8 min
Tasty Morsels of Critical Care 061 | Asthma Tasty Morsels of Critical Care
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- Medicine
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:
* increased work of breathing – dynamic hyperinflation a big part of this
* V/Q mismatch and shunting
* CV instability from intrathoracic pressure
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.
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:
* increased work of breathing – dynamic hyperinflation a big part of this
* V/Q mismatch and shunting
* CV instability from intrathoracic pressure
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.
8 min