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StillAnotherGuest wrote: As an aside, this type of patient would now be below FRC.

SAG

And our magnetometer data should be able to show this decrease.

split_city wrote:In simple terms, FRC is the lung volume at which the outward recoil of the chest is equal and opposite to the inward recoil of the lung.

Well, then, by definition, intrapulmonary P = 0 at that point.

split_city wrote:To understand why, I simply use an airfilled syringe. Please correct me if I'm wrong as this isn't my area, but I would love to learn. Think of the inside of the syringe as the lungs or esophagus..

It's neither of those, you just made a pleural space.

split_city wrote:Put your finger on top of the syringe and pull the plunger down and hold the plunger in place. Say this point is analagous to FRC i.e. the inward recoil (syringe/lungs) is balanced by the outward pull on the syringe (hand/chest).

Actually that would be IC, but go ahead.

split_city wrote:If you let go of the syringe, the syringe would recoil back.

OK, stop right there! That's FRC.

split_city wrote:If you measure the pressure inside the syringe when you held the plunger in place, the value would be negative i.e. what it would be in the lungs at FRC.

Again, you're measuring the pleural pressure. This is a dynamic system, the lungs per se (and for that matter, Pes) are open to air, so if allowed to equilibrate, P will = 0. Pes inflections only occur when the system is in motion. It returns to baseline when it is static. Or perhaps, the slight elevation noted by the collapse of the surrounding structures which must be subtracted as artifact. The elastic recoil of the lungs pertains to the lung itself.

split_city wrote:Yep, I understand that this positive value is an artifact. Unfortunately, we cannot measure pleural pressure.

That's not pleural pressure.

SAG

StillAnotherGuest wrote:

split_city wrote:In simple terms, FRC is the lung volume at which the outward recoil of the chest is equal and opposite to the inward recoil of the lung.

Well, then, by definition, intrapulmonary P = 0 at that point.

Yes, the system is open to atmosphere. Intrapulmonary pressure = airway pressure = 0 at FRC

StillAnotherGuest wrote:

split_city wrote:To understand why, I simply use an airfilled syringe. Please correct me if I'm wrong as this isn't my area, but I would love to learn. Think of the inside of the syringe as the lungs or esophagus..

It's neither of those, you just made a pleural space.

Ok, thanks for clearing that up. It's good to learn new stuff . Now, my understanding is that pleural pressure at FRC is negative because opposite forces acting on it (inwards recoil of lungs and outwards recoil of the chest) acts to pull the lungs from the chest wall. Correct?

After all this discussion, are you suggesting that my negative Pes @ FRC readings are incorrect?? Pes is commonly used as a surrogate measure for pleural pressure. Given that pleural pressure is subatmospheric at FRC, Pes will also be negative. Correct? I have seen a number of papers stating that Pes is negative at FRC. Do you think Pes = intrapulmonary pressure?

split_city wrote:Now, my understanding is that pleural pressure at FRC is negative because opposite forces acting on it (inwards recoil of lungs and outwards recoil of the chest) acts to pull the lungs from the chest wall. Correct?

Intrapleural pressure is normally always negative. When it isn't, the lung turns into a raisin.

split_city wrote:After all this discussion, are you suggesting that my negative Pes @ FRC readings are incorrect??

No, the +20 cmH2O seen during exhalation during a period of baseline breathing.


My point is that that value needs explanation. Either something has caused expiration to go from passive to active (although there's nothing there that would indicate that, like bronchospasm or upper airway obstruction) or the calibration is incorrect.

split_city wrote:Pes is commonly used as a surrogate measure for pleural pressure. Given that pleural pressure is subatmospheric at FRC, Pes will also be negative. Correct? I have seen a number of papers stating that Pes is negative at FRC. Do you think Pes = intrapulmonary pressure?

Is this a trick question? Oh what the hey, I'll go with sure, as long as the patient has no disease that causes loss of compliance.

SAG

StillAnotherGuest wrote:

split_city wrote:Now, my understanding is that pleural pressure at FRC is negative because opposite forces acting on it (inwards recoil of lungs and outwards recoil of the chest) acts to pull the lungs from the chest wall. Correct?

Intrapleural pressure is normally always negative. When it isn't, the lung turns into a raisin.

At full expiration and during forced expiration such as the case during a spirometery test, intrapleural pressure becomes positive. This is why we still have air inside the lungs at RV because the postive pleural pressure compresses the airways, trapping air downstream.

StillAnotherGuest wrote:

split_city wrote:After all this discussion, are you suggesting that my negative Pes @ FRC readings are incorrect??

No, the +20 cmH2O seen during exhalation during a period of baseline breathing.

I have already discussed the reasons why peak Pes is increased. You must remember, this +20cmH20 also includes the +5-10cmH20 artifact caused by the compression of the medialstinal structures. The true peak value is likely to be between 10-15cmH20. All the other patients also had increased peak expiratory Pes during their apneas. I'm pretty sure peak Pes also increased during hypopneas in other patients.

You keep saying baseline breathing. I keep disagreeing with this because the patient is under a high drive state. What would you call his breathing when his airway is patent and there is no flow limitation? Baseline, baseline breathing??

StillAnotherGuest wrote:

My point is that that value needs explanation. Either something has caused expiration to go from passive to active (although there's nothing there that would indicate that, like bronchospasm or upper airway obstruction) or the calibration is incorrect.

I told you why his expiration has become active. The patient is under a high drive state because his airway is acting as a Starling resistor. I have no doubt he was actively recruiting his abdominal muscles.

StillAnotherGuest wrote:

split_city wrote:Pes is commonly used as a surrogate measure for pleural pressure. Given that pleural pressure is subatmospheric at FRC, Pes will also be negative. Correct? I have seen a number of papers stating that Pes is negative at FRC. Do you think Pes = intrapulmonary pressure?

Is this a trick question? Oh what the hey, I'll go with sure, as long as the patient has no disease that causes loss of compliance.

There are no smoke and mirrors. You have clearly stated that you believe that Pes should be zero at FRC.

StillAnotherGuest wrote:so baseline Pes is normally 0 cmH2O

StillAnotherGuest wrote:(and for that matter, Pes) are open to air, so if allowed to equilibrate, P will = 0

What the hey, I'll provide some references to show you that Pes is negative at FRC, thus confirming that Pes does not equal intrapulmonary pressure.

I have said that Pes can be used as an alternative measure for pleural pressure.

Here is a study comparing pleural pressure with Pes in humans

Mead et al (1959) Journal of Applied Physiology 14(1): 81-83

Upright
Mean pleural pressure at end-expiration was -5.1cmH20
Mean esophageal pressure at end-expiration was -4.8cmH20

Supine
Mean pleural pressure at end-expiration was -1.1cmH20
Mean esophageal pressure at end-expiration was +2.6cmH20

They did not mention the BMI of the subjects

Other studies which have shown Pes to be negative at end-expiration include:

Mead et al (1963) Journal of Applied Physiology 18(2): 295-296
Ferris et al (1959) Journal of Applied Physiology 14(4): 521-524
Coulam and Wood (1971) Journal of Applied Physiology 31(2): 277-287

Gillespie et al (1973) Journal of Applied Physiology 35(5): 709-713 showed that Pes correlated well with pleural pressure in the anesthetized dog.

I hope this clears it up for you.

Going back to the first point. Now remember, it has been shown that Pes is considered a relatively good alternative measurement of pleural pressure (in the upright posture anyway), Mead et al (1955), Knowles et al (1959) and Milic-Emili et al (1964) all showed that Pes was positive at RV

split_city wrote:At full expiration and during forced expiration such as the case during a spirometery test, intrapleural pressure becomes positive. This is why we still have air inside the lungs at RV because the postive pleural pressure compresses the airways, trapping air downstream.

As noted:

SAG wrote:Intrapleural pressure is normally...

And those manuevers are not considered "normal".

split_city wrote:I have already discussed the reasons why peak Pes is increased. You must remember, this +20cmH20 also includes the +5-10cmH20 artifact caused by the compression of the medialstinal structures. The true peak value is likely to be between 10-15cmH20.

OK, but you're kinda going back and forth here, quoting a bunch of references documenting negative Pes and then adding in mediastinal pressure artifact when the numbers don't fit. Do a wake supine end-expiratory Pes at the begining of the study and then you can properly account for artifact.

split_city wrote:All the other patients also had increased peak expiratory Pes during their apneas. I'm pretty sure peak Pes also increased during hypopneas in other patients.

SAG is confused. Do you mean increased negative or positive peak expiratory Pes? If it occurs during their apneas then how can you have positive Pes? If there's a brief period of increased positive activity post event, then that should be dismissed as normal artifact.

split_city wrote:The patient is under a high drive state because his airway is acting as a Starling resistor.

And again, the Starling principle only applies during inhalation. The only way you could invoke Starling during exhalation would be if there were another factor applied to expiration, like reactive airways or obstructed airway.

split_city wrote: I have no doubt he was actively recruiting his abdominal muscles.

During that whole period, independent of the surrounding events? I do.

split_city wrote:Here is a study comparing pleural pressure with Pes in humans

Mead et al (1959) Journal of Applied Physiology 14(1): 81-83

Upright
Mean pleural pressure at end-expiration was -5.1cmH20
Mean esophageal pressure at end-expiration was -4.8cmH20

Very impressive, but for the most part, "upright" is not applicable in the sleep laboratory.

split_city wrote:Supine
Mean pleural pressure at end-expiration was -1.1cmH20
Mean esophageal pressure at end-expiration was +2.6cmH20

Don't forget to subtract out the structure compression factor!

split_city wrote:You have clearly stated that you believe that Pes should be zero at FRC.

StillAnotherGuest wrote:so baseline Pes is normally 0 cmH2O

StillAnotherGuest wrote:(and for that matter, Pes) are open to air, so if allowed to equilibrate, P will = 0

What the hey, I'll provide some references to show you that Pes is negative at FRC, thus confirming that Pes does not equal intrapulmonary pressure.

Oh for cryin' out loud! I'll give you a couple of cmH20 +/-. But I ain't gonna give you 20.

split_city wrote:Going back to the first point. Now remember, it has been shown that Pes is considered a relatively good alternative measurement of pleural pressure (in the upright posture anyway), Mead et al (1955), Knowles et al (1959) and Milic-Emili et al (1964) all showed that Pes was positive at RV

Sleep lab patients are rarely upright, and even less so at RV, so that significance is unclear to me. And if you look closely at Knowles, you will see that given practical clinical consideration, patients are a heckuva lot closer to Pes = 0 than anything else.



SAG

StillAnotherGuest wrote:

split_city wrote:At full expiration and during forced expiration such as the case during a spirometery test, intrapleural pressure becomes positive. This is why we still have air inside the lungs at RV because the postive pleural pressure compresses the airways, trapping air downstream.

As noted:

SAG wrote:Intrapleural pressure is normally...

And those manuevers are not considered "normal".

Nor would I call the breathing in the +20cmH20 peak expiratory patient "baseline breathing."

StillAnotherGuest wrote:

split_city wrote:I have already discussed the reasons why peak Pes is increased. You must remember, this +20cmH20 also includes the +5-10cmH20 artifact caused by the compression of the medialstinal structures. The true peak value is likely to be between 10-15cmH20.

OK, but you're kinda going back and forth here, quoting a bunch of references documenting negative Pes and then adding in mediastinal pressure artifact when the numbers don't fit. Do a wake supine end-expiratory Pes at the begining of the study and then you can properly account for artifact.

I was simply quoting negative Pes numbers because it seemed that you thought Pes = 0 at FRC.

So taking into account the compression artifact, is an adjusted peak Pes during expiration of between 10-15cmH20 still too high for you?

StillAnotherGuest wrote:

split_city wrote:All the other patients also had increased peak expiratory Pes during their apneas. I'm pretty sure peak Pes also increased during hypopneas in other patients.

SAG is confused. Do you mean increased negative or positive peak expiratory Pes? If it occurs during their apneas then how can you have positive Pes? If there's a brief period of increased positive activity post event, then that should be dismissed as normal artifact.

I meant a an increase i.e. a more positive peak Pes (try saying that 5 times fast) during active expiratory attempts during apneas when abdominal muscles are cranking away.

StillAnotherGuest wrote:

split_city wrote: I have no doubt he was actively recruiting his abdominal muscles.

During that whole period, independent of the surrounding events? I do.

I will post a snapshot of the patient I had in last night when I next get a chance. He predominantly only had hypopneas during the night. As soon as he fell asleep, he was cranking up is abdominal muscles. Initially, Pes and Pga pressure swings were opposite when he was awake, but Pga peaked during expiration as soon as he went off to sleep.

StillAnotherGuest wrote:

split_city wrote:Here is a study comparing pleural pressure with Pes in humans

Mead et al (1959) Journal of Applied Physiology 14(1): 81-83

Upright
Mean pleural pressure at end-expiration was -5.1cmH20
Mean esophageal pressure at end-expiration was -4.8cmH20

Very impressive, but for the most part, "upright" is not applicable in the sleep laboratory.

So? You didn't define posture in your original argument.

StillAnotherGuest wrote:

split_city wrote:Supine
Mean pleural pressure at end-expiration was -1.1cmH20
Mean esophageal pressure at end-expiration was +2.6cmH20

Don't forget to subtract out the structure compression factor!

Yes, but the initial aim of the study was to determine the effect of posture on both pleural and Pes.

StillAnotherGuest wrote:

split_city wrote:You have clearly stated that you believe that Pes should be zero at FRC.

StillAnotherGuest wrote:so baseline Pes is normally 0 cmH2O

StillAnotherGuest wrote:(and for that matter, Pes) are open to air, so if allowed to equilibrate, P will = 0

What the hey, I'll provide some references to show you that Pes is negative at FRC, thus confirming that Pes does not equal intrapulmonary pressure.

Oh for cryin' out loud! I'll give you a couple of cmH20 +/-. But I ain't gonna give you 20.

Good. I'm glad that's sorted

StillAnotherGuest wrote:Sleep lab patients are rarely upright, and even less so at RV, so that significance is unclear to me. And if you look closely at Knowles, you will see that given practical clinical consideration, patients are a heckuva lot closer to Pes = 0 than anything else.



SAG

That figure doesn't ignore the compression artifact.

BUT

IF you are in the supine position AND you take into account the compression artifact, THEN true Pes will be close to 0 at FRC. In an UPRIGHT posture, Pes will be subatmospheric at FRC. Agreed??

Here's a question for you. FRC decreases in healthy-weight individuals when moving from an upright position to the supine position. This is partially due to mass loading on the abdomen, displacing the diaphragm cranially. If this is true, why is there little to no decrease in FRC in the obese population following the same postural transition?

Can't chat too much right now, gotta bring the Knowles book back to the library (we got the salient point out of that anyway) and go to a football game (real football, not that rolling around in the dirt thing you guys got).

Meanwhile, post the electrical and biophysical Pes calibrations from that 20 cmH2O patient, that should answer most of these questions.

And also, you might wanna rethink this concept:

split_city wrote:I meant a an increase i.e. a more positive peak Pes (try saying that 5 times fast) during active expiratory attempts during apneas when abdominal muscles are cranking away.

SAG

StillAnotherGuest wrote:Can't chat too much right now, gotta bring the Knowles book back to the library (we got the salient point out of that anyway) and go to a football game (real football, not that rolling around in the dirt thing you guys got).

SAG

What game are you talking about? You going to a scoccer game or a gridiron match?

I'd rather watch the paint dry thanks....particularly if you're talking about gridiron

Are you talking about australian rules football or rugby for us when you said "not that rolling around in the dirt thing you guys got"

split_city wrote:....particularly if you're talking about gridiron...

Gridiron...

It even sounds manly...

StillAnotherGuest wrote:

split_city wrote:....particularly if you're talking about gridiron...

Gridiron...

It even sounds manly...

hahahaha...oh the irony!! So manly that the guys who play the game prance around in helmets and padding. Everyone gets so excited when someone passes the ball ten yards. Please let me know when they decide to take off their skirts


Even some of our "old" and "retired" Australian Rules Football players have been recruited over the last few years to play in your manly game.

Anyways, back on topic....

split_city wrote:Even some of our "old" and "retired" Australian Rules Football players have been recruited over the last few years to play in your manly game.

I blame Affirmative Action for that (part of the "Give a Poor Aussie A Job" initiative).

Here's a link to a youtube video of one of our Aussies in the "manly" sport of NFL. Nice hit on Rocca but he just laughs it off. We are used to these types of bumps (without the pansy helmets and padding) in Aussie Rules

http://www.youtube.com/watch?v=cerDBOd_zlg

A video showing a kick-in from Ben Graham, another Aussie over in the States. The kick was 85m (93 yards).

http://www.youtube.com/watch?v=J47ccoM0Dvg

According to Wiki, "on May 22, 2006, the Jets signed Graham to a six-year contract worth US$5.17 million"

A 75m (82yards) kick from Dustin Fletcher:

http://www.youtube.com/watch?v=J47ccoM0Dvg

Sorry, I don't do "YouTube".

Where's my DC and biocals?

SAG

StillAnotherGuest wrote: Sorry, I don't do "YouTube".

Spoilsport

StillAnotherGuest wrote:Where's my DC and biocals?

SAG

Do you simply want me to post some data where I did the calibrations for Pes?