Biomedical subjects

David R Hillman

Publications and source records attributed to David R Hillman.

14 recordsLinked to original sources

PubMed2006

The economic cost of sleep disorders.

STUDY OBJECTIVES: To determine the economic cost of sleep disorders in Australia and relate these to likely costs in similar economies. DESIGN AND SETTING: Analysis of direct and indirect costs for 2004 of sleep disorders and the fractions of other health impacts attributable to sleep disorders, using data derived from national databases (including the Australian Institute of Health and Welfare and the Australian Bureau of Statistics). MEASUREMENTS: Direct health costs of sleep disorders (principally, obstructive sleep apnea, insomnia, and periodic limb movement disorder) and of associated conditions; indirect financial costs of associated work-related accidents, motor vehicle accidents, and other productivity losses; and nonfinancial costs of burden of disease. These were expressed in US dollars (dollar). RESULTS: The overall cost of sleep disorders in Australia in 2004 (population: 20.1 million) was dollar 7494 million. This comprised direct health costs of dollar 146 million for sleep disorders and dollar 313 million for associated conditions, dollar 1956 million for work-related injuries associated with sleep disorders (net of health costs), dollar 808 million for private motor vehicle accidents (net of health costs), dollar 1201 million for other productivity losses, dollar 100 million for the real costs associated with raising alternative taxation revenue, and dollar 2970 million for the net cost of suffering. CONCLUSIONS: The direct and indirect costs of sleep disorders are high. The total financial costs (independent of the cost of suffering) of dollar 4524 million represents 0.8% of Australian gross domestic product. The cost of suffering of dollar 2970 million is 1.4% of the total burden of disease in Australia.

Australia↗

PubMed2006

Anaerobic metabolism of inspiratory muscles in COPD.

OBJECTIVE: The purpose of this study was to determine if the respiratory muscles of patients with COPD could be made to function anaerobically, as evidenced by an increase in arterial blood lactate concentration ([lactate](a)) during specific loading of the inspiratory muscles and, if so, the effect of a programme of high-intensity inspiratory muscle training on this function. METHODS: In seven patients with COPD (FEV(1) = 33 +/- 14% of predicted), measurements of [lactate](a) were made each minute during progressive inspiratory threshold loading to voluntary exhaustion. These tests were performed before and after an 8-week programme of specific high-intensity inspiratory muscle training, combined with general whole-body exercise training. RESULTS: During inspiratory muscle loading small increases in [lactate](a) (0.83 +/- 0.32 mM) were observed in two subjects before training, and in five subjects after training (0.69 +/- 0.57 mM). [Lactate](a) only increased when the inspiratory work rate exceeded 6.9 cm H(2)O L/min per kilogram of body weight, and when baseline maximum inspiratory pressure exceeded 65 cm H(2)O. CONCLUSIONS: The results of this study demonstrated that it is possible for COPD patients to increase inspiratory muscle work rate to a level requiring a major energy contribution from anaerobic glycolytic metabolism. This was only seen when inspiratory muscle strength and endurance were sufficient to allow it. Some patients who failed to demonstrate an increase in [lactate](a) at baseline did so after a programme of high-intensity inspiratory muscle training.

Anaerobic Threshold↗

PubMed2006

Relationship between upper airway and inspiratory pump muscle force in obstructive sleep apnea.

BACKGROUND: Upper airway (UA) patency during inspiration is determined by the balance between dilating forces generated by UA dilator muscle activity and collapsing forces related to the decreased intraluminal pressure that accompanies flow generated by inspiratory muscle activity. It is possible that the relative strengths of UA dilator and inspiratory pump muscles could be an important determinant of the susceptibility to UA collapse during sleep (ie, obstructive sleep apnea [OSA]). METHODS: Measurements of tongue protrusion (TP) force and maximum inspiratory pressure (Pimax) were obtained in 94 patients admitted for overnight polysomnography for suspected OSA, quantified by apnea-hypopnea index (AHI). RESULTS: There was a direct linear relationship between TP force and Pimax (r(2) = 0.37, p < 0.001). A high ratio of TP force to Pimax (greater than group 90th percentile, 0.027 kg/cm H(2)O) appeared to protect against OSA, as moderate-to-severe OSA (AHI > 20/h) was not observed in any individual with a ratio above this threshold. AHI was not linearly related to TP force, Pimax, or the ratio of TP force to Pimax. CONCLUSIONS: UA muscle strength is linearly related to inspiratory pump muscle strength. The ratio of UA muscle strength (TP force) and inspiratory pump muscle strength (Pimax) was not different between individuals with and without OSA; however, a high wakeful ratio of TP force to Pimax appears to be associated with a reduced propensity to moderate-to-severe OSA.

Adult↗

PubMed2005

Quantitative upper airway imaging with anatomic optical coherence tomography.

BACKGROUND: Measurements of upper airway size and shape are important in investigating the pathophysiology of obstructive sleep apnea (OSA) and in devising, applying, and determining the effectiveness of treatment modalities. We describe an endoscopic optical technique (anatomic optical coherence tomography, aOCT) that provides quantitative real-time imaging of the internal anatomy of the human upper airway. METHODS: Validation studies were performed by comparing aOCT- and computed tomography (CT)-derived measurements of cross-sectional area (CSA) in (1) conduits in a wax phantom and (2) the velo-, oro-, and hypopharynx during wakefulness in five volunteers. aOCT scanning was performed during sleep in one subject with OSA. RESULTS: aOCT generated images of pharyngeal shape and measurements of CSA and internal dimensions that were comparable to radiographic CT images. The mean difference between aOCT- and CT-derived measurements of CSA in (1) the wax phantom was 2.1 mm(2) with limits of agreement (2 SD) from -13.2 to 17.4 mm(2) and intraclass correlation coefficient of 0.99 (p < 0.001) and (2) the pharyngeal airway was 14.1 mm(2) with limits of agreement from -43.7 to 57.8 mm(2) and intraclass correlation coefficient of 0.89 (p < 0.001). aOCT generated quantitative images of changes in upper airway size and shape before, during, and after an apneic event in an individual with OSA. CONCLUSIONS: aOCT generates quantitative, real-time measurements of upper airway size and shape with minimal invasiveness, allowing study over lengthy periods during both sleep and wakefulness. These features should make it useful for study of upper airway behavior to investigate OSA pathophysiology and aid clinical management.

Adult↗

PubMed2005

Collapsibility of the upper airway at different concentrations of propofol anesthesia.

BACKGROUND: This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it. METHODS: Upper airway collapsibility was determined from pressure-flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 mug/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 +/- 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects. RESULTS: With increasing depth of anesthesia, (1) critical closing pressure progressively increased (-0.3 +/- 3.5, 0.5 +/- 3.7, and 1.4 +/- 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 microg/ml respectively; P < 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 +/- 9.9% of maximum at 2.5 microg/ml to 0.8 +/- 0.5% of maximum at 6.0 microg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 microg/ml but not at propofol concentrations of 4.0 and 6.0 microg/ml, whereas phasic EMGgg was unchanged. CONCLUSIONS: Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

Adult↗

PubMed2005

Function of the lower esophageal sphincter during and after high-intensity exercise.

INTRODUCTION: Gastroesophageal reflux is commonly reported during high-intensity endurance exercise in otherwise healthy asymptomatic individuals. Although the mechanisms underlying this exercise-induced reflux are unknown, it most likely reflects a failure of the primary barrier to reflux, the lower esophageal sphincter (LES). The aim of this study was to determine the influence of exercise with and without ingestion of fluid on the LES barrier pressure in asymptomatic individuals. METHODS: Seven recreational cyclists (five males) performed four 5-min bouts of cycle exercise at 90% VO2max, each separated by 1-3 min. Before, during, and after exercise, measurements were made of esophageal pressure (Pes), LES pressure (Ples), and gastric pressure (Pg). LES barrier pressure (Pb) was defined as the difference between Ples and Pg. Following exercise bouts 2 and 3, subjects ingested 600 and 200 mL of a sports drink, respectively. RESULTS: Pb before exercise was 13.1 +/- 5.2 cm H2O (+/- SD), decreased to 6.5 +/- 4.6 cm H2O during each of the four bouts of high-intensity exercise (P < 0.05), and remained decreased at 7.4 +/- 3.5 cm H2O after exercise (P < 0.05). CONCLUSIONS: High-intensity exercise reduces LES Pb during exercise in asymptomatic individuals. The magnitude of this exercise-induced impairment in LES function is unaffected by ingestion of a sports drink.

Abdominal Muscles↗

PubMed2004

The effect of learning on ventilatory responses to inspiratory threshold loading in COPD.

BACKGROUND: Progressive threshold loading (PTL) is a common test of respiratory muscle endurance. Healthy naive subjects improve endurance with successive exposures to PTL by altering their breathing responses, thus necessitating a familiarization period before reproducible measures can be obtained. This study sought to determine whether a similar "learning effect" is evident in patients with COPD, and what the mechanism of any such effect may be. METHODS: Ten subjects with COPD (FEV1 34+/-13% predicted) underwent PTL on four occasions (>24 h apart). During PTL measurements were obtained of breathing pattern and maximum threshold pressure (Pthmax) achieved. Maximum inspiratory pressure (PImax) was measured on each occasion. RESULTS: Over the four tests PImax improved by 21+/-16% (SD) (P<0.05) and Pthmax by 32+/-21% (P<0.05) with a plateau in these measures achieved by test three. Pthmax/PImax was unchanged, being 61+/-11% at test one and 67+/-12% at test four. In contrast to healthy subjects, PTL was not associated with increased expiratory time or decreased end-expiratory lung volume. CONCLUSIONS: In contrast to PImax and Pthmax, which changed with successive tests, a single measure of the ratio Pthmax/PImax may present a useful guide to the endurance capacity of the respiratory muscles in patients with COPD.

Adaptation, Physiological↗

PubMed2004

Obstructive sleep apnoea and anaesthesia.

Upper airway obstruction is common during both anaesthesia and sleep, as a result of loss of muscle tone present during wakefulness. Patients with obstructive sleep apnoea (OSA) are vulnerable during anaesthesia and sedation as the effects of loss of wakefulness are compounded by drug-induced depression of muscle activity and of arousal responses, so that they cannot respond to asphyxia. Conversely, those with 'difficult' airways during anaesthesia, either because of problems with maintenance of airway patency without tracheal intubation or because intubation itself is problematic, are at increased risk of OSA. These relationships have clinical importance. On the one hand identification of patients with OSA forewarns the anaesthetist of potential difficulty with airway maintenance intra- and postoperatively, influencing choice of anaesthetic technique and postoperative nursing environment. On the other hand difficulty with airway maintenance during anaesthesia should prompt further investigation for the possibility of OSA.

Airway Obstruction↗

PubMed2004

Dyspnoea in COPD: can inspiratory muscle training help?

Chronic obstructive pulmonary disease (COPD) is a progressive, common and costly condition. Dyspnoea frequently limits activity and reduces health-related quality of life. In addition to impaired lung function, peripheral muscle deconditioning and respiratory muscle dysfunction also contribute to dyspnoea and reduced exercise capacity. Pulmonary rehabilitation using whole body exercise training improves peripheral muscle function and reduces dyspnoea but does not improve respiratory muscle function. Providing that adequate training intensities are utilised, specific loading of the inspiratory muscles with commercially available hand-held devices can improve inspiratory muscle strength and endurance. Several studies have investigated the effects of inspiratory muscle training on dyspnoea in COPD subjects. Results of these studies are conflicting, most likely reflecting methodological shortcomings including insufficient training load, insensitive outcome measures, and inadequate statistical power. This paper describes the origin of dyspnoea in COPD, with particular attention given to the role of inspiratory muscle dysfunction in its genesis and its possible amelioration through inspiratory muscle training.

Breathing Exercises↗

PubMed2004

Physiologic responses to incremental and self-paced exercise in COPD: a comparison of three tests.

OBJECTIVES: To investigate cardiorespiratory and dyspnea responses to incremental and self-paced exercise tests in patients with COPD. DESIGN: A prospective within-subject design was used. PATIENTS: Twenty stable subjects (15 men), with a mean (+/- SD) age of 64.0 +/- 7.5 years and moderate-to-severe COPD (ie, mean FEV(1), 0.8 +/- 0.3 L and 28.9 +/- 7.9% predicted) were studied. METHODS: Each subject completed a 6-min walk test (6MWT), an incremental shuttle walking test (ISWT), and a cycle ergometer test (CET), within a 2-week period. The tests were performed at least 24 h apart. Standardized encouragement was utilized in each test with the aim of maximizing performance. Heart rate (HR) and dyspnea were measured each minute throughout the tests, and pulse oximetric saturation (Spo(2)) was measured before and immediately after each test. The distances walked in the 6MWT and ISWT were compared to peak oxygen uptake (Vo(2)) values from the CET. RESULTS: HR increased linearly with increasing workload during the CET and ISWT, but increased alinearly with a disproportionate increase early in the 6MWT. In contrast, dyspnea scores increased linearly during the 6MWT, but increased alinearly with a disproportionate increase late during the CET and ISWT. Peak HR and dyspnea were not significantly different between tests. Spo(2) was significantly lower at the end of both walking tests compared to that at the end of the CET (p < 0.001). The distance walked in both the ISWT and 6MWT were related to peak Vo(2) values on the CET (for both tests, r = 0.73; p < 0.001). CONCLUSIONS: The patterns of response in HR and dyspnea seen during the 6MWT suggest that patients with COPD titrate exertion against dyspnea to achieve a peak tolerable intensity. This strategy is not possible in an externally paced ISWT or CET. However, it is a limited strategy, with performance converging at higher workloads. Similar peak exercise responses were achieved in the 6MWT, ISWT, and CET. Greater oxygen desaturation was observed during the field walking tests, suggesting that both the ISWT and 6MWT are more sensitive than the CET in detecting exercise-induced hypoxemia and in assessing ambulatory oxygen therapy needs.

Aged↗

PubMed2003

Effect of surface tension of mucosal lining liquid on upper airway mechanics in anesthetized humans.

Upper airway (UA) patency may be influenced by surface tension (gamma) operating within the (UAL). We examined the role of gamma of UAL in the maintenance of UA patency in eight isoflurane-anesthetized supine human subjects breathing via a nasal mask connected to a pneumotachograph attached to a pressure delivery system. We evaluated 1). mask pressure at which the UA closed (Pcrit), 2). UA resistance upstream from the site of UA collapse (RUS), and 3). mask pressure at which the UA reopened (Po). A multiple pressure-transducer catheter was used to identify the site of airway closure (velopharyngeal in all subjects). UAL samples (0.2 microl) were collected, and the gamma of UAL was determined by using the "pull-off force" technique. Studies were performed before and after the intrapharyngeal instillation of 5 ml of exogenous surfactant (Exosurf, Glaxo Smith Kline). The gamma of UAL decreased from 61.9 +/- 4.1 (control) to 50.3 +/- 5.0 mN/m (surfactant; P < 0.02). Changes in Po, RUS, and Po - Pcrit (change = control - surfactant) were positively correlated with changes in gamma (r2 > 0.6; P < 0.02) but not with changes in Pcrit (r2 = 0.4; P > 0.9). In addition, mean peak inspiratory airflow (no flow limitation) significantly increased (P < 0.04) from 0.31 +/- 0.06 (control) to 0.36 +/- 0.06 l/s (surfactant). These findings suggest that gamma of UAL exerts a force on the UA wall that hinders airway opening. Instillation of exogenous surfactant into the UA lowers the gamma of UAL, thus increasing UA patency and augmenting reopening of the collapsed airway.

Adult↗

PubMed2003

Heterogeneous activity of the human genioglossus muscle assessed by multiple bipolar fine-wire electrodes.

Genioglossus (GG) electrical activity [measured by electromyogram (EMGgg)] is best measured by intramuscular electrodes; however, the homogeneity of EMGgg is undefined. We investigated the relationships between EMGgg and the site from which activity was measured to determine whether and to what extent inhomogeneity in activity occurred. Eight healthy human volunteers underwent ultrasound to determine GG depth and width. Four pairs of electrodes were then inserted percutaneously into the left and right GG muscle, anteriorly and posteriorly. Additional configurations were obtained by connecting electrodes across the midline and along each muscle belly. EMGgg activity was simultaneously recorded from these 10 configurations at rest and during various respiratory maneuvers. Heterogeneous behavior of the GG was evidenced by 1) the variable presence of phasic EMGgg at rest, which was undetectable in two subjects but evident in 65% of configurations in six subjects and present in all configurations in all subjects during voluntary hyperventilation; 2) a greater amplitude of EMGgg response to pharyngeal square-wave negative pressure in anterior than posterior configurations (14.1 +/- 7.1 vs. 8.5 +/- 5.1% of maximum, P < 0.05); and 3) variable (linear and alinear) relationships between EMGgg and lingual force within and between subjects. We hypothesize that regional differences in density and type of muscle fiber are the most likely sources of heterogeneity in these responses.

Adult↗

PubMed2002

Comparison of upper airway collapse during general anaesthesia and sleep.

Measurement of the collapsibility of the upper airway while a patient is awake is not a good guide to such collapsibility during sleep, presumably because of differences in respiratory drive, muscle tone, and sensitivity of reflexes. To assess whether a relation existed between general anaesthesia and sleep, we measured collapsibility of the upper airway during general anaesthesia and severity of sleep-disordered breathing in 25 people who were having minor surgery on their limbs. Anaesthetised patients who needed positive pressure to maintain airway patency had more severe sleep-disordered breathing than did those whose airways remained patent at or below atmospheric pressure. Such an association was strongest during rapid-eye-movement (REM) sleep. Our findings suggest that sleep-disordered breathing should be considered in all patients with a pronounced tendency for upper airway obstruction during anaesthesia or during recovery from it.

Adult↗

PubMed2002

Collapsibility of the upper airway during anesthesia with isoflurane.

BACKGROUND: The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. METHODS: To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. RESULTS: The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. CONCLUSIONS: Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

Adult↗