bpap cpap confusion

[coreytayloris]

Hi guys,

I'm doing a critical care rotation as part of my internship atm. I'm having real trouble understanding the mechanism and physiology underpinning bpap and cpap and how different settings alter p02 pc02 etc.does anyone have a good source to read/understand this? Thanks very much

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[jdh71]

Hi guys,

I'm doing a critical care rotation as part of my internship atm. I'm having real trouble understanding the mechanism and physiology underpinning bpap and cpap and how different settings alter p02 pc02 etc.does anyone have a good source to read/understand this? Thanks very much

It's just positive pressure. CPAP is continuous pressure and BiPAP has two different levels of pressure. CPAP helps with oxygen through increase in mean airway (alveolar) pressure, and is like PEEP on a vent. You can obviously also run oxygen though the mask. BiPAP helps with ventilation as the difference between the two pressures "moves air" in and out of the lung improving your minute ventilation (the difference is like increasing the volume on a volume controlled mode on the vent). CPAP is for hypoxic issues (PaO2) and BiPAP is for hypercapnic issues (PaCO2) - though most places don't seem to use pure CPAP for acute situations and just put patients on BiPAP. CPAP is great for pulmonary edema, use with heart failure as intubating an heart failure patient is generally the beginning, not the end, of the woes. Use BiPAP on the bad COPD exacerbation, trial them for an hour and if they make progress on their PaCO2 continue, if not, then intubate. Everything else is much more grab bag as far as "indication" for either modality, though we all almost always try BiPAP on just about everyone who is having some trouble, but not full on respiratory fialure, first prior to making a decision to intubate. We also use it on the DNR/DNI folks. Last caveat BiPAP is a recipe for disater in bad asthma. If the bad asthmatic is retaining CO2, don't trial with BiPAP, intubate, unless the patient refuses (this again is often the beginning fo the woes rather than the end of them, but there are very few things that go south quicker than a bad asthma).

Hope this helps.

 

[Hernandez]

It's CPAP is for hypoxic issues (PaO2) and BiPAP is for hypercapnic issues (PaCO2) - though most places don't seem to use pure CPAP for acute situations and just put patients on BiPAP..

Isn't this the truth. This is how I was trained as a IM resident by a damn good Pulmonologist, when I would do this as a fellow they'd look at me as if I had horns, but what do you expect when it's not uncommon to hear new RT grads stat (and cardiology fellow, cardiologists, and cardiovascular surgeons) state they increased tidal volume to help with the oxygenation.

 

[nephrondoc]

Can use CPAP for hypercapnea as well. For example, if hypercapnea is because of respiratory muscle fatigue from prolonged tachypnea, using CPAP or even increasing CPAP might improve compliance( Eg: Acute CHF) and decrease the work of breathing. Lot of times, if hypercapnea worsens, people just tend to increase IPAP. but, increasing PEEP or CPAP mighe be another worthy strategy as well.

 

[Hernandez]

Can use CPAP for hypercapnea as well. For example, if hypercapnea is because of respiratory muscle fatigue from prolonged tachypnea, using CPAP or even increasing CPAP might improve compliance( Eg: Acute CHF) and decrease the work of breathing. Lot of times, if hypercapnea worsens, people just tend to increase IPAP. but, increasing PEEP or CPAP mighe be another worthy strategy as well.

If you're to that point, NPPV has failed and just intubate.

I'd argue that the CPAP affect on CO2 Often has more to do with increased recruitment and decreasing dead space. Optimize your Vd/Vt will lower PaCO2

 

[turkeyjerky]

. Last caveat BiPAP is a recipe for disater in bad asthma. If the bad asthmatic is retaining CO2, don't trial with BiPAP, intubate, unless the patient refuses (this again is often the beginning fo the woes rather than the end of them, but there are very few things that go south quicker than a bad asthma).

Hope this helps.

Could you expound on this a little bit. I'm inclined to agree but would like to hear your reasoning. Thanks

 

[Mad Jack]

Isn't this the truth. This is how I was trained as a IM resident by a damn good Pulmonologist, when I would do this as a fellow they'd look at me as if I had horns, but what do you expect when it's not uncommon to hear new RT grads stat (and cardiology fellow, cardiologists, and cardiovascular surgeons) state they increased tidal volume to help with the oxygenation.

If an RT ever made it all the way through school and didn't know something that basic, they should be fired immediately. That's like, the foundation of mechanical ventilation- if you don't understand it, you're not safe to practice.

Could you expound on this a little bit. I'm inclined to agree but would like to hear your reasoning. Thanks

The big problem someone in status is having is one of air trapping- they can get air in, but due to the constriction at their bronchioles, they can't get it out. If you use BiPAP, you are increasing their tidal volume, resulting in them having even larger breaths and thus even more air trapping. They trap too much air and their lungs will distend to the point that you end up with venous return and alveolar capillary perfusion decreased to the point that they can't oxygenate anymore and ultimately die. Don't do it, ever.

 

[nephrondoc]

If you're to that point, NPPV has failed and just intubate.

I'd argue that the CPAP affect on CO2 Often has more to do with increased recruitment and decreasing dead space. Optimize your Vd/Vt will lower PaCO2

Didn't i say the same thing as well. Of course, you won't improve compliance without recruiting more lung. I used CHF specifically because CO2 elevation in those patients is mostly due to muscle fatigue. In those patients, no matter how much IPAP you increase without recruiting more lung, WOB and hence, CO2 will not improve. So, at that point, people assume that NPPV failed and intubate the patient. All that the patient needed was an additional PEEP to recruit more and hence improve on compliance. you don't have to work that hard to breathe if your lung compliance improves.

Also, i just said that people tend to increase IPAP when PCO2 goes up and that increasing CPAP/PEEP might be an option as well. No where did i suggest not to intubate. Obviously, if CO2 goes up on optimal NPPV settings, then answer is obvious.

I just can't agree that BiPAP is the treatment for hypercapnea always. It is for most scenarios but not always. CPAP can be used for hypercapnea in selective patients.

 

[Bobblehead]

One point of clarification, while the thread title correctly uses the generic BPAP for bi-level positive airway pressure (ventilation) several of the subsequent replies have been using "BiPAP" which is a registered trademark of the Respironics corporation and specifically refers to their mode of delivering BPAP.

If that's what the replies intended to reference that's fine, but it's something that I've always nitpicked when I see it written in the chart.

 

[Mad Jack]

If you're to that point, NPPV has failed and just intubate.

I'd argue that the CPAP affect on CO2 Often has more to do with increased recruitment and decreasing dead space. Optimize your Vd/Vt will lower PaCO2

Depends on the situation. If they've got CHF and their pH is still over 7.20 but they're working hard to breathe due to V/Q mismatch secondary to their tiring the **** out, sometimes giving them a bit of IPAP can relieve their WOB enough to keep them from getting tubed- they'll still have their rate in the high 20s/low 30s, but they won't be working near as hard to do so, and will be taking larger VTs per breath so you might be able to knock their CO2 down enough to keep them from buying a tube. It's a viable strategy in certain situations, such as when you've got someone with multiple comorbidities that might never come off the vent once they go on, but is definitely a situation that is an exception rather than a rule.

 

[jdh71]

JFC

If I had five dollars for every stupid pedantic cliche point made in this thread about NIPPV, I'd have my dinner paid for tonight.

 

[jdh71]

Didn't i say the same thing as well. Of course, you won't improve compliance without recruiting more lung. I used CHF specifically because CO2 elevation in those patients is mostly due to muscle fatigue. In those patients, no matter how much IPAP you increase without recruiting more lung, WOB and hence, CO2 will not improve. So, at that point, people assume that NPPV failed and intubate the patient. All that the patient needed was an additional PEEP to recruit more and hence improve on compliance. you don't have to work that hard to breathe if your lung compliance improves.

Also, i just said that people tend to increase IPAP when PCO2 goes up and that increasing CPAP/PEEP might be an option as well. No where did i suggest not to intubate. Obviously, if CO2 goes up on optimal NPPV settings, then answer is obvious.

I just can't agree that BiPAP is the treatment for hypercapnea always. It is for most scenarios but not always. CPAP can be used for hypercapnea in selective patients.

CPAP might well be a technical option on hypercapnia but it's simply a stupid strategy when you CAN improve their minute ventilation. You don't get any cool points in the real world for technical points. You get cool points for using the most effective and efficient modalities available to you at the time. And that means treating hypercapnia with bipap.

 

[jdh71]

Depends on the situation. If they've got CHF and their pH is still over 7.20 but they're working hard to breathe due to V/Q mismatch secondary to their tiring the **** out, sometimes giving them a bit of IPAP can relieve their WOB enough to keep them from getting tubed- they'll still have their rate in the high 20s/low 30s, but they won't be working near as hard to do so, and will be taking larger VTs per breath so you might be able to knock their CO2 down enough to keep them from buying a tube. It's a viable strategy in certain situations, such as when you've got someone with multiple comorbidities that might never come off the vent once they go on, but is definitely a situation that is an exception rather than a rule.

I'm with Hern on this one for the most part. If they look that shiitty then you can switch them to the bipap while I get set up for intubation but if they don't settle down fast they get a tube. I'll worry about getting them off a vent later. It's what I do for a living.

 

[Mad Jack]

I'm with Hern on this one for the most part. If they look that shiitty then you can switch them I've to bipap while I get set up for intubation but if they don't settle down fast they get a tube. I'll worry about getting them off a vent later. It's what I do for a living.

I agree- you don't try it for more than 10 minutes, and if it's not working at that point, tube them. But it's worth trying unless they're so far down the tubes that it's emergency territory already.

 

[Mad Jack]

JFC

If I had five dollars for every stupid pedantic cliche point made in this thread about NIPPV, I'd have my dinner paid for tonight.

NIPPV is probably the ventilation modality that is the most "art" and the least cut-and-dry science. It's far less predictable than traditional mechanical ventilation, and far more prone to anecdotes and people that respond in unexpected ways.

 

[Hernandez]

One point of clarification, while the thread title correctly uses the generic BPAP for bi-level positive airway pressure (ventilation) several of the subsequent replies have been using "BiPAP" which is a registered trademark of the Respironics corporation and specifically refers to their mode of delivering BPAP.

If that's what the replies intended to reference that's fine, but it's something that I've always nitpicked when I see it written in the chart.

Nitpick it to another Pulmonologist and you'd probably be told **** you I've got 25 other PTs to see and don't feel like writing the 18 additional other letters it takes to write out bi-level positive pressure ventilation.....

 

[Hernandez]

Didn't i say the same thing as well. Of course, you won't improve compliance without recruiting more lung. I used CHF specifically because CO2 elevation in those patients is mostly due to muscle fatigue. In those patients, no matter how much IPAP you increase without recruiting more lung, WOB and hence, CO2 will not improve. So, at that point, people assume that NPPV failed and intubate the patient. All that the patient needed was an additional PEEP to recruit more and hence improve on compliance. you don't have to work that hard to breathe if your lung compliance improves.

Also, i just said that people tend to increase IPAP when PCO2 goes up and that increasing CPAP/PEEP might be an option as well. No where did i suggest not to intubate. Obviously, if CO2 goes up on optimal NPPV settings, then answer is obvious.

I just can't agree that BiPAP is the treatment for hypercapnea always. It is for most scenarios but not always. CPAP can be used for hypercapnea in selective patients.

Not really, you're point although technically correct as going to confuse the hell out of someone who barely understands the physiology of the lung, it's be like me saying I can increase oxygenation by increasing IPAP which can have some affect buy increasing mean airway pressure but the direct measurable affect of increasing tidal volume or minute ventilation doesn't have much appreciable clinical affect on oxygenation. Or by saying by driving down co2 you skew the AAA grandient and increase oxygenation

Far too often people like patients languish on bipap and need to just get on with it and tube them. Consults where PTs have been on continuous bipap for days annoys me unless there is a dni on the chart

 

[Mad Jack]

Nitpick it to another Pulmonologist and you'd probably be told **** you I've got 25 other PTs to see and don't feel like writing the 18 additional other letters it takes to write out bi-level positive pressure ventilation.....

It's like insisting someone say bag-mask resuscitator instead of ambu-bag. Yeah, it's technically correct, but for the love of god, why?!

 

[nephrondoc]

CPAP might well be a technical option on hypercapnia but it's simply a stupid strategy when you CAN improve their minute ventilation. You don't get any cool points in the real world for technical points. You get cool points for using the most effective and efficient modalities available to you at the time. And that means treating hypercapnia with bipap.

In CHF with hypercapnea, the underlying pathology is fluid in the lungs causing increased WOB. The goal is to get that fluid out of lungs with PEEP and other cardiac interventions. Don't forget that when you open up new alveoli, you are also improving their minute ventilation.

BiPAP = Treating the symptoms because you are just trying to improve numbers aka minute ventilation without worrying about the underlying process.
PEEP/EPAP = treating the cause, because you are trying to correct the primary process which caused hypercapnea to begin with. Increasing IPAP and EPAP both at the same time may work even better at times.

By giving bold statements such as to use BiPAP for hypercapnea always, not only you are misguiding the upcoming medical students but also saying that any other methods that you don't use are rubbish. Like i said in my above posts, BiPAP is the best strategy for hypercapnea on most ocassions but not always. If you don't make medical students think at this stage of their career, they never will.

CPAP is a useful strategy in specific cases, provided you know who those patients are. I am not as busy for the patient as you are. Hence, i don't intubate without properly titrating the settings on NPPV just because i don't have time.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706602/

I will stop my 2cents on this thread here and have no interest in further arguments with you. I accept my defeat if that makes you happy. After all, the attending is always right and i am just a fellow.

 

[Hernandez]

CPAP is a useful strategy in specific cases, provided you know who those patients are. I am not as busy for the patient as you are. Hence, i don't intubate without properly titrating the settings on NPPV just because i don't have time.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706602/

You're getting so far beyond the physiology of what's needed for a medical student (whom asked the initial question) that you're muddling the topic and will promote further confusion,

A medical student needs to know that CO2 is affected by tidal volume and respiratory rate, and that increasing IPAP will help increase tidal volume, hence (usually) dropping CO2, then they need to know that FIO2 and Mean airway pressure (usually in the form of PEEP {another aside CPAP = PEEP} is what drives oxygenation)

You're alluding auto-peep/dynamic hyperinflation is better reserved for vent topics where you can illustrate the issue with scalars, definitely not an easy topic if you're using this

Properly setting NPPV isn't so proper, as mad jack said, it is an art and if you know your physiology you can get to the same point with different methods,

 

[jdh71]

In CHF with hypercapnea, the underlying pathology is fluid in the lungs causing increased WOB. The goal is to get that fluid out of lungs with PEEP and other cardiac interventions. Don't forget that when you open up new alveoli, you are also improving their minute ventilation.

BiPAP = Treating the symptoms because you are just trying to improve numbers aka minute ventilation without worrying about the underlying process.
PEEP/EPAP = treating the cause, because you are trying to correct the primary process which caused hypercapnea to begin with. Increasing IPAP and EPAP both at the same time may work even better at times.

By giving bold statements such as to use BiPAP for hypercapnea always, not only you are misguiding the upcoming medical students but also saying that any other methods that you don't use are rubbish. Like i said in my above posts, BiPAP is the best strategy for hypercapnea on most ocassions but not always. If you don't make medical students think at this stage of their career, they never will.

CPAP is a useful strategy in specific cases, provided you know who those patients are. I am not as busy for the patient as you are. Hence, i don't intubate without properly titrating the settings on NPPV just because i don't have time.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706602/

I will stop my 2cents on this thread here and have no interest in further arguments with you. I accept my defeat if that makes you happy. After all, the attending is always right and i am just a fellow.

Look genius, Bipap also uses all of that CPAP you're all twisted about in your pedantic attempt to try the most right guy in the room. You don't not have CPAP because you're using bipap. The CPAP is still there. And as far as I'm concerned you *ALWAYS* treat hypercapnia with Bipap if you're going to use NIPPV to do something about it. There is simply no reason to **** around with anything else in those situations. It doesn't make any sense to use CPAP because you every once in awhile can when you can just use the gorram bipap. I feel like I'm taking crazy pills in here right now.

The beautiful thing will be some day you'll be done and can use CPAP as little or as much as you like. Where is your god now?!???

 

[Hernandez]

This thread reminds me of post call fellow conferences which also always degraded into dick messuring contests.

 

[Mad Jack]

In CHF with hypercapnea, the underlying pathology is fluid in the lungs causing increased WOB. The goal is to get that fluid out of lungs with PEEP and other cardiac interventions. Don't forget that when you open up new alveoli, you are also improving their minute ventilation.

BiPAP = Treating the symptoms because you are just trying to improve numbers aka minute ventilation without worrying about the underlying process.
PEEP/EPAP = treating the cause, because you are trying to correct the primary process which caused hypercapnea to begin with. Increasing IPAP and EPAP both at the same time may work even better at times.

By giving bold statements such as to use BiPAP for hypercapnea always, not only you are misguiding the upcoming medical students but also saying that any other methods that you don't use are rubbish. Like i said in my above posts, BiPAP is the best strategy for hypercapnea on most ocassions but not always. If you don't make medical students think at this stage of their career, they never will.

CPAP is a useful strategy in specific cases, provided you know who those patients are. I am not as busy for the patient as you are. Hence, i don't intubate without properly titrating the settings on NPPV just because i don't have time.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706602/

I will stop my 2cents on this thread here and have no interest in further arguments with you. I accept my defeat if that makes you happy. After all, the attending is always right and i am just a fellow.

The thing is (and this is just my lame-ass view on it, so take it for what you will) that fluid takes time to go away. And while it's still in there, their juxtacapillary receptors are still going bats***, so you might as well make their life a little easier by giving them some BiPAP to help them along, because even after you correct some of the underlying hypercapnia via recruitment and whatnot, they're still going to be huffing and puffing away until their J receptors chill the **** out. Just giving them CPAP is not optimal on multiple levels. As jdh pointed out, it's not like you've got a limited amount of BiPAP to work with and you're going to run the tank dry- you might as well just use it, because it'll usually help clinically on several levels, and it'll make the patient feel better, which actually matters. Symptom control is big- once they start to freak out, they're going to get themselves into a spiral and get tubed, so anything you can do to make them feel better is a huge step in the right direction.

 

[jdh71]

This thread reminds me of post call fellow conferences which also always degraded into dick messuring contests.

My thoughts exactly.

 

[group_theory]

Makes me glad I'm no longer a fellow and have to deal with these issues ... if someone needs BiPap, put them on BiPap and recheck gas. If they fail, tube them (after discussing with POA/family if time). I've got a 30+ unit to run, plus 5+ patients in the Intermediate on BiPap/Vent, plus a couple in the ED that needs to be seen - don't have time to write "non-invasive bi-level positive pressure ventilation"

 

[deleted547339]

Good lord. There seems to be a ton of mental masturbation here.

 

[PlutoBoy]

Isn't this the truth. This is how I was trained as a IM resident by a damn good Pulmonologist, when I would do this as a fellow they'd look at me as if I had horns, but what do you expect when it's not uncommon to hear new RT grads stat (and cardiology fellow, cardiologists, and cardiovascular surgeons) state they increased tidal volume to help with the oxygenation.

 

[deleted171991]

Actually, increasing tidal volume can help with oxygenation, too, in case of atelectasis or V/Q mismatch secondary to low tidal volumes.

While a low Vt means less trauma, some people overdo it, or let the patient overbreathe the vent without proper PS, resulting in atelectasis and hypoxemia.

If the Vt is too low, PEEP won't help much.

 

[Hernandez]

Actually, increasing tidal volume can help with oxygenation, too, in case of atelectasis or V/Q mismatch secondary to low tidal volumes.

While a low Vt means less trauma, some people overdo it, or let the patient overbreathe the vent without proper PS, resulting in atelectasis (or at least a lot of V/Q mismatch, especially in diseased lungs) and hypoxemia.

When hypoventilation is the cause of hypoxemia, there are two kinds of bad knee-jerk reflexes: increasing the tidal volume in everybody and... increasing the respiratory rate in everybody. So don't laugh if people increase the Vt first to 6-8 ml/kg of IBW, instead of increasing the RR just to ventilate even fewer perfused alveoli.

So what you're saying is that in cases where people don't know how to properly titrate a vent they can on occasion get lucky by making further silly decisions. I know the anesthesia approach is different and yall talk closing volumes and other topics but the medical way is to affect FRC by peep titration and still maintain lower tidal volumes (but again is highly off topic to a medical student level discussion)

I have no issue in increasing tidal volume but without adjusting the peep to increase recruitment first it's silly. I'm still can't believe that things like volumetric capnography hasn't gotten more prevalent to help peep titrate since esophageal manometry is exceedingly difficult to interpret

 

[deleted171991]

WeO

So what you're saying is that in cases where people don't know how to properly titrate a vent they can on occasion get lucky by making further silly decisions. I know the anesthesia approach is different and yall talk closing volumes and other topics but the medical way is to affect FRC by peep titration and still maintain lower tidal volumes (but again is highly off topic to a medical student level discussion)

I have no issue in increasing tidal volume but without adjusting the peep to increase recruitment first it's silly. I'm still can't believe that things like volumetric capnography hasn't gotten more prevalent to help peep titrate since esophageal manometry is exceedingly difficult to interpret

I completely agree that nowadays, with few exceptions, there is no excuse for not having a good PEEP on, and trying to optimize that first. I am just saying that increasing the Vt short-term (even if normal) is not such a bad recruitment manuver. It's probably less traumatic to the lung than the recruitment maneuver the RT would do.

We might work in the OR, but the science is the same. Just the vents differ (especially in not coming with an RT attached - so we get to play a lot with them)

Even more OT: Is there any explanation for the lack of continuous graphical EtCO2 monitors in the ICU? Between those and a pulse oxymeter, there would be much less need for ABGs for vent adjustment (and it would be much faster).

 

[Hernandez]

Even more OT: Is there any explanation for the lack of continuous graphical EtCO2 monitors in the ICU? Between those and a pulse oxymeter, there would be much less need for ABGs for vent adjustment (and it would be much faster).

You're preaching to the choir, I've been actively advocating continuous ETCO2 in my ICU, but like everything people don't fully understand the physiology and don't take into consideration of other issues, and many ICU PTs have significant hemodynamic instability which further complicates the picture, in a hemodynamically stable pt with an unchanged minute ventilation and with stable oxygenation, ETco2 is fine

 

[deleted171991]

You're preaching to the choir, I've been actively advocating continuous ETCO2 in my ICU, but like everything people don't fully understand the physiology and don't take into consideration of other issues, and many ICU PTs have significant hemodynamic instability which further complicates the picture, in a hemodynamically stable pt with an unchanged minute ventilation and with stable oxygenation, ETco2 is fine

The physiology is very simple: the EtCO2 strongly correlates with the PCO2, except in the most unstable patients (from V/Q mismatch standpoint). There is an about 2-5 mmHg physiologic difference between the two, due to dead space ventilation, but it's a great tool to use in any intubated patient. (Even in sick patients, the pulmonary changes don't occur that fast, and after a few ABGs one can figure out the approximate PCO2-EtCO2 difference for that particular patient.) Not only that, but the particular form of its graph can diagnose a number of ventilatory problems. It's a great tool to set or adjust the vent. (ABGs are obviously better, but how many respiratory therapists have you seen using local anesthesia before they stick a patient's artery? It's pretty painful, and pain is the main complaint/memory related to a patient's ICU stay.)

Being hemodynamically unstable doesn't influence the EtCO2 much, until the cardiac output collapses (great tool to notice a significant PE, for example). And it's actually used to adjust MV during anesthesia, without the need for ABGs, in all kinds of unstable patients. It takes about 10 minutes of teaching to learn it, for anybody who understands basic pulmonary physiology. It's use during surgical or procedural anesthesia is required by anesthesia standards of care in any unconscious patient.

Here's what seem to be comprehensive 7-episode tutorial:

Part 1:


Part 2:


Part 3:


Part 4:


Part 5:

 

[Hernandez]

The physiology is very simple: the EtCO2 strongly correlates with the PCO2. There is an about 2-5 mmHg difference between the two, due to dead space ventilation, but it's a great tool to use in any intubated patient. Not only that, but the particular form of its graph can diagnose a number of ventilatory problems. A monitor like that costs a few thousand bucks, peanuts for an ICU budget.

Being hemodynamically unstable doesn't influence the EtCO2 much, until the cardiac output collapses (great tool to diagnose a significant PE, for example). And it's actually used to adjust MV during anesthesia, without the need for ABGs, in all kinds of unstable patients. It takes about 10 minutes of teaching to learn it, for anybody who understands basic pulmonary physiology. It's use is required by anesthesia standards of care in any unconscious patient.

You're anesthisa is showing......as this is not true. And this over simplified explanation is why it will never catch on in medical ICUs.

I can tell you I've seen many docs get annoyed when the ETCO2 is 35 and the PACO2 is 70. The problem is you're assuming a constant dead space fraction of ~20-30% AND you're assuming an unchanging dead space fraction. This is simply a bogus assumption in a medical Icu. @jdh71, how many times you see an ARDS pt's co2 go from 40 to 70 or more in less than 24 hours? I can tell you I've seen Vd/Vt ratio go from 30% to 50% in less than an hour. Much less the bad lungers who's baseline dead space is elevated, I've seen COPD PTs on a incremental stress tests have baseline Vd/Vt of 40%

And while it typically takes massive cardiac collapse to affect elimination of co2 mild hypotension and pressor use can affect you VCO2 production which can also affect your ETCO2 numbers. As will fevers, over supplementation in bad copders etc.

 

[deleted171991]

The last 2 episodes:

 

[deleted171991]

You're anesthisa is showing......as this is not true. And this over simplified explanation is why it will never catch on in medical ICUs.

I can tell you I've seen many docs get annoyed when the ETCO2 is 35 and the PACO2 is 70. The problem is you're assuming a constant dead space fraction of ~20-30% AND you're assuming an unchanging dead space fraction. This is simply a bogus assumption in a medical Icu. @jdh71, how many times you see an ARDS pt's co2 go from 40 to 70 or more in less than 24 hours? I can tell you I've seen Vd/Vt ratio go from 30% to 50% in less than an hour. Much less the bad lungers who's baseline dead space is elevated, I've seen COPD PTs on a incremental stress tests have baseline Vd/Vt of 40%

And while it typically takes massive cardiac collapse to affect elimination of co2 mild hypotension and pressor use can affect you VCO2 production which can also affect your ETCO2 numbers. As will fevers, over supplementation in bad copders etc.

I understand what you are saying, but I can tell you at least one class of patients with no excuse for the lack of EtCO2 monitoring: neuroICU patients intubated for cerebral protection. Also, in the SICU, a good number of intubated patients don't necessarily have such a significant respiratory pathology (especially those who come intubated from the OR).

And it's not just the absolute number. It's the sudden changes (of course, one has to watch it, and I bet nurses are not anxious to have one more thing to worry about) and the aspect of the waveform. The fact that a tool has limits does not mean that it's a bad tool, just that one should be aware of those limits.

 

[Hernandez]

I understand what you are saying, but I can tell you at least one class of patients with no excuse for the lack of EtCO2 monitoring: neuroICU patients intubated for cerebral protection. Also, in the SICU, a good number of intubated patients don't necessarily have such a significant respiratory pathology (especially those who come intubated from the OR).

And it's not just the absolute number. It's the sudden changes (of course, one has to watch it, and I bet nurses are not anxious to have one more thing to worry about) and the aspect of the waveform. The fact that a tool has limits does not mean that it's a bad tool, just that one should be aware of those limits.

I don't disagree with any of this, but it is the treating the medical pt like a surgical or Neuro pt with rarely have pulmonary issues is not applicable and causes mass annoyance with those who don't fully understand what they're measuring and hence why it isn't fully accepted.

And that's before you start talking continuous volumetric capnography.

 

[Mad Jack]

The physiology is very simple: the EtCO2 strongly correlates with the PCO2, except in the most unstable patients (from V/Q mismatch standpoint). There is an about 2-5 mmHg physiologic difference between the two, due to dead space ventilation, but it's a great tool to use in any intubated patient. (Even in sick patients, the pulmonary changes don't occur that fast, and after a few ABGs one can figure out the approximate PCO2-EtCO2 difference for that particular patient.) Not only that, but the particular form of its graph can diagnose a number of ventilatory problems. It's a great tool to set or adjust the vent. (ABGs are obviously better, but how many respiratory therapists have you seen using local anesthesia before they stick a patient's artery? It's pretty painful, and pain is the main complaint/memory related to a patient's ICU stay.)

Being hemodynamically unstable doesn't influence the EtCO2 much, until the cardiac output collapses (great tool to notice a significant PE, for example). And it's actually used to adjust MV during anesthesia, without the need for ABGs, in all kinds of unstable patients. It takes about 10 minutes of teaching to learn it, for anybody who understands basic pulmonary physiology. It's use during surgical or procedural anesthesia is required by anesthesia standards of care in any unconscious patient.

Here's what seem to be a good introduction:



The lecture has 5 more parts (accesible on Youtube).

We had EtCO2 monitoring in our ICUs. It was virtually useless in peds for anything but tracking trends because the kids were so sick. Worked great in adults. The trouble was always getting nurses, residents that were rotating from outside of the medical service, and interns to not freak out about how high some of the EtCO2 readings looked, because they just couldn't make the mental leap required to understand that it doesn't work well in certain patients due to the issues previously mentioned. They'd keep insisting on unnecessary ABGs regardless of the evidence that things were fine.

One of my favorite toys was one of these guys: http://www.radiometer.com/en/products/transcutaneous-monitoring

They took all the guesswork out of things and were quite reliable, cut our need to do heelsticks and ABGs in neonates by a ton. We only used them in NBICU because they're so expensive to operate though...

 

[deleted171991]

I am still shocked when I put the nasal cannula on a patient, for some minor sedation, and the end-tidal reads 60 (usually the nasal EtCo2 is diluted, hence much lower than the real PCO2). There are patients walking around with PCO2's of 70+.

 

[Hernandez]

There are patients walking around with PCO2's of 70+.

Welcome to my world

 

[deleted171991]

You wanna bet those patients are kept in the MICU at a PCO2 of 40, if they get intubated?

 

[Hernandez]

You wanna bet those patients are kept in the SICU at a PCO2 of 40, if they get intubated?

FIFY

 

[jdh71]

You wanna bet those patients are kept in the MICU at a PCO2 of 40, if they get intubated?

Not in my ICU. I can recognize a chronic lunger.

 

[jdh71]

The ETCO2 stuff is . . . well . . . "neat" . . . like an app on my phone that will find me the closest pizza place, and I suppose I'd use it if I had it around, but it's simply unnecessary as it wouldn't change basically anything about my practice in the ICU except give me one more number to look at. Hell, even the neuro patients you can dial in pretty fast and simply don't need to keep looking at the numbers.

I do like ETCO2 and capnography use for conscious sedation though

 

[Boatswain2PA]

The big problem someone in status is having is one of air trapping- they can get air in, but due to the constriction at their bronchioles, they can't get it out. If you use BiPAP, you are increasing their tidal volume, resulting in them having even larger breaths and thus even more air trapping. They trap too much air and their lungs will distend to the point that you end up with venous return and alveolar capillary perfusion decreased to the point that they can't oxygenate anymore and ultimately die. Don't do it, ever.

I'm late to this party, but doesn't the same thing apply to an intubated patient? I work ED, and I'm always terrified to intubate a severe asthmatic because of the significant increase in mortality that is associated with it in asthma. In the past month I have put two severe status patients on BiPap (sorry...BPAP) + ativan and watched them get much better before shipping them to tertiary care. I set the IPAP at 10, and turn the EPAP all the way down, and set the minimum rate at 10. The first patient was the sickest (she had been intubated SEVEN TIMES for asthma), and rapidly improved on BPap. Once she fell asleep she stopped overbreathing the BPAP so much and improved enough to ship. The second one did the same thing, but her rate never really came down below 30.

I haven't seen any studies showing the marked increase in mortality in status patients placed on BPAP like there are for status patients placed on ventilators.

What am I missing?

 

[Mad Jack]

I'm late to this party, but doesn't the same thing apply to an intubated patient? I work ED, and I'm always terrified to intubate a severe asthmatic because of the significant increase in mortality that is associated with it in asthma. In the past month I have put two severe status patients on BiPap (sorry...BPAP) + ativan and watched them get much better before shipping them to tertiary care. I set the IPAP at 10, and turn the EPAP all the way down, and set the minimum rate at 10. The first patient was the sickest (she had been intubated SEVEN TIMES for asthma), and rapidly improved on BPap. Once she fell asleep she stopped overbreathing the BPAP so much and improved enough to ship. The second one did the same thing, but her rate never really came down below 30.

I haven't seen any studies showing the marked increase in mortality in status patients placed on BPAP like there are for status patients placed on ventilators.

What am I missing?

I'm too tired to answer this. @jdh71 halp.

Very briefly though, from what I understand, the studies that showed an increase in mortality with intubation were older, most done in the 80s and 90s. A lot has changed since then so far as medication and how we ventilate patients since then. Truthfully, we really sucked at mechanical ventilation until very recently. Here's a more recent moderate-sized study on asthmatics requiring intubation: http://www.ncbi.nlm.nih.gov/pubmed/18773325

As to your strategy, it's anecdotes, so it's hard to say. Your first example probably had a severe anxiety component to their disease, which you provided relief for by diminishing their WOB and providing ativan. Your latter patient, it would be impossible to say without knowing the full course of their admission- it's possible they were at the brink of tiring out when you threw them on BiPAP and it was just enough to keep them over the hump for a little while. Whether they ultimately completely tired out or if the medications were enough to get them to break we don't really know. And whether BiPAP is effective or safe in asthmatics is also difficult to know- there has yet to be a strong multi center study that I know of that has explored the issue. Here's a recent paper examining the question, that ultimately doesn't come to any real conclusion aside from "more research is needed:"

http://err.ersjournals.com/content/19/115/39.long

I've done BiPAP on asthmatics, usually while running continuous albuterol at 20 mg/hr, and seen good results- the theory being that the extra IPAP helps the medication penetrate deeper into the lungs, while also diminishing WOB. On some patients, it works like a charm. On others, not so much. I think it's worth trailing certain patients on BiPAP (keep in mind I am not a doctor, just a med student and former RT, so take my recommendations with a grain of salt) briefly, with settings on the low side (10/5) and either continuous or q20 minute albuterol nebs. If they don't look better within 15 minutes (gas deteriorating, anxiety increasing, sats dropping) tube 'em. The caveat here is you don't wait if their pH already looks like ****- BiPAP in asthmatics is great for WOB but terrible for correcting CO2 due to the air trapping component.

Usually our rough order of treatment for a bad asthmatic was Albuterol q2>Albuterol q1> Continuous neb 5-20mg/hr (you kind of play starting dose by ear)>BiPAP+Continous if their gas was relatively okay>intubate if BiPAP fails or their gas is bad.

 

[Boatswain2PA]

Thank you for the links. In my environment I doubt there are any true ventilator experts for 250 miles in any direction. I'm certainly not one, yet I feel more proficient than the flight or ground crews that will be caring for them in transit. A few years ago a CRNA manage an intubated asthmatic kid who wound up dieing in my shop, and I'm relatively convinced it was due to poor vent management (stacking). Because of this I consider it a success if I can manage them on bipap alone without intubation. But of course, if they didn't improve on the bipap, then I would have intubated them bbefore transport.

Both these patients had their gasses improve with bipap in my shop, both were flown to tertiary, neither were intubated in their course of stay, and both are back in my little community waiting for the next time their smoking habit tries to kill them. One thing that bothers me though is I can't figure out why the second patient's rate never dropped. Her Sats (pulse ox and PaO2) improved, and her PaCO2 significantly improved as well, yet she kept overbreathing......

 

[Mad Jack]

Thank you for the links. In my environment I doubt there are any true ventilator experts for 250 miles in any direction. I'm certainly not one, yet I feel more proficient than the flight or ground crews that will be caring for them in transit. A few years ago a CRNA manage an intubated asthmatic kid who wound up dieing in my shop, and I'm relatively convinced it was due to poor vent management (stacking). Because of this I consider it a success if I can manage them on bipap alone without intubation. But of course, if they didn't improve on the bipap, then I would have intubated them bbefore transport.

Both these patients had their gasses improve with bipap in my shop, both were flown to tertiary, neither were intubated in their course of stay, and both are back in my little community waiting for the next time their smoking habit tries to kill them. One thing that bothers me though is I can't figure out why the second patient's rate never dropped. Her Sats (pulse ox and PaO2) improved, and her PaCO2 significantly improved as well, yet she kept overbreathing......

I've got some theories, but it's really hard to say.

I've seen some downright criminal vent management at a community hospital in the past- 10 cc/kg on all patients with zero PEEP and mid-30s PIP when initiating a vent levels of bad. The ICU director didn't "believe" in PEEP unless it was "absolutely necessary." That right there is exactly why critical care trained physicians should be running units. Bad vent management will straight up kill your patients.

 

[Mad Jack]

Did your second patient's CO2 normalize at a rate of 30 or was she hypocarbic?

 

[jdh71]

I'm late to this party, but doesn't the same thing apply to an intubated patient? I work ED, and I'm always terrified to intubate a severe asthmatic because of the significant increase in mortality that is associated with it in asthma. In the past month I have put two severe status patients on BiPap (sorry...BPAP) + ativan and watched them get much better before shipping them to tertiary care. I set the IPAP at 10, and turn the EPAP all the way down, and set the minimum rate at 10. The first patient was the sickest (she had been intubated SEVEN TIMES for asthma), and rapidly improved on BPap. Once she fell asleep she stopped overbreathing the BPAP so much and improved enough to ship. The second one did the same thing, but her rate never really came down below 30.

I haven't seen any studies showing the marked increase in mortality in status patients placed on BPAP like there are for status patients placed on ventilators.

What am I missing?

You think it's the vent in those bad asthmatics in those studies that increased mortality or maybe it was just that folks who are really really sick get intubated and really really sick people tend to die more often because they are really really sick people.

I used to have a similar discussing with the BMT folks and diffuse alveolar hemorrhage. They'd tell me that BMT patient with DAH that got intubated did worse.



Really? So you mean that people who had DAH that so bad it caused a hypoxia that couldn't be treated with noninvasive methods because their lungs were full of blood from all of the things we did to them. Those people with the lungs full of blood did worse?!??? Are you see my point here?? These patients have a very bad problem and it's not actually the vent. The fact that vented patients die more often us because they are sicker and needed a vent.

Same with asthma. Bipap can decrease the work of breathing and buy you some time if you need it and to be honest of you don't know what you're doing with a vent and a bad asthmatic maybe Bipap is the best solution until you can get them to someone who can if you can so it quick. However in asthma when the resp failure happens and it will happen in an instant *BOOM!* you're going to want that tube in place.

 

[Hernandez]

I'm late to this party, but doesn't the same thing apply to an intubated patient? I work ED, and I'm always terrified to intubate a severe asthmatic because of the significant increase in mortality that is associated with it in asthma. In the past month I have put two severe status patients on BiPap (sorry...BPAP) + ativan and watched them get much better before shipping them to tertiary care. I set the IPAP at 10, and turn the EPAP all the way down, and set the minimum rate at 10. The first patient was the sickest (she had been intubated SEVEN TIMES for asthma), and rapidly improved on BPap. Once she fell asleep she stopped overbreathing the BPAP so much and improved enough to ship. The second one did the same thing, but her rate never really came down below 30.

I haven't seen any studies showing the marked increase in mortality in status patients placed on BPAP like there are for status patients placed on ventilators.

What am I missing?

It depends on lots of variables. But at end of day it's more to do as jack said lack of actually doing the studies. Thankfully in this day and age this horrific asthma is uncommon and really tends to be limited to poverty inner city populations. I haven't seen an asthmatic die in years, it's even been since my 1st year fellowship since I had to break out an Anesthisia machine for a status pt.

Every pt is different and I'm a huge proponent of looking at the scalars and adjusting based off that, but I'm probably contradicting myself from a previous post, but on a bipap asthma pt Id probably start just opposite as what you have done, either pure cpap to start or a higher EPAP with a IPAP only a few cm above EPAP. Because the underlying physiology is basically auto-peep and on a spontaneously breathing pt on bipap you don't have as much control over TV or RR so you need to help "stint" open the airways to relieve some of the dynamic hyperinflation. The cleveland clinic journal of medicine had a good review article for auto-peep and in asthma PTs that would be kinda where I start and adjust from there depending on scalars and clinical appearance. .....and then give some ketamine.....