Ecmo

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"extracorporeal membrane oxygenation" AND outcomes

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Here is a thorough overview of ECMO drawn from authoritative textbook sources:

Extracorporeal Membrane Oxygenation (ECMO)

What Is ECMO?

ECMO (also called extracorporeal life support) is a form of prolonged cardiopulmonary bypass that oxygenates and removes CO2 from the blood outside the body, providing support when the heart and/or lungs fail. Its origins trace back to Gibbon's extracorporeal circuit first used successfully for open-heart surgery in 1953.
The basic circuit consists of:
  • An inflow cannula - drains blood from the patient
  • A centrifugal pump - maintains blood flow (magnetically levitated, preload-dependent, afterload-sensitive)
  • A membrane oxygenator - gas exchange surface (~2 m² vs. ~143 m² in the human lung)
  • An outflow cannula - returns oxygenated blood to the patient
  • A heat exchanger - prevents heat loss across the oxygenator
  • Continuous heparin infusion to prevent thrombosis
Basic ECMO circuit diagram
Basic ECMO circuit - Fishman's Pulmonary Diseases and Disorders

Two Main Types

1. Veno-Venous (VV) ECMO

  • Purpose: Lung support only
  • Cannulation: Venous drainage and venous return (e.g., femoral vein in, internal jugular vein out via dual-lumen cannula)
  • Indication: Severe acute respiratory failure (ARDS, pneumonia, bridging to lung transplant)
  • Advantage: Preserves native cardiac output; lower risk of limb ischemia
  • Limitation: Does not provide hemodynamic (cardiac) support

2. Veno-Arterial (VA) ECMO

  • Purpose: Heart AND lung support
  • Cannulation: Venous drainage (femoral/internal jugular), arterial return (femoral artery, or via subclavian graft)
  • Indications: Cardiogenic shock, cardiac arrest, refractory hypoxemia, bi-ventricular failure, myocarditis, myocardial stunning
  • Key concern: Can cause pulmonary edema and LV fluid overload because it bypasses the LV without unloading it. Often requires additional strategies: inotropes, vasodilators, IABP, or Impella to unload the LV
  • Bridges to recovery, VAD placement, or heart transplant

3. Hybrid Configurations

  • VAV ECMO and Oxygenated RVAD (Protek Duo): Used when RV failure accompanies respiratory failure (e.g., ARDS with cor pulmonale)

Indications

ConditionMode
Severe ARDS / acute respiratory failureVV ECMO
Bridge to lung transplantVV ECMO (awake, ambulatory preferred)
Cardiogenic shockVA ECMO
Refractory cardiac arrest (E-CPR)VA ECMO
Myocarditis / myocardial stunningVA ECMO
Biventricular failure + hypoxemiaVA or VAV ECMO
RV failure + ARDSOxygenated RVAD / VAV ECMO

Circuit Physiology & Key Parameters

  • To achieve adequate O2 delivery (~260 mL O2/min) with post-oxygenator PaO2 >300 mmHg, blood flow of ~4 L/min must be maintained
  • CO2 removal is efficient even at low flow rates (<1 L/min with high sweep gas)
  • Transmembrane pressure drop should not exceed 30 mmHg (inlet ~250 mmHg, outlet ~220 mmHg)
  • Tubing length/surface area matters: activates the inflammatory cascade, consumes clotting factors, and alters pharmacokinetics of antibiotics, opioids, and sedatives

Anticoagulation

Anticoagulation is required continuously to prevent circuit thrombosis:
AgentNotes
Unfractionated heparin (UFH)Most common; easy reversal, familiar monitoring (PTT/ACT); risks: heparin resistance, HIT
BivalirudinDirect thrombin inhibitor; lower HIT risk; renally cleared; t½ ~25 min; no FDA-approved reversal
ArgatrobanDirect thrombin inhibitor; hepatically cleared; t½ ~45-50 min
A single-center retrospective study found bivalirudin significantly reduced major bleeding events (11.7% vs. 40.7% with heparin) and decreased circuit thrombosis.

Complications

Hemorrhagic

  • Epistaxis, GI bleeding (most common)
  • Rare: intracranial hemorrhage, pulmonary hemorrhage
  • Mechanism: thrombocytopenia, platelet destruction, clotting factor consumption, anticoagulation

Thrombotic

  • Circuit thrombosis (clot in oxygenator or tubing)
  • Arterial embolism (especially with VA ECMO)

Hemodynamic (VA ECMO specific)

  • LV distension and pulmonary edema (LV cannot eject against the increased afterload from arterial return)
  • North-South syndrome (mixing of deoxygenated native LV output with oxygenated ECMO return)

Circuit/Technical

  • Pneumothorax and arterial injury during cannulation
  • Hemopericardium from guidewire cardiac injury
  • Air embolism (especially with awake VV ECMO cannulation)
  • Hemolysis (increases exponentially if a second extracorporeal circuit, e.g., CRRT, is added)
  • Oxygenator failure (monitor by pressure drop and post-membrane gas values)

Systemic

  • Inflammatory cascade activation (cytokine storm)
  • Altered drug pharmacokinetics (sequesters antibiotics, sedatives, opioids in tubing)
  • Acute kidney injury requiring CRRT (associated with OR 6.5 for in-hospital mortality)

Monitoring & Imaging

  • TEE (Transesophageal echocardiography): Before and during cannulation to assess RV/LV function, detect PFO/ASD/VSD, rule out pericardial effusion, guide cannula tip position
  • Fluoroscopy: Guides stiff wire and cannula placement
  • Ultrasound: Linear surface ultrasound for percutaneous vascular access
  • Pre/post-membrane pressure sensors + flow monitoring: Continuous circuit surveillance; transmembrane pressure >30 mmHg signals oxygenator failure

Bridge Strategies

GoalNotes
Bridge to recoveryDays to weeks; heart/lungs recover; device removed
Bridge to VADTransition to durable LVAD or BiVAD when no cardiac recovery
Bridge to transplantVV ECMO as bridge to lung transplant (5% of lung transplants as of 2017, rising); awake ambulatory preferred to avoid ventilator-induced injury
Lung transplant outcomes with VV ECMO bridge: 88% survival to discharge were alive at 1 year; 83% alive at 5 years (Tipograf et al., n=70 successfully transplanted).

Limitations

  • VA ECMO does not compensate for severely impaired LV function and may worsen pulmonary congestion
  • Not a permanent solution; prone to infection and complications with prolonged use
  • Highly institution-dependent: deployment, monitoring, and troubleshooting require dedicated, experienced teams
  • Large prime volume causes acute hemodilution at initiation
  • Allosensitization risk if blood-primed in pre-transplant patients

Recent Evidence


Sources: Fishman's Pulmonary Diseases and Disorders (Chapter 149, pp. 2641-2660); Fischer's Mastery of Surgery 8th ed. (pp. 345-346)
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