It is hard to propose an universal regime. Other additional pathologies may forbid completelly such attempts (head injuries and similar). The aim is that the patient produces tidal volumes that assure sufficient oxygenation and that the work of breathing does not compromise his cardiovascular capacities and metabolic reserves. Therefore, I think as soon as the patient can produce some tidal volume you may start thinking of permitting some training that does not compromises his cardiovascular system and energy reserves. The sooner the better. In the beginning for some patients may be only 5-10 seconds 2-3 times per day.

I think it is different from patient to patient according to the severity of ARDS, new trend nowadays is to paralyze your patient for 48 hours then start him/her on SIMV mode,with the lung protective mechanism(strategy) that we all know.

I believe when on ECMO, there is no need to stop breathing, or be asleep!

I like to see signs of resolution of the inflammatory response that indicate the triggers that put the alveolus at injury from over distention are abating. I like to see that they are tolerating reductions of PEEP and need less pressors. 

I agree with what's been said. I would only add that the duration of neuromuscular blockade (NMB) of 48 hours was an experimental design decision, which I would not rigidly adhere to. I typically assess patient-ventilator interactions after a few hours as i back of  NMB dosing and if the patient synchronizes with the vent I back off further and let him assist the vent.  I do not consider this weaning- just a means to provide safe ventilation

There are much controversies on when to start spontaneous ventilation (SV) in severe ARDS (P/F

Luc

Are our ARDS patients the same? The patients that I have in mind need very high inspiratory pressure to manage their Vt and they cannot generate it for long time by themselves. Yet they need some training to prevent disuse atrophy of the respiratory muscles. This is the objective for trying to have them bread spontaneously during relatively short sequences of time quite early.

Thanks for your point. Actually I was expecting the question. So thanks again ! Yes our patient do generate very high Vt upon arrival to the emergency department or CCU (and high RR too so the work of breathing WOB is very high). Presumably they generate very high transpulmnary pressure although regretably we do not insert espohageal catheter ("balloon"). The reason for that is that they need to reopen on each cycle their alveoli : this is exhausting indeed ! and require an immediate intervention. but is the intervention 

a) intubation 

b) or high PEEP ? 

this is the issue. if you look at Katz, Anesthesiology, 1985, 63, 598-607, he explains very well that the driving pressure needs to be very small when the lung is on its "appropriate" P-V curve. This is also explained by Brochard (ARJCCM, 1995, 152, 121-8) and Froese  (CCM, 1997, 25, 906-8) : the lung need a very low driving pressure when the lung is "appropriately" open (no RV failure thanks to Jardin). Actually this is beautifully demonstrated by Grasso in the last issu eof Anesthesiology (nov 2015). When he increases PEEP, the driving pressure decreases. All fits provided that the PEEP is OK.

Practically, we pre-oxygenate our ARDS patients with a very low SaO2 (50-70%, P/F=40-70) in the ED or CCU with non invasive ventilation (NIV). Quite often the result is quite compelling. Not only the SaO2 increases back toward 70-80 % but even more compelling the large inspiratory efforts are supressed within minutes : is the WOB just taken up by NIV ? is the lung back on its proper P-V curve ? I do not know. The key here is to use high PEEP levels : I start with 10 cm H2O, goes up to 20 within 10-30 minutes, just looking at the sternal notch retraction and the thoraco-abdominal dyscoordination and the Vt, while I get ready for intubation. Sometimes, I have to back down and stop the intubation because the patient is getter better and just need NIV (Pichot, Anaesth Intens Ther 2015, 47, 138-42).

As I said previously, the picture is not rosy all the time. this (NIV or early SV in intubated patient) works beautifully with single organ failure (focal ARDS, acute chest syndrom, etc.). If the patient is already in early multiple organ failure (septic shock acute kidney injury), then the key issue is to re-stabilize the patient before heading to SV  : i.e. serial echocardiography and arterial and venous blood gases to optimize the circulation, early extra renal replacement to normalize the H+. Again see Jardin :(“As soon as some improvement was observed, pressure support ventilation was started », CCM, 2003, 31, 765-9).

By the way, another point is : when does the intensivist see the patient ? if you get the patient "fresh" from home, it makes everything easier. if the intensivist sees the patient after a few days at home plus a few days in the emergency department, then the intensivist is left only with nuclear weapons at hand...the stabilization of the acute cardio-ventilatory distress may take 12 or 24 h. Then lowering VO2 (again : NMB, paracetamol, surface cooling, sedation with alpha-2, etc.)  is key to head toward normalization then SV.

To sum up 

a) put the lung on its proper P-V curve

b) normalize H+

It is easier said than done : the night is long ! see Gattinoni (Minerva Anesth 2014, 80, 1046-57).

:) 

Luc

Your handling of literature is impressive! Regional inequality of ventilation that is time and patient position dependent make all your efforts really difficult. You are probably on the right track though. Good luck!

Thanks, Dragan.  I insist on the fact that

ARDS is a complex problem i.e. we need to analyze every bit and piece of physiology and pharmacology within the considered patient to address in the clinical setting at 03 00 am what we can do, simply, for the patient, without the recourse to stem cells :). I call this analytical management for now i.e looking at the patient as a physiologist will do, and with the hands on as a clinician.

ARDS cannot be addressed alone; Jardin again is helpful (CCM, 2003, 31, 765-9) because the first take-home message of his paper is that the circulation should be cured before heading to cure ARDS : "avoid low PvO2" effect. As we are now some 10 years later we should say avoid the CO2 gap effect (De Backer ICM 2015, in press).

This approach calls for a lot of flexibility for the clinician, moving back and forth from orthodoxy (plan B) to heterodoxy (plan A) and back. This implies giving it a try to the approach proposed above but this implies also back tracking to orthodoxy if something is wrong. Gattinoni Minerva 2014 is very helpful because he addresses acute cardio-ventilatory distress on Friday night : "friday night ventilation" :)

We have to demonstrate all what I delineated : analysis and preliminary results in some 50 patients is one thing. demonstration in a double blind RCT trial with enough patients is another thing...

Dear Marcello Schmidt

My experience is about ARDS in patients undergoing open heart surgery as a sequel of CPB, or, in the postoperative patient with cardiogenic shock, sepsis, or multiple organ failure.

My first successful experience was about a 46-year-old man with ARDS after cardiac surgery whose arterial oxygenation was surprisingly improved 1 hour after using volume-controlled inverse ratio ventilation (VC-IRV). (Middle East J Anaesthesiol. 2009 Oct;20(3):457-60.). During these years I have treated several patients with the same method. But the onset of spontaneous breathing was different. I start weaning of patient from the ventilator after observing the improvement of oxygenation by ABG (at least 2-3 ABG every 2 hour) and based on patient tolerance. The tolerance in patients from 8 hours to 72 hours have been different. The most important factors were age and heart condition.

Despite the already excellent and thorough  responses to your relevant question I would like to add some comments. 

Transition to spontaneous breathing in ARDS patients is one of the most difficult parts of their ventilatory treatment and the point in time to do so is still under debate. 

It is impossible to set fixed rules but was has been discussed so far are all good advices. It is important to have the precipitating cause of ARDS under good clinical control and to have witnessed an improvement in lung function such as less needs for FiO2, increasing compliance, decreased PEEP needs to maintain the same ventilation targets. It is very difficult to give general threshold values  as this vary from patient to patient. This improvement is generally seen after 2 - 3 days of controlled lung protective mechanical ventilation. 

The transition to spontaneous breathing has to be smooth as the lung is still  very susceptible to suffer from mechanical stress and it is essential to prevent a second hit mechanism at this stage. 

So independently of when it is decided to transit the patient to spontaneous breathing the following must be taken into account: 

Avoid patient-ventilator asynchrony by choosing modes or settings that enhance synchrony. 

Check for increased work of breathing. Prevent the patients from vigorous inspiratory efforts or high respiratory drive as this may cause large transpulmonary pressure changes in different regions of the lung. If this cannot be controlled it might be too soon to transition the patient to spontaneous breathing.   

Controlling tidal volumes is difficult as patients are contributing with their own Pmus Compliance is hard to interpret as the ventilator does not "see" the patient's contribution. In this circumstance a smooth breathing pattern and a low driving pressure may be the best indicators of an appropriate spontaneous breathing.