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Herz 2017 · 42:27–44DOI 10.1007/s00059-016-4523-4Published online: 26 January 2017© The Author(s) 2016. This article is available atSpringerLink with Open Access.

L. C. Napp1 · C. Kühn2 · J. Bauersachs1

1 Cardiac Arrest Center, Acute and Advanced Heart Failure Unit, Department of Cardiology and Angiology,Hannover Medical School, Hannover, Germany

2Department of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School,Hannover, Germany

ECMO in cardiac arrestand cardiogenic shock

Cardiogenic shock and cardiac arrest arelife-threatening emergencies with a highmortality rate despite numerous effortsin diagnosis and therapy. For a longtime medical therapy – at the forefrontwith catecholamines, vasodilators andothers – and mechanical ventilation, ifnecessary, were the standard of care forcardiogenic shock. Oxygen supply andperfusion are critically reduced duringshock and arrest, and both are physicalprocesses that are in principle amenableto (temporary) extracorporeal mechan-ical support. Early pioneering workto prove this principle was performedin animals as early as 1937 [1] and inhumans 20–30 years later [2, 3]. Withthe seminal paper by Hill and coworkers[4], extracorporeal membrane oxygena-tion (ECMO), which can provide bloodflow support and extracorporeal gas ex-change at the same time, was introducedinto the clinic. Since then, technicalimprovements have contributed to thecurrent worldwide use of ECMO forsevere respiratory and cardiorespiratoryfailure refractory tomedical therapy. Re-cently, there has been some discussionon initiating mechanical support evenearlier, with the intention to avoid mul-tiorgan failure associated with excessivecatecholamine doses and/or aggressiveventilator settings. By analogy withthe concept of veno-venous ECMO andlung-protective ventilation for treatmentof acute respiratory distress syndrome,the goal of mechanical support in car-diogenic shock is myocardial rest whileprotecting end organ perfusion.

In the following, we review ECMOsupport in the context of cardiogenic

shock and refractory cardiac arrest, witha special focus on technical aspects ofveno-arterial ECMO. Of note, the fol-lowing statements are primarily true forpercutaneous ECMO with femoral can-nulation and may not necessarily be di-rectly transferable to central or upper-body cannulation.

Cardiogenic shock and cardiacarrest

Cardiogenic shock is the main cause ofearly mortality in patients with acutemyocardial infarction [5]. Other condi-tions leading to shock comprise acutelydecompensated chronic heart failure,decompensated valvular heart disease,myocarditis, Takotsubo syndrome, acutepulmonary embolism, acute allograftfailure, incessant arrhythmia, peripar-tum cardiomyopathy [6], and others [7].During cardiogenic shock not only theheart itself suffers from pump failure,but even more end organs such as thebrain, kidney, liver, and gut are at riskdue to insufficient perfusion (multior-gan dysfunction syndrome) [8], and therate of congestion-associated pneumoniaincreases. Beyond blood pressure andheart rate as classic shockmarkers, serumlactate, central venous oxygenation, liverenzyme levels, and urine output are sur-rogate markers of circulatory failure andmultiorgan dysfunction [9]. Reducedcoronary perfusion further decreasescardiac output, and multiorgan dysfunc-tion/failure is further complicated bymetabolic acidosis and acute coagulopa-thy. All of these conditions aggravateeach other in a fatal vicious circle [8, 9].

Out-of-hospitalcardiacarrest(OHCA)occurs with an estimated incidence of500,000 per year in Europe [10, 11],with two thirds having a primary car-diac cause [12]. Mortality after OHCAremains high despite interventional ther-apy and modern intensive care. Only10–15% of those who arrive at the nor-mal hospital survive [13, 14], of whomabout 50–80%have a favorable neurolog-ical prognosis [15, 16]. In this context,immediate bystander CPR and area-wide availability of automated externaldefibrillators are essential to increasesurvival and prognosis. The first elec-tric shock should be applied as earlyas possible [17] to minimize the timeof hypoperfusion, associated LV pumpfailure, and consecutive development ofshock [18]. After return of spontaneouscirculation (ROSC), the patient needs tobe transferred to an experienced center,which holds all required diagnostic andtherapeutic tools [19]. In clinical routine,the first 24 h after resuscitation often

AbbreviationsCPR Cardiopulmonary resuscitation

ECMO Extracorporeal membraneoxygenation

ECPR Extracorporeal cardiopulmonaryresuscitation

IABP Intra-aortic balloon pump

LV Left ventricle

LVAD Left ventricular assist device

OHCA Out-of-hospital cardiac arrest

ROSC Return of spontaneous circulation

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Table 1 Strategies ofmechanical circulatory support

Strategy Indication (examples) Principle Goal

Bridge-to-recovery Acute heart failure(myocarditis, acutemyocardial infarction)

Stabilize systemic circulation, ensure end organ perfusion and reducepreload until myocardial recovery

Recovery

Bridge-to-transplantation

Terminal heart failure Stabilize systemic circulation, ensure end organ perfusion until hearttransplantation

Transplantation

Bridge-to-destination

Terminal heart failure Stabilize systemic circulation, ensure end organ perfusion until LVADimplantation

LVAD

Bridge-to-surgery Acute pulmonary embolismwith shock (and contraindi-cation for fibrinolysis)

Reduce preload and stabilize systemic circulation until emergent em-bolectomy

Embolectomy

Bridge-to-decision Extracorporeal CPR Stabilize systemic circulation, ensure end organ perfusion until (neuro-logical) re-evaluation and decision on therapeutic strategy

Re-evaluation

Refractory cardiogenicshock

ECMO implantation at the referral center by the ECMO team and trans-port to the tertiary center for further therapy

Transfer

CPR cardiopulmonary resuscitation, ECMO extracorporeal membrane oxygenation, LVAD left ventricular assist device

decide on the outcome, and guidelinesrecommend cardiac catheterization inmost cases early after OHCA [20, 21].Therefore, primary admission to a ter-tiary center should be preferred overadmission to a regional hospital andsecondary transfer to a tertiary center,when progression of shock has alreadyoccurred.

The majority of patients after OHCAdevelop post-cardiac arrest syndrome[22, 23] in a vicious circle: Cardiac ar-rest leads to ischemia of the myocardiumand end organs, which results in adversemetabolism, acidosis, and vasoplegia.The hypoperfused heart is not able torespond to the circulatory needs, whichin turn aggravates peripheral ischemia[24]. Therefore, restoration of systemicperfusion is essential – particularly in theimmediate and early phase after ROSC– in order to limit multiorgan dysfunc-tion [25], which can also be considereda “whole-body reperfusion syndrome.”In this context, complete cardiac revas-cularization is recommended [12, 26],but care of other end organs such asthe brain, intestine, liver, and kidneys isequally important [23].

As outlined, cardiogenic shock andcardiac arrest share many pathophysio-logical features and evoke many similarresponses. Thus, itwasnot surprisingbutvery important to prove that the progno-sis of both conditions is equally adverse:In a recent study of 250 consecutive pa-tients from Denmark, 130 were admit-ted to a tertiary center with cardiogenic

shock, while 118 had OHCA. Interest-ingly, both groups had the same dismaloutcomewith60%1-weekmortality [27].This underlines the urgent need for noveltherapeutic strategies for patients withcardiogenic shock and arrest.

Restoration of systemiccirculation

Formanyyearscatecholamineshavebeenused for stabilizationof patientswith car-diogenic shock. Inotropes such as dobu-tamine are given with the intention toincrease cardiac output by their posi-tive inotropic and chronotropic function.In contrast, vasopressors such as nore-pinephrine are administered for increas-ing blood pressure by vasoconstrictionand indirect effects such as increasedpreload. Epinephrine shares features ofboth drug classes. However, inotropicdrugs increase myocardial oxygen con-sumption, heart rate, arrhythmogenicity,and inflammation in the already diseasedheart [28]. Beta1-adrenoceptor agonistshave been associated with energy deple-tion, oxidative stress, and adverse out-come in acute heart failure [29]. Va-sopressors increase myocardial afterloadand potentially impair peripheral tissueperfusion. Thus, from a pathophysio-logical perspective, inotropes as well asvasopressors are associated with adverseeffects on the heart and other end organswhile these organs should recover. Con-sistently, current guidelines recommendcatecholamines as a short-term bridge in

the acute situation (only class IIb, levelof evidence C), but clearly mention thedisadvantages of such drugs, also in lightof the paucity of clinical studies demon-strating a survival benefit [25, 30, 31].In clinical routine, catecholamines areoften “effective” in terms of increasingblood pressure, but linked to impairedmicrocirculation and multiorgan failure,and thus not sufficient for sustained andharmless stabilizationof patients with se-vere cardiogenic shock and resuscitation.In this context, beta-blockers and cal-cium antagonists taken by the patientbefore arrest might further contribute tothe limited efficacy of catecholamines.

Therefore, it is increasingly being dis-cussed to initiate mechanical circulatorysupport as a powerful tool for bridgingearlier and more frequently, in order toimprove the prognosis of patients withsevere cardiogenic shock or refractoryarrest [32]. However, this trend is basedon data from many registries and retro-spective/observational studies, while evi-dence fromprospective randomized con-trolled studies is lacking.

Mechanical circulatory support

Several modes and devices of mechani-cal support are currently available [32],of which each has its own features andadvantages.

The intra-aortic balloonpump (IABP)consists of a catheter-mounted balloonthat inflates during diastole and deflatesduring systole in the descending tho-

28 Herz 1 · 2017

racic aorta. By this, coronary perfu-sion should be enhanced during diastole,while afterload should be decreased dur-ing systole when the left ventricle (LV)ejects. Notwithstanding the attractivepathophysiological principle, augmenta-tion by IABP depends on LV output, andthe potential of support decreases withlower LV output. Several studies havedemonstrated that IABP support is notfavorable in infarct-related cardiogenicshock [33, 34]. Therefore, current guide-lines have retracted the recommendationof IABP use [31].

TheTandemHeart®consists of a pumpand two cannulas, of which one is in-serted via venous access and transseptalapproach into the left atrium (LA),and the other one via arterial accessinto the femoral artery. By this, theTandemHeart® introduces a right-to-left shunt, reduces LV preload by LAdrainage, but increases afterload by ret-rograde flow support toward the aorta.The TandemHeart® is not widely usedin Europe and requires experiencedtransseptal cannula placement, which isassumed to harbor considerable risk inthe acute situation.

Transaorticmicroaxialpumps(Impel-la®, Heartmate PHP®) are introduced viaarterial access through the aorta acrossthe aortic valve into the LV. These de-vices directly unload the LV, transportthe drained volume inside of the pumptoward the aorta and eject into the aor-tic root. This elegant approach, whichfollows the physiological blood flow di-rection, is comprehensively described inthe same issue of this journal (Schäfer A,Bauersachs J, doi: 10.1007/s00059-016-4512-7). However, microaxial pumps donot offer gas exchange or temperaturecontrol.

Probably, the most often used form ofmechanical circulatory support today isECMO.Originating fromcardiac surgeryand initially developed for temporarylung replacement, ECMOsupport is nowbroadly established for cardiorespiratorysupport [35]. Notwithstanding its enor-mous support potential, ECMO has sev-eral special features and harbors certainspecific risks, whichwill be reviewedhere(see next sections).

Abstract · Zusammenfassung

Herz 2017 · 42:27–44 DOI 10.1007/s00059-016-4523-4© The Author(s) 2016. This article is available at SpringerLink with Open Access.

L. C. Napp · C. Kühn · J. Bauersachs

ECMO in cardiac arrest and cardiogenic shock

AbstractCardiogenic shock is an acute emergency,which is classically managed by medicalsupport with inotropes or vasopressors andfrequently requires invasive ventilation.However, both catecholamines and ventila-tion are associatedwith a worse prognosis,and many patients deteriorate despite allefforts. Mechanical circulatory support isincreasingly considered to allow for recoveryor to bridge until making a decision or definitetreatment. Of all devices, extracorporeal

membrane oxygenation (ECMO) is the mostwidely used. Here we review features andstrategical considerations for the use of ECMOin cardiogenic shock and cardiac arrest.

KeywordsCardiogenic shock · Cardiac arrest · Suddencardiac death · Cardiopulmonary resus-citation · ECMO · Mechanical circulatorysupport · Microaxial pump · Extracorporealresuscitation

ECMO bei Herz-Kreislauf-Stillstand und kardiogenem Schock

ZusammenfassungDer kardiogene Schock ist ein akut lebens-bedrohlicher Notfall, der klassischerweisemedikamentös (u. a. Inotropika und ggf.Vasopressoren) behandelt wird und häufigeine invasive Beatmung erfordert. Katecho-lamine und Beatmung sind jedoch mit einerungünstigen Prognose assoziiert, und vielePatienten sind mit konservativen Maßnah-men nicht zu stabilisieren. MechanischeKreislaufunterstützung wird immer öfter her-angezogen, um den Kreislauf zu stabilisieren,dem erkrankten Herzen Zeit zur Erholung zuverschaffen oder eine Überbrückung bis zurdefinitiven Therapie zu etablieren. Das aktuellweltweit am häufigsten eingesetzte System

zur mechanischen Kreislaufunterstützung indiesemZusammenhang ist die extrakorporaleMembranoxygenierung (ECMO). In dervorliegenden Übersicht fassen die Autorendie speziellen Eigenschaften dieses Systemssowie strategischeÜberlegungen im Kontextdes kardiogenen Schocks und des Herz-Kreislauf-Stillstands zusammen.

SchlüsselwörterKardiogener Schock · Herz-Kreislauf-Still-stand · Plötzlicher Herztod · Wiederbelebung ·ECMO · Mechanische Kreislaufunterstüt-zung · Mikroaxialpumpe · ExtrakorporaleReanimation

In general, mechanical support can beused with different strategies (. Table 1).In patients with severe cardiogenicshock from myocardial infarction ormyocarditis, mechanical support is rou-tinely employed in a bridge-to-recoveryapproach. In the case of acute de-compensated chronic heart failure, thepotential for recovery may be limited,which sometimes results in a bridge-to-destination approach. In resuscitatedpatients, a bridge-to-decision strategyis usually required, as further therapiessuch as LVAD surgery, ICD implantationetc. are postponed until awakening ofthe patient allows for estimating neuro-logical recovery and eligibility.

Veno-arterial ECMO

Technical aspects

ECMO is a modified form of cardiopul-monary bypass [36], and has undergonea dramatic technical evolution since thewidely known publication by Hill andcoworkers in 1972 [4]. In principle,ECMO drains venous blood througha cannula and tubing and returns itvia another tubing and cannula into thebody, both driven by a rotor unit. DuringECMO passage the blood becomes oxy-genated, decarboxylated, and warmedin an extracorporeal gas exchange unit.In nonsurgical application in adults,peripheral cannulation of the femoraland/or jugular vessels is the standardtechnique, usually with 21–25 French

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Table 2 Technical features of VA-ECMO

Implantation Cannulation of femoral artery (15–19 Fr) and vein (21–15 Fr) with modi-fied Seldinger’s technique takes about 10min until circuit starts

Mobility Inter- and intrahospital transfer, up to air-bridge (flight transfer)

Hemodynamiceffect

Increased systemic perfusion by retrograde flow support

Preload reduction

Afterload increase

Flow rates Up to 7 l/min, depending on cannulas and rotor/oxygenator

Gas exchange Highly efficient oxygenation and decarboxylation of reinfused blood

Contraindications Ethical considerations, patient’s will

No perspective of a bridging strategy

Severe peripheral artery disease (iliac)

(Severe) aortic regurgitation

Aortic dissection

Left ventricular thrombus (relative)

Uncontrolled bleeding disorder (relative)

Potentialcomplications

Leg ischemia

Bleeding

Vascular complications

Two-circulation syndrome

LV distension

Hyperfibrinolysis

Embolism

Fr French, VA-ECMO veno-arterial extracorporeal membrane oxygenation

draining and 15–19 French returningcannulas (. Table 2). Veno-venous (VV)ECMO drains from and returns to theright atrium. It is used for replacementof lung function, typically during acuterespiratory distress syndrome, and is notfurther discussed here.

In contrast, veno-arterial (VA)ECMOdrains blood from the right atrium andreturns to the arterial system, typicallyto the iliac arteries toward the aorta(. Fig. 1). By this, VA-ECMO reducespreload and increases aortic flow andend organ perfusion [36]. With arterialcannulation, placement of a dedicatedsheath for antegrade perfusion of thecannulated leg (. Fig. 1) is recommendedto prevent leg ischemia [37], which isstandard in many centers.

Agreat advantageofVA-ECMOis thatcannulationmaybeperformednearly ev-erywhere, as the system and all parts aretransportable. Thus, an unstable patientcan receive ECMO support in the emer-gency room, on theward, in the catheter-ization laboratory, the operating theater,or even in the field [38, 39]. In contrastto other support systems, fluoroscopy

or echocardiography guidance is – al-beit helpful – not required for successfulimplantation. Once ECMO is running,the patient can be transferred with thewhole unit, which is another advantageover other systems. Therefore ECMO isfrequently used for transport of unsta-ble patients by car, helicopter, or even byplane as an air-bridge [40].

VA-ECMO establishes a massiveright-to-left shunt by draining venousblood and returning it to the iliac artery.This flow support, which can reach7 l/min with large cannulas and con-temporary rotors, results in a significantincrease inbloodpressure as long as thereis enough vascular resistance (pressure =flow × resistance). The massive venousdrainage effectively reduces preload andthus leads to venous decongestion. Arte-rial reinfusion to the systemic circulationstrongly enhances perfusion of end or-gans and is therefore attractive duringsevere cardiorespiratory failure or re-suscitation. Of note, at the same timeretrograde flow support increases LVafterload (see next section).

Contraindications andcomplications

Notwithstanding the fast set-up of thesystem and the efficient hemodynamicsupport, VA-ECMO has contraindica-tions and harbors a significant risk ofcomplications (. Table 2). Most con-traindications are relative owing to thelifesaving nature of ECMO support,which in turn underlines that ECMOshould only be initiated when ethicalaspects or the patient’s wish do not pre-clude mechanical support. Uncontrolledbleeding is a contraindication, as ECMOrequires heparin for anticoagulation atleast for longer support. In selectedpatients, however, this contraindicationis relative, if ECMO is the only strategyto save the life of the patient. There areindeed centers that run ECMO supportin high-risk patients without any anti-coagulation (off-label) for a limited time(such as in severe trauma [41] or diffusealveolar hemorrhage [42]). A nearly ab-solute contraindication is severe aorticregurgitation: The retrograde flow sup-port of VA-ECMO would cause severeLV distension and pulmonary edema.VA-ECMO results in LV distension evenin patients with moderate aortic regur-gitation [43]. Further contraindicationsare listed in . Table 2.

ECMO support is an invasive pro-cedure with profound changes of bodyoxygenation and circulation, and inher-ently associated with potentially severecomplications [37, 44]. Among theseare vascular complications, leg ischemia,bleeding, hyperfibrinolysis, stroke, andair embolism (. Table 2). These are an-ticipated and in most cases effectivelycontrolled in tertiary centers. This em-phasizes that initiation, maintenance,weaning, and removal of ECMO re-quires a strong theoretical and practicalexpertise and should be performed inhigh-volume centers only.

Pathophysiology: watershed

The retrograde ECMO output meets theantegrade LV output at a zone calledthe “watershed” [36, 45, 46]. In mostcases the watershed occurs somewherebetween the aortic root and the di-

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Fig. 18 Veno-arterial (VA) ECMO. VA-ECMOdrains venous blood (blue) from the right atriumand returns an equal volume after reoxygena-tion anddecarboxylation (red) to the iliac arterytoward the aorta. Note the positionof the drain-ing venous cannula tip in themid right atrium.Femoral arterial cannulation requires an extrasheath for antegrade perfusion of the leg (in-set). (Modified fromNapp&Bauersachs [49]; ©L. C. Napp, J. Bauersachs 2016. This publicationis an open access publication, available on inte-chopen.com)

aphragm (. Fig. 2), depending on thenative output of the heart: The higher theLV output relative to ECMO output, themore distal the watershed [46]. Sincethe output of most ECMO devices isnonpulsatile, pulse pressure measuredat the right radial artery serves as anestimate of LV output [46]. For example,a blood pressure of 80/70 mmHg at anECMOflowof 4.5 l/min suggests awater-shed in the aortic root, whereas a bloodpressure of 140/70 mmHg at the sameECMO flow suggests a watershed in thedescending thoracic aorta. Blood fromthe ECMO is usually well oxygenated;however, oxygenation of blood from theLV depends on the respiratory functionof the lung. Therefore the position ofthe watershed is critical for oxygena-tion. Aortic root oxygenation cannot becontinuously measured with standardequipment. If the watershed is locatedin the ascending aorta and blood fromthe LV has an oxygen saturation of, e. g.,

Fig. 28 Watershedphenomenonduring VA-ECMO. Computed tomography.Antegrade blood flow(low contrast) from the heart competeswith retrograde blood flow (high contrast) from the ECMO inthe aorta, resulting in awatershedphenomenon (arrowhead).Here computed tomography of a pa-tientwith pulmonary embolismand reduced cardiac output demonstrates a rather proximal water-shed, leadingtoperfusionoftherightcarotidarterywith“heartblood”(dark)andthe leftcarotidarterywith“ECMOblood” (bright, arrows). Upper panel: sagittalobliquemaximumintensityprojection (MIP);middle panel: coronal obliqueMIP; lower panel: transverse plane. (FromNapp et al. [36]; © L. C. Napp,C.Kühn,M.M.Hoeperet al. 2015. This publication is anopenaccesspublication, availableonspringer-link.com)

56% during lung failure, then the heartitself may be perfused for hours or dayswith an extremely insufficient oxygensaturation from the lungs in the presenceof sufficient oxygenation of all other or-gans from the ECMO. In this context,the extreme form of dismal circulation isthe “two-circulation-syndrome” [47]: Ifthe venous cannula is incorrectly placedin the inferior caval vein, so that onlyblood from the lower body is drained,

blood from the upper body goes throughthe lungs to the ascending aorta. Thenvenous drainage from and the perfusionof the upper body are both disconnectedfrom that of the lower body. This resultsin a “Harlequin”-like appearance of thepatient, with upper-body hypoxia andlower-body hyperoxia.

As outlined, circulation and oxy-genation are overall subject to profoundchanges during VA-ECMO. Therefore

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Table 3 Monitoring of patients on VA-ECMOa

Parameter Reason/surrogate

Hemodynamics

PA catheter: Mean PA pressure, PC wedge pres-sure

Efficacy of preload reduction

Central venous pressure Efficacy of preload reduction

Right radial pulsatility LV output

Right radial mean blood pressure Perfusion pressure

Consider CCO catheterb LV output

Central venous oxygen saturation Systemic circulation

Urine output Renal perfusion and function

Lab: liver enzymes Venous decongestion

Respiratory support

Right radial blood gases Brain oxygenation, decarboxylation

Lactate End organ ischemia

Transcutaneous continuous near-infrared spec-troscopy

Tissue oxygenation (independent of pulsatil-ity)

Pulse oximetry (right hand finger or ear) Tissue oxygenation (largely dependent ofpulsatility)

Acral perfusion (clinical) Tissue perfusion

ECMO outflow blood gases Control of oxygenator capacity

Imaging

Echocardiography LV distension

Aortic regurgitation

Pericardial effusion

RV function

LV thrombus

Chest X-Ray Pulmonary edema, pneumothorax

Pleural sonography Pleural effusion

Coagulation

D-dimer, fibrinogen, platelet count Hyperfibrinolysis

Free hemoglobin, LDH Hemolysis

Activated clotting time (POCT) Anticoagulation

Blood cell count Anemia, thrombopenia

Leg perfusion

Clinical perfusion assessment Ischemia of the cannulated leg

General critical care monitoring

CCO continuous cardiac output, LDH lactate dehydrogenase, LV left ventricle, PA pulmonary artery,PC pulmonary capillary, POCT point of care testingaPeripheral femoro-femoral cannulationbClassic thermodilution is not reliable owing to right atrial drainage

multiple parameters have to be moni-tored in a patient on VA-ECMO at thesame time (. Table 3; [48]).

Triple cannulation

VA-ECMO delivers powerful circulatoryand respiratory support (. Table 2). Car-bon dioxide elimination by the ECMOis nearly always sufficient, thus hyper-capnia is nearly never a problem in pa-

tients on ECMO support – in contrast to(differential) hypoxia. As outlined ear-lier, the high oxygen content of ECMOoutput reaches only organs below thewatershed. Thus, under normal condi-tions the lower extremities, gut, kidneys,liver etc. are well oxygenated during VA-ECMO support. An additional effect onorgan oxygenation results from a higheramount of oxygen delivered to the lowerbody and an associated higher venous

backflow oxygen: Depending on oxy-genation settings, ECMO outflow pO2usually equals at least 200–300 mmHg,compared with 50–100 mmHg in arte-rial blood oxygenated in the lungs ofa standard ventilated shock patient. Thisresults in a higher total oxygen deliveryto the body, which may have an effectalso on organs perfused by LV blood, yetthe relevance of this effect is unclear todate.

However, in some patients on VA-ECMO support secondary lung failuredevelops. This is a dangerous situation:Depending on the watershed position,all organs perfused by blood from theheart are prone to severe ischemia in thepresence of ECMO support, in particu-lar the heart and brain. If lung failureis due to pulmonary edema, ultrafiltra-tion and active LV unloading (see later)are sufficient to achieve decongestion.However, in many patients with lungfailure on VA-ECMO support, the prob-lemresults fromanARDS-like condition,which cannot be or should not be effec-tively solved by aggressive ventilation ordecongestion. Inthesepatientsanelegantand very effective treatment is upgradingthe ECMO circuit to a triple-cannulatedECMO, with one venous-draining, onearterial-supplying, and one venous-sup-plying cannula (“VAV-ECMO”, . Fig. 3;[36, 49]). In addition to the VA cir-cuit, the additional venous cannula addspreoxygenated blood to the lungs andthereby establishes a “VV component.”This ensures sufficient oxygen content ofblood ejected by the heart and allowsfor lung protective ventilation. Of note,VAV-ECMOrequires sufficient RV func-tion, otherwise it may be necessary to re-locate the venous-supplying cannula intothe pulmonary artery [49] for bypassingthe RV. Retrospective studies suggest ef-ficacy of VAV cannulation for rescue ofbody oxygenation and recovery of lungfailure [50–52], but prospective studiesare needed to confirm the observed ben-efit.

Pathophysiology: afterload,decompression

During acute heart failure, the diseasedLV has impaired ability to eject, and

32 Herz 1 · 2017

Fig. 38 Veno-arterial-venous (VAV) ECMO.VAV-ECMOdrains venous blood (blue) from theright atrium and returns balanced volumes ofblood after reoxygenation anddecarboxylation(red) to the iliac artery toward the aorta and tothe right atrium toward the pulmonary circu-lation. For this purpose, the ECMOoutflow isdivided by a Y-connector. Flow through the re-turning cannulae is balancedwith an adjustableclamp andmonitoredwith a separate flow sen-sor on the upper return cannula. (Modified fromNapp&Bauersachs [49]; © L. C. Napp, J. Bauer-sachs 2016. This publication is an openaccesspublication, available on intechopen.com)

stroke work andmyocardial oxygen con-sumption are increased [30, 53]. Whenbridge-to-recovery is the therapeuticgoal (e. g., myocarditis or myocardialinfarction), stroke work and myocardialoxygen consumption have to be reducedto facilitate regeneration. However,notwithstanding the immediate massivehemodynamic and respiratory supportand the reduction of preload, VA-ECMOincreases LV afterload [53–57]. Thismayresult in increased LV filling pressures,wall stress, and severe pulmonary con-gestion despite reduction of preload.Moreover, ECMO is often ascribeda positive effect on coronary perfusion;however, human data are lacking anddata from animal studies are conflicting[58, 59]. From a pathophysiologicalperspective, a high LV pressure duringdiastole impairs coronary perfusion byreducing the transcoronary perfusion

Fig. 48 VA-ECMO and active LV unloading byusing an Impella®microaxial pump. In additionand in contrast to VA-ECMO,which delivers ret-rograde flow support to the aorta, the Impella®pumpdrains the LV and supplies the blood tothe ascending aorta. This “unloads” the LV andfacilitatesmyocardial recovery andpulmonarydecongestion. (Modified fromNapp&Bauer-sachs [49]; © L. C. Napp, J. Bauersachs 2016.Thispublication is an open access publication, avail-able on intechopen.com)

gradient. In patients with extremely lowsystolic LV function and in all patientswith ongoing arrest, VA-ECMO supportresults in a functionally closed aorticvalve without relevant transaortic bloodflow. This potentially results in severe LVdistension [54] and pulmonary conges-tion in the presence of sufficient systemiccirculation.

Thus, LV unloading, prevention of LVdistension, reduction of myocardial wallstress, and enhancementof coronaryper-fusion are important goals during me-chanical circulatory support for bridge-to-recovery. Unloading (= “venting”)can be achieved by different methods.One way is venting through the atrialseptum, either by atrioseptostomy [60,61] or placement of an additional drain-ing cannula through the atrial septum[62], both of which are potentially haz-ardous [61] particularly in the already

critically ill patient. Another possibil-ity is transvalvular unloading across theaortic valve, which has already been per-formed inanexperimental approachwitha transvalvular coronary catheter con-nected to the venous draining ECMOcannula [63]. However, simple drain-ing of the LV has no direct effect oncoronaryperfusionanddoesnot increaseantegrade transaortic blood flow. There-fore pumps have been developed that arepercutaneously inserted, drain the LV,and eject into the ascending aorta. Theirfirst use (Hemopump®) was publishedas early as in 1990 [64], but the clin-ical breakthrough took nearly 20 yearsto occur, mainly attributed to technicalimprovement of the device. Today, theonly transvalvular microaxial pump ap-proved in the United States and Europeis the Impella® device (Abiomed, Dan-vers, USA), which is the current device ofchoice of most centers for active LV un-loading, also combined with VA-ECMO(. Fig. 4).

The frequency of the combined use ofECMO and Impella® varies greatly be-tween centers. Of note, it is unclear todatewhichpatientshaveabenefitofaddi-tional Impella® support in parallel toVA-ECMO. There are two published stud-ies reporting combined support [65, 66].Their data point to a benefit of dual sup-port, but further studies are unequivo-callyneeded. . Fig. 5showsaproposal forthe management of VA-ECMO and po-tential unloading, based on pathophysi-ological considerations and clinical prac-tice in our center. In general, the lowersystolic LV function is in a given patient,the sooner active LV unloading shouldbe considered.

VA-ECMO for cardiogenic shock

Despite the broad use of ECMO in expe-rienced centers, data from larger studiesare limited. Most studies are retrospec-tive series or registry studies. Some yearsago, IABP was used in many countriesalmost routinely for patients with severecardiogenic shock, but later on random-ized studies demonstrated the noneffec-tiveness of routine IABP support [33].With this in mind, the decision for oragainst mechanical support and the de-

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Main topic

Fig. 59 Manage-ment of VA-ECMOfor bridge-to-re-covery in cardio-genic shock. Pro-posal ofmechani-cal support strate-gies for patientswith cardiogenicshock andprospectof cardiac recovery.LVEDP left ventric-ular end-diastolicpressure, RR arte-rial bloodpressure,VAV-ECMO venoar-teriovenous extra-corporealmem-brane oxygenation

cision for a specific device should takeinto account several different factors suchas RV and LV function, valve status,and lung function. The available devices(ECMO, Impella®, TandemHeart®) eachhave unique features, and there is nouniform device covering all types of car-diogenic shock. This is one of the ma-jor limitations of nearly all retrospectivestudies.

From clinical experience, ECMO ini-tiation is rather easy and fast, and ECMOis a very effective tool for enhancing andensuring systemic circulation and pro-vide gas exchange. As such, it should beprimarily considered in patients with se-vere acute cardiorespiratory failure (the“crash and burn” patient). In addition,some specific indications exist, such asdecompensated pulmonary arterial hy-pertension and pulmonary embolism.. Table 4 lists selected studies [67–72] ofVA-ECMO in cardiogenic shock.

From a pathophysiological perspec-tive, VA-ECMO should be favored forbridge-to-destinationorbridge-to-trans-plantation, when recovery is not the pri-mary goal and LVAD or transplantationwill follow. VA-ECMO is also favor-able for bridge-to-surgery, especially forembolectomy. In resuscitated patients

VA-ECMO is the commonly used de-vice for bridge-to-decision. By contrast,VA-ECMOmay not be the ideal supportform for isolated LV dysfunction withpotential for recovery (acute myocardialinfarction, myocarditis, Takotsubo syn-drome, etc.), since afterload increasesand recovery may be hampered [53].Of note, these are considerations fromdaily clinical routine and pathophysiol-ogy, but dedicated studies are urgentlyneeded to prospectively compare the dif-ferent support forms. One such studyis the prospective, open-label, multicen-ter, randomized, controlled “ANCHOR”trial (Assessment of ECMO inAcuteMy-ocardial Infarction with Non-reversibleCardiogenic Shock to Halt Organ Fail-ure and Reduce Mortality), which is cur-rently investigating the use of ECMO incardiogenic shock during myocardial in-farction. In this context, an interestingtool that is already mentioned in cur-rent heart failure guidelines [31] is the“SAVE” score to estimate theprognosis ofpatients with cardiogenic shock on VA-ECMO [73]. Another promising score isthe “ENCOURAGE” score [72].

VA-ECMO for extracorporealresuscitation

. Table 5 lists a selection of studies[74–86] on extracorporeal CPR (ECPR),i. e., ECMO for refractory resuscitation.Of note, to date there is no prospec-tive randomized study on ECMO forthis indication, also for ethical reasons.A comprehensive review of retrospectivestudies has been recently published else-where [87]. Taken together, the availableliterature on ECPR suggests that ECMOis sufficient toensure systemic circulationin refractory arrest. However, mortalityvaries between centers, and four factorsappear to critically determine ECPR suc-cess: patient selection criteria, a detailedstandard operating procedure, immedi-ate and sufficient bystander CPR, andtime from arrest to ECMO.. Table 6 listsa proposal for inclusion and exclusioncriteria for ECPR. Of note, such criteriacan only set a frame for decision, butmay need to be adjusted for individualpatients. A standard operating proce-dure for ECPR needs to incorporate allelements from circulatory arrest andbystander CPR over professional CPR,early contact with the ECMO center,team approach by anesthesiologists, car-diologists, and intensivists, high-levelintensive care medicine, and optimal re-habilitation. A proposal for a prospectivestudy considering all these factors has re-cently been published [88]. The time-to-ECMO interval is consistently associatedwith mortality [78, 84], very likely dueto the increased incidence and severityof post-resuscitation metabolism withdelayed extracorporeal support. Thus,a dedicated program for ECPR needsto put all efforts into earliest ECMOimplantation and optimal preclinicalCPR.

Conclusion

Mechanical support is increasingly usedin cardiogenic shock to minimize oravoid catecholamines and to facilitateregeneration of the diseased heart. Re-fractory cardiac arrest is an emergingindication for mechanical support, andrecently more centers have developedECPR programs. Cardiogenic shock and

34 Herz 1 · 2017

Table4

Selected

stud

ieso

fVA-ECM

Oforcardiog

enicshock

Refer-

ence

Origin

Design

Compa

rison

Etiology

Patien

ts(N)

Age

Implan

tation

LVEF

Outcome

Complications

Sheu

etal.

[67]

Taiwan

Prospective

observa-

tional

ECMO+IABP

vs.IABP

100%

STEM

Iinbo

thgrou

ps46

vs.25

sexno

trepo

rted

65.1±

10.6years

vs.67.2±

11.1years

(mean,

SD)

Inthecathlab(prob-

ablyshortly

afterPCI,

buttim

epointno

texactly

repo

rted)

Datanot

repo

rted

30d-survival60.9%ECMO-I-

ABP

vs.28.0%

IABP

Bleeding

orvascularcompli-

catio

ns39.1%

Tsao

etal.

[68]

Taiwan

Retro-

spective

ECMO+IABP

vs.IABP

ECMO+IABP:54.5%

STEM

I,45.5%NSTEM

I(93.9%

hadIABP

)IABP:44.0%

STEM

I,56.0%NSTEM

I(100%

hadIABP

)

33vs.25

84.8%

vs.64.0%

men

74.1±

12.2years

vs.70.1±

17.0years

(mean,

SD)

Intheem

ergency

room

orcathlab

ECMO+IABP:

38±10%

IABP:39±

14%

Successfulweaning

81.8%

inECMO+IABP

vs.44.0%

inIABP

survivalto

discharge

66.7%inECMO+IABP

vs.

32.0%inIABP

1-yearsurvival

63.6%inECMO+IABP

vs.

24.0%inIABP

Datanotreported

Sakamoto

etal.

[69]

Japan

Retro-

spective

nodevice

comparison

allhad

VA-ECM

O

100.0%

ACS,36.7%

hadcardiacarrest

beforeECMO95.9%

received

emergency

revascularization

98 66.3%

men

72±

12years

(mean,

SD)

44.9%implanton

admission

,33.7%

implantduringPC

I,20.4%implantaf-

terPCI.95.9%

had

additio

nalIABP

Datanot

repo

rted

Successfulweaning

55.1%

survivalto

discharge32.7%

35.7%ECMO-related

compli-

catio

ns23.5%cann

ulasitecomplica-

tions

4.1%

retrop

erito

nealhemor-

rhage

7.1%

lowerlim

bischem

ia3.1%

cerebralhemorrhage

Sattler

etal.

[70]

Germany

Retro-

spective

ECMOvs.

IABP

ECMO:66.7%

STEM

I,33.3%NSTEM

I,with

66.7%OHCA

and

16.7%IHCA

IABP:83.3%

STEM

I,16.7%NSTEM

I,with

41.7%OHCA

and

16.7%IHCA

12vs.12

83.3%

men

inbo

thgrou

ps

54.8±

13.3

yearsvs.

68.3±

12.2years

(mean,

SD)

1pat.beforePC

I9pat.im

mediately

afterPCI

2pat.24

and48

hafterPCIandIABP

ECMO:48±

10%

IABP:32±

13%

30d-survival67.0%ECMO

vs.33.0%

IABP

3/12

bleeding

2/12

compartmentsyndrom

ehemolysiswith

21.0±12.4

packed

redbloodcelltransfu-

sion

sperpatie

nt

Herz 1 · 2017 35

Main topic

Table4

Selected

stud

ieso

fVA-ECM

Oforcardiog

enicshock(Con

tinued)

Refer-

ence

Origin

Design

Compa

rison

Etiology

Patien

ts(N)

Age

Implan

tation

LVEF

Outcome

Complications

Aso

etal.

[71]

Japan

Register

nodevice

comparison

allhad

VA-ECM

O

42.2%Ischem

icheart

disease(IH

D),34.8%

Heartfailure(HF),

13.7%Valvularheart

disease(VHD),4%

Myocarditis(MYO

),4.1%

Cardiomyopathy

(CMP),0.7%Takot-

subo

synd

rome(TS),

0.3%

Infectious

endo

-carditis(IE)

Patientsw

hohad

cardiacarrest:All

47%,IHD25.0%,HF

15.0%,VHD2.7%

,MYO

1.4%

,CMP2.5%

,TS

0.3%

,IE0.06%

4,658

73.0%

men

All64.8±

13.7years

(mean,

SD)

Datanotreported

60.8%hadIABP

prior

toor

inparallelto

VA-ECM

O

Datanot

repo

rted

Survivaltodischarge

allpatients2

6.4%

,IHD

20.9%,HF32.2%,VHD

23.0%,M

YO43.0%,CMP

26.9%,TS35.3%,IE25.0%

Datanotreported

Muller

etal.

[72]

France

Prospective

observa-

tional

nodevice

comparison

allhad

VA-ECM

O

100%

acutemyocar-

dialinfarctio

n13.8%received

VA-ECM

Odu

ring

CPRand43.5%after

CPR

138

79.7%

men

55 (46–63)

years

(median,

IQR)

10.1%beforeand

89.9%afterPCI

69.6%hadIABP

paralleltoECMO

2.2%

hadIm

pella

and

ECMO

11.6%weresw

itched

tocentralECM

Ocann

ulation

20 (15–25)%

(median,

IQR)

Successfulweaning

35.5%

6-mon

thssurvival41.3%

39.1%ECMOcomplications:

12.3%bleeding

10.9%leg

ischem

ia11.6%accesssitein-

fection3.6%

hemolysis11.6%

overtp

ulmon

aryedem

aon

ECMO

CPRcardiopulmonaryresuscitation,EC

MOextracorporealm

embraneoxygenation,EC

PRextracorporealC

PR,IAB

Pintra-aortic

balloon

pump,IQRinterquartilerange,LVEF

leftventricularejectionfraction,

NSTEM

INon-ST-elevationmyocardialinfarction,pa

t.patients,PC

Ipercutaneouscoronaryintervention,STEM

IST-elevationmyocardialinfarction

36 Herz 1 · 2017

Table5

Selected

stud

ieso

fVA-ECM

Oforcardiac

arrest

Refer-

ence

Origin

Design

IHCA

/OHCA

Etiology

Patien

ts(N)

Age

Bystan

der

CPR

Initial

rhythm

Time-to-

ECMO

Initialp

HInitial

lactate

Outcome

ECMO-related

complications

Pred

ictorsof

mortality

Chen

etal.

[74]

a

Taiwan

Retro-

spective

96.5%/

3.5%

24.6%po

stcardiotomyall

cardiacorigin,

furtherd

etails

notreported

57 59.6%

men

57.1±

15.6

years

(mean,

SD)

96.5%

VF 47.4%,

VT 14.0%,

PEA/

asystole

38.6%

47.6±

13.4min.

(mean,

SD)

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMO66.7%

overallsurvival

31.6%

post-cardiotom

y57.1%

non-po

st-

cardiotomy23.3%

Massive

retrop

eri-

tonealhematom

a1.8%

limbam

puta-

tionafterECM

Ocann

ulation1.8%

furtherd

atano

trepo

rted

Aspartate

aminotrans-

ferase

onday3lactate

onday3

Massetti

etal.

[75]

France

Retro-

spective

87.5%/

12.5%

40%AC

S,10%

HF,15%In-

toxicatio

n,10%RH

Y,10%po

st-car-

diotom

y,7.5%

PE,5%MYO

40 57.5%

men

42±15

years

(mean,

SD)

Datanot

repo

rted

Data

notre-

ported

105±

44min.

(mean,

SD)

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMO30%

survivaltodis-

charge

20%

Vascularcompli-

catio

ns12.5%

legischem

ia2.5%

bleeding

7.5%

,pu

lmon

aryhem-

orrhage12.5%

Time-to-

ECMO

Sung

etal.

[76]

South

Korea

Obser-

vatio

nal

100%

/0%

36.3%coro-

naryartery

disease,36.3%

aftercardiac

surgery,9%

HF,9%

others,

4.5%

PE,4.5%

MYO

22 54.5%

men

62.5±

14.0

years

(mean,

SD)

Datanot

repo

rted

Data

notre-

ported

48.5±

29.0min.

(mean,

SD)

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMO59.1%

survivaltodis-

charge

with

good

neurolog

icalou

t-come40.9%

13.6%bleeding

4.5%

vascular

complications

Datanot

repo

rted

Chen

etal.

[77]

a

Taiwan

Prospec-

tive

observa-

tional

100%

/0%

62.7%AC

S,10.2%HF,

8.5%

MYO

,11.9%po

st-

cardiotomy,

1.7%

PE,5.1%

others

59 84.7%

57.4±

12.5

years

(mean,

SD)

Datanot

repo

rted

(alth

ough

100%

witn

essed

arrest)

VT/VF

49.2%,

PEA

28.8%,

Asystole

22.0%

52.8±

37.2min.

(mean,

SD)

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMO49.2%

survivaltodis-

charge

28.8%

1-yearsurvival

18.6%

Datanotreported

Time-to-ECM

Oinitialrhythm

otherthan

VT/VF

Herz 1 · 2017 37

Main topic

Table5

Selected

stud

ieso

fVA-ECM

Oforcardiac

arrest(Con

tinued)

Refer-

ence

Origin

Design

IHCA

/OHCA

Etiology

Patien

ts(N)

Age

Bystan

der

CPR

Initial

rhythm

Time-to-

ECMO

Initialp

HInitial

lactate

Outcome

ECMO-related

complications

Pred

ictorsof

mortality

Kagawa

etal.

[78]

Japan

Retro-

spective

IHCA

vs.

OHCA

49.4%/

50.6%

IHCA

55%

ACS,3%

HF,

5%MYO

,16%PE,21%

others

OHCA

56%

ACS,5%

HF,

3%MYO

,15%PE,21%

others

38vs.39

58%/85%

men

68 (58–73)

years

vs.

56 (49–64)

years

(me-

dian,

IQR)

92%in

IHCA

72%in

OHCA

IHCA

VT/VF

26%,

PEA

68%,

Asystole

5% OHCA

VT/VF

49%,

PEA

36%,

Asystole

15%

IHCA

25(21–43)

min.

OHCA

59(45–65)

min.

(median,

IQR)

IHCA

7.24

(7.09–7.39)

OHCA

7.02

(6.90–7.14)

(median,

IQR)

Datanot

repo

rted

Weaning

offECMOIHCA

61%,

OHCA

36%

good

neurolog

ical

outcom

eatdis-

charge

IHCA

26%,

OHCA

10%

30-dayssurvival

IHCA

34%,O

HCA

13%

legischem

iaIHCA

18%,O

HCA

21%

Bleeding

orhematom

aIHCA

68%,O

HCA

59%

Time-to-ECM

Oinitialrhythm

otherthanVF

Le Guen

etal.

[79]

France

Prospec-

tive

observa-

tional

0%/

100%

86%cardiac

(nofurther

details),6%

trauma,4%

drug

over-

dose,2%

respiratory,

2%others

51 90%

men

42±15

years

(mean,

SD)

Datanot

repo

rted

VF63%,

Asystole

29%,

PEA8%

120

(102–149)

min.

(median,

IQR)

6.93

±0.17

(mean,SD

)19.9±6.7

(mean,SD

)24

h-survival

40%48

h-survival

12%survivalwith

good

neurolog

ical

outcom

eatday

284%

14%severehem-

orrhagefurther

datanotreported

Lactateat

baseline

end-tid

alCO

2tim

e-to-ECM

O

Avalli

etal.

[80]

Italy

Retro-

spective

IHCA

vs.

OHCA

57.1%/

42.9%

IHCA

37%

ACS,33%po

stcardiotomy,

13%PE,9%

HF,9%

others

OHCA

67%

ACS,5%

HF,

11%RH

Y,17%

others

24vs.18

67%/94%

men

67 (61–73)

years

vs.46

(37–64)

years

(me-

dian,

IQR)

IHCA

100%

OHCA

55%

IHCA

VT/VF

50%,

PEA/

Asystole

50%

OHCA

VT/VF

89%,

PEA/

Asystole

11%

IHCA

55(40–70)

min.

OHCA

77(69–101)

min.

(median,

IQR)

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMOIHCA

58%,

OHCA

16%

28-dayssurvival

IHCA

46%,

OHCA

5%

IHCA

46%vascu-

larcom

pl.

OHCA

33%vascu-

larcom

pl.

Datanot

repo

rted

38 Herz 1 · 2017

Table5

Selected

stud

ieso

fVA-ECM

Oforcardiac

arrest(Con

tinued)

Refer-

ence

Origin

Design

IHCA

/OHCA

Etiology

Patien

ts(N)

Age

Bystan

der

CPR

Initial

rhythm

Time-to-

ECMO

Initialp

HInitial

lactate

Outcome

ECMO-related

complications

Pred

ictorsof

mortality

Chun

getal.

[81]

Taiwan

Prospec-

tive

observa-

tional

100%

/0%

27.6%STEM

I,11.9%

NSTEM

I,22.4%po

st-

surgery,

10.5%HF,

19.4%MYO

,6.0%

post-PCI,

2.2%

others

134

77.6%

men

51.8±

20.5

years

(mean,

SD)

100%

VT/VF

27.6%,

further

data

notre-

ported

Datanot

repo

rted

Datanot

repo

rted

Datanot

repo

rted

Weaning

offECMO50.7%

survivaltodis-

charge

42.5%

survival30

days

54.5%

Overall21.6%

perip

herallimb

ischem

ia3.0%

furtherd

atano

trepo

rted

APACH

E-II-

Score≥22

unsuccessful

weaning

offECMO

Haneya

etal.

[82]

Germa-

nyRetro-

spective

69.4%/

30.6%

30.6%AC

S,15.3%

HF,17.6%

post-PCI/TAV

I,16.5%PE,

2.4%

HYPO,

5.9%

TRA,

11.6%oth-

ers.Post-

cardiotomy

patientsw

ere

exclud

ed

85 71.8%

men

59±16

years

(mean,

SD)

Datanot

repo

rted

VT/VF

29.4%,

PEA

42.4%,

Asystole

28.2%

51±

35min.

(mean,

SD)

All7.01

±0.22

IHCA

7.09

±0.18

OHCA

6.85

±0.24

(mean,SD

)

All11

±6.9

IHCA

7.2±

5.6

OHCA

14.7±9.1

(mean,SD

)

Weaning

offECMO47.1%

(IHCA

57.6%,

OHCA

23.1%)

survivaltodis-

charge

34.1%

(IHCA

42.4%,

OHCA

15.4%)

93.1%with

outse-

vereneurolog

ical

deficitam

ongdis-

chargedpatie

nts

Overall32.9%

legischem

ia16.5%

bleeding

3.5%

cann

ulationcom-

plications

12.9%

pH,CPR

duratio

n

Fagn

oul

etal.

[83]

Belgium

Prospec-

tive

observa-

tional

41.7%/

58.3%

29.2%AC

S,20.8%RH

Y,12.5%PE,

8.3%

TRA,

8.3%

Intoxi-

catio

n,12.5%

HYPO,8.3%

others

24 58.3%

men

48 (38–55)

years

(median,

IQR)

91.7%

VT/VF

41.7%,

PEA/

Asystole

58.3%

58 (45–70)

min.

(median,

IQR)

Survivors

7.22

±0.23

non-survi-

vors7.06

±0.22

(mean,SD

)

Survivors

9.8±5.3

non-survi-

vors14.9±

4.85

(mean,SD

)

Weaning

offECMO29.2%

survivaltoICU

discharge25.0%

Majorbleeding

onECMOsite

29.2%

diffu

sebleeding

41.7%

Time-to-ECM

O(non

-sig-

nificant

trend)

Herz 1 · 2017 39

Main topic

Table5

Selected

stud

ieso

fVA-ECM

Oforcardiac

arrest(Con

tinued)

Refer-

ence

Origin

Design

IHCA

/OHCA

Etiology

Patien

ts(N)

Age

Bystan

der

CPR

Initial

rhythm

Time-to-

ECMO

Initialp

HInitial

lactate

Outcome

ECMO-related

complications

Pred

ictorsof

mortality

Leick

etal.

[84]

Germany

Retro-

spective

0%/

100%

53.6%AC

S,21.4%HF,

23.1%septic

shock,7.1%

Takotsub

osynd

rome,

3.6%

PE,3.6%

MYO

28 53.6%

men

53.9±

15.9

years

(non

-sur-

vivors)

60.3±

9.6

years

(sur-

vivors)

(mean,

SD)

Datanot

repo

rted

VF 28.6%,

Asystole

21.4%,

PEA

39.3%,

10.7%

notre-

ported

44.0

(31.0–

45.0)

min.(sur-

vivors)

53.0

(40.0–

61.3)

min.

(non

-sur-

vivors)

(median,

IQR)

Survivors

7.2

(7.05–7.4)

non-survi-

vors7.1

(7.0–7.3)

(median,

IQR)

Survivors

4.5

(3.9–9.3)

non-survi-

vors4.7

(3.6–7.8)

(median,

IQR)

30-day

survival

39.3%

legischem

ia3.6%

bleeding

32.1%

Time-to-ECM

O

Stub

etal.

[85]

Australia

Prospec-

tive

observa-

tional

57.7%/

42.3%

53.8%AC

S,7.7%

HF,

11.5%Ar-

rhythm

ia,

7.7%

PE,7.7%

respiratory,

11.5%others

26 77%

men

52 (38–60)

years

(median,

IQR)

Datanot

repo

rted

VF 73.1%,

PEA

15.4%,

Asystole

11.5%

56 (40–85)

min.

(median,

IQR)

all6.9

(6.7–7.1)

survivors

7.0

(6.8–7.1)

non-survi-

vors6.8

(6.7–7.0)

(median,

IQR)

all10

(7–14)

survivors8

(6–12)

non-survi-

vors13

(9–14)

(median,

IQR)

Weaning

offECMO54.1%

survivaltodis-

charge

53.8%

Bleeding

69.2%

perip

heralvascu-

larissues3

8.5%

vascularsurgery

41.7%

Time-to-ECM

O,

pH,tropo

nin

Jung

etal.

[86]

Germany

Retro-

spective

70.9%/

29.1%

23.1%VT

/VF

inHF,40.2%

VT/VFin

ACS,28.1%

post-surgery/

-interventio

n,9.4%

others

117

68.4%

men

61 (51–74)

years

(median,

IQR)

Datanot

repo

rted

VT/VF

63.2%,

further

data

notre-

ported

Datanot

repo

rted

Datanot

repo

rted

all9.0

(4.5–14.5)

survivors

4.5

(2.9–6.2)

non-

survivors

11.7

(5.5–14.9)

(median,

IQR)

Weaning

offECMO52.1%

30-dayssurvival

23.1%

good

neurolog

ical

outcom

e14.5%

Datanotreported

Lactate,

hemog

lobin

ACSacutecoronarysyndrome,CP

Rcardiopulmonaryresuscitation,EC

MOextracorporealm

embraneoxygenation,HFheartfailure,H

YPOaccidentalhypothermia,IHCA

in-hospitalcardiac

arrest,IQRinterquartile

range,MYO

myocarditis,NSTEM

Inon-ST-elevationmyocardialinfarction,OHCA

out-of-hospitalcardiac

arrest,PEpulmonaryem

bolism,PEA

pulselesselectricalactivity,RHYarrhythm

ia,SDstandarddeviation,

STEM

IST-elevationmyocardialinfarction,TR

Atraum

a,VF

ventricularfibrillation,VT

ventriculartachycardia

a Nooverlappingpatients

40 Herz 1 · 2017

Table 6 Proposed criteria for extracorporeal CPR (ECPR)

Inclusion criteria (all need to bemet)

Witnessed circulatory arrest

Bystander CPR

Age <75 yearsa

No ROSC after 10 min of professional CPRb

Exclusion criteria (one criterion is sufficient)

Severe comorbidity (cancer, end-stage liver cirrhosis, etc.)

Preexisting cognitive impairment/brain damage

Preclinical CPR >1hc

Optional exclusion criteria

pH at baseline <6.8

Lactate at baseline >15 mmol/l

Exceptions for criteria above

Accidental hypothermia

CPR cardiopulmonary resuscitation, ECMO extracorporeal membrane oxygenationaAge limit depends on comorbidities and biological agebExcellent CPR until ECMO is an essential prerequisite for successcMay be extended in single cases, when very young patients need time for transfer and have optimalCPR

arrest share many pathophysiologicalfeatures, and in this context VA-ECMOis a powerful extracorporeal life supportsystem, as long as it is initiated early.VA-ECMO use requires a dedicatedbridging strategy, such as bridge-to-re-covery, bridge-to-decision, or bridge-to-destination, and complications need tobe anticipated. Retrograde flow supportincreases LV afterload and may result inLV distension, which can be preventedand resolved by LV venting or activeLV unloading. Prospective controlledstudies are needed to develop specificprotocols for defined clinical conditions,in order to find the optimal mechanicalsupport strategy in a given situation.

Corresponding address

L. C. Napp, MDCardiac Arrest Center, Acute and AdvancedHeart Failure Unit, Department of Cardiologyand Angiology, Hannover Medical SchoolCarl-Neuberg-Str. 1, 30625 Hannover, Germanynapp.christian@mh-hannover.de

Compliance with ethicalguidelines

Conflict of interest. L. C. Napp received travel sup-port outside thiswork fromAbbott, Abiomed, Bayer,Biotronik, Boston Scientific, Cordis, Lilly,Medtronic,

Pfizer, Servier andVolcano, and lecture honoraria fromMaquet. C. Kühn received lecture honoraria fromMa-quetandJ.Bauersachs received lecturehonoraria fromAbiomed.

This article does not contain any studieswith humanparticipants or animals performedby anyof the au-thors.

OpenAccessThis article is distributedunder the termsof the Creative CommonsAttribution 4.0 InternationalLicense (http://creativecommons.org/licenses/by/4.0/), which permits unrestricteduse, distribution,and reproduction in anymedium, provided yougiveappropriate credit to the original author(s) and thesource, providea link totheCreativeCommons license,and indicate if changesweremade.

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Fachnachrichten

Steigerung auf hohem NiveauDeutscher Herzbericht 2016

Der Herzbericht stellt der deutschenHerz-Medizin ein gutes Zeugnis aus.Zwar zeigen die Statistiken, dassHerzerkrankungen weiter zu denhäufigsten Gründen für eine Kran-kenhausaufnahme zählen, jedochüberleben immer mehr Betroffene.

„Noch 1990 starben 324,8 von 100.000Einwohnern an den häufigsten Herzerkran-

kungen, 2014 waren es 256,1“, erklärt der

Präsident der Deutschen Gesellschaft fürKardiologie, Prof. Dr. Hugo Katus (Unikli-

nikum Heidelberg). „Dieser Rückgang um

21,15 % dokumentiert auf eindrucksvolleWeise den Stellenwert und die Fortschritte

der deutschen Herz-Medizin.“Angeführt wird die Statistik von Krankhei-

ten, die auf angeborene Fehlbildungen

zurückgehen. Im Vergleich zu 1990 gingdie Zahl der dadurch bedingten Todes-

fälle pro 100.000 Einwohner (Sterbeziffer)

um 66,67 % zurück. Es folgen die beidenhäufigsten Herzerkrankungen: An einer

Herzinsuffizienz starben 2014 um 33,05 %weniger Patienten als 1990, bei Patienten

mit koronaren Herzerkrankungen (Angina

Pectoris, Herzinfarkt) um 31,02 %. „We-gen der Erkrankungshäufigkeit haben die

Entwicklungen bei diesen beiden Krank-

heitsbildern wesentlich zur reduziertenGesamt-Sterblichkeit bei Herzerkrankun-

gen beitragen“, so Prof. Katus.„Besonders erfreulich ist, dass selbst auf

hohem Niveau noch Verbesserungen er-

zielt werden konnten,“ zieht Prof. KatusBilanz. So zeigt sich, dass die Sterbeziffer

der häufigsten Herzkrankheiten 2014 um

4,76 % unter dem Wert von 2013 liegt –ein Trend, der sich bei nahezu allen Er-

krankungsformen zeigt: Bei Fehlbildungensank die Sterbeziffer von 2013 auf 2014 um

16,67 %, bei den koronaren Herzerkran-

kungen um 6,46%, bei Herzinsuffizienz um3,17 % und bei den Rhythmusstörungen

um 2,16 %. Lediglich bei den Herzklappen-

Krankheiten blieb die Sterbeziffer mit 19,7bzw. 19,8 praktisch konstant.

Quelle: Deutscher Herzbericht /Deutsche Gesellschaft für Kardiologie

Weitere Infos: www.dgk.orgBerlin/Düsseldorf, 25.1.2017

Herz 1 · 2017 43

Hier steht eine Anzeige.

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