Critical Care Section Newsroom
December 10, 2025

Immediate Post-ECPR Management Strategies for the Emergency Physician

Ella Purington, MD
Chief Resident, University of Michigan Department of Emergency Medicine

Extracorporeal cardiopulmonary resuscitation (ECPR) – or, the application of veno-arterial extracorporeal membrane oxygenation (VA ECMO) to a patient with active or recent cardiac arrest –  has been shown to improve outcomes in select patients suffering OHCA refractory to conventional cardiopulmonary resuscitation (CPR), and is increasingly utilized in the emergency department (ED) setting .1-3 The goals of post-resuscitation management for patients who receive ECPR are similar to those for patients who have been resuscitated using conventional CPR, with the added factors of major post-cardiac arrest syndrome due to longer low flow durations, VA ECMO support, and associated possible complications.4-6 After initiation of VA ECMO, ED providers should focus on identifying and treating the precipitating cause of the cardiac arrest, maintaining adequate end-organ perfusion, optimizing oxygen delivery, and preventing the cardiac and noncardiac complications associated with VA ECMO.

Post-resuscitation management of ECPR patients begins once adequate VA ECMO flow has been initiated. Chest compressions should be discontinued once on circuit. When at all possible right radial arterial access should be obtained, to allow continuous hemodynamic monitoring and assessment of cerebral oxygenation and carbon dioxide management. An arterial blood gas from the right upper extremity is necessary to ensure adequate oxygenation while minimizing hyperoxia.7,8 If this is not able to be quickly achieved in the ED, a pulse oximetry device on the right hand is a good temporary substitute. Proper location and depth of the ECMO cannulas should be evaluated via imaging (e.g. x-ray, ultrasound). The tip of the drainage (venous) cannula should be located at the junction of the inferior vena cava and right atrium and the tip of the return (arterial) cannula located within the lower aorta or iliac artery. Proper securement of the ECMO cannulas should be confirmed and insertion sites should be evaluated for any immediate complications prior to application of sterile dressings.

Circulation

Following initiation of ECPR, the RPMs of the circuit can be increased to meet the needs of the patient. While clinical scenarios vary, generally aiming for ECMO blood flow of > 3 L/min.9,10 V-AECMO flow should be titrated to maintain a central venous oxygenation greater than 65% and a mean arterial pressure of > 65 mmHg.  Once adequate V-A ECMO flows are achieved, mean arterial pressure (MAP) should be optimized to balance adequate end organ perfusion and cardiac/circuit afterload (target MAP 65 - 80 mmHg).11 If adequate MAP is not able to be immediately achieved through VA ECMO support alone, vasopressors may be added. Norepinephrine is often considered the first-line vasopressor in ECPR patients given the balanced vasoconstrictive effects and minimal arrhythmogenic potential.6,12 One of the most common early complications post-ECPR, drainage insufficiency is a mismatch between the negative pressure in the drainage cannula and the supplied preload from the surrounding central vein, which may occur as a result of inadequate preload or excessively negative drainage pressures. It can frequently be seen as “chugging” or movement of the ECMO tubing. If chugging is encountered, or venous pressure alarms are less than -100 mmHg (when Pven measurements are available), the volume status of the patient should be evaluated and the circuit thoroughly assessed. Many etiologies can be rapidly diagnosed at the bedside with an ultrasound. Finally, during ECPR cannulation patients often receive a bolus of heparin (5,000 – 10,000 units) based on local protocols. In the absence of bleeding, an activated partial thromboplastin time (aPTT) of 50 – 70 seconds (2 – 2.5 times the midpoint of the normal range) is often the goal of ECPR patients immediately post-cannulation.13

Airway and Ventilation

Endotracheal intubation should be a priority across systems of care as recommended by the 2020 AHA guidelines for out of hospital cardiac arrest (OHCA).14 However, initiation of ECPR initiation should not be delayed for intubation and may occur in parallel. Lung-protective ventilation, utilizing a low tidal volume strategy (6-8 mL/kg), is recommended given the high prevalence of acute respiratory distress syndrome (ARDS) in patients suffering OHCA.15 A high positive end expiratory pressure (PEEP) strategy, beginning with at least 10 cm H2O, is advised by some for patients supported by VA ECMO due to the risk of hydrostatic pulmonary edema and the salutary hemodynamic effects of offloading the left ventricle.16 The fraction of supplied O2 (FsO2) through the ECMO circuit should be titrated to a peripheral arterial oxygen saturation (SpO2) goal of 92-97%. PaO2 should be kept < 300 mmHg as hyperoxemia has been inversely associated with survival and positive neurologic outcomes in ECPR patients.8-10 A PaCO2 goal of 35-45 mmHg should be targeted on the patient’s ABG, and the sweep of the ECMO circuit adjusted accordingly. While hypercapnia in and of itself has not been significantly associated with adverse outcomes, a large change in PaCO2 immediately following cannulation has been linked with decreased survival.8

Ventricular Arrhythmia Management

Successful defibrillation of shockable rhythms increases after ECPR initiation due to improved coronary perfusion pressure and oxygen delivery.17 For refractory ventricular arrhythmias, double sequential defibrillation and vector change may be considered.18,19 While the literature on the management of ventricular arrhythmias in the ECPR population is limited, aggressive medical management utilizing antiarrhythmics such as amiodarone and lidocaine should be pursued. For all arrhythmias, established standards of care for OHCA patients are recommended, which include treatment of reversible causes, optimization of electrolytes, and continuous cardiac monitoring.20 Once the patient returns to an organized rhythm, an electrocardiogram should be obtained to evaluate for ST-segment elevation myocardial infarction, occlusion myocardial infarction, and other intervenable abnormalities.

Temperature Control Strategy

Evidence for temperature control strategy (TCS) in ECPR patients is mixed. A meta-analysis of randomized and observational studies failed to show a significant difference in mortality or survival with good neurologic outcome for ECPR patients treated with TCS.21 However, among ECPR patients receiving  TCS in a retrospective analysis of the ELSO database, achieving a temperature of 34–36 °C for 12 to 48 hours was associated with lower in-hospital mortality and improved neurologic survival.22,23 Non-ECMO centers should avoid actively rewarming patients with mild hypothermia (>32°C) after resuscitation during the first 48 hours of the post-ECPR period. Slow rewarming by the ECMO circuit may be considered for ECPR patients with moderate (28 - 32°C) to profound (<28°C) hypothermia. Hyperthermia should be avoided.

Sedation and analgesia

The ECMO circuit alters the pharmacokinetics and volume of distribution of many medications, resulting in an increased sedation requirement.24-26 Additionally, the circuit can sequester drugs, making some medications more effective than others. ECPR patients may require higher levels of sedation and analgesia to optimize cardiopulmonary support and decrease metabolic demand.25 Hydromorphone is a frequent analgesic used for VA ECMO support secondary to its limited sequestration, whereas there is evidence that fentanyl and propofol may be sequestered and potentially less effective.25-29 It is important that short-acting sedatives are used at the lowest effective dose to facilitate rapid weaning and accurate neuroprognostication during post-cardiac arrest care.

VA ECMO Troubleshooting Checklist

Drainage insufficiency

A mismatch between the negative pressure in the drainage cannula and the supplied preload from the surrounding central vein, which may occur as a result of inadequate preload or excessively negative drainage pressures; often results in “chugging” or temporary loss of ability to flow

  • Goal pVen > -80 mmH
    • Consider reducing ECMO flow if patient will tolerate
    • Give volume
  • Chatter/Chugging or Loss of Flow
    • Decrease RPM until able to flow
    • Give intravenous bolus of fluid
    • Prepare to support patient with vasoactive agents, ventilator, volume
    • Slowly increase RPM until back to goal flow
    • Search for cause:
      • Circuit obstruction (kinked drainage lines)
      • Increased intrathoracic/abdominal pressure (PTX, HTX, tamponade, gastric distension, frequent coughing/baring down, agitation)
      • Bleeding
      • Displaced drainage cannula

Left Ventricular Overload

Peripheral ECMO theoretically increases LV afterload due to retrograde flow in the aorta, which may result in increased LV end diastolic pressure and LV distension.
  • Goal LVEDD
    • Males: 4.2-5.9 cm
    • Females: 3.9-5.0 cm
  • Consider initiation of dobutamine or epinephrine, aim for a pulse pressure >10 – 15 mmHg
  • May need additional mechanical circulatory for LV offloading (e.g., Impella device)
    • Alert receiving hospital of concerns for LV overload

Bleeding

The most common complication of ECPR following OHCA, occurring in 30% of all patients. Cannula insertion sites are the most common sources of bleeding, but retroperitoneal, intraabdominal, and mediastinal sources should also be considered.

  • Signs of hemorrhagic shock in ECPR patient
    • Hypotension
    • Tachycardia
    • Decreased flow
    • Chatter of ECMO circuit
  • Management of bleeding
    • Direct pressure or hemostatic dressing at cannulation site
    • Transfusion of blood products (goal 7-8 u/L)
    • Platelet goal >50k if concerns for bleeding
    • Fibrinogen goal > 100
    • Tranexamic acid can be considered for severe bleeding

Differential Oxygenation

This can develop in peripherally cannulated patients when a functioning LV ejects poorly oxygenated blood into the ascending aorta, where it mixes with retrograde flow of well oxygenated blood from the ECMO circuit. The creation of dual circulation can lead to hypoxemic blood entering proximal vessels on the aortic arch.
  • Identified with pulse oximetry being measured as proximal off the aortic arch
    • R arm > R ear lobe > forehead
  • Goal: optimize blood flow and blood oxygenation through pulmonary bed
    • Optimize MAP
    • Consider increasing ECMO flow
    • Decreasing inotropes
    • Decrease LV offloading device support if able
    • Increase PEEP
  • Weaning inotropes/LV offloading devices can lead to LV distension

Pump Failure

This can occur for several reasons including power loss, clot formation, air embolism, or decoupling of the centrifugal pump.
  • Transition to hand crank to provide ECMO flow
  • May need to increase vasopressor and ventilator support
  • May need to switch out staff during hand cranking

Unintentional Decannulation

This is the most feared complication with ECMO and can result in rapid patient deterioration and death.  Transfer of patients is a high-risk period, when the cannulas are at risk of becoming dislodged during frequent movements.

  • One provider should be designated for monitoring cannulas during transfer
  • “Off ECMO” is called when dislodged
    • Clamp both return and drainage limbs
    • Immediate hemorrhage control
    • Pharmacologic support (vasopressor and inotropy support)
    • Escalate ventilator support
    • Blood and/or volume transfusion

Sources:

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