Welcome back to the tasty morsels of critical care podcast.
Today we’re looking at asthma. In reality I find this is much more commonly discussed than seen in real life. No doubt this is due in part, to an improvement in asthma care chronically which is of course a good thing. I think it gets discussed and comes up on exam papers so much partly because it is such a nice illustration of physiology and ventilation.
I am guilty of over teaching this myself having delivered not one, but 2 talks on the subject, and even a prior tasty morsel of EM on the subject.
Oh’s manual devotes a whole chapter, number 35 to the subject.
We definitely see much less of this than we used to. I suspect that’s largely due to better access and provision of primary care but there remains a cohort of fairly brittle folk out there who will occasional crop up in resus or the ICU.
To begin with, let’s cover some aetiology and pathophysiology, asthma has well described allergic and atopic associations as we all learn in medical school but also some important environmental triggers such as the infamous “thunderstorm asthma” that occurred in Australia some years back with 1000s of patients affected.
There are several major consequences of severe asthma that Oh describes:
Status asthmaticus is a term commonly found in textbooks but I don’t think it has anywhere near the utility of it’s Latin equivalent status epilepticus. Oh applies the term to those not responding to nebulised bronchodilators which could be fairly broad.
For management of asthma like this, the mainstay of treatment is inhaled beta agonists with a chaser of ipratropium and some steroid. There is plenty of evidence suggesting simple inhaled beta agonist with an MDI can be as effective as neublisation but for ICU level asthma (which this post is aimed at) you will be reaching for an oxygen driven nebuliser aiming to get particle sizes somewhere in the 1-3um range. however it is well known that <10% of the drug gets delivered to target and it is likely that in the most severe asthmatics where very little gas is moving that the drug delivery is even worse. Hence the existence of the IV therapies.
All of these are controversial on some level and I am not here to advocate for one or the other but more to provide a pithy line or two on each that one could reasonably throw into an SAQ or a viva answer and look somewhat smart.
IV salbutamol is commonly used in the UK and Ireland but like pretty much all of these therapies could not be said to have a robust evidence base. Concerns have been expressed that it adds a significant metabolic load to the work of breathing with the inevitable rise in lactate and fall in BE leading to an increased minute volume and an increase burden of respiration.
IV magnesium is likely more benign and given out extremely commonly in these cases but once again the evidence base is hardly stellar.
IV adrenaline is a common go to and has some physiolgoic rationale beyond flogging the already overstimulated beta agonists. It’s alpha agonist effect may have beneficial effects on secretion burden and plugging.
Aminophylline continues to be used though anecdotally I’ve not seen it to be that helpful
Heliox often crops up in the text books as it allows for the goldilocks phenomenon of laminar flow. However given the limtations on FiO2 at ~30% (generally 30:70 seems to be the mix) it’s not a great option in a population where hypoxia is a real concern.
No post would be complete without mention of crowd favourite ketamine and its potential bronchodilating properties. It is likely overstated but as an induction drug would seem reasonable. Inhalational anaesthetics are somewhat similar but importantly likely to be inaccessible when you need them.
Let’s say you’ve failed all these therapies and a tube has gone in. How would one ventilate such a patient. The answer should be “with great difficulty”. If it turns out they’re completely easy to ventilate with normal pressures and no gas trapping then you have just intubated someone with vocal cord dysfunction, sometimes known as paradoxical vocal cord motion. Worth another post perhaps but can be a common mimic of life threatening asthma.
More likely you’ll find yourself faced with a ventilator complaining loudly that all the pressures are too high. If lucky you’ll sort things before the inevitable CV collapse from intrathoracic pressures or tension pneumo. The emergent response if you’re faced with high pressures and hypotension is disconnect the patient from the vent. If high intrathoracic pressures are the problem then decompressing the thorax through the ETT may be sufficient to temporarily fix the problem. If they have a PTX they’ll need a decompression of the pleural space of some kind.
Disconnecting the vent is of course not a long term solution so how should we appropriately ventilate these patients. The simple answer is probably “very slowly”. The best thing I’ve seen on this is Dave Tuxen’s paper from the late 1980s and the more recent podcast he recorded with the Intensive Podcast. A fairly simple summary is keep the minute volume low ie 6-7L/min at most. If you try harder you’ll cause harm. You can get this with a resp rate of around 10-12/minute with a Vt of ~500-600mls. Without even touching the I:E ratio you’ll end up with an expiratory time around 4 seconds. Tuxen argues that there’s little to be gained by prolonging expiration beyond this or lowering your minute volume below this. The 1980s paper provides some data to back this up. You will undoubtedly get high peak pressures on the vent that reflect airway resistance rather than the pressure being felt at the alveoli. Plateau pressures here are important here to ensure safe pressures and an aspirational goal of <25 cmH20 seems reasonably. Volume vs pressure control is a great debate it seems but my own preference would probably be volume control for what it is worth.
Finally my preference would be to have these people deeply sedated and even paralysed but there is an association between paralysis and a necrotic myositis that can be an issue in weaning and rehab and this is distinct from the usual ICU acquired weakness and myopathy.
David Tuxen on intensive podcast
Tuxen, D. V. & Lane, S. The Effects of Ventilatory Pattern on Hyperinflation, Airway Pressures, and Circulation in Mechanical Ventilation of Patients with Severe Air-Flow Obstruction. Am Rev Respir Dis 136, 872–879 (1987).