Apneic Oxygenation

[RxBoy]

Question for the anesthesia buffs out there...

My understanding is that as long as there is fresh 02 flow, normal capillary-alveolar membrane diffusion, normal hemoglobin, and normal cardiac output a person can maintain there oxygen saturation without having to ventilate. I also know that the first minute of non ventilation yields an average increase in PaCO2 by 6 followed by 3-4 for each additional minute.

My question... Presuming someone was on supplemental oxygen and not ventilating, typically how long could a healthy person last before succumbing to death? And if they died what would be some of the top causes? I would presume it would be a dysrhythmia from hypercarbia or CO2 narcosis.

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[RockLee]

CO2 would be your limiting factor.

I think someone told me once that if you do the calculation, it comes out to something crazy like 2-3 hrs - given no other CO2 side effects other than it lowers the amount of O2 in your lungs overtime

 

[deleted126335]

Question for the anesthesia buffs out there...

My understanding is that as long as there is fresh 02 flow, normal capillary-alveolar membrane diffusion, normal hemoglobin, and normal cardiac output a person can maintain there oxygen saturation without having to ventilate. I also know that the first minute of non ventilation yields an average increase in PaCO2 by 6 followed by 3-4 for each additional minute.

My question... Presuming someone was on supplemental oxygen and not ventilating, typically how long could a healthy person last before succumbing to death? And if they died what would be some of the top causes? I would presume it would be a dysrhythmia from hypercarbia or CO2 narcosis.

They would need to be on more than "supplemental oxygen"
Think intubated, FRC filled with 100% oxygen and attached to an anesthesia circuit filled with 100% oxygen and replenished by having the fresh gas flow on. I think that in a young, fit, healthy person, death would eventually be by asphyxia, eventually the lungs would be filled with CO2 resulting in a hypoxic mixture.

How long? Don't know. An hour or two wouldn't surprise me. Particularly if paralyzed (NMBs dramatically lower oxygen consumption)

 

[InductionAgent]

Question for the anesthesia buffs out there...

My understanding is that as long as there is fresh 02 flow, normal capillary-alveolar membrane diffusion, normal hemoglobin, and normal cardiac output a person can maintain there oxygen saturation without having to ventilate.

One other key factor required is a patent airway. Otherwise the fresh O2 flow cannot get into the patient's lungs. I had a thin, demented elderly patient with myasthenia gravis who postoperatively developed severe CO2 narcosis. He was not completely apneic, but very close. I believe simple diffusion of O2 could have been an important factor in his oxygenation. He was holding his sats 97% and above on face mask O2. However, pCO2 was over 100 and pH on ABG was about 6.9. So I reintubated him, sent him to SICU. They gave him his pyridostigmine via NGT, let him recuperate, and extubated him the next day, and he was back to his demented combative self.

Contrast this to the obese, bull-necked patient who desats on induction despite the fact that you're holding an O2 mask on his face. In addition to higher metabolic demands causing desaturation, there is no apneic oxygenation, because there is no way for the O2 to diffuse through his obstructed airway.

 

[RxBoy]

Thanks for the input guys

Contrast this to the obese, bull-necked patient who desats on induction despite the fact that you're holding an O2 mask on his face. In addition to higher metabolic demands causing desaturation, there is no apneic oxygenation, because there is no way for the O2 to diffuse through his obstructed airway.

I was particularly thinking of this situation in which a patient was very deep with something like propofol and fentanyl on board tolerating an oral airway with basic 02 mask on high flow but were completely apneic.

Not that I wouldn't do something in this situation such as narcan, shut off the propofol, bag mask ventilate... possibly intubate/LMA. But what if I didn't, how long would I have.

I am guessing 20 to 30 minutes.

 

[Bertelman]

I was particularly thinking of this situation in which a patient was very deep with something like propofol and fentanyl on board tolerating an oral airway with basic 02 mask on high flow but were completely apneic.

I think you'll need more than just a simple mask to ensure actual flow into the lungs. Again, depending on habitus (chest wall compliance), it may take some force for the O2 to make it into the alveoli. Think about one lung ventilation. If the pt. becomes too hypoxic, one solution is to attach O2, with CPAP 5 to the down lung. You won't get a CPAP of 5 with a simple mask until your flows hit like 50 L/min.

 

[lushmd]

Check out this paper from Anesthesiology.

 

[RxBoy]

Check out this paper from Anesthesiology.

Wow very interesting study. Even though it was published in 1959. Then again it would be tough to replicate a study like this nowadays seeing as inducing and paralyzing someone while only offering oxygen flow via an endotrachael tube could be viewed as cruel.

Although the sample size was really small (8), it seems that humans can tolerate a large amount of respiratory acidosis (one subject had a PaCO2 of 250 and pH 6.7) as long as there isn't a concurrent hypoxia. And as I suspected one of the earlier signs of hypercarbia was dysrhythmia (premature venticular contractions). Most of these people were apenic longer than 30 minutes and one was even 55 minutes.

Nice find.

 

[proman]

For what it's worth, the current world record for static apnea with preoxygenation is 20:10 minutes by Stig Severinsen on 4/1/2010. That's with up to 30 minutes of pre-breathing 100% oxygen and hyperventilating.

 

[Jeff05]

For what it's worth, the current world record for static apnea with preoxygenation is 20:10 minutes by Stig Severinsen on 4/1/2010. That's with up to 30 minutes of pre-breathing 100% oxygen and hyperventilating.

by the time your pco2 is 90 (pco2 increases by 6 first minute of apnea and 3-4 each minute after that) ph is 7.0 (presume starting 40/7.4). obviously there is some acute metabolic compensation...
K+ increases by 0.5 for every 0.1 decrease in pH so assuming starting 5, it is now 7.

therefore, you can have someone perfectly well oxygenated and still code due to hypoventilation, which results in hypercarbia, which results in acidosis and hyperkalemia --> arrhythmia --> death.

 

[jwk]

Unless you have some positive pressure, atelectasis will begin fairly quickly. Less gas exchange, then HPV, even less gas exchange. O2 goes down, CO2 goes up.

This is what we do all the time at the end of a case. Pt on 100% O2, don't ventilate them so the CO2 will build up, but after a couple minutes, the SaO2 starts to drift down.

If you aren't ventilating the patient, there is no flow - they're simply existing on an oxygen-enriched environment. Why do we pre-oxygenate? You think you have 2-3 hours to get the tube in once your NMB hits?

 

[wine thief]

If you aren't ventilating the patient, there is no flow - they're simply existing on an oxygen-enriched environment. Why do we pre-oxygenate? You think you have 2-3 hours to get the tube in once your NMB hits?

This is not correct. With apneic oxygenation, oxygen exchange is still occurring at the alveolar level. If you supply O2 and have a patent airway, oxygenation will occur in the absence of ventilation.

 

[RiskyFugu]

CO2 would be your limiting factor.

I think someone told me once that if you do the calculation, it comes out to something crazy like 2-3 hrs - given no other CO2 side effects other than it lowers the amount of O2 in your lungs overtime

I’m a medical student, so bear with me. If my reasoning is wrong, please correct me.

As I understand it, an excess of ventilation affects CO2 more than it does O2 for to reasons: 1. Because ventilating more will drop our PAO2 below 40 and increase diffusion of CO2 out of the alveolar capillaries, and because CO2 diffuses more readily across the capillary-alveolar barrier than O2 does. Also, O2 diffusion itself is more limited because 1. our blood has a limit on its oxygen content and 2. O2 does not diffuse as readily across the barrier as CO2 does. and 3. hyperventilating will create a V/Q mismatch and effectively more dead space (i.e. ventilation without the perfusion to match it).

But, it would seem reasonable to me that an absence of ventilation would cause us to become hypoxemic before we became hypercarbic (or suffer from respiratory acidosis). Under normal conditions, we have a PAO2 of 100 to keep our hemoglobin saturated. Not being able to mechanically move expired air out of our lungs and bring in fresh air into them would probably cause our PAO2 to drop well below 100mmHg. It would also cause our PACO2 to rise, but again, CO2 diffuses across out more completely than O2 diffuses in and thus O2 would become a problem faster than CO2 would.

Again, please correct me if I’m wrong.

 

[RiskyFugu]

Unless you have some positive pressure, atelectasis will begin fairly quickly. Less gas exchange, then HPV, even less gas exchange. O2 goes down, CO2 goes up.

This is what we do all the time at the end of a case. Pt on 100% O2, don't ventilate them so the CO2 will build up, but after a couple minutes, the SaO2 starts to drift down.

If you aren't ventilating the patient, there is no flow - they're simply existing on an oxygen-enriched environment. Why do we pre-oxygenate? You think you have 2-3 hours to get the tube in once your NMB hits?

JWK, why would atelectasis occur? If there is surfactant and if the intrapleural pressure remains lower than the pressure in the alveoli, shouldn't the alveoli remain un-collapsed?

 

[pgg]

JWK, why would atelectasis occur? If there is surfactant and if the intrapleural pressure remains lower than the pressure in the alveoli, shouldn’t the alveoli remain un-collapsed?

Absorption atelectasis is going to be an issue with 100% oxygen and no CPAP.

If you aren't ventilating the patient, there is no flow

That's not correct; with apneic oxygenation there is bulk flow of O2 into the alveoli without ventilation.

 

[BobBarker]

You can do it with just a good mask seal, high flows, and an oral airway helps. Pts sat dropped to about 85 (didn't really preoxygenate), and then increased to 100 with no ventilation within 2 minutes.

 

[RxBoy]

I’m a medical student, so bear with me. If my reasoning is wrong, please correct me.

As I understand it, an excess of ventilation affects CO2 more than it does O2 for to reasons: 1. Because ventilating more will drop our PAO2 below 40 and increase diffusion of CO2 out of the alveolar capillaries, and because CO2 diffuses more readily across the capillary-alveolar barrier than O2 does. Also, O2 diffusion itself is more limited because 1. our blood has a limit on its oxygen content and 2. O2 does not diffuse as readily across the barrier as CO2 does. and 3. hyperventilating will create a V/Q mismatch and effectively more dead space (i.e. ventilation without the perfusion to match it).

But, it would seem reasonable to me that an absence of ventilation would cause us to become hypoxemic before we became hypercarbic (or suffer from respiratory acidosis). Under normal conditions, we have a PAO2 of 100 to keep our hemoglobin saturated. Not being able to mechanically move expired air out of our lungs and bring in fresh air into them would probably cause our PAO2 to drop well below 100mmHg. It would also cause our PACO2 to rise, but again, CO2 diffuses across out more completely than O2 diffuses in and thus O2 would become a problem faster than CO2 would.

Again, please correct me if I’m wrong.

As a med student, I thought like you. I was under the assumption that you need to ventilate to oxygenate. However, provided there is supplemental oxygen, ventilation is a function of CO2 exchange not oxygenation.

Don't get me wrong, ventilation is required to bring room air (FiO2 of 21%) into your alveoli which will bring oxygen rich gas to your alveolar capillary membrane IF you were just breathing room air. However we are talking specifically about providing supplemental oxygen so that you don't need to inspire in order to bring in fresh O2. As long as someone has a high FiO2 with high flows, non collapsed alveoli, normal hemoglobin, and normal cardiac output, your body does not need to inspire to bring fresh oxygen because its being supplemented with high flow which will bind to hemoglobin.

However, expiration is a passive process that is required to eliminate CO2. As long as you are not expiring, you will build up CO2. As PaCO2 builds up, it will equilibrate with PACO2 in the alveloi which will not allow gas exchange between blood CO2 and the airspace. PaO2 will always be lower than the PAO2 being delivered so gas exchange will be present. However as more and more CO2 builds up, it will displace oxygen from the airspace which will eventually cause hypoxia. With health lungs, this could take 30 minutes to an hour.

 

[sevoflurane]

Just to add a bit to this thread.

FRC=2500ml
VO2= 3ml/kg or roughly 250cc/min

Fully pre-oxygenated, without supplemental O2 would equal:

2500ml/(250cc/min) = maximum of about 10 minutes.