"please keep me updated about oximeters "
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Question For The Sleep Techs AND RRT/RPSGTs
When you are doing a PSG titration ... does the software you are using indicate inspiration and expiration VOLUME? Does it indicate inspiration EFFORT? i.e. does it just tell you that the chest and abdomen are moving or is there an indication of the strength or effort of that movement??
I would expect that COPD could affect both inspiration volume AND inspiration effort. Well, even expiration effort and volume as well.
I would expect that COPD could affect both inspiration volume AND inspiration effort. Well, even expiration effort and volume as well.
Views: 14
Replies to This Discussion
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Permalink Reply by Judy on
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Duane, just because one has COPD and OSA one isn't necessarily eligible for an insurance-paid bi-level. My original sleep doctor (sleep/pulmonary/critical care credentialed) was well aware that I had COPD before I even had my evaluation PSG. Bi-level is actually handwritten at the top of my PSG results report. Evidently the results weren't severe enough to qualify immediately for a bi-level. Many insurances, including Medicare, require a patient to "fail" CPAP therapy BEFORE they will pay for a bi-level except under specific circumstances. Evidently my results didn't meet the criteria as my equipment order was for a straight CPAP (I insisted it be fully data capable). It took 17 months of CPAP and a loaner APAP and 3 pressure changes BEFORE I was brought back in for a bi-level titration and switched to a bi-level (again I insisted on it being fully data capable). Medicare paid for both the original straight CPAP and the VPAP Auto,
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Permalink Reply by Duane McDade on
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All I hear is a frenchie saying I surrender, I surrender, I surrender.
Mollete said:Duane McDade said:
"So is your name Mollete or Holly? Are you French? palay vuxe 4 barrel"
Oui, je suis! Parlez-vous français? Vous devez être bilingue ici simplement pour survivre! Ou même trois langues! L'étude du sommeil est si intéressant. Ne pensez-vous pas ainsi? J'étudie chaque minute que je ne suis pas de travail à la conserverie de poisson.
Je vous dis une chose, monsieur, l'utilisation de ce langage "html" est une douleur dans le cul!
mollete
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Permalink Reply by RockRpsgt on
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I believe that is what Duane was trying to say. With COPD you have to be able to prove complex apnea to get the pt the right treatment for the pt.
Judy said:Duane, just because one has COPD and OSA one isn't necessarily eligible for an insurance-paid bi-level. My original sleep doctor (sleep/pulmonary/critical care credentialed) was well aware that I had COPD before I even had my evaluation PSG. Bi-level is actually handwritten at the top of my PSG results report. Evidently the results weren't severe enough to qualify immediately for a bi-level. Many insurances, including Medicare, require a patient to "fail" CPAP therapy BEFORE they will pay for a bi-level except under specific circumstances. Evidently my results didn't meet the criteria as my equipment order was for a straight CPAP (I insisted it be fully data capable). It took 17 months of CPAP and a loaner APAP and 3 pressure changes BEFORE I was brought back in for a bi-level titration and switched to a bi-level (again I insisted on it being fully data capable). Medicare paid for both the original straight CPAP and the VPAP Auto,
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Aw right, you guys. Now REALLY go ahead and confuse me!!! I thought Complex Sleep Apnea was a mixture of CENTRAL apneas AND OBSTRUCTIVE apneas. I haven't had 10 Central Apneas total in ALL my PSGs, evaluation AND titration, combined. At least not that have been reported in the printed full data summary results reports. And, yeah, that includes those called "mixed apneas".
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The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respirations.
Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself
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Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure, the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy, after the obstructive component has been eliminated. This has long been seen in sleep laboratories, and has been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating Cheyne-Stokes breathing, however, no longitudinal studies have yet been published, nor have any results been generated which suggest any differential outcomes versus standard CPAP therapy.
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Okay. Last I knew I was NOT yet a CO2 retainer. But then I've only had 2 ABGs and I'm unsure just how much, if any, value PFT or Spriometry results are for indication of CO2 retention. My last ABG was long enough ago I doubt that its results have much pertience today.
I just had a Spirometry in June. Would any of these be any indication? IF so, which one?
FVC absolute? FVC % p/c? FEV1 absolute? FEVI % p/c? FEV1/DVC absolute? FEF 25-75%? FEF 25-75% % p/c? FEF Max absolute?
And I notice you are ALL ignoring my "brilliant theory" on the LCD screen VT ratio that I posted on page 1 of this thead about 8:30 EDT this morning. Tsk, tsk. I'm going to assume since none of you discouraged this theory that you agree that it might be the key. Nyah, nyah! Damned if you do and damned if you don't, guys! *wicked grin*
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who cares Mollete I was trying to get the info to the forum. People pull info from other sites all of the time. Half of the text books for sleep are word for word from one another. I am getting pretty sick of you calling people out. Either you are here to help or you are not. My view is that you are a pretty lonely person to have the time to research everyone's post. I am done with you. I will not participate in anymore discussions that you are involved in. You are here to show of your brain more than you are to help.
Mollete said:Rock Hinkle said:The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respirations.
Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself
Plagiarism!!
http://en.wikipedia.org/wiki/Hypoxic_drive
"The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respirations.
Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself."
Wikipedia, fer cryin' out loud.
mollete
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ALLOW ME ROCK .... I'M ON THE FONTLINE BATTLING SLEEP APNEA 5 NIGHTS A WEEK! I DON'T HAVE TO, BUT I WANT TO. THE PROBLEM WITH BOOKS /RESEARCH PAPERS ETC, ETC.....IS MOST OF THE TIME OK 99.9 % THE INFORMATION IS WORTHLESS AND IS NEVER APPLIED, NEVER! EVERY PATIENT IS UNIQUE, AND MUST BE TREATED AS NEEDED. ALL THE INFORMATION IN ALL THE BOOKS AND PAPERS WILL NOT PRODUCE A "SILVER BULLET" FOR TREATING SLEEP APNEA IN ALL ITS SPLENDER. WALK A MILE IN A SLEEP TECHS SHOES , AND FIND OUT JUST HOW WORTHLESS "WORDS" ARE. THE JOB IS THE BEST TEACHER. ANY COMPANY THAT MAKES A PRODUCT THAT TREATS OR DETECTS SLEEP APNEA WILL MAKE CLAIMS THAT THIS PRODUCT WILL DO THIS AND GIVE YOU 1000-5000 WORDS THAT TRY TO MAKE YOU BELIEVE. LETS GET REAL HERE. ALL I WANT IS FOR PEOPLE TO GET BETTER. I HELP I DON'T HAVE TIME TO ARGUE! I KNOW FROM 7 YEARS OF DOING THIS THAT I DO THE BEST I CAN TO HELP FOLKS SOLVE THET'RE ISSUES AT THE LAB I WORK AT, AND THE PEOPLE ON THIS FORUM WHO WANT ADVISE. TOO MUCH INFORMATION CAN BE BAD. AND IN THE WRONG HANDS DANGEROUS!
Rock Hinkle said:who cares Mollete I was trying to get the info to the forum. People pull info from other sites all of the time. Half of the text books for sleep are word for word from one another. I am getting pretty sick of you calling people out. Either you are here to help or you are not. My view is that you are a pretty lonely person to have the time to research everyone's post. I am done with you. I will not participate in anymore discussions that you are involved in. You are here to show of your brain more than you are to help.
Mollete said:Rock Hinkle said:The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respirations.
Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself
Plagiarism!!
http://en.wikipedia.org/wiki/Hypoxic_drive
"The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr.
In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respirations.
Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself."
Wikipedia, fer cryin' out loud.
mollete
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I LOVE TO SHOUT!! I READ THE AASM SLEEP REPORT MAGAZINE, AND NO MOST OF THE INFORMATION IS SUPERFICAL, AND DONE FOR CREDITS AND GRANTS. I MEAN THE EFFECTS OF AMBIEN ON RATS WITH BLACK SPOTS AND WHITE MICE. PLEASE! WHEN THEY HAVE SOME USEFUL IDEAS I'LL LOOK...IF I HAVE TIME YOU SEE I'M VERY BUSY DO SLEEP STUDIES. THEY ARE NOT. IN FACT I SPEND MOST OF MY TIME EXPLAINING IN HUMAN NOT DOCTOR NO WORDS OVER 8 LETTERS LONG, WHAT A SLEEP STUDY IS AND WHAT WE LOOK FOR AND THEN TELL THEM TO SLEEP. DO YOU THINK THEY CARE ABOUT THEY'RE CHEMOREPORTORMSYPETETORIUMS, FOR GODS SAKE!!!!!!!!!!!!!!!!!!!!!!!!!!!1
Mollete said:Duane McDade said:
Well you don't have to shout.ALLOW ME ROCK .... I'M ON THE FONTLINE BATTLING SLEEP APNEA 5 NIGHTS A WEEK! I DON'T HAVE TO, BUT I WANT TO. THE PROBLEM WITH BOOKS /RESEARCH PAPERS ETC, ETC.....IS MOST OF THE TIME OK 99.9 % THE INFORMATION IS WORTHLESS AND IS NEVER APPLIED, NEVER! EVERY PATIENT IS UNIQUE, AND MUST BE TREATED AS NEEDED. ALL THE INFORMATION IN ALL THE BOOKS AND PAPERS WILL NOT PRODUCE A "SILVER BULLET" FOR TREATING SLEEP APNEA IN ALL ITS SPLENDER. WALK A MILE IN A SLEEP TECHS SHOES , AND FIND OUT JUST HOW WORTHLESS "WORDS" ARE. THE JOB IS THE BEST TEACHER. ANY COMPANY THAT MAKES A PRODUCT THAT TREATS OR DETECTS SLEEP APNEA WILL MAKE CLAIMS THAT THIS PRODUCT WILL DO THIS AND GIVE YOU 1000-5000 WORDS THAT TRY TO MAKE YOU BELIEVE. LETS GET REAL HERE. ALL I WANT IS FOR PEOPLE TO GET BETTER. I HELP I DON'T HAVE TIME TO ARGUE! I KNOW FROM 7 YEARS OF DOING THIS THAT I DO THE BEST I CAN TO HELP FOLKS SOLVE THET'RE ISSUES AT THE LAB I WORK AT, AND THE PEOPLE ON THIS FORUM WHO WANT ADVISE. TOO MUCH INFORMATION CAN BE BAD. AND IN THE WRONG HANDS DANGEROUS!
The obvious fault in your statement is that the literary accounts that you mention are simply compilations of other people's own work and experience. Are you totally discounting their thoughts, opinions and expertise? I would respectfully submit that the reverse is true-- 99.9% of the information is or can be helpful, it simply depends on how or when you're going to use it.
I do, however, think that when someone goes through the trouble of doing some research and publishes it, that they be given proper credit for it.
mollete
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Yes and when I'm falling out of an airplane and don't have a Parachute I wish I had a Book or reference material that would tell me how many times I could flap my arms before I hit the ground. Maybe how my family might bennifit and the statistics on how double policy payoffs...... BLAH BLAH BLAH. What are you trying to prove??? Mollete. Wait, (Duane takes out a Pad of Paper, and Readies his Pen) Tell me about your , Mother?
Mollete said:Article points out:
"However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect..."
Attributing this to Haldane Effect never made any sense to me. While arterial pO2 would increase in the face of oxygen supplementation, venous pO2 wouldn't really change, so CO2-Hbcombined wouldn't change either. Once you got to lung and increased pO2 is seen, localized or not, it would unload as it's supposed to, perhaps even aided by Haldane, not hindered.
By that same rationale, are we saying that "Yeah, let's keep 'em dangerously acidotic, cause if we fix that, it will shift oxyhemoglobin dissociation curve via Bohr?" Are we saying that treatment in general is specifically designed to make everybody worse? What are they going to blame on all these dead scientists that aren't around to defend themselves next? World hunger?
To my previous point, as long as you're breathing and have some reserve, this would occur. If you're not breathing (as seen in critically ill patients) then there's certainly the potential for some issues.
mollete
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NO BUT LAST NIGHT I STAYED AT THE HOLIDAY INN!
Mollete said:OK, I have a question for you, there, Duane. Are you one of those previously-mentioned "RPSGT"s?
mollete
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