Despite the acknowledged importance of nutritional support for COPD patients, it is difficult to accomplish in acutely stressed individuals. A randomized trial of nutritional supplementation during an acute exacerbation was carried out in 16 hospitalized patients for a 2 week period. Six control patients consumed a standard diet supplying 1,951 $ pm$ 130 (mean $ pm$ SEM) kcal and 80 $ pm$ 6 g protein/d, while ten treatment patients, in addition to the usual diet received oral supplements (Ensure) or snacks, resulting in an intake of 2,516 $ pm$ 129 kcal (p = 0.012) and 99 $ pm$ 6 g protein/d (p = 0.059). Although the treatment subjects improved their intake over the control group, no significant improvement in nutritional status occurred in either group. / Forced vital capacity (FVC % predicted) improved significantly over the study period in treated vs control subjects (+11.10 $ pm$ 4.63 vs $-$4.50 $ pm$ 2.14; p = 0.026). Nitrogen balances were calculated for 9 subjects, and all were in negative balance ($-$8.42 $ pm$ 1.74 g nitrogen/d) with no difference between groups. / Because of the high doses of methylprednisolone administered (69.6 $ pm$ 8.3 mg/d), and their known catabolic effects, we examined whether the dose affected nitrogen balance and muscle strength. Both nitrogen balance (r = $-$0.73; p = 0.025) and grip strength (r = $-$0.76; p $<$ 0.001) worsened with higher doses of steroids. The catabolic process may have resulted from elevated energy requirements, inadequate intake of protein and energy or been induced by high doses of steroids. / Hospitalized COPD patients are highly stressed and catabolic, and the means to preventing protein wasting during an acute exacerbation of their disease remains to be established. (Abstract shortened by UMI.)

Pulmonary patients attending outpatient rehabilitation experience an enhanced ability for physical activity. The current study assessed and characterized domestic physical activity levels of new and maintenance patients to 1) compare physical activity levels of pulmonary patients on rehabilitation and non-rehabilitation days, 2) to identify factors that may contribute to low physical activity levels and 3) to compare step count levels between 2 activity monitors.Eighteen patients (age, 66.2 ± 8.8 y; FEV1, 52.1 ± 11.8%) participating in pulmonary rehabilitation wore an accelerometer and pedometer for 7 consecutive days. Patients new to pulmonary rehabilitation and maintenance patients participated in the study. Upon returning the monitors, patients returned a log sheet with the times monitors were put on and taken off each morning and night.The participants who completed the one week assessment had an average step count of 3,800 ± 1,651 steps/day, with a significant difference (p < .05) between rehabilitation days (5,468 ± 2,810 steps/day) and non-rehabilitation days (2,874 ± 1,490 steps/day). The number of minutes/day spent in moderate walking activities was also significant (p < .05) between rehabilitation (10.9 ± 16.0 minutes/day) and non-rehabilitation days (3.1 ± 5.8 minutes/day). Male waist circumference and occupational status were significantly correlated with low physical activity levels. The pedometer and accelerometer step count values were not significantly different from each other.Patients participating in pulmonary rehabilitation have significantly different activity levels between rehabilitation and non-rehabilitation days. To increase activity benefits, patients with COPD should increase activity levels on rehabilitation and non-rehabilitation days. Special consideration should be taken to help patients increase physical activity levels on non-rehabilitation days.(key words: chronic obstructive pulmonary disease, pedometer, accelerometer, pulmonary rehabilitation. / School of Physical Education, Sport, and Exercise Science

Chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF) patients show a marked reduction in exercise capacity compared to that of healthy age-matched individuals. While inadequate gas exchange and resulting hypoxemia appears as the primary factor in COPD, an impaired cardiac output is the predominant explanation for the reduced oxygen delivery in CHF. However, the extent of the contributions of other systemic factors remains unclear. In light of the potential interactions between cardiac output (Qc) and pulmonary hyperinflation, there is surprisingly little data thus far on ventilatory constraints in CHF and on the role of blood flow delivery in COPD which may further limit the exercise capacity. Thus, the purpose of this study was to compare the slope of the Qc versus oxygen uptake (VO2) response through several submaximal cycling loads in patients with moderately severe COPD and with that of moderate to severe CHF patients as well as age-matched healthy control subjects (CTRL). Also examined was the possibility that ventilatory constraints such as dynamic hyperinflation contribute to an abnormal stroke volume response in both diseases. Cardiac output was measured using the CO 2-rebreathing equilibrium technique during baseline conditions and cycling at 20, 40 and 65% of peak power in 17 COPD (Age: 64 +/- 8 yrs; FEV 1/FVC: 37 +/- 11%; FEV1: 41 +/- 15 % predicted), 10 CHF (Age: 57+/- 10 yrs; FEV1/FVC: 73.8 +/- 5.6%; FEV 1: 93 +/- 13% predicted) and 10 age-matched CTRL subjects. Inspiratory capacity (IC) was also measured for the determination of dynamic hyperinflation during the steady state exercise bouts. The results indicate that while the absolute Qc values are lower in COPD and in CHF than in CTRL during 65% peak power cycling (11.30 +/- 2.38 vs 12.40 +/- 2.08 vs 15.63 +/- 2.15 L&bull;min-1 respectively, p &lt; 0.01), likely due to their lower exercise metabolic demand. The Qc/VO2 response to increasing levels of exercise intensity was lower or normal in CHF patients compared to CTRL, while normal or hyperdynamic in most COPD patients. Indeed, the majority of patients with COPD exhibited Qc/VO2 slopes greater than 7.0, which may be indicative of a peripheral muscle bioenergetic disturbance that may drive the need for greater oxygen delivery, and thus result in an exaggerated central circulatory response.

Total body fat and muscle mass depletion has been reported in some patients with COPD. This study used simple anthropometric measurements to compare the body composition of patients with moderate-severe COPD to that of healthy controls, and examines relationships between body composition, disease severity, habitual physical activity and resting and exercise energy expenditure. Results show no significant differences in overall Heath-Carter somatotype characteristics, percent body fat, fat free mass and girth measurements between COPD and control subjects although when stratified by gender, female COPD patients exhibited a greater body fat component. Measured VO2 (L/min) at rest or during steady-state exercise was not significantly different between COPD and control subjects despite a higher exercise ventilation in patients. Neither resting or exercise energy expenditure was related to body composition, however it was related to DLCO/VA (ml·min-1·mmHg -1·L-1). Findings from this study suggest that COPD patients capable of participating in dynamic exercise studies do not exhibit total body fat and muscle depletion. Findings in women suggest that the relative decrease in FFM may be related to a relatively higher proportion of body fat and not a decrease in absolute muscle mass.

Background: Chronic obstructive pulmonary disease (COPD) is a devastating illness that affects 4.3% of the population of British Columbia over the age of 45 years. Asthma is known to coexist in 10-20% of individuals with obstructive lung disease, and adds to the substantial burden of illness posed by COPD alone. Inhaled corticosteroids (ICS) are currently recommended for the management of COPD among individuals with frequent exacerbations; however, the ability of inhaled corticosteroids to reduce death and hospitalizations among individuals with COPD is controversial. Less is known about the effectiveness of ICS among individuals who are afflicted with both COPD and asthma. Methods: We used a retrospective cohort study design and administrative data to estimate the relative effectiveness of ICS in reducing hospitalizations or death among individuals with concomitant asthma and COPD, compared with individuals with COPD alone. We used an extended Cox model to estimate this association, with a time-varying measure of exposure to ICS. Results: We did not find any association between ICS and hazard of death or hospitalization among individuals with COPD alone (HR = 0.99; 95% CI: 0.94 – 1.05), however the hazard was 18% lower (HR = 0.82; 95% CI: 0.69-0.99) among individuals with concomitant disease. Conclusions: Individuals with combined COPD and asthma show significant benefit from the use of ICS and are more responsive to the effects of ICS than individuals with COPD alone.

Obstructive sleep apnoea (OSA) is a common respiratory disorder characterised by repetitive periods of upper airway (UA) collapse during sleep. OSA is more common in males and the obese but the reasons why remain poorly understood. Abdominal obesity, particularly common in males, is likely to indirectly modulate the amount of tension (tracheal traction) exerted on the UA by the trachea and other intrathoracic structures, potentially leading to increased UA collapsibility. Other factors such as lung volume changes with obesity, altered drive to UA muscles and exaggerated arousal responses are also likely to contribute to UA instability. An investigation of these potential contributing factors forms the basis of this thesis. In the first study, the effect of external abdominal compression on UA collapsibility during sleep was investigated in a group of obese male OSA patients. A large pneumatic cuff wrapped around the abdomen was inflated to increase intra-abdominal pressure, aiming to produce an upward force on the diaphragm, designed to reduce axial tension on the UA. Abdominal compression increased end-expiratory gastric (PGA) and end-expiratory transdiaphragmatic (PDI) pressure by ~50% and produced a significant rise in UA collapsibility compared to the cuff deflated condition. These data support that increased intra-abdominal pressure has a negative effect on UA function during sleep. This effect may help explain why obesity is the leading risk factor for OSA and why OSA affects men more than women, given that abdominal obesity is particularly common in obese males. In the second study, differences in minimum expiratory (tonic) diaphragm activity during wakefulness were compared between 8 obese OSA patients and 8 healthyweight controls. Changes in tonic diaphragm activity and lung volume following sleep onset were also compared between the two groups. There was no evidence of increased tonic diaphragmatic activity during wakefulness in obese OSA patients to support significant diaphragmatic compensation for abdominal compressive effects of obesity. There were small decrements in lung volume following sleep onset in both groups (<70 ml), with significantly greater lung volume and diaphragmatic EMG decrements when sleep onsets were immediately followed by respiratory events. While lung volume decrements at sleep onset were relatively small, this does not discount that UA function is not more sensitive to effects of reduced lung volume in obese OSA patients. To more closely investigate the potential interactive effects of obesity on physiological variables likely influencing UA function, the third study investigated the temporal relationships between a comprehensive range of relevant physiological variables leading into and following the termination of obstructive apnoeas during sleep in 6 obese OSA patients. Prior to UA obstruction, diaphragm and genioglossus muscle activity decreased, while UA resistance increased. Lung volume and end-expiratory PGA and end-expiratory PDI also fell during this period, consistent with diaphragm ascent. There was a substantial increase in ventilation, muscle activity and lung volume immediately following the termination of obstructive events. Respiratory events and arousals occurred in close temporal proximity prior to and following obstructive apnoeas, supporting that cyclical respiratory events and arousals may both help to perpetuate further events. The results from this study support that there is a ‘global’ loss in respiratory drive to UA dilator and pump muscles precipitating obstructive respiratory events. The associated decreases in UA dilator muscle activity and lung volume may therefore both contribute to the propensity for the UA to obstruct. In summary, increased intra-abdominal pressure was shown to negatively impact UA airway collapsibility during sleep. A decrease in lung volume at sleep onset and prior to UA obstruction further support that lung volume decrement, coincident with a decline in overall respiratory drive, potentially contributes to the propensity for airway obstruction. Further studies are needed to elucidate the relative contribution of relatively small changes in lung volume versus changes in respiratory and UA muscle activity per se on UA patency in OSA patients. / Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2010

Masters of Science in Medicine / The relationship between COPD and laryngopharyngeal sensitivity has not been previously determined. Limited research into the relationship between COPD and swallow function suggests that patients with COPD are at increased risk of aspiration. One possible mechanism for this is a reduction in laryngopharyngeal sensitivity (LPS). Reduced laryngopharyngeal sensitivity (LPS) has been associated with an increased risk of aspiration in pathologies such as stroke, however impaired LPS has not been examined with respect to aspiration risk in COPD. The Aims of this study were to investigate the effect of COPD on laryngopharyngeal sensation using Laryngopharyngeal Sensory Discrimination Testing (LPSDT) and to determine whether a relationship between LPS and swallow function in patients with proven COPD exists. Method: 20 patients with proven COPD and 11 control subjects underwent LPSDT utilising an air-pulse stimulator (Pentax AP4000) via a nasendoscope (Pentax FNL10AP). The threshold of laryngopharyngeal sensation was measured by the air pressure required to elicit the laryngeal adductor reflex (LAR). A number of further examinations were also completed for COPD subjects. These included respiratory function testing, self-reporting questionnaire on swallowing ability (SSQ), bedside clinical examination of swallowing (MASA) and endoscopic assessment of swallowing (EAS). Results: subjects with COPD had a significantly higher LAR threshold when compared to their normal healthy counterparts (p<0.001). Positive correlations were identified for the relationships between MASA score and EAS results for presence of laryngeal penetration / aspiration (p<0.04), vallecular residue (p<0.01) and piriform residue (p<0.01). Conclusion: Patients with COPD have significantly reduced mechanosensitivity in the laryngopharynx. Patients with COPD also have impaired swallow function characterised primarily by pharyngeal stasis. These changes may place patients with COPD at increased risk of aspiration.

Doctor of Philosophy (Medicine) / Sleepiness is an important source of morbidity in the community, with potentially catastrophic consequences of occupational or driving injuries or accidents. Although many measures of sleepiness exist, there is no gold standard. The electroencephalograph (EEG) has been studied as an indicator of sleep pressure in the waking organism, or sleep depth. A mathematical model has been developed, relating the observed EEG to interactions between groups of neurons in the cortex and thalamus (Robinson, Rennie, Rowe, O'Connor, & Gordon, 2005; Robinson, Rennie, & Wright, 1997). These interactions are thought to be important in the transition from wake to sleep. Sleepiness is common in obstructive sleep apnea (OSA). The measurement of sleepiness would have great utility in quantifying the disease burden, measuring treatment response, or determining fitness for work or driving. This study will evaluate parameters derived from the EEG mathematical model as a measure of sleepiness. It is divided into the following four parts: 1. Subjects with likely OSA based on symptoms and demographics from an international database were compared with matched non-OSA controls. The OSA group showed deficits in executive function and abnormalities on evoked response potential testing. 2. Outcomes from a cross-sectional study in a sleep-clinic OSA population were aggregated by factor analysis into a five summary variables relevant to sleepiness: subjective sleepiness, mood & anxiety, memory & learning, driving, and executive functioning. 3. EEG mathematical model parameters from wake EEG recordings were related to the five summary outcomes. Executive function correlated with a parameter Z, representing the negative feedback loop between the thalamic reticular nucleus and the thalamocortical relay nuclei. 4. EEG model parameters during first NREM sleep cycle of 8 subjects with regular sleep architecture were studied. Net cortical excitation (parameter X) is predicted to increase across the cycle, while there was, as predicted, a greater inhibitory effect of the thalamic reticular nucleus upon thalamocortical relay cells (parameter Z). In this preliminary assessment, EEG model parameters reflecting thalamocortical interactions are sensitive to prefrontal lobe tasks such as executive function, which are known to be vulnerable to sleep loss and sleepiness, and these parameters also show variation with increasing sleep depth.

Thesis (Ph. D.)--Virginia Commonwealth University, 2006. / Prepared for: School of Nursing. Bibliography: leaves 117-143. Also available online via the Internet.

Diss. (sammanfattning) Umeå : Univ., 2004. / Härtill 6 uppsatser.