Couple of vent questions.

[redy]

1) PRVC aims to give the target Tv with the least PIP, right? So in a patient with huge inspiratory efforts, as the pt will pull in tv without much pressure requirements from the vent, he is basically doing his own WOB without much vent assistance right?

This comes from a patient of mine who on PRVC with target Tv of 500 is pulling Tv of 700 (he is having a high minute vent requirement due to increased dead space from post sarcoidosis fibrocystic disease). The RT says the pip is 8, same as peep of 8 which is indicative of the fact that the machine is not giving any assistance as he is getting all his tv with 0 of pip (which is the least pressure in this case to achieve target volume). Is this all correct?

2) If all of that is correct, then what mode is his WOB least? Pressure support?

3) which leads to my final question. What is the difference in pressure support vs. pressure control? Flow cycled vs time cycled? What does that mean in practical terms?

4) obviously I need to read more on the intricacies of mech vent and the different modes. Suggested reading material?



Thanks a lot.

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[jdh71]

The mode where WOB is least is the mode where WOB is least. That's NOT a typo. Play around with the modes. If the patient is still dysynchronous think about your sedation and if you have enough and if they are so out of control you can't deal with it using your vent modes and sedation, paralyze them and see what the hell is going on. If they need to be parsluzed to keep them from killinh themselves, then freaking parsluze thfm for 24 to 48 hoors shile the critical illness calms down if need be. We all prefer lower tidal volumes even in lungs with normal compliance but sometimes if the patient wants big volumes and its not harming their pressures let them have what they want.

This isn't an algorithm it's an art.

 

[redy]

The mode where WOB is least is the mode where WOB is least. That's NOT a typo. Play around with the modes. If the patient is still dysynchronous think about your sedation and if you have enough and if they are so out of control you can't deal with it using your vent modes and sedation, paralyze them and see what the hell is going on. If they need to be parsluzed to keep them from killinh themselves, then freaking parsluze thfm for 24 to 48 hoors shile the critical illness calms down if need be. We all prefer lower tidal volumes even in lungs with normal compliance but sometimes if the patient wants big volumes and its not harming their pressures let them have what they want.

This isn't an algorithm it's an art.

Thanks for the reply. I appreciate the art aspect of it but I am trying to better understand the science of it here.

The patient's not really dysynchronous with the vent unless pulling in huge Tv is dysynchrony. He is pulling them for a reason though so I want to let him have what he wants. My question was how best to deliver what he wants while minimizing his WOB? Pressure support or volume assist/control? The question came about because I didn't think his WOB was that bad despite pulling bigger Tv when on PRVC till the RT pointed out how he was doing all the WOB in PRVC (as I said above). So I am asking are there issues in the other modes too which might mean I am not helping his WOB as much as I think I am.

 

[Hernandez]

1) PRVC aims to give the target Tv with the least PIP, right? So in a patient with huge inspiratory efforts, as the pt will pull in tv without much pressure requirements from the vent, he is basically doing his own WOB without much vent assistance right?

PRVC isn't a standard moniker and different vents handle it differently. But my main understanding is that it's primary use is to adjust delivery to attempt to still give a set volume in patients who tend have higher peak pressures. If they aren't peaking out, the vent usually still behaves as a VACV vent.

Honestly I do not use this mode, its trying to bastardized 2 different modes and frankly I'd rather "**** or get off the pot" and either fix VACV or go with another mode.

This comes from a patient of mine who on PRVC with target Tv of 500 is pulling Tv of 700 (he is having a high minute vent requirement due to increased dead space from post sarcoidosis fibrocystic disease). The RT says the pip is 8, same as peep of 8 which is indicative of the fact that the machine is not giving any assistance as he is getting all his tv with 0 of pip (which is the least pressure in this case to achieve target volume). Is this all correct?

Incorrect. If I understand you, it isn't that the vent isn't giving support, it's that the patient is generating such a negative force that the vent isn't able to keep up with flow/pressure that he needs. You can tweak this by either increasing flow, pressure, tidal volume or increasing sedation

2) If all of that is correct, then what mode is his WOB least? Pressure support?

Completely depends on the situation. At times if it's say....a profound GI bleed who is developing lactic acidosis with relatively normal lung architecture I will place them on pressure support and adjust the PSV based on clinical scenarios. If they're in ARDS or have ****ty lungs, I'll tend to either sedate/paralyze or use PCV, if I can't get them to settle down and they still have a very high rate, this the patient population where I like bilevel and will utilize a normal I:E, I just did this this week.

3)which leads to my final question. What is the difference in pressure support vs. pressure control?

One is support and one is control, duh. In pressure SUPPORT, there is not mandated breath, if you're apnic you're apnic, in PCV, well, the easiest way to think about it is that it is CMV that modulates pressure not volume. There are a few minor differences but for all practical purposes VACV = PACV, and an experienced user can make either mode 99% equivalent

Flow cycled vs time cycled? What does that mean in practical terms?

Nothing you should concern yourself with. However, short explanation depends on patient effort. Time cycle refers to a mandatory breath. Let's say someone is brain dead and has no respiratory drive, if the vent is set on volume control, 12x500 50%+5. If there is no patient initiated breath by the 5 second interval; the machine will initiate a breath. In flow cycled (and also pressure cycled) if you have a patient with the same setting as above who initiates a breath by generating a negative flow (usually 2L/min), the machine will initiate a breath, same for pressure, and in this day and age, most vents are a combination of both time and flow/pressure cycled. If ya wanted to get nit picky, you could describe a volume control vent as a flow cycled, volume regulated, with a time cycle back up assist control ventilation.

4) obviously I need to read more on the intricacies of mech vent and the different modes. Suggested reading material?



Thanks a lot.

Tobin's.

 

[jdh71]

Thanks for the reply. I appreciate the art aspect of it but I am trying to better understand the science of it here.

The patient's not really dysynchronous with the vent unless pulling in huge Tv is dysynchrony. He is pulling them for a reason though so I want to let him have what he wants. My question was how best to deliver what he wants while minimizing his WOB? Pressure support or volume assist/control? The question came about because I didn't think his WOB was that bad despite pulling bigger Tv when on PRVC till the RT pointed out how he was doing all the WOB in PRVC (as I said above). So I am asking are there issues in the other modes too which might mean I am not helping his WOB as much as I think I am.

You don't think pulling in huge tidal volumes when you have it set to a certain volume isn't a bit "off" from what you're trying to do clinically?

This is one reason I'm not a huge fan of PRVC and similar modes. The patient's flow demands can end up delivering more volume than you want. Which is why I'm definitely with hern: decide what you *really* want, pressure or volume, controlled, set your vent accordingly.

Set the vent to the patient and what you're trying to do the rest is pretty "academic" for the most part.

 

[Bostonredsox]

Sort of on topic with the excess tv based on pt initiated breaths.

If you have a bad ards pt who you have on say vacv24, 390ml, 80% and 16...And they're pulling TVs of 550-600+...do you increase sedation/paralyze them to bring the TV down to 6ml/kg? I'm monitoring pPlat to ensure its under 30 and pH >7.2. But if whilst meeting those criteria,they are pulling TVs far above my set tv(I'm set @6-7ml/kg, they're pulling upwards of 9-10) I don't reflexively paralyze them. Should I be doing this differently?

 

[jdh71]

Sort of on topic with the excess tv based on pt initiated breaths.

If you have a bad ards pt who you have on say vacv24, 390ml, 80% and 16...And they're pulling TVs of 550-600+...do you increase sedation/paralyze them to bring the TV down to 6ml/kg? I'm monitoring pPlat to ensure its under 30 and pH >7.2. But if whilst meeting those criteria,they are pulling TVs far above my set tv(I'm set @6-7ml/kg, they're pulling upwards of 9-10) I don't reflexively paralyze them. Should I be doing this differently?

Turn off the autoflow first if you're using a drager. Turn off the "PRVC" on other vents. Set to a strict volume control mode. If you're not sure which setting this is on your vent ask the RT to show you.

 

[Hernandez]

Turn off the autoflow first if you're using a drager. Turn off the "PRVC" on other vents. Set to a strict volume control mode. If you're not sure which setting this is on your vent ask the RT to show you.

Also make sure the RT hasn't left an active nebulizer on the circuit on a vent that doesn't have the nebulizer function; the extra flow can screw with breath trigger and your tv numbers.

And many times, I will give extra sedation and a one time push of vec for these PTs

 

[jdh71]

Also make sure the RT hasn't left an active nebulizer on the circuit on a vent that doesn't have the nebulizer function; the extra flow can screw with breath trigger and your tv numbers.

And many times, I will give extra sedation and a one time push of vec for these PTs

I also like the single dose of paralytic to get a more accurate sense if what you are dealing with. Because the pressure is basically measured at the mouth, if you've got a patient actively creating negative intrathoracic through their own work your vent will show you falsely low peaks and plateaus

 

[Hernandez]

I also like the single dose of paralytic to get a more accurate sense if what you are dealing with. Because the pressure is basically measured at the mouth, if you've got a patient actively creating negative intrathoracic through their own work your vent will show you falsely low peaks and plateaus

Completely agree, my personal bias is on these PTs also is that if their airway pressures are high and they're a little dyschronous, I usually only need 1-2 pushes of vec and that usually shows then and they settle down and dot need more.

 

[Bostonredsox]

I'm with you on the single push of vec. I give it frequently on patients I can't get sedated post intubation where I'm giving big doses of fentantyl, versed and propofol, they're pressure is getting low yet there still thrashing around very dysynchronus. That push of vec byes about 30minutes of quiet and allows all the sedation to catch up and then they do not require any paralytic after that.

Your answers all make sense to me. I'll have to play around with the vents a bit we have a couple knowledgable RTs I can go over it with.

 

[redy]

Thanks for the answers. Appreciate it.

As a follow up on jdh statement on strict volume control mode, if I am not mistaken a pt can always pull in tv over what you have set in any mode, right or wrong?

 

[Hernandez]

Thanks for the answers. Appreciate it.

As a follow up on jdh statement on strict volume control mode, if I am not mistaken a pt can always pull in tv over what you have set in any mode, right or wrong?

This is one the historical differences between control mode ventilation and assist/control. Most new vents will allow some over breathing of tidal volumes, but the older drägers my shop is replacing is ridiculous how much they will give above the set volume.

 

[Hernandez]

Pimp question time.....why is VTe usually larger than VT?

 

[redy]

Pimp question time.....why is VTe usually larger than VT?

Nebulized bronchodilators using compressed air.

 

[europeman]

I like PRVC:

However, depending on your software, a patients OWN spontaneous breath while on PRVC can be supported in different ways. In our shop, their spontaneous breaths while on prvc are simply supported with pressure support (at whatever level you set).

Let me ask you something though. Aside from the fact you may need more sedation, as long as your mean airway pressures are okay, why do you care if your patient is "pulling 700cc"?

When a patient does ther own inspiratory effort, the flow tends to go into basilar and posterior segments. If the patient pulls this in, there isn't positive pressure forcing it down.... So you don't have to worry, per se, of Baro-trauma. In short, a patient with tidal volume of 800 with say peep 5 and pressure support 5 is VERY different alvear and lung physiology than a patient on a set tidal vol of 800 not spontaneously breathing.

 

[Hernandez]

I like PRVC:

However, depending on your software, a patients OWN spontaneous breath while on PRVC can be supported in different ways. In our shop, their spontaneous breaths while on prvc are simply supported with pressure support (at whatever level you set).

Let me ask you something though. Aside from the fact you may need more sedation, as long as your mean airway pressures are okay, why do you care if your patient is "pulling 700cc"?

In an ARDS pt, it matters, otherwise I tend to adjust for pt comfort.

Which vents offer PS for a pressure regulated volume control modality for a pt initiated breath?

 

[europeman]

My question was more rhetorical.

I disagree.

To ascribe to the notion that ardsnet means that it is harmful for patients SPONTanEOUS breaths to have big tidal volumes is a huge leap.

It's different physiology. Baro-trauma happens from vents which over distend alveola, collapse, and then over distend. That's ardsnet with positive pressure.

That's not what happens with spontaneous breathing with minimal pressure support..... Even In ARDS.

What do you think the patient is doing? Sucking down the tube hard enough to cause Baro-trauma? Of course not.

 

[Hernandez]

My question was more rhetorical.

I disagree.

To ascribe to the notion that ardsnet means that it is harmful for patients SPONTanEOUS breaths to have big tidal volumes is a huge leap.

It's different physiology. Baro-trauma happens from vents which over distend alveola, collapse, and then over distend. That's ardsnet with positive pressure.

That's not what happens with spontaneous breathing with minimal pressure support..... Even In ARDS.

What do you think the patient is doing? Sucking down the tube hard enough to cause Baro-trauma? Of course not.

One of us is confused...and I'm not sure it's me. We're talking pressure regulated volume Control...this isn't a spontaneous mode of ventilation, it remains a control mode ventilation strategy. So yes, in that light, tidal volume seems far more important variable than pressure , so unless you're using a vent with a different style of delivering PRVC, which is why I asked which vent uses PSV....it sounds to me that you're referring to Pressure Release Ventilation,

Excessive negative pressure inspiratory forces can be deleterious, in increasing oxygen consumption upwards of 50% of carrying capacity! and I'm sure it can cause micro alveolar leakage, and other effects such as any negative pressure pulm edema scenerio

 

[Hernandez]

Nebulized bronchodilators using compressed air.

Nope, heat and humidity, increase volume size

 

[europeman]

When you are on PRVC.... It's technically a volume targeted PRESSURE control mode for the set breaths.

What I'm saying is that in addition to whatever rate you say; let's say RR of 4 for the purpose of this example, the question is.... What happens during the other PATiENT initiated breaths?

Well it depends on the way it's set up. If pRVC is set at rate of 4 (and tidal of say 450) but Patient breathing spontaneously at 8, then those additional 4 breaths can be accomplished in a few ways. In our shop, those additional breaths are simply pressure supported breaths (set at whatever amount you want). So if it's set at PS of 10 and they only pull 200.... Well then 4 of their breaths in a minute will be prvc breaths at around 450cc and the additional will be 200 if that's all they pull. Alternatively, you can set it to simply support them always to a targeted volume of 450. Whatever.

Thats not the point. The question is if you have a patient pulling 800 with minimal pressure support.... Is that bad? When someone said "yes if they have ARDS" then I disagree, because, that implies there is Baro-trauma as a function of the high volume. And that's just not true.


That said, OF COURSE a patient persistently pulling 800 is problematic unless you are about to extubate them because clearly they are not in a mode appropriate for them or have sedation issues etc.... And of course they are waisting energy. I agree. But Baro-trauma is not the issue.


You can't get negative Pulm pressure edema while intubated. That's a phenomenon of extubation when glottis is closed

 

[Mad Jack]

Turn off the autoflow first if you're using a drager. Turn off the "PRVC" on other vents. Set to a strict volume control mode. If you're not sure which setting this is on your vent ask the RT to show you.

Pretty sure Autoflow on a Drager is similar to Demand Flow on our Aveas. Disabling it is a double-edged sword. By fixing the flow, you can increase a patient's work of breathing (as they pull harder in an attempt to get more flow than the vent will deliver), increase your peak pressures (try sucking on a straw with your finger covering one end- you get a similar effect to a patient pulling against a fixed flow valve, as once they exceed the set flow, the gas in the circuit ends up being compressed with a resulting increase in pressure), and end up with a lot of breath stacking (as they continue to attempt to pull flow after the breath ends). A lot of the time you end up with patients that look like they're struggling to breathe and are dyssynchronous with the vent. We just sedate the hell out of them around here.

 

[jdh71]

Pretty sure Autoflow on a Drager is similar to Demand Flow on our Aveas. Disabling it is a double-edged sword. By fixing the flow, you can increase a patient's work of breathing (as they pull harder in an attempt to get more flow than the vent will deliver), increase your peak pressures (try sucking on a straw with your finger covering one end- you get a similar effect to a patient pulling against a fixed flow valve, as once they exceed the set flow, the gas in the circuit ends up being compressed with a resulting increase in pressure), and end up with a lot of breath stacking (as they continue to attempt to pull flow after the breath ends). A lot of the time you end up with patients that look like they're struggling to breathe and are dyssynchronous with the vent. We just sedate the hell out of them around here.

How do you figure more negative intrathoracic pressure (which occurs with more work of breathing) is going to make peak pressures higher at the mouth??

 

[Hernandez]

When you are on PRVC.... It's technically a volume targeted PRESSURE control mode for the set breaths.

.

On some vents, yes, the problem as I alluded to in my first post is every manufacture approaches this mode differently. What you describe sounds more like the Maquet method. You can do this IMV type with PB as well, but I mainly used it in a A/C style mode, Hamilton also has an adaptive support modality which is pure PSV.

Thats not the point. The question is if you have a patient pulling 800 with minimal pressure support.... Is that bad? When someone said "yes if they have ARDS" then I disagree, because, that implies there is Baro-trauma as a function of the high volume. And that's just not true.

While we don't have a fully clear view of all of the factors that go into lung injury, I disagree that larger volumes even with lower pressures isn't a danger, and there is plenty of data to suggest in ARDS pt that higher volumes is detrimental, regardless of the pressures involved, figure 2 next to last page,

And not only that, but there is a decent number of us who target tidal volumes ranges on oressure control, I can't remember if is was Macintire or Marini's point/counter point in chest that they touch on this or not,

You can't get negative Pulm pressure edema while intubated. That's a phenomenon of extubation when glottis is closed

Not entirely true, why the moniker neg pressure pulm edema is reserved for negative pressures against a closed glottis, negative pressures can cause issues on lungs no matter how they're generated, have you never cause re-expansion pulmonary edema with a thora? I've seen patients so dyschrony us that they generate negative pressures more than -40torr on he he pressure curve fighting the vent Granted, as long as your peep is set above the lower inflection point it likely isn't a real concern,

 

[Mad Jack]

How do you figure more negative intrathoracic pressure (which occurs with more work of breathing) is going to make peak pressures higher at the mouth??

When you shut off Demand Flow you are disabling the flutter valve in the vent. This means that if a patient is trying to pull in 60 of flow but the vent is delivering only 40, you end up compressing the circuit with all of the force that was trying to pull in that extra -20 of flow. If you get ahold of a manomoeter with a mouthpiece for measuring NIFs, you can experience it yourself. Just clamp your nose, put the mouthpiece in your mouth, and take a breath. Pay attention to how your diaphragm is moving as you take a few breaths- obviously it'll be dropping an then your accessory muscles pull your chest wall outward as your breath gets larger. Now cover the end opposite the mouthpiece, and try to take a breath. You'll feel your diaphragm contract and your abs tighten, and the air within your lungs compress. Try dropping your diaphragm and taking a breath. No matter how little flow you try to pull, you're going to increase the pressure of the gas within your lungs by compressing it as you try to generate enough NIF to inhale. Sure, you're pulling with 20 of flow or whatever against the wall of your hand, but it's the same net effect as if you were trying to pull 60 of flow while 40 is being delivered. If you've got a really good respiratory departmetn, they might have the gear you need to hook a mouthpiece up to a vent, so you can actually try pulling breaths against flow set lower than you are trying to generate, and watch what it does to the pressures on the vent itself.

 

[jdh71]

When you shut off Demand Flow you are disabling the flutter valve in the vent. This means that if a patient is trying to pull in 60 of flow but the vent is delivering only 40, you end up compressing the circuit with all of the force that was trying to pull in that extra -20 of flow. If you get ahold of a manomoeter with a mouthpiece for measuring NIFs, you can experience it yourself. Just clamp your nose, put the mouthpiece in your mouth, and take a breath. Pay attention to how your diaphragm is moving as you take a few breaths- obviously it'll be dropping an then your accessory muscles pull your chest wall outward as your breath gets larger. Now cover the end opposite the mouthpiece, and try to take a breath. You'll feel your diaphragm contract and your abs tighten, and the air within your lungs compress. Try dropping your diaphragm and taking a breath. No matter how little flow you try to pull, you're going to increase the pressure of the gas within your lungs by compressing it as you try to generate enough NIF to inhale. Sure, you're pulling with 20 of flow or whatever against the wall of your hand, but it's the same net effect as if you were trying to pull 60 of flow while 40 is being delivered. If you've got a really good respiratory departmetn, they might have the gear you need to hook a mouthpiece up to a vent, so you can actually try pulling breaths against flow set lower than you are trying to generate, and watch what it does to the pressures on the vent itself.

All of that decreases the total pressure in the system not increasing it. What you are describing is increasing work not an increase in the pressure the lungs see in an elevated fashion. All that work decreases total pressure because its negative. All other things being equal less volume will decrease the pressure compared to the autoflow giving more volume.

 

[Mad Jack]

All of that decreases the total pressure in the system not increasing it. What you are describing is increasing work not an increase in the pressure the lungs see in an elevated fashion. All that work decreases total pressure because its negative. All other things being equal less volume will decrease the pressure compared to the autoflow giving more volume.

You're totally right (obviously, you're the pulmonologist lol). It just seems really counterintuitive because you are compressing the same volume of gas into a space that seems to be growing smaller (or at least smaller relative to its rate of expansion), but it is still negative inspiratory force, not positive, so you wouldn't have higher peak pressures. Usually these same patients stack their breaths though, which explains the higher pressures we tend to see in them overall (they are still pulling in at the end of those breaths trying to get more flow, generating a good amount of negative force in the attempt, and all it takes is a bit of NIF to trigger another breath). Cranking the flow up works for some of them, but some just end up stacking their breaths because their Ti is so short with the volumes you are giving using ARDSNet that they are still inhaling when the delivery of their tiny breath ends.

 

[jdh71]

You're totally right (obviously, you're the pulmonologist lol). It just seems really counterintuitive because you are compressing the same volume of gas into a space that seems to be growing smaller (or at least smaller relative to its rate of expansion), but it is still negative inspiratory force, not positive, so you wouldn't have higher peak pressures. Usually these same patients stack their breaths though, which explains the higher pressures we tend to see in them overall (they are still pulling in at the end of those breaths trying to get more flow, generating a good amount of negative force in the attempt, and all it takes is a bit of NIF to trigger another breath). Cranking the flow up works for some of them, but some just end up stacking their breaths because their Ti is so short with the volumes you are giving using ARDSNet that they are still inhaling when the delivery of their tiny breath ends.

You are correct though that if a patient is trying to kill themselves with the vent they need more sedation and if that's not cutting it then paralysis.

 

[europeman]

Hernandez! Thank you for the thoughts! You make some great points for sure.

I guess I should rephrase that Baro-trauma is a complicated phenomenon. If you prevent over-dissension AND prevent alveolar collapse/opening/collapse with a mode like ApRV, I'm a form believer that this is not Baro-traumatic despite a higher than 8cc/kg tidal which u will get (since u will have more recruited ling). Of course, until the Hibashi study comes out proving this, the best evidence indeed is ARDSNET. However, just like EGDT.... I personally never believed many of the individual things in the protocol (like cvp or transfusion requirements)..... Yet for years and years people were saying "oh that's the best evidence."

ARDSnet compared a "lower" tidal to frankly an absurd tidal volume on AC and showed a benefit. That doesn't mean necessarily that higher than 8cc/kg vol causes Baro trauma in other modes. It just doesn't.


I appreciate your paper. Still doesn't prove causation at all.


Can you tell I'm an ApRV fan though? Granted... It's a mode which is VERY mis-understood and wrongly utilized. I'm not a proponent of wide spread aprv.... Too complicated and wouldn't be good!!! Ardsnet all the way! Easy! AC tidal 400 and u are done! But at the tertiary centers with expertise.... Individual patients require different things and prescribing ARDSnet to everyone frankly is not what is best in those cases.

 

[jdh71]

If I had a dollar for every surgeon who thought APRV was magic . . .

 

[ORL10]

If I had a dollar for every surgeon who thought APRV was magic . . .

I second that. SICU uses APRV if someone plugs and desats during a nursing turn. I will say many patients who have been dyschronous on LPV (high peep, low tv protocol)have tolerated APRV more comfortably, has this been others experience? I do feel like it jacks up my TTE views, especially IVC collapsibility.

 

[Mad Jack]

MICU: ARDSNet is magic.
SICU: APRV is magic.
ED: BiPAP is magic.
Newborn: CPAP is magic. (Or HFOV, depending on the day)
CTICU: SIMV is magic.
CCU: Oh my god what is this machine please send them to MICU STAT!

 

[jdh71]

I second that. SICU uses APRV if someone plugs and desats during a nursing turn. I will say many patients who have been dyschronous on LPV (high peep, low tv protocol)have tolerated APRV more comfortably, has this been others experience? I do feel like it jacks up my TTE views, especially IVC collapsibility.

That's kind of what APRV was designed to do, let the patient breathe however they want above the two levels of peep with the release providing enough ventilation to keep the pH from getting ******ed. In my experience its a reasonable try for the dysynchronous patient and sometimes patients hate it just as much.

 

[Hernandez]

@europeman. Do y'all use APRV in hypercapnic PTs who require very high minute ventilation?

 

[europeman]

Mad jack... Hahaha funny post!


Hernandez..... I don't understand your question? I guess if you are asking about managing co2 with aprv then the answer is that it works great! The problem though is its more complicated than simple changing thr minute ventilation that is calculate on the screen. In the poly-trauma patient with significant tbi that requires a co2 between 30-35 it works fine.

I find aprv to be more efficient than other modes at removing co2. For example if you have a patient on AC with minute vent of say 10...... Then that same patient will maintain that co2 it's aprv minute vent of 7 or 8. So it allows leeway. Many people that don't have lot of familiarity with aprv will, for example, decrease t high in order to increase the frequency of releases in order to lower co2 when in fact if they have recruitable lung you will actually get rid of more co2 by extending thr t high plus minus increasing the pressure high.

Aprv very very mis understood. Many papers out there about it, but most if you look closely have mis management of the vent and bastardized versions of it. One per peeve of mine is having a p low of anything other than zero. Also setting t2 is not easy if you aren't trained.

So yes. If your aprv is set in a way whereby thr p high is so high that you are hyper inflating alveoli and collapsing your ivc, then your issue isn't aprv.... It's your bad settings on that mode. Same is true with any mode. Except aprv more complicated.

Reminds me of antibiotics.... So many docs prescribe them.... Very very few know what they are doing

 

[Hernandez]

10L/min minute ventilation is nothing for an ARDS pt, I can do hit that as a requirement while straining to take a man sized poop. What I'm asking is that is not uncommon at all for me to see an ARDS pt with minute ventilation requirements of 20+L/min who still have ****ty PaCO2 & pHs, how can you reasonably increase MV that high on someone on APRV, especially if you have a background I:E of 3:1 or longer?

I fully understand the recruitment benefits on improving ventilation, and my personal favorite Are volumetric end tidal CO2 monitors to help optimize peep titration, and I also use the step titration and Ppeak method a lot as well (both of which are IMHO, far better than esophageal manometry), so I understand how to titrate recruitment there, but all I've ever really heard from people on how they titrate not just minute ventilation but airway pressures and release times on APRV amounts to hand waving and broad generalities that I'm too stupid to get, which means APRV is not a panacea and should be just as limited to tertiary centers as ECMO remains. So at the end of the day, I do use APRV, but On PTs with high intrensic rates for no apparent reason, low overall minute ventilation requirements, and a ALI clinical picture and here I tend to do a bastardized approach somewhere between my approach on HFOV, And PCV to titrate the settings. I do however use what I refer to as BiLevel, which I use to mean, APRV with normal background I:E, not infrequently.

So, I guess what I'm getting at, is you keep referring to how APRV tends to be used wrongly, then where might one get an overview of the right way?

Also, about Plow, I actually have some issues with Plow of zero on theoretical issues with atelectrauma, and I think I had discussed with JDH almost a year ago one of my ideas for a bench study was to do a rat model on APRV settings and compare post mortum specimens on lungs with the traditional Habashi peep 0 vs a "physiologic" peep of 3-5cm in he he setting of blatant over distinction and regular distinction to see if there were any pathological differences, because we do know in regular VACV that peep is somewhat protective on the lungs in these extremes.

 

[ORL10]

I always find it entertaining when physicians assume other doctors have no idea what they are doing, and that they "the experienced doctors" are the only ones capable of correctly using a particular technology or mode of ventilation. Sometimes setting the vent is trial and error, plain and simple.

Also i'm also fairly certain that NO ONE knows how to use antibiotics perfectly. Tracheobronchitis, VAP, HCAP, HAP, feculent aspiration how many days (ok maybe for VAP we have some idea) which abx, double cover gram negatives when, can you use CAP for most HCAPs? How long, when can you stop vanco, should anyone use procalcitonin? No one knows the answer to all of these questions in individual patients, and a lot depends on your experience combined with a patients clinical picture.

 

[europeman]

My previous post I didn't intend to sound patronizing. My apology. Not my intention. Rather my point is aprv is a mode with inherent more nuances and complexities than other modes and, for that reason alone in my opinion, I agree with you is not the be all end all mode for everywhere.

When I gave the example of fixing co2 with aprv.... There isn't hand waving. It's just not simple like AC where you up the volume and/or frequency.

Not to be patronizing again, but your comment of aprv pLow peep of zero causing atelectrauma reflects a common misunderstanding of of the p low. The patient NEVER gets to a peep of zero! Ever. It's NOT Analagous to peep of zero on AC or even bilevel where of course the alveoli would see peep of zero and cause collapse.

You set your t low so that the "release" stops when the exploratory flow hits 75% of the peek flow (that's pretty good time to start.... Depends on patients physiology. COPD patient may require longer release time so you would set it at say 50%). That's how you keep everything recruited on the release. Your release heads TOWARDS zero but never actually gets even close to there since you don't give it enough time to do so (ie setting t low).

The purpose of having the p low at zero is so the release is more efficient. Setting it at day peep of 5 decreases efficiency as well as some other problems. End of the world for most patients? Of course not.

I think APRV is best done by Habashi. While he didn't invent it, the inventor called him the perfecter. So I think if you want to learn how to do aprv, learn from him.

And I agree with you.... If you don't have practice managing aprv then using it on a traumatic head patient isn't very smart to start! But my point is if you have the experience the co 2 management is fine.

 

[Hernandez]

That's my biggest question no one has a good explanation for, just how do you determine Expiratory flow, even on the marqet vents, no one has been able to show me how to quantify this, so I have seen a great many vents set up were they do indeed go to a peep of zero, especially in patients who are more hypercapnic than hypoxemic and need higher levels of minute ventilation. Hence my original question of using APRV in pts who need higher minute ventilation. The usual answer I get is "oh you eyeball it on the scalars"

Where I trained no one had a good handle on how to use APRV, we had a trauma guy come in who trained with some big names on it but he wasn't able to really clarify my questions either. So I'm left with what I can find to read on how to use APRV which I like the potential benefits and the mode itself makes sense but the caveats of setting up don't translate well to written form. So I'm left with base experience of pulm attendings placing a pt on APRV......then Paralyzing the pt....which I thought sounds counter to what APRV is suppose to be

 

[europeman]

Okay.... Now I get you. Yes it's annoying because people are sometimes so cryptic.... I think it's cuz they don't really know what they are doing frankly.

If you send me a private text With your email I'll be glad to send you over some EASY to read steps to setting up your aprv settings.

It's actually very clear and easy. It's just very different than other ways of setting up modes.

So the answer is in order to set the t2, make sure your p low is zero. Start at 0.5 seconds say.

Then watch your flow curves. Depending on your machine, interrogate the flow curve so you can determine what the peak exploratory flow is. If, just to use a number, the peak exploratory flow is 50Liters/min, then adjust the length of the expiration:release (ie the 0.5second t2) so that it ends/stops at 75% of this. So that would be at 37.5L/min on the flow curve. For sake of example, let's just say this actually is 0.5 seconds.

So in those 0.5 seconds the patient releases...... Flow starts fast at 50L/s and the slows as the recoil of the chest/expiration force comes down. So say at 0.1s the flow rate is 45, then at 0.2 it's 40...... At 0.5 it's 37.5L/s (bingo!) so releAse stops and you go back to your p high. You are NEVER allowed to release that extra stuff in your lung...... (If you did you would de-recruit at a peep of zero!). If your next patient had more recoil on their lungs.... He may need the t2 set at 0.4 seconds. Next patient with copd needs more time to release may need 0.7 seconds. But again those times are set so the release ends at 50-75% of the peak flow.

The beauty of setting the p low at zero is by doing that, you are able to observe the true lung physiology of the release.

 

[Hernandez]

This is going to sound ******ed, but I know I've had 4 hands on sessions with different docs and vent reps who couldn't tell me how to quantify and if they could measure exp flow, they were very cryptic on how to adjust the 75% of expiratory flow, so I just sat down with a pt I have on a vent and sure enough, it's burried but my vents do automatically list PEF, now I feel rather stupid, and that tiny amount of information could have saved me a lot of annoyance with that mode. Sadly my fellowship failed me on this aspect. Thank you making it painfully obvious what I've been missing on setting his up (no sarcasm present)

 

[europeman]

No problem. Tks for the kind words.

One tip: try and actually get the numbers off the machine manually by using the flow/time graph. What kind of machine do you use? If you are able to actually graph the flow over time curves, then you may see the reported peak value to be higher than the real peak because of valve phenomena. That is, you will see on the graph that the real peak is lower because the graph looks like it's spiking.... Does this make sense? If not I'll send you a pic on Tuesday when I'm back at hospital.

Also, you need to see the graph in order to determine how long to set your t2. I usually just start at 0.5 and then you look at the graph And record the peak and record the rate when the t2 is over (ie at 0.5 seconds since we started there). If the rate at the end is less than 75% of the peak flow then u know u need to tighten (ie shorten) your t2 and vice versa.

 

[europeman]

.

On some vents, yes, the problem as I alluded to in my first post is every manufacture approaches this mode differently. What you describe sounds more like the Maquet method. You can do this IMV type with PB as well, but I mainly used it in a A/C style mode, Hamilton also has an adaptive support modality which is pure PSV.



While we don't have a fully clear view of all of the factors that go into lung injury, I disagree that larger volumes even with lower pressures isn't a danger, and there is plenty of data to suggest in ARDS pt that higher volumes is detrimental, regardless of the pressures involved, figure 2 next to last page,

And not only that, but there is a decent number of us who target tidal volumes ranges on oressure control, I can't remember if is was Macintire or Marini's point/counter point in chest that they touch on this or not,



Not entirely true, why the moniker neg pressure pulm edema is reserved for negative pressures against a closed glottis, negative pressures can cause issues on lungs no matter how they're generated, have you never cause re-expansion pulmonary edema with a thora? I've seen patients so dyschrony us that they generate negative pressures more than -40torr on he he pressure curve fighting the vent Granted, as long as your peep is set above the lower inflection point it likely isn't a real
concern,

I reviewed the paper thank you. This paper doesn't show, despite the title, that volume per se is the issue which causes atelectrauma.... Is shows higher mortality with high volume with *conventional ventilation.*. Apples and oranges.

That's an important point. I agree that over dissention of an alveoli isn't good! And of course if u put too much volume into an individual alveoli you will over distend it with more volume. Of course.

But the lung isn't a single alveoli. They are interdependent through pores of Kahn, cannals of lambert, etc.

If u simply change the vent settings on this study to a recruitable mode (eg aprv.), over time at the same pressure u will recruit more alveoli and then have more volume. And you will have less Baro trauma because extending the time at the inspiratory high (say on pressure control) doesn't in itself over distend single alveoli. That's been shown.

Of course with standard settings then you will have better results with low volumes cuz u will do less Baro trauma to a smaller group of alveoli (ie the only ones still open).

It's comparing apples to oranges.

Also of course if u have standard modes and have high and low volumes the higher volumes will more drastically cause atelectrauma becUse the individual alveoli will collapse and open and collapse and open...... Baro trauma

On another note..... I have a question. In ARDSnet the patients were divided into groups. I think it was around 6000 eligible patients and those were split into an excluded and included group. In the included group there was. A benefit of 6cc versus 12 cc group. But the excluded group (who were vented at 10cc/kg) had the SAME mortality as the 6cc group.

Why is that???

 

[Hernandez]

I reviewed the paper thank you. This paper doesn't show, despite the title, that volume per se is the issue which causes atelectrauma.... Is shows higher mortality with high volume with *conventional ventilation.*. Apples and oranges.

Uhm, are we reading the same study, as they were adjusting their analyses to see if the data supported the thought that it is airway PRESSURES are the issue, so they do some multi-regression voodoo that shows it isn't just the Pplat that impact mortality, as people argued that who cares what the tidal volume as as long as the Pplat is less than 30? This cements in my mind that it isn't just volume and it definitely isn't just pressure.

you can say apples/oranges all you want but you can't just claim your modality is special and this doesn't apply in the absence of data . I've hear many a convincing argument for HFOV compared to CMV/PCV/APRV, they even have a nice video about how much the alveoli derecruit on a release breath on APRV vs HFOV that is mighty convincing. but rigorous studies don't bare out the hypothetical benefit as reality. And in my mind APRV is in the same boat as HFOV was prior to THE OSCAR/OSCILLATE studies,

 

[europeman]

Hi. Tks for response.

I'll have longer one later..... My short answer is this: I agree that good human data on aprv lacking. But the animal data is more convincing than the animal data was for low tidal.... Data which is what initially led to the huge ardsnet trial. Not only that.... The actual physiologic explanation of low tidal volume AC just doesn't make sense..... Whereas aprv does . I think good science isn't just taking the results and going with it.... But rather having some sort of explanation. The concept that low tidal vol "protects alveoli from vol-trauma" is physiologically naive and is just not what happens in the lung. If you take your vent and connect it to a balloon.... The concept makes sense. If you take the vent and connect it to an actual lung (eg animal lung with actual alveoli) there is clearly more to the picture .

Since mortality is still so high with ards, I think it is therefore prudent among us not to shut out other ideas. If ardsnet protocols had ards morality rates of zero, then I'll be first to abandon aprv. But the mortality is still absurd! We can't be comfortable yet with our outcomes.

Now, that said..... Many people had fundamental problems with the xigris early studies, the early goal directed study, glycemic control , etc etc. ARDSnet will fall into this same category too. The study was seriously flawed. Again, the excluded patients with 10cc/kg had the same mortality as the 6cc!

Also, of course, what you believe clinically is in part related to what you see. I happen to be at an institution with expert ApRV docs and RTs. Of course that makes a difference. And I acknowledge that!