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Its not Apnea but.....
#1
...we think you would benefit from trying out a Dreamstation.
Thats what the folks that analyzed my study said.
My AHI on this study was only 3 but my SP02 was 99% of the time below 90%

The one month trial will cost me $200
The Dreamstation suggested was not priced but I am thinking (based on a previous conversation) in excess of $2500 because I was told the equipment "starts" at $2500
This is Canadian $
When I told her I could not afford this and would look in the used market, she got very luke warm and pretty much ended the conversation.

So to my questions
Whats the success rate of folks increasing their SP02 using CPAP or APAP equipment
Should I get a used machine and use it in auto mode and monitor, based on the fact I can likely resell it if not working (I would still be likely to be out less money)
I have two machines available to me in my budget, a resmed S9 Autoset and a respironics Remstar Auto C-Flex, which might be the better option?

I have not fully read the information here concerning the self adjustments to treat oneself but feel confident that I can do so (The remstar comes with 2 different and brand new masks)

EDIT: Would I be better to ask the Doc to prescribe oxygen?

Thanks for any and all advice and information.
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#2
Rather than a CPAP, you might want to talk with a pulmonologist about an oxygen concentrator. You also might want additional testing to determine the reasons for your condition.

And what Chill says below: it would be a really good idea to see a cardiologist.
                                                                                                                                                                                  
Please organize your SleeyHead screenshots like this.
I'm an epidemiologist, not a medical provider. 
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#3
I agree, with SPO2 that low and an AHI of 3 you need a different kind of doctor not a CPAP machine.  Who knows, maybe that is normal for you?  A pulmonologist and and cardiologist seem like a good place to start.
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#4
CPAP can have a very beneficial effect on oxygenation, and is probably preferable to supplemental oxygen.  The mechanisms of this improvement are complex, so I'm going to let someone else explain it below, but a small amount of positive  pressure INCREASES THE POSITVE END EXPIRATORY PRESSURE (PEEP) in the lungs, and this is a basic pulmonary principle your doctor is aware of.

CPAP is a valid and economical way to improve profusion and oxygenation. That said, when not treating for sleep apnea, you don't need auto adjusting pressure or data and other bells and whistles. You can find a CPAP that reliably provides a fixed pressure for low cost, especially on the used market, and I would not hesitate to order from Supplier #2 (secondwindcpap) who has basic CPAPs selling for a little as $95, although I'd encourge you to go for the S8 or S9 Elite CPAPs in the $200-$300 USD range. Still, that is ownership at the cost of a month or so of rent. All you need is the prescription.


Quote:Physiology of Ventilation
To understand how CPAP works, providers should begin with an understanding of the physiology of the pulmonary system. The lower airways resemble an inverted tree extending from the trachea through the bronchi to the alveolar sacs.

Alveoli form the primary constituent of lung tissue. An average adult has 300–600 million alveoli, each of which measures about 1/3 mm in diameter. Alveolar walls consist of a single layer of cells and elastin fibers that permit stretching and contracting during ventilation.

The internal surface of each alveolus is covered by a thin film of fluid containing surfactant that decreases surface tension and keeps alveolar walls from collapsing and sticking together on expiration. This reduces the work of reopening them with each breath.

Surfactant production diminishes when lungs are hypoperfused and hypoxic. Without adequate surfactant, alveoli collapse and atelectasis develops. The lungs become stiff, and alveoli ultimately fill with fluid.

The alveolar-capillary surface area available for gas exchange is about 1 sq. meter/kg of body weight in the average adult. Normally, the blood-gas barrier is one cell thick. Every red blood cell circulating through the lungs spends about one second in the pulmonary capillary network. During that time, it goes through two to three alveoli and picks up its full complement of (O2) in one-fifth of a second.

The brief time each red blood cell spends in the pulmonary capillary network is normally sufficient for adequate gas exchange. However, this isn’t the case in states of disease, such as emphysema and lung cancer, when the gas exchange surface area is reduced by more than two-thirds and the membranes are thicker, or interstitial or alveolar fluid is present. In this situation, O2 diffusion will be inadequate to meet the body’s demands at rest, and carbon dioxide (CO2) won’t be adequately eliminated.

The relationship between pressure inside the pulmonary system and atmospheric pressure determines the direction of airflow, and the amount of air moved into the lungs depends on airway resistance and lung compliance.

Airway Resistance
Several factors determine airway resistance. These include airway diameter, motor nerve impulses, the length of the airway, lung volume, tissue resistance, compliance and work of breathing. We’ll discuss each here.

Airway diameter: If the airway radius is narrowed by half, the resistance through it increases by 16. There’s a reduction in airflow to the fourth power. Airway diameter is affected by receptors in the trachea and large bronchi that are activated by irritants or immune system responses.

Motor nerve impulses: Resistance may greatly increase due to airway secretions or bronchial constriction. The vagus nerve constricts bronchioles and sympathetic stimulation dilates bronchioles. Release of histamine causes constriction of smooth muscle resulting in bronchoconstriction.

Length of the airways: If length doubles, resistance doubles.

Lung volume
: Diminished lung volume results in increased airway resistance. Small airways may close completely. Patients with increased airway resistance often breathe at high volumes to help decrease airway resistance.

Tissue resistance: Tissue resistance accounts for about 20% of the total airway resistance in young patients, although it may be increased with some diseases.

Compliance: This is the ability of the lungs and thorax to expand easily with inhalation. Good compliance means easy expansion. A normal breath of 500 mL requires a distending pressure of less than 3 cm of water (H2O). A child’s balloon may need a pressure of 300 cm of water for the same change in volume.

***To demonstrate and appreciate compliance, chew some bubble gum. See how easy it is to blow a bubble after only a minute of chewing. This is great compliance. Compare that to the difficulty in blowing a bubble after an hour when gum elasticity has diminished. This demonstrates poor compliance.

Work of breathing: In healthy persons, the energy required for normal quiet breathing is small (only 3% of the total body expenditure). Loss of surfactant, increased airway resistance, decreased compliance, airflow obstruction and lung hyperinflation increase the work of breathing. As lungs become “stiffer,” respiratory muscles become fatigued, resulting in ventilatory failure. Anything that increases functional reserve capacity (FRC) will improve lung mechanics and enable more work to be generated for the same effort.

Although work of breathing is difficult to measure at the bedside, it’s easy to appreciate clinically. EMS providers can do this by observing the patient for tripoding, use of accessory muscles and retractions. O2 consumption increases as ventilatory reserves decrease. As the amount of O2 needed becomes excessive, the body becomes hypoxic. See Table 1 for symptoms and diseases that increase work of breathing.

How CPAP Works
Patients who benefit from CPAP frequently present with a chief complaint of dyspnea. Dyspnea can be caused by cardiac, pulmonary, neuromuscular, psychologic/social/spiritual etiologies or any combination of them. The severity varies widely among patients. EMS providers should get a good baseline assessment to trend improvement. See Table 2 for a modified Borg Dyspnea Scale, which rates the intensity.

CPAP gets many patients with severe inspiratory muscle fatigue through their acute crisis without the need for intubation. CPAP delivers a constant positive pressure to the airways of a spontaneously breathing patient during inspiration and expiration through a noninvasive mask. CPAP raises inspiratory pressure above atmospheric pressures and then applies PEEP to exhalation.

Intrinsic PEEP (auto-PEEP) is usually about 5 cm water. It must be overcome before negative pressure can be generated to inhale more air. If one exhales against resistance, smaller, dependent airways are “splinted” open at the end of expiration, and small bronchi and alveoli don’t collapse. Keeping these structures open on exhalation allows the muscles that were working to keep them open (the ones exerting auto-PEEP) to be recruited into inspiration. When alveoli stay open, inspiratory effort doesn’t have to be expended to reinflate them. This reduces inspiratory work, relieves respiratory muscle fatigue and decreases work of breathing.

Increased pressure in the airways also allows for better distribution of gases, which leads to an increase in alveolar pressure and reexpansion of collapsed alveoli. This reverses micro-atelectasis. In addition, maintaining inspiratory and expiratory pressures above normal levels results in improved functional reserve capacity, better lung compliance and bronchodilation. This positively affects the ventilation/perfusion (V/Q) ratio.

As alveoli stay open, gas-exchange time can double. This increases oxygen levels in the blood and decreases CO2 levels—as long as respiratory diffusion and pulmonary perfusion dynamics work properly. This reduces hypoxia and reverses hypercarbic ventilatory failure.(1)

CPAP changes alveolar/hydrostatic pressure dynamics. An increase in alveolar pressures will counterbalance interstitial or capillary hydrostatic pressures and will slow or stop movement of fluid into the alveoli. Positive airway pressure pushes fluid out of the alveoli in pulmonary edema and will stop further influx.

It also improves cardiac output. When pulmonary capillary wedge pressures (PCWP) are less than 23, cardiac output is determined by preload (venous filling pressures). Thus, increased preload equals increased cardiac output.

In cardiogenic pulmonary edema due to heart failure, PCWP is already maxed out. If greater than 23, cardiac output is dependent on afterload. CPAP increases pressures throughout the thorax, including pressure surrounding the left ventricle (LV). This makes it easier to eject blood out of the heart. Similarly, pressure surrounds the thoracic cavity but not the abdominal aorta, giving the impression of reduced LV afterload outside of the thoracic cavity. This will increase cardiac output unless PEEP levels are too high. High intrathoracic pressures greatly reduce preload to the right heart and will reduce the blood pressure.

CPAP produces an increase in tidal volume with a subsequent reduction in the work of breathing. Stabilization of minute ventilation with an increase in FRC should improve ventilation-perfusion relationships and potentially reduce oxygen requirements. This allows for an increase in available O2 for tissue perfusion and a decrease in CO2 levels.

If CO2 elimination from the lungs decreases, CO2 levels in the blood will rise. This condition, called hypercarbia, occurs with respiratory depression or hypoventilation, which can be caused by airway obstruction, respiratory muscle impairment or pulmonary obstructive diseases, among other pathologies. EMS providers should correct hypercarbia by increasing ventilation and attempting to correct the underlying cause. Improved ventilation and gas exchange are major benefits of CPAP.

Conclusion
Prehospital crews have been without the capabilities offered by CPAP and had to watch dyspneic patients decline, requiring intubation. Patients who are still awake during intubation often experience anxiety and discomfort and need to remain sedated. They can’t talk with the tube passing through their vocal cords, and the aspiration risk is high with open cords. Intubated patients are also more susceptible to VAP, MRSA and Klebsiella than non-intubated ones.

Consideration of these complications, as well as the cost of equipment and a mandatory ICU admission, makes avoiding intubation by administering CPAP an attractive option.

CPAP should be the first line of respiratory therapy in carefully selected patients based on local protocols. It relieves symptoms but should be used in concert with appropriate medications in patients with asthma, chronic obstructive pulmonary disorder (COPD) and heart failure. This will address specific underlying pathology.

Remember, CPAP isn’t a ventilator. Patients must be monitored carefully (vital signs, SpO2, capnography and clinical responses) after CPAP application to detect improvement in condition or lack of improvement that may indicate the need for intubation and assisted ventilations, as well as for signs of complications that may signal the need to remove the CPAP mask.
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#5
(03-16-2017, 07:00 PM)bexiesbruv Wrote: My AHI on this study was only 3 but my SP02 was 99% of the time below 90%

That could be flow limitation. As you no doubt have discovered, all of the information can be overwhelming. But I want to talk about the most common affliction for which CPAP therapy is prescribed, which is officially called obstructive sleep apnea. This is where the upper airway collapses and no air enters the lungs. A less severe event is a hypopnea, where the airway remains partially open, but not enough to get adequate air flow. Both obstructive apneas and hypopneas count in the apnea-hypopnea index (AHI). But flow limitation is an even less severe restriction of the airway that does not count in the AHI, and this may be what you have. If so, a CPAP machine should be the fix.

Quote:The one month trial will cost me $200

I would go for that, simply because it will likely include mask fittings. It's sometimes hard to find a mask that fits well, and that trial-and-error process can get expensive if you're paying out of pocket for the masks.

Quote:The Dreamstation suggested was not priced but I am thinking (based on a previous conversation) in excess of $2500 because I was told the equipment "starts" at $2500

At that point you can make the decision about getting your own machine on your own. You'll be much better informed by then. Meanwhile, study up on the different types of machines.

http://www.apneaboard.com/wiki/index.php...ne_Choices
Sleepster
Apnea Board Moderator
www.ApneaBoard.com


INFORMATION ON APNEA BOARD FORUMS OR ON APNEABOARD.COM SHOULD NOT BE CONSIDERED AS MEDICAL ADVICE. ALWAYS SEEK THE ADVICE OF A PHYSICIAN BEFORE SEEKING TREATMENT FOR MEDICAL CONDITIONS, INCLUDING SLEEP APNEA. INFORMATION POSTED ON THE APNEA BOARD WEB SITE AND FORUMS ARE PERSONAL OPINION ONLY AND NOT NECESSARILY A STATEMENT OF FACT.
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#6
If you don't have apnea and your oxygen is so low, I don't understand why you weren't referred to a specialist to identify why the oxygen shortage?

My average oxygen is 86% without the cpap. I have very little apnea, but have a slow heart rate and as such my oxygen drops all night long. It now averages 91% with the cpap - not fabulous, but I don't feel the need for naps most days. I'll be getting a pacemaker in the future. My family member has an average of 76% oxygen without bipap. He has zero apnea but does have lung issues. With bipap, his average oxygen is 95%.

I did ask my doc about oxygen and they avoid that until they absolutely can't because it creates a host of other problems. So, as long as the cpap works alone, that's what we go with.

I recommend getting one with apap. You have a choice of apap or cpap modes. My family member can only use the bipap mode, not the auto mode, while I can use the auto mode but have to have a higher lower limit than the auto would indicate. It would help, I think, in your situation, to get a recording oximeter to test what your lower limit should be.

I will say though that different machines may actually work differently for you. With the Respironics 560 series, the auto mode just didn't work for me, so I had to switch that to cpap and straight pressure. When my replacement Resmed auto came in, that algorithm worked fine for me, so it's been auto most of the time.
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#7
What is your spo2 while awake? If that is less than ideal, then definitely it's an issue beyond Cpap type machines.

Since you have a very low ahi, For raising spo2 levels, a straight bilevel machine is a better choice than a Cpap or an apap. The pressure support(PS) in a bilevel will improve spo2. More the PS, more the o2 level improvement in general.

If bilevel is not available then a resmed machine with epr is a better choice since epr at 3 is close to a PS of 3cm.

The respironics apap's Aflex or Cpap's cflex+ is closer to a PS of 2cm.

Definitely see a pulmonologist and a cardiologist.
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#8
(03-17-2017, 12:33 AM)AshSF Wrote: What is your spo2 while awake? If that is less than ideal, then definitely it's an issue beyond Cpap type machines.

Awake and moving its low-mid 90's


Awake and moving its low-mid 90's
When I run, its higher but I lose the reading too often to make total sense of the readings.

The sleep folks told me 95% was average for Alberta

Thats so far with the information given, I really do appreciate all the replies.

My (now I have read through these replies) revised plan is to get back to the folks at the sleep place and set up the $200 trial
I already have an appointment with my Doc later today and will ask for a referral to a cardiologist or pulmonary specialist
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#9
Another possibility.  See Pickwickian syndrome
INFORMATION ON APNEA BOARD FORUMS OR ON APNEABOARD.COM SHOULD NOT BE CONSIDERED AS MEDICAL ADVICE. ALWAYS SEEK THE ADVICE OF A PHYSICIAN BEFORE SEEKING TREATMENT FOR MEDICAL CONDITIONS, INCLUDING SLEEP APNEA. INFORMATION POSTED ON THE APNEA BOARD WEB SITE AND FORUMS ARE PERSONAL OPINION ONLY AND NOT NECESSARILY A STATEMENT OF FACT.
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#10
I'm not obese, although I think I might have been. I started losing fat mass about 3 years ago. I was only 170lbs back then but maybe 30% body fat.
I currently weigh in at 155 and maybe about 20-22 % body fat.

One thing to mention is that my aerobic/anaerobic capacity over the past couple of months has fallen.
I have lost 10 beats off my resting heart rate and a similar number from my "easy" running pace. Also 10 beats off my max heart rate
So, my resting heart rate is mid 60's (and frankly, I dont mind that at all)
My easy run pace has changed my heart rate from 118-120 to 128-130
My "all out" pace is down from 171 to 160

I decided to start lifting and do some high intensity interval training which is helping improve my blood pressure control (with associated meds, a calcium channel blocker)
So I am not currently focusing on my aerobic capacity but it was how I figured my anaerobic has changed.

This might be too much info but someone reading might make sense of it.
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