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CPAP Rentals & Sales

The provision of CPAP therapy can only be prescribed by a recognised sleep or respiratory physician, Peninsula Sleep Laboratory will not supply anyone who does not have an appropriate prescription.

To view the extensive range of CPAP machines and masks that are carried by Peninsula Sleep Laboratory visit here.

For more information about Rentals and Sales visit here.

CPAP Troubleshooting.

If you are experiencing difficulties with your CPAP mask or want some tips on cleaning the mask, please visit our CPAP Troubleshooting page here.

However in all instances it is important to contact the CPAP Clinic to resolve any issues you are experiencing. If you are not a patient of Peninsula Sleep Laboratory or have purchased CPAP equipment elsewhere there is a consultation fee. $50 for a half an hour appointment and clinic visits are by appointment only, so please contact Peninsula Sleep Laboratory to book. Contact details here.

More information about the Peninsula Sleep Laboratory CPAP Clinic can also be found here.

Peninsula Sleep Laboratory Holiday Hours.

Peninsula Sleep Laboratory will be shut over the Christmas and New Year period. The laboratory will be closed from Thursday the 23rd of December 2010 and will resume normal hours from Monday the 10th of January 2011.

For any CPAP supplies or repairs during this holiday shut down period please contact the supplier directly. For their contact information please follow the links: ResMed, Phillips Respironics, Fisher & Paykel.

From everyone at Peninsula Sleep Laboratory we wish you a Merry Christmas and Happy New Year.

An Objective Assessment Of The Effectiveness Of Mandibular Advancement Devices In Home Use.

Keith Burgess (1,2), Andrew Burgess (2,3), Hedi Lamy (2), (1).Department of Medicine, University of Sydney. Sydney. NSW. 2050, (2).Peninsula Sleep Laboratory. Sydney. NSW. 2086, (3).Faculty of Medcine, Notre Dame University. Sydney. NSW. 2010, Australia

ABSTRACT Background: Mandibular Advancement Devices (MADs) are now used more frequently to treat Obstructive Sleep Apnoea (OSA). Their effectiveness in practice is uncertain. Currently they are often thought of as providing treatment success in only 50% of patients. We suspected that using a second polysomnogram (PSG) to guide final adjustment would improve effectiveness.

Aim: To objectively assess in the home the effectiveness of MADs in moderate severity OSA using our paradigm. Methods: We invited 200 subjects treated by the same algorithm to be restudied in their home environment. [Paradigm = Initial PSG, MAD advanced till “snoring controlled”, repeat PSG, further adjustment based on 2nd PSG]. 50 subjects (age 63±10, M:F 33:17) were studied with the MAD insitu by unattended PSG in their homes. (Somte PSG. Compumedics. Melbourne). All studies were scored by a certified technician not involved in the study, using R & K rules and “Chicago criteria”. (Snoring loudness was scored: 0=nil, 1=mild, 2=moderate, 3=loud, 4=very loud). The home studies with MAD in situ were compared to the original PSGs for sleep related variables and potential confounders. A variety of devices were used, though 65% were Somnodent. Treatment success was defined as normalisation of AHI or more than 50% reduction in AHI.

Results: Total sleep time increased from 331±73 mins to 381±56 (P<001). Despite an increase in REM sleep from 15.8 ± 5.4% to 17.5 ± 4.9% (P=0.02), arousal index fell from 28 ± 13/hr sleep to 17 ± 8/hr at home (P<0.001). AHI fell from 21.8 ± 14/hr to 9.5 ± 9.8/hr (P<0.001), Desaturation below 90% fell from 4.7±12.4% sleep time to 2.3±4.9% (P=0.1). Snoring Score was reduced from 2.5 ± 0.7 to 1.7 ± 0.8 (P< 0.001), BMI was unchanged at 28.6 ± 4.2. Supine sleep % was unchanged @ 38±26.

Conclusions: In the home environment MADs reduced RDI by 56%, & desaturation below 90% by 51%. Treatment success occurred in 65% initially then in 70% subjects after final adjustment. There were no identified confounders. Conflict of interest: Yes

Peninsula Sleep Laboratory Educational Evening "Sleep. Who needs it?" – March 2nd 2010

Associate Professor Keith Burgess MB BS, M.Sc, Ph.D, FRACP, FRCP, FACP (Respiratory and Sleep Disorders Physician) talked about "Manipulating Sleep at High Altitude" and "New Data on Dental Devices in OSA". Dr Dianne Richards B Soc. Sc (Sleep Psychologist) spoke about "Non Pharmacological Treatment for Insomnia". The evening attracted 40 General Practitioners, Dentists and Specialists and was a great success. For GP's that are interested in talks, please visit the GP's page to download a copy of the talks.

TRANSFORMATION OF OBSTRUCTIVE SLEEP APNOEA AT SEA LEVEL TO CENTRAL SLEEP APNOEA AT HIGH ALTITUDE; INFLUENCE OF CEREBRAL BLOOD FLOW

Under special circumstances Obstructive Sleep Apnoea (OSA) and Central Sleep Apnoea (CSA) can occur in the same patient at different times; the transformation of OSA at sea level to CSA at high altitude and simulated high altitude have been reported (1). Those reports lacked measures of ventilatory response or cerebral blood flow that might help explain the underlying physiological mechanisms. Here, we report data from one otherwise healthy subject (54 years) who participated in experiments investigating the effects of pharmacological-induced alterations in cerebral blood flow velocity (CBFv) during sleep monitored with full polysomnography. At sea-level he had mild OSA (AHI = 14/hr) which was completely resolved at high altitude (5,050m) and replaced with severe CSA (AHI = 108/hr). During wakefulness, whilst his resting CBFv was unaltered at high altitude from that at sea-level, his cerebrovascular response to CO2 was reduced by 38 % and the ventilatory response to hypercapnia was elevated (0.1 to 1.0 l/min/mmHg); PaCO2 fell from 40 to 25 mmHg following ascent to altitude. Since reductions in CBF-CO2 sensitivity are important determinates of eupnoeic ventilation, hypercapnic ventilatory sensitivity and breathing stability, these factors may partly explain the exacerbation of CSA. Although the mechanisms by which OSA is replaced with CSA at altitude are unclear, hypoxic-induced alterations in chemoreflex stability and upper airway muscle activity are likely to be critical factors.

1. Burgess et al Respirology 2004

This study was supported by the Otago Medical Research Foundation, Peninsula Health Care p/l, Air Liquide p/l and the Italian National Research Council who kindly provided use of the EV-K2-CNR research laboratory.

Separate Effects Of Acclimatisation And Cerebral Blood Flow On Central Sleep Apnea At High Altitude

Keith R. Burgess, Andrew Dawson, Kelly Shepherd, Marianne Swart, Kate N. Thomas, Jui-Lin Fan, Rebekah A. I. Lucas, Samuel J. E. Lucas, James D. Cotter, Karen C. Peebles, Rishi Basnyat, Philip N. Ainslie. University of Sydney, Sydney, NSW, Australia. Peninsula Sleep Laboratory, NSW, Australia; University of Otago, Dunedin, New Zealand; Nepal International Clinic, Kathmandu, Nepal.

Exposure to high altitude causes a universal increase in central sleep apnea (CSA), mediated by alterations in ventilatory control and possibly in cerebral blood flow (CBF). The extent to which CSA changes over time at high altitude, and the extent to which it can be altered by pharmacologically induced alterations in CBF is unclear.

We hypothesised that partial acclimatisation and pharmacologically induced alteration of CBF would have separate effects on the frequency and duration of central apneas during sleep at high altitude. We studied 12 normal volunteers on four occasions over a three week period at 5050m, at Lobuje in northern Nepal. Measurements included overnight polysomnography with transcranial Doppler measurement of CBF, non invasive hemodynamics and ABG analysis at the Pyramid Research Station. They were studied at the beginning and end of their stay, to control for acclimatisation, and in between the control nights they were studied after pharmacological intervention. All subjects received oral Indomethacin 100mg and iv Acetazolamide (10mg/kg) 2 hours before sleep, in random order with placebo controls, at approximately 4 day intervals. The data from the pharmacological intervention nights were compared to the mean data from the control nights.

After Indomethacin, CBF fell by 22 ± 8% and the apneas lengthened from 13.9 ± 2.2 to 15.4 ± 3.3secs (p<0.01). Central Sleep Apnea Index (CSAI) increased from 96.4 ± 30.3 to 101 ± 28.2 apneas/hr (NS).

After Acetazolamide, CBF increased by 31 ± 6% , which had no effect on apnea duration but the CSAI fell from 96.4 ± 30.3 to 53.7 ± 45.7 apneas/hr (p<0.001).

During partial acclimatisation, CSAI increased from 76.9 ± 48.9 to 115.9 ± 20.2 /hr over the 12 day period (p=0.01), and apnea duration lengthened from 13.1 ± 2.6 to 14.6 ± 2.2 secs (p<0.02). Over the same period PaCO2 declined from 29±3 to 26±2mmHg, and the rise (25±10%) in CBF upon initial exposure (days 1-4) returned to its sea-level values. We propose that the increase in apnea length with Indomethacin was due to reductions in CBF and cerebrovascular reactivity and increase in “loop gain”. However the lengthening of the apneas due to acclimatisation must be due to mechanisms that are independent of CBF.

This study was supported by the Otago Medical Research Foundation, Peninsula Health Care p/l, Air Liquide p/l and the Italian National Research Council who kindly provided use of the EV-K2-CNR research laboratory.