Case report - Special issue: Acute Coronary Syndromes

Rescue venoarterial ECMO in cardiogenic shockcomplicated by refractory cardiac arrest duringpercutaneous coronary intervention

Rihard Knafelj a, Primoz Trunk b, Simon Terseglav c, Maja Sostaric b,Marko Noc a,*aCenter for Intensive Internal Medicine, University Medical Center, Ljubljana, SloveniabDepartment of Cardiovascular Surgery, University Medical Center, Ljubljana, SloveniacDepartment of Cardiology, University Medical Center, Ljubljana, Slovenia

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3

a r t i c l e i n f o

Article history:

Received 4 January 2014

Received in revised form

31 January 2014

Accepted 1 February 2014

Available online 6 March 2014

Keywords:

Cardiogenic shock

Cardiac arrest

Coronary intervention

Extracorporeal membrane

oxygenation

a b s t r a c t

Cardiogenic shock represents the leading cause of death in hospitalized patients with acute

coronary syndromes. Immediate revascularization, either percutaneous or surgical, cur-

rently represents the only intervention of proven benefit. Despite the lack of such proof,

intraaortic balloon pump (IABP) and vasoactive drugs are typically used to improve hemo-

dynamic stability on top of revascularization. Mechanical circulatory support devices

beyond IABP such as Impella, TandemHeart and venoarterial extracorporeal membrane

oxygenation (VA ECMO) are hemodynamically even more effective. Despite the lack of

proven survival benefit, this technology might be lifesaving in case of profound hemody-

namic deterioration in the catheterization laboratory. We describe a case of profound

cardiac shock due to complicated coronary artery disease, recurrent cardiac arrest during

PCI, intraarrest PCI intra-aortic balloon pump insertion and successful resuscitation after

venoarterial ECMO placement. Complete revascularization was achieved following ECMO

insertion and patient was discharged home on day 29 with no neurological sequelae with

ejection fraction of 40%.

# 2014 The Czech Society of Cardiology. Published by Elsevier Urban & Partner Sp. z o.o.

All rights reserved.

Available online at www.sciencedirect.com

ScienceDirect

journal homepage: http://www.elsevier.com/locate/crvasa

.

1. Introduction

Cardiogenic shock represents the leading cause of death inhospitalized patients with acute coronary syndromes. Imme-diate revascularization, either percutaneous or surgical,currently represents the only intervention with a randomized

* Corresponding author at: Center for Intensive Internal Medicine, UnTel.: +386 1 522 22 96; fax: +386 1 522 22 96.

E-mail address: marko.noc@mf.uni-lj.si (M. Noc).http://dx.doi.org/10.1016/j.crvasa.2014.02.0010010-8650/# 2014 The Czech Society of Cardiology. Published by Else

proof of benefit [1]. Despite the lack of such evidence, intra-aortic balloon pump (IABP) and vasoactive drugs are typicallyused to improve hemodynamic stability on top of revasculari-zation [2,3]. Mechanical circulatory support devices beyondIABP such as Impella, TandemHeart and venoarterial extra-corporeal membrane oxygenation (VA ECMO) are hemody-namically more effective and, despite the lack of proven

iversity Medical Center, Zaloska 7, 1000 Ljubljana, Slovenia.

vier Urban & Partner Sp. z o.o. All rights reserved..

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3 e349

survival benefit, this technology is frequently used as a rescuestrategy in patients with profound hemodynamic collapse [4–11]. We herein report the case of a patient with cardiogenicshock complicated by refractory cardiac arrest during percu-taneous coronary intervention (PCI) in whom percutaneous VAECMO insertion in the catheterization laboratory proved to belifesaving.

2. Case report

A 52-year-old active smoker with hyperlipidemia but withouthistory of coronary artery disease was brought to thecommunity hospital by emergency prehospital team. Hiscomplaint was severe dyspnea and chest pain escalatingduring the last 3 days. Except for acetylsalicylic acid 100 mgand ezetimibe 10 mg/simvastatin 20 mg, he was not taking anyregular medication. Electrocardiogram (ECG) recorded by theprehospital unit revealed ST elevation in V1–3 and, notably,elevation in aVR together with depression in V5–6 (Fig. 1a). Anevolving pulmonary edema was diagnosed and since it wasrefractory to morphine, furosemide and oxygen, endotrachealintubation was performed and mechanical ventilation initiat-ed soon after hospital admission. Because of hypotension,norepinephrine infusion was also added. Repeat ECG revealedresolution of ST-elevation in precordial leads but not in aVR,and ST-depression in several other leads (Fig. 1b). Cardiactroponin T (TnT) was only slightly elevated (0.32 mmol/L,normal <0.013 mmol/L). Our hospital was alerted for immedi-ate coronary angiography and the patient was transported byambulance within 50 min.

On the admission to our hospital, transesophageal echo-cardiography was immediately performed to exclude possiblemechanical defect (i.e. mitral chordae or papillary musclerupture). Apical akinesia and diffuse hypokinesia of ante-rolateral wall with left ventricular ejection fraction below 30%and significant mitral regurgitation without flail leaflet weredocumented. The patient was then transported to thecatheterization laboratory. Despite norepinephrine and dobu-tamine, initial aortic pressure was 100/75 and heart rate of130 bpm. Coronary angiography revealed severe diffuseobstructive coronary disease with eccentric 60% ostial leftmain (LM) stenosis, occlusion of left anterior descending artery(LAD) after the first septal branch with some collaterals to thedistal vessel (Rentrop 1–2), occluded first diagonal branch, long90–95% ostial stenosis of medium sized first obtuse marginalbranch, 99% stenosis of large second obtuse marginal branchwith TIMI 3 and proximal chronic total occlusion of thedominant right coronary artery (RCA) with predominately leftto right collaterals (Fig. 2). Based on prehospital ECG andechocardiography with evidence of apical akinesia/anterolat-eral hypokinesia, LAD was considered as a culprit vessel. Theplan was to restore LAD patency and improve hemodynamicstatus followed by PCI of second obtuse marginal. The patientreceived unfractioned heparin according to activated clottingtime and JL 4 6 Fr guiding catheter was used to engage leftcoronary artery without ventricularization of pressure tracing.A standard working horse guide-wire (Advance, AbbottVascular) was passed across the occlusion with the supportof Minitrack 2.0 mm � 15 mm balloon (Abbott Vascular).

Following a few balloon inflations, patency of LAD with TIMI1–2 was restored. Despite this, hemodynamic status furtherdeteriorated to pulseless electrical activity. Chest compressionwas initiated, epinephrine boluses administered and norepi-nephrine infusion increased. Effectiveness of chest compres-sion was assured by continuous monitoring of the aorticpressure. After approximately 5 min, spontaneous circulationwas restored. Intraaortic balloon pump (IABP) using 7.5 Fr 40 cclinear balloon catheter (Maquet Getinge Group) was insertedthrough the left femoral artery and epinephrine infusionadded to already existing vasopressor/inotropic support.Transient hemodynamic stabilization was followed by recur-rent cardiac arrest which was this time refractory toconventional cardiac life support. During ongoing cardiopul-monary resuscitation which only transiently restored sponta-neous circulation, VA ECMO was implemented. In brief,guiding catheter was removed from right femoral artery and6 Fr sheath exchanged for 17 Fr arterial cannula after sequen-tial dilatation using Seldinger technique. The tip of the arterialcannula was placed at the aortic bifurcation. Anterogardepuncture of ipsilateral superficial femoral artery for sheathinsertion to prevent limb ischemia was, due to urgency of thesituation and lack of pulsative flow, abandoned. A 21 Fr venouscannula was inserted through the left femoral vein using thesame percutaneous technique. The tip was positioned at theentry into the right atrium. VA ECMO (CardioHelp, MaquetGetting Group) was started and ‘‘rpm’’ increased to 3600resulting in 3.54 L/min retrograde aortic flow. IABP wasmaintained at 1:1 ratio. The total time from onset of refractorycardiac arrest to VA ECMO ‘‘jump start’’ was 30–35 min.Because of prolonged cardiac resuscitation and persistentcoma despite reestablishment of cerebral perfusion, coolingusing VA ECMO circuit was initiated to reach a targettemperature between 32 and 34 C [12]. Cardiac surgeon wascalled to the catheterization laboratory and a decision wasmade to proceed with emergency CABG. Since all operatingrooms were occupied, the patient was transiently transportedto cardiac intensive care unit. Epinephrine infusion could havebeen discontinued and norepinephrine/dobutamine signifi-cantly reduced. Excessive urinary output (600 mL) wasdocumented already within initial 2 h. Arterial lactate, whichwas within normal limits in referring hospital, increased to amaximum of 9.5 mmol/L (Fig. 3). Cardiac troponin I (TnI) beforeCABG was 3.99 mmol/L (normal <0.06 mmol/L). After 4 h inintensive care unit, the patient was transported to theoperating room. Levosimendan infusion was started and VAECMO was replaced with conventional heart–lung machineusing the same cannulas. LAD was grafted by LIMA. Largeobtuse marginal and RCA were grafted by safenous vein grafts.Since left ventricular function did not improve after CABG, VAECMO and IABP were re-started and the patient transferred tointensive care unit. Arterial lactate normalized within 30 h(Fig. 3) and urinary output was normal. TnI increased to amaximum of 22.48 during the first postoperative day.Postoperative course was complicated by bleeding at the siteof arterial cannula requiring intervention on the secondpostoperative day, malignant ventricular arrhythmias withventricular fibrillation requiring coronary angiography toconfirm grafts patency on day 3, nosocomial infectionsrequiring treatment with several antimicrobial drugs and

Fig. 1 – Prehospital electrocardiogram (a) and electrocardiogram after hospital admission, intubation, mechanical ventilationand norepinephrine infusion.

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3e350

Fig. 2 – Immediate coronary angiography of the left (a) andright (b) coronary artery.

Fig. 3 – Arterial lactate concentration during initial 30 h afterfirst presentation.

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3 e351

paroxysmal atrial fibrillation/undulation treated with amio-darone. Left ventricular function gradually improved andallowed successful weaning from ECMO on day 14 facilitatedby IABP which was removed on day 15. Mechanical ventilationfollowed by tracheal extubation was discontinued on day 20.The total duration of intensive care stay was 24 days. Thepatient was discharged from our hospital 29 days after theindex event with normal neurocognitive status. Except forlimited area of akinesia of the apical part of inter-ventricularseptum, echocardiography revealed normalization of ejectionfraction and only non-significant mitral regurgitation. Fivemonths after the index event, the patient is living his normallife (NYHA) and has an ejection fraction of 40%.

3. Discussion

We herein describe a previously healthy man with acutecoronary syndrome and very complex coronary diseasepresenting with pulmonary edema followed by cardiogenicshock and refractory cardiac arrest during PCI attempt. Afterfailure of advanced cardiac life support, VA ECMO waslifesaving and allowed for urgent CABG, reversal of cardiogenicshock within 24 h and bought time for myocardial recoveryfollowing revascularization.

Looking retrospectively, the best solution for this patientwould have probably been immediate hemodynamic supportby IAPB or VA ECMO followed by complete surgical revascu-larization without PCI attempt. The reason for hemodynamicdeterioration during PCI might have been accidental deepengagement of the guiding catheter into the stenosed LMduring PCI or balloon withdrawal. Despite successful initialresuscitation, cardiac arrest undoubtedly worsened alreadyexisting cardiogenic shock which ultimately progressed torefractory cardiac arrest. Despite the lack of randomized data,we can speculate that this complication might have beenavoided by implementation of hemodynamic support prior toPCI attempt [13,14] or if we immediately decided foremergency CABG without PCI attempt.

After hemodynamic stabilization with VA ECMO, we werefaced with the dilemma regarding the timing of CABG since‘‘acute heart team’’ in the catheterization laboratory felt thatfurther PCI attempts would not represent the optimalrevascularization option. At that point, one possibility wasto wait with CABG for few days to reverse cardiogenic shock byECMO and document neurological recovery after cardiacarrest. However, since we suspected LAD occlusion to beacute, such delay may have resulted in large, unreperfusedanterior infarction. Since peak TnI increased only to 22 mmol/Lafter CABG, which is 10–20 times less what we usuallyexpected in such acute LAD occlusion, the infarct was eitherlargely aborted by timely CABG or LAD occlusion has not beenthe culprit despite initial ECG, echocardiography and ability tocross occlusion without dedicated CTO wire. Indeed, theculprit might have been also large obtuse marginal branchwith spontaneous re-perfusion before coronary angiography.

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3e352

However, it is important to notice that in the setting of socomplex multi-vessel disease, the culprit lesion may not beunequivocally identified, and in fact, multiple culprits are alsopossible [15]. From the interventional point of view, however,we believe that correct identification of culprit lesion isimportant since this lesion should be primary treated followedby non-culprit lesions advised by the guidelines [15]. Completerevascularization seems to be important also in cardiogenicshock complicated by cardiac arrest which was the case in ourpatient [15]. Since this could have been hardly achieved duringindex PCI, emergency CABG was decided by the our ‘‘acuteheart team’’ and should not be forgotten as a potential solutionin the presence of complex coronary disease despite profoundhemodynamic collapse.

Nowadays, there is increasing evidence predominantlycoming from far east that refractory cardiac arrest, even inthe prehospital setting, may be successfully stabilized by VAECMO which buys time for subsequent revascularization withremarkable 10–20% survival with good neurological outcome[16,17]. In fact, such hyper-invasive strategy in patients without-of-hospital cardiac arrest and no return of spontaneouscirculation is currently being tested in the randomized fashion[18]. If such catastrophic situation occurs in the cath laboratorysuch as in our patient, immediate VA ECMO insertion can befaster and more easily accomplished than either on the field orin emergency department [4–7]. Instead of surgical cut down,percutaneous insertion of cannulas by interventional cardiolo-gist without is rather straight forward and safe even in theabsence of pulsative flow since X-ray may be used to controlposition of the wire and advancement of ECMO cannulas evenduring ongoing chest compression. It is very important toemphasize, however, that delay between cardiac arrest and‘‘jump start’’ by VA ECMO should be as short as possible becausethis will reduce the severity of post-resuscitation brain injuryand post-resuscitation systemic inflammatory response lead-ing to multiple organ dysfunction. Since pre-primed ECMO israrely available, ECMO priming should be performed in parallelwith insertion of arterial and venous cannulas by additionalteam. Assist devices such as Impella, which is inserted into theleft ventricle and does not need oxygenator, are even more userfriendly [11]. We therefore believe that temporary circulatoryassist devices may in the near future become a standard of carein ‘‘24-7’’ catheterization laboratories treating patients withacute coronary syndromes. This would allow for hemodynamicstabilization followed by PCI also in patients with profoundcardiogenic shock and cardiac arrest thereby providing arealistic chance for survival [18,19].

Conflict of interest

All authors (Rihard Knafelj, Primoz Trunk, Simon Terseglac,Maja Sostaric, Marko Noc) declare no conflict of interestconsidering case report, methods, materials or equipment used.

Funding body

All authors (Rihard Knafelj, Primoz Trunk, Simon Terseglac,Maja Sostaric, Marko Noc) declare that none of the materials or

equipment described in article was funded by the industry.There was no financial support from industry regardingpreparation this paper.

Ethical statement

All authors (Rihard Knafelj, Primoz Trunk, Simon Terseglac,Maja Sostaric, Marko Noc) declare that treating the patientdescribed in case-report strict ethical principles were applied.

Informed consent

Since the paper submitted is not characterized as a researchpaper we did not search for nor obtained informed consent.

r e f e r e n c e s

[1] J.S. Hochman, L.A. Sleeper, J.G. Webb, et al., Earlyrevascularization in acute myocardial infarctioncomplicated with cardiogenic shock. SHOCK Investigators.Should we emergently revascularize occluded coronariesfor cardiogenic shock, New England Journal of Medicine 341(1999) 625–634.

[2] H. Thiele, U. Zeymer, F.J. Neumann, et al., Intraaorticballoon support for myocardial infarction with cardiogenicshock, New England Journal of Medicine 367 (2012)1287–1296.

[3] S.R. Finfer, J.L. Vincent, Circulatory shock, New EnglandJournal of Medicine 369 (2013) 1726–1734.

[4] M.R. Mooney, K.V. Arom, L.D. Joyce, et al., Emergencycardiopulmonary bypass support in patients with cardiacarrest, Journal of Thoracic and Cardiovascular Surgery 101(1991) 450–454.

[5] J.G. Powney, R.S. Bonser, S. Lentini, Emergencycoronary artery surgery after refractory cardiac arrest:a single centre experience, British Heart Journal 67 (1992)392–394.

[6] Y. Mori, K. Ueno, A. Hattori, et al., Emergencycardiopulmonary bypass in patients with cardiac arrestcaused by myocardial infarction, Artificial Organs 18 (1994)698–701.

[7] M.J. Ricciardi, M. Moscucci, B.P. Knight, et al., Emergencyextracorporeal membrane oxygenation (ECMO)-supportedpercutaneous coronary interventions in fibrillating heart,Catheterization and Cardiovascular Interventions 48 (1999)402–405.

[8] H. Sunami, Y. Fujita, T. Okada, et al., Successfulresuscitation from prolonged ventricular fibrillation using aportable percutaneous cardiopulmonary support system,Anesthesiology 99 (2003) 1227–1229.

[9] Y. Matsunari, H. Imanaka, M. Takeuchi, et al., Recoveryfrom fatal ventricular fibrillation after immediateapplication of percutaneous cardiopulmonary support,Masui 53 (2004) 795–798.

[10] K. Sung, Y.T. Lee, P.W. Park, et al., Improved survival aftercardiac arrest using emergent auto-priming percutaneouscardiopulmonary support, Annals of Thoracic Surgery 82(2006) 651–656.

[11] V.K. Mukku, Q. Cai, S. Gilani, et al., Use of Impela ventricularassist device in patients with severe coronary arterydisease presenting with cardiac arrest, InternationalJournal of Angiology 21 (2012) 163–166.

c o r e t v a s a 5 6 ( 2 0 1 4 ) e 3 4 8 – e 3 5 3 e353

[12] The Hypothermia After Cardiac Arrest (HACA) Study Group,Mild therapeutic hypothermia to improve the neurologicaloutcome after cardiac arrest, New England Journal ofMedicine 346 (2002) 549–556.

[13] D. Perera, R. Stables, M. Thomas, et al., Elective intra-aorticballoon counter-pulsation during high-risk percutaneouscoronary intervention, Journal of the American MedicalAssociation 304 (2010) 867–874.

[14] W.W. O'Neill, N.S. Kleiman, J. Moses, et al., A prospective,randomized clinical trial of hemodynamic support withImpela 2.5 versus intra-aortic balloon pump in patientsundergoing high-risk percutaneous coronary intervention.The PROTECT II study, Circulation 126 (2012) 1717–1727.

[15] D. Mylotte, M.C. Morice, H. Eltchaninoff, et al., Primarypercutaneous coronary intervention in patients with acutemyocardial infarction, resuscitated cardiac arrest andcardiogenic shock: the role of primary multivesselrevascularization, JACC: Cardiovascular Interventions 6(2013) 115–125.

[16] K. Nagao, N. Hayashi, K. Kanmatsuse, et al.,Cardiopulmonary cerebral resuscitation using emergency

cardiopulmonary bypass, coronary reperfusion therapy andmild hypothermia in patients with cardiac arrest outsidethe hospital, Journal of the American College of Cardiology36 (2000) 776–783.

[17] Y.S. Chen, A. Chao, H.Y. Yu, et al., Analysis and resultsof prolonged resuscitation in cardiac arrest patientsrescued by extracorporeal membrane oxygenation,Journal of the American College of Cardiology 41 (2003)197–203.

[18] J. Belohlavek, K. Kucera, J. Jarkovsky, et al., Hyperinvasiveapproach to out-of-hospital cardiac arrest usingmechanical chest compression device, prehospitalintraarrest cooling, extracorporeal life support and earlyinvasive assessment compared to standard care. Arandomized parallel groups comparative study proposal.‘‘Prague OHCA study’’, Journal of Translational Medicine 10(2012) 163.

[19] S.A. Bernard, T.W. Gray, M.D. Buist, et al., Treatment ofcomatose survivors of out-of-hospital cardiac arrest withinduced hypothermia, New England Journal of Medicine346 (2002) 557–563.