The V-A ECMO Ward Round

Author: Emma King
Peer reviewers: Jessica Wang, Chris Nickson

Everything ECMO 022

 A 56-year-old man is on peripheral V-A ECMO following an out of hospital cardiac arrest 2 days ago.

His supports are:

  • ECMO: Blood flow 4 L/min with 2995 rpm, fresh gas flow (FGF) 3 L/min.
  • Inotropes: milrinone 15 mcg/min, adrenaline 1 mcg/min and noradrenaline 14 mcg/min to maintain a blood pressure of 68/62 mmHg (MAP 64 mmHg).

He remains ventilated with tidal volumes of 400mls, RR 12, PEEP 15 and FiO2 0.6. His oxygen saturation in his right hand is 98% and his lactate is 1.2. His end-tidal CO2 is 10. He is warm and well perfused on examination. He is on continuous renal replacement therapy (CRRT) for acute kidney injury.

Q1. You are doing your morning ward round. What are the main ECMO related questions that you need to ask?

Is he adequately supported?

  • Is the ECMO flow adequate?
  • Is his native circulation optimised?

Have complications developed?

  • Does he have any patient-related complications?
  • Have any ECMO circuit related complications developed?

How do we move forward?

  • Can we remove any supports?
    • Is he ready for the ECMO to be weaned?
    • Can he be extubated?
  • What is the overall plan?
    • Is ECMO being used as a bridge to recovery, or a bridge to VAD/transplant?
    • Is he deteriorating and palliation is required?

Q2. How do you assess if the patient is adequately supported?

There are two things to consider: the ECMO circuit and the patient’s native circulation.

The ECMO circuit

Inadequate ECMO flow results in a shocked patient.  Excessive ECMO flow will lead to complications such as raised left ventricular (LV) afterload and haemolysis due to high pump speeds.

It is important to assess for signs of adequate patient perfusion:

  • Is the MAP within target?
    • > 60 mmHg is a typical goal. MAPs exceeding 80 will lead to complications from increased LV afterload and will make it difficult to achieve adequate ECMO flow due to increased impedance in the circuit.
  • Is there evidence of organ hypoperfusion?
    • Is the lactate within normal range?
    • If renal failure is not an issue, is the urine output adequate?
    • Is the skin cold, blue or mottled?
    • If the patient is extubated – is conscious state normal?

The native circulation

If there is little to no native cardiac output this may lead to:

  • LV stasis, resulting in LV thrombus
  • LV distension, preventing myocardial recovery and reducing coronary perfusion pressure
  • Worsening of pre-existing aortic regurgitation (as blood is being “pushed” back into the heart by the ECMO circuit), leading to LV distension
  • Increased left atrial LA pressures resulting in pulmonary oedema.

If the native cardiac output is too high:

  • ECMO may not be providing an opportunity for myocardial rest and recovery
  • High inotrope requirements may lead to complications, such as digit necrosis
  • Differential hypoxia may develop if there is co-existing lung pathology (see Everything ECMO 007: What is different about hypoxia on V-A ECMO).

Ensuring the native circulation is optimized can be a balancing act. Daily checks include:

  • Reviewing the inotrope requirement
    • The least amount possible to ensure some pulsatility and minimise the risk of complications
  • Ensuring the risk of LV stasis and distension is reduced
    • Look for pulsatility on the arterial trace
    • Echo assessment of LV dimensions and valvular regurgitation can be essential in guiding management.
  • Ensuring the pre-load to the RV and the LV is optimized

Q3. Do you think this patient is adequately supported?

Yes. His examination and investigation are consistent with adequate perfusion. There is pulsatility present suggesting a small amount of native cardiac output.

Q4. What patient-related complications can develop on ECMO?


  • This is a common complication. Consider all sources including devices (e.g., IABP) and the ECMO circuit. These are nosocomial infections that should be covered broadly and may include pathogens such as yeast, and may not be resolved until decannulation and removal of ECMO occurs.


  • Patients are typically anticoagulated whilst on ECMO support unless bleeding complications are present.
  • Bleeding may be a particular issue in V-A ECMO with dual antiplatelet use.
  • Check for bleeding around the cannulae sites or other lines
  • Other sources of bleeding include retroperitoneal, intrathoracic or intra-abdominal
    • Difficult femoral cannulation and thoracic procedures (such as chest drain insertion) make this more likely
    • Trauma from CPR (e.g., liver/spleen lacerations) may also be a source of bleeding
  • This may be due to problems with the clotting mechanism
    • Thrombocytopenia
    • Disseminated intravascular coagulation
    • Hyperfibrinolysis and acquired von Willebrand syndrome (see below)

Pulmonary oedema

  • LV distension due to LV stasis or aortic regurgitation will lead to increased LA pressure and result in pulmonary oedema. If significant aortic regurgitation is present this complication may be fatal.


  • Signs include reducing pulsatility, rising CVP and access insufficiency

Thrombus (in the patient)

  • LV thrombus, arterial thrombus or DVT/PE.
  • If heparin-induced thrombotic thrombocytopenia (HITT) is a concern, an alternative anticoagulation agent will need to be considered (see Everything ECMO 016: Holy HITTS!)

Differential hypoxia

Problems with limb perfusion

  • Hyperperfusion may occur if both the access and return cannula are in the same limb. The venous outflow will be partially obstructed and unable to cope with the high blood flow received into the leg via the backflow cannula
  • Hypoperfusion may occur in the leg with the return cannula if there are problems with the backflow cannula
    • Monitoring of Doppler pulses is essential

Neurological complications

  • These include: delirium, coma, cerebrovascular accident, intracerebral haemorrhage

Renal failure

  • Consider a relatively low threshold to start renal replacement therapy for fluid management

Multiorgan failure

  • Particularly if V-A ECMO support was commenced relatively late, multiorgan failure may result in an unsupportable patient. 

Q5. What ECMO circuit complications can develop?

It is important to assess the whole circuit (cannulae, tubing, pump, oxygenator) in addition to considering the effect on the patient.

ECMO complications related to the circuit include:

  • Access insufficiency
    • see Everything ECMO 003
    • Signs include kicking of the access line, dropping and fluctuating ECMO blood flow rates, and increasingly negative access pressures (if using the HLS console)
    • Haemolysis may occur as a consequence
  • Thrombus
    • Most patients are anticoagulated with unfractionated heparin, but may have factors that prevent therapeutic levels being achieved.
    • Pump head thrombosis (change circuit urgently)
      • There may be noise or white fibrin deposit in the pump head
    • Oxygenator thrombosis
      • Clots may be visible in the oxygenator (more prominent on the proximal side)
      • As the oxygenator fails the transmembrane pressure gradient will increase and the function will decrease (seen as a low PaO2 on the post oxygenator gas). (**worth having a diagram/picture here to illustrate transmembrane gradient?)
      • Circuit change should occur if:
        • The transmembrane pressure is >10 mmHg / litre of ECMO blood flow or >50 mmHg in total. Note that while these are the maximum acceptable values although they are usually much less than this.
        • The post oxygenator gas PaO2 is < 200 mmHg
      • Patient trajectory should also be taken into account and circuit change may be required before these values are achieved
    • Clots developing in the cannulae, circuit, or backflow tubing should be aspirated or the circuit should be changed
  • Haemolysis
    • see Everything ECMO 004 and LITFL CCC – Haemolytic Anaemia
    • Daily attention to signs of haemolysis can help detect problems early
      • Plasma free Hb > 0.1 g/dL, elevated bilirubin, LDH and K+, dark urine or red effluent in patients on CRRT
    • Treatment of significant ECMO related haemolysis is to treat the cause
  • Bleeding
    • Circuit driven fibrinolysis (see Everything ECMO 012)
      • This results in increased bleeding associated with rising D-dimers, fibrinogen <1.5 g/L, and stable or decreasing platelet levels
    • Over anticoagulation
    • Acquired von Willebrand syndrome
  • Cannulae and tubing
    • Check the cannulae for malposition
      • Make sure the position of the cannulae have not moved at the skin insertion
      • Position of the access cannula can be checked on CXR, but tip position may differ depending on lung inflation or upright position of the patient. Echocardiography is a more reliable method of determining cannula tip position.
    • Make sure the cannulae and tubing is well secured and there are no kinks in the tubing to minimise turbulent flow and the risk of complications

Q6. Do you think this patient is ready to be weaned from V-A ECMO?


His inotropic requirement and ECMO blood flow of 4 L/min is still a significant amount of support. In addition, he has little pulsatility and end-tidal CO2 remains low, suggesting that myocardial recovery has not occurred.

Weaning from V-A ECMO is further discussed in Everything ECMO 008: Weaning from V-A ECMO.

Q7. What other details would you document in your daily ward round note?

Key details to note are:

  • Type of ECMO support (V-A vs V-V, peripheral vs central), location of cannulae, the number of days on ECMO support and circuit age
  • The patient’s overall trajectory
  • Key parameters and haemodynamic targets
    • MAP target, ECMO blood flow range, vasopressor and inotrope range, SaO2 target, fluid balance target, transfusion triggers, sedation target
  • Anticoagulation plan; this should take into consideration the patient’s bleeding and thrombosis risk and will change with time
  • The daily plan and objectives
  • Any key factors for handover to the out of hours team


  1. 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. The annals of thoracic surgery. 2014;97(2):610-616 [pubmed]
  2. Murphy DA, Hockings LE, Andrews RK, et al. Extracorporeal membrane oxygenation – hemostatic complications. Transfusion Medicine Reviews. 2015;29(2):90-101 [pubmed]

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