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  Does long term humidifier use affect lungs?
Posted by: Russatrice - Yesterday 10:31 PM - Replies (4)

I haven't slept well recently so maybe I'm over thinking things in the middle of the night, but my question is, does the nightly practice of having humid air pumped into the lungs for several hours at a time cause any health problems after long term use? Thinking of being more prone to bronchitis or pneumonia, maybe?
My humidifier is set to 3, btw, so average humidity plus slightly heated tube, but I might want to up that to 4 as the air gets drier with the winter heating.

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  TOO MUCH PRESSURE
Posted by: markhy - Yesterday 07:44 PM - Replies (12)

Can not adjust the air pressure ....

Checked and reset settings

Deleted card data

Ramp set at 20 mins -pressure still blasts out when turned on

ResMed S9 autoset

HELP !!!

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  Newbie - need advice on settings and machine
Posted by: tmc712 - Yesterday 01:43 PM - Replies (11)

Hi,

I'm hoping someone can steer me in the right direction here. I was recently diagnosed with severe OSA and got an ResMed AirSense 10 AutoSet on September 27. I've been using it consistently since then. At first, I was getting horrible AHI numbers, in the teens or even 20s. (My sleep test AHI was 32.)

After several mask changes, and having my DME rep change my settings a couple times, I seem to have *somewhat* adapted and according to SleepyHead, my AHI over the last 53 days has ranged from 2.11 to 8.81 (average was 5.06). My pressure range is 4-16, and I have EPR set to 3. The max pressure each night is almost always is less than 13, usually somewhere in the 10-12 range.

I'm feeling better than I was about a month ago, but honestly I don't really feel any better than before I got my machine. I rarely sleep through the night without waking at least once. It's quite possible there are non-apnea related things going on with me - I tend to be a very anxious person and I'm a light sleeper. However, I'd like to see if there are any changes to my settings I can try to see if some of my insomnia is apnea-related.

I should also mention that my DME rep noticed shortly after I got my machine that I was having a lot of central apneas, so he recommended a BiPAP titration study. (My original study was a home study, and my original diagnosis was just obstructive, not complex/central.) I went to the lab in early November and honestly had the worst night of sleep I've had in a very long time. The inhalation time was set to about 2.5 to 3 seconds, and when I'm trying to fall asleep, I tend to take long deep breaths to calm myself. Basically the machine kept cutting off my inhalations and I started to panic. Somehow I eventually fell asleep for a few hours, and my AHI during that time was 6.1. They concluded that I needed a BiPAP setting of 8/4 and I should get an ST machine.

I haven't been contacted by my DME about getting this machine yet, which is good because I'm really hesitant to go through with it, mainly because with my current machine I usually get better numbers, fall asleep more easily, and feel better in the morning (but still not great). And my centrals, while not zero, seem to be decreasing in general.

So, to sum up, I have three questions:

(1) If you were me, would you get the ST machine, or hold off on that?

(2) Are there any settings changes that you'd recommend on my current machine that might help improve my sleep quality? I think I'm finally brave enough to change the settings myself with the DME's "approval."

(3) Any thoughts on whether the "for her" algorithm might work better for me? (Not that I have access to it on my current machine, but I've been wondering about it.)

I'd be happy to post data. Just let me know what would be helpful. I've already gotten a lot of help just reading though others' questions and posts.

Thank you!

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  New to this - I'm not getting enough air
Posted by: Alan Adler - 12-03-2016 11:26 PM - Replies (16)


Hello board. I am new to this. But I'm technical, an engineer with many patents. I have been diagnosed with RLS (Restless Leg Syndrome) which wakes me up with painful arms and legs after as little as 10 minutes sleep. I have developed a hypothesis that this condition is due to oxygen deprivation and my hypothesis has been endorsed by leading physicians in this field.

I've found that if I drowse, partially awake, I do not develop the pain. So, despite my not having apnea, I decided to try CPAP. I purchased a DSX500 DreamStation Auto CPAP and 3 nasal masks (DreamWear, Nuance Pro, Wisp).

The DreamWear was uncomfortably tight and is not adjustable. It gave me a sore nose in 2 hours. During that time pressure went very slowly from 4 to 11 (ramp was not activated). It wasn't until pressure reached about 10 that I felt I was getting enough air.

Next I tried Nuance Pro mask. It's very comfortable. But pressure only rose from 4 to 6, then drifted back down to 4.1 over a one hour session. At no time did I feel I was getting sufficient air.

I am a patient of the Kaiser Permanente system, so I will soon consult with a provider. But I'll bet some of you members know more than providers. So I've joined here, seeking your expertise.

I've already learned from this board how to access the provider menu, so I can program the machine to start higher. But prior to that I'd like to learn more.

Thank you for your help and suggestions
.

Alan

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  sensitive teeth tooth ache
Posted by: alfiepops - 12-03-2016 09:43 PM - Replies (6)

Is anyone else experiencing tooth ache due to their cpap machine sometimes all my teeth ache when I wake up or start to very soon after waking its driving me mad all my teeth aching at once.....[/size][/font]

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  2015 peer reviewed article comparing a bench test of 11 APAPs
Posted by: robysue - 12-03-2016 07:47 PM - Replies (2)

All APAPs Are Not Equivalent for the Treatment of Sleep Disordered Breathing: A Bench Evaluation of Eleven Commercially Available Devices by Kaixian Zhu, MS,1,2,3 Gabriel Roisman, MD, PhD,2 Sami Aouf, MD,1 and Pierre Escourrou, MD, PhD2 published at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4481055/

The article describes a bench test of 11 commercially available APAPs, including the F&P Icon+ APAP, PR System 1 Auto CPAP and the Resmed S9 AutoSet. In the article, each of the eleven tested APAPs is given a code name. Throughout the article:

    D6 = F&P Icon+ Auto
    D7 = PR System 1 Auto
    D8 = Resmed S9 AutoSet
The Auto algorithms for the Resmed AirSense 10 AutoSet and PR Dreamstation Auto CPAP are similiar enough to the algorithms used for the S9 and System One respectively that this article is still of some use in comparing and contrasting how these three APAPs behave.

Contents of the article are included below, but without the large number of images and tables, it will be hard to understand what the paper is talking about. Use the link to read the article and look at the figures.


***************Article Contents******************
Abstract
Study Objectives:

This study challenged on a bench-test the efficacy of auto-titrating positive airway pressure (APAP) devices for obstructive sleep disordered breathing treatment and evaluated the accuracy of the device reports.

Methods:

Our bench consisted of an active lung simulator and a Starling resistor. Eleven commercially available APAP devices were evaluated on their reactions to single-type SDB sequences (obstructive apnea and hypopnea, central apnea, and snoring), and to a long general breathing scenario (5.75 h) simulating various SDB during four sleep cycles and to a short scenario (95 min) simulating one sleep cycle.

Results:

In the single-type sequence of 30-minute repetitive obstructive apneas, only 5 devices normalized the airflow (> 70% of baseline breathing amplitude). Similarly, normalized breathing was recorded with 8 devices only for a 20-min obstructive hypopnea sequence. Five devices increased the pressure in response to snoring. Only 4 devices maintained a constant minimum pressure when subjected to repeated central apneas with an open upper airway. In the long general breathing scenario, the pressure responses and the treatment efficacy differed among devices: only 5 devices obtained a residual obstructive AHI < 5/h. During the short general breathing scenario, only 2 devices reached the same treatment efficacy (p < 0.001), and 3 devices underestimated the AHI by > 10% (p < 0.001). The long scenario led to more consistent device reports.

Conclusion:

Large differences between APAP devices in the treatment efficacy and the accuracy of report were evidenced in the current study.

Citation:

Zhu K, Roisman G, Aouf S, Escourrou P. All APAPs are not equivalent for the treatment of sleep disordered breathing: a bench evaluation of eleven commercially available devices. J Clin Sleep Med 2015;11(7):725–734.

Keywords: auto-titrating continuous positive airway pressure, obstructive sleep apnea, bench test, central sleep apnea, device report
Obstructive sleep apnea syndrome is caused by repetitive closure of the upper airway during sleep that leads to episodes of arterial oxygen desaturation and interrupted sleep. Continuous positive airway pressure (CPAP) delivered via a nasal mask is an effective treatment for obstructive sleep apnea (OSA).1 It is the reference treatment for patients with moderate-to-severe OSA2,3 and has been shown to improve nocturnal and diurnal symptoms of OSA, objective and subjective measures of daytime somnolence, quality of life, and also been demonstrated to reduce driving accidents.4–6 When hypertension coexists with OSA, CPAP may reduce blood pressure.7 As with many therapies for chronic conditions, compliance is a major issue. It ranges in the literature from 20% to 83%.8–12

As opening airway pressure may vary during the night with position, sleep stage, drug or alcohol use, attempts to improve compliance and treatment efficacy have included the use of auto-titrating CPAP (APAP). These devices are designed to vary and achieve the necessary pressure to maintain airway patency throughout the sleep. Their mechanism of action proposes that the reduction in mean pressure minimizes side effects of CPAP, improving tolerance and increasing associated usage.13

BRIEF SUMMARY

Current Knowledge/Study Rationale: Auto-titrating positive airway pressure devices are designed to adjust the therapeutic pressure to maintain the upper airway patency and treat the obstructive sleep disordered breathing. The efficacy of treatment is questioned and clinical evaluations are curtailed by the variability of disease in patients.

Study Impact: All APAPs performed differently when subjected to simulated sleep disordered breathing patterns on a bench-test. Large differences exist in the treatment efficacy and accuracy of the device report data between APAP devices.

But studies to date have not identified a statistically significant difference between APAP and fixed CPAP devices in compliance or in Epworth Sleepiness scores.14 Patruno et al.15 favored fixed pressure over APAP for reducing cardiovascular risk, although data on blood pressure outcomes were limited.

The clinical efficacy of APAP has also been questioned by some studies showing a large residual apnea-hypopnea index (AHI) with some devices.16 Reports of residual events obtained by the devices have also been questioned by some authors.17–22 Moreover, FDA approval for introducing a new APAP device to the market does not guarantee its effectiveness and safety, as manufacturers may gain entry to the market by “510(k) premarket notification,” which relies on a “substantial equivalence” to an existing device, or by demonstrating safety and effectiveness with limited clinical studies.23 Since clinical studies are curtailed by the variability between patients and study conditions, an overall picture of their results is not clear. Bench studies are advantageous over clinical ones as they allow evaluating devices in standardized and quite reproducible conditions.24,25

As many APAP devices are now released on the market, we wished to evaluate their functioning and the validity of their reports that are often used by physicians as measures of efficacy. Eleven devices were evaluated on a new bench using patient-simulated events and disease scenarios close to the actual observations in patients.

Go to:
METHODS
Materials

The bench model is mainly composed of an active lung simulator ASL5000 (IngMar Medical, Pittsburgh, USA) and a Starling resistor (Figure 1).25,26 It is able to reproduce normal and disordered breathing patterns, e.g., obstructive and central apneas and hypopneas.

Figure 1
Figure 1
Principle of the bench model.
The Starling resistor within a cylindrical transparent chamber (180 mm long, 28 mm internal diameter) consisted of a compliant rubber tube (120 mm long between two 15-mm external diameter connectors at each side of the cylinder). The chamber was connected to a pressure control system (MFCS-4C-70 and MFCS-NEG-4C-70, Fluigent, Villejuif, France), which supplied continuous positive and negative pressures around the tube inside the chamber (Pch). The Pch regulated the opening state of the rubber tube that represented the pharynx, and this pressure was monitored by a manometer (MECOSMARTD-06, Mesureur, Chilly-Mazarin, France). The upper airway obstruction and snoring were triggered and synchronized to the breathing via a transistor-transistor logic (TTL) signal sent by the ASL5000 at the beginning of breathing cycles, in order to mimic the pathophysiology of OSA. During obstructive apneas, the critical closing pressure and the full opening pressure measured at the mask were 6 and 11 cm H2O, respectively.

The APAP device was connected to a calibrated leak port (24 L/min at 10 cm H2O) built in the patient circuit,25,26 which presented a standardized intentional leak at the mask.27 A linear pneumotachograph (series 4700A, Hans Rudolph, Shawnee, USA) was connected downstream to the leak port. The mask pressure and airflow were measured by PA-1 flow instrumentation (series 1110A, Hans Rudolph). A wireless speaker (UE984-000298, Logitech) was placed in a hermetic chamber connected to the mask to generate snoring.

All data were transferred to a PC via a NI USB-6210 card (National Instruments, Austin, USA), and a LabView (National Instruments) program was developed for data acquisition and instrument control. All the recorded signals were sampled at 20 Hz for further analysis.

Bench Model Principles

The breathing flow patterns resulted from the interactions of the ASL5000 with the Starling resistor.26 The following settings were applied to the lung model: uncompensated residual capacity = 0.5 L, compliance = 80 mL/cm H2O, resistance = 5 cm H2O/L/s, and inspiratory flow amplitude of normal breathing = 20 L/min. To maintain the inspiratory efforts during obstructive sleep disordered breathing (SDB) events, the ASL5000 was switched to flow pump mode and produced normal breathing flow. The lung was set as passive during central apneas (central apneas in this paper refer to the ones without cardiac oscillation if not specified). All central apneas occurred with an open upper airway. For obstructive apnea, the pressure inside the chamber of the Starling resistor (Pch) was set at 9 cm H2O. By modifying the settings of the lung simulator and the Pch, different waveforms of airflow could be achieved (Figure 2). All the SDB patterns were produced at 4 cm H2O airway pressure as minimal default value of APAP devices. For normal breathing and central apneas, the Pch was −8 cm H2O and the upper airway was fully opened.

Figure 2
Figure 2
Airflow waveforms of the obstructive hypopnea.
The snoring sound was extracted from a patient sleep recording. The high-frequency elements were filtered out and its peak power was at 46 Hz.

The presence of cardiac oscillations on the airflow may be considered as an indicator of open upper airway in central apneas and may be used in some APAP algorithms.28 The cardiac oscillations were simulated by the active lung as 1-Hz sinusoidal airflow of 2 L/min (10% of baseline amplitude).

The opening of the upper airway at the resumption breathing after the obstructive apneas might result in a so-called “obstructive pressure peak” at mask.29 To produce this signal, the upper airway was opened with a 0.5-sec delay with regard to the TTL signal, i.e., the flow pump started breathing prior to the opening of the upper airway.

Devices under Study

Eleven APAP devices were included in the study: iCH Auto (Apex, New Taipei City, Taiwan), RESmart Auto (BMC, Beijing, China), iSleep20i (Breas, Mölnlycke, Sweden), Floton Auto (Curative, Beijing, China), SleepCube Auto (Devilbiss, Somerset, USA), ICON+ (Fisher & Paykel, Auckland, New Zealand), PR1 Remstar Auto P-Flex (Philips Respironics, Murrysville, USA), S9 AutoSet (Resmed, Sydney, Australia), DreamStar Auto (Sefam, Viller-lès-Nancy, France), Transcend Auto (Somnetics, New Brighton, USA), and SOMNOBalance-e (Weinmann, Hamburg, Germany). These devices were numbered from D1 to D11. Treatment reports were extracted through the corresponding software of each device.

The minimum and maximum pressures of the devices were set at 4 and 20 cm H2O, respectively. Pressure ramp and comfort mode were disabled.

Test Protocols

Single-Type SDB Event Sequences

Five flow sequences of single-type SDB events were developed. Brief descriptions of these sequences are summarized in Table 1. Illustrations of these sequences are shown in Figures 2​2–4.

Table 1
Table 1
Sequence of single-type SDB events.
Figure 3
Figure 3
Illustration of single-type SDB event sequences and results: obstructive apnea (left column) and hypopnea (right column).
Figure 4
Figure 4
Illustration of single-type SDB event sequences and results: snoring (left column) and central apnea without cardiac oscillations (right column).
General Scenarios

In addition to repetitive single-type SDB events, we developed 2 breathing scenarios, which included a distribution of mixed SDB events to simulate clinical and complex conditions (Figure 5). The long scenario lasted 5.75 h, including a 6-min normal breathing session, which corresponded to awake state of patient, and 4 complete sleep cycles each lasting about 1.4 h. The breathing rate and the frequency of SDB events were adapted to the sleep stages as observed in sleep disorders. The duration of the events also varied. For example, the first sleep cycle consisted of a 4-min “N1 sleep stage” at 12 bpm breathing rate with few events, a 60-min “N2+N3 sleep stages” at 12 bpm with numerous events of all types including central apneas, and a 20-min “REM sleep stage” with variable breathing rate (Figure 5A). Most SDB events were set up in the N2+N3 stages. A 10-min normal breathing session was placed at the end of N2+N3 part in order to verify if the absence of SDB events could prompt a gradual decrease in pressure. The 20-min REM sleep was composed of 4 alternated 5-min sessions of “phasic” and “tonic” REM, where the breathing rate varied from 10 to 15 bpm in “phasic” REM and remained steady at 12 bpm in “tonic” REM with predominantly obstructive SDB events. For the entire scenario, the total AHI set on the bench was 51.4/h, of which 75% of events were obstructive (obstructive AHI = 38.6/h) and 25% were central. Of note, snoring, “obstructive pressure peak” signals, and cardiac oscillations were not simulated in this scenario. For the first sleep cycle part in the general scenario (the first 95-min session), the total AHI was equal to 44.8/h, of which 73% of events were obstructive (obstructive AHI = 32.8/h). The short scenario lasted 95 min, which corresponded to the first sleep cycle of the long scenario.

Figure 5
Figure 5
Illustration of the general scenarios and results.
Methodology

For reproducibility, tests of single-type SDB events and of the long scenario were repeated twice. A third test was executed if the coefficient of variation of the first 2 tests was > 10%. Tests of the short scenario were repeated 3 times for each device. For each sequence or scenario, a baseline reference test was completed with a fixed CPAP = 4 cm H2O.

Data Analysis

For the obstructive apnea and hypopnea sequences, mask pressure (Pm) and airflow-derived peak-to-peak flow amplitude (ΔV', derived by calculating the upper and lower envelops of the flow curve) were recorded and calculated. Pm curves were uniquely presented for the snoring and central apnea sequences. Regarding the general scenarios, the mean/median pressure and P90/95 were calculated from the Pm. Residual AHI was scored by analyzing the flow curve. Precisely, the residual events were scored by considering both the amplitude reduction and the corresponding duration, i.e., ΔV' ≤ 10% of normal baseline: apnea; 10% < ΔV' ≤ 70%: hypopnea, with a duration ≥ 10 seconds.26,30 All the analyses mentioned above were performed with MATLAB (MathWorks Inc., Natick, USA).

The differences in treatment efficacy (residual AHI) and in therapy pressure between devices and between bench-assessed and device-reported data were investigated by repeated measures analysis of variance (rANOVA) with these 2 factors. Further rANOVA was conducted for each device to compare the bench-assessed and device-reported AHI if the global difference was found significant (Medcalc Software, Mariakerke, Belgium).

For an overview, each device was scored based on its treatment efficacy and accuracy of device-reported residual AHI. Also, devices were classified according to specific clinical profile, such as treatment of snoring, apneas of obstructive and central mechanisms. The following results were normalized and chosen as criteria: (1) the percentage of normalized obstructive events for the long general scenario (denoted as treatment efficacy, normalized as TE = 1 − residual obstructive AHI / 38.6); (2) the consistency in residual AHI between bench and device (denoted as scoring accuracy, normalized as = 1 − |Δ Residual total AHI|, in which Δ Residual total AHI = (AHI report − AHI bench) / AHI bench × 100%); (3) reactions to snoring, and (4) reactions to central apneas (graded as Yes or No).

Go to:
RESULTS
Single-Type SDB Event Sequences

Obstructive Apnea Sequence

According to the resultant flow, in percentage of the normal baseline amplitude, at the end of the sequence, the devices fell into 3 categories: (A) resultant flow > 70%: D3, D6, D7, D8, and D10—especially D3 and D8—fully normalized the breathing flow; (B) 10% < resultant flow ≤ 70%, i.e., hypopneas still remained: D1, D2, D4, and D9; © resultant flow ≤ 10%: D5 and D11 (Figure 3).

The time to reach the maximum pressure varied from device to device. In category A, D8 reached the maximum pressure most rapidly, at 14.8 min, i.e., before the middle of the sequence, D10 increased its pressure most slowly and the airflow was normalized only at the end of the sequence. D3 reached the highest pressure (13.5 cm H2O) among all the devices. Two devices in category C did not change their pressure during the entire tests (D5 and D11). Of note, D11 performed differently when the “obstructive pressure peak” signal was presented: the ΔV' was enhanced to 70.2% and its pressure reached at 11.4 cm H2O with a delay of 20.1 minutes (Figure 3).

Obstructive Hypopnea Sequence

Similarly to the obstructive apnea test, the devices fell into 2 categories according to the resultant flow at the end of the 20-min sequence: (A) resultant flow > 70%: D1, D2, D3, D5, D6, D7, D8, and D11—of which D3 and D11 fully normalized the breathing flow; (B) resultant flow ≤ 70%: D4, D9, and D10, of which D4 did not change its pressure during the tests (Figure 3). In category A, D2, D6, D8, and D9 reached the maximum pressure before the middle of the sequence; of these, D8 increased its pressure most rapidly. D3 recorded the highest pressure (12.6 cm H2O) among the devices.

Snoring Sequence

Devices were divided into 2 categories according to the pressure change when snoring was presented. (A) D2, D5, D7, D8, and D11 increased the pressure; (B) D1, D3, D4, D6, D9, and D10 kept their pressure at the initial value (Figure 4).

Central Apnea Sequence with/without Cardiac Oscillations

Devices fell into 2 categories according to the pressure change during central apneas: (A) D5, D7, D8, and D11 kept the same EPAP during the test; (B) D1, D2, D3, D4, D6, D9, and D10 increased their pressure. In category B, D1, D4, and D6 limited their maximum pressures around 10 cm H2O. The Pm curves are shown on Figure 4.

For central apneas with cardiac oscillations, all the devices reacted in the same way as for the central apneas without cardiac oscillation.

General Scenarios

All devices decreased their pressure after a 10-min normal breathing session in the first sleep cycle except D3 (Figure 5B). D9 decreased its pressure most rapidly by 4.8 cm H2O during the 10-min normal breathing session (Figure 5B).

In the long scenario, bench-measured mean/median treatment pressures and P90/95 differed between devices (p < 0.001, Figure 6A, ​A,66B). D1, D3, D4, and D10 had a mean treatment pressure > 10 cm H2O (Figure 6A). D10 showed the highest P90 = 19.5 cm H2O (Figure 6B). The residual obstructive AHI on the bench that revealed the efficacy of treatment also differed significantly between devices (p < 0.001): D1, D3, D4, D6, and D10 obtained a residual obstructive AHI < 5/h, among which D3 totally eliminated the obstructive SDB events (Figure 6C). The Pm and flow curves are shown in Figure 5. For all devices, the differences between bench-assessed and device-reported AHI and pressure data were not significant.

Figure 6
Figure 6
Comparison between bench-measured and device-reported results of the long general scenario.
In the short scenario, significant differences were found in mean/median pressure and in P90/95 (p < 0.001 for each). D3 and D6 had a mean pressure > 10 cm H2O. Device-reported mean/median pressure data were different from measured pressure (p < 0.001). D1 overestimated the mean therapy pressure by > 10% (p = 0.01). Residual obstructive AHI differed between devices (p < 0.001, Table 2): only D3 and D6 obtained a residual obstructive AHI < 5/h. For D3, the residual obstructive AHI = 0 (Table 2). Device-reported AHI were different to bench-assessed ones (p < 0.001). D1, D8, and D10 underestimated the AHI by 39%, 23%, and 11%, respectively (p < 0.05 for each).

Table 2
Table 2
Bench-assessed and device-reported AHI in short general scenario.
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DISCUSSION
This study is the most extensive evaluation of APAP devices to date using a new closed-loop respiratory bench model taking into account not only the mechanical properties of human upper airway, but also the lung characteristics, such as compliance and resistance. With this bench test, eleven currently marketed APAP devices were challenged by three different protocols: short sequences of constant repetitive single-type SDB events, as well as by two general breathing scenarios including a variety of events to approach actual clinical conditions. The devices were investigated on both the performance and on the accuracy of the device reports. The main findings were as follows: (1) most devices responded to simulated obstructive apneas (except D5 and D11) and obstructive hypopneas (except D4), but their reaction time and their treatment efficacy considerably differed. D11 only responded to the obstructive apneas when “obstructive pressure peak” signals were added; (2) 5 devices raised the pressure when subjected to the snoring sound (D2, D5, D7, D8, D11); (3) when central apneas were simulated, only 4 devices did not rise the pressure (D5, D7, D8, D11); (4) For the long scenario, efficacy varied between devices: only 5 devices obtained a residual obstructive AHI < 5/h (D1, D3, D4, D6, D10); (5) For the short scenario, significant differences were found in therapy pressure and in efficacy between devices and between bench-assessed and device-reported data: only 2 devices obtained a residual obstructive AHI < 5/h (D3, D6) whereas 3 devices underestimated the AHI by > 10% (D1, D8, D10).

Regarding the long scenario, only 5 of 11 devices (D1, D3, D4, D6, and D10) showed effectiveness, i.e., the residual obstructive AHI < 5/h, owing to their higher therapy pressure (Figure 6A, ​A,66B). Noteworthy, their prompt responses in pressure were linked to the inability to differentiate between central and obstructive apneas (Figure 5). Also, only D3 did not decrease the pressure when the normal breathing resumed. However, when the pressure dropped too fast, the treatment that resumed after the normal breathing session was insufficient (e.g., D9, Figure 5). These differences between devices in residual AHI were probably due to the inconsistencies between the definitions of SDB events in airflow amplitude in comparison to the recommendations regarding the flow amplitude thresholds.30 The treatment was not always efficient for the short scenario. Some devices resulted in a high amount of residual obstructive SDB events even when their pressure increased, as they reached the equilibrium with a significant lag time (e.g., D1, D4, and D10).

Device D5 did not respond to any simulated apnea. Such an apnea with the flow amplitude lower than 5% was considered as a non-obstructive SDB event according to the manufacturer's definition.31 Also, the “obstructive pressure peak” signal, which was considered by D11 as a surrogate for obstructive apnea, was only reported in 67% of cases, while no sensitivity or specificity was indicated,29 and the clinical application of this method remained questionable. Other techniques of upper airway patency evaluation were applied by some devices, such as forced oscillation technique32 for D8 and pulse pressure method for D7. For D9, the upper airway patency identification relied on the detection of cardiac oscillations in airflow at mask. However, D9 raised the pressure during central apneas despite the presence of simulated “cardiac” oscillations. A potential explanation could be a misdetection of amplitude or frequency of these physiological oscillations. Of note, the sensitivity of cardiac oscillation was reported as only 60% for central apnea diagnosis.28 As a “trivial” solution, D9 allows users to set a maximum pressure for apneas in order to prevent a high pressure level during central apneas. It is noteworthy that the APAP devices showed better performance and treatment effectiveness for obstructive hypopnea than for apnea, especially for D5 and D11. Hence, these devices may be better adapted to mild obstructive SDB patients.

The reported results may bear a considerable significance due to the current clinical practice, which relies on unattended auto-titrating methods to set up constant pressure in patients as a way to save the cost of in-lab titration. Auto-titration could be used to select an effective EPAP or an appropriate EPAP range,14,33 in order to shorten the lag time for reaching the pressure equilibrium for APAP treatment and to avoid unnecessary pressure variations that could induce microarousals in patients,34,35 or ineffective adjustment of pressure which might be observed in patients with high number of alternation between sleep and wake periods.36

Concerning the outcomes of treatment, the poor performances of some devices may explain the observation of a poorer control of blood pressure with APAP, which was associated with a higher residual AHI.15 More recent studies have also underlined a less beneficial effect of APAP on autonomic nervous system activation measurements such as heart rate variability37,38 or pulse wave amplitude.39 The observed differences in residual AHI between bench values and device-reported ones bear considerable clinical implications, as the current follow-up of patient often rely on device-reported residual AHI which may be very different from actual patient values.17–21,39 Table 3 is intended to provide a general overview on the performance of each device and a classification according to patients' SDB profiles. D1, D3, D4, D6, and D10 showed a treatment efficacy > 90% (Table 3). In addition, D3, D5, D6, D8, D9, D10, and D11 showed an accuracy of device-reported AHI > 90% (Table 3). However, the inability of central-mechanism detection should be highlighted for the following devices: D1, D2, D3, D4, D6, D9, and D10. These devices should be used with cautions in patients with coexisting central SDB events.

Table 3
Table 3
Scoring and classification of APAP devices.
Limitation of the Study

On the current bench, the obstructive SDB patterns were characterized by the mechanical properties of the upper airway. Compared to the clinical trials, the variety of specific airflow patterns was limited, and the critical closing pressure for the upper airway (6 cm H2O) was positive as observed, particularly in severe obstructive patients. Also, the reported device performance only relies on the simulated patient's condition, i.e., the general scenarios, which were created to more closely simulate clinical variations within sleep-stage distribution.

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CONCLUSIONS
This study using reproducible and standardized SDB events evidenced large differences between all APAP devices in performance and treatment efficacy. Both bench studies and clinical evaluations are necessary to test the devices in full range of patients' spectrum of diseases and should be implemented in the registration of devices.

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DISCLOSURE STATEMENT
This was not an industry supported study. This research was supported by a CIFRE grant to K. Zhu, from the French Ministry of Higher Education and Research. The authors have indicated no financial conflicts of interest.

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ABBREVIATIONS
AHI apnea-hypopnea index
APAP auto-titrating positive airway pressure
OSA obstructive sleep apnea
CPAP continuous positive airway pressure
SDB sleep-disordered breathing
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REFERENCES
1. Sullivan CE, Issa FG, Berthon-Jones M, McCauley VB, Costas LJ. Home treatment of obstructive sleep apnoea with continuous positive airway pressure applied through a nose-mask. Bull Eur Physiopathol Respir. 1984;20:49–54. [PubMed]
2. Giles TL, Lasserson TJ, Smith B, White J, Wright JJ, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;(1):CD001106. [PubMed]
3. Scottish Intercollegiate Guidelines Network. Edinburgh: Scottish Intercollegiate Guidelines Network; 2003. Management of obstructive sleep apnoea/hypopnoea syndrome in adults.
4. Engleman HM, Martin SE, Kingshott RN, Mackay TW, Deary IJ, Douglas NJ. Randomised placebo controlled trial of daytime function after continuous positive airway pressure (CPAP) therapy for the sleep apnoea/hypopnoea syndrome. Thorax. 1998;53:341–5. [PMC free article] [PubMed]
5. Jenkinson C, Davies RJ, Mullins R, Stradling JR. Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised prospective parallel trial. Lancet. 1999;353:2100–5. [PubMed]
6. George CF. Reduction in motor vehicle collisions following treatment of sleep apnoea with nasal CPAP. Thorax. 2001;56:508–12. [PMC free article] [PubMed]
7. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet. 2002;359:204–10. [PubMed]
8. Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis. 1992;145:841–5. [PubMed]
9. Nino-Murcia G, McCann CC, Bliwise DL, Guilleminault C, Dement WC. Compliance and side effects in sleep apnea patients treated with nasal continuous positive airway pressure. West J Med. 1989;150:165–9. [PMC free article] [PubMed]
10. Rolfe I, Olson LG, Saunders NA. Long-term acceptance of continuous positive airway pressure in obstructive sleep apnea. Am Rev Respir Dis. 1991;144:1130–3. [PubMed]
11. Waldhorn RE, Herrick TW, Nguyen MC, O'Donnell AE, Sodero J, Potolicchio SJ. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest. 1990;97:33–8. [PubMed]
12. Weaver TE, Grunstein RR. Adherence to continuous positive airway pressure therapy. Proc Am Thorac Soc. 2008;5:173–8. [PMC free article] [PubMed]
13. Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;(4):CD005308. [PubMed]
14. Smith I, Lasserson TJ. Pressure modification for improving usage of continuous positive airway pressure machines in adults with obstructive sleep apnoea. Cochrane Database Syst Rev. 2009;(4):CD003531. [PubMed]
15. Patruno V, Aiolfi S, Costantino G, et al. Fixed and autoadjusting continuous positive airway pressure treatments are not similar in reducing cardiovascular risk factors in patients with obstructive sleep apnea. Chest. 2007;131:1393–9. [PubMed]
16. Meurice JC, Cornette A, Philip-Joet F, et al. Evaluation of autoCPAP devices in home treatment of sleep apnea/hypopnea syndrome. Sleep Med. 2007:695–703. [PubMed]
17. Desai H, Patel A, Patel P, Grant BJB, Mador MJ. Accuracy of autotitrating CPAP to estimate the residual Apnea-Hypopnea Index in patients with obstructive sleep apnea on treatment with autotitrating CPAP. Sleep Breath. 2009;13:383–90. [PubMed]
18. Denotti AL, Wong KKH, Dungan GC, 2nd, Gilholme JW, Marshall NS, Grunstein RR. Residual sleep-disordered breathing during autotitrating continuous positive airway pressure therapy. Eur Respir J. 2012;39:1391–7. [PubMed]
19. Ikeda Y, Kasai T, Kawana F, et al. Comparison between the apnea-hypopnea indices determined by the REMstar Auto M series and those determined by standard in-laboratory polysomnography in patients with obstructive sleep apnea. Intern Med. 2012;51:2877–85. [PubMed]
20. Cilli A, Uzun R, Bilge U. The accuracy of autotitrating CPAP-determined residual apnea-hypopnea index. Sleep Breath. 2013;17:189–93. [PubMed]
21. Ueno K, Kasai T, Brewer G, et al. Evaluation of the apnea-hypopnea index determined by the S8 Auto-CPAP, a continuous positive airway pressure device, in patients with obstructive sleep apnea-hypopnea syndrome. J Clin Sleep Med. 2010;6:146–51. [PMC free article] [PubMed]
22. Berry RB, Kushida CA, Kryger MH, Soto-Calderon H, Staley B, Kuna ST. Respiratory event detection by a positive airway pressure device. Sleep. 2012;35:361–7. [PMC free article] [PubMed]
23. The 510(k) Program: Evaluating Substantial Equivalence in Premarket Notifications [510(k)] - Guidance for Industry and Food and Drug Administration Staff [Internet] [Date last accessed: December 19, 2014]. Available from: http://www.fda.gov/MedicalDevices/Device...404770.htm Document issued on: July 28, 2014.
24. Farré R, Montserrat JM, Rigau J, Trepat X, Pinto P, Navajas D. Response of automatic continuous positive airway pressure devices to different sleep breathing patterns: a bench study. Am J Respir Crit Care Med. 2002;166:469–73. [PubMed]
25. Abdenbi F, Chambille B, Escourrou P. Bench testing of auto-adjusting positive airway pressure devices. Eur Respir J. 2004;24:649–58. [PubMed]
26. Zhu K, Kharboutly H, Ma J, Bouzit M, Escourrou P. Bench test evaluation of adaptive servoventilation devices for sleep apnea treatment. J Clin Sleep Med. 2013;9:861–71. [PMC free article] [PubMed]
27. ISO 17510-1: 2007 Sleep apnoea breathing therapy - Part 1: Sleep apnoea breathing therapy equipment.
28. Ayappa I, Norman RG, Rapoport DM. Cardiogenic oscillations on the airflow signal during continuous positive airway pressure as a marker of central apnea. Chest. 1999;116:660–6. [PubMed]
29. Ruhle KH, Domanski U, Nilius G. Obstructive pressure peak: a new method for differentiation of obstructive and central apneas under auto-CPAP therapy. Sleep Breath. 2013;17:111–5. [PubMed]
30. Iber C, Ancoli-Israel S, Chesson AL, Quan SF. 1st ed. Westchester, IL: American Academy of Sleep Medicine; 2007. The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications.
31. DeVilbiss Healthcare. Clinical overview: DeVilbiss IntelliPAP AutoAdjust [Internet] [Date last accessed: June 30, 2014]. Available from: http://www.devilbisshealthcare.com/files...4_Web.pdf. Last update: 2010.
32. Armitstead JP, Richards GN, Wimms A, Benjafield AV. Central sleep apnea detection and the enhanced AutoSet algorithm [Internet] [Date last accessed: June 30, 2014]. Available from: http://www.resmed.com/fr/assets/document...paper.pdf. Last update: 2010.
33. Morgenthaler TI, Aurora RN, Brown T, et al. Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: an update for 2007. An American Academy of Sleep Medicine report. Sleep. 2008;31:141–7. [PMC free article] [PubMed]
34. Fuchs FS, Wiest GH, Frank M, et al. Auto-CPAP therapy for obstructive sleep apnea: induction of microarousals by automatic variations of CPAP pressure? Sleep. 2002;25:514–8. [PubMed]
35. Marrone O, Insalaco G, Salvaggio A, Bonsignore G. Role of different nocturnal monitorings in the evaluation of CPAP titration by autoCPAP devices. Respir Med. 2005;99:313–20. [PubMed]
36. Lévy P, Pépin JL. Autoadjusting continuous positive airway pressure: what can we expect? Am J Respir Crit Care Med. 2001;163:1295–6. [PubMed]
37. Patruno V, Tobaldini E, Bianchi AM, et al. Acute effects of autoadjusting and fixed continuous positive airway pressure treatments on cardiorespiratory coupling in obese patients with obstructive sleep apnea. Eur J Intern Med. 2014;25:164–8. [PubMed]
38. Karasulu L, Epöztürk PÖ, Sökücü SN, Dalar L, Altın S. Improving heart rate variability in sleep apnea patients: differences in treatment with auto-titrating positive airway pressure (APAP) versus conventional CPAP. Lung. 2010;188:315–20. [PubMed]
39. Bakker JP, Campbell AJ, Neill AM. Pulse wave analysis in a pilot randomised controlled trial of auto-adjusting and continuous positive airway pressure for obstructive sleep apnoea. Sleep Breath. 2011;15:325–32. [PubMed]

The bench tests were conducted with "test" breathing patterns (artificially generated) and each machine set wide open---i.e. the machines were running with pressure set 4-20. There's a lot of technical details about how the test breathing patterns were set up so that they mimicked both REM and non REM sleep breathing patterns.

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  2015 peer reviewed article on how xPAPs score events and auto algorithms respond
Posted by: robysue - 12-03-2016 07:12 PM - Replies (1)

Treatment of sleep-disordered breathing with positive airway pressure devices: technology update by Karin Gardner Johnson and Douglas Clark Johnson published on-line at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4629962/

The above link is to a highly technical article about all of the ins and outs of the various algorithms used by Resmed S8, S9, A10 xPAPs, PR System One xPAPs, the DeVilbass IntelliPAP AutoAdjust, and the DeVilbass IntelliPAP AutoAdjust 2. The PR Dreamstations came out after this paper was written, but there good reason to assume that most (or all) of the design of the S1 Auto algorithms has been carried over to the Dreamstations.

The original article has a number of very important figures and tables. In particular, "Table 2" gives a synopsis of the actual differences between the families of xPAPs when it comes to how they determine "baseline" ventilation, how they score events, and how they respond to the events. The PR "search" algorithm is briefly described in the table.

I would encourage you to read the article by clicking on the link rather than reading what I've copied below because I have not taken the time to correct any of the formating errors created by the copy and paste. Hence what is below is going to be harder to read and it doesnot contain the tables.

************Contents of Article************************
Abstract
Many types of positive airway pressure (PAP) devices are used to treat sleep-disordered breathing including obstructive sleep apnea, central sleep apnea, and sleep-related hypoventilation. These include continuous PAP, autoadjusting CPAP, bilevel PAP, adaptive servoventilation, and volume-assured pressure support. Noninvasive PAP has significant leak by design, which these devices adjust for in different manners. Algorithms to provide pressure, detect events, and respond to events vary greatly between the types of devices, and vary among the same category between companies and different models by the same company. Many devices include features designed to improve effectiveness and patient comfort. Data collection systems can track compliance, pressure, leak, and efficacy. Understanding how each device works allows the clinician to better select the best device and settings for a given patient. This paper reviews PAP devices, including their algorithms, settings, and features.

Keywords: BiPAP, CPAP, iVAPS, AVAPS, ASV, positive pressure respiration, instrumentation, treatment algorithm
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Introduction
Positive airway pressure (PAP) is the primary treatment of sleep-disordered breathing including obstructive sleep apnea, central sleep apnea, and sleep-related hypoventilation. The most common form – continuous positive airway pressure (CPAP) – maintains a continuous level of PAP in a spontaneously breathing patient. Other forms that provide noninvasive positive pressure ventilation include bilevel positive airway pressure (BiPAP), adaptive servoventilation (SV), and volume-assured pressure support (VAPS). This review will highlight the differences in the device types as well as features that help with the functioning and comfort.

PAP equipment involves three basic parts: a device with a motor, a mask that covers either or both the mouth and nose, and a tube that connects the device to the mask. PAP has improved greatly since Colin Sullivan invented CPAP in June 1980 in Australia, using a paint compressor attached to pool tubing and a mask made from a plaster cast glued to the patient’s face. Major landmarks in the evolution of PAP are the first commercially available units by Respironics in 1985 and the self-sealing “bubble mask” in 1990.1

Current noninvasive positive pressure ventilation units are much more complex and may include an air filter, sensors (motor speed, gas volumetric flow rate, pressure, snore transducer), microprocessor-based controller, data storage, multilingual displays, and humidifier with heated tubing.

We reviewed literature from the manufacturers, patents, and published literature to provide an understanding of the different algorithms, features, and clinical applications of the various PAP devices.

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Overview of device types
CPAP maintains a continuous PAP throughout inspiration and expiration. Autoadjusting (Auto) CPAP can gradually increase or decrease the pressure based on respiratory events, but similarly maintains the same pressure throughout the respiratory cycle. This can be helpful for patients who may need a higher pressure in rapid eye movement (REM) or supine position, but cannot tolerate the higher pressure through the entire night. AutoCPAP can also be used diagnostically to determine a fixed pressure setting.2

BiPAP provides a higher pressure during inspiration and lower pressure during expiration. This may improve tolerance and help with ventilation. A backup rate can be added to give a breath with weak or absent respiratory effort. AutoBiPAP may adjust either the expiratory positive airway pressure (EPAP) and inspiratory positive airway pressure (IPAP) with a fixed pressure support (PS) or may adjust them independently.

SV is a bilevel system that continuously changes the inspiratory PS on a breath-by-breath basis in order to achieve a target ventilation or flow for a more constant breathing pattern, especially in the treatment of periodic breathing or Cheyne–Stokes respiration (CSR). Auto forms of SV also increase EPAP in response to obstruction.

Volume-assured pressure support (VAPS) is a variable bilevel PAP that allows the target volume or ventilation to be programmed, which allows more control of ventilation. This is useful for patients with combined periodic breathing and hypoventilation or patients with REM-related hypoventilation related to conditions like chronic obstructive pulmonary disease (COPD), neuromuscular disorders, or obesity, who may need different PS levels at different times.

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Motor/flow generator and transducers
In order to provide a constant desired pressure at the patient’s airway, adjustments in flow must be made to account for the loss of pressure between the flow generator and the patient’s airway, as well as for breathing fluctuations and leak.

Transducers monitor the motor speed, airflow, and the pressure at a fixed point downstream from the flow generator. Because the sensor is within the device and not in the mask, the device must calculate the predicted pressure at the mask based on the flow measurements at a different point in the system. The pressure at two points varies with the flow. For turbulent flow, this can be calculated by Flow (q) = constant√(p1 − p2).3 The length and diameter of the tubing and mask characteristics affect the constant value, and so the technician must input the mask and tube type for the microprocessor to make the correct calculations. The mask flow can also be calculated by subtracting the flow through the exhaust of the device from the flow through the tubing.4

In order to maintain a stable mask pressure, the microprocessor must adjust the turbine speed in response to deviations in pressure that occur from leak or normal swings in air pressure from breathing. The flow signal is sent through low and high pass filters to separate the respiratory flow signal from artifacts. Low pass filters exclude large quick deviations in flow (eg, coughs or sneezes) and high pass filters exclude cardiogenic fluctuations. Feedback limits determine if the flow or pressure is beyond the expected range of flow variation at a particular motor speed (eg, break in the tubing), and prevent the device from delivering too much or too little pressure.5 With increasing altitude, fan speed needs to be increased to maintain the same pressure.6 Many devices adjust automatically to altitude.

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Leak compensation
Unlike invasive ventilation, leak is an important factor that must be compensated for. Leak affects aspects of performance including pressure delivered, cycle and trigger thresholds, and respiratory event determination. Leak compensation works by constantly monitoring flow and looking for deviations from the expected respiratory flow and will compensate the motor speed for the leak. Because there are normal variations in the patient’s breathing cycle the expected leak is usually averaged over several breaths. If leak is high, auto devices may compensate by lowering the pressure, which may seal the mask and reduce leak.

The leak can be determined from the flow rate at the end of exhalation.7 Normal leak includes that from exhalation ports on the mask, which varies by mask type and pressure level, and unintentional leak from the mouth or around the mask. In general, leak should be under 24 L/min in nasal masks and under 36 L/min in full face masks.

The lips and tongue sometimes act like a one-way valve opening during exhalation, when the pharyngeal pressure is highest. This is called valve leak or expiratory puffs. Expiratory puffs may falsely imply flow limitation, which can cause auto devices to increase pressures unnecessarily. Some algorithms place less reliance on flow limitation when large leak or expiratory puffs are present.8

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Respiratory cycle determination
Determination of the inspiratory and expiratory cycles is essential not only to provide bilevel PAP but also for expiratory pressure relief and determination of inspiratory flow limitation in auto algorithms. The start of inspiration is marked by a switch from negative to positive flow (relative to baseline). The point at which the flow signal switches from positive to negative flow is the start of expiration.

SV and some auto devices use more continuous respiratory cycle determination. ResMed’s servoventilator microprocessor uses fuzzy inference rules looking at the flow rate (relative to mean flow), direction, and size to determine the phase of the respiratory cycle9 (Table 1). Respironics’ servoventilator determines the length of inspiration and expiration of recent breaths to predict the future breath duration and divides the breaths into short time segments (64 ms) to determine the expected mid-inspiration and other points of the cycle.10

Table 1
Table 1
ResMed’s fuzzy logic for phase determination
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CPAP
Most CPAP devices allow for pressure settings between 4 and 20 (all pressures in cm⋅H2O). An EPAP of 4 is the lowest pressure needed to provide enough flow to clear the dead space from the device, tubing, and airway to prevent rebreathing of exhaled air.11 The goal of CPAP is to increase upper airway pressure enough to provide a pneumatic splint to open the airway, which may collapse during inspiration. Typically, the pressure is set to prevent hypopnea, apnea, snoring, flow limitation, and arousals. By providing positive end expiratory pressure, CPAP may recruit alveoli and improve ventilation.

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AutoCPAP
The aim of AutoCPAP is to adjust the pressure in response to respiratory events without adjustment to artifacts caused by leak or other factors. AutoCPAP from different companies and different models by the same company have varying definitions of events, responses to obstructive events, and protocols for decreasing the pressure once the breathing stabilizes. These variations are important to understand for appropriate clinical care as they affect the patient’s tolerance of the devices and the clinical efficacy.12–14 If a patient enters REM sleep or changes position, the degree of obstruction may suddenly increase and by the time the device is able to adjust to the needed pressure the patient may have had desaturations or arousals. This is why most studies reporting the equivalence of AutoCPAP to in-lab titration recommend changing the EPAP minimum to the pressure the device is at or below 90–95% of the time.2,15 In our experience, many patients left on AutoCPAP 4–20 are undertreated and may present with awakenings a couple hours into sleep, residual symptoms, or difficulty tolerating PAP. Some patients are sensitive to the pressure changes, so if patients are not doing well with AutoCPAP, fixed CPAP should be tried.

Some of the first AutoCPAPs, like Virtuoso LX smart and SOMNOsmart, only detected vibration-based snore changes making them unresponsive to many significant events.16 Most new AutoCPAP systems use snore detection in combination with flow detection. The flow is sampled many times per second, scaled with a low pass filter to remove artifact, and then a mean flow can be determined for any time length. Peak flow can be a poor measure of breath volume, which can lead to over- or underestimation of an apnea or hypopnea. Respironics uses a weighted peak flow (WPF) method to estimate ventilation, while ResMed uses a scaled low-pass-filtered absolute value of respiratory flow and uses a root mean squared (RMS) technique of the variance of the flow from the mean to compare one moving time period to another. DeVilbiss Intellipap AutoAdjust uses a scaled peak amplitude, while AutoAdjust 2 uses RMS and other filtering techniques to adjust for artifacts in peak flow.

Respironics’ WPF method first determines the inspiratory period, then the inspiratory volume and the points on the inspiratory flow curve that correspond to the 20% and 80% volume. The average flow of all points between the 20% and 80% points is used as the WPF, a measure of ventilation. This method uses WPF values over the prior 4 minutes and determines the average of values between the 80th and 90th percentile. This baseline is used to compare with the current WPF to look for decrease in amplitude, which would indicate apnea or hypopnea.17

ResMed’s RMS method determines ventilation from variance of the flow throughout the entire breath by comparing individual flow points to the mean airflow over a defined time period. The mean airflow is the zero-point between inspiration and expiration, thus variance from this mean divided by two equals the amplitude of the inspiratory flow. By taking the square root of the variance squared, outlying values receive less weight. A moving short time period (eg, one breath or 2 seconds) can be compared to a moving longer period (eg, 5 minutes) to evaluate for apnea or hypopnea.18 Apneas and hypopneas are typically defined as a reduction in ventilation below a percentage of recent breathing for at least 10 seconds, with varying methods used by different devices (Table 2).

Table 2
Table 2
AutoCPAP algorithms
Since responding to central apneas can lead to over titration, testing for airway patency allows for differentiation of central from obstructive apneas. Two methods used to test for airway patency include cardiogenic pulsation testing and device-generated pressure oscillations. The first method looks for cardiogenic pulse artifact in the flow, which is only present if the airway is open. In the second method, the device provides single pressure pulse or small oscillation in the flow (eg, 1 cm, 4–5 Hz or forced oscillation technique), which is only reflected back to the flow sensors if the airway is closed.18–20 Respironics uses pressure pulses and also defines an obstructive apnea if there is a larger than expected breath after apnea termination. A mixed apnea can be determined if the airway is open for only part of the flow. ResMed from >9 onward uses force oscillation technique to define central apneas and defines central apneas if leak is >30 L/min.18 DeVilbiss Autoadjust 2 uses a modulating micro-oscillation to determine airway patency during apneas.

In order to evaluate flow limitations, Respironics determines roundness, flatness, skewness, and WPF to rate the most recent four breaths as better, worse, or the same compared to baseline. Roundness is determined by the similarity of the WPF between 5% and 95% values to a sine wave. Flatness is determined by the absolute value of the variance between 20% and 80% of inspiratory flow from the average of all the values in the same period, divided by 80% volume point. Skewness is determined by dividing the average of the highest 5% of flows in the mid third of the breath by the average of the highest 5% of flows in the first third of the breath.17

ResMed also determines flow limitation. S8 AutoSet defines flow limitation using flatness of an inspiratory breath. The flatness index is calculated by the RMS deviation from unit scaled flow calculated over the middle 50% of a normalized inspiratory breath.4 From the S9 onward, flow limitation is calculated using a combination of flatness index, breath shape index, ventilation change, and breath duty cycle. Ventilation change is the ratio of the current breath ventilation to recent 3-minute ventilation. Breath duty cycle is the ratio of current breath time of inspiration to total breath time of recent 5 minutes. If a breath is severely flow limited, the flow limitation index will be closer to one and when the breath is normal or round, the flow limitation index will be zero.8

Table 2 summarizes the differences between the algorithms for the ResMed AutoSet device,4,8 ResMed AutoSet for Her,8 Respironics System One REMstar Auto,17 and DeVilbiss IntelliPAP AutoAdjust and AutoAdjust 2.21 ResMed AutoSet evaluates flow every breath looking for apneas, snore, and flow limitation, but responds to flow limitation on a 3-breath average, has faster decreases in the absence of flow limitation and has a higher rate of pressure change to all responses (apnea, snore, and flow limitation) than AutoSet for Her.8,18

In comparison, ResMed AutoSet for Her evaluates the flow for every breath looking for apneas, snore, and flow limitation, and delivers a proportional increase in pressure depending on the degree of deviation of the event from normal, modulated by the current pressure setting and leak rates. If pressure is >10, then the response to flow limitation reduces and a louder snore is required to produce a response.8 Both AutoSet for Her and AutoSet respond less as leak gets higher.

Respironics REMstar Auto uses layers of control including ramp, leak, snore, apnea/hypopnea, variable breathing, and flow limitation. If there is no snore, apnea/hypopnea, variable breathing, or flow limitation breathing for 3–5 minutes, it will enter a testing period in which it will first decrease the pressure until either Pminimum or the flow characteristics (peak, flatness, roundness, and skew) worsen, which is the Pcritical, then quickly increase by 1.5 and holds for 10 minutes unless further events or flow limitation occurs. If there is snore, apnea/hypopnea, variable breathing or flow limitation, the pressure increases by 0.5/min until there is no further improvement or worsening, then decreases by 1.5, which is set as the Poptimal pressure. REMstar also uses several mechanisms to avoid over titration, which include nonresponsive apnea/hypopnea logic, variable breathing, and leak control (Table 2).17,22

Most devices start at the set EPAP minimum (EPAPmin) each night. Respironics REMstar Pro and REMstar Auto have CPAP check mode, which checks the 90% pressure every 30 hours, then decides whether to leave the EPAP unchanged, or changes the EPAP up or down by one but not more than three from set EPAP.23

DeVilbiss’s IntelliPAP AutoAdjust allows setting of amplitude and duration cut-points for apneas and hypopneas to change sensitivity. AutoAdjust does not detect flow limitation and defines central apneas as <5% of airflow for 10 seconds.21 It continuously scores events, but only decides once per minute whether to adjust pressures. AutoAdjust 2 similarly adjusts pressures once per minute, but also responds to flow limitation based on inspiratory flatness. It uses modulating micro-oscillation during apneas to test for patency and has an algorithm to define periodic breathing, looking for cyclic breathing as short as a 20-second cycle. AutoAdjust 2 holds or lowers pressures in response to central apneas and periodic breathing.

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BiPAP
BiPAP provides a higher pressure during inhalation and lower pressure during exhalation. Pressures generally range from EPAP minimum of four to IPAP maximum of 25–30. Most devices use a flow trigger to determine when to change to IPAP. The trigger is set above zero flow to sense a significant patient effort. Different methods including flow, shape, and volume are used to cycle to EPAP in efforts to minimize dyssynchrony. The flow cycle algorithm changes to EPAP when the flow drops below a percentage (eg, 25%) of the peak flow so the patient will not encounter resistance to exhalation.24 Shape cycling algorithm uses shape of flow,25 and volume cycle algorithm uses exhaled volume to cycle to EPAP. There can be significant variation between devices in terms of how quickly pressure levels are met and whether a device has a delay or premature cycle, especially in the setting of leaks.26 If there is a mismatch between the patient’s respiratory cycle and the device control cycle there can be patient discomfort.

In older BiPAP devices, the motor was braked at the transition point from higher to lower pressures and the motor was accelerated when the device transitioned from lower to higher pressure, which affected synchrony and tolerability. One method to improve comfort is to allow the blower motor to spin freely on transition between inspiration and expiration. Newer devices allow for a smoother transition in pressure changes, and waveforms can be square, exponential, ramp, or sinusoidal. ResMed has a sharkfin-shaped “Easy-Breathe” waveform.27 The shape of the waveform may be affected by the compliance and resistance of the patient’s respiratory system and the breathing effort, as well as mechanical constraints of blower momentum and propagation delays. In general, BiPAP provides a square wave of PS, but manual or automatic adjustments can give more of a smooth pressure change, which may help with comfort. Most BiPAP devices allow for adjustment of the rise time (angle of the pressure change) from 100 ms to 600 ms.

Some BiPAP devices include cycle, trigger, inspiration time, and rise time settings, which can be adjusted to enhance effectiveness and patient comfort, especially for patients with COPD or neuromuscular disorders25 (Table 3). Typically the rise time should be kept shorter in COPD patients to allow lungs to fill more quickly and give enough time to exhale. A longer rise time in patients with neuromuscular weakness helps ensure adequate tidal volume and gas exchange (Figure 1).

Figure 1
Figure 1
Rise time.
Table 3
Table 3
Suggested PAP settings
Because of the delay in detecting the onset of inspiration and delivery of the pressure adjustment, it is common for the inspiratory pressure needed for BiPAP settings to prevent obstruction during early inspiration to be higher than the CPAP pressure needed to prevent the same. For example, a patient requiring CPAP 8, may require BiPAP 10/6 so that a pressure of 8 is reached early enough in the inspiration to keep the airway open.

Trigger sensitivity refers to the degree of inspiratory flow change needed to change the pressure cycle from EPAP to IPAP. At high sensitivity, small changes in inspiratory flow will bring changes to IPAP. If the trigger is too sensitive (too high), then the device may force a breath in response to artifacts like leak or abnormally strong heartbeat due to cardiogenic oscillations in the breathing. Low trigger sensitivity is recommended if the patient complains the breath occurs before exhalation is complete or before the patient starts inhalation. High setting is recommended for patients with weak respiratory effort, such as in neuromuscular disorders (Figure 2).

Figure 2
Figure 2
Trigger and cycle sensitivities.
Inspiration time typically ranges from 0.3 seconds to 2 seconds, often with a default of 1.5 seconds. The higher the baseline respiratory rate, the shorter the inspiratory time (Ti) recommended. Short Ti settings can be helpful for COPD patients for whom pressure does not quickly equilibrate throughout the lung, so the patient may need to actively exhale to cycle the end of expiration. Not only can this cause dyssynchrony and discomfort, it may also lead to air trapping and reduced tidal volume if expiration time is too short.25

Cycle sensitivity sets the level of inspiratory flow below which the device changes from IPAP to EPAP. High cycle setting is recommended when shortened Ti is needed, such as for COPD or if the patient complains that the breaths are too long. Low cycle is recommended when longer Ti is needed for neuromuscular diseases, weak respiratory effort, or stiff lungs, or if the patient complains that the pressure seems to switch from IPAP to EPAP too quickly.

BiPAP can be triggered by spontaneous, timed or spontaneous/timed (ST) modes. In spontaneous mode, inspiration is only triggered when the device senses a flow change. Large leak may cause the trigger to fail if the device does not appropriately adjust. Timed mode triggers at a fixed rate and makes no attempt to synchronize with the patient’s breathing, which can result in breath stacking and patient discomfort. ST mode changes pressures with spontaneous breathing efforts, but if the patient has not triggered a breath by a set respiratory rate, then the device will trigger a breath.

ST mode is most often used for primary central apnea or central apneas due to respiratory depression. ST mode may also be used for neuromuscular disease patients, whose respiratory efforts fall during REM sleep, which may make them unable to trigger inspiration.28 Timed mode is often used for patients with severe neuromuscular weakness or spinal cord injury, who are unable to trigger inspiration.

BiPAP may worsen central apneas due to CSR by increasing breath size of spontaneous breaths and forcing a triggered breath during the apneic portion, which is when the partial pressure of carbon dioxide (PCO2) level is already at its lowest.29 By further decreasing the PCO2, respiratory drive is reduced further and the duration of the apnea will often lengthen, although the oxygenation may improve with the deeper or forced breath. Sometimes the improved oxygenation and PS will help to eventually stabilize the patient’s breathing,30 but in our experience patients with CSR often find BiPAP intolerable or still have a suboptimal clinical response including fluctuations in the respirations and electroencephalogram.

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AutoBiPAP
Like AutoCPAP, not all AutoBiPAP devices work in the same way. Some devices only allow a fixed PS, others set a PS maximum (PSmax), and others allow for both PS minimum (PSmin) and PSmax. Thus AutoBiPAP may not provide adequate ventilator support if PSmin cannot be set. AutoBiPAP devices generally do not have an ST option, so are not recommended for central apneas.

ResMed’s VPAP AutoBiPAP and DeVilbiss AutoBiPAP have a fixed set PS. Respironics Series 50 AutoBiPAP fixes PSmin at two and allows setting PSmax, while Series 60 AutoBiPAP allows setting both PSmin and PSmax. Within the limits of PSmin and PSmax, Respironics AutoBiPAP changes EPAP in response to apneas (two apneas or one apnea and one hypopnea) and snoring, and IPAP in response to hypopneas (two hypopneas) and flow limitation, with algorithms similar to REMstar AutoCPAP.31

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Adaptive servoventilation
Because higher PAP pressures and high PS can induce periodic breathing and CSR, devices have been developed to try to even out the breathing over several breaths. These devices include ResMed VPAP AdaptSV (equivalent to Teijin AutoSet CS) with ASV setting, AirCurve ASV, which has been renamed AirCurve CS PaceWave with ASV and ASVAuto settings, and Respironics BiPAP AutoSV Advanced. Another device, SOMNOvent CR, is available outside of the US from Weinmann (Table 4).

Table 4
Table 4
SV algorithms
ResMed’s standard ASV uses a set fixed EPAP, samples flow 50 times per second, and alters IPAP throughout inspiration to achieve target minute ventilation. The PS range can be 0–20, but default is usually a PSmin of three and PSmax of 15. The device calculates a target minute ventilation based on the recent average weighted minute ventilation, weighted toward the last 3 minutes. ASV uses fuzzy logic to determine the part of the respiratory cycle and whether the current ventilation is below or above the desired target and then adjusts the PS throughout the cycle to achieve that target, thus avoiding abrupt pressure changes. The change in pressure is calculated by multiplying a gain of 0.3 cm H2O/L/min/s by the difference between the target minute ventilation and the actual minute ventilation. An automatic backup rate starts with the current spontaneous rate based on moving average calculated over several breaths and gradually adapts during an apnea to 15 bpm.9 ASVAuto also adjusts the EPAP level similar to the AutoSet algorithm in response to obstructive apneas, flow limitation, and snoring.32

The hope is that by stabilizing breathing, the periodic breathing pattern will subside. If the device is cycling the pressures frequently to maintain the target ventilation, it indicates that the underlying periodic pattern is still present and often the patient will either not tolerate the device or there will be a suboptimal clinical response.33

Respironics BiPAP AutoSV Advanced is set with EPAP minimum and maximum, PSmin and PSmax, max pressure, and auto or fixed rate. Ti, rise time, and Bi-Flex can also be set for comfort. The level of PS is targeted based on instantaneous average inspiratory flow, which is the sum of the inspiratory flows during a time divided by the number of samples during a time in order to adjust for spurious values. The target peak flow is generally set at 90%–95% of the mean peak flow of the last 4 minutes. In an attempt to stabilize breathing in the setting of obstructive features (apnea [<20% flow], hypopnea [20%–60% flow], and snoring), the target peak flow increases from 95% of the mean inspiratory peak flows over the last 4 minutes to the 60th percentile of the inspiratory peak flow values. The target peak flow is also increased to 60th percentile if CSR features are noted based on a CSR index, which measures similarity to a CSR pattern or a flow index that measures fluctuations in breath size.34

The respiratory cycle of AutoSV Advanced is determined by using the average length of the breathing cycle over recent breaths and calculating the expected midpoint of inspiration. Compared to multiple small adjustments in the PS throughout the breath cycle with ResMed’s ASV, the inspiratory PS is determined based on the prior breath’s PS plus a gain based on a moving average of the pressure needed in the prior 30 breaths multiplied by the difference between the target peak inspiratory flow and the current breath’s peak inspiratory flow. An intrabreath PS is given if the actual flow is less than target flow in the 100 ms prior to the expected halfway point of the inspiration of the current breath. If actual flow is larger than target flow, the PS will be decreased for the following breath.34

The EPAP adjustment algorithm of AutoSV Advanced is similar to REMstar Auto algorithm, but uses a triggered breath rather than forced oscillation to differentiate obstructive from open airway events.32 The automatic backup rate of AutoSV Advanced is determined based on a moving window of the last 12 spontaneous breaths. A mandatory breath is given if the breath does not occur within certain parameters, with a minimum breath rate of 8–10 bpm. A fixed backup rate can also be set.

The older BiPAP AutoSV did not automatically titrate the expiratory pressure, and the algorithm for the automatic backup rate was not proportional to the baseline breathing rate, but it would give a breath if no spontaneous breath occurred within 8 seconds of end of expected breath length or within 4 seconds, if there was recent triggered breath.35 Respironics BiPAP AutoSV Advanced has been found to be more effective than the older BiPAP AutoSV.35 SV, which targets recent ventilation (ASV) or recent peak flow (AutoSV) is not appropriate for managing patients with respirator insufficiency, for whom BiPAP or VAPS should be considered.

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Volume-assured pressure support
Respironics AVAPS (average VAPS) and ResMed iVAPS (intelligent VAPS) adjust the PS in order to maintain target average ventilation over several breaths (Table 5). This mode of PAP is often helpful for patients with respiratory insufficiency due to neuromuscular and restrictive conditions in which respiratory effort varies during sleep or who need PAP during the day, COPD patients with risk of hypoventilation, and for obesity hypoventilation patients who may need compensation based on positional and sleep stage changes. Because many patients have much worse hypoventilation in REM, BiPAP with a fixed PS may provide too much pressure in NREM, which may lead to intolerance or complex sleep apnea and may not provide enough PS in REM to control PCO2 levels. Benefits of VAPS over BiPAP can include maintaining volumes in the setting of altered patient effort based on sleep stage or altered lung mechanics related to position. Lesser PS during wake may increase comfort and aid sleep onset, reduce risk of barotrauma, and lower pressures for most of the time.36 A randomized trial of iVAPS vs BiPAP found that iVAPS delivered a lower mean PS for the oxygenation and transcutaneous PCO2 level and had better adherence than BiPAP.37

Table 5
Table 5
VAPS algorithms
Both AVAPS and iVAPS adjust PS and respiratory rate to reach a defined target with the goal of stabilizing the PCO2, which relates directly to alveolar ventilation. With a target tidal volume (eg, AVAPS), if there is a large variance in the respiratory rate, there can be fluctuations in the alveolar ventilation and thus PCO2. By targeting estimated alveolar ventilation (minute ventilation–estimated dead space ventilation; eg, iVAPS), variations in respiratory rate should not affect alveolar ventilation or PCO2 as long as the estimated dead space equals physiologic dead space. The device estimates the anatomic dead space using height.38 However, patients with lung diseases, such as emphysema, have increased physiologic dead space that would be underestimated by the above equation, and thus their alveolar ventilation can be much lower than the estimated alveolar ventilation. Thus, emphysema patients may require high target alveolar ventilation to achieve an adequate actual alveolar ventilation. Alternatively, the “height” can be entered artificially high for emphysema patients, thus the calculated dead space will be closer to physiologic dead space, and therefore iVAPS more closely maintains the actual alveolar ventilation.

Respironics AVAPS targets an average tidal volume over several breaths. Typically, the target tidal volume is set based on 6–10 mL/kg ideal body weight. It calculates the average PS provided to the patient over the prior 2 minutes in order to achieve a particular tidal volume. If average recent ventilation is less than target volume, IPAP for the next breath is increased. PS will change at a rate of 2/min if there is unstable breathing and 1/min if there is stable breathing. AVAPS-AE model (and also AVAPS on Trilogy 100 Ventilator) can set maximum rate of pressure change from 1/min to 5/min. AVAPS uses square waveform with Ti and rise time settings. EPAP is fixed with AVAPS, but AVAPS-AE adjusts EPAP similar to Respironics REMstar Auto with a searching protocol between EPAP minimum and maximum. AVAPS either uses a fixed rate or auto backup rate set at 2 bpm lower than the rate of the last six spontaneous breaths.39

ResMed iVAPS uses a similar servoventilator with fuzzy logic for determining respiratory phase as adaptive SV. Unlike adaptive SV, the goal ventilation is set to a target alveolar ventilation, which is defined as minute ventilation minus anatomical dead space ventilation. iVAPS alters the gain every 8/50th second throughout the inspiratory cycle to achieve the target ventilation with a smooth parabolic transition that can be modified with rise time, Ti, and cycle and trigger sensitivities. EPAP is fixed like adaptive SV.40

iVAPS’ intelligent backup rate function uses two-third of the set target patient rate as the backup rate during spontaneous breathing and switches during apneas to the set patient target rate apnea. This reduces potential dyssynchrony during spontaneous breathing, while providing ventilation during apneas at a lower PS than if the backup rate remained lower.41

The iVAPS ventilation and rate targets can be configured using the Learn Target feature. While the patient is awake and comfortably breathing at rest, the clinician initiates the Learn Target session, which typically lasts between 15 minutes and 20 minutes and monitors the breathing while on a base EPAP pressure of 6. It uses the average respiratory rate, and since metabolic rate decreases in sleep, it uses 90% of the average estimated alveolar ventilation of the last 5 minutes of the session to propose a target patient rate and target alveolar ventilation, which can then be set by the clinician.42

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Other features of PAP
Humidification, heated tubing, ramp, automatic start and stop functions, alarms, and expiratory pressure relief are device functions that are designed to improve patient comfort and compliance (Table 6).

Table 6
Table 6
Other PAP features
Humidifiers include a water chamber with a heating plate through which the airflow is blown. Increasing the warmth of the heating plate increases humidification. Temperature sensors or humidification sensors allow for regulation of temperature or humidification level. Increasing humidification in the air helps reduce nasal irritation and congestion that can result from the airflow on the nasal passages.43 If the humidified air cools in the tubing, water may condense in the tube or mask, commonly referred to as “rainout”. Insulation sleeves that wrap around the tubing or heated tubing, which includes a heating element in the tubing, can increase humidification and eliminate “rainout”. The controls for the heated tubing are often linked to the warming level of the plate, but some devices allow for dissociation of the controls, which may further help with comfort in some patients. Different amounts of humidification may be needed depending on the external humidity and temperature.

For travel, standard PAP devices can be used with external battery packs or with converters to allow them to be powered by a car, boat, or other vehicles. There are also small battery-powered units weighing around 10 oz, such as Z1 CPAP and Z1 Auto from HDM, compared to 48 oz for Respironics System One and 44 oz for ResMed AirSense S10.

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Data collection and display
Data from the device can be retrieved on the interface with a data card, cable, and wireless or by cellular and bluetooth to an online platform. Data cards can either be used to download locally or to an online website, which allows for sharing. Summary data from the last month is often viewable on the device. DeVilbiss IntelliPAP devices use codes that represent different data sets that their website uses to generate a report.

Data collected varies among devices and can include pressure settings, leak, average, 90%–95% pressures and maximum pressures, PS, tidal volumes, minute ventilation, and apnea hypopnea index. Some devices report more detailed data about respiratory events, which may include central, mixed, obstructive and undetermined apneas, hypopneas, flow limitation, snoring, expiratory puffs, percentage of time in periodic breathing, tidal volume, and minute ventilation. Reports can show summary data over days and months as well as detailed data with the timing of events over the course of one night. Often data can be searched for a 30 day compliance period having over 4 hours of use on 70% of the nights. Respironics System One devices can also show full night waveform tracings with scored events and pressure settings. An oximetry module can be connected to ResMed’s AirSense device to allow for saturation data. More data about adherence tracking systems are available in a review by Schwab et al.44

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Conclusion
There are a wide range of PAP devices and a wide range of different algorithms used to provide PAP to treat sleep-disordered breathing. For this reason, devices in the same category may differ greatly in their clinical efficacy and comfort. Understanding how PAP devices function can help the clinician select the best PAP device, appropriately titrate, troubleshoot, and optimize settings for a particular patient. Many comfort features have improved the function and performance of devices, which allows many patients who have been unable to tolerate PAP in the past to become compliant. Many devices track compliance and provide important clinical data to help care for the patients.

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Acknowledgments
We thank ResMed and DeVilbiss for providing information about their algorithms.

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Footnotes
Disclosure

The authors report no conflicts of interest in this work.

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References
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  hose valve noise
Posted by: ArtistEd - 12-03-2016 05:26 PM - Replies (2)

The hose valve to my full mask had become unbearably clicky and so I just took it off and pushed the hose in the mask hole. I can tell you, that was the best sleep I've had since I've been using the CPap for about 2 mos. My AHI went from 12-15 to 4.6 last night, while the pressure went from 10-12 to 14 last night.
My question is, do I need that valve?

Thanks, Ed

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  Respironics blower failure
Posted by: SleepyinMTL - 12-03-2016 12:38 AM - Replies (2)

My Respironics System One (a backup unit I use while traveling) just died in the middle of the night.

I suspect it is the blower due to the noise it makes while attempting start-up.

Is there a built-in diagnostic tool and code that would confirm this ??

Unit has about 9500 hours of usage.

I figured it would cost $200+ to have it repaired and just ordered a Resmed

Airstart 10 Auto as a replacement for about $400 with overnight delivery.

My home machine is a Resmed Airsense 10 Auto.

How common is it for a blower to die after about three years usage ?

Do the Resmed blowers typically last longer ?

Thanks !

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  Upset about central apnea
Posted by: sleepytimegal - 12-03-2016 12:17 AM - Replies (6)

I've been looking at my Sleepyhead results for the first time these last couple of days. (I had to get a new hard drive to get it downloaded.) I was surprised to see that I have so many central apneas. Well, not really a lot since my AHI is pretty low with treatment. But, without counting, it seems like the central and obstructive events are pretty equal on the graph most days. My sleep doctor never mentioned that to me and just told me I have OSA. I was wondering if the SleepyHead data would be accurate on that account. I didn't sleep long during my sleep study - about 4.5 hours, so maybe those results weren't that comprehensive.

I guess my question is this: would you believe the Sleepyhead data about central apena to be accurate? I suppose that sounds silly - I guess I just didn't want to have central apnea - it sounds more scary to me. I was just getting used to being 'very severe' and now this makes it seem even worse. Any thoughts?

Thanks in advance for your responses.

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