Preliminary Data - Current project (exciting!)

StillAnotherGuest wrote: Assessment of supine PFT need not necessarily be performed in all obese patients, but could be of great value in in those patients where orthopnea occurs and /or unusual values of positive Pes are observed, suggesting expiratory flow limitation or fixed obstructed airway (however, still waiting for those callibrations to rule out errors in measurement and/or extent of artifact).

Sorry, I haven't performed any calibration of the recording device. The only other useful data I would have would be the baseline breathing while awake, to determine Pes artifact.

StillAnotherGuest wrote:Another key point is also insuring that all other potential sources of othopnea have been ruled out, including those of cardiac origin. Any signs of right-sided heart failure?
SAG

Not that I'm aware of. I will have a look at my notes.

EDIT:

Original "+20cmH20 patient" --> Aged 56, BMI 34, no cardiac problems

"Abdo crunching" guy --> Aged 41, BMI 30, hypertension (no other heart complications)

split_city wrote:Maybe this tonic activity is lost at sleep onset, allowing the diaphragm to ascend, resulting in a reduction in FRC. This decrease in FRC will likely increase upper airway collapsibility.

Right, translating all this to the sleep state(s) is critical. For instance, as you know, as soon as give these guys anesthesia, they go right down the tubes:

Perioperative Changes in Functional Residual Capacity in Morbidly Obese Patients
G. Damia, D. Mascheroni, M. Croci, L. Tarenzi
Br. J. Anaesth. (1988), 60, 574-578

Functional residual capacity (FRC) was measured before and after induction of anaesthesia for jejunoileal bypass surgery in 30 morbidly obese patients. The onset of anaesthesia was associated with a 51% reduction in FRC from 2.2 litre to 1.0 litre. Eighteen of the patients were investigated more extensively; in these subjects FRC was reduced below the control values of residual volume (RV) with the onset of anaesthesia, but recovered towards baseline after laparotomy incision. Reduction in FRC is related to baseline vital capacity (VC) and FRC and is much greater than that reported for patients of normal weight.

split_city wrote:Moving all the equipment around just to cater for a supine test probably isn't really worth it. The room I do my testing in really isn't that big.

Oh c'mon. If these guys can do it...

Lung volumes during sustained microgravity on Spacelab SLS-1
A. R. Elliott, G. K. Prisk, H. J. Guy and J. B. West
J Appl Physiol 77: 2005-2014, 1994

Gravity is known to influence the mechanical behavior of the lung and chest wall. However, the effect of sustained microgravity (mu G) on lung volumes has not been reported. Pulmonary function tests were performed by four subjects before, during, and after 9 days of mu G exposure. Ground measurements were made in standing and supine postures. Tests were performed using a bag-in-box-and-flowmeter system and a respiratory mass spectrometer. Measurements included functional residual capacity (FRC), expiratory reserve volume (ERV), residual volume (RV), inspiratory and expiratory vital capacities (IVC and EVC), and tidal volume (VT). Total lung capacity (TLC) was derived from the measured EVC and RV values. With preflight standing values as a comparison, FRC was significantly reduced by 15% (approximately 500 ml) in mu G and 32% in the supine posture. ERV was reduced by 10-20% in mu G and decreased by 64% in the supine posture. RV was significantly reduced by 18% (310 ml) in mu G but did not significantly change in the supine posture compared with standing. IVC and EVC were slightly reduced during the first 24 h of mu G but returned to 1-G standing values within 72 h of mu G exposure. IVC and EVC in the supine posture were significantly reduced by 12% compared with standing. During mu G, VT decreased by 15% (approximately 90 ml), but supine VT was unchanged compared with preflight standing values. TLC decreased by approximately 8% during mu G and in the supine posture compared with preflight standing. The reductions in FRC, ERV, and RV during mu G are probably due to the cranial shift of the diaphragm, an increase in intrathoracic blood volume, and more uniform alveolar expansion.

SAG

StillAnotherGuest wrote:

split_city wrote:Maybe this tonic activity is lost at sleep onset, allowing the diaphragm to ascend, resulting in a reduction in FRC. This decrease in FRC will likely increase upper airway collapsibility.

Right, translating all this to the sleep state(s) is critical. For instance, as you know, as soon as give these guys anesthesia, they go right down the tubes:

Perioperative Changes in Functional Residual Capacity in Morbidly Obese Patients
G. Damia, D. Mascheroni, M. Croci, L. Tarenzi
Br. J. Anaesth. (1988), 60, 574-578

Functional residual capacity (FRC) was measured before and after induction of anaesthesia for jejunoileal bypass surgery in 30 morbidly obese patients. The onset of anaesthesia was associated with a 51% reduction in FRC from 2.2 litre to 1.0 litre. Eighteen of the patients were investigated more extensively; in these subjects FRC was reduced below the control values of residual volume (RV) with the onset of anaesthesia, but recovered towards baseline after laparotomy incision. Reduction in FRC is related to baseline vital capacity (VC) and FRC and is much greater than that reported for patients of normal weight.

Changes in diaphragm position following the induction of anesthesia remains controversial. Some studies have shown a cranial displacement of around 2cm, particularly in the most posterior regions of the diaphragm. Others studies have shown a cranial movement of the posterior region, while the anterior region moved caudally. Consequently, the overall change in FRC attributed to an altreation in diaphragm position was nil.

Here's something which puzzles me. A few studies have stated that they believe that the reason for the cranially displacement of the diaphragm during anesthesia, is due to a loss in muscle tone. However, as I said previously, the diaphragm is generally considered to already be relaxed at the end of expiration. What "tone" is being lost IF it's already relaxed??

Anyways, we plan to look at the changes in FRC right at the wake-sleep transition AND preceding, during and post apnea. I am currently in the process of time-matching the Compumedics system and the computer which recorded A-P and Lateral chest and abdominal dimensions. Furthermore, I am also matching the scored events e.g. apneas, hypopneas, arousals etc with the lung and abdominal compartmental volume data. It looks like I was correct in stating that the lines in the below picture correspond to oscillations in apneas (decrease in A-P dimensions) and arousals (increase in A-P dimensions)

split_city wrote:Moving all the equipment around just to cater for a supine test probably isn't really worth it. The room I do my testing in really isn't that big.

StillAnotherGuest wrote:Oh c'mon. If these guys can do it...

Lung volumes during sustained microgravity on Spacelab SLS-1
A. R. Elliott, G. K. Prisk, H. J. Guy and J. B. West
J Appl Physiol 77: 2005-2014, 1994

Gravity is known to influence the mechanical behavior of the lung and chest wall. However, the effect of sustained microgravity (mu G) on lung volumes has not been reported. Pulmonary function tests were performed by four subjects before, during, and after 9 days of mu G exposure. Ground measurements were made in standing and supine postures. Tests were performed using a bag-in-box-and-flowmeter system and a respiratory mass spectrometer. Measurements included functional residual capacity (FRC), expiratory reserve volume (ERV), residual volume (RV), inspiratory and expiratory vital capacities (IVC and EVC), and tidal volume (VT). Total lung capacity (TLC) was derived from the measured EVC and RV values. With preflight standing values as a comparison, FRC was significantly reduced by 15% (approximately 500 ml) in mu G and 32% in the supine posture. ERV was reduced by 10-20% in mu G and decreased by 64% in the supine posture. RV was significantly reduced by 18% (310 ml) in mu G but did not significantly change in the supine posture compared with standing. IVC and EVC were slightly reduced during the first 24 h of mu G but returned to 1-G standing values within 72 h of mu G exposure. IVC and EVC in the supine posture were significantly reduced by 12% compared with standing. During mu G, VT decreased by 15% (approximately 90 ml), but supine VT was unchanged compared with preflight standing values. TLC decreased by approximately 8% during mu G and in the supine posture compared with preflight standing. The reductions in FRC, ERV, and RV during mu G are probably due to the cranial shift of the diaphragm, an increase in intrathoracic blood volume, and more uniform alveolar expansion.

SAG

eehh.....I'll study my patients in the supine postion if I want to look at the effect of posture on lung function. My main focus is on the overnight study..... sticking tubes and wires in... not fussing over supine PFT measurements.

I was thinking more along the lines of shipping the whole thing upstairs:

Microgravity Reduces Sleep-disordered Breathing in Humans
ANN. R. ELLIOTT, STEVEN A. SHEA, DERK-JAN DIJK, JAMES K. WYATT, EYMARD RIEL, DAVID F. NERI, CHARLES A. CZEISLER, JOHN B. WEST, and G. KIM PRISK
Am. J. Respir. Crit. Care Med., Volume 164, Number 3, August 2001, 478-485

Where they reaffirm

Spaceflight is associated with a reduction in end-expiratory lung volume (5), which would normally serve to reduce upper airway cross-sectional area.

but go on to discover

The most striking findings of this experiment were the dramatic reduction in the number of sleep-related breathing disturbances, the reduction in the amount of time spent snoring, and the reduced number of arousals associated with these respiratory related events during microgravity.

and conclude:

The results are probably due to the passive elimination of the gravitationally induced changes in the upper airway anatomical structures rather than changes in lung volume, ventilatory chemosensitivity, upper airway muscle control, or circadian timing. From this data we can infer that gravity plays a dominant role in the increase in upper airway resistance and obstruction that occurs after the transition to the supine posture and during all stages of sleep.

So one must wonder, in the myriad of forces at work in SDB, of the relative contribution of tracheal traction.

If you use the Space Shuttle for SDB, do they give you monitoring software?

SAG

StillAnotherGuest wrote: I was thinking more along the lines of shipping the whole thing upstairs:

Microgravity Reduces Sleep-disordered Breathing in Humans
ANN. R. ELLIOTT, STEVEN A. SHEA, DERK-JAN DIJK, JAMES K. WYATT, EYMARD RIEL, DAVID F. NERI, CHARLES A. CZEISLER, JOHN B. WEST, and G. KIM PRISK
Am. J. Respir. Crit. Care Med., Volume 164, Number 3, August 2001, 478-485

Where they reaffirm

Spaceflight is associated with a reduction in end-expiratory lung volume (5), which would normally serve to reduce upper airway cross-sectional area.

but go on to discover

The most striking findings of this experiment were the dramatic reduction in the number of sleep-related breathing disturbances, the reduction in the amount of time spent snoring, and the reduced number of arousals associated with these respiratory related events during microgravity.

and conclude:

The results are probably due to the passive elimination of the gravitationally induced changes in the upper airway anatomical structures rather than changes in lung volume, ventilatory chemosensitivity, upper airway muscle control, or circadian timing. From this data we can infer that gravity plays a dominant role in the increase in upper airway resistance and obstruction that occurs after the transition to the supine posture and during all stages of sleep.

lol...probably?? Oh that's really reassuring...

Anyways, yes, their results do go against the trend. They have shown that a reduction in lung volume (well, they didn't measure it, but FRC is known to be lower in microgravity), led to a DECREASE in AHI. This is the opposite to what happens here on Earth. Mind you, the pre-flight AHI was 8.3 while it was 3.4 during the flight. It would be interesting to see what happens to patients with severe OSA.

Nevertheless, the reduction in AHI looks to be the result of gravitational effects on upper airway structure. Perhaps they need an MRI machine in the SpaceLab as well? Get some images of the airway while they are sleeping

StillAnotherGuest wrote:So one must wonder, in the myriad of forces at work in SDB, of the relative contribution of tracheal traction.

SAG

I'll raise your microgravity study with this study:

Thorax. 2006 May;61(5):435-9. Epub 2006 Feb 20. Links
Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea.Heinzer RC, Stanchina ML, Malhotra A, Jordan AS, Patel SR, Lo YL, Wellman A, Schory K, Dover L, White DP.

BACKGROUND: Previous studies have shown that changes in lung volume influence upper airway size and resistance, particularly in patients with obstructive sleep apnoea (OSA), and that continuous positive airway pressure (CPAP) requirements decrease when the lung volume is increased. We sought to determine the effect of a constant lung volume increase on sleep disordered breathing during non-REM sleep. METHODS: Twelve subjects with OSA were studied during non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. The increase in lung volume due to CPAP (at a therapeutic level) was determined with four magnetometer coils placed on the chest wall and abdomen. CPAP was then stopped and the subjects were studied for 1 hour in three conditions (in random order): (1) no treatment (baseline); (2) at "CPAP lung volume", with the increased lung volume being reproduced by negative extrathoracic pressure alone (lung volume 1, LV1); and (3) 500 ml above the CPAP lung volume(lung volume 2, LV2). RESULTS: The mean (SE) apnoea/hypopnoea index (AHI) for baseline, LV1, and LV2, respectively, was 62.3 (10.2), 37.2 (5.0), and 31.2 (6.7) events per hour (p = 0.009); the 3% oxygen desaturation index was 43.0 (10.1), 16.1 (5.4), and 12.3 (5.3) events per hour (p = 0.002); and the mean oxygen saturation was 95.4 (0.3)%, 96.0 (0.2)%, 96.3 (0.3)%, respectively (p = 0.001). CONCLUSION: An increase in lung volume causes a substantial decrease in sleep disordered breathing in patients with OSA during non-REM sleep.

Some of the comments made in this paper:

"Previous animal and human studies suggest that the
mechanism underlying these results is probably an increase
in upper airway stiffness and size with increased lung volume
due to caudal traction on the pharyngeal airway"

"Because the subjects we studied were overweight or obese
(like most patients with OSA), we suspect that their
diaphragm was pushed upwards (cranially) when lying on
their back. The negative extrathoracic pressure applied in the
lung almost certainly pulled the diaphragm and trachea to a
more caudal position, thereby increasing the traction on the
upper airway and making it less collapsible."

"The supine posture is usually the position in which the
greatest respiratory disturbances are recorded, possibly in
part due to abdominal fat applying pressure on the
diaphragm leading to decreased lung volume and decreasing
the traction on the upper airway by the trachea. If this
assumption is correct, it is possible that, when subjects lie on
their side or are prone, the effect of negative extrathoracic
pressure would be smaller."

"Although an iron lung may well be
more cumbersome than nasal CPAP therapy, our data suggest
that increments in lung volume may be one of the
mechanisms by which sleep disordered breathing is improved
by CPAP."

CPAP does many things to improve SDB 1) acts as a pneumatic splint 2) reduces airway edema (not a lot of work in this area) and 3) increases lung volume

Now, changes the pressure inside the shell may have also acted on the patients' neck, but.....

"Finally, a direct effect of the iron lung negative pressure on
the neck and upper airway cannot be completely excluded. A
decrease in the pressure around the neck when lung volume
was increased could have ‘‘unloaded’’ the upper airway
making it less collapsible. However, when the pressure in the
iron lung was decreased, the webbing forming the seal
around the neck was shifted inside the chamber which would
only further decrease the neck area potentially exposed to the
negative pressure in the lung. We therefore doubt that this
contributed to the reduction in sleep disordered breathing"

So, this study showed that changing lung volume directly influenced SDB.

Raphael Heinzer also ran this study:

Am J Respir Crit Care Med. 2005 Jul 1;172(1):114-7. Epub 2005 Apr 7. Links
Comment in:
Am J Respir Crit Care Med. 2005 Nov 15;172(10):1349-50; author reply 1350-1.
Lung volume and continuous positive airway pressure requirements in obstructive sleep apnea.Heinzer RC, Stanchina ML, Malhotra A, Fogel RB, Patel SR, Jordan AS, Schory K, White DP.
Division of Sleep Medicine, Sleep Disorders Program @ BI, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. rheinzer@rics.bwh.harvard.edu

Previous studies have demonstrated that lung volume during wakefulness influences upper airway size and resistance, particularly in patients with sleep apnea. We sought to determine the influence of lung volume on the level of continuous positive airway pressure (CPAP) required to prevent flow limitation during non-REM sleep in subjects with sleep apnea. Seventeen subjects (apnea-hypopnea index, 42.6 +/- 6.2 [SEM]) were studied during stable non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. An epiglottic pressure catheter plus a mask/pneumotachometer were used to assess flow limitation. When lung volume was increased by 1,035 +/- 22 ml, the CPAP level could be decreased from 11.9 +/- 0.7 to 4.8 +/- 0.7 cm H(2)O (p < 0.001) without flow limitation. The decreased CPAP at the same negative extrathoracic pressure yielded a final lung volume increase of 421 +/- 36 ml above the initial value. Conversely, when lung volume was reduced by 732 +/- 74 ml (n = eight), the CPAP level had to be increased from 11.9 +/- 0.7 to 17.1 +/- 1.0 cm H(2)O (p < 0.001) to prevent flow limitation, with a final lung volume decrease of 567 +/- 78 ml. These results demonstrate that relatively small changes in lung volume have an important effect on the upper airway in subjects with sleep apnea during non-REM sleep.

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI, seal

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI, seal

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI, seal

No, this conclusion is absolutely NOT a done deal.

These studies are only concerned with NREM, where altered chemosensitivity runs rampant.

Yes, they increased FRC and improved SDB, but changing lung volumes to that extent also creates significant changes in ventilation/perfusion.

As soon as I saw the Boston group, a simple Ctrl F brought me to:

Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea wrote:Another possibility is that an increase in EELV led to an overall increase in the SaO2 due to improved ventilation/perfusion matching that could lead to decreased SaO2 fluctuations. This reduction in chemical stimuli fluctuations may have stabilised respiratory control, decreasing the risk of cyclic breathing.

You do that traction thing in REM and then you'll have something.

I sure would like to see what the heck their Pes was doing, if active exhalation was present or not.

And a Shop-Vac? Really.

SAG

.....grab hold of the trachea in humans, stretch it (without manipulating lung volume) and assess changes in airway collapsibility. We can only go by animal studies.

It will be interesting to see the lung volume results from my abdominal compression study. Recall, airway collapsibility increased by about 0.6cmH20 following a ~50% increase in Pga.

Lung volume may have remain unchanged if the outwards movement of the chest balanced the cranial displacement of the diaphragm.

Unfortunately, there isn't an easy way to visualize tracheal movement during sleep. Can't say that a loss in tension was a definate cause for the increased airway collapsibility.

Nor can we say that the increased collapsibility was due to edema.

Whatever the case, my study was the FIRST to show that compressing the abdomen, thus increasing Pga, caused the airway to become more collapsible. We can only speculate how this occurred.

Anyways, what does a 0.6cmH20 increase in airway collapsibility mean in a clinical sense? There really hasn't been any work looking at the relationship between airway collapsibility (in cmH20) versus RDI.

StillAnotherGuest wrote: I sure would like to see what the heck their Pes was doing, if active exhalation was present or not.

I can ask them as I know Amy Jordan (PhD student from our lab) and have been in contact with Raphael in the past via email.

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CPAPopedia Keywords Contained In This Post (Click For Definition): RDI

split_city wrote:

StillAnotherGuest wrote:I sure would like to see what the heck their Pes was doing, if active exhalation was present or not.

I can ask them as I know Amy Jordan (PhD student from our lab) and have been in contact with Raphael in the past via email.

And also, if present, when it disappeared (I think that pretty much anything that causes it will disappear with a low-level PAP of some sort)(then you gotta wonder if the air-trapping and consequently FRC would then dip. It's endless)

split_city wrote:.....grab hold of the trachea in humans, stretch it (without manipulating lung volume) and assess changes in airway collapsibility. We can only go by animal studies.

And even then, you only got maybe two that are close to humans. And with one of them, people get cranky when you take 'em apart. Especially if you can't get 'em back together again.

Meanwhile, I'm working on a CPT Code for the Space Shuttle. I think the Miscellaneous Code will work (none of the PAP codes will work, cause there's no "PAP" in outer space) but the co-pay looks to be about $2,134,874,657.27.

Disposables (LiOX, LiH) will be another couple bucks. Like about 600,000,000 of them.

SAG

Right, now I have time-matched our magnetometer data with the scored events. Here's a snapshot showing changes in A-P and Lat dimensions of the chest and abdomen during apneas/hypopneas and following arousals.

Top trace: Chest A-P
Second Trace: Chest Lat
Third Trace: Abdo A-P
Fourth Trace: Abdo Lat

Blue areas: apneas/hypopneas
Red areas: arousals



I haven't yet determined the actual changes in lung and abdominal compartmental volumes.