Resmed vs. Respironics - Help

rested gal wrote: heheh, yeahhhhh, riiiiight.

Bet there are a few people you'd like to use that on!!

A post in 2004 on a board many sleep techs frequent:

One of the techs asked:
Several years ago it seemed like esophageal pressure monitoring (Pes) was becoming a standard in polysomnography. I haven't heard much about it lately. Are many centers/labs still using Pes or is this invasive procedure fading out?


Among the replies by other techs was this:
In the center I ran there was a physician who wanted to do this. He did not know, could not tell me, what the normal values would be so, he decided he would wer one and be monitored all night to establish a baseline. He showed the technologist how to place the catheter, on me. Then the technologist nervously placed it on him. He had it in for about 15 seconds, tossed his cookies then exclaimed he would never put a patient through that.

Too be honest, esophageal catheters and the diaphragm EMG catheter mentioned in previous study, really aren't all that bad. You are aware that they are there, but they don't generally cause discomfort. It's just the initial "OMG, that's going where?" thought that turns some people off.

I have a catheter about 3.2mm is diameter. Small electrode rings bring that up to about 3.6mm in certain places. The catheter also hase two balloons attached so I can measure esophageal and gastric pressure. I have put this down approximately 40 people, not to mention about 7 times down myself! Once in, it is fine. It's only a problem if the patient has a bad gag reflex. If they do, you just can't get the catheter in. Only two out of the 40 or so subjects I have put it down have had a reflex which prevented me from getting it down.

Nonetheless, while I believe Pes is a far more sensitive measurement of effort compared to effort bands, I don't think catheters will be introduced as a standard piece of PSG equipment

split_city wrote:No, not at all. However, the general consensus from several studies is that closing pressure is <5cmH20 in even the most severe OSA patients. Furthermore, this is generally classified as the passive collapsing pressure i.e. under no influence of dilator muscle activity. This pressure is lower i.e. closer to atmospheric pressure when dilator muscles are active.

There are certainly times where the airway collapses above this pressure. But the number of events would be much lower.

It can also go the other way. There are times in which a lower closing pressure or even -ve pressure for that matter is required to collapse the airway. For example, I had this patient who generally had a closing pressure of about 3cmH20. However, there was a couple of instances where his airway remained patent even when mask pressure reached -6cmH20. This was despite the fact that the patient was in the same sleep stage and he remained in the same posture.

Split_city would you be willing to reference some of those studies showing that collapse doesn't occur at pressures above 5 cm pressure?

I suspect that there might be additional illuminating information there about the specific conditions under which those results were obtained.

Regards,
Bill

NightHawkeye wrote:

split_city wrote:No, not at all. However, the general consensus from several studies is that closing pressure is <5cmH20 in even the most severe OSA patients. Furthermore, this is generally classified as the passive collapsing pressure i.e. under no influence of dilator muscle activity. This pressure is lower i.e. closer to atmospheric pressure when dilator muscles are active.

There are certainly times where the airway collapses above this pressure. But the number of events would be much lower.

It can also go the other way. There are times in which a lower closing pressure or even -ve pressure for that matter is required to collapse the airway. For example, I had this patient who generally had a closing pressure of about 3cmH20. However, there was a couple of instances where his airway remained patent even when mask pressure reached -6cmH20. This was despite the fact that the patient was in the same sleep stage and he remained in the same posture.

Split_city would you be willing to reference some of those studies showing that collapse doesn't occur at pressures above 5 cm pressure?

I suspect that there might be additional illuminating information there about the specific conditions under which those results were obtained.

Regards,
Bill

I didn't actually mean that the airway doesn't collapse above 5cmH20, but this represents the upper limit of the average closing pressure.

Here are some references specifically looking at OSA patients:

J Appl Physiol. 2005 Nov;99(5):2020-7. wrote: Respiratory control stability and upper airway collapsibility in men and women with obstructive sleep apnea.Jordan AS, Wellman A, Edwards JK, Schory K, Dover L, MacDonald M, Patel SR, Fogel RB, Malhotra A, White DP.

Pcrit was measured by progressively dropping the continuous positive airway pressure level for three to five breaths until airway collapse. Apnea-hypopnea index-matched women had a higher BMI than men (38.0 +/- 2.4 vs. 30.0 +/- 1.9 kg/m2; P = 0.03), but Pcrit were similar between men and women (Pcrit: 0.35 +/- 0.62 and -0.18 +/- 0.87, respectively, P = 0.63). In the BMI-matched subgroup, women had less severe OSA during non-rapid eye movement sleep (30.9 +/- 7.4 vs. 52.5 +/- 8.1 events/h; P = 0.04) and lower Pcrit (-2.01 +/- 0.62 vs. 1.16 +/- 0.83 cmH2O; P = 0.005).

Chest. 2002 May;121(5):1531-40 wrote: Upper airway collapsibility during sleep in upper airway resistance syndrome.Gold AR, Marcus CL, Dipalo F, Gold MS.

The mean +/- SD Pcrit of the 12 normal subjects was - 15.4 +/- 6.1 cm H(2)O; the mean Pcrit of the 22 UARS patients was - 4.0 +/- 2.1 cm H(2)O; the mean Pcrit of the 37 patients with mild-to-moderate OSA/H (AHI > or = 10/h and < 40/h) was - 1.6 +/- 2.6 cm H(2)O; and the mean Pcrit of the 47 patients with moderate-to-severe OSA/H (AHI > or = 40/h) was 2.4 +/- 2.8 cm H(2)O. The Pcrit of each group differed from that of all other groups (p < 0.01)

Chest. 2000 Oct;118(4):1031-41 wrote: Abbreviated method for assessing upper airway function in obstructive sleep apnea.Boudewyns A, Punjabi N, Van de Heyning PH, De Backer WA, O'Donnell CP, Schneider H, Smith PL, Schwartz AR.

Ten obese patients (body mass index, 32.0+/-5.6 kg/m(2)) with severe OSA (respiratory disturbance index, 63.0+/-14.6 events/h) were studied. Pcrit fell from 1.8 (95% CI, -0.1 to 2.7) cm H(2)O in the supine position to -1.1 cm H(2)O (95% CI, -1.8 to 0.4 cm H(2)O; p = 0.009) in the lateral recumbent position

Am J Respir Crit Care Med. 1999 Jan;159(1):149-57 wrote: Pharyngeal critical pressure in patients with obstructive sleep apnea syndrome. Clinical implications.Sforza E, Petiau C, Weiss T, Thibault A, Krieger J.

As a group, the mean Pcrit was 2.09 +/- 0.1 cm H2O (range, 0 to 4.5)

NightHawkeye wrote: Split_city would you be willing to reference some of those studies showing that collapse doesn't occur at pressures above 5 cm pressure?

I could be very wrong, but I'm guessing split_city was referring to passive airway collapse of the velopharynx.

By contrast, closing pressure of the larynx can presumably be much higher than 5 cm. But this type of apnea is a defensive and thereby entirely active neuromuscular closure. This etiology manifests and scores as obstructive apnea, none the less. An extreme example would be dllfo's VCD-related apneas that currently cannot be resolved at 30 cm.

Interestingly, defensive neurology orchestrates a counterproductive vocal-chord closure at the nadir of many central apneas as well. I suspect these closed-airway central apneas may primarily account for that low 62% sensitivity rating in the 420e (whereby cardiac oscillation cannot be conveyed and measured through the airway utilizing Rapoport's patented method of central-apnea differentiation---based solely on detection of an "open airway"). Even though the vocal chord closures tend to occur at CA nadir, I still suspect the cardiac oscillation signal is effectively diminished beyond reliable detection in many or most cases.


[on edit: I see split_city answered while I was composing my post]

Here is a figure from a paper by Mary Morrell and colleagues:

Progressive Retropalatal Narrowing Preceding Obstructive Apnea
MARY J. MORRELL, YASEEN ARABI, BRIAN ZAHN, and M. SAFWAN BADR
AM J RESPIR CRIT CARE MED 1998;158:1974–1981.

It visually demonstrates that the airway can in fact collapse towards the end of expiration. NOTE: It looks like the airway is still open but the grey looking area is in fact the esophageal pressure sensing catheter.

split_city wrote:Here are some references specifically looking at OSA patients:

J Appl Physiol. 2005 Nov;99(5):2020-7. wrote: ...

Thank you split_city. I'm in assimilation mode this morning as I look through some of this stuff.

I stumbled upon a more recent study from the Journal of Applied Physiology which attempts to quantify differences between passive and active collapse, "Neuromechanical control of upper airway patency during sleep". I believe it contributes to the ongoing discussion.

http://jap.physiology.org/cgi/content/full/102/2/547

There are some interesting charts which are probably worth posting, but since my primary computer died during last night's thunderstorm I'm not in a position to do that right now. (It looks like motherboard failure. I'm congratulating myself on having converted to Linux a while back. I expect full capability again as soon as I get the hardware replaced.)

Regards,
Bill

NightHawkeye wrote: I stumbled upon a more recent study from the Journal of Applied Physiology which attempts to quantify differences between passive and active collapse, "Neuromechanical control of upper airway patency during sleep". I believe it contributes to the ongoing discussion.

http://jap.physiology.org/cgi/content/full/102/2/547

Yep, I have seen that paper. Basically, the authors looked at active and passive airway collapse during sleep in OSA patients and age, sex and BMI-matched control subjects.

This first figure shows what happens during a passive and active Pcrit measurements. The left hand side shows passive collapse. Nasal pressure is dropped rapidly for <10 breaths. As you can see, the GG is not recruited and the airway collapses. The right hand represents active collapse. Nasal pressure is dropped for a longer period of time. This enables time for the GG to be recruited, thus preventing collapse. Consequently, a lower pressure is required to result in airway collapse during active trials.



The second figure show passive and active Pcrit in OSA patients and controls. As expected, the controls had a less collapsible airway under passive conditions. Furthermore, the control subjects were more effective at keeping the airway open under active conditions. This along with the other part of the figure suggests that there might be some sort of impairment with the musculature system in OSA patients.