First watch this:

Now that should be a good start point to realize that there is something most physicians, even those who routinely ventilate patients, overlook. The time constant required to recruit. One can easily picture the rapid derecruitment, then re-recruitment – known as atelectrauma for the novices- which will result not only in only temporary success with recruitment maneuvers (RMs), but likely also contribute to ongoing lung injury. Now in less severe cases of ALI, we “get away with it” and the patient gets better anyway. But when the rate of healing is less than the rate of VILI, we get in trouble. Only – just like aggressive fluid resuscitation – we can be blissfully unaware of the unwitting iatrogenic contribution and feel like “the patient succumbed despite everything we did.” Perhaps, but then again perhaps because as well.

In our shop, with conservative fluid management and aggressive de-resuscitation, ARDS has been seldom seen in the last 10-15 years (versus my first years of practice where I encouraged aggressive resuscitation in the ICU and to my ED colleagues), hence ventilation had become rather uninteresting… But with COVID now I’ve had to dust off my “fancier” ventilation strategies and have been using inverse ratio and APRV (not all our vents can do APRV). It would be fun if it wasn’t for the mortality…

So, what can that little rat lung video teach us?

First, the concepts of pressure-time integral (PTI) and alveolar surface area, things we do not routinely use as mental constructs. As we can see in the video, time is required for the pressure to move into the distal airways and recruit. That is why RMs often run in the 30-60 second range at anywhere from 30 to 40 cm/h2o. We all know that they work, but only transiently, and yes, a higher PEEP is usually used post RM, but this may not represent a sufficient PTI to prevent de-recruitment and continued atelectrauma.

Second, the visual example of heterogeneity. Though the Baby Lung analogy and lung protective concepts still hold, that heterogeneity highlights how a relatively low VT and respecting plateau pressure limits may not sufficiently protect certain more distended alveoli. Indeed, as compliance increases with recruitment, the stress is more evenly distributed across alveoli rather than preferentially in the ones that remain open. Hence a strategy that prevents de-recruitment becomes paramount.

This is where APRV comes in. I used it a bunch a few years ago when working in a center where we received commonly enough and had a bit more ADRS than commonly in my shop.  APRV stands for airway pressure release ventilation, and requires one to completely wipe the mind’s dry-erase board of ventilatory parameters and really just start thinking in terms of pressure-time integral.

APRV is essentially a bilevel ventilation mode over which a patient can take spontaneous breaths, analogous to a CPAP mode with occasional pressure release that allows for ventilation. Though APRV has been around for a long time, the work of APRV guru Nader Habashi and his APRV network have done tremendous work fine tuning their system of time-controlled adaptive ventilation (TCAV) which is a way of setting APRV appropriately to the patient’s physiology. I highly encourage reading their work and resources available – which includes mentoring. APRV isn’t a plug-and-play mode, it is paramount to understand the physiology behind it.

So we need to set P hi, P lo (it’s supposed to be 0 so an easy one), T hi and T lo – and yes FiO2 (at least one familiar one!). So basically you determine how much time the patient spends (this largely determines your respiratory rate) at a certain level of pressure, generally between 20-30 depending on severity of ALI and lung compliance, and how long an expiratory phase they get (really short).  That’s actually the one that needs understanding, because that’s the TCAV sweet spot, how you prevent as much VILI as possible.

You need to think of peak expiratory flow rates (PEFR – yup just like in outpatient asthma!), and adjust the T lo to 75% of the PEFR. This provides what Nader himself describes as the air cushion that remains in the lungs and prevents the alveoli from taking the brunt of the next positive pressure burst, particularly those at the most fragile end of the spectrum.

You need to remember the concept of functional residual capacity (FRC) as this is what we aim for to avoid recruitment-derecruitment.

So, caught your attention? If you have a physiologist’s soul (and if you’re resuscitating patients you really should!), and were not yet using TCAV-APRV, I hope you are thinking about it because it makes sense. And in these COVID patients we may not have the usual margin of safety to do our usual ventilation.

So, please register at the APRV Network, read all their free guideline documents which are great but I will not post as they require you to register (its free), and here are a couple of must-reads by Nader and his group:

dynamic alveolar physiology

history of APRV

And of course Scott has some awesome discussions with Dr. Habashi himself.

Oh yes and as per our Webinar last week, Josh Farkas has been using APRV on his COVID patients with success!

 

please share your COVID ventilation experience!

…and no offense, but please, though open, this is a blog intended for clinicians, not a forum for lay questions or comments. I simply do not have the time to answer them and will not, and I feel rude deleting them (but will do so) but clinical readers need concise information packaging, so please feel free to read or listen in e-silence. Again, I apologize for this recent necessity.

 

cheers

 

Philippe