What to do when the SpO2 stays low on VV-ECMO?

Check for oxygen supply failure – is oxygen is connected and flowing to the ECMO console?

Disconnection of oxygen tubing during transport is an emergency. There is no alarm (!) on the ECMO circuit to highlight a lack of oxygen delivery to the membrane.

Signs of oxygen supply failure include:

1. Lack of colour differential between access and return cannula (see Figure 3 below)
2. Patient desaturation (falling SpO2 – a late sign)
3. Reduced access saturation, displayed on ECMO console (this may generate an alarm depending on the setting, typical if they fall below 40% – also a late sign of oxygen supply failure)

• Increase ECMO flow: This is a good option if there is no access insufficiency and recirculation not a clinical problem. In general, maintain the pump speed < 4000 rpm, although in some circumstances this may need to be increased.
• Tolerate SpO2 >85%: A key consideration during VV ECMO is oxygen delivery. If patient saturations are low but oxygen delivery appears adequate (consider Hb, oxygen saturation, and oxygen extraction and ensure low lactate and no related new organ failure) it is often reasonable to reduce the SpO2 target rather than undertake additional interventions.
• Prone positioning: While not a common intervention patients can be prone positioned during VV-ECMO. This intervention has been shown to reduce mortality in patients with moderate to severe ARDS not receiving ECMO and was suggested to be beneficial in a recent meta-analysis of ECMO patients^1,2. It is currently being further evaluated in ECMO patients³.
• Transfuse to higher haemoglobin target: Increasing Hb concentration will increase oxygen content and oxygen delivery. The extraction ratio will also decrease and mixed venous saturation will increase. As a result less oxygen will need to be added to the blood to achieve a normal saturation. This is a common practice in some ECMO centres^4,5, however the risk/benefit has not been fully assessed. It should be noted that in non-ecmo cohorts (also not hypoxic) that conservative transfusion target have been shown to be equivalent or superior to a liberal transfusion targets^6,7.
• Start Nitric Oxide: Nitric Oxide may improve V:Q matching in the lung and improve saturation but this has not been shown to reduce mortality⁸. The physiologic effect and the added benefit are likely to be negligible in ECMO patients when the tidal volumes are very low.

The likely cause in this patient is increased cardiac output in the setting of septic shock.

Other potential causes of hypoxaemia also need to be considered and excluded (see Everything ECMO 001 for a stepwise approach to hypoxaemia on VV-ECMO). Also note that the unchanged cannulae positions on the chest radiograph and the low pre-oxygenator SO2 exclude recirculation as a clinically significant issue.

Increased cardiac output contributes to hypoxaemia on VV-ECMO as follows:

• During severe respiratory failure the shunt fraction is high.
• Blood passing through the lungs without passing through the ECMO membrane will not be oxygenated effectively.
• As the patient’s cardiac output increases the proportion of the cardiac output passing through the ECMO membrane will decrease resulting in decreased patient saturations (SpO2 and SaO2).

• Ensure current ECMO cannula position and oxygenator function is optimal.
• Treat underlying cause of increased cardiac output: treat sepsis and provide adequate doses of vasopressor^4,5.
• Convert to high flow configuration: a second access cannula is added to achieve higher flow for a given RPM a radiographic example is shown below^4,5. With a well-placed primary access cannula the effect is usually rather small and may add 0.5- 1 L/min blood flow. In the setting of high cardiac output it might be challenging to substantially improve oxygen saturation in this manner.
• Targeted temperature management: lowering patient temperature may decrease oxygen demand and improve oxygen saturations. However, the benefits of this approach are unproven, it has been described in a case report⁹.
• Control cardiac output with beta blockers: The rationale for this strategy is to increase the ratio of ECMO flow (QECMO) to native cardiac output, due to the negative chrontropic and negative inotropic effects of beta blockers. As a result a higher proportion of the cardiac output will be oxygenated by the membrane. There are a few reports of this strategy in the literature and it appears to increase SpO2^10,11. However the concern remains that while SpO2 may increase the reduction in cardiac output may counteract an increase in oxygen content and result in no improvement in oxygen delivery¹². A further factor to consider is that beta-blockers may also reduce oxygen consumption¹³, and there are data suggesting titratable beta blockers may reduce mortality in sepsis^14,15. Further studies are required before this treatment is recommended for hypoxaemia during VV-ECMO.