival (HR 0.47, 95% CI 0.28-0.77, P ¼ .003), and 1-year survival (HR 0.53, 95% CI 0.33-0.83, P ¼ .006) favoring ECMO with CPR over conventional CPR.28 In multivariate analysis, an initial rhythm of ventricular fibrillation/tachycardia and use of ECMO were positively associated with survival to discharge. In a retrospective, single-center, observational study at a tertiary care university hospital in Korea by Shin et al, 406 adult patients with witnessed in-hospital CA receiving CPR for >10
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Table 3. Observational Studies of Patients Receiving ECMO and CPR for Cardiac Arrest. Study
No. Patients ECMO þ CPR
Inclusion Criteria
Clinical Outcome
Chen et al32
135
Witnessed IHCA CPR > 10 min
Avalli et al33
42
IHCA and OHCA
Wang et al34
230
IHCA and OHCA
Sawamoto et al35
26
Accidental hypothermic OHCA
Johnson et al36
26
OHCA
Haneya et al37
85
IHCA and OHCA
Le Guen et al27
51
Witnessed OHCA
Thiagarajan et al38
Leick et al39
295
OHCA
28
OHCA
Time Frame
Miscellaneous
Survival rate with an acceptable neurologic status
At discharge: 34.1% Mortality risk factors: longer CPR duration (probability of survival was 0.5, 0.3, or 0.1 when CPR duration was 30, 60, or 90 min), acute coronary syndrome, and higher organ dysfunction in first 24 hours Survival rate with 6 Months: 38% – good neurological (IHCA) vs 5% outcome (OHCA), P < .05 – Survival At discharge: 31.2% (IHCA) vs 38.7% (OHCA), P ¼ .26 Favorable neurologic At discharge: 25.1% outcome (IHCA) vs 25.8% (OHCA), P ¼ .55 At discharge: 38.5% Factors associated with favorable Survival rate with neurological outcome: absence of favorable asystole, nonasphyxial neurological hypothermia, higher arterial pH, outcome and lower serum lactate Survival rate At discharge: 15% – ECMO-related In-hospital: 69% complication rate (mostly bleeding and ischemic events) Survival rate At discharge: 34% Among survivors, 93% were without ECMO-related In-hospital: 33% severe neurologic deficit. The complication rate survival rate in the IHCA patients receiving ECMO was higher than their OHCA counterparts (42% vs 15%; P < .02). 28 Days: 4% Significant correlation (r ¼ .36, P ¼ Survival rate with a .01) between blood lactate and favorable time delay between CA and neurologic ECMO onset. outcome 90% died within 48 hours of presentation Survival rate At discharge: 27% Factors associated with lower mortality: acute myocarditis compared with noncardiac diagnoses (OR 0.18, 95% CI 0.050.69) and percutaneous cannulation technique (OR 0.42, 95% CI 0.21-0.87). Survival rate 30 Days: 39.3% Door-to-ECMO time was significantly longer in nonsurvivors (42.5 vs 25.0 min, P < .01). Door-to-ECMO time was the only independent predictor of 30-day mortality. KM survival analysis demonstrated a benefit favoring patients with a door-to-ECMO time 6 cm/s were successfully weaned.79 Upon additional administration of heparin, the circuit is usually clamped for approximately 10 minutes during which time, blood pressure, heart rate, pulmonary artery pressures, arterial and mixed venous oxygen saturation, and presence of any arrhythmias are looked for to assess hemodynamic stability. If a patient is deemed to be hemodynamically stable, the patient can be weaned from ECMO and the cannulae can be removed by manual compression or surgically. However, if the patient is deemed unstable, the circuit should be declamped and circulatory support should immediately be resumed.
Conclusion Contemporary advances in extracorporeal technology have led to increasing use of ECMO in the setting of CA. Although the feasibility and efficacy of ECMO for adults with in-hospital CA has been reported (in nonrandomized trials), the safety and efficacy of ECMO for out-of-hospital patients with CA remain unknown. Rates of favorable recovery remain low in refractory patients with CA, despite treatment with ECMO. Delineation of the optimal patient population and optimal timing in relation to the time of CA must still be addressed. Randomized controlled trials of adequate sample size are warranted to evaluate the impact of this technology (compared to conventional resuscitation methods) on adults with CA. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.
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