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The aim of this chapter is to discuss the indication and the role of a venoarterial extracorporeal membrane oxygenation (VA-ECMO) in the refractory cardiogenic shock and cardiac arrest.
Geneva University Hospitals, Intensive Care, Department of Anesthesiology, Pharmacology and Intensive Care, Genève, Switzerland
Carlo Banfi
University Hospitals, Division of Cardiovascular Surgery, Department of Surgery, Geneva, Switzerland
Raphaël Giraud
Geneva University Hospitals, Intensive Care, Department of Anesthesiology, Pharmacology and Intensive Care, Genève, Switzerland
*Address all correspondence to: marie-eve.brunner@hcuge.ch
1. Introduction
Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is a temporary technique for supporting the cardiac and the pulmonary system in patients suffering from refractory cardiogenic shock [1]. It allows time for reversible forms of cardiac failure to recover and can prevent end-organ damage from under perfusion.
Cardiogenic shock (CS) is defined as critical end-organ hypoperfusion due to low cardiac output and myocardial contractile dysfunction without hypovolemia [2]. CS has a broad spectrum from mild hypoperfusion to refractory CS. Experts’ recommendations for the management of adult patients with cardiogenic shock from the French-Language Society of Intensive Care (Société de Réanimation de Langue Française), with the participation of the French Society of Anesthesia and Intensive Care, the French Cardiology Society, the French Emergency Medicine Society, and the French Society of Thoracic and Cardiovascular Surgery recommend the use of peripheral VA-ECMO if temporary circulatory support is needed with a strong agreement [3]. Five percent of patients with acute myocardial infarction (AMI) develop a CS, with high mortality rates [4]. Despite optimal maximal therapy such as inotropes, Vasoconstrictors, intra-aortic balloon pump (IAPB), revascularization techniques, and mechanical circulatory support, CS remains the most frequent source of hospital death ranging between 60 and 70% compared to patients with AMI without advanced CS which is about 10% [5]. Cardiac arrest (CA) is the main cause of sudden death and occurs in almost 22% of patients with AMI [6]. CA has obviously a poor prognosis, and only a small percentage of the patients can return to a normal lifestyle. The principal causes for very poor outcome and prognosis in CA are an absence of return of spontaneous circulation (ROSC), long CPR, hypoxic encephalopathy, and out-of-hospital CA. In both refractory CS and CA following AMI, which are very critical circumstances, VA-ECMO has been proposed and utilized during the last decades to obtain rapid resuscitation, stabilization, and subsequent triage to bridge treatment. ECMO has remarkably progressed over the recent years; it became an invaluable tool in the care of adults with severe CS refractory to conventional management [7, 8].
The aim of this chapter is to describe VA-ECMO techniques, the more recent indications, and results in the use of the VA-ECMO in patients with refractory CS and CA.
VA-ECMO drains blood from the vascular system, which circulates outside the body by a mechanical pump, and is then re-infused into the circulation. In the circuit, hemoglobin becomes fully saturated with O2, and CO2 is removed. Oxygenation is determined by flow rate, and CO2 elimination can be controlled by adjusting the rate of countercurrent gas flow through the oxygenator.
Figure 1.
Percutaneous femoro-femoral VA-ECMO cannulation.
In CS and CA, where the cardiac circulation needs to be supported, a venoarterial configuration is required. This system includes a membrane oxygenator and a centrifugal pump to supply up to 5 L/min of support. VA-ECMO can be performed either peripherally or centrally. In peripheral VA-ECMO, a venous cannula is inserted via the femoral vein to the right atrium for drainage and an arterial cannula is inserted via the femoral artery into the ascending aorta for perfusion [9] (Figure 1).
Peripheral VA-ECMO cannulation can be performed both surgically by semi-Seldinger cut down and percutaneously. Intensive care physicians, interventional cardiologists, and obviously cardiac surgeons can perform the percutaneous technique whereas only cardiothoracic surgeons can perform central VA-ECMO [10].
There are a number of emergency indications. CS can occur in previously healthy patients or patients with chronic cardiac failure and with acute decompensation.
Refractory CS can take place after a myocardial infarction [11], any cardiomyopathy [12], a fulminant myocarditis [13, 14], intoxication with cardiotoxic drugs, electrical storm [15, 16], valvular insufficiency, massive pulmonary embolism [17], or CA with certain conditions.
Post cardiotomy CS (PCCS) can also occur after a cardiac surgery (heart transplantation for example) when it is not possible to wean from bypass [18].
Four types of situations can be described and are resumed in Table 1: bridge to decision, bridge to recovery, bridge to candidacy , and bridge to transplantation.
Bridge to decision (BTD)
Use of VA-ECMO in patients with drug-refractory acute circulatory collapse and at immediate risk of death to sustain life until a full clinical evaluation can be completed and additional therapeutic options can be evaluated.
Bridge to recovery (BTR)
Use of VA-ECMO to keep patient alive until intrinsic cardiac function recovers sufficiently to remove VA-ECMO.
Bridge to candidacy (BTC)
Use of VA-ECMO to improve end-organ function in order to make an ineligible patient eligible for transplantation/LVAD.
Bridge to transplantation (BTT)
Use of VA-ECMO to keep a patient at high risk of death before transplantation alive until a donor organ becomes available.
Table 1.
VA-ECMO: Types of situations.
Before VA-ECMO implantation, we should have several considerations. First of all, the likelihood of organ recovery has to be weighted. Initiation of VA-ECMO is appropriate only if the organ failure is thought to be reversible. When recovery is not expected, others options as transplantation or long term assist device as bridge to transplant versus destination therapy may be considered. The place of VA-ECMO in CS is shown in Figure 2.
Figure 2.
Place of VA-ECMO in CS.
Cardiogenic shock / Severe cardiac failure due to almost any cause
Myocardialinfarction
Cardiacarrhythmicstorm refractory to other measures
Fulminant myocarditis
Massive pulmonary embolisms
Drug overdose/toxicity with profound cardiac depression
Septic cardiomyopathy
Post-cardiotomy
Inability to wean from cardiopulmonary bypass after cardiac surgery
Post heart transplant
Primary graft failure after heart or heart-lung transplantation
Refractory cardiac arrest (No ROSC despite 30 min of optimal CPR)
Indications:
Age < 65 years
First rhythm: “shockable” rhythm
No flow ≤ 5 min
Witnessed cardiac arrest
EtCO2 per CPR > 10 mmHg
Time to ECMO < 60–90 min
Table 2.
Main VA-ECMO indications for cardiogenic shock and cardiac arrest.
Advanced age, severe brain injury, long time cardiac arrest, disseminated malignancy are considered as contraindications to the institution of VA-ECMO. Finally, aortic insufficiency or aortic dissection are both major contraindications.
Clinical and biological signs as well as therapeutic measures leading to VA-ECMO implantations in cardiogenic shock are resumed in Table 3.
Clinical and biological signs
Therapeutic measures
SBP < 90 mmHg OR MAP < 60 mmHg
Fluid for optimal preload Vasoactive drugs (first choice: norepinephrine)
CI <2.2 l/min/m2 S(c)vO2 < 50% LVEF < 20% VTI < 10 cm
Inotropes (first choice: dobutamine) IABP
SaO2 < 92%
Mechanical ventilation + sedation
Urine output < 30 ml/h
Malignant arrhythmia
IV Loading of amiodarone and/or lidocaïne External electric shock
If despite these measures lactate levels significantly still increase within 2 hours
→ Consider VA-ECMO implantation
Table 3.
Clinical and biological signs of cardiogenic shock as well as therapeutic measures leading to VA-ECMO implantations.
SBP: Systolic blood pressure, MAP: Mean arterial blood pressure, Cl: Cardiac index, S(c)vO2: Mixed/central venous saturation, LVEF: Left ventricular ejection fraction, VTI: Velocity time integral, SaO2: Arterial oxygen saturation, IABP: Intra aortic balloon pump.
A. Refractory CS post myocardial infarction
Refractory CS post myocardial infarction is the main cause of death in hospitalized patients with acute myocardial infarction. It occurs in 5–10% of patients [19]. The use of early PCI in those patients was associated with improved survival [11]. No randomized controlled trials compare VA-ECMO with other mechanical supports, but non-randomized studies show a survival benefit with the early use of VA-ECMO. One study tested the hypothesis that early ECMO offered additional benefits in improving 30-day survival in patients with acute myocardial infarction complicated by profound CS undergoing primary percutaneous coronary intervention. The VA-ECMO group had a significantly lower 30-day mortality (39.1% versus 72%, p=0.008). This study was limited by the fact that the two cohorts were enrolled in two different periods (Non-VA-ECMO Group: 1993–2002, versus VA-ECMO group: 2002–2009) and also because coronary stents were unavailable until 1998 [20]. To date, only case reports or case series showed a benefit in implanting VA-ECMO in refractory cardiogenic shock. It appears essential to implant VA-ECMO before multiorgan failure but no defined criteria are yet available to decide exactly when the device should be implanted. Randomized controlled trials are needed to determine if there is a true benefit in the use of VA-ECMO in CS post myocardial infarction to determine if early VA-ECMO in conjunction with optimal medical treatment would improve clinical outcomes at 30 days as compared with optimal medical treatment alone.
B. Electrical storm induced CS
In electrical storm induced CS, appropriate and timely VA-ECMO support helps to maintain and preserve vital organ perfusion. The period of stability offered by VA-ECMO support can allow optimization of anti-arrhythmic medication particularly the use of anti-arrhythmic agents most of whom have profound negative inotropic and hypotensive effects, and prevents left ventricular dilation [15]. It also prevents the low flow syndrome and multi-organ failure. VA-ECMO implantation should be considered early when conventional maneuvers fail to control the cardiac rhythm [21]. Early-onset VA-ECMO support may be lifesaving and should be considered in the management of hemodynamically unstable arrhythmias when conventional therapy fails to convert refractory ventricular tachycardia [16, 22]. While recommendations for VA-ECMO to handle refractory ventricular tachycardia remain to be set, success in using VA-ECMO in this case rely upon the correct selection of patients in the emergency department, and the prompt implantation before multiple organ failure occurs. Prompt institution of VA-ECMO support achieves the best outcome [21].
C. Fulminant myocarditis
Fulminant myocarditis is a non-ischemic, clinical manifestation of cardiac inflammation with rapid onset and severe hemodynamic compromise. Infective etiologic process is usually the most frequent finding. Inotropic therapy and intra-aortic balloon pump might not be sufficient to treat the pump failure. VA-ECMO support may be required to provide time to enhance heart recovery in this normally self-limiting disease. A recent 5-Year Multi-Institutional Experience showed a VA-ECMO weaning rate of 81% and discharge rate of 72% in the overall patient population [13]. Mirabel et al. shows that patients with fulminant myocarditis, who would have died without emergent initiation of circulatory support, had favorable short- and long-term outcomes with 68% hospital survivors and 46% partial or complete native heart function recovery [14]. In both studies, VA-ECMO implantations were performed when maximal medical therapy failed to improve hemodynamic status. In the study of Lorusso et al., pre-ECMO patient characteristics showed a systolic blood pressure at 61.8 ± 30.4 mmHg, pH at 7.2 ± 0.1 and lactate levels at 12.0 ± 4.6 mmol/L, corresponding to severe cardiogenic shock states [13].
D. Massive pulmonary embolism
A pulmonary embolism (PE) is a common illness that can cause death [23]. Massive acute PE (MAPE) results in CA in 41% of cases and is associated with a high mortality rate [24, 25]. Clinical practice guidelines recommend fibrinolytic therapy for patients with MAPE and CA, although few data are available to guide decisions about the agent, dose, rate, and frequency of administration [26, 27]. Fibrinolysis offers a rapid onset of action and ease of administration, and it is readily available in most hospital settings. The use of fibrinolysis during CPR in patients with presumed pulmonary embolism may improve survival [28, 29]. Fibrinolytic therapy is the first-line treatment in patients with high-risk pulmonary embolism presenting with CS in absence of contraindications. However, in several cases, there are absolute contraindications for this therapy. Catheter-based intervention is recommended for patients with circulatory collapse due to MAPE and is equivalent to surgical embolectomy [30]. Emergent VA-ECMO provides an opportunity for improving the prognosis of an otherwise near-fatal condition and should be considered in the algorithm for managing MAPE in an unstable patient [31]. The survival rate in patients with MAPE who receive VA-ECMO and anticoagulation or surgical embolectomy was 62% [31]. Thus, ECMO can provide lifesaving hemodynamic and respiratory support in critically ill patients with MAPE in patients hemodynamically unstable to support any other interventions or have not responded to medical therapies. Success in ECMO for MAPE is determined by the return of sufficient RV function [32]. ECMO may be considered in early management of patients with MAPE unresponsive or contraindicated to pharmacological treatment [33].
E. Pulmonary arterial hypertension
In addition, VA-ECMO is also a supportive option for patients with decompensated pulmonary arterial hypertension. In fact, pulmonary arterial hypertension is associated with high morbidity and mortality, particularly in patients with progressive RV failure. In this case, VA-ECMO can be used as a bridge to lung transplant or bridge to recovery when medical therapy is not sufficient to prevent cardiopulmonary failure in the acute setting [34].
F. Post-cardiotomy CS
Post-cardiotomy CS (PCCS) is very rare, but is a lethal complication in post cardiac surgery. PCCS occurs in 2–6% of patients undergoing surgical revascularization or valvular surgery [35, 36]. Approximately 0.5–1.5% of patients is refractory to maximal inotropic and intra-aortic balloon pump (IABP) support [37]. Post-cardiotomy CS occurs in perioperative cardiac surgery in patients with normal preoperative myocardial function as well as those with pre-existing impaired function [38]. Refractory PCCS leads rapidly to multi-organ dysfunction and is nearly always fatal without the use of advanced mechanical circulatory support [35]. VA-ECMO is used to salvage patients who develop refractory PCCS [39]. However, even if outcomes in patients requiring such support for PCCS continue to be poor [40], VA-ECMO may be used as temporary post-operative cardiovascular support.
G. Primary graft failure
Primary graft failure (PGF) after heart transplantation is a detrimental complication, and carries high morbidity and mortality. In a study involving 114 consecutive patients receiving orthotopic heart transplantation, 18 (15.7%) developed PGF requiring VA-ECMO support. Thirteen patients (72.2%) were able to be weaned from the support, and eight of them (44%) were discharged [41]. Thus, as in PGF recovery is usually more frequent than in other cases of PCCS, due to the more probable reversibility of the damage, ECMO support could be used as bridge to graft recovery [42, 43].
H. Septic cardiomyopathy
Septic cardiomyopathy occurs with severe myocardial depression in septic shock. In a retrospective observational study, 14 patients with septic shock refractory to conventional treatment all had a severe myocardial dysfunction at VA-ECMO implantation. Mean LV ejection fraction (LVEF) was 16% and cardiac index was 1.3 L/min/m2 in these patients. At ECMO implantation, mean pH was 7.16 and blood lactate was 9 mmol/L. Twelve patients were weaned off VA-ECMO. Ten patients survived after a follow-up of 13 months and recover a normal LVEF [44]. VA-ECMO may provide benefit to patients with a cardiac failure in the setting of a septic shock, but larger studies are needed.
I. Refractory cardiac arrest
Increasing number of papers has reported encouraging results on the use of VA-ECMO for refractory CA. Extracorporeal circulation ensures an adequate blood flow, time to perform diagnostic and therapeutic interventions even before a return of spontaneous circulation is achieved [43]. For patients with whom conventional advanced life support maneuvers are insufficient and/ or to make specific interventions possible (e.g., coronary angiography and percutaneous coronary intervention (PCI) or pulmonary embolectomy for MAPE), extracorporeal CPR (eCPR) has to be considered as a lifesaving therapy [45]. This practice is evolving and is used for both in-hospital (IHCA) and out-of-hospital (OHCA) CA despite few observational statistics. Observational studies suggest that eCPR for CA is correlated with enhanced survival [46] in case of reversible cause of CA, few comorbidity, witnessed CA, immediate high-quality CPR, and eCPR early implanted (e.g., within 1 h of CA) as well as when VA-ECMO is implanted by emergency physicians and intensivists [47–50]. eCPR involves significant resource and training. It has been correlated with enhanced survival after IHCA in selected patients [47, 51] when compared with manual or mechanical CPR. After OHCA, survival after eCPR is less favorable [52]. However, when deployed during and/or soon after resuscitation attempts, despite variations in practice and heterogeneity of outcomes, these interventions yield a good neurological survival in 12% of adults suffering a refractory OHCA [53]. In a retrospective observational study dividing CA patients in two groups (shockable rhythm and non-shockable rhythm), the authors found that non-shockable rhythms could be considered as a formal contraindication allowing a concentration of efforts on the shockable rhythms, where the chances of success are substantial. They conclude that VA-ECMO for refractory OHCA should be limited due to a very poor neurological outcome [54]. Indications for eCPR are detailed in Table 2. However, there is an urgent need for randomized studies of eCPR and large eCPR registries to identify the circumstances in which it works best, establish guidelines for its use and identify the benefits, costs and risks of eCPR.
Not surprisingly, VA-ECMO is associated with a lot of possible complications that can be lethal. This is why VA-ECMO must be done by well-trained teams in reference centers.
The most common complications listed with the use of VA-ECMO are: major or significant bleeding, re-thoracotomy for bleeding or tamponade, vascular complications as lower limb ischemia, lower limb ischemia requiring fasciotomy or compartment syndrome, lower extremity ischemia requiring amputation, neurologic complications like stroke, acute kidney injury requiring renal replacement therapy, and significant infection.
A. Bleeding
In a recent meta-analyze, 20 studies were analyzed including 1866 patients. Bleeding was the most frequent complications with an estimated rate of 41%. The most frequent source of hemorrhage is the femoral cannula insertion site [55]. In central ECMO, the rate of re-thoracotomy for bleeding or tamponade was 42%. The average number of units of packed red blood cells transfused ranged from 12.7 to 29.0 units. Indeed, bleeding, thrombosis, and hemolysis remain the most common causes of morbidity and mortality for patients receiving ECMO therapy. These adverse effects have to be considered and should be monitored during ECMO therapy. Apart from surgical hemostasis problems, coagulation and inflammatory systems are immediately activated when blood comes in contact with the ECMO circuit, which necessitates systemic anticoagulation [56]. In a recent single center prospective randomized study on adult patients requiring ECMO therapy, hemostasis, anticoagulation, hemolysis, and inflammatory parameters were monitored. The results showed that median platelet count had dropped, prothrombin fragment 1.2, thrombin-antithrombin complex, and D-dimers increased, whereas fibrinogen values dropped [57]. However, antithrombotic therapy is necessary to maintain patency with the ECMO circuit and ultimately reduce the risk of clotting while decreasing the probability of hemorrhage. Currently, the most commonly used antithrombotic therapy is systemic anticoagulation with unfractionated heparin, which is associated with its well-known complications inclusive of bleeding (patient) and clotting (circuit). Systemic anticoagulation complications in ECMO support have not really reduced despite developments in technology and monitoring methods over the last few years.
Moreover, bleeding and thrombosis comprise majority of all side effects that can occur on ECMO, and the inability to mediate and control this effectively can lead to catastrophic complications and increases mortality. Heparin monitoring is very challenging on ECMO. There are actually no universal protocols concerning anticoagulation management; however, some centers propose to target 45–60 s for aPTT and 0.2–0.3 IU/ml for heparinemia (anti-Xa activity) [58]. Hemoglobin threshold for red cell transfusion should be 7–8 g/dl and only severe thrombocytopenia complicated by bleeding should be corrected. There is no single test that correctly monitors all of the factors influencing the anticoagulation, including the heparinization. As a result, over time and experience, a variety of tests are used. More recently, the Extracorporeal Life Support Organization (ELSO) proposed guidelines for management of the anticoagulation with ECMO. The main parameters monitored during ECMO are the activated coagulation time (ACT), the antifactor Xa assay (anti-Xa), and the activated partial thromboplastin time (aPTT). More recently, the thromboelastography (TEG) or the thromboelastometry (ROTEM) have been introduced to monitor ECMO patients. These tests add information about the phases of coagulation, platelet function, and fibrinolysis, which is very relevant in ECMO patients as they have coagulation abnormalities. While many centers have integrated those tests into their ECMO anticoagulation guidelines, more research is needed to understand the place of TEG and ROTEM monitoring in ECMO patients [59].
B. Vascular complications
Vascular issues are the second more frequent complication. The cumulative rate of lower extremity ischemia is around 17%. The cumulative rate of lower extremity fasciotomy or compartment syndrome is around 10%. The cumulative rate of lower extremity amputation occurs to 7 of 192 (5%) [60]. In another retrospective study, statistics of 100 patients with VA-ECMO inserted via percutaneous femoral approach for CS or refractory CA were examined. A 7-9 Fr percutaneous reperfusion catheter, distal to the arterial cannula, was positioned into the artery, if the leg showed sign of under-perfusion. Thirty patients with early ischemia benefited from a reperfusion cannula to improve perfusion of the limb and it succeeded in 26 of them. Seven patients suffered a compartment syndrome of the leg necessitating urgent fasciotomy. In two of those patients, the ischemia moved to irreversible ischemia necessitating amputation of the limb. The authors concluded that the majority of ischemic episodes were resolved with the insertion of a distal perfusion catheter. They did not observe any mortal vascular complication, nor was any of the observed complications related to increased mortality [61]. However, in another recent study, 84 peripheral VA-ECMO patients were separated into two groups depending on the presence of major vascular complications, defined as patients who required surgical intervention. The authors found that vascular complications negatively affect survival in patients receiving VA-ECMO support by means of femoral cannulation and that distal perfusion catheter can decrease the incidence of complications [62].
C. Hemolysis
Hemolysis during ECMO therapy remains of concern with a reported incidence between 5 and 18% [63–65]. Major contributors are technical-induced hemolysis that may consist of sub lethal damage to erythrocytes by shear stress, high ECMO blood flow particularly high flow velocity through small cannulas, cavitation particularly in case of hypovolemia, pressure changes within the oxygenator particularly in case of fibrin/thrombosis upon the membrane [66–72]. Free plasma hemoglobin (fHb) and lactate dehydrogenase can increase significantly during ECMO support [73, 74] because of red blood cell (RBC) destruction. fHb is cytotoxic causing cell necrosis [73, 75]. It also scavenges nitric oxide, leading to vasoconstriction, endothelial dysfunction, and platelet aggregation [76, 77]. Consequently, renal insufficiency or multiple organ failure can appear [78–80]. Then, prevention and rapid identification of hemolysis are crucial for ECMO patients.
D. Neurological complications
Neurological complications are rather common in patients on VA-ECMO [81]. These complications are generally related to thrombosis with cerebral infarction and intracranial hemorrhage [82]. Intracranial hemorrhage (ICH) in particular has been associated with higher rates of mortality [83]. A review on a large, multihospital database, the Nationwide Inpatient Sample of the Healthcare Cost and Utilization Project of the Agency for Healthcare Research and Quality reviewed patients between 2001–2011 receiving ECMO [84]. The authors showed that 10.9% suffered from neurological complications including seizure (4.1%), stroke (4.1%), and intracranial hemorrhage (3.6%). The outcome between seizure patients and patients without neurological complications did not differ. Patients with stroke or hemorrhage have a higher hospital length of stay, higher probability of discharge to a long-term facility, and patient who suffered of intracranial hemorrhage have a higher mortality rate. More research is still needed to prevent neurologic complications.
E. Infections
The ELSO registry found an overall prevalence of infection of 11.7%, ranging from 7.6% in neonates to 20.9% in adults, with little variation during the 11-year span of the registry data [85]. An increased rate of death was found in patients who acquired infection during VA-ECMO. Bloodstream infections were predominant in most studies that reported the site of infection, followed by surgical site infections, urinary tract infections, and respiratory tract infections [86]. A fungal infection developed in 12% of patients, with surgical site infections reported most commonly [87]. Currently, the ELSO Infectious Disease Task Force does not recommend routine antimicrobial prophylaxis during ECMO. This is confirmed by a recent review stating that there is no evidence to defend prophylactic antibiotics in most patients, even if infections during ECMO are serious complications. Infections should be prevented [86].
F. Refractory pulmonary edema
In case of peripheral VA-ECMO for refractory CS, patients with very low residual cardiac contractility and elevated afterload due to the ECMO can lead to an inadequate decompression of the left ventricle resulting in a refractory pulmonary edema, fatal pulmonary hemorrhage, and left ventricle (LV) clotting [88]. Various methods for left heart decompression are known, but there is no consensus about the appropriate method and timing of decompression. However, in this situation, the first therapeutic measures are the introduction of inotropic drugs associated with an intra-aortic balloon pump to help increase LV contractility allowing the opening of aortic valve, to decrease left ventricular afterload, and thus to unload the LV. Minimally invasive strategies such as percutaneous transseptal left atrial decompression [89] and subxiphoid surgical approaches to drain the left ventricle [90] have been described to reduce LV distension. The residual atrial defect may require correction once the patient has been weaned from mechanical support. Use of a percutaneously inserted VAD (Impella™; Abiomed, Aachen, Germany) to decompress the left ventricle has also been reported in this setting [91], alleviating the need for a high-risk septostomy or surgical venting. However, in some circumstances depending of the patient’s state and local resources, central cannulation with left ventricular decompression may be indicated [92].
G. Harlequin syndrome
Harlequin syndrome is a hypoxemia of the upper body due to a competition of the VA-ECMO flow with the systolic function of the native heart. In a femoro-femoral VA-ECMO, when the heart function recovers, there is a competition between VA-ECMO flow and native cardiac flow in the aorta. In case of significant impairment of pulmonary gas exchange leading to an upper body hypoxemia, despite optimization of the ventilator settings, ECMO configuration has to be adapted. VA ECMO flows can be increased in an attempt to better perfuse the aortic root with retrograde arterialized blood. In addition, the arterial outflow cannulation site can be switched from the femoral artery to the axillary or carotid artery. As they are in closer proximity to the aortic arch, these cannulation sites may be more effective in washing the root with oxygenated blood. However, cannulation of these smaller vessels will require a smaller cannula, which will decrease the maximum achievable flows. A VA-V-ECMO circuit can also be created where a portion of arterialized blood from the arterial outflow cannula is diverted via the right internal jugular artery to the right heart. This enriches the blood traveling through the pulmonary circulation and to the left ventricle to provide better oxygen delivery to the coronary and cerebral circulations. Finally, if cardiac function has recovered sufficiently, VA-ECMO can be converted to VV-ECMO to provide only gas exchange support until the lungs fully recover its function [93].
After a few days of mechanical assistance, patients implanted with VA-ECMO for CS or CA can sometimes be successfully weaned from the device, when they have partially or fully recovered from the condition that indicated ECMO use. Hemodynamic parameters such as invasive arterial pressure and heart rate, intravenous inotropes and vasoactive drugs, blood lactate and blood gas analyses should be monitored. A daily echocardiography should be performed and those criterions are evaluated: LVEF; aortic time–velocity integral (VTI); transmitral early peak (E) and late diastolic velocities; spectral tissue Doppler lateral mitral annulus peak systolic (TDSa); and early diastolic (Ea) annular velocities. LV filling pressures are estimated with the E/Ea ratio. First of all, the patient has to be considered as hemodynamically stable: baseline MAP > 60 mmHg with no or low-dose vasoactive agents and a pulsatile arterial waveform present for at least 24 h, and no compromising of the pulmonary blood oxygenation. Only in these conditions, an ECMO weaning trial can be attempted. ECMO flow is gradually reduced to 66% for 10–15 min, then to 33% and/or to a minimum of 1–1.5 L/min for another 10–15 min. If the patient begins to present hemodynamical instability (MAP dropped under 60 mmHg), the trial is stopped, and ECMO flow has to return to the initial flow. In a study upon 51 patients, the authors assessed a weaning strategy following support for refractory CS to recognize clinical, hemodynamic, and Doppler echocardiography parameters predictive for efficacious ECMO removal. Patients who were considered as hemodynamically stable underwent ECMO flow decrease trials to <1.5 L/min under clinical and Doppler echocardiography monitoring. Patients with partially or fully recovery from severe cardiac failure, weaning trial tolerance, LVEF >20–25% and VTI >10 cm under minimal ECMO support, had ECMO support removed. In this study, 38 patients endured the weaning trial and 20 were finally weaned of the ECMO support.
This study showed that echocardiographic parameters determine weaned and non-weaned patients more than all other factors examined. The authors concluded that patients who tolerate a full ECMO weaning trial and have aortic VTI ≥10 cm, LVEF >20–25%, and TDSa ≥6 cm/s at minimal ECMO flow can be weaned [94].
Survival after VA-ECMO for refractory CS depends on etiology and severity of the patient at the implantation of the VA-ECMO support.
Mirabel et al. described factors associated with unfavorable outcomes in myocarditis related CS as higher body mass index; severe comorbidity; ICU admission Simplified Acute Physiology Score II, Sepsis-Related Organ Failure Assessment, and Glasgow Coma Scale; VA-ECMO placed under cardiopulmonary resuscitation; elevated sodium, troponin Ic and blood lactate; and low hematocrit and arterial pH [14].
Health-related quality of life was also evaluated in those survivors and revealed persistent difficulties with work or other daily activities. Mental health and vitality were deemed satisfactory. Severe anxiety, depression, and PTSD symptoms were reported by 27–38% of the patients after a median follow-up of 18 months.
Despite the high number of refractory CS requiring VA-ECMO, predictive survival modeling has not been reported till 2015 with the SAVE Score: Predicting survival after VA-ECMO for refractory CS [95]. Using a large international cohort of 3846 patients treated with VA-ECMO for CS (Extracorporeal Life Support Organization: ELSO), prognostic factors were identified for hospital survival and created a well-calibrated and reasonably discriminatory in-hospital survival prediction score comprising 13 pre-VA-ECMO variables. Parameters are Acute CS diagnosis group (myocarditis, arrhythmias, post heart of lung transplantation, congenital heart disease or others diagnoses leading to refractory CS), age, weight, acute pre-VA-ECMO organ failure, chronic renal failure, and time of intubation before VA-ECMO implantation. All of them determine a 5-class survival risk with survival rate. A SAVE-score of zero is approximately equivalent to 50% survival with positive scores representing higher chances of survival [95].
While inappropriate VA-ECMO use raises resource utilization and hospital costs and is associated with unacceptably high mortality, early identification of mortality risk factors and detailed analyses of survivors’ long-term outcomes are needed. A two-center retrospective study was designed to identify pre-ECMO factors associated with in-ICU death and then derive a practical mortality risk score that might help physicians to select appropriate acute myocardial infarction (AMI) patients for VA-ECMO.
A study concerning 138 ECMO supporting AMI patients analyzed long-term survivors’ health-related quality of life (HRQOL) and frequencies of anxiety, depression, and post-traumatic stress disorder (PTSD). The survivors were evaluated for HRQOL, psychological and PTSD status 6 months after discharge of ICU. This study showed that nearly 50% of all patients were still alive. The authors developed the ENCOURAGE score on the basis of multivariable logistic regression analyses including seven pre-ECMO parameters: age >60, female sex, body mass index >25 kg/m2, Glasgow coma score < 6, creatinine >150 μmol/L, lactate (<2, 2–8, or >8 mmol/L), and prothrombin activity < 50%. Six months after ECMO, probabilities of survival were 80, 58, 25, 20, and 7% for ENCOURAGE score classes 0–12, 13–18, 19–22, 23–27, and ≥ 28, respectively. The ENCOURAGE score ROC AUC (0.84) was significantly better than those of the SAVE, SAPS II, and SOFA scores. Survivors’ HRQOL evaluated after median follow-up of 32 months revealed satisfactory mental health but persistent physical and emotional related difficulties, with 34% anxiety, 20% depression, and 5% PTSD symptoms reported. The authors concluded that the ENCOURAGE score might be a useful tool to predict mortality of severe CS in AMI patients who received VA-ECMO. However, it now needs prospective validation on other populations than AMI patients [96].
Prognosis is quite different regarding refractory CA patients. Early VA-ECMO implantation has been shown to give a better outcome in patient with CA. Low flow longer than 90 minutes offers a very bad prognosis [47].
In 2008, a French group proposed recommendations to limit the VA-ECMO implantation in case of refractory CA [97]. Our local ECMO alarms criteria for refractory cardiac arrest are shown in Table 4. Patients are evaluated according to these criteria by a multidisciplinary team including emergency physicians, intensivists, anesthesiologists, cardiologists, and cardiac surgeons. A consensual decision to implant a VA-ECMO or not is taken.
ECMO alarm criteria
Indications
Contraindications
No-flow ≤ 3 min OR immediate CPR by professional OR signs of life per CPR OR hypothermia
Finally, some papers are now published about the ethical dimension of ECMO support [98]. In fact, ECMO technology now allows prolonged support with decreased complications, and the need of early implantation, have led to a significant increase in the use of ECMO worldwide. This increasing use of a technology that is not a destination device in itself introduces many ethical dilemmas specific to this technology.
The use of VA-ECMO in patients with refractory cardiogenic shock and cardiac arrest is widely increasing and is now recognized as a standard technique because in these patients the mortality without the ECMO support would be dramatically higher. It seems essential to determine whether ECMO support should be initiated before organ dysfunction advances to preserve organ function. However, even if data in the literature show a progressive increase in the overall outcome, these devices are associated with serious complications such as bleeding, lower limb ischemia, infections, and CNS irreversible damage that remain problematic issues. Efforts to reduce or prevent them are necessary and strongly recommended to improve the outcome. Finally, as inappropriate VA-ECMO use raises resource utilization and hospital costs and is associated with unacceptably high mortality, early identification of mortality risk factors and detailed analyses of survivors’ long-term outcomes are needed.
References
1.Makdisi G, Wang IW. Extra Corporeal Membrane Oxygenation (ECMO) review of a lifesaving technology. J Thorac Dis. 2015;7(7):E166-76.
2.Authors/Task Force m, Windecker S, Kolh P, Alfonso F, Collet JP, Cremer J, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014;35(37):2541-619.
3.Levy B, Bastien O, Karim B, Cariou A, Chouihed T, Combes A, et al. Experts' recommendations for the management of adult patients with cardiogenic shock. Ann Intensive Care. 2015;5(1):52.
4.Shah RU, de Lemos JA, Wang TY, Chen AY, Thomas L, Sutton NR, et al. Post-Hospital outcomes of patients with acute myocardial infarction with cardiogenic shock: findings from the NCDR. J Am Coll Cardiol. 2016;67(7):739-47.
5.Goldberg RJ, Spencer FA, Gore JM, Lessard D, Yarzebski J. Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation. 2009;119(9):1211-9.
6.Brady WJ, Gurka KK, Mehring B, Peberdy MA, O'Connor RE, American Heart Association's Get with the Guidelines I. In-hospital cardiac arrest: impact of monitoring and witnessed event on patient survival and neurologic status at hospital discharge. Resuscitation. 2011;82(7):845-52.
7.MacLaren G, Combes A, Bartlett RH. Contemporary extracorporeal membrane oxygenation for adult respiratory failure: life support in the new era. Intensive Care Med. 2012;38(2):210-20.
8.Shekar K, Mullany DV, Thomson B, Ziegenfuss M, Platts DG, Fraser JF. Extracorporeal life support devices and strategies for management of acute cardiorespiratory failure in adult patients: a comprehensive review. Crit Care. 2014;18(3):219.
9.Abrams D, Combes A, Brodie D. Extracorporeal membrane oxygenation in cardiopulmonary disease in adults. J Am Coll Cardiol. 2014;63(25 Pt A):2769-78.
10.Conrad SA, Grier LR, Scott LK, Green R, Jordan M. Percutaneous cannulation for extracorporeal membrane oxygenation by intensivists: a retrospective single-institution case series. Crit Care Med. 2015;43(5):1010-5.
11.Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS, et al. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA. 2005;294(4):448-54.
12.Bermudez CA, Rocha RV, Toyoda Y, Zaldonis D, Sappington PL, Mulukutla S, et al. Extracorporeal membrane oxygenation for advanced refractory shock in acute and chronic cardiomyopathy. Ann Thorac Surg. 2011;92(6):2125-31.
13.Lorusso R, Centofanti P, Gelsomino S, Barili F, Di Mauro M, Orlando P, et al. Venoarterial extracorporeal membrane oxygenation for acute fulminant myocarditis in adult patients: a 5-year multi-institutional experience. Ann Thorac Surg. 2016;101(3):919-26.
14.Mirabel M, Luyt CE, Leprince P, Trouillet JL, Leger P, Pavie A, et al. Outcomes, long-term quality of life, and psychologic assessment of fulminant myocarditis patients rescued by mechanical circulatory support. Crit Care Med. 2011;39(5):1029-35.
15.Brunner ME, Siegenthaler N, Shah D, Licker MJ, Cikirikcioglu M, Brochard L, et al. Extracorporeal membrane oxygenation support as bridge to recovery in a patient with electrical storm related cardiogenic shock. Am J Emerg Med. 2013;31(2):467 e1-6.
16.Pagel PS, Lilly RE, Nicolosi AC. Use of ECMO to temporize circulatory instability during severe Brugada electrical storm. Ann Thorac Surg. 2009;88(3):982-3.
17.Pavlovic G, Banfi C, Tassaux D, Peter RE, Licker MJ, Bendjelid K, et al. Peri-operative massive pulmonary embolism management: is veno-arterial ECMO a therapeutic option? Acta Anaesthesiol Scand. 2014;58(10):1280-6.
18.Bakhtiary F, Keller H, Dogan S, Dzemali O, Oezaslan F, Meininger D, et al. Venoarterial extracorporeal membrane oxygenation for treatment of cardiogenic shock: clinical experiences in 45 adult patients. J Thorac Cardiovasc Surg. 2008;135(2):382-8.
19.Jeger RV, Radovanovic D, Hunziker PR, Pfisterer ME, Stauffer JC, Erne P, et al. Ten-year trends in the incidence and treatment of cardiogenic shock. Ann Intern Med. 2008;149(9):618-26.
20.Sheu JJ, Tsai TH, Lee FY, Fang HY, Sun CK, Leu S, 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. Crit Care Med. 2010;38(9):1810-7.
21.Tsai FC, Wang YC, Huang YK, Tseng CN, Wu MY, Chang YS, et al. Extracorporeal life support to terminate refractory ventricular tachycardia. Crit Care Med. 2007;35(7):1673-6.
22.Ricciardi MJ, Moscucci M, Knight BP, Zivin A, Bartlett RH, Bates ER. Emergency extracorporeal membrane oxygenation (ECMO)-supported percutaneous coronary interventions in the fibrillating heart. Catheter Cardiovasc Interv. 1999;48(4):402-5.
23.Beckman MG, Hooper WC, Critchley SE, Ortel TL. Venous thromboembolism: a public health concern. Am J Prev Med. 2010;38(4 Suppl):S495-501.
24.Bailen MR, Cuadra JA, Aguayo De Hoyos E. Thrombolysis during cardiopulmonary resuscitation in fulminant pulmonary embolism: a review. Crit Care Med. 2001;29(11):2211-9.
25.Kurkciyan I, Meron G, Sterz F, Janata K, Domanovits H, Holzer M, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-35.
26.Kearon C, Akl EA, Comerota AJ, Prandoni P, Bounameaux H, Goldhaber SZ, et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):e419S-94S.
27.Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S829-61.
28.Bottiger BW, Bode C, Kern S, Gries A, Gust R, Glatzer R, et al. Efficacy and safety of thrombolytic therapy after initially unsuccessful cardiopulmonary resuscitation: a prospective clinical trial. Lancet. 2001;357(9268):1583-5.
29.Fatovich DM, Dobb GJ, Clugston RA. A pilot randomised trial of thrombolysis in cardiac arrest (The TICA trial). Resuscitation. 2004;61(3):309-13.
30.Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011;123(16):1788-830.
31.Maggio P, Hemmila M, Haft J, Bartlett R. Extracorporeal life support for massive pulmonary embolism. J Trauma. 2007;62(3):570-6.
32.Giraud R, Banfi C, Siegenthaler N, Bendjelid K. Massive pulmonary embolism leading to cardiac arrest: one pathology, two different ECMO modes to assist patients. J Clin Monit Comput. 2015.
33.Lebreton G, Bouabdallaoui N, Gauduchon L, Mnif MA, Roques F. Successful use of ECMO as a bridge to surgical embolectomy in Life-Threatening Pulmonary Embolism. Am J Emerg Med. 2015;33(9):1332 e3-4.
34.Abrams DC, Brodie D, Rosenzweig EB, Burkart KM, Agerstrand CL, Bacchetta MD. Upper-body extracorporeal membrane oxygenation as a strategy in decompensated pulmonary arterial hypertension. Pulm Circ. 2013;3(2):432-5.
35.Mohite PN, Sabashnikov A, Patil NP, Saez DG, Zych B, Popov AF, et al. Short-term ventricular assist device in post-cardiotomy cardiogenic shock: factors influencing survival. J Artif Organs. 2014;17(3):228-35.
36.Muehrcke DD, McCarthy PM, Stewart RW, Foster RC, Ogella DA, Borsh JA, et al. Extracorporeal membrane oxygenation for postcardiotomy cardiogenic shock. Ann Thorac Surg. 1996;61(2):684-91.
37.Rastan AJ, Dege A, Mohr M, Doll N, Falk V, Walther T, et al. Early and late outcomes of 517 consecutive adult patients treated with extracorporeal membrane oxygenation for refractory postcardiotomy cardiogenic shock. J Thorac Cardiovasc Surg. 2010;139(2):302-11, 11 e1.
38.Delgado DH, Rao V, Ross HJ, Verma S, Smedira NG. Mechanical circulatory assistance: state of art. Circulation. 2002;106(16):2046-50.
39.Khorsandi M, Shaikhrezai K, Prasad S, Pessotto R, Walker W, Berg G, et al. Advanced mechanical circulatory support for post-cardiotomy cardiogenic shock: a 20-year outcome analysis in a non-transplant unit. J Cardiothorac Surg. 2016;11(1):29.
40.Pokersnik JA, Buda T, Bashour CA, Gonzalez-Stawinski GV. Have changes in ECMO technology impacted outcomes in adult patients developing postcardiotomy cardiogenic shock? J Card Surg. 2012;27(2):246-52.
41.Santise G, Panarello G, Ruperto C, Turrisi M, Pilato G, Giunta A, et al. Extracorporeal membrane oxygenation for graft failure after heart transplantation: a multidisciplinary approach to maximize weaning rate. Int J Artif Organs. 2014;37(9):706-14.
42.Chung JC, Tsai PR, Chou NK, Chi NH, Wang SS, Ko WJ. Extracorporeal membrane oxygenation bridge to adult heart transplantation. Clin Transplant. 2010;24(3):375-80.
43.Patroniti N, Sangalli F, Avalli L. Post-cardiac arrest extracorporeal life support. Best Pract Res Clin Anaesthesiol. 2015;29(4):497-508.
44.Brechot N, Luyt CE, Schmidt M, Leprince P, Trouillet JL, Leger P, et al. Venoarterial extracorporeal membrane oxygenation support for refractory cardiovascular dysfunction during severe bacterial septic shock. Crit Care Med. 2013;41(7):1616-26.
45.Wallmuller C, Sterz F, Testori C, Schober A, Stratil P, Horburger D, et al. Emergency cardio-pulmonary bypass in cardiac arrest: seventeen years of experience. Resuscitation. 2013;84(3):326-30.
46.Xie A, Phan K, Tsai YC, Yan TD, Forrest P. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest: a meta-analysis. J Cardiothorac Vasc Anesth. 2015;29(3):637-45.
47.Chen YS, Lin JW, Yu HY, Ko WJ, Jerng JS, Chang WT, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet. 2008;372(9638):554-61.
48.Stub D, Bernard S, Pellegrino V, Smith K, Walker T, Sheldrake J, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94.
49.Maekawa K, Tanno K, Hase M, Mori K, Asai Y. Extracorporeal cardiopulmonary resuscitation for patients with out-of-hospital cardiac arrest of cardiac origin: a propensity-matched study and predictor analysis. Crit Care Med. 2013;41(5):1186-96.
50.Sakamoto T, Morimura N, Nagao K, Asai Y, Yokota H, Nara S, et al. Extracorporeal cardiopulmonary resuscitation versus conventional cardiopulmonary resuscitation in adults with out-of-hospital cardiac arrest: a prospective observational study. Resuscitation. 2014;85(6):762-8.
51.Shin TG, Choi JH, Jo IJ, Sim MS, Song HG, Jeong YK, et al. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: a comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011;39(1):1-7.
52.Le Guen M, Nicolas-Robin A, Carreira S, Raux M, Leprince P, Riou B, et al. Extracorporeal life support following out-of-hospital refractory cardiac arrest. Crit Care. 2011;15(1):R29.
53.Ortega-Deballon I, Hornby L, Shemie SD, Bhanji F, Guadagno E. Extracorporeal resuscitation for refractory out-of-hospital cardiac arrest in adults: a systematic review of international practices and outcomes. Resuscitation. 2016;101:12-20.
54.Pozzi M, Koffel C, Armoiry X, Pavlakovic I, Neidecker J, Prieur C, et al. Extracorporeal life support for refractory out-of-hospital cardiac arrest: should we still fight for? A single-centre, 5-year experience. Int J Cardiol. 2016;204:70-6.
55.Paden ML, Conrad SA, Rycus PT, Thiagarajan RR, Registry E. Extracorporeal Life Support Organization Registry Report 2012. ASAIO J. 2013;59(3):202-10.
56.Esper SA, Levy JH, Waters JH, Welsby IJ. Extracorporeal membrane oxygenation in the adult: a review of anticoagulation monitoring and transfusion. Anesth Analg. 2014;118(4):731-43.
57.Malfertheiner MV, Philipp A, Lubnow M, Zeman F, Enger TB, Bein T, et al. Hemostatic Changes During Extracorporeal Membrane Oxygenation: A Prospective Randomized Clinical Trial Comparing Three Different Extracorporeal Membrane Oxygenation Systems. Crit Care Med. 2015.
58.Combes A, Bacchetta M, Brodie D, Muller T, Pellegrino V. Extracorporeal membrane oxygenation for respiratory failure in adults. Curr Opin Crit Care. 2012;18(1):99-104.
59.Annich GM. Extracorporeal life support: the precarious balance of hemostasis. J Thromb Haemost. 2015;13 Suppl 1:S336-42.
60.Cheng R, Hachamovitch R, Kittleson M, Patel J, Arabia F, Moriguchi J, et al. Complications of extracorporeal membrane oxygenation for treatment of cardiogenic shock and cardiac arrest: a meta-analysis of 1,866 adult patients. Ann Thorac Surg. 2014;97(2):610-6.
61.Avalli L, Sangalli F, Migliari M, Maggioni E, Gallieri S, Segramora V, et al. Early vascular complications after percutaneous cannulation for extracorporeal membrane oxygenation for cardiac assist. Minerva Anestesiol. 2016;82(1):36-43.
62.Tanaka D, Hirose H, Cavarocchi N, Entwistle JW. The Impact of Vascular Complications on Survival of Patients on Venoarterial Extracorporeal Membrane Oxygenation. Ann Thorac Surg. 2016.
63.Lubnow M, Philipp A, Foltan M, Bull Enger T, Lunz D, Bein T, et al. Technical complications during veno-venous extracorporeal membrane oxygenation and their relevance predicting a system-exchange--retrospective analysis of 265 cases. PLoS One. 2014;9(12):e112316.
64.Murphy DA, Hockings LE, Andrews RK, Aubron C, Gardiner EE, Pellegrino VA, et al. Extracorporeal membrane oxygenation-hemostatic complications. Transfus Med Rev. 2015;29(2):90-101.
65.Zangrillo A, Landoni G, Biondi-Zoccai G, Greco M, Greco T, Frati G, et al. A meta-analysis of complications and mortality of extracorporeal membrane oxygenation. Crit Care Resusc. 2013;15(3):172-8.
66.Green TP, Kriesmer P, Steinhorn RH, Payne NR, Irmiter RJ, Meyer CL. Comparison of pressure-volume-flow relationships in centrifugal and roller pump extracorporeal membrane oxygenation systems for neonates. ASAIO Trans. 1991;37(4):572-6.
67.Lehle K, Philipp A, Zeman F, Lunz D, Lubnow M, Wendel HP, et al. Technical-Induced Hemolysis in Patients with Respiratory Failure Supported with Veno-Venous ECMO - Prevalence and Risk Factors. PLoS One. 2015;10(11):e0143527.
68.Leverett LB, Hellums JD, Alfrey CP, Lynch EC. Red blood cell damage by shear stress. Biophys J. 1972;12(3):257-73.
69.Shimono T, Makinouchi K, Nose Y. Total erythrocyte destruction time: the new index for the hemolytic performance of rotary blood pumps. Artif Organs. 1995;19(7):571-5.
70.Vercaemst L. Hemolysis in cardiac surgery patients undergoing cardiopulmonary bypass: a review in search of a treatment algorithm. J Extra Corpor Technol. 2008;40(4):257-67.
71.Wielogorski JW, Cross DE, Nwadike EV. The effects of subatmospheric pressure on the haemolysis of blood. J Biomech. 1975;8(5):321-5.
72.Williams DC, Turi JL, Hornik CP, Bonadonna DK, Williford WL, Walczak RJ, et al. Circuit oxygenator contributes to extracorporeal membrane oxygenation-induced hemolysis. ASAIO J. 2015;61(2):190-5.
73.Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005;293(13):1653-62.
74.Skogby M, Mellgren K, Adrian K, Friberg LG, Chevalier JY, Mellgren G. Induced cell trauma during in vitro perfusion: a comparison between two different perfusion systems. Artif Organs. 1998;22(12):1045-51.
75.Cappellini MD. Coagulation in the pathophysiology of hemolytic anemias. Hematology Am Soc Hematol Educ Program. 2007:74-8.
76.Jeney V, Balla J, Yachie A, Varga Z, Vercellotti GM, Eaton JW, et al. Pro-oxidant and cytotoxic effects of circulating heme. Blood. 2002;100(3):879-87.
77.Schaer DJ, Buehler PW, Alayash AI, Belcher JD, Vercellotti GM. Hemolysis and free hemoglobin revisited: exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins. Blood. 2013;121(8):1276-84.
78.Betrus C, Remenapp R, Charpie J, Kudelka T, Brophy P, Smoyer WE, et al. Enhanced hemolysis in pediatric patients requiring extracorporeal membrane oxygenation and continuous renal replacement therapy. Ann Thorac Cardiovasc Surg. 2007;13(6):378-83.
79.Gbadegesin R, Zhao S, Charpie J, Brophy PD, Smoyer WE, Lin JJ. Significance of hemolysis on extracorporeal life support after cardiac surgery in children. Pediatr Nephrol. 2009;24(3):589-95.
80.Vermeulen Windsant IC, de Wit NC, Sertorio JT, van Bijnen AA, Ganushchak YM, Heijmans JH, et al. Hemolysis during cardiac surgery is associated with increased intravascular nitric oxide consumption and perioperative kidney and intestinal tissue damage. Front Physiol. 2014;5:340.
81.Mateen FJ, Muralidharan R, Shinohara RT, Parisi JE, Schears GJ, Wijdicks EF. Neurological injury in adults treated with extracorporeal membrane oxygenation. Arch Neurol. 2011;68(12):1543-9.
82.Graziani LJ, Gringlas M, Baumgart S. Cerebrovascular complications and neurodevelopmental sequelae of neonatal ECMO. Clin Perinatol. 1997;24(3):655-75.
83.Risnes I, Wagner K, Nome T, Sundet K, Jensen J, Hynas IA, et al. Cerebral outcome in adult patients treated with extracorporeal membrane oxygenation. Ann Thorac Surg. 2006;81(4):1401-6.
85.Bizzarro MJ, Conrad SA, Kaufman DA, Rycus P, Extracorporeal Life Support Organization Task Force on Infections EMO. Infections acquired during extracorporeal membrane oxygenation in neonates, children, and adults. Pediatr Crit Care Med. 2011;12(3):277-81.
86.O'Horo JC, Cawcutt KA, De Moraes AG, Sampathkumar P, Schears GJ. The Evidence Base for Prophylactic Antibiotics in Patients Receiving Extracorporeal Membrane Oxygenation. ASAIO J. 2016;62(1):6-10.
87.Gardner AH, Prodhan P, Stovall SH, Gossett JM, Stern JE, Wilson CD, et al. Fungal infections and antifungal prophylaxis in pediatric cardiac extracorporeal life support. J Thorac Cardiovasc Surg. 2012;143(3):689-95.
88.Pellegrino V, Hockings LE, Davies A. Veno-arterial extracorporeal membrane oxygenation for adult cardiovascular failure. Curr Opin Crit Care. 2014;20(5):484-92.
89.Aiyagari RM, Rocchini AP, Remenapp RT, Graziano JN. Decompression of the left atrium during extracorporeal membrane oxygenation using a transseptal cannula incorporated into the circuit. Crit Care Med. 2006;34(10):2603-6.
90.Guirgis M, Kumar K, Menkis AH, Freed DH. Minimally invasive left-heart decompression during venoarterial extracorporeal membrane oxygenation: an alternative to a percutaneous approach. Interact Cardiovasc Thorac Surg. 2010;10(5):672-4.
91.Vlasselaers D, Desmet M, Desmet L, Meyns B, Dens J. Ventricular unloading with a miniature axial flow pump in combination with extracorporeal membrane oxygenation. Intensive Care Med. 2006;32(2):329-33.
92.Weymann A, Schmack B, Sabashnikov A, Bowles CT, Raake P, Arif R, et al. Central extracorporeal life support with left ventricular decompression for the treatment of refractory cardiogenic shock and lung failure. J Cardiothorac Surg. 2014;9:60.
93.Chung M, Shiloh AL, Carlese A. Monitoring of the adult patient on venoarterial extracorporeal membrane oxygenation. Scientific World Journal. 2014;2014:393258.
94.Aissaoui N, Luyt CE, Leprince P, Trouillet JL, Leger P, Pavie A, et al. Predictors of successful extracorporeal membrane oxygenation (ECMO) weaning after assistance for refractory cardiogenic shock. Intensive Care Med. 2011;37(11):1738-45.
95.Schmidt M, Burrell A, Roberts L, Bailey M, Sheldrake J, Rycus PT, et al. Predicting survival after ECMO for refractory cardiogenic shock: the survival after veno-arterial-ECMO (SAVE)-score. Eur Heart J. 2015;36(33):2246-56.
96.Muller G, Flecher E, Lebreton G, Luyt CE, Trouillet JL, Brechot N, et al. The ENCOURAGE mortality risk score and analysis of long-term outcomes after VA-ECMO for acute myocardial infarction with cardiogenic shock. Intensive Care Med. 2016;42(3):370-8.
97.Riou B, Adnet F, Baud F, Cariou A, Carli P, Combes A, et al. Recommandations sur les indications de l’assistance circulatoire dans le traitement des arrêts cardiaques réfractaires. 2008;Annales Françaises d’Anesthésie et de Réanimation 28 (2009) 182–186.
98.Abrams DC, Prager K, Blinderman CD, Burkart KM, Brodie D. Ethical dilemmas encountered with the use of extracorporeal membrane oxygenation in adults. Chest. 2014;145(4):876-82.
Written By
Marie-Eve Brunner, Carlo Banfi and Raphaël Giraud
Submitted: 08 November 2015Reviewed: 12 April 2016Published: 14 September 2016
Open access peer-reviewed chapter
