High-Flow Nasal Cannula, Non-intubated

18G

18G

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HFNC has been achieving great results for pre-oxygenation and maintaining oxygen saturation during intubation. I have used a HFNC in a few select patient's with pretty good results as well. One example patient is a CHF exacerbation, increased work of breathing, tachypnea at 28min, was on CPAP at 10, titrated to 12 w/o improvement. Course crackles are present throughout. SpO2 is maintaining 85% only on CPAP. Patient has considerable gastric distention that the RN reports as occurring only after being placed on CPAP. The physician does not want to place an NG tube to decompress which would aid in improving ventilation.

To improve oxygenation, I flowed 15lpm through the capnography N/C and quickly seen a rise in SpO2 that peaked at 96%. The average throughout my care maintained 91-94%.

Has anyone else started to utilize HFNC to aid oxygenation in non-intubating patients?
 
In patients with low sats I use the ETCO2 cannula under the disposable CPAP mask to increase the FiO2. Works like a champ.
 
Just a clarification (for others reading especially, as I suspect you knew this). the phrase "high flow nasal cannula" usually refers to the newfangled humidified thingamagig that will flow more like 60 LPM. I know that 15 LPM is "high flow" for a nasal cannula compared to the usual 2-4ish, but if you see "HFNC" in the literature they're probably talking about the fancy toy.

Silly quibbling aside, nice case!
 
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jrm818 said:
Just a clarification (for others reading especially, as I suspect you knew this). the phrase "high flow nasal cannula" usually refers to the newfangled humidified thingamagig that will flow more like 60 LPM. I know that 15 LPM is "high flow" for a nasal cannula compared to the usual 2-4ish, but if you see "HFNC" in the literature they're probably talking about the fancy toy.

Silly quibbling aside, nice case!
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HFNC really isn't new at all.
 
Remi said:
HFNC really isn't new at all.
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To tell you the truth I wasn't really sure when it came around, but I was pretty sure it's growing use in the emergency world is a relatively new development.

It looks like vapotherm started making their machine in about 2000. I don't know if that qualifies as new or not, but medicine does move slowly.....
 
People just need to be aware of the differences between oxygenation and ventilation. Same as with a patient that has seen improved sats with CPAP but they are still hypoventilating. This is my biggest fear as we roll CPAP out to bls.
And yes, I am familiar with permissive hypercapnea.
 
I get pre intubation passive oxygenation, but don't really understand how a nasal cannula would be useful in a post intubation situation.
 
redundantbassist said:
I get pre intubation passive oxygenation, but don't really understand how a nasal cannula would be useful in a post intubation situation.
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I didn't see anyone advocating using a NC in an intubated patient. It's often used at 15lpm during the peri-intubation phase for apneic oxygenation which allows for longer attempts during difficult airways without severe desaturation.

You're correct though, there's no benefit to using a NC in an intubated patient since their airway is isolated by the cuff.
 
redundantbassist said:
I know. Hovever, I was asking because I saw many demonstrations where the cannula was left in place after the intubation.
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More than likely it was left in place because they either A) forgot to remove it or B) left it in place because they had other things to do and/or would have to disconnect the vent circuit so rather than remove the circuit, remove the cannula and then replace the circuit (which in some cases could be detrimental to the patient if the patient is requiring PEEP to build/maintain alveolar recruitment where disconnecting the circuit could lose those alveoli that have already been recruited and set the patient back) they just left the cannula in place.

Another option is it was left in place on the chance that the tube was dislodged. In that case it would be easy to turn the oxygen back on to the NC and provide apneic oxygenation while they removed the tube and began bagging the patient. Then it's still in place for that apneic oxygenation we keep talking about when the PT is re-intubated.
 
Handsome Robb said:
More than likely it was left in place because they either A) forgot to remove it or B) left it in place because they had other things to do and/or would have to disconnect the vent circuit so rather than remove the circuit, remove the cannula and then replace the circuit (which in some cases could be detrimental to the patient if the patient is requiring PEEP to build/maintain alveolar recruitment where disconnecting the circuit could lose those alveoli that have already been recruited and set the patient back) they just left the cannula in place.

Another option is it was left in place on the chance that the tube was dislodged. In that case it would be easy to turn the oxygen back on to the NC and provide apneic oxygenation while they removed the tube and began bagging the patient. Then it's still in place for that apneic oxygenation we keep talking about when the PT is re-intubated.
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Thanks Robb
 
DEmedic said:
They usually get left on because we forget to take them off and the tubing would be tangled in the Thomas tube holder.
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Anything within 3 feet of the patient's face its gonna get tangled in those damn tube holders. In fact, the number of things tangled in the tube holder is usually inversely proportional to the patient's oxygen saturation as you are trying to urgently reintubate after accidental extubation. Add a multiplier to that formula if it happens in the CT scanner.
 
There was a study published just last month that described a case series of patients in whom the rate of rise of Etc02 was dramatically reduced using very high-flow oxygen for apneic oxygenation during ENT cases. We were all taught to expect a rise of about 8-10 in the first minute of apnea and about 3/min thereafter......this study showed an average rise of just slightly over 1 mmHg/min. Dr. Farkas goes over the paper and explains the physiology of it in his (really excellent, BTW) PulmCrit blog. It sounds as though the mechanism might be similar to that used by high frequency oscillatory ventilation.

There was also another study published out of Australia recently (the Aussies are kicking our butts pretty badly in terms of the rate of producing research on prehospital airway management) that showed a decrease in desaturation events during RSI using apneic oxygenation. To my knowledge, this is the first published study on the technique in the prehospital environment. It showed a significant (though not at all dramatic) decrease in desaturation events of about 6% (22% vs. 16%) after instituting the technique for all RSI's. They also saw faster re-oxygenation. One significant limitation here is that Sidney HEMS had apparently instituted other changes to their RSI protocol at about the same time as adding apneic oxygenation. This was mentioned in the study, but not detailed.
 
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