Version May 2024
INTRODUCTION — Extracorporeal membrane oxygenation (ECMO) is an advanced form of life support that is mostly used in patients with severe respiratory or cardiac failure when conventional treatment fails. Technical advances in ECMO, coupled with accumulating data that describe successful outcomes [1,2], have resulted in increased ECMO use.
This topic will provide an overview of implementation and management of venoarterial (V-A) ECMO in patients with acute cardiac failure. Other ECMO-relevant topics are found elsewhere:
●(See "Extracorporeal life support in adults in the intensive care unit: Overview".)
●(See "COVID-19: Extracorporeal membrane oxygenation (ECMO)".)
●(See "Extracorporeal life support in adults: Extracorporeal carbon dioxide removal (ECCO2R)".)
●(See "Extracorporeal life support in adults in the intensive care unit: Vascular complications".)
TERMINOLOGY — V-A ECMO is a form of extracorporeal life support. V-A ECMO is used for temporary support of patients with acute or acute on chronic cardiac or circulatory failure. The configuration of the circuit in V-A ECMO is comprised of a drainage cannula that removes blood from the right atrium or a large central vein. This blood is oxygenated extracorporeally and reinfused into a major artery. Additional terms are described in the table (table 1) and discussed in detail separately. (See "Extracorporeal life support in adults in the intensive care unit: Overview", section on 'Terminology'.)
CLINICAL APPLICATIONS — Our approach to selecting patients for V-A ECMO is discussed in this section. Guidelines that describe the indications and practice of extracorporeal life support/ECMO are published by the Extracorporeal Life Support Organization (ELSO) [3,4].
We evaluate patients with acute cardiac failure who have not responded to conventional therapy as potential candidates for V-A ECMO. The primary goal of V-A ECMO under these circumstances is mechanical circulatory support, along with oxygenation and carbon dioxide (CO2) removal as needed. The indications for V-A ECMO encompass a variety of etiologies associated with acute cardiac failure including refractory cardiogenic shock, extracorporeal support during cardiopulmonary resuscitation (ECPR), and acute decompensated pulmonary vascular disease. (See 'Refractory cardiogenic shock' below and 'Sudden cardiac arrest (extracorporeal cardiopulmonary resuscitation)' below and 'Acute decompensated pulmonary vascular disease' below and 'Others' below.)
Patients who primarily need respiratory support or patients who only need CO2 removal are typically not suitable candidates for V-A ECMO but may be considered for venovenous ECMO and extracorporeal CO2 removal, respectively. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)" and "Extracorporeal life support in adults: Extracorporeal carbon dioxide removal (ECCO2R)".)
Refractory cardiogenic shock — V-A ECMO has been used successfully in patients with refractory cardiogenic shock (typically Interagency Registry for Mechanically Assisted Circulatory Support [INTERMACS] profile 1 or Society for Cardiovascular Angiography and Interventions [SCAI] stages D and E). Successful ECMO use has been described in patients with cardiogenic shock due to a variety of conditions including the following [5-25] (see "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction", section on 'Prognosis'):
●Acute myocardial infarction (see "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Right ventricular myocardial infarction")
●Acute decompensated heart failure from underlying dilated, restrictive, or congenital cardiomyopathy (see "Restrictive cardiomyopathies", section on 'Treatment')
●Post-cardiac transplant allograft failure (see "Heart transplantation in adults: Graft dysfunction", section on 'Early graft dysfunction')
●Refractory ventricular arrhythmia (see "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy", section on 'Heart failure therapy')
●Cardiotoxic drug intoxication (table 2)
●Fulminant myocarditis (see "Treatment and prognosis of myocarditis in adults", section on 'Heart failure therapy')
●Peripartum cardiomyopathy (see "Peripartum cardiomyopathy: Treatment and prognosis", section on 'Mechanical circulatory support')
●Sepsis- or stress-induced cardiomyopathy (see "Causes and pathophysiology of high-output heart failure", section on 'Sepsis')
●Cardiogenic shock following resuscitated cardiac arrest (see "Intensive care unit management of the intubated post-cardiac arrest adult patient", section on 'Airway, ventilation, and oxygen targets')
●Postcardiotomy shock (see "Postoperative complications among patients undergoing cardiac surgery", section on 'Poor inotropy')
Data to support V-A ECMO in patients with cardiogenic shock that is refractory to conventional management is conflicting.
●Many cohort series and small randomized trials reported benefit [25-31] with survival rates at hospital discharge ranging from 18 to 71 percent. In general, the highest rates of survival are reported in cardiogenic shock due to sepsis-induced cardiomyopathy, fulminant myocarditis, refractory ventricular arrhythmias, and post-cardiac transplant primary graft dysfunction [24,26,27]. As an example, in a multicenter cohort study with propensity score-weighted analysis, those who received V-A ECMO for sepsis-induced cardiomyopathy had significantly higher survival than those managed without ECMO (51 versus 14 percent, adjusted relative risk for mortality 0.57, 95% CI 0.35-0.93) [24].
●In contrast, data on patients with acute myocardial infarction-related cardiogenic shock suggest no meaningful benefit from V-A ECMO [31-35]. Nonetheless, further trials are warranted to improve our understanding as to whether there is a select group of patients in this population who may benefit from V-A ECMO as a life-saving therapy.
•In a randomized trial (ECLS-SHOCK) of 420 patients with acute myocardial infarction complicated by cardiogenic shock for whom early revascularization was planned, early institution of V-A ECMO was associated with a 30-day mortality that was similar to patients who were treated with medical therapy alone (48 versus 49 percent) [32]. Patients treated with V-A ECMO were ventilated for longer (9 versus 7 days) and had higher rates of moderate or severe bleeding (23 versus 10 percent) and peripheral ischemic events (11 versus 4 percent). Additional outcomes were also no different between the two groups (eg, renal replacement therapy, repeat revascularization, myocardial reinfarction, rehospitalization for congestive heart failure, or poor neurologic outcome). A prespecified analysis did not reveal any specific subgroup that benefited more from upfront V-A ECMO, although shock severity was not included in this analysis. Several issues may have biased the results including lack of blinding, crossover between the groups (13 percent in medical treatment group received ECMO; 8 percent in the ECMO group did not receive ECMO), and the potential for institutional-related differences in ECMO care. Furthermore, active left ventricular unloading was quite low in the ECMO group at 5.8 percent compared with 31.6 percent in the control group.
•A meta-analysis of four randomized trials, which included the above trial, reported similar results [33]. Use of V-A ECMO did not reduce the 30-day mortality (odds ratio [OR] 0.93, 95% CI 0.66-1.29) and complication rates were higher for major bleeding (OR 2.44, 95% CI 1.55-3.84) and peripheral vascular ischemia (OR 3.53, 95% CI 1.70-7.34). Prespecified subgroup analyses similarly demonstrated no benefit from V-A ECMO. Because the analysis was heavily weighted by the ECLS-SHOCK trial [32], crossover was a source of bias in favor of the control group.
Predictors of survival are poorly studied [25,26,28-30]. A survival prediction model for those receiving V-A ECMO, derived from the Extracorporeal Life Support Organization (ELSO) Registry, identified the following as risk factors associated with increased mortality [26]:
●Postcardiotomy cardiogenic shock
●Chronic renal failure
●Longer duration of ventilation prior to ECMO initiation
●Pre-ECMO organ failures
●Pre-ECMO cardiac arrest
●Congenital heart disease
●Lower pulse pressure
●Lower serum bicarbonate
Potentially protective factors from the same analysis included the following [26]:
●Younger age
●Lower body weight
●Acute myocarditis
●Heart transplant
●Refractory ventricular tachycardia (VT) or fibrillation (VF)
●Higher diastolic blood pressure
●Lower peak inspiratory pressure
Sudden cardiac arrest (extracorporeal cardiopulmonary resuscitation) — V-A ECMO is increasingly being used in conjunction with cardiopulmonary resuscitation during cardiac arrest, termed extracorporeal cardiopulmonary resuscitation (ECPR).
Initiation of V-A ECMO in this setting provides robust circulatory support that can restore end-organ perfusion during cardiac arrest to allow for institution of effective treatment of the underlying etiology that is leading to cardiac arrest (eg, coronary artery stent, bypass grafting). In addition, it can be continued if persistent cardiogenic shock occurs following return of spontaneous circulation.
Evidence suggests that ECPR may be associated with improved survival with good neurologic outcome in select patients (eg, age <60 years, shockable rhythm, witnessed arrest with bystander CPR, in-hospital arrest) [2,36-45]. Estimates of survival vary, but most studies have reported that approximately one-third of patients survive to hospital discharge (range 20 to 43 percent) [2,38-42]. As an example, in a meta-analysis of 11 studies totaling nearly 10,000 patients who underwent CPR, ECPR was associated with a significant reduction in overall in-hospital mortality (OR 0.67, 95% CI 0.51-0.87) and increased rate of favorable neurologic outcome, both in the short-term (OR 1.65, 95% CI 1.02-2.68) and long-term (OR 2.04, 95% CI 1.41-2.94) [45]. ECPR was also associated with increased survival at three months (OR 3.98, 95% CI 1.12-14.16), six months (OR 1.87, 95% CI 1.36-2.57), and one year (OR 1.72, 95% CI 1.52-1.95). Low center volume was associated with increased risk of death, and the potential benefit of ECPR was confined to patients with in-hospital cardiac arrest (see in-hospital cardiac arrest bullet below).
Preliminary data also suggest that outcomes may be better for in-hospital compared with out-of-hospital cardiac arrest:
●Out-of-hospital cardiac arrest – There are conflicting data describing outcomes in patients with out-of-hospital cardiac arrest:
In one phase 2, open-label randomized trial of 30 patients with out-of-hospital cardiac arrest due to refractory VF, survival to hospital discharge was higher in those who received ECPR compared with those who received standard advanced cardiac life support (ACLS) (43 versus 7 percent) [2].
However, most trials have not found such a benefit from ECPR [43,45-47].
•In a randomized trial of 256 patients with out-of-hospital cardiac arrest of presumed cardiac cause, in-hospital ECPR and rapid invasive evaluation resulted in a nonstatistically significant improvement in six-month survival with functional recovery compared with standard ACLS care (31.5 versus 22.0 percent) [43]. Notably, a subgroup of ECPR patients with CPR duration ≥45 minutes had significantly higher rates of overall six-month survival and survival with neurologic recovery out to 30 days, supporting the concept that ECPR may be successful despite prolonged duration of conventional CPR. In a secondary analysis of patients in this trial who did not achieve prehospital return of spontaneous circulation, ECPR was associated with a significantly lower risk of death at 180 days compared with prolonged conventional ACLS alone (23.9 versus 1.2 percent) [47].
•In another multicenter randomized trial, ECPR was compared with conventional CPR in 134 adults with witnessed out-of-hospital cardiac arrest, an initial shockable rhythm, and failure to regain spontaneous circulation after 15 minutes [46]. At 30 days, there was no significant difference between groups in survival with good neurologic outcome (ECPR group 14 patients [20 percent] versus conventional CPR 10 patients [16 percent]; OR 1.4, 95% CI 0.5-3.5). Adverse events were similar among the groups. In this study, a longer time to cannulation and differences in practice among the participating centers may help explain the discrepancies when compared with studies that demonstrate success with ECPR.
•In the meta-analysis of 11 studies that included the above study [46], a subgroup analysis of patients who had out-of-hospital cardiac arrest reported similar in-hospital mortality when ECPR was compared with conventional CPR (OR 0.76, 95% CI 0.54-1.07) [45].
●In-hospital cardiac arrest – In highly selected patients with in-hospital cardiac arrest (eg, younger age, fewer comorbidities, shockable rhythm, shorter duration of CPR until ECMO initiation), nonrandomized propensity analyses and subsequent meta-analysis have suggested a possible benefit with ECPR [45,48-50]. As an example, in a meta-analysis of 11 studies, a subgroup analysis of patients who had in-hospital cardiac arrest suggested that in-hospital mortality was lower in patients receiving ECPR than in those receiving conventional CPR (OR 0.42, 95% CI 0.25-0.7) [45].
Survival for those who undergo ECPR may decrease with older age (eg, >40 years) [51,52].
ACLS protocols for cardiac arrest are discussed separately. (See "Advanced cardiac life support (ACLS) in adults".)
Acute decompensated pulmonary vascular disease — V-A ECMO has been used successfully in patients with acute decompensated pulmonary vascular disease who are unresponsive to conventional therapy.
This includes acute decompensation in patients with underlying pulmonary hypertension (PH), preoperative stabilization for pulmonary artery endarterectomy in patients with chronic thromboembolic PH, and massive or hemodynamically unstable pulmonary embolism (PE). Conventional therapies for these conditions are described separately. (See "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)", section on 'Management of acute pulmonary hypertensive crisis' and "Chronic thromboembolic pulmonary hypertension: Initial management and evaluation for pulmonary artery thromboendarterectomy", section on 'Operable candidates' and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults", section on 'Hemodynamically unstable'.)
Data to support V-A ECMO for these indications are largely derived from case series [53-61]. Survival to hospital discharge ranged from 30 to 100 percent and varied with the etiology. The highest rates of survival tend to occur in those with hemodynamically significant PE compared with other etiologies [57-59,61]. Increasing age, lower pH, lower diastolic blood pressure, and need for ECPR may be associated with in-hospital mortality [61].
Others — Successful use of V-A ECMO has also been reported in cases of significant trauma, anaphylactic shock, poisoning (table 2), drowning, hypothermia, and pulmonary hemorrhage [62-65].
V-A ECMO has also been used after both cardiac death and brain death to optimize the quality of donor organs for transplantation [66,67]. (See "Heart transplantation in adults: Donor selection and organ allocation", section on 'Role of mechanical circulatory support'.)
INITIAL CLINICAL ASSESSMENT
General assessment — When evaluating patients who have a potential indication for V-A ECMO, as members of an ECMO team, we assess candidacy clinically. The focus of clinical evaluation involves the following:
●We use clinical history and examination to evaluate the etiology of cardiac failure (eg, myocardial infarction, cardiopulmonary arrest, acute PH crisis, pulmonary embolism).
●We assess the relative contribution of respiratory failure to the patient's presentation, if any.
●We inquire about and obtain records that may provide clues to the severity of any underlying illness or comorbidity (eg, pulmonary artery catheter, coronary angiography, and echocardiography records).
●Using this information, we assess the potential for disease reversibility or for targeted intervention (eg, percutaneous coronary intervention, ventricular assist device, cardiac transplantation, pulmonary vasodilators [in the case of PH crisis]), and the prognosis from any underlying comorbidity or complications (eg, cerebrovascular disease, aortic vascular disease, the presence of multiorgan failure).
●We also ensure that ECMO is aligned with the patient goals of care by discussing it with the patient (if feasible) and their surrogate/caregivers. We also explain the alternatives, including conventional medical management, alternative mechanical circulatory support strategies, or palliation. (See "Communication in the ICU: Holding a meeting with families and caregivers".)
Once the ECMO team makes a decision to proceed, a plan is made for cannula insertion, provided there is no contraindication. (See "Extracorporeal life support in adults in the intensive care unit: Overview", section on 'Staffing (ECMO teams)' and 'Contraindications (absolute and relative)' below.)
Contraindications (absolute and relative) — Once indicated, we next assess potential contraindications (listed on the table (table 3)) or challenges associated with administration of V-A ECMO (eg, peripheral or aortic vascular disease or stents, vascular access points, bleeding diathesis, need for ambulation as a bridge to transplant candidacy).
Contraindications that are more specific for patients being evaluated for V-A ECMO include severe aortic insufficiency and aortic dissection (absolute contraindications) and arterial conditions that limit vascular access, such as severe peripheral artery disease (relative contraindication).
Although retrospective data have not demonstrated an association between increased body mass index (BMI) and worse outcomes in V-A ECMO, higher BMI may present challenges in cannulation, pose additional risks during ECMO support, and be a barrier to heart transplantation for those unable to be bridged to either recovery or a destination device [68].
Timing and transfer — Timing and transfer considerations are similar to venovenous (V-V) ECMO.
Although data are sparse, outcomes are generally better when V-A ECMO is instituted relatively early during the course of a patient's illness (eg, following failure to respond to conventional inotropic support, with or without additional mechanical support, such as an intra-aortic balloon pump, but before they have suffered potentially irreversible end-organ damage). However, there is no clear cutoff after which ECMO becomes less beneficial.
This was best illustrated in the ECMO-CS trial [31]. ECMO-CS was a small randomized clinical trial that assessed outcomes of 117 patients with rapidly deteriorating or severe cardiogenic shock (Society for Cardiovascular Angiography and Interventions [SCAI] D-E shock) at four centers in the Czech Republic that were randomized to receive either immediate V-A ECMO or initial conservative therapy. There were no differences in the composite primary endpoint of death from any cause, resuscitated circulatory arrest, and implementation of another mechanical circulatory support device at 30 days between the two groups (63.8 [immediate ECMO] versus 71.2 percent [no immediate ECMO], hazard ratio 0.72, 95% CI 0.46-1.12). All-cause mortality was also comparable between the two groups (50 [immediate ECMO group] versus 47.5 percent [early conservative therapy group]). Notably, 39 percent of the initial conservative therapy arm ended up receiving V-A ECMO for further deterioration. This study highlights the importance of early involvement of a multidisciplinary shock team to help guide decision making in these patients.
Given the hemodynamic instability associated with cardiogenic shock, initiation of ECMO at the referring hospital prior to transfer is expected to be more common with V-A ECMO for cardiogenic shock than it is with V-V ECMO for respiratory failure. Further details are provided separately. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Timing and transfer issues'.)
CATHETER INSERTION
Venoarterial configurations and sites — There are several configurations for V-A ECMO. Choosing among them is at the discretion of the clinical team and institutional practice. The presence of hardware (eg, stent) or vascular pathology (eg, severe peripheral vascular disease) may dictate the choice of sites(s) used in a given patient.
Common configurations — Most commonly, we use a configuration with femoral venous drainage and femoral arterial reinfusion cannulae (femoral V-A ECMO (figure 1)). This is due to the percutaneous accessibility of these vessels at the bedside and the fact that cannulation is often needed under urgent or emergent circumstances [69].
Femoral artery cannulation may not be suitable for some patients. As examples:
●For patients with femoral arterial reconstruction, cannulation of the femoral artery may not be feasible, and in patients with severe occlusive peripheral artery disease or relatively small arteries, femoral artery cannulation increases risk of lower extremity ischemia. In such circumstances, upper body approaches (including central cannulation), insertion of a distal perfusion cannula, or use of an end-to-side graft are options, provided expertise for these techniques are available. (See 'Configurations that avoid or address dual circulation from competitive flow' below and 'Other complications' below.)
●For patients who undergo postcardiotomy ECMO, the cannulae used for cardiopulmonary bypass may be transferred from the cardiopulmonary bypass machine to the ECMO circuit; these configurations typically have a drainage cannula in the right atrium and reinfuse oxygenated blood into the ascending aorta. Reconfiguration to a more traditional femoral V-A ECMO approach may also be appropriate.
●In patients with advanced pulmonary hypertension (PH) who require tight ventricular support, central V-A configurations (eg, subclavian, innominate, aortic, and left atrial (LA) reinfusion configurations, with or without direct right atrial drainage) may be preferred over femoral arterial cannulation, especially when there is preserved left ventricular (LV) function. (See 'Configurations that avoid or address dual circulation from competitive flow' below.)
An alternative, more invasive approach is a pumpless central arteriovenous (A-V) configuration, in which blood passes from the pulmonary artery, through a membrane lung, and returns to the LA. This configuration, which relies upon the LV to propagate the oxygenated blood into the systemic circulation, avoids any increased afterload on the LV from retrograde reinfused blood flow that accompanies most V-A configurations [70].
For those patients with PH who have a pre-existing interatrial septal defect, a single-site, dual-lumen venovenous (V-V) configuration may be considered, with venous blood drained from the superior vena cava, inferior vena cava, or right atrium and the reinfusion port directed across the interatrial defect, creating an oxygenated right-to-left shunt [54,55,71].
Occasionally, for patients who need isolated right ventricular (RV) unloading, a venous pulmonary artery configuration may be considered (eg, RV support after LV assist device implantation). Blood is removed from the right atrium and returned to the pulmonary artery, thereby bypassing the RV (figure 2).
Configurations that avoid or address dual circulation from competitive flow — Dual circulation refers to a phenomenon that can occur in V-A ECMO (particularly in the setting of femoral arterial reinfusion) in which there is competitive flow within the aorta between the anterograde native cardiac output and retrograde ECMO reinfusion flow; the mixing point between the two flows is dynamic and based on the relative strengths of the native and ECMO pumps at any given moment in time. When the mixing point is in the descending aorta and there is impaired native gas exchange, this results in poorer oxygenation in the upper body compared with the lower body (ie, differential oxygenation). (See 'Dual circulation' below.)
Dual circulation can be anticipated or can be encountered as a complication of V-A ECMO. It is most often encountered in those with pulmonary edema and managed with diuresis or venting of the LV (see 'Dual circulation' below). However, if differential oxygenation is sufficiently severe despite these measures or is the result of a noncardiogenic etiology, such as pneumonia or acute respiratory distress syndrome, it may be mitigated with the use of hybrid ECMO configurations or upper body approaches, including central configurations. As examples:
●Hybrid configurations provide both cardiac and respiratory support while mitigating proximal aortic arch hypoxemia. It may be achieved by using a Y-connector to split the reinfused blood flow between the arterial and venous systems. For example, oxygenated blood can simultaneously be supplied to both the femoral artery for hemodynamic support and the right atrium for upper body gas exchange support (referred to as a V-AV configuration (figure 3)) [72].
●Upper body V-A approaches include internal jugular or right atrial drainage with axillary, subclavian, innominate, LA, or aortic reinfusion [73-75].
•Axillary, subclavian, and innominate reinfusion, which are typically achieved with an end-to-side graft, have relatively less differential oxygenation due to the origin of the reinfusion blood flow being close to the aortic arch. However, the most proximal take-offs from the aorta remain at risk (eg, coronary and carotid arteries).
•In aortic reinfusion (which typically involves direct cannulation), there is minimal if any differential oxygenation due to anterograde flow from the aortic root.
•In LA reinfusion (with the cannula typically grafted to a pulmonary vein), there is no differential oxygenation, though such an approach relies upon adequate native LV output to propagate the reinfused oxygenated blood into the systemic circulation.
●Central configurations (ie, aortic and LA reinfusion configurations, with or without direct right atrial drainage), while having the advantage of a more physiologic direction of blood flow, are more invasive (often requiring a sternotomy), which limits their utility in emergent situations unless the patient is undergoing ECMO initiation intraoperatively during cardiac surgery.
Size and insertion technique — In V-A ECMO, we use drainage cannulae that are 23 to 25 French in size, potentially larger if centrally cannulated or if a hybrid configuration is anticipated. We select arterial reinfusion cannulae based on the size of the artery being cannulated for reinfusion and the anticipated amount of support required, typically 15 to 19 French for femoral arterial reinfusion, although a smaller cannula (eg, 14 French) may be used for patients whose arteries cannot safely accommodate a 15 French cannula. If the artery is too small to accommodate a smaller reinfusion cannula, the cannula may be attached to the artery via an end-to-side graft [73,76]. Similar to V-V ECMO and drainage-limited blood flow rates affecting the degree of oxygenation support, the sizes of the cannulae in V-A ECMO can affect the degree of cardiac support provided, with smaller cannulae resulting in lower maximum blood flow rates, potentially leading to less support.
We preferentially use a percutaneous approach via the Seldinger technique under image-guidance as the default approach for cannulation, the details of which are provided separately (see "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Insertion technique'). However, a cutdown approach may be required under certain circumstances.
Other catheters — Arterial lines and pulmonary artery catheters (PACs) are often placed in ECMO patients for monitoring and management of hemodynamics and gas exchange.
●Arterial lines – For patients supported with a configuration involving femoral arterial reinfusion, an arterial line should be placed in the right upper extremity for purposes of arterial blood gas monitoring. Measuring gas exchange from this location is the most reliable method of identifying differential oxygenation or differential carbon dioxide tension that may result from dual circulation (see 'Measuring oxygenation' below and 'Dual circulation' below). When the ECMO circuit consists of arterial reinfusion through the right axillary, right subclavian, or innominate artery, the arterial line should be placed in the left upper extremity with the same rationale. Depending on the urgency of ECMO cannulation, the arterial line may be placed before or immediately after cannulation. (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation".)
●PACs – PACs are often already in place in patients with cardiogenic shock prior to ECMO cannulation. For patients without a PAC in place and who are undergoing cannulation in the cardiac catheterization lab, we will typically place a PAC at the time of cannulation. For those without a PAC and in whom cannulation is performed elsewhere, we consider PAC placement on a case-by-case basis. (See "Pulmonary artery catheters: Insertion technique in adults".)
INITIAL SETTINGS AND TITRATION — Following cannulation, the patient is connected to the ECMO circuit (typically the pump, the membrane lung, the monitor) and oxygen is infused into the membrane lung.
There are no universally agreed upon initial settings for V-A ECMO. Typical settings are dictated by the degree of support that may be needed. As an estimate, we typically use the following, achieved incrementally over the first few minutes after initiation:
●Pump speed to achieve an extracorporeal blood flow of 3 to 4 L/minute (an approach we consider to be 'partial flow' relative to total cardiac output) [77]
●Sweep gas flow to achieve a typical range of 1 to 10 L/minute, with initial settings usually at the lower end of that range
●Fraction of delivered oxygen of 1.0 (typically not titrated during V-A ECMO)
Immediately following initiation, we perform the following:
●We increase blood flow rate until we achieve adequate end-organ perfusion or support (eg, decreasing blood lactate level, decreasing creatinine with an increased urine output and a decreased need for vasopressors and inotropic support) and an appropriate oxygen saturation (taking into consideration the effect of dual circulation and differential oxygenation). The amount of blood flow to achieve these goals may continue to be 'partial flow' or may require 'full flow' (ie, in the range of calculated cardiac output) in some instances.
●In general, we titrate sweep gas flow with a target of near-normal pH to the region of the body supplied by ECMO blood flow, provided there is not a substantial concomitant metabolic acidosis (in order to avoid reinfusing blood into the systemic circulation with excessively low partial pressure of arterial carbon dioxide). Importantly, because blood flow in V-A ECMO bypasses the lungs, sweep gas flow should never be titrated below 0.5 L/minute even in the presence of ongoing regional alkalemia since cessation of sweep gas flow (which includes oxygen) will result in shunt physiology and worsen oxygenation in the region of the reinfused blood.
If an unacceptable degree of alkalemia (eg, pH >7.5) persists in the region of the body supplied by ECMO blood flow despite being at minimal sweep gas flow, the following approaches may be considered (depending on the underlying etiology of alkalemia):
•Treat the cause of respiratory alkalosis (if present) and/or reduce the patient's alveolar ventilation (particularly in the setting of invasive mechanical ventilation where ventilator settings are contributing to upper body respiratory alkalosis)
•Correct metabolic alkalosis as tolerated (eg, with carbonic anhydrase inhibitors)
•Add carbon dioxide to the sweep gas composition (uncommonly used)
It is important to be aware of the potential for differential carbon dioxide tension because of dual circulation, in which increases or decreases in sweep gas flow rates will only modify carbon dioxide tension within the ECMO circulation and not within the native circulation, with implications for metabolic compensation. In peripheral V-A ECMO with a mixing point above the renal arteries, when the kidneys are perfused by ECMO blood flow with too low a sweep gas flow rate (resulting in a regional respiratory acidosis), the result will be a compensatory metabolic alkalosis by the kidneys that will lead to upper body alkalemia. To correct the resultant upper body metabolic alkalosis, one must increase (not decrease) the sweep gas flow rate to generate the desired renal response [78].
Within an hour of cannulation, we generally obtain routine laboratories, systemic arterial blood gas (ABG; eg, radial ABG, preferably from the right upper extremity when femoral V-A ECMO is used), coagulation studies, and pre- and post-membrane lung blood gases.
Daily assessment and circuit monitoring are discussed separately. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Daily assessment and circuit monitoring'.)
SUPPORTIVE THERAPIES
Concomitant respiratory failure — Many patients receiving V-A ECMO receive invasive mechanical ventilation in the setting of severe hemodynamic instability or concomitant respiratory failure. Respiratory failure may be due to cardiogenic pulmonary edema or other etiologies, such as aspiration, infectious pneumonia, or acute respiratory distress syndrome.
●For patients receiving V-A ECMO who require invasive mechanical ventilation, despite the lack of an agreed-upon approach, we use a lung-protective strategy that minimizes ventilator-induced lung injury, using the same principles as for venovenous (V-V) ECMO. We treat all potential reversible etiologies and have a low threshold to add a venous reinfusion limb for severe hypoxemia or hypercapnia (ie, venoarteriovenous ECMO (figure 3)). (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Invasive mechanical ventilation' and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Management of refractory hypoxemia during ECMO'.)
●Unlike patients who require V-V ECMO for acute respiratory failure, there is a greater likelihood of avoiding or removing invasive mechanical ventilation in patients receiving V-A ECMO for cardiac failure (eg, patients with isolated cardiogenic shock with preserved gas exchange and ability to protect their airway, patients with acute pulmonary hypertension [PH] crisis as a bridge to transplant). We advocate for prompt endotracheal extubation whenever possible. Weaning mechanical ventilation should follow the standard approach in that institution. (See "Weaning from mechanical ventilation: Readiness testing" and "Initial weaning strategy in mechanically ventilated adults" and "Extubation management in the adult intensive care unit".)
Anticoagulation — In patients receiving V-A ECMO, the approach to anticoagulation is generally similar to that in V-V ECMO, the details of which are provided separately. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Anticoagulation'.)
However, in the absence of bleeding, we typically target an activated partial thromboplastin time (aPTT) that is approximately twice the control (ie, a target higher than what we typically use in V-V ECMO), with further tailoring of anticoagulation goals based on the clinical scenario. The rationale for this higher target is that the risks of arterial embolization, left ventricle (LV) thrombus formation, and circuit thrombosis are greater than that in V-V ECMO due to arterial cannulation, turbulent flow with retrograde arterial reinfusion, and lower blood flow rates.
Other routine measures — Other supportive strategies are mostly discussed in the linked topics below:
●Fluid management – Fluid management can be challenging in patients receiving V-A ECMO and varies with the indication. As examples:
•Cardiogenic shock with LV failure – In our experience, an initial positive fluid balance may be required to counteract the early systemic inflammatory response and capillary leak characteristic of severe early cardiogenic shock during the initial 48 to 72 hours. A negative fluid balance may be targeted, thereafter. We typically use a pulmonary artery catheter to help guide fluid management in this patient cohort.
•Decompensated pulmonary vascular disease/right ventricle (RV) failure – In patients with acute PH crisis with RV failure, we generally avoid excessive volume unless patients are overtly hypovolemic. (See "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)", section on 'Management of acute pulmonary hypertensive crisis' and "Right heart failure: Causes and management", section on 'Monitoring and sodium and fluid restriction' and "Right heart failure: Causes and management", section on 'Approach to refractory volume overload'.)
●Sedation, analgesia, mobilization – We use a similar strategy to that described in V-V ECMO. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Routine measures' and "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)
In some patients, sedation may be weaned off successfully, especially when the goal is early mobilization for patients who need V-A ECMO as a bridge to heart, lung (in the case of PH), or heart-lung transplantation. However, femoral cannulation configurations and other concomitant mechanical circulatory support devices (eg, intra-aortic balloon pump or transaortic microaxial continuous flow pump) may preclude such activity [75,79-82]. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Invasive mechanical ventilation'.)
●Transfusion strategies – (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Transfusion'.)
●Ventilator-associated pneumonia precautions – (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults".)
●Nutritional support – (See "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription" and "Nutrition support in intubated critically ill adult patients: Enteral nutrition" and "Nutrition support in intubated critically ill adult patients: Parenteral nutrition".)
●Glucose control – (See "Glycemic control in critically ill adult and pediatric patients".)
●Stress ulcer prophylaxis – (See "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention" and "Management of stress ulcers".)
●Hemodynamic monitoring – (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and "Novel tools for hemodynamic monitoring in critically ill patients with shock".)
●Fever management – (See "Fever in the intensive care unit", section on 'Outcomes'.)
●Early physical therapy – (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Routine measures' and "Post-intensive care syndrome (PICS): Treatment and prognosis", section on 'Early ambulation/physical therapy'.)
●Tracheostomy – (See "Tracheostomy: Rationale, indications, and contraindications" and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Routine measures'.)
DAILY ASSESSMENT AND CIRCUIT MONITORING
Routine — Daily assessment and monitoring is similar to that in patients receiving venovenous ECMO and is typically performed by a multidisciplinary cardiogenic shock team. Further details on monitoring are provided separately. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Daily assessment and circuit monitoring'.)
Measuring oxygenation — In femoral V-A ECMO, we measure oxygen saturation from an arterial sample or peripheral oximeter in the right upper extremity. The rationale for this approach is explained by the phenomenon of dual circulation where fully saturated blood infused into the femoral artery from the ECMO circuit perfuses the lower extremities and the abdominal viscera and blood ejected from the heart (with potentially lower oxygen saturation, particularly in the case of impaired native gas exchange) selectively perfuses the heart, brain, and upper extremities. Cardiac and cerebral hypoxia could exist and be unrecognized if oxygenation is monitored using only blood from the lower extremities or the left upper extremity. However, if oxygenation is adequate in the right upper extremity, reflective of blood flow to the innominate artery, then it is reassuring that blood flow to the aortic arch, and thus the carotid and coronary arteries, is likely sufficiently oxygenated. Note that the same issues may arise with differential carbon dioxide tension as a result of dual circulation. (See 'Dual circulation' below.)
When arterial reinfusion occurs through the right axillary, subclavian, or innominate artery, peripheral oxygenation should be measured from the left upper extremity, with the same rationale that this will be more reflective of oxygenation in the aortic arch from reinfused blood that reaches the aorta despite competitive flow.
The phenomenon of dual circulation, complications that arise from it, and management strategies for it are discussed separately. (See 'Dual circulation' below and 'Configurations that avoid or address dual circulation from competitive flow' above.)
Monitoring for left ventricle distension — Because the most common configurations of V-A ECMO involve retrograde blood flow within the aorta, resulting in increased afterload on the left ventricle (LV), patients are at risk of developing LV distension and, consequently, pulmonary edema or intracardiac/aortic thrombosis.
We monitor LV output by examining the following:
●Continuous monitoring of the pulsatility in the arterial line's waveform (typically from an arterial line in the right upper extremity). We generally attempt to maintain an arterial pulse pressure (ie, difference) of at least 10 mmHg in the absence of an LV venting device (eg, intra-aortic balloon pump or transaortic microaxial continuous flow pump). (See "Intra-arterial catheterization for invasive monitoring: Indications, insertion techniques, and interpretation" and "Intraaortic balloon pump counterpulsation".)
●Monitoring right- and left-sided filling pressures and cardiac output using a pulmonary artery catheter. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)
●Bedside echocardiography, the frequency of which is dictated by the clinical scenario (eg, in the context of worsening hemodynamics or assessing for recovery). (See "Transesophageal echocardiography in the evaluation of the left ventricle".)
Managing LV distension is discussed below. (See 'Low pulsatility' below.)
Monitoring for limb ischemia — We use examination and near infrared spectroscopy monitoring of the extremities to assess distal tissue perfusion of the lower extremities [83,84]. (See 'Peripheral arterial complications' below and "Extracorporeal life support in adults in the intensive care unit: Vascular complications", section on 'Acute limb ischemia'.)
V-A ECMO-SPECIFIC COMPLICATIONS — Complications of V-A ECMO are similar to those that can occur in venovenous ECMO and are shown in the table (table 4). Additional complications that are either more common in or specific to V-A ECMO are discussed below.
Physiologic complications — It is important for the clinician to understand, recognize, and manage V-A-specific phenomena of dual circulation and left ventricle (LV) distension so they can be treated promptly.
Dual circulation — During femoral V-A ECMO, when there is minimal to no LV output, the reinfused extracorporeal blood flows retrograde up the aorta and across the aortic arch, perfusing the entire body including the cerebral and coronary vascular beds. However, in the presence of native LV ejection, a mixing point will develop between the reinfused blood from the ECMO circuit and that from the native cardiac output. The mixing point is dynamic depending on the relative strengths of the native and extracorporeal pumps, a phenomenon known as competitive flow. If the mixing point occurs in the descending aorta, then upper body oxygenation will be supplied by native cardiac output while the lower body is supplied by the ECMO circuit, effectively establishing dual circulations. If the native cardiac output ejects poorly oxygenated blood (eg, in the setting of impaired native gas exchange from cardiogenic pulmonary edema or acute respiratory distress syndrome), then the upper body, and most importantly, the coronary and cerebral circulations may be inadequately oxygenated while the lower body is well-oxygenated, referred to as differential oxygenation. Dual circulation may similarly result in differential carbon dioxide tension between the upper and lower body.
Axillary, subclavian, and innominate arterial reinfusions have relatively less differential oxygenation due to the origin of the reinfusion blood flow being close to the aortic arch. In aortic reinfusion (eg, ascending aorta directly cannulated), there is minimal if any dual circulation or differential oxygenation due to anterograde flow from the aortic root; and in left atrial (LA) reinfusion, there is no dual circulation or differential oxygenation because the LV is ejecting the well-oxygenated blood reinfused from the ECMO circuit.
Detecting and monitoring for differential oxygenation and use of configurations to manage it are discussed separately. (See 'Measuring oxygenation' above and 'Configurations that avoid or address dual circulation from competitive flow' above.)
Low pulsatility — A low or absent pulse pressure (ie, low "intrinsic pulsatility") may be an indication that there is insufficient LV preload and/or impaired LV contractility with LV distension. Our assessment relies upon pulmonary artery catheter (PAC) and bedside echocardiography findings to determine the etiology of low pulsatility. Interpretation of PAC findings is discussed separately. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".):
●Insufficient LV preload – Insufficient LV preload is often a contributing factor immediately following peripheral cannulation since the process of ECMO itself involves the removal of venous blood for extracorporeal circulation that is returned to the arterial side. Additional contributors include systemic inflammation and relative intravascular volume depletion that may accompany early refractory cardiogenic shock as well as initiation of ECMO itself. It may be suspected based upon PAC findings.
Severe right ventricular failure, if present, may also result in or contribute to insufficient LV preload and limited LV ejection. The latter would be evident on echocardiography and be associated with high right-sided pressures on PAC.
●Impaired LV contractility and LV distention – Impaired LV contractility in the face of ventricular stunning (common with cardiogenic shock due to acute myocardial infarction, fulminant myocarditis, refractory ventricular arrhythmias, or post-cardiac arrest) plus increased afterload due to the reinfused ECMO blood flow is usually the predominant mechanism underlying LV distention and low pulsatility in patients with cardiogenic shock. This can result in stasis of blood in the aortic root and LV and ultimately lead to subendocardial ischemia, pulmonary edema, ventricular arrythmias, and LV or aortic root thrombosis. LV distention is most often seen in those receiving femoral V-A ECMO, particularly following cardiac arrest. In support of this phenomenon are elevated left-sided pressures on the PAC and poor LV contractility on echocardiography.
There is no consensus on the best approach to low pulsatility in patients receiving V-A ECMO. We suggest the following:
●Patients without evidence of pulmonary edema or LV volume overload: Intravenous fluids and inotropes – In patients without overt evidence of pulmonary edema or LV volume overload who have lack of pulsatility particularly early after cannulation, it is our general practice to give isotonic crystalloid fluids (or blood in the case of ongoing bleeding). At the same time, inotropic therapy is typically initiated to increase LV contractility and LV ejection while preparations are made for placement of an LV "unloading" (also known as "venting") device.
●Patients with evidence of pulmonary edema or LV distension: LV venting device – Temporary mechanical circulatory support devices that are commonly used to manage LV distention include intra-aortic balloon pumps (IABP) for indirect LV venting and transaortic microaxial continuous flow pumps or less commonly surgical methods for direct LV venting. Choosing among these options is often institution- and patient-specific and depends upon factors including the presence of an existing device or thrombus.
•IABP and transaortic microaxial continuous flow pump – While an IABP can augment intrinsic pulsatility, clinicians should be aware that LV distension and pulmonary edema may still persist. This phenomenon is less likely to occur when a transaortic microaxial continuous flow pump is used since it drains blood from the LV and pumps it anterograde into the aorta, making the latter approach more suitable in patients with particularly severe LV stunning; however, the use of such a device should be avoided in patients with LV thrombus. Importantly, IABP can be placed percutaneously at the bedside whereas transaortic microaxial continuous flow pumps require placement in the cardiac catheterization lab and transaortic microaxial continuous flow pumps may be associated with a higher rate of adverse events.
•Direct surgical methods – Direct LV venting may also be achieved via surgical approaches. We often employ a surgical venting strategy as a transition from an initial percutaneous approach when prolonged need for ECMO support at higher blood flow rates is anticipated, particularly as a bridge to durable LV assist device (LVAD) or heart transplantation. Our favored approach to surgical LV venting is an LVAD integrated with V-A ECMO, termed Ec-VAD [85,86]. In brief, Ec-VAD is configured with LV apical cannulation via mini-thoracotomy combined with femoral or internal jugular venous cannulation as drainage with reinfusion to the axillary artery or ascending aorta.
Other complications
Peripheral arterial complications — Complications associated with peripheral arterial cannulation include limb ischemia, thrombosis, pseudoaneurysm formation, arterial dissection, and compartment syndrome, any of which may require vascular surgical intervention. More detailed discussion of the vascular complications of ECMO are provided separately. (See "Extracorporeal life support in adults in the intensive care unit: Vascular complications".)
Coronary or cerebral hypoxia — During femoral V-A ECMO, dual circulation may result in cardiac and cerebral hypoxia if the coronary and cerebral vascular beds are supplied with poorly oxygenated blood from the LV in the setting of impaired native gas exchange. This phenomenon can be detected when there is a difference between oxygen saturation measured in the upper and lower extremities. Coronary and cerebral hypoxia can lead to additional complications including cardiogenic pulmonary edema, anoxic brain injury, encephalopathy, and seizures. The concepts of dual circulation, competitive flow, differential oxygenation, and configurations that address them are discussed above. (See 'Dual circulation' above and 'Configurations that avoid or address dual circulation from competitive flow' above.)
Pulmonary edema and hemorrhage — Pulmonary edema and hemorrhage can occur in patients who have severe LV distention during V-A ECMO, typically when the LA pressure exceeds 25 mmHg. LA pressure is often estimated by measuring pulmonary capillary wedge pressure or pulmonary arterial diastolic pressure in the absence of significant pre-capillary pulmonary hypertension. Treatment is discussed separately. (See 'Low pulsatility' above.)
Cardiac or aortic thrombosis — Intracardiac or aortic thrombosis can occur due to retrograde blood flow in the ascending aorta with subsequent stasis of blood in the LV or aortic root. Treatment typically involves increasing anticoagulation targets (if feasible and as tolerated) and treating LV distension. (See 'Low pulsatility' above.)
Neurologic injury — Neurologic complications are common among patients receiving V-A ECMO [87,88]. The types of neurologic injury reported include coma of uncertain cause, encephalopathy, anoxic brain injury, ischemic myoclonus, spinal cord infarction, ischemic stroke, intracranial bleeding, and brain death.
It is important to realize that these findings may be due to the condition that prompted ECMO or a sequela of ECMO itself, including anticoagulation, thrombocytopenia, and hemolysis.
WEANING — We use the following criteria to indicate readiness to wean from V-A ECMO [89]:
●Recovering clinical condition
●Improving end-organ function
●Partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2:FiO2) ratio >100 mmHg (some experts have a higher threshold; eg, >200 mmHg on FiO2 0.3 to 0.4)
●Low-level vasopressor and inotrope support (eg, norepinephrine ≤4 mcg/minute, dobutamine <5 mcg/kg/minute)
Once the above criteria are met, we utilize a three-step approach to weaning [89]:
●Daily weaning assessment with reduction in ECMO blood flow – We incrementally decrease ECMO blood flow by 0.5 L/minute increments, every one to two minutes, to target a flow of 2 L/minute. We typically maintain ECMO flow at 2 L/minute for at least eight hours as tolerated (some experts use shorter periods).
●Decannulation readiness assessment – If reduced ECMO flow is tolerated, we perform bedside assessment for decannulation by transiently reducing ECMO blood flow to target 1 to 1.5 L/minute for at least one minute (some experts may extend the trial for longer).
●Final assessment with circuit clamping and decannulation – If the above is tolerated, we decrease blood flow gradually and clamp the circuit (for a short period of time, such as one minute), with plans for immediate decannulation if tolerated. Pulmonary artery catheter and echocardiography findings may aid in assessing tolerance of blood flow reductions and predicting weaning success (eg, LV ejection fraction >20 percent [90]).
At each step, any of the following criteria constitutes failure of a weaning trial, which should prompt a return to the last stable blood flow rate:
●Mean arterial pressure falls below 65 to 70 mmHg or decreases by more than 10 mmHg from baseline
●Significant increase in intracardiac filling pressures
●Deterioration in vital signs, respiratory status, or mental status
Transition from V-A ECMO to venovenous ECMO can be considered if biventricular function has sufficiently recovered but gas exchange remains inadequate. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute extremity ischemia".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Extracorporeal membrane oxygenation (ECMO) (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Terminology – Venoarterial (V-A) extracorporeal membrane oxygenation (ECMO) is a form of extracorporeal life support. V-A ECMO is mostly used for temporary support of patients with acute cardiac/circulatory failure. The term V-A refers to the configuration of the circuit, which is comprised of a drainage cannula that removes blood from the right atrium or a large central vein (V-A). This blood is oxygenated extracorporeally and reinfused into a major artery (V-A) (table 1). (See 'Terminology' above and "Extracorporeal life support in adults in the intensive care unit: Overview", section on 'Terminology'.)
●Patient selection – We evaluate patients with acute cardiac failure who have not responded to conventional therapy as potential candidates for V-A ECMO. (See 'Clinical applications' above and 'Initial clinical assessment' above.)
•Common indications include refractory cardiogenic shock due to a variety of etiologies, extracorporeal support during cardiopulmonary resuscitation, and acute decompensated pulmonary vascular disease. Others include significant trauma, anaphylactic shock, drowning, hypothermia, pulmonary hemorrhage, and donor optimization for organ donation. (See 'Clinical applications' above.)
•Absolute and relative contraindications are listed in the table (table 3). Contraindications that are specific for patients being evaluated for V-A ECMO include severe aortic insufficiency and aortic dissection (absolute contraindications) and arterial conditions that limit vascular access, such as severe peripheral arterial disease (relative contraindication). (See 'Contraindications (absolute and relative)' above.)
●Catheter insertion – Most commonly, a femoral V-A ECMO configuration is used (figure 1). If avoidance of competitive flow is desired, we consider hybrid configurations (figure 3) or use upper body approaches (eg, internal jugular or right atrial drainage with axillary, subclavian, innominate, left atrial, or aortic reinfusion). Drainage cannulae are typically 23 to 25 French, larger if centrally cannulated, and we select arterial reinfusion cannulae based on the size of the artery being cannulated for reinfusion, typically 15 to 19 French for femoral arterial reinfusion. We use a percutaneous approach via Seldinger technique under image-guidance as the default approach for cannulation, the details of which are provided separately. (See 'Catheter insertion' above and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Insertion technique'.)
●Initial settings and titration – Following cannulation, the patient is immediately connected to the ECMO circuit. Although variable, typical initial settings are the following, achieved incrementally over the first few minutes after initiation (see 'Initial settings and titration' above):
•Pump speed to achieve an extracorporeal blood flow of 3 to 4 L/minute output. We target adequate end-organ perfusion or support (eg, decreasing blood lactate level, decreasing creatinine with increased urine output, and a decreased need for vasopressors and inotropic support), and an appropriate oxygen saturation (taking into consideration the effect of dual circulation and differential oxygenation).
•Sweep gas flow typically ranges from 1 to 10 L/minute. Sweep gas flow is titrated to a target of near-normal pH (unless there is either severe metabolic acidosis or differential carbon dioxide tension as a result of dual circulation) and should never fall below 0.5 L/minute since this can worsen oxygenation.
•Fraction of delivered oxygen of 1.0. This is not usually titrated.
Within an hour of cannulation, we generally obtain routine laboratories, systemic arterial blood gas (ABG; eg, radial ABG), coagulation studies, and pre- and post-membrane lung blood gases.
●Supportive care
•Mechanical ventilation – For patients on V-A ECMO who require invasive mechanical ventilation, we use a similar strategy to that outlined for patients receiving venovenous (V-V) ECMO and have a low threshold to add a venous reinfusion limb for severe hypoxemia or hypercapnia (venoarteriovenous ECMO (figure 3)). Further details are provided separately. (See 'Concomitant respiratory failure' above and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Invasive mechanical ventilation'.)
•Anticoagulation – Patients receiving V-V ECMO require anticoagulation due to the high risk of systemic and circuit thrombosis. In patients receiving V-A ECMO, the approach to anticoagulation is similar to that in V-V ECMO. However, in the absence of bleeding, we suggest targeting an activated partial thromboplastin time (aPTT) that is twice the control (Grade 2C). The higher aPTT is warranted due to the higher risk of thrombosis in the V-A ECMO population (in particular arterial embolization, left ventricle thrombus, and circuit thrombosis) compared with V-V ECMO. Further details are provided separately. (See 'Anticoagulation' above and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Anticoagulation'.)
●Monitoring – Daily assessment and monitoring is similar to that in patients on V-V ECMO. (See "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Daily assessment and circuit monitoring'.)
Specific to V-A ECMO is the following:
•For patients receiving femoral V-A ECMO, we ensure that oxygen saturation is measured from the right upper extremity while for right axillary, subclavian, or innominate artery reinfusion configurations, we measure oxygenation from the left upper extremity. The rationale is that this approach assesses the phenomenon of dual circulation that results from competitive flow between native and ECMO circuits, which may lead to oxygenation differences in different regions of the body. (See 'Measuring oxygenation' above and 'Dual circulation' above and 'Configurations that avoid or address dual circulation from competitive flow' above and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Daily assessment and circuit monitoring'.)
•We also monitor the pulsatility in the arterial line's waveform, cardiac pressures on pulmonary artery catheter (PAC), and bedside echocardiography and treat insufficient preload or poor LV function accordingly. (See 'Low pulsatility' above.)
●Complications – Other than dual circulation and low pulsatility, complications of V-A ECMO are similar to those that can occur in V-V ECMO and are shown in the table (table 4). Complications that are more common in or specific to V-A ECMO include peripheral arterial complications (eg, limb ischemia, arterial dissection), myocardial or cerebral ischemia, pulmonary edema or hemorrhage, cardiac or aortic thrombosis, and neurologic complications. (See 'V-A ECMO-specific complications' above and "Extracorporeal life support in adults: Management of venovenous extracorporeal membrane oxygenation (V-V ECMO)", section on 'Complications'.)
●Weaning – Weaning is considered when the patient's clinical condition is compatible with recovery, end-organ function is improving, the partial pressure of arterial oxygen to fraction of inspired oxygen ratio is >100 mmHg, and vasopressors and inotropes are at low levels. It involves an incremental reduction in blood flow and eventual clamping of the circuit, which, if tolerated, is followed by decannulation. PAC and echocardiography findings may aid in assessing tolerance of blood flow reductions. (See 'Weaning' above.)
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