rss
6

Sleep Apnea: Causes, Effects, Symptoms, and Treatments From a Sleep Disorder Technician

Just some information for those who have or suspect they have sleep apnea. I am both an EMT and a Senior Sleep Disorder Technician working at several different labs in and around Salt Lake City (one company, many labs), and have spent a long time learning everything I can about sleep apnea first hand.
-
Please let me know if you found this helpful and if you have further questions please ask, I have been helping people better understand this condition face to face for years in our labs, and like trying to teach people how to tell if they might have apnea and why treating it will extend their lives.
-
This is a first draft, and ironically I wrote it in my free time at the lab tonight, so if any major errors or omissions are brought to my attention I will revise them ASAP.

Weight and age are the number one causes of sleep apnea.

As you get older, particularly above 40, the tissues in your throat become looser and therefore more likely to obstruct your airway when you are laying down or asleep. This obstruction is what causes snoring. If severe enough, it periodically stops snoring as the obstruction wins out. This happens most often on an out breath, and can stop someones breathing for around thirty seconds if it is severe enough. See how long you can hold your breath on an out breath, and imagine doing it 60 times per hour every night of your life (I have seen up to 120 times per hour, which is once every thirty seconds, for anywhere to 15-20 seconds each time). I would estimate 5 to 10% of the adults we see for sleep apnea have this level of severity.  This type of apnea is known as obstructive sleep apnea, and is the most common type. The inside of everyones throat is different in size and shape, and it is estimated about 60% of the population in the US has apnea, while around 90% of them don’t know it (those may be old stats, sorry).

The second type of apnea is central apnea, which I don’t plan to go into in much depth in this article because it has different symptoms and treatments, but the diagnosis process for obstructive apnea will also cover central apnea. I will simply say that if you have central apnea you may not snore or be heavy (so don’t swear off a sleep test if you don’t snore or are not overweight!), but you will still feel unrested in the morning. Central apnea is caused by the brain rather than an obstruction, and is most common in those over 60 or those who have incurred head or neck trauma at some point in their life. Though it can be present at any age, we will usually only see it in younger people if they have a mental disability such as autism or down syndrome or cerebral palsy. Other conditions such as multiple sclerosis can greatly increase the likelihood that a person has both central and obstructive apneas.

To return to obstructive apnea, as you gain weight, there is more weight on your chest while you sleep, this means that your lungs have to work harder to take a deep breath, and each time you breath your lungs lift the extra weight on your torso. This is why sleep disordered breathing is usually (but not always) worse when a person is on their back, because the majority of the weight on their torso is right on top of their lungs, making them take shorter breaths (the chest cannot rise as high because of the weight).

23
Liked it
RSSComments: 6  |  Post a Comment  |  Trackback URL
  1. This article is very informative.My mom has gone thru the polysomnography test and we are waiting for the rreports.
    This info has helped me to prepare myself for her.

  2. Her reports hve shown a disturbance in the oxygen level and choking of the cord.The article given above is very informative so please all shd go thru it.It helped me to be prepared for the reports.

  3. Thankyou for the article. I am the Grandmother of a 7 yr old male. He has an unknown genetic syndrome. So we have been told. It is very frustrating to not have any real diagnosis. He is none verbal. Although he did learn his first word “no” this past summer. He has had many many respitory infections beginning at about the age of 14 months, including pnemonia and bronchitis many times. We also have just discovered that he also has allergies. So far we know that he is allergic to dust mites, on a scale from 1 to 5, dust mites are a 5. Dogs are a 3 and 3 different types of grasses also being a 3. More testing for allergies will be done next month. He can not blow out of his mouth, as if blowing out a candle. He can not take in a deep breath, as to breath in and hold your breath. He also can not blow in or out of his nose. This has been so very frustrating. My daughter noticed 2 yrs ago that he stopped breathing during sleep. We took him to the ENT department at Childrens. They did a xray on his throat, it did not show any enlargement of his tonsils or adnoids. The Dr. ordered a sleep study. He has both central and obstructive sllep apnea. Dr. wanted to take out tonsils and adnoids even though the was no enlargement, That was scheduled and then cancelled because of abnormal blood tests. Then after many more ENT visits, with nothing really being done, mainly because Luke is always sick. DR. decided to try a CPAP sleep study. I have enclosed at the bottom the report from that. After waiting many months again and me having to really get into it with him about this issue not being taken care of. He ordered the CPAP for home. He sent us to get Luke set up for the CPAP. That Dr. said that she was uncomfortable giving Luke the CPAP because she feels that Luke did not have enough apneas to be causing his very low oxygen saturation levels, which the ENT Dr. never informed us of. She feels that there might be another reason for his low oxygen saturation, something with his lungs. So, now she is sending us to another clinic that has both an ENT and a Pulmonologist. This is being dragged out way to long. I am very concerned for my grandson. He now is starting to cough all of the time. I would be so grateful to you if you would read the report with the CPAP and give me your opinion. I do not have the report of the first sleep study without the CPAP. Thankyou so much, Robin
    , LUKE
    MRN
    DOB 01/19/2002
    DOS 09/12/2009
    AGE 7 years
    REFERRING PHYSICIAN MD
    DATE OF RECORDING 09/1 212009
    DATE OF FINAL REPORT 09/18/2009
    MEDICATIONS None reported
    PRE-TESTING DIAGNOSIS Obstructive sleep apnea
    BMI 19.3
    COMMENTS: This is a 7 year old male with a history of developmental delay, an unknown genetic disorder, and adenotonsillar hypertrophy in for initial CPAP titration. Het had a PSG in August, 2008 that revealed mild OSA with a central component. He was scheduled for a T\T\A but the surgery was cancelled because of “abnormal blood work” and a CPAP trial was ordered. Of note, the patient has never had desensitization to the CPAP interface, which is important in children. He was very easy to set up, but became quite anxious when the mask was put on. The study began at a CPAP of 4 cm H20 pressure (cwp) with the patient wearing a Petite Comfort Gel nasal mask and chin strap. The humidifier was bypassed because the technician could not control the leak at the humidifier chamber.
    An attended diagnostic polysomnogram with CPAP titration was performed. Frontal, central and occipital EEG, right and left EOG, and chin EMG, were recorded. Additionally, the following parameters were monitored: leg movements (anterior tibialis EMG), snoring (piezo sensor), heart rate with EKG (Lead II), arterial oxygen saturation, respiratory effort pattern by inductance plethysmography (including rib cage, abdominal, sum, and dvt channels), expired ETCO2, nasal airflow (including thermistor and nasal pressure transducer), and body position. The study was performed and scored in accordance with pediatric criteria based on AASM 2007 Manual for Scoring of Sleep and Associated Events. The technical quality of the study was good.
    The record available for analysis displays 483.5 minutes of total recording time, with 456 minutes of sleep time. Sleep Onset occurred in 9 minutes and persistent sleep occurred within 14 minutes, indicating normal sleep latency. Sleep efficiency was normal at 94.3%. Wake after sleep onset was 18.5 minutes. Sleep architecture showed 11.5% stage REM sleep (decreased), 0.9% stage Ni sleep, 36.7% stage N2 sleep, and 50.9% stage N3 sleep (slow wave sleep). The latency to REM Onset was at the lower limits of normal at 76.5 minutes.
    Arousals occurred at an abnormal frequency, with an arousal index of 13.7/hour, and an arousal plus awakening index of 14.3/ hour. Snoring was intermittently present. Paradoxical efforts were not reported.
    Analysis of the respiratory pattern shows that there were 7 central apneas, with a Central Apnea Index of 0.9 per hour. There were 0 mixed apneas, 0 obstructive apneas and 5 obstructive hypopneas. The Obstructive Apnea and HypOpnea index was 0.7 per hour. The Apnea Index was 0.9 per hour, the Hypopnea Index was 0.7 per hour, and the total Apnea-Hypopnea Index (AHI) was 1.6 per hour. Arousals occurred with apnea and hypopnea at a rate of 0.9/hour.
    Arterial oxygen saturation while awake averaged 96%. Apneas and hypopneas were associated with arterial desaturation to as low as 79%. Arterial oxygen saturation ranged from 90 to 98% during NREM sleep, with a mean of 97%. Arterial oxygen saturation ranged from 79 to 98% during REM sleep, with a mean of 96%. Arterial saturation was >89% during 97.6% of sleep time, and ranged from 80 – 89% during 0.1% of sleep time; during the remainder of sleep time the probe did not register saturation due to movement.
    End tidal carbon dioxide level (ETCO2) ranged from 30 to 50 mmHg while awake. During sleep, ETCO2 ranged from 32 to 57 mmHg. Carbon dioxide retention was not observed. The leg movement index was 1.7/hour, and the leg movement-with-arousal index was 0.0/hour. The leg movement index was normal.
    The mean heart rate was 95 beats/minute awake, and 86 beats/minute when asleep. Bradycardia was not observed. The resting respiratory rate was 20 breaths/minute and irregular. Beginning and ending blood pressures were 105/53 and 78/47 mmhg respectively. An increase in blood pressure overnight may reflect sympathetic stimulation due to upper airway obstruction.
    The patient was titrated to 7 cwp. He looked very good except his C02 was steady around 51 mmhg (though high waking C02 values were noted) and his respiratory rate ranged 9 to 20 bpm. The technician ran a trial of BiPAP but the patient had increased snoring and central apneas. The patient was returned to CPAP and the study ended with the patients pressure at 9 cwp. Leak was generally well maintained though not easy to establish (and may be not easy to replicate at home). The petite comfort gel mask was almost too big for the patient and its possible that he may be better fit with a “Mini-Me”. During sleep, some occipital EEG slowing was observed. Despite initiation of CPAP, REM was ioorly maintained.
    CONCLUSION: Successful titration study. Obstructive sleep apnea was well treated with final settings of:
    Mask: Petite Respironics Comfort Gel Nasal Mask WI Chin Strap
    Final Pressure: Cpap 9 Cwp, C-Flex 2
    No Humidity Added To Circuit.
    In addition to the results of this study, the use of other clinical information is recommended to help make decisions regarding therapy, monitoring, and further evaluation.

  4. Thankyou for the article. I am the Grandmother of a 7 yr old male. He has an unknown genetic syndrome. So we have been told. It is very frustrating to not have any real diagnosis. He is none verbal. Although he did learn his first word \”no\” this past summer. He has had many many respitory infections beginning at about the age of 14 months, including pnemonia and bronchitis many times. We also have just discovered that he also has allergies. So far we know that he is allergic to dust mites, on a scale from 1 to 5, dust mites are a 5. Dogs are a 3 and 3 different types of grasses also being a 3. More testing for allergies will be done next month. He can not blow out of his mouth, as if blowing out a candle. He can not take in a deep breath, as to breath in and hold your breath. He also can not blow in or out of his nose. This has been so very frustrating. My daughter noticed 2 yrs ago that he stopped breathing during sleep. We took him to the ENT department at Childrens. They did a xray on his throat, it did not show any enlargement of his tonsils or adnoids. The Dr. ordered a sleep study. He has both central and obstructive sllep apnea. Dr. wanted to take out tonsils and adnoids even though the was no enlargement, That was scheduled and then cancelled because of abnormal blood tests. Then after many more ENT visits, with nothing really being done, mainly because Luke is always sick. DR. decided to try a CPAP sleep study. I have enclosed at the bottom the report from that. After waiting many months again and me having to really get into it with him about this issue not being taken care of. He ordered the CPAP for home. He sent us to get Luke set up for the CPAP. That Dr. said that she was uncomfortable giving Luke the CPAP because she feels that Luke did not have enough apneas to be causing his very low oxygen saturation levels, which the ENT Dr. never informed us of. She feels that there might be another reason for his low oxygen saturation, something with his lungs. So, now she is sending us to another clinic that has both an ENT and a Pulmonologist. This is being dragged out way to long. I am very concerned for my grandson. He now is starting to cough all of the time. I would be so grateful to you if you would read the report with the CPAP and give me your opinion. I do not have the report of the first sleep study without the CPAP. Thankyou so much, Robin
    , LUKE
    MRN
    DOB 01/19/2002
    DOS 09/12/2009
    AGE 7 years
    REFERRING PHYSICIAN MD
    DATE OF RECORDING 09/1 212009
    DATE OF FINAL REPORT 09/18/2009
    MEDICATIONS None reported
    PRE-TESTING DIAGNOSIS Obstructive sleep apnea
    BMI 19.3
    COMMENTS: This is a 7 year old male with a history of developmental delay, an unknown genetic disorder, and adenotonsillar hypertrophy in for initial CPAP titration. Het had a PSG in August, 2008 that revealed mild OSA with a central component. He was scheduled for a T\\T\\A but the surgery was cancelled because of “abnormal blood work” and a CPAP trial was ordered. Of note, the patient has never had desensitization to the CPAP interface, which is important in children. He was very easy to set up, but became quite anxious when the mask was put on. The study began at a CPAP of 4 cm H20 pressure (cwp) with the patient wearing a Petite Comfort Gel nasal mask and chin strap. The humidifier was bypassed because the technician could not control the leak at the humidifier chamber.
    An attended diagnostic polysomnogram with CPAP titration was performed. Frontal, central and occipital EEG, right and left EOG, and chin EMG, were recorded. Additionally, the following parameters were monitored: leg movements (anterior tibialis EMG), snoring (piezo sensor), heart rate with EKG (Lead II), arterial oxygen saturation, respiratory effort pattern by inductance plethysmography (including rib cage, abdominal, sum, and dvt channels), expired ETCO2, nasal airflow (including thermistor and nasal pressure transducer), and body position. The study was performed and scored in accordance with pediatric criteria based on AASM 2007 Manual for Scoring of Sleep and Associated Events. The technical quality of the study was good.
    The record available for analysis displays 483.5 minutes of total recording time, with 456 minutes of sleep time. Sleep Onset occurred in 9 minutes and persistent sleep occurred within 14 minutes, indicating normal sleep latency. Sleep efficiency was normal at 94.3%. Wake after sleep onset was 18.5 minutes. Sleep architecture showed 11.5% stage REM sleep (decreased), 0.9% stage Ni sleep, 36.7% stage N2 sleep, and 50.9% stage N3 sleep (slow wave sleep). The latency to REM Onset was at the lower limits of normal at 76.5 minutes.
    Arousals occurred at an abnormal frequency, with an arousal index of 13.7/hour, and an arousal plus awakening index of 14.3/ hour. Snoring was intermittently present. Paradoxical efforts were not reported.
    Analysis of the respiratory pattern shows that there were 7 central apneas, with a Central Apnea Index of 0.9 per hour. There were 0 mixed apneas, 0 obstructive apneas and 5 obstructive hypopneas. The Obstructive Apnea and HypOpnea index was 0.7 per hour. The Apnea Index was 0.9 per hour, the Hypopnea Index was 0.7 per hour, and the total Apnea-Hypopnea Index (AHI) was 1.6 per hour. Arousals occurred with apnea and hypopnea at a rate of 0.9/hour.
    Arterial oxygen saturation while awake averaged 96%. Apneas and hypopneas were associated with arterial desaturation to as low as 79%. Arterial oxygen saturation ranged from 90 to 98% during NREM sleep, with a mean of 97%. Arterial oxygen saturation ranged from 79 to 98% during REM sleep, with a mean of 96%. Arterial saturation was >89% during 97.6% of sleep time, and ranged from 80 – 89% during 0.1% of sleep time; during the remainder of sleep time the probe did not register saturation due to movement.
    End tidal carbon dioxide level (ETCO2) ranged from 30 to 50 mmHg while awake. During sleep, ETCO2 ranged from 32 to 57 mmHg. Carbon dioxide retention was not observed. The leg movement index was 1.7/hour, and the leg movement-with-arousal index was 0.0/hour. The leg movement index was normal.
    The mean heart rate was 95 beats/minute awake, and 86 beats/minute when asleep. Bradycardia was not observed. The resting respiratory rate was 20 breaths/minute and irregular. Beginning and ending blood pressures were 105/53 and 78/47 mmhg respectively. An increase in blood pressure overnight may reflect sympathetic stimulation due to upper airway obstruction.
    The patient was titrated to 7 cwp. He looked very good except his C02 was steady around 51 mmhg (though high waking C02 values were noted) and his respiratory rate ranged 9 to 20 bpm. The technician ran a trial of BiPAP but the patient had increased snoring and central apneas. The patient was returned to CPAP and the study ended with the patients pressure at 9 cwp. Leak was generally well maintained though not easy to establish (and may be not easy to replicate at home). The petite comfort gel mask was almost too big for the patient and its possible that he may be better fit with a “Mini-Me”. During sleep, some occipital EEG slowing was observed. Despite initiation of CPAP, REM was ioorly maintained.
    CONCLUSION: Successful titration study. Obstructive sleep apnea was well treated with final settings of:
    Mask: Petite Respironics Comfort Gel Nasal Mask WI Chin Strap
    Final Pressure: Cpap 9 Cwp, C-Flex 2
    No Humidity Added To Circuit.
    In addition to the results of this study, the use of other clinical information is recommended to help make decisions regarding therapy, monitoring, and further evaluation.

  5. Also I forgot to say that the Dr. that we went to to get Luke set uo for the CPAP feels that he might need oxygen instead of the CPAP. That is my concern . Also in your article you do not recommend it. Thankyou, Robin

  6. Robin- I’m sorry it has taken me so long to respond. I just noticed that you had commented. It seems to me that these results indicate that a CPAP might benefit your grandson, but I would definitely take a doctor’s advice over my own. Much of his report is normal, but what is odd is that he has a very low number of apneas per hour, yet a very large oxygen decrease per apnea. What this means is that he is having an average of 1 apnea per hour, but when it happens he is dropping very low. Oxygen might correct this, but for a child so young it is not recommended. You really have a tough situation, but if you can find a sleep clinic rather than an ENT, you’re bound to get more specialized results. Kids with genetic disorders are all different, but usually as they get older they need actual CPAP rather than oxygen. Also, think about the developing lungs of a 7 year old- if your lungs get all the air they need when barely breathing, they have no reason to try breathing deeply and the muscles of the diaphragm may not be growing properly. I’m no expert on oxygen in children, but I have seen kids who have been on o2 since they were young and they’re rarely in a good situation. Again, sorry it took me so long, I would recommend a specialist for pediatrics and sleep. Unfortunately, such specialists are often few and far between. I know there is a lab in Salt Lake that is called Utah Sleep and Pulmonary Specialists, and they’re really good, but that might not be an option for your grandson…

    Good luck!
    Kris

RSSPost a Comment
comments powered by Disqus
-->