Mechanical circulatory support in the intensive care unit : International Anesthesiology Clinics

Secondary Logo

Journal Logo

Review Articles

Mechanical circulatory support in the intensive care unit

Sommer, Philip MDa; Nunnally, Mark MDb

Author Information
International Anesthesiology Clinics: Fall 2022 - Volume 60 - Issue 4 - p 46-54
doi: 10.1097/AIA.0000000000000381
  • Free

Goals for mechanical circulatory support (MCS) have grown from facilitating surgical procedures1 and supporting respiratory dysfunction2,3 to minimizing iatrogenic harm, facilitating rehabilitation, and sustaining patients in cardiogenic shock. MCS in the intensive care unit (ICU) should be thought of as a complete clinical service more than a technology because of the numerous clinical care issues that need to be assessed/addressed.

While intra-aortic balloon counterpulsation (IABP), percutaneous MCS devices and left ventricular assist devices are quite common in the ICU setting, this review will focus mainly on use of extracorporeal membrane oxygenation (ECMO) in the ICU.


A major area of innovation and expanded indications concerns ECMO. The use of ECMO in particular has evolved as a treatment for acute respiratory distress syndrome (ARDS). The CESAR randomized trial renewed interest for ECMO after results suggested a mortality benefit if patients with severe respiratory failure were treated at centers with ECMO experience.4 In 2009, H1N1 influenza-associated ARDS allowed for comparison of conventional low tidal volume ventilation with supplementation of ECMO. A number of countries reported significant mortality benefits in patients treated at ECMO specialized centers.5,6 The results of the 2018 multicenter randomized EOLIA trial once again suggested promising results for those patients with severe ARDS who were treated with ECMO compared with conventional therapy.7 The results of these trials have spurred the continued growth and ubiquity of ECMO for a variety of conditions.

ECMO configurations

All ECMO circuits operate by draining blood from a central vein through a cannula and mechanical pump, passing it through an oxygenator, and then returning it to the body through a cannula into either the venous or arterial system. A blood gas interface exists inside the oxygenator that allows for the removal of carbon dioxide (CO2) and direct oxygenation of blood. This interface of gas exchange is controlled by a blender which allows alteration of partial pressure of CO2 and oxygen and controls diffusion into blood. The infusion site of blood into the venous or arterial side of the patient determines if the patient is on venovenous ECMO (VV-ECMO) or venoarterial ECMO (VA-ECMO). VA ECMO can be either done with central or peripheral cannulation techniques (Figs. 1, 2). Central VA ECMO requires venous cannulation usually from the right atrium and an arterial cannula that resides in the aorta.10 Central cannulation most commonly occurs in post cardiotomy patients who fail to wean from cardiopulmonary bypass despite inotropic support.11 Peripheral cannulation involves usually the right internal jugular vein or femoral vein for drainage with an arterial outflow cannula in the femoral artery being the most common.12

Figure 1:
Venoarterial extracorporeal membrane oxygenation with peripheral cannulation showing blood being drained from the inferior vena cava, going through the circuit, and then returning into the femoral artery. From Chaves et al.8 Reproduced under the terms of the Creative Commons Attribution License 4.0.
Figure 2:
Venoarterial extracorporeal membrane oxygenation with central cannulation. The venous drainage from the patient comes from the cannula placed in the right atrium and the return cannula is placed in the ascending aorta. From Chung et al.9 Reproduced under the terms of the Creative Commons Attribution License 4.0.

VV ECMO is used for patients with a significant respiratory disease requiring removal of CO2 and infusion of oxygen. Cannulation typically involves a drainage cannula in the femoral vein and a return cannula carrying oxygenated blood into an internal jugular vein (Fig. 3).13 Single-site bicaval cannulation in the right internal jugular has promise in patients with respiratory failure with the potential advantages of allowing for more mobility, reducing recirculation of blood, and less cannula-related bleeding.14

Figure 3:
Diagram of venovenous extracorporeal membrane oxygenation showing that the blood is being extracted through the patient’s femoral vein, traveling through the circuit, and oxygenated blood is returned into the superior vena cava through the right internal jugular vein. From Chaves et al.8 Reproduced under the terms of the Creative Commons Attribution License 4.0.


ECMO cannulae continue to evolve, but their basic purpose has not changed: provide an adequate amount of blood flow to the circuit, minimize inflammatory responses that instigate thrombosis, and minimize damage to the native blood vessels. Many modern ECMO cannulae are coated with heparin to try and make them more biocompatible.15 The use of heparin coating reduces activation of the clotting cascade, reduces complement activation, and has potential anti-inflammatory benefitss.16 One drawback of using heparin is the potential for the development of heparin-induced thrombocytopenia (HIT).17 Due to this concern, newer biocompatible coatings such as the “Balance Biosurface” (Medtronic Inc., Minneapolis, MN) and Terumo X coating (Terumo Cardiovascular Systems Corporation, Ann Arbor, MI) have been developed to mimic native endothelium with the benefit of reducing platelet adhesion and decreasing complement pathway activation.18–20 Use of synthetic polymers and phospholipids to coat the ECMO cannulae may reduce inflammation and coagulation cascade which may reduce the risk of HIT.16

Length of the cannule will depend on the patient and the insertion location. In VV ECMO, it is recommended that the distance between the cannulae tips is 8 to 10 cm to prevent recirculation,21 a situation in which returning oxygenated blood is removed by the drainage cannula, preventing it from entering systemic circulation and decreasing the effectiveness of the ECMO circuit in terms of the percentage of cardiac output (CO) that is oxygenated by the circuit. Proper positioning of the femoral drainage cannula is usually at the atrial-inferior vena cava junction while the reinjection cannula will enter the superior vena cava and go to the right atrium.22,23 Cannulae will have radiographic material on them so their position can be confirmed by radiography/fluoroscopy but can also be confirmed with echocardiography and/or fluoroscopy.

Cannulae size depends on sex, height, pre-existing peripheral vascular disease, and flow needs for the patient. Typically in VA ECMO, arterial cannulae size ranges from anywhere between 14 and 21 Fr.24 If full circulatory support is required, 15 Fr is usually the minimum size required for VA ECMO.25 While larger cannulae can provide increased flow rates, complications such as limb ischemia, bleeding, and thrombosis increase as cannulae size increases.26 Using manufacturer-provided pressure/flow curves, the correct size cannula can be determined for optimal blood flow.27,28 The correct sized cannula must be able to provide enough ECMO flow relative to the native CO to overcome the physiological derangements while minimizing recirculation and avoiding iatrogenic injury.11

ECMO pumps

Both centrifugal and roller blood pumps are commercially available for ECMO use in both pediatric and adult patients.29 Centrifugal pumps utilize a magnetic suspension system that will levitate an impeller that rotates at high speeds, creating a vortex effect and a pressure differential that drives blood out of the patient, through the circuit, and back to the patient.30 Roller pumps function by serially compressing the length of tubing to create positive displacement and blood flow. Recently, advancements in centrifugal pump technology has lead them to overtake roller pumps in overall usage throughout the United States.31 Roller pumps have some significant disadvantages. They require extra volume for circuit priming, at high flow rates shear forces and hemolysis become significant, and tubing wear requires changing every few days.32,33


Most blood oxygenators are membrane oxygenators. They have a hollow bundle fiber design that allows blood to flow externally around the fibers while the sweep gas flows internally though the fibers. This configuration is referred to as extraluminal flow and is the most common configuration of oxygenators available.34 Separation of the blood and gas phases is necessary to reduce inflammatory activation and coagulation. Initially, silicone-coated microporous polypropylene membranes were the choice for long-term ECMO support.35 Recently, poly-methl-pentene membranes have been developed and with their use have come improvements, such as less plasma leakage, smaller priming volumes, better gas exchange, and reduced physical size of the oxygenator. The new poly-methl-pentene membranes are associated with reduced markers of inflammation, improved longevity, and reduced blood product transfusion requirements.36,37 Internal resistance to blood flow is a property of the oxygenator and is measured by the decrease in pressure across the oxygenator with Pressurein (Pin)−Presureout (Pout).38 The Pin is measured after the pump but before the oxygenator while the Pout is measured after the oxygenator before returning to the patient.39 An increase in the transmembrane pressure is a common sign of platelet-thrombin complexes that attach to the exchanger.40 This increase in pressure can affect blood flow rates as well as the gas exchange properties of the oxygenator. Continued monitoring of oxygenator function includes assessment of preoygenator and postoxygenator blood gas samples. Setting the fraction of inspired oxygen on the sweep gas will determine the partial pressure gradient between the sweep gas and the patient’s blood. As the blood flow increases through the oxygenator and the circuit, more oxygenated blood will circulate as a part of the patient’s CO. If blood flow across the oxygenator is within the manufacturer’s range, the oxyhemoglobin saturation post-membrane oxygenator should be 100%. If the arterial partial pressure of oxygen (PaO2) postoxygenator is <300 mm Hg, it could mean that the membrane oxygenator is not functioning properly. Inspection of the membrane oxygenator to look for the platelet-thrombin complexes, which will appear as white areas on the oxygenator, should occur daily. Blood clots can occur in any area of the circuit and will appear as dark red deposits. Usually, no intervention is required if the size of the clot is <5 mm and they are not growing in size. If derangements in gas exchange or changes in transmembrane pressures are seen with visible clots, an oxygenator exchange may need to be performed with the assistance of perfusionists, intensivists, nursing, and/or cardiothoracic surgeons. Elevated D-dimer levels are associated with the need for exchange and can represent the burden of clot within the oxygenator.41,42 Low fibrinogen levels, decreasing platelets, and decreasing levels of heparin required for anticoagulation can also indicate membrane oxygenator dysfunction.43

Hyperoxia is a danger that can come from the use of VV and VA ECMO. Several studies suggest that in a number of scenarios an association between hyperoxia and worse outcomes, including mortality, for patients on ECMO.44–46 Ideally, the PaO2 of the patient from their arterial line should be maintained between 60 and 100 mm Hg.

In VA ECMO, there can be circumstances where native CO is sufficient to perfuse vessels arising from the proximal aorta, in particular the right arm and cerebral vessels.47 Poor gas exchange in the lungs may result in these vessels receiving hypoxic perfusion while more distal arteries are supplied by fully oxygenated ECMO flow (Fig. 4). This condition is referred to as “North-Southing,” or the “Harlequin Syndrome.”49 Left untreated, it can lead to critical limb or cerebral ischemia. Detection is most commonly through monitoring of arterial oxygenation in the right upper extremity, but cerebral oximetry can be helpful. Therapies include reducing native CO by increasing ECMO flow to reduce cardiac preload or reducing cardiac function through negative chronotropes or inotropes. In refractory cases, a central venous outflow cannula can be inserted to enrich the oxygenation of the blood entering the right atrium as a hybrid VA/VV ECMO configurartion.50

Figure 4:
Venoarterial extracorporeal membrane oxygenation (ECMO) peripheral cannulation strategy has the possibility of creating North South or “Harlequin” syndrome. In this scenario, blood that has passed through the ECMO circuit that is high in oxygen content is sent back to the patient through the femoral artery and travels up retrograde towards the heart and aortic arch. If the patient’s native heart function is recovering and is able to pump blood through lungs, a mixing cloud (*) can occur between the anterior flow of the native heart and the retrograde flow of the ECMO circuit. Relatively deoxygenated blood may then be the predominate perfusing flow to the brain and upper limbs causing ischemia of the tissues. Monitoring can be done with the use of arterial blood gases from a right radial arterial line. From Tsangaris et al.48 Reproduced under the terms of the Creative Commons Attribution License 4.0.

Clearance of CO2 happens more efficiently than that of oxygen across the membrane. Because of this efficiency of removal, CO2 concentration is not as affected by flow through the circuit as oxygen is. Utilizing higher rates of flow on the sweep gas is the most efficient way to remove CO2 when the native lung function is abnormal. By relying on adjustments of sweep gas for CO2 removal and flow adjustments for oxygen input, the VV ECMO circuit can allow for lung protective ventilation while maintaining normal physiological values.

Heat exchanger

The function of heat exchangers is to maintain a patient at normothermia. They are usually located within the membrane oxygenator in a separate compartment. Unsterile water from the heater is separated from the blood by different materials, such as stainless steel or polyurethane.51 The integrity of this separation between the two compartments is critical to maintain sterility. Heat exchangers are tested for integrity by allowing water to recirculate through them for 10 minutes to look for water leaks.52 Recommendations are to test the heat exchanger, either with water or with pressurized air across the chamber, before initiating ECMO.

Monitoring patient hemodynamics

Patients on VA ECMO invariably have some degree of cardiac dysfunction that requires specific patient monitoring and management goals for a successful ECMO outcome. Some of those hemodynamic goals for patients on VA ECMO include unloading of the left ventricle (LV) to promote myocardial recovery, restore acid-base status and oxygenation, promote LV ejection to prevent thrombosis, balance the need for anticoagulation versus the risk of bleeding, and maintain oxygen and nutrient supply to major organs. An arterial line is essential for management of patients on VA and VV ECMO. In patients on VA ECMO with peripheral cannulation, a right-sided arterial line in the arm is ideal as it is more representative of cerebral oxygen concentration. This concept is because of the possibility of heterogenous oxygenation of arterial blood (Harlequin Syndrome). Arterial line pulsatility is a measure of the amount of blood being ejected by the LV. Decreasing pulsatility can indicate worsening LV function or reduced filling while increasing pulsatility can represent ventricular recovery or enhanced filling.

The measurement of mixed venous oxygen (MVO2) saturation provides a global assessment of perfusion status throughout the body. Unfortunately, in VV ECMO, accurate measurement of MVO2 saturation is elusive. Central venous blood is already enriched from the circuit and sampling from the preoxygenator flow may contain recirculated enriched blood. In both circumstances, saturations will be higher than the true “native” values that reflect deoxygenated blood returning from the periphery. In VA ECMO, the MVO2 saturation is accurate and can be used for clinical decisions when taken from the venous line before the oxygenator. Low venous oxygen saturation on VA ECMO is associated with increasing mortality rates.53 Low MVO2 saturation requires interventions that address supply and demand of oxygen to tissues. Supply can be increased by increasing ECMO flows, maintaining adequate mean arterial pressure (MAP), ensuring adequate oxygenation, and appropriate hemoglobin levels. Demand alterations focus on decreasing metabolic rate by using sedation or decreasing consumption by addressing infection using neuromuscular blockade, or treating shivering.54

Lactate is a byproduct of cellular anaerobic metabolism and can be associated with inadequate oxygen delivery to tissues. While the lactate level is important to monitor during VA ECMO support, monitoring lactate clearance is an important prognostic indicator for outcomes.55 Hyperlactemia is not always the byproduct of inadequate tissue oxygenation and in fact lactate can be produced secondary to adrenergic stimulation and catecholamine release.56 A lactate level that continues to be elevated or is rising after initiation of ECMO therapy warrants a full examination of the patient to rule out causes such as bleeding, sepsis, or organ ischemia.

Lactate, MVO2 saturation, and MAP are all global markers of end-organ perfusion.57 However, regional peripheral perfusion may be compromised as well. Monitoring for Harlequin syndrome is important in VA ECMO, but other vessels may be impaired because of the properties of the cannulae, in particular by reducing flow to the legs through the femoral arteries. The clinical examination is a reliable indicator of end-organ perfusion. Derangements in neurological status, mottled skin, decreased capillary refill, and decreased urine output are clinical signs of malperfusion that can be valuable additions to labs and monitors.

To look at regional blood flow and oxygen delivery, systems such as near-infrared spectroscopy (NIRS) have been developed to monitor cerebral oxygen saturation. The NIRS system is a noninvasive monitor that detects tissue oxygenation saturation. Oxyhemoglobin and deoxyhemoglobin absorb different wavelengths of near infrared light that allows for the ratio of oxygenated hemoglobin to total hemoglobin to be calculated.58 NIRS valves can be altered by several variables including temperature, sedation levels, ECMO flow rates, CO2, and others. Differences in NIRS readings between the right and left cerebral hemispheres or an overall sudden decrease in values can indicate neurological injury in patients on VA ECMO.59 NIRS monitoring can be used on the peripheral tissues as well. As limb ischemia is a major concern in VA ECMO, following the trends and noting the difference in NIRS between the cannulated limb and non-cannulated limb can indicate lower extremity ischemia.60

Monitoring the flow of blood on VA ECMO is critical since cardiogenic shock is characterized by a low flow output state leading to end-organ dysfunction. During VA ECMO support, the CO and flow to tissues is the sum of flow from the VA ECMO circuit and the remaining CO from the native heart. When starting on VA ECMO, flow parameters should be set to 50 to 70 mL/kg/min while maintaining a MAP >60 mm Hg.44 This flow can be titrated up and down to satisfy the metabolic needs of the body while allowing for cardiac recovery. Inotropes such as dobutamine and epinephrine can be used to help augment native cardiac function in order to achieve MAP and perfusion goals.

The type of pump on the ECMO circuit will determine flow characteristics of the circuit being used. Centrifugal pumps are preload dependent and afterload sensitive. While the most direct way to increase flow on ECMO is to increase the revolutions-per-minute, flows can be affected by other factors such as the sudden decrease in preload or change in afterload. Alterations in preload or afterload can come from a variety of factors such as bleeding, sepsis, thrombus in the oxygenator, or clot in the arterial cannula. To monitor contribution to the CO by the native heart and risk of Harlequin Syndrome, arterial line waveforms can be used but echocardiography is first-line tool for cardiac evaluation,61 and right upper extremity oxygenation measurement is the preferred method for detecting heterogeneous arterial oxygenation.

Left ventricular distention

A common problem during management of VA ECMO is LV distention from retrograde flow from the arterial ECMO canula up the aorta. This flow opposes a LV that has decreased function and is unable to overcome the added pressure, leading to increased afterload and distention. As retrograde flows from VA ECMO begin, there is a simultaneous increase in LV systolic and diastolic pressures. This increased pressure in combination with decreased cardiac performance of the native heart creates a situation of LV overdistention. CO of the native heart should be assessed on a regular basis using echocardiography, especially to help determine cardiac chamber size. If the LV is distended, oxygen demand increases, cardiac ischemia worsens, and recovery is compromised. Assessment of valves, especially the aortic valve, is equally important. If the aortic valve fails to open and eject blood, blood can become stagnant in the LV and form thrombus. Use of thermodilution CO measurement in VA ECMO are unreliable due to blood flow alterations.

In circumstances of LV distention, LV unloading is used to help improve cardiac function and decrease distention, thereby reducing myocardial oxygen demand and promote cardiac recovery. Options for unloading the LV are IABP, Impella (Abiomed Inc., Danvers, MA), percutaneous atrial septostomy, or central VA ECMO.62 Use of Impella for relieving LV distention may improve survival, but with the downside of more bleeding and ischemic complications than treatment with VA ECMO alone.63 Echocardiography is particularly useful in this situation to determine degree of distention and if unloading of the LV has occurred after intervention.

Limb ischemia

As mentioned, blood flow disruption to the lower limbs is common, especially when the femoral artery is used as the cannulation vessel. Dissection of the common femoral artery, thrombus, pseudoaneurysm formation, and embolism can put the ipsilateral lower limb at risk for ischemia. Similar concerns apply for cannulation configurations involving vessels supplying the upper extremities. Lower extremity ischemia complicates 17% of patients receiving VA ECMO with femoral artery cannulae, leading to fasciotomy and even amputation.64 Extremity complications are associated with poor outcomes.65 In order to maintain flow to the lower extremity, a distal perfusion catheter can be placed at the time of cannula insertion or percutaneously after insertion of the cannula. Targets for cannulation for the distal perfusion catheter include the common femoral artery, superficial femoral artery, and the posterior tibial artery (retrograde flow).66 After placement of the catheter, blood flow and oxygenation can be monitored by checking doppler pulses in the lower extremity or with NIRS. Studies looking at effectiveness of distal perfusion catheters are difficult to interpret due to variability in placement location, timing, indication, and monitoring, but use is associated with a reduction in lower limb ischemia.67 Limb ischemia can lead to compartment syndrome in the lower extremities. The neurovascular exam of the potentially affected area should include an assessment for swelling or change in color of the skin, decreased capillary refill, weakening pulses, pain to light palpation, and loss of motor function or sensation. While compartment syndrome is a clinical diagnosis, an intra-compartmental pressure greater than 30 mmHg indicates the need for fasciotomy to release the pressure and restore blood flow to the threatened limb.


One of the biggest issues that face patients and clinicians when on MCS is the delicate balance of the need for anticoagulation to prevent clotting versus the risk of bleeding. Bleeding and thrombosis continue to be major causes of morbidity and mortality in ventricular assist devices, VV, and VA ECMO. Autopsy examinations of patients who were on ECMO suggest thromboembolic events are underrecognized.68 Anticoagulation is generally preferred during long-term ECMO and early in the management of left ventricular assist devices. Heparin has historically been the initial choice for anticoagulation. The proper dose of heparin that is required to prevent thrombosis is variable between different institutions and differs between patients. Monitoring is possible by assessing the activated partial thromboplastin time (aPTT), anti-Xa levels, and the activated clotting time. Less aggressive strategies of anticoagulation have been validated in ECMO. There were more thrombotic events, including oxygenator thrombosis, but also lower rates of bleeding incidents when targeting aPTT levels of 35 to 40 seconds compared with 45 to 55 seconds.69 Anti-Xa levels are unaffected by the state of generalized inflammation common in critical illness, owing to its direct measurement of heparin activity.70 Anti-Xa activity is more accurate with heparin dosing than the activated clotting time, making it the preferred test for patients on ECMO, with a target goal of 0.3 to 0.7 U/mL.71 Using anti-Xa levels, as opposed to aPTT, decreased time to target the anticoagulation goal and lessened the amount of heparin given to patients.72 When the results of the anti-Xa and the aPTT tests are discordant, clinical risks of bleeding and thrombosis must be balanced. As the aPTT approaches values >70 seconds, major bleeding increases even in the setting of therapeutic anti-Xa levels.73,74 Due to specificity of the anti-Xa assay, a therapeutic anti-Xa value with a low aPTT should be interpreted as the patient being appropriately anticoagulated (Fig. 5).

Figure 5:
Using anti-Xa levels and activated partial thromboplastin time (aPTT) in combination can minimize the risks of thrombosis and bleeding in patients on ECMO. This figure is an example of a heparin dosing protocol for patients who are on ECMO with the target levels of anti-Xa between 0.15 and 0.7 U/mL and the aPTT <70 seconds. In this protocol, 5000 U of IV heparin are given before the initiation of ECMO and a heparin infusion started at 500 U/h when the aPTT is <70 seconds with no signs of bleeding. Reproduced with author’s permission.

One factor limiting use of heparin in some patients is development of HIT, which develops when heparin binds to platelet factor-4 (PF4) and the complexes act as immunogens that promote production of IgG antibodies, resulting in IgG-heparin- platelet factor-4 complexes that activate platelets and create a pro-thrombotic state.75 Argatroban and bivalrudin are direct thrombin inhibitors and have been used as alternatives for patients with HIT.76 Bivalrudin has a relatively short half-life of 25-30 minutes and is mostly cleared by enzymatic activity.77 Despite only about 20% of bivalrudin being renally cleared, lower starting doses are recommended in those patients with renal dysfunction.78 Monitoring of therapeutic bivalrudin levels is done by following the aPTT. The half-life of argatroban is 45 minutes and its use is limited to those patients with hepatic impairment. It was non-inferior to heparin in terms of bleeding and thrombosis when used for anticoagulation in VV ECMO.79 Efficacy of bivalrudin and argatroban is measured by aPTT levels, like heparin. The need for anticoagulation continues to change as advances from heparin coated cannulas, improved oxygenator materials, and centrifugal pumps have decreased the pro-coagulant response of ECMO. It has been possible to maintain patients on VV ECMO without use of systemic anticoagulation. In such cases, flow rates should be maintained at least 3 L/min. Using these parameters, patients have been managed with no increased risk of thrombosis and a decreased risk of gastrointestinal bleeding (GIB) and blood transfusion.80

Neurological complications

Some of the most devastating complications for patients on ECMO are neurological events. The rate of neurological complications in VA ECMO patients is ~15%, including brain death, cerebral infarction, seizures, and intracranial hemorrhage.81 This rate of complication will be expected to vary, depending on comorbidities, and indication and timing of VA ECMO initiation.82 Patients who suffer any form of neurological complication have significantly higher rates of in-hospital mortality than those who do not. Those who survive frequently face crippling neurological deficits. In comparison, the neurological complication rate of patients on VV ECMO is ~7%, most commonly manifested as intracranial hemorrhage, followed by brain death and seizures.83


Another common complication during ECMO is GIB. A number of factors other than anticoagulation make patients prone to GIB, including acquired von Willebrand syndrome, thrombocytopenia, and hypofibrinogenemia. The location of the GIB can be from duodenal ulcers, gastritis, esophagitis, or arterio-venous malformations. Wherever the bleed is, endoscopic evaluation should be considered to gain control over bleeding and if possible, anticoagulation should be held or reversed if the GIB is causing hemodynamic instability.

Additional management issues

Sedation practices for patients on ECMO have evolved significantly in the past 20 years. Previously, patients were kept deeply sedated to minimize the possibility of dislodging cannulae and to allow for minimal metabolic demands. Current recommendations emphasize early sedation after cannulation to allow for flow targeting and titration and minimizing oxygen consumption, followed by an approach of the minimum sedation necessary.84 There is no consensus as to what medications to use for sedation but many institutions rely on a multimodal approach utilizing narcotics such as fentanyl and hydromorphone and sedating agents like propofol and dexmedetomidine. Modern sedation techniques aim to have a patient who is “calm and comfortable.” Titrating sedation medications to achieve this can be challenging due to change in the pharmacodynamic and pharmacokinetic properties that the ECMO circuit introduces. Components such as the cannulae and tubing, oxygenator, and pump increase the volume of distribution of certain medications.85 Pharmakokinetic properties, such as protein binding, lipophilicity, and molecular size will play a role in how the drugs are metabolized through the ECMO circuit. Under these circumstances, titration is helpful to avoid over-sedation and drug accumulation. Light sedation strategies have the added benefit of being able to liberate patients from the ventilator faster, facilitate physical therapy, and improve physical functioning at time of discharge.86 Choice and method of sedation should be done in conjunction with a mutlidisciplinary team consisting of nursing, intensivists, pharmacists, and surgeons.

Patient mobilization is important in any ECMO patient and ability to mobilize is sometimes a benefit of ECMO itself through reduced sedation requirements. Atrophy and weakness, along with neuropathy and clinical myopathy, are common in patients who are critically ill on ECMO or who have received other forms of prolonged MCS.87 Physical therapy is important for a patient’s recovery and fundamental as a pre-habilitation step in patients who are awaiting either heart or lung transplant on MCS. Many centers have had success with early mobilization and rehabilitation, including patients with femoral cannulation configurations. Through collaboration between physical therapy, nurses, and physicians, patients can have safe physical therapy programs that will aid in recovery without putting them at increased harm. Screening of patients should be done before initiation of physical therapy to ensure patient safety and precautions should be established to ensure adequate flow with hip flexion in patients with femoral cannulas.87

A core principle of “respiratory” ECMO is prevention of further lung injury. While light sedation allows for work with physical therapy and more interactions with family and staff, many patients on VV ECMO will require increased sedation to prevent ventilator-induced lung injury (VILI). Respiratory management of patients on VA and VV ECMO are often different due to the etiology requiring ECMO. In patients with respiratory failure, the goal is to allow maximum lung rest and recovery while utilizing ECMO for gas exchange. Traditionally this has meant the use of proning, sedation, paralysis, and lung protective ventilation. Use of extracorporeal carbon dioxide removal (ECCO2R) now allows for sedated patients to achieve ultra-low tidal volumes (less than 4 cc/kg of ideal body weight), maximizing lung protection.88 While there is conflicting evidence supporting use of the ultra-low tidal volumes in ARDS with ECMO, it appears there may be a benefit to allow maximum lung rest with low driving pressures, minimizing respiratory rate, while allowing gas exchange to occur through the circuit.89,90 Ventilator strategies for patients who have a cardiogenic shock on VA ECMO may not call for lung volumes as low as those used in VV ECMO, although these patients are also at high-risk for developing ARDS. Standard tidal volumes for 6-8 cc/kg are recommended along with a relatively modest positive end-expiratory pressure (PEEP), around 10 cmH2O. These settings must be adjusted to optimize preload and afterload so the native heart can continue to function without excess oxygen demand.

In patients who fail to liberate from the ventilator, the decision to perform a tracheotomy while on ECMO is an important step in their management. Traditionally, patients on ECMO would have the tracheotomy performed in the operating room. Using the operating room requires additional manpower and resources to move a patient on ECMO while placing them at risk for an adverse event during transport. ICU bedside tracheotomy has advantages and can be performed safely. Percutaneous dilatational tracheotomy (PDT) techniques facilitate placement of a tracheotomy at the bedside.91 Bleeding, tracheal injury, and esophageal injury are possible complications of tracheotomy that must be weighed against the potential benefits of less sedation, easier communication, better oral care, and potential for lower rates of pneumonia.92 Between an open tracheotomy and a PDT procedure, there appears to be no difference in rate of significant bleeding or adverse events.93 Bleeding may be from a number of factors, including anticoagulation use, thrombocytopenia, hypofibrinogenemia, and platelet dysfunction. The incidence of major bleeding after tracheotomy varies significantly depending on patient population, type of procedure, and preoperative anticoagulation management, and ranges from 8% to 43%.94,95

Discontinuation of ECMO

Liberation from VV ECMO is usually on the guidance of expert opinion rather than true guidelines. Institutions vary in practices for when and how they decide to taper support. Timing of when to start liberation trials is based on when lung recovery begins to occur. One method is to compare tidal volumes on the ventilator while using the same driving pressures. As the tidal volumes increase, the CO2 will begin to fall. Decrease in CO2 should prompt an adjustment in the blender to decrease the sweep gas flow to maintain a normal pH. During this time, frequent arterial blood gas measurements ensure that the patient does not have a respiratory alkalosis or acidosis. With VV ECMO, there is little utility in decreasing the flows on the circuit since the gas exchange will mostly be determined by makeup of sweep gas from the blender.96 When using lung protective ventilation settings, ventilator adjustments should be made to improve gas exchange while maintaining protective ventilation parameters, such as low driving pressures. If adequate oxygenation and ventilation can be maintained utilizing lung protective ventilation strategies with minimal circuit contribution to gas exchange, the patient is ready for decannulation from ECMO. Instead of tapering ECMO respiratory support, some patients on VV ECMO may be able to liberate from the ventilator. After initiation of ECMO and stability has been achieved, sedation should be decreased to facilitate spontaneous breathing trials. Care must be taken to ensure that the patient’s respiratory efforts are not inducing VILI. Support in the form of increasing sweep gas flow can be used to support gas exchange during the breathing trials. If the patient is able to meet criteria for extubation while on ECMO support, they are ready for a trial of extubation. There are multiple benefits to extubation, including lower rates of pneumonia, easier communication, less sedation, and increased ability to work with physical therapy. While specific recommendations do not exist for VV ECMO liberation, a protocol can be created with a multi-disciplinary team to ensure common goals, procedural expectations, and contingencies when patients are liberated.

Liberation from VA ECMO encompasses a more involved look at not just elements of gas exchange, but also evaluation of hemodynamics, end-organ perfusion, and patient cooperation. As with VV ECMO liberation, there are no formal guidelines for how to taper VA ECMO support. Common criteria that are assessed to see if a patient is acceptable for liberation include arterial line pulsatility, signs of ventricular recovery on echocardiography, stable low levels of inotropes, low-dose pressors to maintain MAP >65 mm Hg, and sufficient end-organ perfusion by the native heart. There are no specific hemodynamic targets, but generally include the cardiac index should be >2 L/min/m2, the central venous pressure be ~8 to 12 mm Hg, the pulmonary capillary wedge pressure be less than 18 mm Hg, and demonstration of a normal lactate and stable signs of end-organ perfusion, including liver function tests and creatinine. If these targets can be met, decreasing flows through the ECMO circuit and monitoring indices of perfusion is a standard method. One technique is to place the patient on flows of 2 L/min for 8 hours to look for stability. After that time, flows can be dropped by 0.5 L/min every few hours to a goal a flow of 1 L/min. If the patient remains hemodynamically stable at 1 L/min for a short period of time, flows will be turned up to 2 L/min to prevent circuit clotting and preparations can be made for decannulation. It is important to not keep flows at low values for extended periods due to risk of thrombosis. Arterial blood gas results should be checked frequently during this tapering period to look for poor gas exchange or acidosis from hypoperfusion. Use of echocardiography during tapering is important to monitor patient’s cardiac status in real-time. Cardiac function monitoring is much more important when decreasing VA ECMO than VV ECMO support. In cases where a patient has a device such as an Impella or IABP in place to help with LV venting, it is usually beneficial to discontinue ECMO first and maintain additional MCS so that afterload can be reduced. This order can be modified depending on the clinical situation.


MCS in the ICU has directly and indirectly led to improvements in multiple components of ICU care. Respiratory and circulatory support allow patients to be sedated less, mobilized, and strengthened. Advances in devices and techniques are improving outcomes and reducing complications. Recent experience with the SARS-2 coronovirus pandemic suggest respiratory ECMO support is now a standard in carefully selected patients.97 MCS devices sustain patients with more severe pathophysiology and facilitate corrective procedures that can salvage formerly irrecoverable states, such as cardiogenic shock. These therapies underscore the constantly innovative evolving nature of critical care. Most importantly, they underscore the importance of an interdisciplinary service for improving patient outcomes.

Conflict of interest disclosure

The authors declare that they have nothing to disclose.


1. Gibbon J. Artificial maintenance of circulation during experimental occlusion of pulmonary artery. Arch Surg. 1937;34:1105–1131.
2. Kolobow T. The promise of the membrane artificial lung. Int J Artif Organs. 1978;1:15–20.
3. Hill JD, O’Brien TG, Murray JJ, et al. Prolonged extracorporeal oxygenation for acute post-traumatic respiratory failure (shock-lung syndrome). Use of the Bramson membrane lung. N Engl J Med. 1972;286:629–634.
4. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet. 2009;374:1351–1363.
5. Australia and New Zealand Extracorporeal Membrane Oxygenation (ANZ ECMO) Influenza Investigators, Davies A, Jones D, Bailey M, et al. Extracorporeal Membrane Oxygenation for 2009 Influenza A(H1N1) Acute Respiratory Distress Syndrome. JAMA. 2009;302:1888–1895.
6. Freed DH, Henzler D, White CW, et al. Extracorporeal lung support for patients who had severe respiratory failure secondary to influenza A (H1N1) 2009 infection in Canada. Can J Anaesth. 2010;57:240–247.
7. Combes A, Hajage D, Capellier G, et al. Extracorporeal membrane oxygenation for severe acute respiratory distress syndrome. N Engl J Med. 2018;378:1965–1975.
8. Chaves RCF, Rabello Filho R, Timenetsky KT, et al. Extracorporeal membrane oxygenation: a literature review. Rev Bras Ter Intensiva. 2019;31:410.
9. Chung M, Shiloh AL, Carlese A. Monitoring of the adult patient on venoarterial extracorporeal membrane oxygenation. ScientificWorldJournal. 2014;2014:393258.
10. Jayaraman AL, Shah P, Ramakrishna H. Cannulation strategies in adult veno-arterial and veno-venous extracorporeal membrane oxygenation: techniques, limitations, and special considerations. Ann Card Anesth. 2017;20:S11–S18.
11. Rupprecht L, Flörchinger B, Schopka S, et al. Cardiac decompression on extracorporeal life support: A review and discussion of the literature. ASAIO J. 2013;59:547–553.
12. Wrisinger WC, Thompson SL. Basics of extracorporeal membrane oxygenation. Surg Clin North Am. 2022;102:23–35.
13. Brodie D, Bacchetta M. Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011;365:1905–1914.
14. Colombier S, Prêtre R, Iafrate M, et al. Double-stage venous cannulation combined with Avalon® cannula for potential prolongation of respiratory ECMO in end-stage pulmonary disease. Perfusion. 2016;31:593–597.
15. Biran R, Pond D. Heparin coatings for improving blood compatibility of medical devices. Adv Drug Deliv Rev. 2017;112:12–23.
16. Wendel HP, Ziemer G. Coating-techniques to improve the hemocompatibility of artificial devices used for extracorporeal circulation. Eur J Cardiothorac Surg. 1999;16:342–350.
17. Steinlechner B, Kargl G, Schlömmer C, et al. Can heparin-coated ECMO cannulas induce thrombocytopenia in COVID-19 patients? Case Reports Immunol. 2021;2021:6624682.
18. Kohler K, Valchanov K, Nias G, et al. ECMO cannula review. Perfusion. 2013;28:114–124.
19. Tanaka M, Motomura T, Kawada M, et al. Blood compatible aspects of poly (2-methoxyethylacrylate) (PMEA)—relationship between protein adsorption and platelet adhesion on PMEA surface. Biomaterials. 2000;21:1471–1481.
20. Saito N, Motoyama S, Sawamoto J. Effects of new polymer-coated extracorporeal circuits on biocompatibility during cardiopulmonary bypass. Artif Organs. 2000;24:547–554.
21. Abrams D, Bacchetta M, Brodie D. Recirculation in venovenous extracorporeal membrane oxygenation. ASAIO J. 2015;61:115–121.
22. Rich PB, Awad SS, Crotti S, et al. A prospective comparison of atrio-femoral and femoro-atrial flow in adult venovenous extracorporeal life support. J Thorac Cardiovasc Surg. 1998;116:628–632.
23. Banfi C, Pozzi M, Siegenthaler N, et al. Veno-venous extracorporeal membrane oxygenation: cannulation techniques. J Thorac Dis. 2016;8:3762–3773.
24. Kim J, Cho Y, Sung K, et al. Impact of cannula size on clinical outcomes in peripheral venoarterial extracorporeal membrane oxygenation. ASAIO J. 2019;65:573–579.
25. Werdan K, Gielen S, Ebelt H, et al. Mechanical circulatory support in cardiogenic shock. Eur Heart J. 2014;35:156–167.
26. Shaheen A, Tanaka D, Cavarocchi NC, et al. Veno-venous extracorporeal membrane oxygenation (V V ECMO): indications, preprocedural considerations, and technique. J Card Surg. 2016;31:248–252.
27. Romagnoli S, Zagli G, Ricci Z, et al. Cardiac output: a central issue in patients with respiratory extracorporeal support. Perfusion. 2017;32:44–49.
28. Takayama H, Landes E, Truby L, et al. Feasibility of smaller arterial cannulas in venoarterial extracorporeal membrane oxygenation. J Thorac Cardiovasc Surg. 2015;149:1428–1433.
29. Extracorporeal Life Support Organization. ECLS Registry Report, International Summary. Ann Arbor, MI: Extracorporeal Life Support Organization; 2019:1–37.
30. Masuzawa T, Onuma H, Kim S, et al. Magnetically suspended centrifugal blood pump with a self bearing motor. ASAIO J. 2002;48:437–442.
31. Lawson S, Ellis C, Butler K, et al. Neonatal extracorporeal membrane oxygenation devices, techniques and team roles: 2011 survey results of the United States’ Extracorporeal Life Support Organization centers. J ExtraCorp Technol. 2011;43:236–244.
32. Palanzo D, Qui F, Baer L, et al. Evolution of the extracorporeal life support circuitry. Artificial Organs. 2010;34:869–873.
33. Kurusz M, Christman EW, Williams EH, et al. Roller pump induced tubing wear: another argument in favor of arterial line filtration. J ExtraCorp Technol. 1980;12:49–59.
34. Brogan TV. ECMO Specialist Training Manual , 4th ed. Ann Arbor, MI: Extracorporeal Life Support Organization.
35. Peek GJ, Killer HM, Reeves R, et al. Early experience with a polymethyl pentene oxygenator for adult extracorporeal life support. ASAIO J. 2002;48:480–482.
36. Khoshbin E, Roberts N, Harvey C, et al. Poly-methyl pentene oxygenators have improved gas exchange capability and reduced transfusion requirements in adult extracorporeal membrane oxygenation. ASAIO J. 2005;51:281–287.
37. Khoshbin E, Dux AE, Killer H, et al. A comparison of radiographic signs of pulmonary inflammation during ECMO between silicon and poly-methyl pentene oxygenators. Perfusion. 2007;22:15–21.
38. Sidebotham D. Troubleshooting adult ECMO. J Extra Corpor Technol. 2011;43:P27–P32.
39. Lequier L, Horton SB, McMullan DM, Bartlett RH. Extracorporeal membrane oxygenation circuitry. Pediatr Crit Care Med. 2013;14(suppl 1):S7–S12.
40. Blomback M, Kronlund P, Aberg B, et al. Pathologic Fibrin formation and cold-induced clotting of membrane oxygenators during cardiopulmonary bypass. J Cardiothorac Vasc Anaesth. 1995;9:34–43.
41. Lubnow M, Philipp A, Dornia C, et al. D-dimers as an early marker for oxygenator exchange in extracorporeal membrane oxygenation. J Crit Care. 2014;29:473.e1–473.e4735.
42. Dornia C, Philipp A, Bauer S, et al. D-dimers are a predictor of clot volume inside membrane oxygenators during extracorporeal membrane oxygenation. Artif Organs. 2015;39:782–787.
43. Basken R, Cosgrove R, Malo J, et al. Predictors of oxygenator exchange in patients receiving extracorporeal membrane oxygenation. J Extra Corpor Technol. 2019;51:61–66.
44. Keebler ME, Haddad EV, Choi CW, et al. Venoarterial extracorporeal membrane oxygenation in cardiogenic shock. JACC Heart Fail. 2018;6:503–516.
45. Kilgannon JH, Jones AE, Parrillo JE, et al. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation. 2011;123:2717–2722.
46. Sznycer-Taub NR, Lowery R, Yu S, et al. Hyperoxia is associated with poor outcomes in pediatric cardiac patients supported on venoarterial extracorporeal membrane oxygenation. Pediatr Crit Care Med. 2016;17:350–358.
47. Hoeper MM, Tudorache I, Kühn C, et al. Extracorporeal membrane oxygenation watershed. Circulation. 2014;130:864–865.
48. Tsangaris A, Alexy T, Kalra R, et al. Overview of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) support for the management of cardiogenic shock. Front Cardiovasc Med. 2021;8:686558.
49. Rao P, Khalpey Z, Smith R, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest. Circ Heart Fail. 2018;11:e004905.
50. Cakici M, Gumus F, Ozcinar E, et al. Controlled flow diversion in hybrid venoarterial-venous extracorporeal membrane oxygenation. Interact Cardiovasc Thorac Surg. 2018;26:112–118.
51. Hawkins JL. Membrane oxygenator heat exchanger failure detected by unique blood gas findings. J Extra Corpor Technol. 2014;46:91–93.
52. Hamilton C, Stein J, Seidler R, et al. Testing of heat exchangers in membrane oxygenators using air pressure. Perfusion. 2006;21:105–107.
53. Han L, Zhang Y, Zhang Y, et al. Risk factors for refractory septic shock treated with VA ECMO. Ann Transl Med. 2019;7:476.
54. Zwischenberger JB, Kirsh MM, Dechert RE, et al. Suppression of shivering decreases oxygen consumption and improves hemodynamic stability during postoperative rewarming. Ann Thorac Surg. 1987;43:428–431.
55. Mungan İ, Kazanci D, Bektas S, et al. Does lactate clearance prognosticates outcomes in ECMO therapy: a retrospective observational study. Bmc Anesthesiol. 2018;18:152.
56. Garcia-Alvarez M, Marik P, Bellomo R. Stress hyperlactataemia: present understanding and controversy. Lancet Diabetes Endocrinol. 2014;2:339–347.
57. Choi MS, Sung K, Cho YH. Clinical pearls of venoarterial extracorporeal membrane oxygenation for cardiogenic shock. Korean Circ J. 2019;49:657–677.
58. Hogue CW, Levine A, Hudson A, et al. Clinical applications of near-infrared spectroscopy monitoring in cardiovascular surgery. Anesthesiology. 2021;134:784–791.
59. Khan I, Rehan M, Parikh G, et al. Regional cerebral oximetry as an indicator of acute brain injury in adults undergoing veno-arterial extracorporeal membrane oxygenation—a prospective pilot study. Front Neurol. 2018;9:993.
60. Steffen RJ, Sale S, Anandamurthy B, et al. Using near-infrared spectroscopy to monitor lower extremities in patients on venoarterial extracorporeal membrane oxygenation. Ann Thorac Surg. 2014;98:1853–1854.
61. Douflé G, Roscoe A, Billia F, et al. Echocardiography for adult patients supported with extracorporeal membrane oxygenation. Crit Care. 2015;19:326.
62. Schrage B, Becher PM, Bernhardt A, et al. Left ventricular unloading is associated with lower mortality in patients with cardiogenic shock treated with venoarterial extracorporeal membrane oxygenation: results from an international, multicenter cohort study. Circulation. 2020;142:2095–2106.
63. Cheng A, Swartz MF, Massey HT. Impella to unload the left ventricle during peripheral extracorporeal membrane oxygenation. ASAIO J. 2013;59:533–536.
64. Cheng R, Hachamovitch R, Kittleson M, 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;97:610–616.
65. Jia D, Yang I, Ling R, et al. Vascular complications of extracorporeal membrane oxygenation: a systematic review and meta-regression analysis. Crit Care Med. 2020;48:e1269–e1277.
66. Makdisi G, Makdisi T, Wang IW. Use of distal perfusion in peripheral extracorporeal membrane oxygenation. Ann Transl Med. 2017;5:103.
67. Juo YY, Skancke M, Sanaiha Y, et al. Efficacy of distal perfusion cannulae in preventing limb ischemia during extracorporeal membrane oxygenation: a systematic review and meta-analysis. Artif Organs. 2017;41:E263–E273.
68. Rastan AJ, Lachmann N, Walther T, et al. Autopsy findings in patients on postcardiotomy extracorporeal membrane oxygenation (ECMO). Int J Artif Organs. 2006;29:1121–1131.
69. Seeliger B, Döbler M, Friedrich R, et al. Comparison of anticoagulation strategies for veno-venous ECMO support in acute respiratory failure. Crit Care. 2021;24:701.
70. Al-Jazairi A, Raslan S, Al-Mehizia R, et al. Performance assessment of a multifaceted unfractionated heparin dosing protocol in adult patients on extracorporeal membrane oxygenator. Ann Pharmacother. 2021;55:592–604.
71. Delmas C, Jacquemin A, Vardon-Bounes F, et al. Anticoagulation monitoring under ECMO support: a comparative study between the activated coagulation time and the anti-xa activity assay. J Intensive Care Med. 2020;35:679–686.
72. Kulig CE, Schomer KJ, Black HB, et al. Activated partial thromboplastin time versus anti-factor Xa monitoring of heparin anticoagulation in adult venoarterial extracorporeal membrane oxygenation patients. ASAIO J. 2021;67:411–415.
73. Arnouk S, Altshuler D, Lewis TC, et al. Evaluation of anti-Xa and activated partial thromboplastin time monitoring of heparin in adult patients receiving extracorporeal membrane oxygenation support. ASAIO J. 2020;66:300–306.
74. Aubron C, DePuydt J, Belon F, et al. Predictive factors of bleeding events in adults undergoing extracorporeal membrane oxygenation. Ann Intensive Care. 2016;6:97.
75. Greinacher A. Clinical practice. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373:252–261.
76. Koster A, Weng Y, Böttcher W, et al. Successful use of bivalirudin as anticoagulant for ECMO in a patient with acute HIT. Ann Thorac Surg. 2007;83:1865–1867.
77. Warkentin TE, Koster A. Bivalirudin: a review. Expert Opin Pharmacother. 2005;6:1349–1371.
78. Robson R. The use of bivalirudin in patients with renal impairment. J Invasive Cardiol. 2000;12(suppl):33–36.
79. Fisser C, Winkler M, Malfertheiner MV, et al. Argatroban versus heparin in patients without heparin-induced thrombocytopenia during venovenous extracorporeal membrane oxygenation: a propensity-score matched study. Crit Care. 2021;25:160.
80. Kurihara C, Walter JM, Karim A, et al. Feasibility of venovenous extracorporeal membrane oxygenation without systemic anticoagulation. Ann Thorac Surg. 2020;110:1209–1215.
81. Lorusso R, Barili F, Mauro MD, et al. In-hospital neurologic complications in adult patients undergoing venoarterial extracorporeal membrane oxygenation: results from the Extracorporeal Life Support Organization Registry. Crit Care Med. 2016;44:e964–e972.
82. Zangrillo A, Landoni G, Biondi-Zoccai G, et al. A meta-analysis of complications and mortality of extracorporeal membrane oxygenation. Crit Care Resusc. 2013;15:172–178.
83. Lorusso R, Gelsomino S, Parise O, et al. Neurologic injury in adults supported with veno-venous extracorporeal membrane oxygenation for respiratory failure: findings from the Extracorporeal Life Support Organization Database. Crit Care Med. 2017;45:1389–1397.
84. Extracorporeal Life Support Organization. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support Version 14. Ann Arbor, MI: Extracorporeal Life Support Organization; 2017.
85. Cheng V, Abdul-Aziz MH, Roberts JA, et al. Optimising drug dosing in patients receiving extracorporeal membrane oxygenation. J Thorac Dis. 2018;10(suppl 5):S629–S641.
86. Patel M, Altshuler D, Lewis TC, et al. Sedation requirements in patients on venovenous or venoarterial extracorporeal membrane oxygenation. Ann Pharmacother. 2020;54:122–130.
87. Wells CL, Forrester J, Vogel J, et al. Safety and feasibility of early physical therapy for patients on extracorporeal membrane oxygenator: University of Maryland Medical Center Experience. Crit Care Med. 2018;46:53–59.
88. Combes A, Fanelli V, Pham T, et al. European Society of Intensive Care Medicine Trials Group and the “Strategy of Ultra-Protective lung ventilation with Extracorporeal CO2 Removal for New-Onset moderate to severe ARDS” (SUPERNOVA) investigators. Feasibility and safety of extracorporeal CO2 removal to enhance protective ventilation in acute respiratory distress syndrome: the SUPERNOVA study. Intensive Care Med. 2019;45:592–600.
89. McNamee JJ, Gillies MA, Barrett NA, et al. Effect of lower tidal volume ventilation facilitated by extracorporeal carbon dioxide removal vs standard care ventilation on 90-day mortality in patients with acute hypoxemic respiratory failure: the REST Randomized Clinical Trial [published correction appears in JAMA. 2021;326:1013–1023.
90. Bein T, Weber-Carstens S, Goldmann A, et al. Lower tidal volume strategy (≈3 ml/kg) combined with extracorporeal CO2 removal versus “conventional” protective ventilation (6 mL/kg) in severe ARDS: the prospective randomized Xtravent-study. Intensive Care Med. 2013;39:847–856.
91. Ciaglia P, Firsching R, Syniec C. Elective percutaneous dilatational tracheostomy. A new simple bedside procedure; preliminary report. Chest. 1985;87:715–719.
92. Charlesworth M, Szentgyorgyi L, Ashworth AD, et al. Tracheostomy insertion during venovenous extracorporeal membrane oxygenation: do the benefits outweigh the risks? J Cardiothorac Vasc Anesth. 2018;32:e69–e70.
93. Salas De Armas IA, Dinh K, Akkanti B, et al. Tracheostomy while on extracorporeal membrane oxygenation: a comparison of percutaneous and open procedures. J Extra Corpor Technol. 2020;52:266–271.
94. Salna M, Tipograf Y, Liou P, et al. Tracheostomy is safe during extracorporeal membrane oxygenation support. ASAIO J. 2020;66:652–656.
95. Kruit N, Valchanov K, Blaudszun G, et al. Bleeding complications associated with percutaneous tracheostomy insertion in patients supported with venovenous extracorporeal membrane oxygen support: a 10-year institutional experience. J Cardiothorac Vasc Anesth. 2018;32:1162–1166.
96. Broman LM, Malfertheiner MV, Montisci A, et al. Weaning from veno-venous extracorporeal membrane oxygenation: how I do it. J Thorac Dis. 2018;10(suppl 5):S692–S697.
97. Kon ZN, Smith DE, Chang SH, et al. Extracorporeal membrane oxygenation support in severe COVID-19. Ann Thorac Surg. 2021;111:537–543.
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.