Peep

[bkell101]

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Two ARDS patients not doing well in the micu right now....

PEEP is all the way up to 17. Is there a max on peep?

Can too much peep create dead space ventilation by creating such high alveolar pressure and ceasing flow in the arteries passing by?

 

[rsgillmd]

Two ARDS patients not doing well in the micu right now....

PEEP is all the way up to 17. Is there a max on peep?

Can too much peep create dead space ventilation by creating such high alveolar pressure and ceasing flow in the arteries passing by?

I don't do critical care in the units, so I don't know what the current literature says. However, if you go high enough on your ventilation pressures you can start to impair cardiac output. Optimal PEEP/Best PEEP is defined as the best compromise between ventilation and cardiac output. I've seen PEEP around 20 or so a few times before. Not unusual.

There is a good article from the summer or fall of 2004 in NEJM that describes the use of low tidal volume, high PEEP ventilation. There is a table in that article that gives some suggested ventilatory strategies. It may give some indication of how high they went on PEEP.

ARDS is definitely an interesting topic. Besides high PEEP/low tidal volumes, you can go into other things such as use of muscle relaxants, alternative modes of ventilation (such as APRV), permissive hypercapnia, prone position ventilation (I've never seen it in the ICU), etc. But that is starting to go off topic.

Keep reading and asking questions.

 

[bigdan]

The ARDSnet protocol describes adjusting your PEEP and FiO2 in concert with one another; their little protocol card gives examples up to PEEP of 24. Check it out on the Google. Agree with above regarding"best PEEP".

 

[Stellar Clouds]

Could always try VDR if your ICU has them

Or it is at least worth you looking up

 

[Bostonredsox]

Peep increases intrathoracic pressures thus at high levels it produces a tamponade effect and can markedly diminish cardiac output as well as worsen hypotension. That said ARDS is a special beast. I have seen peeps approaching 30 in bad cases. There's a good synopsis of current guidelines in ventilation strategys in ARDS from CHEST you should look into.

 

[Idiopathic]

the keys are tolerating hypercarbia and possibly treating acidosis with medical therapies, being realistic with your oxygenation goals (like PO2>60) until the capillary leak and fluid sequestration have improved and preventing barotrauma and atalectrauma with big intrapulmonary pressure shifts (i.e. the process of ventilation). the benefts of high PEEP arent really noticed if you cant keep your peak pressures under 35, so PEEP to 30, as mentioned, would not only not be expected to benefit in long term outcomes, it could also lead to significant right heart dysfunction.

if you cant keep your oxygen saturation at 90 with PEEP of 20 then I think you should be thinking of VDR/prone or both

 

[Idiopathic]

Two ARDS patients not doing well in the micu right now....

PEEP is all the way up to 17. Is there a max on peep?

Can too much peep create dead space ventilation by creating such high alveolar pressure and ceasing flow in the arteries passing by?

to directly answer your question, yes high PEEP will increase dead space ventilation, BUT this is better than large shunt, which is what happens when you allow the lung to be compressed and have atalectasis. so overdistending the alveoli allows the ones that are well perfused to ventilate/exchange oxygen and CO2, and allows ones that are overdistended to not shunt as much blood through their regional circulation. this helps oxygenation, but you then will need to focus on therapies to tolerate the inevitable hypercarbia (high CO2) that will result - because you are right, you will increase dead space, but improve your shunting.

 

[bobow98]

Just a med student here but should you probably keep an eye on the cardiac output when increasing peep significantly?

Sent from my ADR6425LVW using SDN Mobile

 

[Idiopathic]

Just a med student here but should you probably keep an eye on the cardiac output when increasing peep significantly?

Sent from my ADR6425LVW using SDN Mobile

sure, but you should always keep an eye on the cardiac output, right? use of hemodynamic tools such as blood pressure, heart rate, and metabolic variables such as lactate and base deficit are usually good ways to ensure that you arent doing too much damage to the CO, and are maintaining organ perfusion. some cases will benefit from more direct monitoring like arterial lines and pulmonary artery catheters. also its important that these patients have good filling pressures to tolerate the intrathoracic pressure, but too much intravenous fluid administration is a common problem, and correlates with poor outcomes. definitely a line to be walked here

 

[seinfeld]

You are right, too much peep and you will loose the benefit of the decreased shunt secondary to increased dead space ventilation. I have personally also accomplished this with aggressive diuresis as well, leaving essential no perfusion to West Zones I,II.

Although ETCO2 is not accurate in ARDS it can be used as a sign of over distention and increasing dead space. Some ventilators you can have them do a "best" peep using this technology. Essentially you adjust peep until you see a dramatic decline in ETCO2 indicating that you have lost gas exchange secondary to over distention.

What you should be looking at is the MEAN airway pressure. You can have lower PEEP but higher MAPs secondary to adjustment in Inspiratory time or secondary to ventilator Flow characteristics (square wave versus decelerating flow). High MAP are the idea behind Oscillators (hopefully these last 2 NEJM articles put the technology back in the closet) and APRV.

Having said all that, i will echo what others say. Keep Plateau pressure around 25 or the Change in airway pressure (delta P, the difference between plateau and PEEP) somewhere around 15. Peep and improved Oxygenation have not been shown to improve mortality, so biggest thing you can do is to not further harm the patient. If the patient is young and otherwise healthy consider early ECMO or a transfer to a center which treats a lot of ARDS.

 

[bigdan]

consider early ECMO or a transfer to a center which treats a lot of ARDS.

Spoken like a Michigan Man! I'm gonna start my ICU fellowship there in June - can't wait!

 

[rsgillmd]

.........What you should be looking at is the MEAN airway pressure. You can have lower PEEP but higher MAPs secondary to adjustment in Inspiratory time or secondary to ventilator Flow characteristics (square wave versus decelerating flow). High MAP are the idea behind Oscillators (hopefully these last 2 NEJM articles put the technology back in the closet) and APRV.......

Seinfeld, can you elaborate a little bit on mean airway pressure. Either I am searching wrong or looking in the wrong places. I never got a good explanation of what mean airway pressure refers to, what factors go into it, and what to do with the information. It's usually just a one liner like you mentioned -- that maintaining a high mean airway is the idea behind oscillators. Do I need to pick up a NICU book? Can you point me to some resources?

Peak and plateau pressure I understand. That's usually covered fairly well in our anesthesia textbooks. Mean airway pressure is something that has eluded my understanding.

Thanks.

 

[Hernandez]

You are right, too much peep and you will loose the benefit of the decreased shunt secondary to increased dead space ventilation. I have personally also accomplished this with aggressive diuresis as well, leaving essential no perfusion to West Zones I,II.

Although ETCO2 is not accurate in ARDS it can be used as a sign of over distention and increasing dead space. Some ventilators you can have them do a "best" peep using this technology. Essentially you adjust peep until you see a dramatic decline in ETCO2 indicating that you have lost gas exchange secondary to over distention.

What you should be looking at is the MEAN airway pressure. You can have lower PEEP but higher MAPs secondary to adjustment in Inspiratory time or secondary to ventilator Flow characteristics (square wave versus decelerating flow). High MAP are the idea behind Oscillators (hopefully these last 2 NEJM articles put the technology back in the closet) and APRV.

Having said all that, i will echo what others say. Keep Plateau pressure around 25 or the Change in airway pressure (delta P, the difference between plateau and PEEP) somewhere around 15. Peep and improved Oxygenation have not been shown to improve mortality, so biggest thing you can do is to not further harm the patient. If the patient is young and otherwise healthy consider early ECMO or a transfer to a center which treats a lot of ARDS.

I'm much bigger fan of Volumetric ET CO2 for this purpose, if you have a NICO monitor. Is much more sensitive and you will see a decrease in VCO2 before it effects ETCO2.

I'd also add for shipping for ECMO, I'd suggest sending to an ELOS accreditided facility .

Seinfeld, can you elaborate a little bit on mean airway pressure. Either I am searching wrong or looking in the wrong places. I never got a good explanation of what mean airway pressure refers to, what factors go into it, and what to do with the information. It's usually just a one liner like you mentioned -- that maintaining a high mean airway is the idea behind oscillators. Do I need to pick up a NICU book? Can you point me to some resources?

Peak and plateau pressure I understand. That's usually covered fairly well in our anesthesia textbooks. Mean airway pressure is something that has eluded my understanding.

Thanks.

You can titrate your peep to the point where the mean pressures start increasing, then you're likely starting to over distend.

 

[Idiopathic]

Seinfeld, can you elaborate a little bit on mean airway pressure. Either I am searching wrong or looking in the wrong places. I never got a good explanation of what mean airway pressure refers to, what factors go into it, and what to do with the information. It's usually just a one liner like you mentioned -- that maintaining a high mean airway is the idea behind oscillators. Do I need to pick up a NICU book? Can you point me to some resources?

Peak and plateau pressure I understand. That's usually covered fairly well in our anesthesia textbooks. Mean airway pressure is something that has eluded my understanding.

Thanks.

mean airway pressure is just what it sounds like. its the pressure in the airways over time, and the simplest depiction of it is

MawP = [(peak pressure * time at peak pressure or time in inspiration) +(PEEP * time at PEEP or time in expiration)] / time of one breath cycle

SO, if you spend 1 minute not ventilating but maintain a PEEP of 20 then your men is 20, if you have a PEEP of 20 and take 15 breaths at a pressure of 10 over PEEP and at a 1:3 ratio of in:ex then your mean is calculated this way

[(30 * 1) + (20 * 3)]/4 = 90/4 or 22.5

if you breathe at a 1:1 ratio but at the same pressures, then your mean goes up to

[(30 * 1) + (20 * 1)]/2 = 50/2 or 25, which makes sense since you spend half your time at 30 and half your time at 20, so your mean will be halfway between the two. so, this is why APRV and inverse ratio (or bi-level) ventilation augment your mean airway pressure without increasing your peak airway pressures, and why they are go-to maneuvers for challenging hypoxia.

the more subtle changes to mean pressures come from adjusting the waveform, or changing the slope of the rise up or down during ventilation. for instance if you spend more time decreasing your PIP down to PEEP during expiration (or slowing the expiratory phase) then you will functionally raise your mean airway pressure. important to remember that these maneuvers will often have a price to pay with retention of CO2 and this is why it is suggested that you tolerate hypercapnia to achieve oxygenation in all but the worse cases (i.e. severely raised ICP)

sorry if this is basic, its a good med student/resident review

 

[Idiopathic]

.

 

[rsgillmd]

mean airway pressure is just what it sounds like. its the pressure in the airways over time, and the simplest depiction of it is

MawP = [(peak pressure * time at peak pressure or time in inspiration) +(PEEP * time at PEEP or time in expiration)] / time of one breath cycle

SO, if you spend 1 minute not ventilating but maintain a PEEP of 20 then your men is 20, if you have a PEEP of 20 and take 15 breaths at a pressure of 10 over PEEP and at a 1:3 ratio of in:ex then your mean is calculated this way

[(30 * 1) + (20 * 3)]/4 = 90/4 or 22.5

if you breathe at a 1:1 ratio but at the same pressures, then your mean goes up to

[(30 * 1) + (20 * 1)]/2 = 50/2 or 25, which makes sense since you spend half your time at 30 and half your time at 20, so your mean will be halfway between the two. so, this is why APRV and inverse ratio (or bi-level) ventilation augment your mean airway pressure without increasing your peak airway pressures, and why they are go-to maneuvers for challenging hypoxia.

the more subtle changes to mean pressures come from adjusting the waveform, or changing the slope of the rise up or down during ventilation. for instance if you spend more time decreasing your PIP down to PEEP during expiration (or slowing the expiratory phase) then you will functionally raise your mean airway pressure. important to remember that these maneuvers will often have a price to pay with retention of CO2 and this is why it is suggested that you tolerate hypercapnia to achieve oxygenation in all but the worse cases (i.e. severely raised ICP)

sorry if this is basic, its a good med student review

Thanks for the explanation. It is greatly appreciated.

 

[Idiopathic]

yeah i guess its more of a resident/fellow review, however. i certainly didnt learn it in med school

 

[bkell101]

You are right, too much peep and you will loose the benefit of the decreased shunt secondary to increased dead space ventilation. I have personally also accomplished this with aggressive diuresis as well, leaving essential no perfusion to West Zones I,II."

Reading through west zones is exactly what provoked my question. Crazy too I had a Hall question that basically pointed out hypotension/too much lasix could lead to inc dead space.

"Although ETCO2 is not accurate in ARDS it can be used as a sign of over distention and increasing dead space. Some ventilators you can have them do a "best" peep using this technology. Essentially you adjust peep until you see a dramatic decline in ETCO2 indicating that you have lost gas exchange secondary to over distention. "

This is really interesting we have end tidal monitors available. I'll try it out in the future if my attending allows me. Would it ever be prudent to do a recruitment maneuver before going to really high levels of peep to improve that you have recruit able alveoli and have a chance to improve shunting...I think the up to date article touched on this concept.

 

[bkell101]

mean airway pressure is just what it sounds like. its the pressure in the airways over time, and the simplest depiction of it is

MawP = [(peak pressure * time at peak pressure or time in inspiration) +(PEEP * time at PEEP or time in expiration)] / time of one breath cycle

SO, if you spend 1 minute not ventilating but maintain a PEEP of 20 then your men is 20, if you have a PEEP of 20 and take 15 breaths at a pressure of 10 over PEEP and at a 1:3 ratio of in:ex then your mean is calculated this way

[(30 * 1) + (20 * 3)]/4 = 90/4 or 22.5

if you breathe at a 1:1 ratio but at the same pressures, then your mean goes up to

[(30 * 1) + (20 * 1)]/2 = 50/2 or 25, which makes sense since you spend half your time at 30 and half your time at 20, so your mean will be halfway between the two. so, this is why APRV and inverse ratio (or bi-level) ventilation augment your mean airway pressure without increasing your peak airway pressures, and why they are go-to maneuvers for challenging hypoxia.

the more subtle changes to mean pressures come from adjusting the waveform, or changing the slope of the rise up or down during ventilation. for instance if you spend more time decreasing your PIP down to PEEP during expiration (or slowing the expiratory phase) then you will functionally raise your mean airway pressure. important to remember that these maneuvers will often have a price to pay with retention of CO2 and this is why it is suggested that you tolerate hypercapnia to achieve oxygenation in all but the worse cases (i.e. severely raised ICP)

sorry if this is basic, its a good med student/resident review

This is awesome, ill have to take some time to digest this...

 

[bkell101]

One patient...the airway pressures were going up with the peep, we turned down the peep and the blood gases are showing pretty decent improvement in oxygenation

The other patient is now proned....now down to 80 percent fio2....my Attending (Michigan trained as well) says we'll try echo if no further improvement

Really interesting cases with good application of vent and lung mechanics, hopefully they become less interesting and start improving though

I believe We have a journal club coming up on how low airways pressures/ low tvv improved mortality independent of high peep strategy ....should be interesting

 

[Idiopathic]

the first case is probably overdistension that was relieved, allowing improvement in cardiac output and right to left flow, so that is a good lesson there - more PEEP can have deleterious effects

remember, its all about keeping the patient alive and oxygenating while the primary injury heals itself - its unlikely ecmo will have a mortality benefit in the second case, although if done earlier may have had a morbidity benefit. just my 0.02

 

[UBCmed09]

An important goal in titrating PEEP in lung-injured patients is to optimize the balance between recruiting atelectatic lung units and thus avoiding the damage done by cyclic recruitment and derecruitment. Esophageal manometry (although still with its critics) has shown some promise as a surrogate marker of transpulmonary pressure thus allowing arguably more rational titration of PEEP. I've seen it used in both morbid obese patients requiring ventilation as well as ARDS patients with sometimes remarkable results. I would suspect most large ICUs are at least occasionally using esophageal manometry. I can't recall his name but a prominent Boston intensivist makes quite a compelling case for using this in the most challenging ARDS patients.

Cheers,
UBCmed09

 

[Idiopathic]

An important goal in titrating PEEP in lung-injured patients is to optimize the balance between recruiting atelectatic lung units and thus avoiding the damage done by cyclic recruitment and derecruitment. Esophageal manometry (although still with its critics) has shown some promise as a surrogate marker of transpulmonary pressure thus allowing arguably more rational titration of PEEP. I've seen it used in both morbid obese patients requiring ventilation as well as ARDS patients with sometimes remarkable results. I would suspect most large ICUs are at least occasionally using esophageal manometry. I can't recall his name but a prominent Boston intensivist makes quite a compelling case for using this in the most challenging ARDS patients.

Cheers,
UBCmed09

i wouldnt use it routinely, but I can see how it might help in someone who is not responding as expected to appropriate Vt and PEEP. Honestly, I think knowing that someone had uncorrectably high intrathoracic pressures that you would have to overcome to oxygenate would help you decide to shift to VDR, go prone 🙂scared🙂, or go to ECMO quicker, although your supermorbid population in whom this is likely to provide beneficial information is also the population that will struggle with the last two modes of support

 

[Hernandez]

i wouldnt use it routinely, but I can see how it might help in someone who is not responding as expected to appropriate Vt and PEEP. Honestly, I think knowing that someone had uncorrectably high intrathoracic pressures that you would have to overcome to oxygenate would help you decide to shift to VDR, go prone 🙂scared🙂, or go to ECMO quicker, although your supermorbid population in whom this is likely to provide beneficial information is also the population that will struggle with the last two modes of support

VDR? Volumetric Diffusive Respiration? People still use that?

 

[Stellar Clouds]

VDR? Volumetric Diffusive Respiration? People still use that?

Yes it is still used. I had a patient on it for about a week when I was in the ICU back in November.

 

[Hernandez]

Yes it is still used. I had a patient on it for about a week when I was in the ICU back in November.

In what pt population?

 

[Idiopathic]

In what pt population?

Adult patients with ARDS? Severe inhalational injuries? It provides for better airway mechanics and better gas exchange in a more dynamic environment without the severely high delta in pressures needed with conventional modes. It also allows for better mobilization of secretions, although you sometimes have to leave the cuff down which makes me all

 

[Stellar Clouds]

In what pt population?

Cancer pt s/p pneumonectomy who developed ARDS. Couldn't maintain his o2 sat despite increases in FiO2 and airway pressures.

 

[seinfeld]

GREAT clinical discussion

Go Blue!!

 

[Bostonredsox]

Cancer pt s/p pneumonectomy who developed ARDS. Couldn't maintain his o2 sat despite increases in FiO2 and airway pressures.

Thats because your only ventialting one lung and that lung has develped ARDS. Hes toast my friend, use whatever modality you want.

I agree, this has been a nice and informative discussion. However, My shop has almost none of these nice toys available lol. it all translates to a transfer...can't wait for fellowship somewhere else 🙁

 

[Stellar Clouds]

Thats because your only ventialting one lung and that lung has develped ARDS. Hes toast my friend, use whatever modality you want.

I agree, this has been a nice and informative discussion. However, My shop has almost none of these nice toys available lol. it all translates to a transfer...can't wait for fellowship somewhere else 🙁

We all thought he was toast too. He was on VDR for about a week, switched back to a regular vent, and was weaned less than a week later.

 

[Bostonredsox]

We all thought he was toast too. He was on VDR for about a week, switched back to a regular vent, and was weaned less than a week later.

file that in your win column as an 'upset'. they dont come that often.

 

[Idiopathic]

We all thought he was toast too. He was on VDR for about a week, switched back to a regular vent, and was weaned less than a week later.

yeah thats a patient that i wouldnt even mess around with standard ventilation on, if they start to look bad they get VDR or ECMO if they are a reasonable ECMO candidate.

 

[Bostonredsox]

yeah thats a patient that i wouldnt even mess around with standard ventilation on, if they start to look bad they get VDR or ECMO if they are a reasonable ECMO candidate.

/nod...i ship that to the nearest facility with ECMO capabilities as soon as I see the xry.

 

[Hernandez]

Adult patients with ARDS? Severe inhalational injuries? It provides for better airway mechanics and better gas exchange in a more dynamic environment without the severely high delta in pressures needed with conventional modes. It also allows for better mobilization of secretions, although you sometimes have to leave the cuff down which makes me all

I don't think I've seen any data on VDR use in the pulm literature in the last 5 years and it only has a small blurb in tobin's. I'd bet that if placed to same level of scrutiny as HFOV it'll loose out to ARMA Protocol as well.

 

[Idiopathic]

I don't think I've seen any data on VDR use in the pulm literature in the last 5 years and it only has a small blurb in tobin's. I'd bet that if placed to same level of scrutiny as HFOV it'll loose out to ARMA Protocol as well.

we typically use it only for those patients off pathway or for who traditional ARDS strategies arent working. ECMO and proning have no significant proven benefit either, but they have been advocated for as well.

 

[Hernandez]

we typically use it only for those patients off pathway or for who traditional ARDS strategies arent working. ECMO and proning have no significant proven benefit either, but they have been advocated for as well.

Do you reserve this for failure for APRV as well? Or do you manage to get better minute ventilation using this so is it better in the pt population where HFOV and APRV would run a significant resp acidosis?

 

[Idiopathic]

Do you reserve this for failure for APRV as well? Or do you manage to get better minute ventilation using this so is it better in the pt population where HFOV and APRV would run a significant resp acidosis?

i typically lump in APRV/bilevel with conventional ventilation in this situation, even though I make sure my trainees realize the distinctions.

you definitely CAN get better minute ventilation, and save a lot of the barotrauma. its rescued several of my patients before when all other modes were failing, and ive paired it with prone ventilation as well, in an extreme case. I typically find that VDR is much better at allowing for the mobilizing of intrapulmonary secretions, which can be a good and bad thing, but definitely will need to happen to reduce the mismatch. ultimately, it allows you to use your mean airway pressure more effectively, i believe.

 

[fakin' the funk]

My mental shortcut for thinking about Mean Airway Pressure is that it's the pressure "pushing" the oxygen molecules into the pulmonary capillaries. Raise the Pmaw, you increase the pressure "pushing" those molecules in, and improve oxygenation.

This isn't really how it works physiologically, but it's a quick and dirty explanation how high-Pmaw techniques like APRV, inverse-ratio, and high-PEEP conventional volume control assist with oxygenation.

 

[fakin' the funk]

Can too much peep create dead space ventilation by creating such high alveolar pressure and ceasing flow in the arteries passing by?

This is why there's an "ideal" amount of lung distension with PEEP, where the tidal cycling is occurring between the Lower Inflection Point and the Upper Inflection Point on a pressure-volume curve.

If you overdistend with too much PEEP, you get a system with lower-than-ideal compliance and predispose to volutrauma/barotrauma. Same thing with tidal cycling below the LIP, but here you get atelectrauma.

My question for the practicing ICU people out there, is anyone actually constructing pressure-volume loops on real patients? Or is that just some theoretical BS I read in books?

 

[Idiopathic]

My mental shortcut for thinking about Mean Airway Pressure is that it's the pressure "pushing" the oxygen molecules into the pulmonary capillaries. Raise the Pmaw, you increase the pressure "pushing" those molecules in, and improve oxygenation.

This isn't really how it works physiologically, but it's a quick and dirty explanation how high-Pmaw techniques like APRV, inverse-ratio, and high-PEEP conventional volume control assist with oxygenation.

overly simplistic, in my opinion, but whatever works for you. i describe it as the pressure keeping the distal airways open, since we associate that both with positive effects such as oxygenation (decreased atalectasis) and with negative effects such as decreased capillary flow and barotrauma from too much pressure.

 

[Idiopathic]

This is why there's an "ideal" amount of lung distension with PEEP, where the tidal cycling is occurring between the Lower Inflection Point and the Upper Inflection Point on a pressure-volume curve.

If you overdistend with too much PEEP, you get a system with lower-than-ideal compliance and predispose to volutrauma/barotrauma. Same thing with tidal cycling below the LIP, but here you get atelectrauma.

My question for the practicing ICU people out there, is anyone actually constructing pressure-volume loops on real patients? Or is that just some theoretical BS I read in books?

yes but this just deals with pulmonary mechanics and not with cardiac output. you can be in ideal zone and still compromise cardiac output and right to left flow. i mainly use the loops when i am concerned about auto-PEEP that I cant appreciate from the ventilator screen

 

[RxBoy]

This is why there's an "ideal" amount of lung distension with PEEP, where the tidal cycling is occurring between the Lower Inflection Point and the Upper Inflection Point on a pressure-volume curve.

If you overdistend with too much PEEP, you get a system with lower-than-ideal compliance and predispose to volutrauma/barotrauma. Same thing with tidal cycling below the LIP, but here you get atelectrauma.

My question for the practicing ICU people out there, is anyone actually constructing pressure-volume loops on real patients? Or is that just some theoretical BS I read in books?

Its been found to not work well because you are constructing a static value on a dynamic system. Lungs exhibit hystersis when you add PEEP.

Surfactant allows alveoli to stay at higher volumes during expiration than inspiration. This is why expiration deflates slower on pressure volume loops and characteristically above the inspiratory curve instead of simply retracing it on the way down. As you add peep you arrive at a different FRC by the end of expiration than you had at the beginning. Hence there will be a new pressure-volume curve with different inflection points at the next tidal volume. I'll stop there because the details explaining these mechanics are incrediably confusing and more importantly essentially meaningless in clinical practice.

Long story short, you cant just use inflection points.