What can affect O2 readings?

[LisaV]

Links fixed

 

[LisaV]

Links fixed

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Thanks for the links! The ebay one was actually extremely informative with regard to my original question. This is the type of information I'm coming across when I do searches as well, most written about the accuracy of O2 readings while moving, exercising, sweating, etc. to begin with.

However, assuming my monitor is accurate 100%, I wonder if there are actual studies or literature showing effects of pollution, chest congestion, etc. on O2 levels? I haven't been able to find any online. I'm just curious in general. This would be a great study to do. <img src="i/expressions/face-icon-small-smile.gif" border="0">

Anyway, thanks for the great links, LisaV!!

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[ladybug]

Ask and ye shall receive! LOL

This study does look at pollution... yikes!

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/content/abstract/159/2/365">http://ajrccm.atsjournals.org/...ent/abstract/159/2/365</a>

Here's the whole article:

<a target=_blank class=ftalternatingbarlinklarge href="http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf">http://ajrccm.atsjournals.org/cgi/reprint/170/4/383.pdf</a>

Here is an excerp from an article on asthma and GERD regarding oxygen saturation and reflux:

Stimulation of esophageal mucosal receptors giving rise to vagally mediated reflex bronchospasm has emerged as the leading hypothesis. Prolonged reflux-clearance-time often causes symptomatic esophageal disease and esophagitis. The epithelial layer of the mucosa becomes eroded, exposing vagal nerve endings. Consequently, esophageal receptors become increasingly sensitive to refluxed material. Once stimulated, the receptors transmit a signal that results in constriction of the bronchioles. Mansfield and colleagues[12] noted that the total respiratory resistance increased by 10% in asthmatic subjects with a positive Bernstein test (acid perfusion test) after esophageal acid stimulation. Kjellen and colleagues[13] found that esophageal acid caused a decrease in vital capacity of 0.2 L and an increase in alveolar plateau by 0.9% in asthmatics with GERD. Wright and colleagues[14] noted significant decreased airflow and arterial oxygen saturation before and after esophageal acid perfusion. Atropine pretreatment abolished these findings, providing more evidence for an acid-induced vagally mediated esophagobronchial reflex.

The above-mentioned is from this article:
<a target=_blank class=ftalternatingbarlinklarge href="http://www.medscape.com/viewarticle/457853_2">http://www.medscape.com/viewarticle/457853_2</a>

I just wish there were more articles on this stuff.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.

 

[LisaV]

Well, that's the thing, Sonia. So much can effect your O2 levels. My late husband had the pseudo/MRSA-colonized bronchiectasis I mention in my tag, and also severe asthma, and mitral valve prolapse, and slightly enlarged aortic valve (but not large enough for replacement), some sleep apnea, and eventually pulmonary hypertension. On a bad day all of these things would feed into each other and lower his sats.

Of course, he took meds for the things you can take meds for (calcium channel blockers, asthma meds, the usual CF inhaler things, antibiotics, etc) and they tested him regularly to see that the meds were working as well as they could.

But finally the docs could never know for sure which of these might be the "primary" cause of his low sats, but they did know for sure that he needed to be on O2 (first during sleep, later during exercise, finally all of the time). And being on O2 let him stay active and involved with life for a long long time.