2L low flow nc in bronchiolitis

[sliceofbread136]

Keep getting er admits for bronchiolitis who apparantly are working when they come in but with a good oxygen sat. They suction and put on 2L low flow and tell me that he needs to come in because he requires O2. I usually end up taking it off them when they get to the floor and discharge them in the morning if they don’t require excessive suctioning.

I’ve asked twice what they think low flow is doing for these kids without hypoexemia. One answer was “it’s our hospital guideline”, I checked that and it isn’t.

Another attending told me that even though they are not having desaturations they are compensating for an “Aa gradient” which is why the low flow nc helps them which I have a hard time buying. ive always thought the compensation for any mild V/Q mismatch would be done be through lung perfusion and not through increased ventilation as I see kids persist at 88% without increased work of breathing all the time...

in my mind I’ve always seen bronchiolitis as an airway resistance issue and if they have atelectasis and mucous plugging then a pulmonary parenchyma compliance issue. What I’ve seen help are hfnc and suctioning and obviously if they need it actual positive pressure.

Am I missing something with this low flow nasal oxygen for work of breathing in bronchiolitis? Is there something it actually does?

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[BigRedBeta]

Depends on how small the kid is. And in my mind "low flow" vs high flow cannula is a misnomer - flow is flow despite what the Optiflow and vapotherm reps may try to convince you of. If you're overcoming their minute ventilation then by definition you are on "high flow" regardless of what the cannula is labeled. So the 4kg kid with a RR of 60 and an assumed tidal volume of 7ml/kg (for a MV of ~1.6 L) may derive benefit from even 2LPM.

In bigger kids though, I agree that 2LPM is not going to do much unless they are hypoxic. WOB of breathing is multifactorial but far more likely to be related to pulmonary compliance and the relationship between FRC and closing volumes. Additionally mucous plugging and atelectasis is not a static process. As the kids move and cough, they are going to be affecting airways across a spectrum of disease involvement. Move that snot to the wrong distal airway and you can lose access to a relatively healthier set of alveoli. Stays there too long and the alveoli deflates and now your cumulative atelectasis has moved you that much farther away from your ideal FRC. Thrown in changes to radial traction with neighboring alveoli and you can end up with a cascading effect, but move that mucus and things can improve readily if the affected alveoli are otherwise unscathed. Likewise, as those relative resistances change, you may overinflate some number of alveoli.

I wouldn't conflate V/Q mismatch with work of breathing at all. And I disagree to an extent with your thought that V/Q mismatch is going to be remedied by lung perfusion once you've gone past normal physiologic V/Q matching (eg what's needed when going from supine to upright or what happens during exercise). In my mind, there gets to be a certain point within the pathophysiology of bronchiolitis where your West Zones kind of go out the window and everything becomes significantly more heterogenous with well matched areas (typical of Zone 2) and really poorly matched areas throughout the lungs without any real rhyme or reason. The body is going to respond in it's stereotypical patterns regardless of whether they are desirable for the situation or not. And of course, unless you're in the CVICU or the PICU with very specific patients, it's not like you are going to target your pulmonary vascular resistance for intervention anyway.

Lastly, very few people outside of the intensivists really take any time to think about physiology. And there are plenty of times when things get done that appear to help but physiologically they don't make any sense. I can't for the life of me tell you why blow by O2 seems to help anyone, and yet, there are undoubtedly 100kg teenagers who somehow benefit from having a bag mask pointed at their face and an alveolar FiO2 that can't be much more than 0.213 (if that) but damned if they don't desat the moment you take it away.

 

[sliceofbread136]

Depends on how small the kid is. And in my mind "low flow" vs high flow cannula is a misnomer - flow is flow despite what the Optiflow and vapotherm reps may try to convince you of. If you're overcoming their minute ventilation then by definition you are on "high flow" regardless of what the cannula is labeled. So the 4kg kid with a RR of 60 and an assumed tidal volume of 7ml/kg (for a MV of ~1.6 L) may derive benefit from even 2LPM.

In bigger kids though, I agree that 2LPM is not going to do much unless they are hypoxic. WOB of breathing is multifactorial but far more likely to be related to pulmonary compliance and the relationship between FRC and closing volumes. Additionally mucous plugging and atelectasis is not a static process. As the kids move and cough, they are going to be affecting airways across a spectrum of disease involvement. Move that snot to the wrong distal airway and you can lose access to a relatively healthier set of alveoli. Stays there too long and the alveoli deflates and now your cumulative atelectasis has moved you that much farther away from your ideal FRC. Thrown in changes to radial traction with neighboring alveoli and you can end up with a cascading effect, but move that mucus and things can improve readily if the affected alveoli are otherwise unscathed. Likewise, as those relative resistances change, you may overinflate some number of alveoli.

I wouldn't conflate V/Q mismatch with work of breathing at all. And I disagree to an extent with your thought that V/Q mismatch is going to be remedied by lung perfusion once you've gone past normal physiologic V/Q matching (eg what's needed when going from supine to upright or what happens during exercise). In my mind, there gets to be a certain point within the pathophysiology of bronchiolitis where your West Zones kind of go out the window and everything becomes significantly more heterogenous with well matched areas (typical of Zone 2) and really poorly matched areas throughout the lungs without any real rhyme or reason. The body is going to respond in it's stereotypical patterns regardless of whether they are desirable for the situation or not. And of course, unless you're in the CVICU or the PICU with very specific patients, it's not like you are going to target your pulmonary vascular resistance for intervention anyway.

Lastly, very few people outside of the intensivists really take any time to think about physiology. And there are plenty of times when things get done that appear to help but physiologically they don't make any sense. I can't for the life of me tell you why blow by O2 seems to help anyone, and yet, there are undoubtedly 100kg teenagers who somehow benefit from having a bag mask pointed at their face and an alveolar FiO2 that can't be much more than 0.213 (if that) but damned if they don't desat the moment you take it away.

thanks a lot! I love picking more experienced folks brains on here

 

[SurfingDoctor]

Does your ER have a 24 hour observation unit housed within?

 

[sliceofbread136]

Does your ER have a 24 hour observation unit housed within?

nope. That would be great though

 

[SurfingDoctor]

nope. That would be great though

Well, that’s why they slap them on oxygen. It’s a way to force an observation.

 

[sliceofbread136]

Well, that’s why they slap them on oxygen. It’s a way to force an observation.

yup makes sense