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J Hedner,
L Grote,
M Bonsignore,
W McNicholas,
P Lavie,
G Parati, P Sliwinski,
F Barbé,
W De Backer,
P Escourrou, [......],
M Pretl,
R Riha,
D Rodenstein,
T Saaresranta,
R Schulz,
R Tkacova,
G Varoneckas,
A Vitols,
H Vrints,
J Zielinski
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ABSTRACT: The European Sleep Apnoea Database (ESADA) reflects a network of 22 sleep disorder centres in Europe enabled by a COST action B26 programme. This ongoing project aims to describe differences in standard clinical care of patients with obstructive sleep apnoea (OSA) and to establish a resource for genetic research in this disorder. Patients with suspected OSA are consecutively included and followed up according to local clinical standards. Anthropometrics, medical history, medication, daytime symptoms and sleep data (polysomnography or cardiorespiratory polygraphy) are recorded in a structured web-based report form. 5,103 patients (1,426 females, mean±sd age 51.8±12.6 yrs, 79.4% with apnoea/hypopnoea index (AHI) ≥5 events·h(-1)) were included from March 15, 2007 to August 1, 2009. Morbid obesity (body mass index ≥35 kg·m(-2)) was present in 21.1% of males and 28.6% of females. Cardiovascular, metabolic and pulmonary comorbidities were frequent (49.1%, 32.9% and 14.2%, respectively). Patients investigated with a polygraphic method had a lower AHI than those undergoing polysomnography (23.2±23.5 versus 29.1±26.3 events·h(-1), p<0.0001). The ESADA is a rapidly growing multicentre patient cohort that enables unique outcome research opportunities and genotyping. The first cross-sectional analysis reveals a high prevalence of cardiovascular and metabolic morbidity in patients investigated for OSA.
European Respiratory Journal 05/2011; 38(3):635-42. · 5.89 Impact Factor
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I Fietze,
T Penzel,
A Alonderis,
F Barbe,
M R Bonsignore,
P Calverly,
W De Backer,
K Diefenbach,
V Donic,
M M Eijsvogel, [......],
P Steiropoulos,
J Svaza,
Z Tomori,
P Tonnesen,
G Varoneckas,
J Verbraecken,
J Vesely,
A Vitols,
J Zielinski,
W T McNicholas
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ABSTRACT: In Europe, the services provided for the investigation and management of obstructive sleep apnoea (OSA) varies from country to country. The aim of this questionnaire-based study was to investigate the current status of diagnostic pathways and therapeutic approaches applied in the treatment of OSA in Europe, qualification requirements of physicians involved in diagnosis and treatment of OSA, and reimbursement of these services.
Two questionnaires were sent to 39 physicians in 22 countries in Europe. In order to standardize the responses, the questionnaire was accompanied by an example.
Sleep centers from 21 countries (38 physicians) participated. A broad consistency among countries with respect to the following was found: pathways included referral to sleep physicians/sleep laboratories, necessity for objective diagnosis (primarily by polysomnography), use of polygraphic methods, analysis of polysomnography (PSG), indications for positive airway pressure (PAP) therapy, application of standard continuous PAP (CPAP) therapy (100% with an CPAP/APAP ratio of 2.24:1), and the need (90.5%) and management of follow-up. Differences were apparent in reimbursement of the diagnostic procedures and follow-up, in the procedures for PAP titration from home APAP titration with portable sleep apnea monitoring (38.1%) up to hospital monitoring with PSG and APAP (85.7%), and in the qualification requirements of sleep physicians.
Management of OSA in different European countries is similar except for reimbursement rules, qualification of sleep specialists and procedures for titration of the CPAP treatment. A European network (such as the one accomplished by the European Cooperation in Science and Technology [COST] B26 Action) could be helpful for implementing these findings into health-service research in order to standardize management in a cost effective perspective.
Sleep Medicine 02/2011; 12(2):190-7. · 3.40 Impact Factor
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A Prejbisz,
M Makowiecka-Ciesla,
K Paschalis-Purtak,
B Pucilowska-Jankowska,
P Bielen,
M Kluk,
G Kowalewski,
I Cendrowska-Demkow,
E Florczak,
T Buchner, P Sliwinski,
A Januszewicz
Journal of Hypertension - J HYPERTENSION. 01/2010; 28.
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K Popko,
E Gorska,
O Potapinska,
M Wasik,
A Stoklosa,
R Plywaczewski,
M Winiarska,
D Gorecka, P Sliwinski,
M Popko,
T Szwed,
U Demkow
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ABSTRACT: Obesity is one of the most commonly identified factors for the obstructive sleep apnea syndrome (OSAS). Adipose tissue is the source of many cytokines, among them there are IL-6, IL-1, and TNF-alpha. The level of inflammatory cytokines increases in people with OSAS and obesity. The aim of this study was to evaluate the distribution of genotypes in inflammatory cytokine genes in people with obesity-related OSAS. The examined group consisted of 102 person with obesity related-OSAS and 77 normal weight person without OSAS. Genotyping of DNA sequence variation was carried out by restriction enzyme (IL-1: Taq I, IL-6: Lwe I, TNF-alpha: Nco I) analysis of PCR amplified DNA. The study revealed a significant correlation between polymorphism located in the promoter region of inflammatory cytokine genes and obesity-related OSAS.
Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 01/2009; 59 Suppl 6:607-14. · 2.27 Impact Factor
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A Alonderis,
F Barbé,
M Bonsignore,
P Calverley,
W De Backer,
K Diefenbach,
V Donic,
F Fanfulla,
I Fietze,
K Franklin, [......],
D Rodenstein,
A Sanna,
R Schulz,
E Sforza, P Sliwinski,
Z Tomori,
P Tonnesen,
G Varoneckas,
J Zielinski,
K Kostelidou
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ABSTRACT: Sleep apnoea syndrome (SAS), one of the main medical causes of excessive daytime sleepiness, has been shown to be a risk factor for traffic accidents. Treating SAS results in a normalized rate of traffic accidents. As part of the COST Action B-26, we looked at driving license regulations, and especially at its medical aspects in the European region.
We obtained data from Transport Authorities in 25 countries (Austria, AT; Belgium, BE; Czech Republic, CZ; Denmark, DK; Estonia, EE; Finland, FI; France, FR; Germany, DE; Greece, GR; Hungary, HU; Ireland, IE; Italy, IT; Lithuania, LT; Luxembourg, LU; Malta, MT; Netherlands, NL; Norway, EC; Poland, PL; Portugal, PT; Slovakia, SK; Slovenia, SI; Spain, ES; Sweden, SE; Switzerland, CH; United Kingdom, UK).
Driving license regulations date from 1997 onwards. Excessive daytime sleepiness is mentioned in nine, whereas sleep apnoea syndrome is mentioned in 10 countries. A patient with untreated sleep apnoea is always considered unfit to drive. To recover the driving capacity, seven countries rely on a physician's medical certificate based on symptom control and compliance with therapy, whereas in two countries it is up to the patient to decide (on his doctor's advice) to drive again. Only FR requires a normalized electroencephalography (EEG)-based Maintenance of Wakefulness Test for professional drivers. Rare conditions (e.g., narcolepsy) are considered a driving safety risk more frequently than sleep apnoea syndrome.
Despite the available scientific evidence, most countries in Europe do not include sleep apnoea syndrome or excessive daytime sleepiness among the specific medical conditions to be considered when judging whether or not a person is fit to drive. A unified European Directive seems desirable.
Sleep Medicine 06/2008; 9(4):362-75. · 3.40 Impact Factor
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ABSTRACT: Leptin is an adipocyte-derived hormone regulating energy homeostasis and body weight. Leptin concentration is increased in patients with the obstructive sleep apnea syndrome (OSAS). Leptin receptor (LEPR) is a single transmembrane protein belonging to the superfamily of cytokine receptors related by a structure to the hemopoietin receptor family. The aim of the present study was to evaluate the frequency of distribution of leptin receptor gene polymorphism GLN223ARG in OSAS patients compared with healthy controls. The examined group included 179 subjects: 102 OSAS patients (74 men and 28 women) and 77 non-apneic controls (39 men and 38 women). Genomic DNA was isolated with the use of a column method and genotyping of DNA sequence variation was carried out by restriction enzyme analysis of PCR-amplified DNA. The results revealed a significant correlation between the polymorphism of LEPR and OSAS. Carriers of Arg allele in homozygotic genotype Arg/Arg and heterozygotic genotype Gln/Arg were more often obese and developed OSAS than the group of carriers of homozygotic Gln/Gln genotype. This tendency was observed in the whole examined population and in the group of obese women. We also found the highest levels of total cholesterol, LDL, HDL, and triglycerides in the group of homozygotic Arg/Arg genotype carriers, lower in heterozygotic Gln/Arg genotype carriers, and the lowest in the group of persons carring homozygotic Gln/Gln genotype. The presence of Arg allel seems linked to a higher risk of obesity and higher lipid levels in OSAS patients. OSAS may have a strong genetic basis due to the effects from a variety of genes including those for leptin receptor.
Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 12/2007; 58 Suppl 5(Pt 2):551-61. · 2.27 Impact Factor
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Revue des Maladies Respiratoires 10/2001; 18(4 Pt 2):S15-7. · 0.59 Impact Factor
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ABSTRACT: Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V E) was 12.2 +/- 1.9 L/min (mean +/- SD) at rest, and increased progressively (p < 0.001) to 31.0 +/- 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 +/- 3% of TLC at end-exercise. Pdi at rest was 9.4 +/- 3.2 cm H(2)O and increased during the first two thirds of exercise (p < 0.001) to plateau at about 13 cm H(2)O. EAdi was 24 +/- 6% of voluntary maximal at rest and increased progressively during exercise (p < 0.001) to reach 81 +/- 7% at end-exercise. In conclusion, dynamic hyperinflation during exhaustive exercise in patients with COPD reduces diaphragm pressure-generating capacity, promoting high levels of diaphragm activation.
American Journal of Respiratory and Critical Care Medicine 06/2001; 163(7):1637-41. · 11.08 Impact Factor
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ABSTRACT: Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients.
European Respiratory Journal 11/2000; 16(4):684-90. · 5.89 Impact Factor
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ABSTRACT: We studied three professional flautists while playing to determine: (1) what respiratory muscles and percent vital capacity (%VC) were used; (2) how mouth pressure (Pm), embouchure resistance (Rem), embouchure aperture (Aem), flow (V) and velocity (Vel) affect sound loudness (I) and frequency (F). We measured Pm, esophageal, gastric, transdiaphragmatic, transpulmonary (PL) pressures, diaphragmatic EMG, sound and chest wall displacements directly. Lung volume (VL) was estimated from PL during playing and the static deflation PL-VL curve measured separately; V from Delta VL/Delta t; Rem from Pm/(Delta VL/Delta t). Staccati and sustained notes at different F and I were performed. I increased mainly with V and F with Vel. V and Vel are independently controlled by Pm and Aem. The variation of mean Pm was small (6-11 cm H(2)O) and large for VC (72-83%) suggesting braking inspiratory muscle activity while playing. However, rib cage (RC) and abdominal (Ab) motion were different for each subject. One displaced Ab>RC at high VL and RC>Ab at low VL, another the opposite pattern; the third was in between. We conclude that while different flautists use different strategies to control Pm, the results are similar. Independent control of V and Vel by Pm and Aem allow flautists to control I and F regardless of how Pm is generated.
Respiration Physiology 06/2000; 121(1):33-44.
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ABSTRACT: It is suggested that oxygen flow be increased by 1 L/min during sleep in COPD patients undergoing long-term oxygen therapy (LTOT) in order to avoid nocturnal desaturations. The purpose of this study was to investigate the occurrence of nocturnal desaturations while breathing oxygen in COPD patients receiving LTOT.
Inpatient/university hospital.
We studied 82 consecutive COPD patients. Their functional characteristics were as follows (mean +/- SD): FVC, 2.15 +/- 0.69 L; FEV(1), 0.87 +/- 0.33 L; PaO(2), 51.6 +/- 5 mm Hg; and PaCO(2), 47 +/- 8 mm Hg.
Overnight pulse oximetry (PO) was performed twice: (1) while breathing air and (2) while breathing supplemental oxygen assuring satisfactory diurnal resting oxygenation (mean PaO(2) during oxygen breathing, 67 +/- 6 mm Hg; mean arterial oxygen saturation [SaO(2)] during oxygen breathing, 93%).
PO performed while patients were breathing air showed a mean overnight SaO(2) of 82.7 +/- 6.7%. Patients spent 90% of the recording time with an SaO(2) of < 90%. While breathing oxygen, 43 patients (52.4%) remained well oxygenated. Their mean overnight SaO(2) while breathing oxygen was 94.4 +/- 2.1%, and time spent with saturation < 90% was 6.9 +/- 8.6%. Thirty-nine patients (47.6%) spent > 30% of the night with an SaO(2) of < 90% while breathing supplemental oxygen. Their mean overnight SaO(2) while breathing oxygen was 87.1 +/- 4.5%, and time spent with an SaO(2) of < 90% was 66.1 +/- 24.7% of the recording time. Comparison of ventilatory variables and daytime blood gases between both groups revealed statistically significantly higher PaCO(2) on air (p < 0.001) and on oxygen (p < 0. 05), and lower PaO(2) on oxygen (p < 0.05) in the group of patients demonstrating significant nocturnal desaturation.
We conclude that about half of COPD patients undergoing LTOT need increased oxygen flow during sleep. Patients with both hypercapnia (PaCO(2) > or = 45 mm Hg) and PaO(2) < 65 mm Hg while breathing oxygen are most likely to desaturate during sleep.
Chest 03/2000; 117(3):679-83. · 5.25 Impact Factor
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ABSTRACT: Ten normal and four moderate to severe stutterers participated in the study. Pleural (Ppl) and abdominal (Pab) pressure was studied using oesophageal and gastric balloon catheter systems and VL (VL) was studied using magnetometry. The classical Campbell diagram was modified by plotting Pab versus VL. In a preliminary study we determined whether a surrogate curve could be substituted for the true curve in the Campbell diagram. We obtained true relaxation curves in six subjects. We obtained surrogate chest wall relaxation curves by joining the Pab value at functional residual capacity (FRC) to a point on the dynamic expiratory Pab, VL curve where Pab had decreased to half its maximum inspiratory excursion. In order to obtain the mirror image of the elastic recoil curve of the lung subjects breathed slowly from FRC to total lung capacity. Dynamic Pab, VL and Ppl, VL measurements during quiet breathing and speech were superimposed on static lung and chest wall curves. The simultaneous plot of Ppl and Pab provided a continuous measure of transdiaphragmatic pressure as a function of VL. We inferred non-diaphragmatic muscle recruitment vis-à-vis the diaphragm by the relationship of Pab to Ppl and Pab to the relaxation curve. We compared dynamic Ppl during phonation with that during breath-holding with the glottis open at the same VL, as an estimate of subglottic pressure (Psg). Analysis of variance testing showed that the true, surrogate and predicted relaxation slopes were not significantly different. The strategies that stutterers used to speak were either higher or lower VL than normal subjects and they had a different pattern of respiratory muscle recruitment. Stutterers were unable to achieve the appropriate degree of recruitment to develop and maintain a normal Psg for conversational speech and this contributed to dysfluency. We conclude that the quiet breathing loops can provide a reasonable approximation to the relaxation curve in normal healthy subjects and that modifications to the Campbell diagram provide useful means of measuring Psg and assessing respiratory muscle recruitment patterns.
Respirology 10/1999; 4(3):213-22. · 2.42 Impact Factor
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ABSTRACT: During exercise, dynamic hyperinflation-induced intrinsic positive end-expiratory pressure (PEEPi) and decreased dynamic lung compliance (CL,dyn) of patients with chronic obstructive pulmonary disease (COPD) increase the elastic work of inspiration (Wi) more than would be predicted from the increase in tidal volume (VT). This contributes significantly to their exertional breathlessness. In 10 stable patients with COPD, the dynamic Wi was measured during incremental bicycle exercise to exhaustion. The total Wi was then partitioned into the portion required to overcome PEEPi (Wi,PEEPi) and nonPEEPi elastic load (Wi,nonPEEPi). The latter is used to overcome the increase in the total respiratory system elastance during inflation. From resting breathing to peak exercise, Wi more than doubled (p<0.001). This increase was largely due to Wi,PEEPi, which significantly rose from 1.7+/-0.3 to 5.3+/-0.8 L x cm H2O(-1) (p<0.001). In comparison, Wi,nonPEEPi increased from only 3.0+/-0.4 to 5.1+/-0.5 L x cm H2O(-1) (p<0.01). Consequently, Wi,PEEPi as a fraction of total Wi increased from 35.5+/-5.6 to 51.0+/-3.3% (p<0.02). In addition, the measured Wi,nonPEEPi at peak exercise, when expressed as a percentage of its value during resting breathing, was 25% more than that predicted from the increase in VT alone. Assuming a constant chest wall compliance, this can be attributed to the exercise-induced decrease in CL,dyn, which was 0.27+/-0.04 and 0.17+/-0.02 L x cm H2O(-1) (p<0.01), respectively, during resting breathing and peak exercise. In conclusion, the dynamic hyperinflation-induced intrinsic positive end-expiratory pressure is more important than the increase in tidal volume in raising the work of inspiration during exercise in patients with chronic obstructive pulmonary disease; the decrease in dynamic lung compliance plays a definite but less important role.
European Respiratory Journal 02/1998; 11(2):416-21. · 5.89 Impact Factor
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ABSTRACT: We measured pressures and power of diaphragm, rib cage, and abdominal muscles during quiet breathing (QB) and exercise at 0, 30, 50, and 70% maximum workload (Wmax) in five men. By three-dimensional tracking of 86 chest wall markers, we calculated the volumes of lung- and diaphragm-apposed rib cage compartments (Vrc,p and Vrc,a, respectively) and the abdomen (Vab). End-inspiratory lung volume increased with percentage of Wmax as a result of an increase in Vrc,p and Vrc,a. End-expiratory lung volume decreased as a result of a decrease in Vab. DeltaVrc,a/DeltaVab was constant and independent of Wmax. Thus we used DeltaVab/time as an index of diaphragm velocity of shortening. From QB to 70% Wmax, diaphragmatic pressure (Pdi) increased approximately 2-fold, diaphragm velocity of shortening 6.5-fold, and diaphragm workload 13-fold. Abdominal muscle pressure was approximately 0 during QB but was equal to and 180 degrees out of phase with rib cage muscle pressure at all percent Wmax. Rib cage muscle pressure and abdominal muscle pressure were greater than Pdi, but the ratios of these pressures were constant. There was a gradual inspiratory relaxation of abdominal muscles, causing abdominal pressure to fall, which minimized Pdi and decreased the expiratory action of the abdominal muscles on Vrc,a gradually, minimizing rib cage distortions. We conclude that from QB to 0% Wmax there is a switch in respiratory muscle control, with immediate recruitment of rib cage and abdominal muscles. Thereafter, a simple mechanism that increases drive equally to all three muscle groups, with drive to abdominal and rib cage muscles 180 degrees out of phase, allows the diaphragm to contract quasi-isotonically and act as a flow generator, while rib cage and abdominal muscles develop the pressures to displace the rib cage and abdomen, respectively. This acts to equalize the pressures acting on both rib cage compartments, minimizing rib cage distortion.
Journal of Applied Physiology 11/1997; 83(4):1256-69. · 3.75 Impact Factor
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ABSTRACT: Nine healthy subjects (age 31 +/- 4 yr) exercised with and without expiratory-flow limitation (maximal flow approximately 1 l/s). We monitored flow, end-tidal PCO2, esophageal (Pes) and gastric pressures, changes in end-expiratory lung volume, and perception (sensation) of difficulty in breathing. Subjects cycled at increasing intensity (+25 W/30 s) until symptom limitation. During the flow-limited run, exercise performance was limited in all subjects by maximum sensation. Sensation was equally determined by inspiratory and expiratory pressure changes. In both runs, 90% of the variance in sensation could be explained by the Pes swings (difference between peak inspiratory and peak expiratory Pes). End-tidal PCO2 did not explain any variance in sensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects, during normal as well as expiratory flow-limited exercise, the pleural pressure generation of the expiratory muscles is equally related to the perception of difficulty in breathing as that of the inspiratory muscles.
Journal of Applied Physiology 10/1997; 83(3):936-47. · 3.75 Impact Factor
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ABSTRACT: Inspiratory muscles are weak and contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). Differential inspiratory pressure contributions from the diaphragm and inspiratory rib cage muscles (RCMs) during exercise in patients with COPD patients are insufficiently described. We measured, in 16 patients with COPD, the global inspiratory muscle pressure (delta Pmus) and transdiaphragmatic pressure (delta Pdi) during an incremental bicycle exercise to exhaustion. The pressures needed to overcome the elastic load were further partitioned into portions for overcoming the PEEPi-imposed inspiratory threshold load (before the beginning of inspiratory flow) and for inflating the respiratory system (between the beginning and end of inspiratory flow). The delta Pdi/delta Pmus ratio was used to quantify the pressure contribution from RCMs relative to that from the diaphragm for a given inspiratory effort. We observed that in patients with COPD during exercise (1) there is a progressive increase in total inspiratory pressure contribution from RCMs relative to that of the diaphragm, and the magnitude of this increase appears to depend on the RCMs reserves during resting breathing; (2) most of the diaphragmatic pressure contribution occurs before the beginning of inspiratory flow, to overcome the PEEPi-imposed inspiratory threshold load; (3) RCMs pressure contribution predominates during the period of inspiratory flow once PEEPi is neutralized, not only for overcoming the elastic load caused by increased tidal volume, but also for compensating for the diaphragmatic pressure contribution during this interval that was gradually lost with increasing exercise work load.
American Journal of Respiratory and Critical Care Medicine 10/1997; 156(3 Pt 1):807-13. · 11.08 Impact Factor
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ABSTRACT: Although fatigue of the inspiratory muscles has been well documented, its prevalence in patients with chronic obstructive pulmonary disease (COPD) and its influence on mortality are unknown, because of the lack of a simple, clinically available diagnostic test. The hypothesis and experimental evidence relating inspiratory muscle dysfunction to the development of hypercapnia and hypercapnic ventilatory failure are reviewed. Since a poor prognosis in COPD is associated with carbon dioxide retention, inspiratory muscle weakness and/or fatigue may have an association with survival in these patients.
Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 09/1997; 52(4):380-3.
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ABSTRACT: The inspiratory capacity (IC) maneuver is increasingly used to monitor exercise-induced dynamic hyperinflation in patients with COPD. However, the reliability of this method in patients with COPD exercising to symptom limitation has not been systematically studied and presented. The purpose of the present study was therefore to evaluate the reliability of the IC maneuver in assessing changes in end-expiratory lung volume (EELV) by assessing the pressure developed during IC maneuvers, in patients with COPD during incremental bicycle exercise to exhaustion. Fifteen patients with stable COPD performed bicycle exercise to symptom limitation. During the experiment, the patients performed IC efforts during resting breathing and at the end of each exercise work load. Esophageal pressure (Pes) measured at peak inspired volume plateau (zero flow) was -13.5 +/- 1.9 and -13.4 +/- 1.9 cm H2O (p = 0.79) during IC maneuvers at resting breathing and during the final exercise work load, respectively. When the Pes values at the peak inspired volume plateau during IC efforts at each exercise level were expressed as a percentage of those during resting breathing, the great majority of the ratios were above 90% with the lowest at 84%, and these ratios were independent of exercise intensity. Despite a constant Pes during IC, there was a progressive decrease in IC with increasing exercise work load in most patients, suggesting an increase in EELV. At the highest exercise work load achieved, delta EELV calculated as the decrease in IC was 0.26 +/- 0.06 L (p < 0.001). We conclude that repeated IC maneuver is a simple and reliable method for estimating EELV changes during exercise to exhaustion in patients with COPD.
American Journal of Respiratory and Critical Care Medicine 07/1997; 156(1):55-9. · 11.08 Impact Factor
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ABSTRACT: It has previously been reported that the duration of obstructive apneas increases from the beginning to the end of the night (M. Charbonneau, J. M. Marin, A. Olha, R. J. Kimoff, R. D. Levy, and M. Cosio. Chest 106: 1695-1701, 1994). The purpose of this study was to test the hypothesis that stimulation of upper airway (UA) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening. We studied seven patients (six men, one woman) with severe obstructive sleep apnea (apnea-hypopnea index = 93 +/- 26 events/h) during two consecutive nights of polysomnographic monitoring. On one night (random order), we performed topical UA anesthesia with 0.2% tetracaine and on the control night, sham anesthesia. We measured apnea duration, esophageal pressure (Pes) during apneas, and apneic O2 desaturation. Consistent with previous findings, apnea duration, number of efforts per apnea, and peak Pes at end apnea increased from the beginning to the end of the control nights. UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night. Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights, but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights. These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal, leading to apnea prolongation.
Journal of Applied Physiology 01/1997; 81(6):2618-26. · 3.75 Impact Factor
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ABSTRACT: Intrinsic positive end-expiratory pressure (PEEPi) due to dynamic hyperinflation has been measured as a plateau airway opening pressure during airway occlusion (PEEPi,stat). PEEPi has also been dynamically determined as a fall in esophageal pressure (Pes) before the inspiratory flow starts (PEEPi,dyn). The aims of the current study were to systematically compare PEEPi,stat and PEEPi,dyn and to explain the underlying mechanisms of their difference. The study was performed in healthy subjects with dynamic hyperinflation induced by expiration through a Starling resistor. The Campbell diagram was constructed for each subject by determining the static pressure-volume curves of the lung (Pst,[l]) and chest wall (Pst,[w]). For a given end-expiratory volume, PEEPi,stat was measured on the Campbell diagram as the pressure difference between Pst(w) and -Pst(l). PEEPi,dyn was measured as mentioned above. The effects of respiratory muscle recruitment on PEEPi,dyn were estimated by the Pes values when Pes started to fall relative to Pst(w). We found that: (1) there was a great variability of the PEEPi,dyn/PEEPi,stat ratio among and within subjects; (2) expiratory muscle recruitment was evident on most occasions; (3) persistent inspiratory muscle activity during expiration was present in some subjects; (4) the Pes values at the start of inspiratory flow were frequently on the left of -Pst(l), which contributed to the difference between PEEPi,stat and PEEPi,dyn and implied a greater dynamic than static elastance presumably due to viscoelastic properties; (5) chest wall distortions characterized by inflation of the abdomen with deflation of the rib cage during the initial inspiratory efforts were observed in three subjects. In conclusion, interpretation of PEEPi,dyn needs to be cautious because both expiratory and tonic inspiratory muscle activities that lead to significant over- or underestimation of PEEPi by PEEPi,dyn, respectively, are associated with acute dynamic hyperinflation. In addition, the effects of viscoelastic properties and chest wall distortions on PEEPi,dyn need to be further investigated.
American Journal of Respiratory and Critical Care Medicine 11/1996; 154(4 Pt 1):938-44. · 11.08 Impact Factor
