100,517 research outputs found
Nutritional assessment and support of the stable COPD patient
This reference reviews strategies used to assess, treat, and manage patients in each phase of chronic obstructive pulmonary disease (COPD), including the latest diagnostic modalities to identify and distinguish its components in the earlier stages. The 45 contributions discuss therapeutic approaches to enhance quality of life and modify the course of COPD, solutions to common surgical dilemmas, techniques to increase stability and facilitate rehabilitation in patient care, depression and anxiety in patients, pathophysiological factors contributing to dyspnea and exercise limitation, and pharmacotherapy. Edited by Similowski and Jean-Philippe Derenne (both of Groupe Hospitalier Pitié- Salpetrière), and William A. Whitelaw (pulmonary medicine, U. of Calgary). Annotation c. Book News, Inc., Portland, OR (booknews.com
Postural lung volume reduction, expiratory flow limitation, and orthopnoea in diaphragmatic weakness: Preliminary observations
Effects of venous compression of the legs on overnight rostral fluid shift and obstructive sleep apnea
The amount of fluid displaced overnight from the legs into the neck as a consequence of lying recumbent
correlates with the number of apneas and hypopneas per hour of sleep (AHI). Sedentary living promotes
dependent fluid accumulation in the legs that can be counteracted by venous compression of the legs
(compression stockings). We hypothesized that, in non-obese sedentary men with obstructive sleep
apnea (OSA), wearing compression stockings during daytime will reduce the AHI by reducing the amount
of fluid available for the displacement into the neck overnight. Polysomnography and measurement of
overnight changes in leg fluid volume and neck circumference were performed at baseline and after one
day of legs venous compression. The median AHI decreased from 30.9 (interquartile range 19.6–60.4) to
23.4 (12.9–31.8) (P = 0.016) in association with a median 40% reduction in the change in leg fluid volume
(P = 0.016) and a median 42% reduction in the increase in neck circumference (P = 0.016). These results
provide proof-of-principle that overnight fluid displacement into the neck plays a causative role in OSA
Letter, [Author unclear] to Paulina T. Merritt
Handwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Nutritional assessment and support of the stable COPD patient
This reference reviews strategies used to assess, treat, and manage patients in each phase of chronic obstructive pulmonary disease (COPD), including the latest diagnostic modalities to identify and distinguish its components in the earlier stages. The 45 contributions discuss therapeutic approaches to enhance quality of life and modify the course of COPD, solutions to common surgical dilemmas, techniques to increase stability and facilitate rehabilitation in patient care, depression and anxiety in patients, pathophysiological factors contributing to dyspnea and exercise limitation, and pharmacotherapy. Edited by Similowski and Jean-Philippe Derenne (both of Groupe Hospitalier Pitié- Salpetrière), and William A. Whitelaw (pulmonary medicine, U. of Calgary). Annotation c. Book News, Inc., Portland, OR (booknews.com
Dynamic hyperinflation and flow limitation during methacholine-induced bronchoconstriction in asthma
The best peak expiratory flow is flow-limited and effort independent in normal subjects.
Postural preinspiratory cortical activity, genioglossus activity and fluid shift in awake obstructive sleep apnoea patients
The anatomy and mechanical properties of the upper airway (UA) depend on posture. Lying in a supine position causes cephalad fluid shift to the neck, thus narrowing the UA and pre- disposing the individual to obstructive sleep apnoea (OSA). Increased UA dilator muscle activity during wakefulness prevents the UA collapse but the underlying mechanism has not yet been elucidated. In the sitting position during wakefulness, some OSA patients exhibit preinspiratory cortical activity (preinspiratory potential, PIP) probably related to UA abnormalities. The aim of this study was to investigate changes in the preinspiratory cortical activity and UA dilator muscle in OSA patients during postural challenge. An electroencephalogram was used to detect PIP, and the genioglossus electromyographic activity and ventilation were analysed in 17 awake, male OSA patients while they were sitting, just after lying down, and then in response to leg positive pressure to enhance cephalad fluid shift. The prevalence of PIP decreased from 53% (sitting) to 12% (supine) (P = 0.002) in association with increased genioglossus activity (tonic from median (25th, 75th centiles) 2.3 (1.8, 2.8)% to 3.6 (1.7, 5.0)% of voluntary deglutition, P = 0.019; phasic from 2.3 (1.9, 2.8)% to 3.7 (2.0, 6.1)%, P = 0.024), and with increased transcutaneous carbon dioxide pressure (from 43.0 (42.4, 44.2) to 44.6 (43.5, 45.2) mmHg). No change was observed during leg-positive-pressure application. Moving from the sitting position to the supine position reduces respiratory-related premotor cortical activity in awake OSA patients. The concomitant increase in genioglossus activity, therefore, is not driven by cortical respiratory activity
Electroencephalographic evidence for pre-motor cortex activation during inspiratory loading in humans
Faced with mechanical inspiratory loading, awake animals and anaesthetized humans develop
alveolar hypoventilation, whereas awake humans do defend ventilation. This points to a
suprapontine compensatory mechanism instead of or in addition to the ‘traditional’ brain-
stem respiratory regulation. This study assesses the role of the cortical pre-motor representation
of inspiratory muscles in this behaviour. Ten healthy subjects (age 19–34 years, three men)
were studied during quiet breathing, CO2-stimulated breathing, inspiratory resistive loading,
inspiratory threshold loading, and during self-paced voluntary sniffs. Pre-triggered ensemble
averaging of Cz EEG epochs starting 2.5 s before the onset of inspiration was used to
look for pre-motor activity. Pre-motor potentials were present during voluntary sniffs in all
subjects (average latency (±S.D.): 1325 ± 521 ms), but also during inspiratory threshold loading
(1427 ± 537 ms) and during inspiratory resistive loading (1109 ± 465 ms). Pre-motor potentials
were systematically followed by motor potentials during inspiratory loading. Pre-motor
potentials were lacking during quiet breathing (except in one case) and during CO2-stimulated
breathing (except in two cases). The same pattern was observed during repeated experiments
at an interval of several weeks in a subset of three subjects. The behavioural component of
inspiratory loading compensation in awake humans could thus depend on higher cortical motor
areas. Demonstrating a similar role of the cerebral cortex in the compensation of disease-related
inspiratory loads (e.g. asthma attacks) would have important pathophysiological implications:
it could for example contribute to explain why sleep is both altered and deleterious in such
situations
Effect of salbutamol on dynamic hyperinflation in chronic obstructive pulmonary disease patients.
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