Difference between revisions of "Justifying Advanced PAP Machines"

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Justifying ASV

ASV or Adaptive servo-ventilation (ASV)

Central Sleep Apnea (CSA) is the cessation of respiratory effort result in a lack of respiratory movements. During sleep, your breathing is disrupted regularly because of how your brain functions, your brain simply doesn't tell your body to breathe, and therefore you don't try to breathe.

Apnea: 80% to 100% reduction in airflow for >= 10 seconds Hypopnea: 50% to 80% reduction in airflow for >= 10 seconds Flow Limitation: <50% reduction in airflow for >= 10 seconds

Five types of Central Sleep Apnea

per the Mayo Clinic Central sleep apnea occurs when your brain fails to transmit signals to your breathing muscles. Central sleep apnea can be caused by a number of conditions that affect the ability of your brainstem — which links your brain to your spinal cord and controls many functions such as heart rate and breathing — to control your breathing. The cause varies with the type of central sleep apnea you have.

Types include:

• Cheyne-Stokes breathing. This type of central sleep apnea is most commonly associated with congestive heart failure or stroke. This condition is characterized by a gradual increase and then decrease in breathing effort and airflow. During the weakest breathing effort, a total lack of airflow (central sleep apnea) can occur.
• Drug-induced apnea. Taking certain medications such as opioids — including morphine sulfate (Ms Contin, others), oxycodone (Oxycodone HCL, Oxycontin, others) or codeine sulfate — may cause your breathing to become irregular, to increase and decrease in a regular pattern, or to temporarily stop completely.
• High-altitude periodic breathing. A Cheyne-Stokes breathing pattern may occur if you're exposed to a very high altitude. The change in oxygen at this altitude is the reason for the alternating rapid breathing (hyperventilation) and underbreathing.
• Complex sleep apnea. Some people with obstructive sleep apnea develop central sleep apnea while using continuous positive airway pressure (CPAP) for their sleep apnea treatment. This condition is known as complex sleep apnea because it's a combination of obstructive and central sleep apneas.
• Medical condition-induced central sleep apnea. Several medical conditions may give rise to central sleep apnea of the non-Cheyne-Stokes variety.
• Idiopathic (primary) central sleep apnea. The cause of this uncommon type of central sleep apnea isn't known.

Diagnosis of Central Apnea

1. Must have clinical symptoms to make the diagnosis - Sleepiness, insomnia, snoring, apneas, awakening with Shortness of Breath, A‐fib, CHF, or neurological disorder (such as stroke, MS)
2. Central AHI >5
3. Central apneas and Central hypopneas >50% of total AHI
4. Not better explained by another sleep disorder

Hypopneas - Obstructive and Central

To determine the statistics for Central apneas and Central hypopneas >50% of total AHI above we need to determine which hypopneas are central in nature. The description below defines the difference between obstructive and central hypopneas.

An obstructive hypopnea contains one or more of the following:

1. An increase in PAP flow signal
2. Snoring during the event
3. Paradoxical breathing

A central hypopnea will have none of the above.

Central Hypopnea. Central hypopneas are associated with reductions of purely in-phase thoracic and abdominal effort or movement signals, followed by an increase in chest and belly movements at the end. There is no evidence of phase shifting or paradoxical breathing, no airflow flattening, and no snoring throughout the entire central hypopnea.

A Central AHI is composed of Central Apnea and Central Hypopnea. The Central Apnea numbers are easily extracted from modern PAP machines which report detailed efficacy data. We need to concentrate on Central Hypopnea numbers to demonstrate a Central AHI >5 and that Central apneas and Central hypopneas >50% of total AHI

Central Hypopnea. Central hypopneas are associated with reductions of purely in-phase thoracic and abdominal effort or movement signals, followed by an increase in chest and belly movements at the end. There is no evidence of phase shifting or paradoxical breathing, no airflow flattening, and no snoring throughout the entire central hypopnea.

Paradoxical Breathing explanation: The chest and abdomen should expand when they inhale and contract when they exhale. If the chest and abdomen contract while inhaling and expand while breathing out, a person may have paradoxical breathing.

Charts identifying Central Hypopneas

Failed Sleep Studies

Demonstrations of significant Central Apneas at Trial pressures

Although the conclusion of your study is severe obstructive apnea, your diagnostic study before PAP shows predominately central apnea, but enough OA that this would lead to a likely diagnosis of complex or mixed apnea in the severe range. Central events were more numerous and longer in duration than obstructive, with an event actually going more than 1-1/2 minutes. Bet you couldn't hold your breath that long if your were awake! Your BiPAP titration did reduce OA and helped significantly with your sleep architecture and some of the effects of apnea such as snoring; however, the report concedes you continue to have CA. The CA "improved" with final pressure but was not resolved.

A glance at the charts on page 4 shows that at the beginning of the night you had predominately OA events. You seemed to do pretty good at CPAP pressure of 11/11 for about 15 minutes during N2 sleep. They moved you to 16/12 bipap during a wake period that transitioned to N2 sleep. They then dropped pressure to 10/6 and you immediately had abundant CA, which transitioned to OA and back to CA as bipap pressure increased. A 15 minute period at 14/9 just after 1:00 had no apnea, but you were recorded as awake. Pressure increased to 15/10 then 19/14 with a brief drop-out of events. It appears that this period may be the basis of your titrated BiPAP pressure.

My impression is that you are headed for ASV (hopefully soon). This titration shows you were not successfully treated at any of the pressures attempted, and no trial lasted longer than 15 minutes. Your BiPAP titration is the best compromise found, with none being in a range that would be considered effective. Your results since the titration demonstrate that you will not succeed at bilevel without a backup to treat centrals, and your treated complex apnea remains in the high moderate to severe range. The titration study tells me, that there is not an effective pressure range any of us can recommend to you that will result in an acceptable AHI for any long-term.

I'm sorry to say, there is nothing I can suggest to improve your results other than you need to be sure your doctor is aware that you continue to have severe mixed sleep apnea, with many central and obstructive events, and for you to push to obtain ASV at the earliest possible time.

Sleep Study on BiPAP determined events rated according to the machine data remains very high with mixed events. The machine data suggest the results are much worse than the untreated AHI. You should tell them you have looked at the results of the tests and don't really see how it was determined (1) that you have obstructive apnea, and (2), how it was determined that you had a "good response" to bipap pressure of 15/10. At 1:15 at 14/9 and 15/10 shows central abundant apnea (approximately 30 AHI to numerous to count). At 1:45 to 2:15 15/10 was tried for 30 minutes with 11 apnea (AHI 22) with the longest apnea of the night at 2:00 at 15/10. A final period of 15/10 was tried at about 4:30, lasting about 15 minutes (deducting for wake) with 2 OA events (AHI 8) No sustained period of efficacy (ahi<5) was found. Your ongoing machine data confirm any efficacy found during the titration study may have been coincidental or an anomaly. You should flatly say in your opinion BiPAP at the prescribed pressures is not working, and explain any symptoms you feel (fatigue, frequent awakenings, whatever).

CSA-and-ASV-Updated-Morgan.pdf

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