Prospective Students

Broad Research Area:

Mechanisms and Consequences of Sleep Disordered Breathing

There are several clinically important breathing problems during sleep. These range from sudden infant death syndrome ("cot death") to sleep apnoea in middle aged adults (repeated obstructive breathing events in sleep in otherwise healthy subjects) to asphyxial episodes or sleep hypoventilation in patients with known respiratory muscle weakness or lung disease.

Breathing disturbance and sleep fragmentation have important daytime consequences including severe daytime sleepiness, neurocognitive impairments and a substantially increased risk of traffic and other accidents. Obstructive sleep apnoea is also associated with cardiovascular disease (eg hypertension and heart disease).

Supervisors

Prof Doug McEvoy
T: 8275 1187 F: 8277 6890
E: doug.mcevoy@rgh.sa.gov.au

 

Dr Peter Catcheside
T: 8275 1187 Ext: 1309 F: 8277 6890
E: peter.catcheside@rgh.sa.gov.au

 

Dr Stuart Baulk
T: 8275 1098 F: 8275 1114
E: stuart.baulk@rgh.sa.gov.au
W: Click to go to Stuart's UniSA Homepage

Institutions

Honours and PhD studies can be undertaken at AISH through the following institutions:

Honours

Honours Projects offered in 2008

  1. Respiratory control stability during wakefulness and sleep in obstructive sleep apnoea patients versus healthy controls. Read more...
  2. Vulnerability to driving and neurocognitive impairment in obstructive sleep apnoea. Read more...
  3. The effect of sex hormones on the ventilatory & cardiovascular response to brief arousal from sleep. Read more...
  4. A randomised controlled trial of oral surfactant for the treatment of obstructive sleep apnoea & snoring in Sjogrens patients. Read more...
  5. Mechanisms of inspiratory load detection. Read more...

We are happy to discuss students' suggestions for projects that fall within our research interests.

Scholarships & Employment:

A $3000 stipend is available from AISH. Many of our students also obtain employment in the Sleep Lab as clinical sleep technicians.
To apply: Contact one of the supervisors, and your institution's honours program coordinator for further details of how to apply.

1. Respiratory control stability during wakefulness and sleep in obstructive sleep apnoea patients versus healthy controls

Respiratory control factors, such as an inherently unstable respiratory control system, may play a key role in the pathophysiology of OSA. The aim of this study is to compare respiratory control stability between OSA patients on treatment and healthy individuals during both wakefulness and sleep. We will use a technique called pseudo random binary stimulation (PRBS) to measure respiratory system "loop gain", a measure of respiratory control system stability. This technique treats the respiratory system as a negative feedback control system and employs random modulation of inhaled CO2 to probe and quantify the response of the system to perturbations within the normal physiological range.

Relevant Publications

  • Khoo MC, Kronauer RE, Strohl KP, Slutsky AS. Factors inducing periodic breathing in humans: a general model. J Appl Physiol. 1982;53:644-59.
  • Khoo MC, Gottschalk A, Pack AI. Sleep-induced periodic breathing and apnea: a theoretical study. J Appl Physiol. 1991;70:2014-24.
  • Hudgel DW, Gordon EA, Thanakitcharu S, Bruce EN. Instability of ventilatory control in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 1998;158:1142-9

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2. The effect of sex hormones on the ventilatory & cardiovascular response to brief arousal from sleep

Female sex hormones such as progesterone have a strong influence on ventilation and are thought to play a role in explaining the much lower prevalence of OSA in women compared to men. Obstructive and central sleep apnoeas are very frequently associated with brief arousal from sleep and an associated hyperventilatory "overshoot-undershoot" response that leads to low ventilatory drive around the time of the return to sleep. This period of low drive provides ideal conditions for a subsequent apnea/arousal cycle such that the ventilatory response to arousal may be key for initiating and then perpetuating cyclical breathing disturbances in sleep.

Our group has shown that the hyperventilatory response to arousal from sleep is greater in men versus women; both in healthy individuals and in OSA patients. This may indicate a protective role of female sex hormones on post-arousal ventilatory control stability. The purpose of this study is to explore this hypothesis further by examining if the ventilatory response to brief arousal from sleep in healthy women is different between the follicular and luteal phases of the menstrual cycle.

Relevant Publications

  • Jordan AS, Eckert DJ, Catcheside PG, McEvoy RD. The ventilatory response to brief arousal from NREM sleep is greater in men than in women. Am. J. Resp. Crit. Care Med. 168: 1512-1519, 2003.
  • Jordan AS, McEvoy RD, Edwards JK, Schory K, Yang CK, Catcheside PG, Fogel RB, Malhotra A, White DP. The influence of gender and upper airway resistance on the ventilatory response to arousal in obstructive sleep apnoea. J. Physiol. (Lond). 558: 993-1004, 2004.

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3. A randomised controlled trial of oral surfactant for the treatment of obstructive sleep apnoea & snoring in Sjogrens patients

Sjogren's syndrome (SS) is one of the most common chronic auto-immune diseases and is characterised by inflammation of the lacrimal and salivary glands leading to, amongst other symptoms, a dry mouth and upper airway. Our group has found some preliminary evidence that SS patients have a high prevalence of OSA suggesting that airway dryness may lead to stickier airway secretions and an upper airway more prone to collapse.

The aim of this study is to test this hypothesis further by comparing respiratory disturbance indices during sleep in SS patients receiving airway surfactant to lower airway surface tension forces versus a placebo in a randomised cross-over trial.

Relevant Publications

  • Hilditch, C.J., McEvoy, R.D., George, K.E., Thompson, C.C., Ryan, M.K., Rischmueller, M., Catcheside, P.G. Upper airway surface tension but not upper airway collapsibility is elevated in primary Sjögren's syndrome. Sleep, 2008; 31(3): 367-374.
  • Gudbjornsson B, Broman JE, Hetta J and Hallgren R. Sleep disturbances in patients with primary Sjögren's syndrome. Br J Rheumatol 32:1072-1076, 1993.
  • Jokic R, Klimaszewski A, Mink J and Fitzpatrick MF. Surface tension forces in sleep apnoea: The role of a soft tissue lubricant : A randomized double-blind, placebo controlled trial. Am J Respir Crit Care Med 175:1522-5, 1998.
  • Kirkness JP, Madronio M, Stavrinou R, Wheatley JR and Amis TC. Relationship between surface tension of upper airway lining liquid and upper airway collapsibility during sleep in obstructive sleep apnoea hypopnea syndrome. J Appl Physiol 95:1761-1766, 2003.
  • Morrell MJ, Arabi Y, Zahn BR, Meyer KC, Skatrud JB, Safwan Badr, M. Effect of surfactant on pharyngeal mechanics in sleeping humans: implications for sleep apnoea. Eur Respir J 20: 451–457, 2002.
  • Van der Touw, T, Crawford AB and Wheatley, JR. Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects. J Appl Physiol 82(1): 78–85, 1997.

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4. Vulnerability to driving and neurocognitive impairment in obstructive sleep apnoea

Increased public and medical awareness is leading to the identification of large numbers of OSA patients but the ability of road safety and health care professionals to assess motor-vehicle accident risk and advise on risk reduction is lagging seriously behind. For example, while data suggest that patients with severe OSA are at increased risk, little is known about MVA risk and driving performance in patients with mild-moderate disease. We know that healthy, young adult drivers are prone to fall-asleep accidents after partial sleep deprivation, and that low-dose alcohol acts synergistically with sleep loss to markedly impair driving. The vulnerability of OSA patients to these additional insults is unknown - yet they are common and likely to be important. Treatment of severe OSA improves driving performance and accident risk, but treatment response in certain functional domains (eg sleepiness, response time) is often incomplete, raising the spectre of ongoing driving impairment. We are currently comparing driving simulator performance in a large sample of OSA patients with that in healthy, matched controls. We are also comparing the vulnerability of patients and controls to separate conditions of sleep deprivation and low dose alcohol, and will determine the effects of CPAP treatment in a sub-sample of severely affected patients. The findings of these studies will significantly improve the clinical management of OSA, and will help inform government education and awareness campaigns, and fitness to drive regulations.

Within this larger project there is scope for a physiology honours project, focussing on one of several different aspects of vulnerability in obstructive sleep apnoea (OSA).

Relevant Publications

  • Vakulin, A., Baulk, S.D., Catcheside, P.G., Anderson, R., van den Heuvel, C.J., Banks, S. & McEvoy, R.D. Effects of moderate Sleep Deprivation and Low dose alcohol on driving simulator performance and perception measures in young men. Sleep, 2007; 30(10): 1327-33. 
  • Horne, J.A. & Baulk, S.D. (2004) Awareness of Sleepiness when Driving. Psychophysiology, 41(1): 161-5.
  • Banks, S., Catcheside, P., Lack, L., Grunstein, R.R., & McEvoy, R.D. (2004) Low Levels of Alcohol Impair Driving Simulator Performance and Reduce Perception of Crash Risk in Partially Sleep Deprived Subjects. Sleep, 27(6): 1063-7.
  • Barrett, P.R., Horne, J.A., & Reyner, L.A. (2004) Alcohol continues to affect sleepiness related driving impairment, when breath alcohol levels have fallen to near-zero. Hum Psychopharmacol Clin Exp, 19: 421-3.

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5. Mechanisms of inspiratory load detection

Humans can detect the presence of impediments to breathing with considerable acuity. The sensory mechanisms underlying these sensations likely contribute to the modulation of respiratory effort in the presence of breathing load, and may importantly contribute to key survival responses such as initiating medical treatment in asthma and waking from sleep in obstructive sleep apnoea. Almost all of the research to date concerning respiratory load detection acuity is based on the assumption that these sensations primarily arise from inspiratory muscle "length-tension inappropriateness" (i.e. flow- or volume-pressure changes). However, some data suggest that tension changes alone may primarily account for these sensations.

A greater understanding of the sensory mechanisms underlying respiratory load detection and perception has important implications for the interpretation of studies examining the effects of various interventions on respiratory sensations.

This study aims to explore the physical characteristics of breathing load most closely associated with the detection of resistive, elastic and static-pressure loads. The specific hypothesis to be tested is that load detection acuity is more closely related to changes in pressure than to changes in resistance (flow vs pressure) or elastance (volume vs pressure). This hypothesis will be tested using detailed respiratory measurements in a group of healthy volunteers who will be asked if they can detect and distinguish between differing load types of varying intensities.

Relevant Publications

  • Hlavac MC, Catcheside PG, McDonald R, Eckert DJ, Windler S, McEvoy RD. Hypoxia impairs the arousal response to external resistive loading and airway occlusion during sleep. Sleep 29(5): 624-631, 2006.
  • Eckert DJ, Catcheside PG, McDonald R, Adams AM, Webster KE, Hlavac MC, McEvoy RD. Sustained hypoxia depresses sensory processing of respiratory resistive loads. Am J Respir Crit Care Med. 172(8):1047-54, 2005.
  • Eckert DJ, Catcheside PG, Smith JH, Frith PA, McEvoy RD. Hypoxia suppresses symptom perception in asthma. Am. J. Resp. Crit. Care Med. 169(11): 1224-1230, 2004.
  • Orr RS, Jordan AS, Catcheside P, Saunders NA, McEvoy RD. Sustained isocapnic hypoxia suppresses the perception of the magnitude of inspiratory resistive loads. J Appl Physiol 2000; 89: 47-55.

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