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Emergency Cardiac Support With Extracorporeal Membrane Oxygenation for Cardiac Arrest

      Abstract

      A 46-year-old woman with no major medical history presented to the emergency department with chest pain and evidence of anterior, anterolateral, and inferior ST-elevation myocardial infarction. Her condition quickly deteriorated into cardiogenic shock with ventricular arrhythmia. Despite revascularization of the left anterior descending artery and intravenous inotrope and antiarrhythmic therapy, her unstable hemodynamics and arrhythmias persisted. Early emergency initiation of venoarterial extracorporeal membrane oxygenation (ECMO) led to prompt hemodynamic and rhythm stability; however, adequate endogenous cardiac output did not ensue, and she was not able to be weaned from ECMO until hospital day 8. She subsequently recovered and continues to do well in the outpatient setting. This case demonstrates the remarkable hemodynamic and rhythm stability that early initiation of ECMO can provide in the setting of unstable myocardial infarction.

      Abbreviations and Acronyms:

      CPR (cardiopulmonary resuscitation), ECMO (extracorporeal membrane oxygenation), IABP (intra-aortic balloon pump), LAD (left anterior descending), LM (left main), MI (myocardial infarction)
      During acute myocardial infarction (MI), cardiogenic shock and refractory ventricular arrhythmias may persist despite revascularization and maximal medical and intra-aortic balloon pump (IABP) support. We present the case of a woman with ST-elevation MI who, despite successful and prompt percutaneous intervention, continued to remain electrically and hemodynamically unstable despite repeated defibrillation, intravenous antiarrhythmic inotropic drugs, and use of an IABP. Emergency establishment of venoarterial extracorporeal membrane oxygenation (ECMO) led to immediate electrical and hemodynamic improvement with subsequent patient survival and recovery. From this experience, we demonstrate that ECMO can be a lifesaving approach in the catheterization laboratory for emergency treatment of patients with cardiogenic shock and refractory ventricular arrhythmias due to acute MI; thus, ECMO should be considered early during resuscitation.

      Report of a Case

      A previously healthy 46-year-old woman presented to the emergency department with a 28-hour history of acute-onset chest pressure and dyspnea. She appeared severely distressed, with ongoing chest pain, nausea, vomiting, and diaphoresis. Her vital signs included a blood pressure of 129/96 mm Hg, heart rate of 124 beats/min, and respiratory rate of 24 breaths/min.
      Her electrocardiogram demonstrated sinus tachycardia with ST elevation in leads V3 through V6, II, III, and aVF suggestive of anterior, anterolateral, and inferior myocardial injury (Figure 1, A). Her baseline electrical activity was unstable, and an electrocardiogram 4 minutes later demonstrated nonsustained ventricular tachycardia (Figure 1, B). Her initial troponin T level was 0.95 ng/mL (reference range, <0.01 ng/mL [to convert to μg/L, multiply by 1]).
      • Jaffe A.S.
      2001–a biomarker odyssey.
      She was diagnosed as having an ST-elevation MI and referred for emergency coronary angiography after the administration of oral aspirin, oral clopidogrel, and intravenous unfractionated heparin.
      Figure thumbnail gr1
      Figure 1A, Electrocardiogram (ECG) at presentation showing sinus tachycardia with ST elevation in leads V3 through V6, II, III, and aVF suggestive of anterior, anterolateral, and inferior myocardial injury. B, An ECG 4 minutes after the initial ECG, showing rhythm instability and ventricular tachycardia.
      On arrival in the cardiac catheterization laboratory, the patient experienced ventricular fibrillation and required cardiac defibrillation, tracheal intubation, and controlled ventilation with 100% oxygen. Left coronary angiography revealed mobile thrombus in the left main (LM) coronary artery, 100% ostial occlusion of the left anterior descending (LAD) artery, and thrombus embolization into the circumflex artery (Figure 2 and Supplemental Video 1 [available online at http://www.mayoclinicproceedings.org]). The LM and LAD arteries were treated with aspiration thrombectomy and angioplasty with restoration of perfusion to the LM and mid-LAD arteries (Figure 3 and Supplemental Video 2 [available online at http://www.mayoclinicproceedings.org]). Intravenous eptifibatide therapy was also initiated during the intervention to maximize platelet inhibition.
      Figure thumbnail gr2
      Figure 2Right anterior oblique caudal view of the left coronary system with thrombus noted in the distal left main artery (arrow), and an occluded left anterior descending artery and thrombus in the obtuse marginal branch of the circumflex artery (hatched arrow).
      Figure thumbnail gr3
      Figure 3Right anterior oblique cranial view of the left coronary system with an intracoronary wire placed in the previously occluded left anterior descending artery and improved perfusion.
      Throughout the procedure, the patient required cardiopulmonary resuscitation (CPR) for recurrent cardiac arrest and received a total of 10 shocks for recurrent ventricular arrhythmias. Adequacy of chest compressions throughout the resuscitation were assessed by arterial waveforms monitored via a catheter in the right femoral artery. To prevent fatigue while performing CPR, causing a deterioration in CPR efficacy, chest compressors were changed at 2-minute intervals during brief rhythm analysis or when chest compression cadence decreased below 100/min. The patient's profound electrical and hemodynamic instability persisted despite administration of amiodarone, vasopressin, intravenous epinephrine, and the placement of an IABP. Severe pulmonary vascular congestion and pulmonary edema, as evidenced in the anesthesia circuit, contributed to her persistent hypoxemia.
      Advanced percutaneous left ventricular assist devices were considered for circulatory support but not used out of concern that they might not have provided the immediate improvement in oxygenation or increase in cardiac output necessary to protect neurologic and myocardial viability. Instead, a venoarterial ECMO system was placed via the right femoral artery and vein. The vein was cannulated with a 25F cannula that extended into the right atrium, and the artery was cannulated with a 17F cannula. Serial vascular dilators were used to enable percutaneous placement of these large-caliber cannulas. Immediate pre-ECMO arterial blood analysis revealed a pH of 6.82 and a base deficit of less than −25 mmol/L. Initiation of ECMO led to immediate electrical and hemodynamic stability, and no further CPR was required. However, IABP support was continued to improve diastolic perfusion of the coronary arteries. Initial echocardiography demonstrated a left ventricular ejection fraction of 10%. Figure 4 demonstrates the documented course of events from arrival in the catheterization laboratory.
      Figure thumbnail gr4
      Figure 4Timeline of events after the patient's arrival to the catheterization laboratory (cath lab). CPR = cardiopulmonary resuscitation; ECMO = extracorporeal membrane oxygenation; IABP = intra-aortic balloon pump.
      The patient was transferred to the intensive care unit, cooled to 34°C for 24 hours, and maintained on ECMO at a cardiac index of 1.8 to 2.0. She demonstrated progressive neurologic recovery and awoke at 24 hours. Her hemodynamics improved during the subsequent week but not enough that ECMO could be discontinued. Her peak creatine kinase–MB level was 358 ng/mL (reference range, <3.8 ng/mL) (to convert to μg/L, multiply by 1), and her peak troponin level was 12.6 ng/mL. She was successfully weaned from ECMO on day 8, and low-dose epinephrine and vasopressin were continued as intravenous infusions. She had minimal bleeding but no other ECMO-associated complications. The IABP was continued while she was receiving ECMO to increase blood flow to the coronary arteries and brain and to counteract the increased afterload effects of ECMO. The IABP was removed on day 9, and she was extubated soon after. Her subsequent hospital course was complicated by a pulmonary embolism and splenic vein thrombosis. Gastrointestinal bleeding and the presence of a thrombotic mass in her ascending colon necessitated a partial colectomy with benign disease documented on pathology. Dilation and curettage were also performed for endometrial thickening. Thrombophilia and hematology evaluation suggested that she had an acquired thrombophilia due to thrombocytosis secondary to iron deficiency anemia. We speculate that her coronary thrombi were likely formed at the site of an unstable atherosclerotic lesion in the ostium of the LAD artery, with fragments subsequently embolizing within the circumflex artery. She was discharged from the hospital 30 days after her MI with intact neurologic status, and she continues to do well as an outpatient (last assessed in January 2013). At her last echocardiogram evaluation 2 months after her event, the left ventricular ejection fraction was 30% to 35%.

      Discussion

      Cardiogenic shock related to ongoing MI that persists despite revascularization may lead to subsequent multiorgan failure. Injured myocardium may retain substantial viability after successful revascularization, but functional recovery often lags by several days, thereby necessitating extrinsic hemodynamic support. The American College of Cardiology and American Heart Association guidelines recommend placement of an IABP in the setting of cardiogenic shock or ischemia-related intractable ventricular arrhythmias (Class IIa, Level of Evidence of B).
      • Antman E.M.
      • Anbe D.T.
      • Armstrong P.W.
      • et al.
      ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction).
      However, in the patient we described, pharmacologic therapy and insertion of an IABP failed to resolve the life-threatening, persistent cardiogenic shock and refractory ventricular arrhythmias after coronary revascularization. Instead, we relied on ECMO as a bridge therapy to sustain hemodynamics until the patient’s heart fully recovered. This case is unique in that ECMO was considered early and initiated effectively in the catheterization laboratory, resulting in immediate hemodynamic and rhythm stability. Given the severity of metabolic abnormality, the degree of hypoxemia with fulminant pulmonary edema, and the prolonged duration of CPR, one would not have predicted whether a full recovery was possible, and termination of resuscitation would have been justified. Our experience with the inadequacy of the IABP support is consistent with the recent Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) II trial, which failed to demonstrate significant reduction in 30-day mortality in patients with acute MI and cardiogenic shock treated with an IABP placement.
      • Thiele H.
      • Zeymer U.
      • Neumann F.
      • et al.
      Intraaortic balloon support for myocardial infarction with cardiogenic shock.
      Extracorporeal membrane oxygenation can provide oxygenation and circulatory support and may have a distinct advantage over purely hemodynamic support devices, especially in the setting of persistent hypoxemia and severely reduced cardiac function. Although data are limited regarding its utility in acute MI and cardiogenic shock, smaller studies have indicated a potential benefit. One single-center, retrospective series of 33 patients who received ECMO support in the setting of persistent cardiogenic shock, despite the use of vasopressors and IABP placement, suggested improved survival compared with 25 patients with similar clinical characteristics treated with IABP alone.
      • Tsao N.W.
      • Shih C.M.
      • Yeh J.S.
      • et al.
      Extracorporeal membrane oxygenation-assisted primary percutaneous coronary intervention may improve survival of patients with acute myocardial infarction complicated by profound cardiogenic shock.
      There is also evidence of improved 30-day survival in patients presenting in severe shock during MI, with a 33% absolute risk reduction and a 45.8% relative risk reduction of death associated with ECMO therapy.
      • Sheu J.J.
      • Tsai T.H.
      • Lee F.Y.
      • et al.
      Early extracorporeal membrane oxygenator-assisted primary percutaneous coronary intervention improved 30-day clinical outcomes in patients with ST-segment elevation myocardial infarction complicated with profound cardiogenic shock.
      Another single-center, retrospective study of 98 patients receiving extracorporeal life support for cardiogenic shock during acute coronary artery syndrome found that 32.7% survived to hospital dismissal. This study included 41 patients who had pulseless electrical activity and/or asystole, which seemed to be an independent indicator of inpatient mortality.
      • Sakamoto S.
      • Taniguchi N.
      • Nakajima S.
      • Takahashi A.
      Extracorporeal life support for cardiogenic shock or cardiac arrest due to acute coronary syndrome.
      In a study of 35 patients, ECMO benefit did not differ among revascularization strategy (percutaneous intervention vs coronary bypass).

      Wu MY, Tseng YH, Chang YS, et al. Using extracorporeal membrane oxygenation to rescue acute myocardial infarction with cardiopulmonary collapse: the impact of early coronary revascularization [published online ahead of print January 7, 2013]. Resuscitation. doi:10.1016/j.resuscitation.2012.12.019.

      Overall, these are small studies with multiple confounders, but they indicate the potential value of ECMO support in patients with unstable acute coronary syndrome.
      In the United States specifically, ECMO has been used on a limited basis for supporting adults. According to the International Extracorporeal Life Support Organization, the only reporting registry for ECMO, 876 US adults who received extracorporeal CPR within the past 20 years (without accounting for cardiogenic shock) had a 26% survival. Extracorporeal membrane oxygenation for pure cardiac support was used in 709 adult patients documented in 2012, with an overall survival of 39%.

      Extracorporeal Life Support Organization (ESLO) Registry Report, International Summary. ESLO website. http://www.elsonet.org. Accessed April 6, 2013.

      Extracorporeal membrane oxygenation is still of limited use throughout the world for cardiac support in adults and even less for adult extracorporeal CPR. Nonetheless, its use is becoming more frequent and is potentially lifesaving, such as in this patient.
      Likewise, data are limited regarding other percutaneously placed left ventricular assist devices, such as Impella (Abiomed, Inc) or TandemHeart (CardiacAssist, Inc). In one randomized trial comparing 12 patients treated with Impella to 13 patients treated with IABP, the improvement in the cardiac index was greater in the Impella group, but the 30-day mortality remained the same for both groups.
      • Seyfarth M.
      • Sibbing D.
      • Bauer I.
      • et al.
      A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction.
      Similarly, a meta-analysis of 3 studies that compared IABP to percutaneous left ventricular assist devices (TandemHeart or Impella) failed to demonstrate improvement in 30-day mortality for patients in cardiogenic shock. Although the hemodynamics improved with the 2 left ventricular assist devices, there was a greater risk of bleeding with TandemHeart and higher levels of observed hemolysis with Impella.
      • Cheng J.M.
      • den Uil C.A.
      • Hoeks S.E.
      • et al.
      Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials.

      Conclusion

      This case demonstrates the value of venoarterial ECMO in the setting of cardiogenic shock and refractory ventricular arrhythmias precipitated by an acute MI. In our case, ECMO resolved the patient's ventricular arrhythmia and stabilized her hemodynamics until cardiac recovery. At 4 months after MI, the patient was asymptomatic and had a left ventricular ejection fraction of 30% to 35%. When available in the catheterization laboratory for emergency use, ECMO may serve as an ancillary lifesaving measure for patients with cardiogenic shock and refractory ventricular arrhythmias in the setting of an acute MI. Moreover, it should be considered early during the resuscitative efforts to optimize potential benefit, including the stabilization of arrhythmias and limiting additional organ injury.

      Supplemental Online Material

      • Supplemental Video 1

        Angiogram of presenting coronary occlusion. Right anterior oblique caudal view of the left coronary system with mobile thrombus in the left main (LM) artery, 100% ostial occlusion of the left anterior descending (LAD) artery, and thrombus embolization into the circumflex artery.

      • Supplemental Video 2

        Angiogram after percutaneous intervention. Right anterior oblique cranial view of the left coronary system with an intracoronary wire down the previously occluded left anterior descending artery and improved perfusion.

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      1. Wu MY, Tseng YH, Chang YS, et al. Using extracorporeal membrane oxygenation to rescue acute myocardial infarction with cardiopulmonary collapse: the impact of early coronary revascularization [published online ahead of print January 7, 2013]. Resuscitation. doi:10.1016/j.resuscitation.2012.12.019.

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        • Seyfarth M.
        • Sibbing D.
        • Bauer I.
        • et al.
        A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction.
        J Am Coll Cardiol. 2008; 52: 1584-1588
        • Cheng J.M.
        • den Uil C.A.
        • Hoeks S.E.
        • et al.
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