Hypoxia on VV

Approach to hypoxia

Hypoxia on VV ECMO is a common problem and requires some key considerations.

  • Oxygen consumption of the patient
  • Basics of oxygen delivery ECMO circuit – setting of ECMO blood and fresh gas flow
  • Exclude significant recirculation
  • Restauration of circulatory volume
  • Evaluate change in patient native cardiac output

Basic checks

  • Colour differential present
  • Oxygen delivery to the oxygenator
    • Oxygen connected and running if from oxygen cylinder
    • Checking connections, blender FiO2 at 1.0, flow calibration
  • Oxygenator function – post oxygenator gas PO2 >300 mmHg (very minimum >200)
  • Is there access insufficiency interfering with oxygen delivery to the patient?
  • Change in cardiac output? explaining change of oxygen saturations
  • Substantial change in ventilator settings, compliance suggesting new findings e.g. pneumothorax

Beyond basic checks

Key questions to answer beyond the basic checks are:

  • What is the tolerable SpO2 / arterial pO2 for this individual patient at the stage of their disease?
  • What is the trajectory and likely time period of low oxygen levels?
  • Is the oxygen delivery adequate for this patient?

Clinical experience suggests that young patients will tolerate short episodes of hypoxia without sequelae. Even longer periods on pO2 of 55 mmHg seem safe but there is little data to be confident at lower levels and management will reflect the assessment of the bedside intensivist and the ECMO consultant at the time. Individual patient considerations are key e.g. a patient with chest injuries with a moderate TBI as the primary reason for VV support versus patient with community acquired pneumonia

Change in patient native cardiac output

Cardiac output may change gradual or sudden. The heart rate may serve as an indicator (if the stroke volume is relatively unchanged) the fraction of cardiac output that is captured by the ECMO circuit is decreased and may lead to desaturation depending on the native lung function.

This can be as simple as the patient waking up, bleeding or any other cause for increase in HR including PE and always think of sepsis if there is no obvious alternative diagnosis.

It is important to take note that the opposite may also pose a threat to the patient in the absence of hypoxia. Silently progressive right heart failure whilst on VV ECMO may not present with hypoxia (despite an increase in heart rate) given the generally decreasing cardiac output. Or any other factor that may decrease cardiac output e.g. bleeding, cardiac tamponade.

Recirculation

Recirculation is the phenomenon observed during venovenous ECMO in which a portion of the reinfused blood from the circuit is returned immediately back to the circuit through the drainage cannula instead of flowing through the patient.

Recirculation may occur immediately after insertion or change in cannula position including modification of configuration or may only become relevant with progressive disease and oxygenation requirements. Excessive blood flows in itself may enhance recirculation hence a lower RPM should be trialed. Otherwise if considered relevant to the patient’s oxygenation only further separation between access and return cannula will resolve this. Since we are trying to avoid advancing cannulae after post insertion, the favoured option would be to withdraw the access cannula a fraction 1-2cm. The risk being that access flow could worsen.

Management

Management may differ depending on the trajectory and the above discussed individual patient goals for SpO2. Faster deterioration is more likely to require provision for change in management/ support. However, it is generally worthwhile to consider the following:

Quick reference hypoxia

  • Ensure FiO2 at the blender is set to 1.0
  • Check connections and oxygen delivery to the oxygenator with colour differential present
  • Increase ECMO blood flow – consider reasons for access insufficiency if limited at low levels
  • Balance potential fluid administration with potential further deterioration in lung function
  • Increase ventilator FiO2
  • Judge degree of recirculation, a pre-oxygenator gas will help to assess this (HLS gives reads an oxygen saturation in the venous limb) implication for cannula position
  • Ensure post oxygenator pO2 >300 mmHg (<200 should definitely trigger a circuit change, but even less than 300 should trigger thoughts about potential oxygenator pathology/ insufficiency)
  • Correct anaemia more liberally than the usual threshold of Hb<70 g/L, in particular if concerned about the overall oxygen delivery this becomes a priority intervention and Hb of 90 or even >100 g/L is been targeted
  • Check for haemolysis – plasma free haemoglobin does not contribute significantly to oxygen transport and has numerous deleterious effects
  • Pre-oxygenator gas may also help to judge the significance of recirculation phenomena
  • Revision of cannula position
  • Consideration of 2nd access cannula – high flow configuration

Often mentioned but generally NOT recommended include

  • Treatment with beta-blockade to slow intrinsic cardiac output – danger of compromising oxygen delivery
  • Increasing RPM without checking effectiveness – potential for haemolysis and exaggerated hypoxia if recirculation relevant
  • Trialing dual-lumen cannulae in this setting

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