The V-V ECMO Ward Round

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

Everything ECMO 023

A 36-year-old female is on V-V ECMO for influenza A and a secondary Staphylococcus aureus pneumonia. It is day 3 of support. This morning she has the following examination:


  • HR 120 bpm, BP 95/52 mmHg, SpO2 84%
  • Fully sedated but not paralysed, with slightly blue fingers and toes

ECMO settings:

  • Blood flow rate: 3.8 L/min on 3995 rpm. Kicking of the line occurs if the rpm is increased.
  • Fresh gas flow (FGF) rate: 4 L/min

Ventilator settings:

  • Pressure control ventilation with Pinsp 10 cmH2O, PEEP 15 cmH20,  FiO2 1.0 and Vt 80 mls

Inotropic requirements:

  • Adrenaline 2 mcg/min
  • Noradrenaline 36 mcg/min
  • Vasopressin 2 units/hrABG:
  • pH 7.20, PaO2 56 mmHg, PaCO2 53 mmHg, HCO3 19, lactate 2.5

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

Is she adequately supported?

  • Is oxygen delivery adequate?
  • Is PaCO2 controlled?

Is her lung function and recovery optimised?

  • Are the ventilation settings appropriate?
    • Is a lung protective ventilation strategy still required?
    • Are her lungs recovering and we can allow spontaneous respiratory effort?
  • Is the underlying pathology being treated?
  • Is fluid balance optimised?

Have complications developed?

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

How do we move forward?

  • Can we wean the ECMO?
  • What is the overall plan?
    • Is ECMO being used as a bridge to recovery or a bridge to transplant?
    • Is she deteriorating and is palliation required?

Q2. Do you think the patient is appropriately supported?


Her examination, low oxygen saturation and lactic acidosis suggests poor oxygen delivery to her tissues. The respiratory component of her mixed acidosis suggests that the FGF is not adequate to clear her CO2.

Q3. What are the factors that determine oxygenation in V-V ECMO?

Consider the oxygen delivery equation:

DO2 = CaO2 x CO                     [Oxygen delivery = oxygen content x cardiac output]

CaO2 = (Hb  x 1.39 x SaO2) + (0.003 x pO2)

Oxygen delivery must be able to meet oxygen demands/consumption (VO2). It is therefore important to consider the ECMO output (or blood flow), haemoglobin, oxygen saturation, and patient oxygen requirements.

  • Optimal values for these parameters are not well established in the literature. The most recent ELSO Guideline recommends a goal DO2:VO2 > 3 (corresponding to an SvO2 25-30% less than the SaO2)1
  • V-V ECMO blood flow is recommended to start at 50-80 ml/kg/min1. At our institution, most of our patients are maintained on 4-5 L/min*(check this fact…)
  • An SaO2 >85% or PaO2 >55 mmHg is generally considered acceptable1,2. However, saturations of 75-80% may be adequate depending on patient oxygen consumption and other oxygen delivery variables1.
  • There is some evidence to suggest maintaining a Hb >70 g/L may be acceptable3. Higher thresholds may be considered if there is failure to improve oxygen delivery despite optimization of other parameters.
  • In patients with high cardiac output, the circuit may not be able to capture and oxygenate a high enough proportion of the patient’s cardiac output (see Everything ECMO 011).
    • Strategies to decrease oxygen consumption in addition to sedation (e.g., beta blockade, cooling) may be considered, but are not frequently employed at our institution.

Q4. How would you optimise oxygen delivery on V-V ECMO?

Optimise ECMO blood flow:

  • Minimise access insufficiency by:
    • Giving a fluid bolus
    • Paralysis
    • Changing the patient’s position
  • Convert to high flow configuration to increase the proportion of the patient’s cardiac output being captured by the ECMO circuit (see Everything ECMO 011)

Reduce oxygen consumption by:

  • Treating fevers
  • Paralyzing the patient
  • Consider reducing inotropes if possible
  • Consideration of beta-blockade or active cooling (see discussion above)

Consider pulmonary vasodilators (NO/PGI2) to minimise V/Q mismatch

Q5. Why should you improve her CO2 clearance?

Controlling the patient’s PaCO2 will

  • Minimise the patient’s acidosis
  • Avoid further contributing to lung injury by minimising respiratory drive and allowing lung protective ventilation goals to be achieved.

Q6. How would you improve her CO2 clearance?

Increase the FGF (or sweep) to increase CO2 clearance. This is a very efficient process in ECMO and preferable to increasing ventilator settings to unsafe limits.

Q7. How do you ensure lung function and recovery is optimized?

Ventilation strategies (discussed further in Everything ECMO 002: V-V ECMO Ventilation and Weaning):

  • Early in the disease process, it is important to ensure lung protective ventilation strategies:
    • Vt <6 ml/kg
    • Pinsp <30 cmH20
    • FiO2 <0.6
    • Consideration of maintaining a driving pressure (Pplat-PEEP) of <15
    • To achieve this patients often need to be heavily sedated and paralysed.
  • As patients transition to the recovery phase and their compliance improves they can be allowed to breathe spontaneously.
  • Other strategies:
  • Continue to manage the patient’s underlying pathology.
  • Maintain a restrictive fluid strategy.

Q8. What patient-related complications can develop on ECMO?


  • This is common. Consider all sources including the ECMO circuit. These are nosocomial infections that 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.
  • 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 (including injuries from CPR) 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)

Barotrauma and pneumothorax

  • May occur if sedation is not adequate, or V-V ECMO is instituted relatively late.
  • Avoid intervention with chest drains if possible due to the high risk of bleeding complications


  • Signs include reducing pulsatility, rising CVP and access insufficiency

Thrombus (in the patient)

  • This may occur as DVT/PE or arterial thrombus if a PFO is present.
  • If heparin-induced thrombotic thrombocytopenia (HITT) is a concern, an alternative anticoagulation agent will need to be considered (see Everything ECMO 016).

Neurological complications

  • Delirium, coma, cerebrovascular accident, intracerebral haemorrhage

Renal failure

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

Multiorgan failure

Q9. 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: An ECMO Earthquake?
    • Signs include kicking of the access line, dropping/fluctuating ECMO blood flow, and increasingly negative access pressures (if using the HLS console)
    • Haemolysis may occur as a consequence
  • Problematic recirculation
    • If the access and return cannulae are too close recirculation can occur
    • The patient’s SpO2 will be low whilst the pre-oxygenator SaO2 will be >80%
  • Thrombus
    • Most patients 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 in the cannulae or circuit tubing should be aspirated or the circuit should be changed
  • Haemolysis
    • see Everything ECMO 004: Why is the bag turning red? 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: Turn and face the circuit… ch-ch-change it! )
      • 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 can also 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 cannulae 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

Q10. When can the patient can be safely weaned from V-V ECMO?

It is important to ensure that the underlying condition is improved

  • Lung compliance and CXR improving
  • PaCO2 remains in the normal range with safe ventilation strategies and a gradual reduction in fresh gas flow

Weaning is discussed further inEverything ECMO 002: V-V ECMO Ventilation and Weaning.


  1. Agerstrand CL, Burkart KM, Abrams DC, Bacchetta MD, Brodie D. Blood conservation in extracorporeal membrane oxygenation for acute respiratory distress syndrome. Ann Thorac Surg. 2015;99(2):590-5. [pubmed]
  2. Combes A, Bacchetta M, Brodie D, Müller T, Pellegrino V. Extracorporeal membrane oxygenation for respiratory failure in adults. Curr Opin Crit Care. 2012;18(1):99-104. [pubmed]
  3. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support. Extracorporeal Life Support Organization, Version 1.4 August 2017. Ann Arbor, MI, USA.

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