Session 1 – Antonio Pesenti, Refractory Hypoxaemia Therapuetic Strategies
Before deciding on support, first need to know what targets. One might be PaO2? If you climb up a mountain it’s low? Is this important – not according to Grocott in NEJM 2009 where low levels were compensated for by higher Hb.
Rx hypoxia broadly divided as follows
- Treat cause – antibiotics, thrombolysis, etc, etc
- Increase FiO2
- Reduced atelectasis – PEEP
- Increase pulmonary blood flow
- Reduce venous admixture – ECMO
PEEP prevents collapse = recruitment manoeuvres are needed to open collapsed lung. Indeed main difference between traditional IPPV & HFOV/APRV is high airway pressure – theory being more recruitment AND retention.
Don’t forget effects of heart + shunt upon O2 but iNO doesn’t work.
The benefits of proning extend beyond its effects on PaO2 – failure to improve this variable does not mean you should stop doing it.
Session 2 – Jan Bakker, Haemodynamic effects upon ECMO
When considering you need to ask:
- What other support have you got?
- What configuration are you using?
Peripheral VA-ECMO can significantly increase after load – first consider dilators, then increase forward flow whilst remember to treat acidodsis/anaemia. If that doesn’t work, add an IABP.
With VV-ECMO, RV afterload will fall with PVR effect because of beneficial effects upon CO2/PAO2.
Session 3 – Weaning from ECMO Giacomo Grasselli
No science to this – lack of definite criteria, indications from guidelines and local protocol and personal experience
- wean ECMO, then vent
- Emergency discontinuation, e.g. bleed
- First wean vent, then ECMO
Weaning from VV is weaning gas flow – you don/t need to reduce flow
You need haemodynamic stability as well as respiratory improvement. Measure oxygen delivery – the target is tissue oxygenation NOT PaO2.
How long do you keep the gas off? – Karolinska say 4 hours
Some authors propose leaving cannulae in place for put to 48 hours flushed with heparinised solution – practice VARIABLE
How to decannulate VV?
- Stop/reduce heparin
- Put purse string around insertion cannula
- Clamp lines
- Stop pump
- Remove pipe allowing small amount of leakage to red air embolism
- Manual compression 20 min for venous and 30 min for arterial.
- Close monitoring distal perfusion for arterial and consider vascular ultrasound in both as high incidence of clot or injury
Keynote – Michael QUINTEL, 50 years of ECMO
ECLS first developed by John Gibbon and Mali in 1936 in response to sudden death young patient with PE and first used in ORD for ASD repair May 1953
CESAR trial goo.gl/T6tdEL
First oxygenators bubble before developed hollow fibre oxygenator
The development of heparin-coated circuits allowing limiting APTT was one the major steps in reducing morbidity and mortality
Single centres such as Michigan have led the way – now more adult/paed, less neonates
Then H1N1 prompted exploration http://ja.ma/2xp301Q
H1N1 make worldwide excessive use of the technology but there is no new real data.
Reasonable data about risk/benefit ratio does not exist. Cerebral micro emboli are universal. 85% get DVT.
Pro: Is ECMO always an Option? Steffen Weber-Carstens
Similar International Consensus Position Paper by Coombes and colleagues on what defines an ECMO centre
Triage essentially as duration IPPV significant risk factor of deaths.
Con: Giacomo Bellani
In one series, 87% of referrals had at least one relative contraindication
25% of patients in CESAR didn’t get it
EOLIA trial has not reported and is ongoing – we are in the infancy of what we know
Why use more resources when you can achieve the same thing with less? LungSafe shows we still don’t get optimium PEEP, NMBA, fluid balance and supportive care in ARDS.