Bellani says that any T1RF normally warrants a trial of helmet free flowing CPAP to see if they improve by monitoring with RR and paO2
Jaber says no, just get the FiO2 to >92% and then get them to ICU and see what you need…NIV..HiFlo etc
So now what if the patient is on 30L/min and SaO2 not achieving outcomes….
Roca says to asks if the situation is flow dependent (eg work of breathing) then he would first try actual HiFlo (60L/min)
And they ask should we ask patient?
Roca says yes, even considering loss of
?reliable patient insight with C19, asking is still important
Bellani talks about monitoring and says that low paCO2 in these patients is important and shouldn’t be ignored…
He feels people often forget to use the CO2
Jaber reminds us any patient on NIV needs intubation plan. If you’re doing trial NIV need to have *looked at* airway
and I presume also know if you *would* offer intubation, which seems a bigger deal to me - as a famous wizard said, pick when what is right and what is easy
but nobody mentions that
Then Gattinoni asks how we decide to shift plans and know that mechanical ventilation is now the least dangerous approach…when the patient just stays the same / small change
Bellani says it depends on the FiO2 and if the P/F is around 20 then we *can* wait and see…but that
It also depends what the diagnosis is because that dictates if you have a treatment that’s likely to lead to improvement over time
And then we mentioning proning…
Papazian said he would try proning in a cooperative patient - says 95% the literature though I’d about C-19
But they ask why?? does this just not delay intubation?
…Papazian says recent trials have shown differences in rate of ventilation, but not in mortality
But Roca says the meta-trial showed that awake prone positioning did *not* change the time to failing (intubation)
So they press the panel to be specific about when they pick the time to intubate
Roca says you can never take a decision based on a number
The number identifies the risk
—> points towards ROX score
An audience member asks whether recent experience means we need to reassess our targets… allowing permissive hypoxaemia
Bellani believes the risk of induced lung injury in these circumstances is too high
And we then leave pts to crash in middle of the night with no reserve
…in these situations there is no benefit to not intubating them
So it’s not about the fact SaO2 is ~85% but about the injury/process that’s behind that number
Gattinoni - we don’t often die from gas exchange, we die from the cost of the process that got you there
The decision is what is right or wrong
It’s what is less harmful
An audience member asks why not use awake sedation to mitigate for self induced lung disease ….Bellani says yes, they sometimes use low dose dexmeditomidine or remifentanyl (only in the ICU)
So to close there is no second answer but Gattinoni says we need to ask
What is the stress of the strain we apply?
What lung volumes?
At which cost to pressure?
And at which rate?
And until we measure all of these together, we are driving at night
🧠 Heading here this morning for joint @ERC_resus session ‘How do I predict neurological outcome after cardiac arrest” at #LIVES2022
This is a core part of my day to day and frequent conversation I have with the junior team so interested to listen …
So far the audience have been asked four times to move closer to the front. Nobody moves.
The first q is ‘how do you do it’.
Sandroni says Neuron specific enolase (NSE) for 3 days, clinical exam from day 3, EEG starting early…used later, CT is repeated in patients with prolonged unconsciousness and MRI in those that aren’t waking up..
🫁 🧬 ARDS in Sepsis - Are biomarkers helpful? #LIVES2022
(The answer for me is - minimally…I rarely have access to them at the beside 🛌 but I presume the answer from JM Constantin has meat to it, so I’m here to listen)
We start here by asking is ARDS due to sepsis the same as that due to peritonitis or pneumonia?
And he has now changed the title to Are biomarkers helpful in ARDS?