New to APAP. Very, very interesting!

[Aether087]

The primary determinant of respiratory drive is pH of 1) CSF centrally (pons), and 2) blood peripherally (carotid bodies and aortic arch). Increased arterial CO2 decreases pH and decreased arterial CO2 increases pH. Low pH stimulates respiration; high pH depresses respiration. Arterial oxygen concentration is a secondary drive that works predominantly when the CO2 response is "blunted" as in chronic CO2 retainers. Pulmonary stretch receptors also play a role.

My previous post regarding pressure and tidal volume (VT) was a vast oversimplification. A little more info: VT can be divided into at least 2 fractions. Fraction 1 is deadspace ventilation; this is ventilation of tissues that DO NOT participate in gas exchange. Such tissues are the naso- and oro- pharynx, larynx, trachea, bronchi, bronchioles, etc. The second fraction is alveolar ventilation. This is where gas exchange occurs. Think of the lungs as one big balloon covered by a mesh of lichens. These lichens represent the pulmonary capillaries. Gas exchange occurs at the alveolar-pulmonary capillary interface. As the alveoli expand and contract with inspiration and expiration, the pressure in the alveoli is transmitted to the surrounding pulmonary capillaries. If the intra-alveolar pressure and resulting distention is great enough, flow through the pulmonary capillaries can decrease or even stop. This may convert alveolar ventilation (good for CO2 washout) into deadspace ventilation (good for CO2 retention). At what pressure does this conversion occur? Very variable but likely to be somewhere in the 8 cmH2O to 20 cmH2O pressure range. Beginning to see how this works?

Straight CPAP and CPAP with lower EPR values (1 cmH2O relief) MAY promote increased deadspace ventilation and CO2 retention. CPAP with higher EPR values (3 cm H2O) MAY promote increased alveolar ventilation and CO2 washout resulting in increased central apnea (normal response to decreased CSF and arterial pH). Mask volume and flow in the mask has little to do with this UNLESS the fresh gas flow into the mask is too low to prevent rebreathing of exhaled CO2; very unlikely.

Hope this helps. Sorry for the long post.

[Sleeprider]

I don't want to hijack this thread, but the O.P. has good knowledge of ventilation and probably knows the answer.

The primary determinant of respiratory drive is pH of 1) CSF centrally (pons), and 2) blood peripherally (carotid bodies and aortic arch). Increased arterial CO2 decreases pH and decreased arterial CO2 increases pH. Low pH stimulates respiration; high pH depresses respiration. Arterial oxygen concentration is a secondary drive that works predominantly when the CO2 response is "blunted" as in chronic CO2 retainers. Pulmonary stretch receptors also play a role.

My previous post regarding pressure and tidal volume (VT) was a vast oversimplification. A little more info: VT can be divided into at least 2 fractions. Fraction 1 is deadspace ventilation; this is ventilation of tissues that DO NOT participate in gas exchange. Such tissues are the naso- and oro- pharynx, larynx, trachea, bronchi, bronchioles, etc. The second fraction is alveolar ventilation. This is where gas exchange occurs. Think of the lungs as one big balloon covered by a mesh of lichens. These lichens represent the pulmonary capillaries. Gas exchange occurs at the alveolar-pulmonary capillary interface. As the alveoli expand and contract with inspiration and expiration, the pressure in the alveoli is transmitted to the surrounding pulmonary capillaries. If the intra-alveolar pressure and resulting distention is great enough, flow through the pulmonary capillaries can decrease or even stop. This may convert alveolar ventilation (good for CO2 washout) into deadspace ventilation (good for CO2 retention). At what pressure does this conversion occur? Very variable but likely to be somewhere in the 8 cmH2O to 20 cmH2O pressure range. Beginning to see how this works?

Straight CPAP and CPAP with lower EPR values (1 cmH2O relief) MAY promote increased deadspace ventilation and CO2 retention. CPAP with higher EPR values (3 cm H2O) MAY promote increased alveolar ventilation and CO2 washout resulting in increased central apnea (normal response to decreased CSF and arterial pH). Mask volume and flow in the mask has little to do with this UNLESS the fresh gas flow into the mask is too low to prevent rebreathing of exhaled CO2; very unlikely.

Hope this helps. Sorry for the long post.

Okay, my post was understatement of the year.

[surferdude2]

Very good information, especially for those like me who are suffering from emphysema. I now have a better understanding of how the blood gas exchange takes place. My care givers have not taken the time to do that other than to say that exhaling against a moderate pressure, such as pursed lips, will give some relief when shortness of breath occurs.

So we were indeed talking about two different kinds of washout; one being the washout of CO₂ in the mask dead air space, the other being washout of the CO₂ in the alveoli.

Thank you for taking the time.

Dude

[surferdude2]

To me, this begs another question. I have been made aware that CPAP has been indicated for treatment of COPD by some professionals. The article I read didn't go into the matter in depth so I'm left wondering about the details.

I'm primarily wondering what the recommended pressure setting would be when there is no flow limitations that normally establish that level. I assume the higher the better but the limiting factor would likely be discomfort with exhaling against high pressures and leak management. Those same problems bedevil sleep apnea sufferers and usually are overcome by time and effort on the part of the user. The body seems to be able to acclimate to exhalation pressures that initially seem impossible to overcome.

Possibly there can be no recommended pressure for treating emphysema with CPAP. It may well be a matter of starting low and gradually working up to the maximum tolerable pressure after an extended period of acclimation. Possibly anywhere between 8 cm H₂O to 20 cm H₂O based on whatever the user can stand.

Any thoughts?

Dude

[Aether087]

"Pursed-lip" breathing works like CPAP to prevent collapse of small airways allowing the alveoli to participate in gas exchange.

Regarding CO2 washout: CO2 contained within the mask should not be a factor. With my device, the fresh airflow is such that there is always flow out of the vent ports on the mask and the flow is quite vigorous. This will carry away any exhaled CO2.

I really think that we are talking primarily about CO2 that is not removed from the blood in the lungs so that it can be exhaled AND a little about CO2 remaining in the airways (bronchioles, bronchi, trachea, naso- and oro- pharynx) that is leftover after an exhalation. The gas in the airways at end-exhalation is a mix of CO2 and air. The total deadspace volume in the average adult human is 150 ml. With my VTs being in the 650 ml range, the CO2/air mix in my deadspace is a minimal contributor to my overall arterial PaCO2. Primary respiratory drive is pH reflecting PaCO2 level in CSF and blood. CO2 "washout" is thus lowered CO2 in the blood due to hyperventilating.

[Sleeprider]

To me, this begs another question. I have been made aware that CPAP has been indicated for treatment of COPD by some professionals. The article I read didn't go into the matter in depth so I'm left wondering about the details.

I'm primarily wondering what the recommended pressure setting would be when there is no flow limitations that normally establish that level. I assume the higher the better but the limiting factor would likely be discomfort with exhaling against high pressures and leak management. Those same problems bedevil sleep apnea sufferers and usually are overcome by time and effort on the part of the user. The body seems to be able to acclimate to exhalation pressures that initially seem impossible to overcome.

Possibly there can be no recommended pressure for treating emphysema with CPAP. It may well be a matter of starting low and gradually working up to the maximum tolerable pressure after an extended period of acclimation. Possibly anywhere between 8 cm H₂O to 20 cm H₂O based on whatever the user can stand.

Any thoughts?

Dude

Dude, I think for restrictive lung disease like COPD positive air pressure my be helpful in improving gas exchange and dealing with any comorbidity of OSA. The real trick to helping these people (and perhaps you) get better volume is through the use of pressure support. COPD patients may require considerable positive pressure to help them inflate the lungs, and machines intended for that application have IPAP pressures up to 30 cm. They also need low exhalation resistance, so EPAP pressure is minimized to facilitate exhalation, while preventing airway collapse. Unlike central or complex apnea patients, they usually don't need ASV or ST ventilation, but the pressure support can be important. Lots of articles come up using keywords bilevel COPD or BiPAP COPD. This summary briefly shows how large PS can significantly help these people. http://www.sciencedirect.com/science/art...3814200458

Pressure support, not fixed pressure, can unload the burden of inflating inelastic, restrictive lungs from the chest muscles using the pressure differential of the PAP ventilator to take on some of the work. Have you ever tried bilevel?

[Aether087]

NIPPV or PPV support for patients with COPD is much more challenging than is ventilatory support for OSA. Support for COPD patients may (should) involve pharmacologic measures to manage airway and lung tone in addition to ventilatory support.

We have sophisticated ventilators in the ICU that allow us control over many ventilatory parameters. These vents also have sophisticated software and displays that show us flow-volume-pressure-time plots that tell us how the patient's lungs and airways are responding to the treatment. I do not know if such tools are available in the average sleep lab.