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Bei obstruktiven Lungenerkrankungen kann es neben einer statischen, anatomisch fixierten Lungenuberblahung auch zu einer funktionellen Uberblahung kommen, die reversibel ist. In diesem Kapitel werden Techniken der Entblahung beschrieben.Bei obstruktiven Lungenerkrankungen kann es neben einer statischen, anatomisch fixierten Lungenuberblahung auch zu einer funktionellen Uberblahung (»dynamic hyperinflation«) kommen, die reversibel ist. Diese fuhrt zu einer Kaudalisierung und Verkurzung des Zwerchfells und kann durch physiotherapeutische Interventionen repositioniert werden. Durch das ungunstigere Langen-Spannungs-Verhaltnis bei einer Uberblahung reduziert sich die Funktion des Zwerchfells. Die diaphragmale Dysfunktion fuhrt oft zu einer ventilatorischen Insuffizienz unter Zuhilfenahme der Atemhilfsmuskulatur, was bei Lungenpatienten oft Verspannungen und Erschopfungszustande im Schulter-Nacken-Bereich verursacht.

Eine sorgfaltige Anamnese ist die Grundlage einer angemessenen physiotherapeutischen Intervention. In diesem Kapitel werden die wichtigsten Aspekte einer umfassenden Anamnese dargelegt. Die komplexe Atiopathogenese der chronisch-obstruktiven Lungenerkrankung (COPD) mit den vielen systemischen Auswirkungen und den von Patienten subjektiv unterschiedlich empfundenen Konsequenzen macht es schwierig, den aktuellen Status des Patienten zu erfassen und darzustellen. Eine sorgfaltige Anamneseerhebung erlaubt oftmals Ruckschlusse auf Risikofaktoren und kausale Zusammenhange. Haufig ist allein durch eine sorgfaltige Anamnese eine physiotherapeutische Diagnose moglich, welche Voraussetzung einer sachgerechten physiotherapeutischen Behandlung ist. Einen ersten Hinweis auf COPD geben die so genannten AHA-Leitsymptome.

Dieses Kapitel befasst sich mit Dysbalancen der sekundaren Atemmuskulatur. Die Muskulatur des Menschen hat sowohl Halte- wie auch Bewegungsfunktion: In Haltefunktion halt der Muskel seine Lange trotz von ausen einwirkender Krafte konstant. In Bewegungsfunktion passt sich der Muskel standig an die variierende Muskellange und -spannung an. Propriozeptoren registrieren Spannungszustand und Lange der Skelettmuskulatur. Die durch die propriozeptiven Sensoren in Muskeln, Sehnen und Gelenken gewonnene Information dient der Koordination von schnellen, uber Ruckenmarksneurone vermittelten Reflexen zur Korperstabilisierung und -bewegung. Die Ruckenmarksreflexe erleichtern dem zentralen motorischen System die Planung und Ausfuhrung von Bewegungen, da ein breites Repertoire an grundlegenden Bewegungselementen bereits vorhanden ist

Die Herzfunktion bei COPD-Patienten ist beeintrachtigt. Hier wird der pathophysiologische Zusammenhang beschrieben. COPD ist eine Erkrankung, die chronisch und systemisch ist und mit systemisch erhohten Markern der Inflammation einhergeht. Wahrend die pulmonale Inflammation ursachlich fur die Atemwegsobstruktion zeichnet, gibt es zunehmende Hinweise fur ein »spill over« von Mikroorganismen in dem systemischen Kreislau«. Dies fuhrt zu einer extrapulmonalen – systemischen – Entzundung mit Beeinflussung multipler Organsystem. Die bekannteste Auswirkung von Lungenerkrankungen auf die Herzfunktion ist die Belastung des rechten Herzventrikels durch eine pulmonale Hypertonie mit Ausbildung eines Cor pulmonale.

Harninkontinenz ist eine haufige Komorbiditat bei Patienten mit COPD. Chronischer Husten steigert den Druck im Bauchraum, und bewirkt dadurch einen erhohten Druck auf die Blase, der den Schliesmechanismus der Blase beeintrachtigt. Das physiotherapeutische Assessment erfasst die Problematik mit krankheitsspezifischen Fragebogen, standardisierten Pad-Tests und einem Miktionstagebuch. Muskelfunktionstests dienen der Beurteilung der Beckenbodenmuskulatur und der Erfassung der Inkontinenzsymptome. Das physiotherapeutisch geleitete Kontinenztraining umfasst die Patientenedukation mit dem Ziel der Optimierung des Trink- und Entleerungsverhaltens. Das Training der Beckenbodenmuskulatur dient der Schulung der Sensomotorik, sowie der Verbesserung der Ausdauerleistung, Reaktionsfahigkeit und Kraft. Sinnvoll ist eine Integration der Beckenbodenkontrolle in Alltagsbewegungen, insbesondere bei Husten. Um eine langfristige Verbesserung der Blasenkontrolle zu erzielen sollte anschliesend ein Erhaltungstraining als Bestandteil der Lungenrehabilitationsprogramme moglichst in der Gruppe durchgefuhrt werden.

Sleep-disordered breathing (SDB) and respiratory failure (RF) are complications of acid maltase deficiency (AMD), a rare hereditary myopathy.To define the relationship between lung and respiratory muscle function, to establish incidence and patterns of SDB, and to determine daytime predictors of SDB.Sitting and supine lung and respiratory muscle function tests were obtained in 27 subjects with juvenile and adult AMD (aged 39 +/- 19 years) and compared with outcomes of polysomnography.Ventilatory restriction was present in 17/27 subjects. Inspiratory vital capacity (IVC) correlated (p0.005) with peak inspiratory muscle pressure (PIP, R = 0.61), respiratory muscle strain (P(0.1)/P(0.1max), R = -0.68), and gas exchange by day (PaO(2): R = 0.71; PaCO(2): R = -0.64) and night (SaO(2): R = 0.73; P(tc)CO(2): R = -0.75). Diaphragm weakness (DW) was present in 13 subjects, 10 of whom had hypercapnic RF (PaCO(2) 65 +/- 7 mm Hg), and was associated with longer disease course. SDB was found in 13 subjects, 12 with DW. It was characterized by REM-sleep hypopneas that, as ventilatory restriction worsened, were complemented by hypoventilation (P(tc)CO(2)50 mm Hg) first in REM sleep, then in non-REM sleep (p0.005). SDB was predicted by DW (sensitivity 80%, specificity 86%) and nocturnal hypoventilation by IVC40% (sensitivity 80%, specificity 93%). Noninvasive ventilation, instituted for daytime respiratory failure or nocturnal hypoventilation, normalized daytime and nocturnal gas exchange (p0.005).Vital capacity correlates with respiratory muscle function in AMD. Diaphragm weakness is the major cause of SDB and RF. SDB and nocturnal hypoventilation are predictable from daytime function tests.

The prevalence of obstructive sleep apnoea (OSA) following stroke is high and OSA is associated with increased morbidity, mortality and poor functional outcome. Nasal continuous positive airway pressure (nCPAP) is the treatment of choice for OSA, but its effects in stroke patients are unknown.The effectiveness and acceptance of treatment with nCPAP in 105 stroke patients with OSA, admitted to rehabilitation was prospectively investigated. Subjective wellbeing was measured with a visual analogue scale in 41 patients and 24-;h blood pressure was determined in 16 patients before and after 10 days of treatment. Differences were compared between patients who did and did not accept treatment.There was an 80% reduction of respiratory events with concomitant increase in oxygen saturation and improvement in sleep architecture. No serious side-effects were noticed. Seventy-four patients (70.5%) continued treatment at home. Nonacceptance was associated with a lower functional status, as measured by the Barthel Index, and the presence of aphasia. Ten days after initiation of nCPAP, compliant users showed a clear improvement in wellbeing (differences in visual analogue scale (ΔVAS) mean±sd 26±26 mm)versusnoncompliant patients (ΔVAS 2±25 mm, p=0.021). Only the compliant group had a reduction in mean nocturnal blood pressure (ΔBP; −8±7.3 mmHgversus0.8±8.4 mmHg, p=0.037).Stroke patients with obstructive sleep apnoea can be treated effectively with nasal continuous positive airway pressure and show a similar improvement and primary acceptance to obstructive sleep apnoea patients without stroke. Continuous positive airway pressure acceptance is associated with improved wellbeing and decreased nocturnal blood pressure.

Adaptive servo-ventilation (ASV) is a novel method of ventilatory support designed for Cheyne-Stokes respiration (CSR) in heart failure. The aim of our study was to compare the effect of one night of ASV on sleep and breathing with the effect of other treatments. Fourteen subjects with stable cardiac failure and receiving optimal medical treatment were tested untreated and on four treatment nights in random order: nasal oxygen (2 L/min), continuous positive airway pressure (CPAP) (mean 9.25 cm H(2)O), bilevel (mean 13.5/5.2 cm H(2)O), or ASV largely at the default settings (mean pressure 7 to 9 cm H(2)O) during polysomnography. Thermistor apnea + hypopnea index (AHI) declined from 44.5 +/- 3.4/h (SEM) untreated to 28.2 +/- 3.4/h oxygen and 26.8 +/- 4.6/h CPAP (both p < 0.001 versus control), 14.8 +/- 2.3/h bilevel, and 6.3 +/- 0.9/h ASV (p < 0.001 versus bilevel). Effort band AHI behaved similarly. Arousal index decreased from 65.1 +/- 3.9/h untreated to 29.8 +/- 2.8/h oxygen and 29.9 +/- 3.2/h CPAP, to 16.0 +/- 1.3/h bilevel and 14.7 +/- 1.8/h ASV (p < 0.01 versus all except bilevel). There were large increases in slow-wave and rapid eye movement (REM) sleep with ASV but not with oxygen or CPAP. All subjects preferred ASV to CPAP. One night ASV suppresses central sleep apnea and/or CSR (CSA/CSR) in heart failure and improves sleep quality better than CPAP or 2 L/min oxygen.

The plasma level of fibrinogen is felt to be an independent risk factor for vascular events. Obstructive sleep apnea (OSA) has a high prevalence in patients with stroke and may also be an independent risk factor. The aim of our study was to determine the association between OSA and plasma levels of fibrinogen in patients with stroke. Polysomnography was performed during neurological rehabilitation in 113 patients (82 men, 31 women, age 58 +/- 11.1 yr, mean +/- SD) with ischemic stroke. OSA was absent (RDI5) in 44 patients, 42 had mild OSA (5or = RDI20), and 27 had moderate to severe OSA (RDIor = 20). Parameters of OSA (respiratory disturbance index [RDI], oxygen indices) were correlated to plasma levels of fibrinogen, measured in the morning after admission to rehabilitation. Fibrinogen was positively correlated with RDI (r = 0.24, p = 0.007), duration of the longest apnea (r = 0.18, p = 0.049), and negatively correlated with several oxygen indices including average minimal oxygen saturation (r = -0.41, p0.001). Correlation coefficients were slightly higher when excluding patients with stroke of presumed cardiac origin. Multiple linear regression identified minimal mean oxygen saturation and sex as independent predictors of fibrinogen level. The correlation between severity of coexisting OSA and fibrinogen level in patients with stroke suggests a possible pathophysiological mechanism for an increased risk of stroke in patients with OSA.

Mouth leak is common during nasal ventilatory assistance, but its effects on ventilatory support and on sleep architecture are unknown. The acute effect of sealing the mouth on sleep architecture and transcutaneous carbon dioxide tension (Ptc,CO2) was tested in 9 patients (7 hypercapnic) on longterm nasal bilevel ventilation with symptomatic mouth leak. Patients slept with nasal bilevel ventilation at their usual settings on two nights in random order. On one night, the mouth was taped closed. Leak was measured with a pneumotachograph. Median leak fell from 0.35+/-0.07 (mean +/- SEM) L x s(-1) untaped to 0.06+/-0.03 L x s(-1) taped. Ptc,CO2 fell in 8/9, including all hypercapnic patients. Across all patients, the mean Ptc,CO2 fell by 1.02+/-0.28 kPa (7.7+/-2.1 mm Hg) with taping (p = 0.007). Arousal index fell in every patient. Mean arousal index fell from 35.0+/-3.0 to 13.9+/-1.2 h(-1) (p

Biochemical markers in sarcoidosis are closely related to the immunological events and the activity of inflammatory effector cells at sites of granuloma formation. The markers can be measured in serum, then reflecting whole body concentration, or in BAL fluid, then indicating activity in the lung. Only calcium and ACE serum levels have gained a proven value in the clinical field.

Hypercapnic respiratory failure in patients with COPD frequently requires mechanical ventilatory support. Extracorporeal CO2 removal (ECCO2R) techniques have not been systematically evaluated in these patients.This is a pilot study of a novel ECCO2R device that utilizes a single venous catheter with high CO2 removal rates at low blood flows. Twenty hypercapnic patients with COPD received ECCO2R. Group 1 (n = 7) consisted of patients receiving noninvasive ventilation with a high likelihood of requiring invasive ventilation, group 2 (n = 2) consisted of patients who could not be weaned from noninvasive ventilation, and group 3 (n = 11) consisted of patients on invasive ventilation who had failed attempts to wean.The device was well tolerated, with complications and rates similar to those seen with central venous catheterization. Blood flow through the system was 430.5 ± 73.7 mL/min, and ECCO2R was 82.5 ± 15.6 mL/min and did not change significantly with time. Invasive ventilation was avoided in all patients in group 1 and both patients in group 2 were weaned; PaCO2 decreased significantly (P.003) with application of the device from 78.9 ± 16.8 mm Hg to 65.9 ± 11.5 mm Hg. In group 3, three patients were weaned, while the level of invasive ventilatory support was reduced in three patients. One patient in group 3 died due to a retroperitoneal bleed following catheterization.This single-catheter, low-flow ECCO2R system provided clinically useful levels of CO2 removal in these patients with COPD. The system appears to be a potentially valuable additional modality for the treatment of hypercapnic respiratory failure.

Background Accumulating evidence suggests a role of obstructive sleep apnoea (OSA) as a risk factor for coronary atherosclerosis. This study aimed i) to assess the prevalence of OSA in the general population and ii) to analyse the association of this disorder with traditional cardiovascular disease risk factors and subclinical coronary atherosclerosis. Methods In a cross-sectional analysis of the Heinz Nixdorf Recall study a subgroup of 1604 subjects (791 men, age 50–80 years) underwent OSA screening. Furthermore, coronary artery calcium (CAC) was measured. OSA was defined as apnoea-hypopnoea index (AHI) ≥ 15/h. Results OSA was observed in 29.1% of men and 15.6% of women. In a multiple linear regression analysis adjusted for risk factors AHI was associated with CAC in men aged ≤65 years (estimated log-transformed increase of CAC = 0.25, 95% confidence interval (CI) = −0.001–0.50, p = 0.051) and in women of any age (estimated log-transformed increase = 0.23, 95% CI = 0.04–0.41, p = 0.02). Doubling of the AHI was associated with a 19% increase of CAC in men aged ≤65 years and with a 17% increase in women of any age. Conclusions In the general population aged ≥50 years OSA is associated with subclinical atherosclerosis in men aged ≤65 years and in women of any age, independent of traditional cardiovascular risk factors.

Tracheal stenosis due to either benign or malignant disease is a situation that the pulmonary physicians and thoracic surgeons have to cope in their everyday clinical practice. In the case where tracheal stenosis is caused due to malignancy mini-interventional interventions with laser, apc, cryoprobe, balloon dilation or with combination of more than one equipment and technique can be used. On the other hand, in the case of a benign disease such as; tracheomalacia the clinician can immediately upon diagnosis proceed to the stent placement. In both situations however; it has been observed that the stents induce formation of granuloma tissue in both or one end of the stent. Therefore a frequent evaluation of the patient is necessary, taking also into account the nature of the primary disease. Evaluation methodologies identifying different types and extent of the trachea stenosis have been previously published. However; we still do not have an effective adjuvant therapy to prevent granuloma tissue formation or prolong already treated granuloma lesions. There have been proposed many mechanisms which induce the abnormal growth of the local tissue, such as; local pressure, local stress, inflammation and vascular endothelial growth factor overexpression. Immunomodulatory agents inhibiting the mTOR pathway are capable of inhibiting the inflammatory cascade locally. In the current mini-review we will try to present the current knowledge of drug eluting stents inhibiting the mTOR pathway and propose a future application of these stents as a local anti-proliferative treatment.

Die hier vorgestellten, aktuellen Forschungsergebnisse zur COPD sind einer neuen Qualitat in der klinischen Wissenschaft zu verdanken. Es sind vor allem zwei neue Datenquellen, die in den letzten Jahren erschlossen wurden: grose populationsbasierte, retrospektive Beobachtungsstudien mit bis zu 5-stelligen Fallzahlen einerseits und sehr intensiv untersuchte, prospektive Kohorten andererseits. In einem der Beitrage dieses Artikels wird das neben der amerikanischen ECLIPSE-Kohorte in Deutschland entstehende COSYCONET vorgestellt. Hier kann sich der Leser einen Eindruck uber den wissenschaftlichen Umgang mit einer prospektiven Kohorte verschaffen. Die Flut neuer Daten hat auch dazu beigetragen, dass die Aussagen des internationalen GOLD-Komitees komplexer geworden sind. Klinisch wichtig sind der Verzicht auf das Ergebnis des Bronchospasmolysetests als Diagnosekriterium der COPD und die Verwendung von Symptomfragebogen – neuerdings auch des CCQ-Scores – als neue Dimension in der Beschreibung der Erkrankungsschwere. Auserdem wird die Bedeutung schwerer akuter Exazerbationen fur das weitere Schicksal der Patienten hervorgehoben. Die im GOLD-Update von 2011 erstmals vorgestellten COPD-Typen I bis IV waren zunachst lediglich eine Expertenmeinung. Daher sind die jetzt vorliegenden Daten uber die prognostische Relevanz der Klassifikation dringend notwendig. Das Hauptthema der Tagung waren die kardiovaskularen Aspekte der COPD. Es wird deutlich, dass fur Patienten mit COPD – uber die Komorbiditat zweier haufiger chronischer Erkrankungen hinaus – kardiovaskulare Ereignisse von besonderer Bedeutung sind. Umgekehrt ist die fortgeschrittene COPD ein wichtiger Risikofaktor bei Erkrankungen des Herzens und der Gefase. Diese gegenseitige Beeinflussung gilt sowohl fur den Langzeitverlauf als auch fur akute Komplikationen wie die COPD-Exazerbation und den Myokardinfarkt, und sie macht sich in harten Endpunkten wie der Letalitat bemerkbar. In den folgenden Beitragen wird das Thema im Hinblick auf die Epidemiologie, die kardiovaskulare Biologie und im Besonderen auf seine Bedeutung in der COPD-Exazerbation untersucht. Die kardiovaskulare Toxizitat der Pharmakotherapie der COPD wird ebenso neu bewertet wie mogliche protektive Effekte von Pharmaka mit kardiovaskularer Indikation (Statine und Betarezeptorenblocker) bei Patienten mit COPD.

Snoring worsens with high alcohol consumption. It is unclear whether moderate alcohol intake worsens sleep and breathing in subjects with obstructive sleep apnoea syndrome (OSAS), and whether alcohol increases the pressure requirement for nasal continuous positive airway pressure (CPAP). Fourteen adult males with untreated OSAS but without heart or lung disease were studied (age 53+/-9 yrs, body mass index (BMI) 33+/-5 kg x m(-2) (mean+/-SD). The subjects underwent overnight polysomnography on four occasions: control, alcohol, CPAP, and alcohol + CPAP. On the alcohol nights, the subjects drank 1.5 mL x kg(-1) body weight (BW) vodka (40% alcohol by volume) (blood alcohol with and without CPAP 0.45+/-0.1 and 0.47+/-0.2 mg x mL(-1) (mean+/-SD)). On the CPAP nights, the pressure required to prevent apnoea, snoring, and silent inspiratory airflow limitation was determined using an autotitrating nasal CPAP system (ResCare AutoSet). Alcohol and control nights were performed in random order. Without CPAP, alcohol produced a small non-significant decrease in the percentage of rapid eye movement (REM) sleep (control 11+/-2 vs alcohol 8+/-1% (mean+/-SEM)), but with CPAP there was no such effect (control 15+/-2 vs 17+/-2%; CPA x alcohol interaction p=0.015). With CPAP, slow-wave sleep in the first 2 h increased slightly with alcohol (control 39+/-6 vs alcohol 51+/-4%; p=0.004). Arousal index without CPAP increased slightly with alcohol (control 43+/-5 vs alcohol 49+/-6 events x h(-1); p=0.02). There was little or no effect of alcohol on other sleep stages, arousal index, apnoea index, apnoea/hypopnoea index, mean or longest event duration, mean or worst arterial oxygen saturation, with or without CPAP, either for the full night or for the first 2 h. There was no change in the pressure requirement for CPAP (full night: control 11.9+/-0.9 vs alcohol 12.5+/-0.9 cm H2O; first 2 h: 10.9+/-0.6 vs 11.1+/-0.8 cm H2O). Moderate alcohol intake (in the form of vodka) has little effect on breathing or saturation during sleep in subjects with mild-to-severe obstructive sleep apnoea, and no effect on the pressure required for continuous positive airway pressure in order to prevent apnoea, snoring, and flow limitation. These results cannot be extrapolated to other doses or forms of alcohol, or to subjects with concurrent heart or lung disease.

The presence of asbestos bodies (ABs) in sputum specimens of individuals with occupational asbestos exposure has been well-documented. The aim of this study was to determine their clinical relevance in comparison to the concentration of AB in bronchoalveolar lavage (BAL) and lung tissue. Subjects were included following a well-documented exposure of asbestos history (n = 93) or BAL fluid analysis positive for ABs (n = 42). The subjects with a well documented history of AB exposure were divided into three groups: heavy (Group 1, n = 29); moderate (Group 2, n = 31); or occasional exposure (Group 3, n = 33). BAL fluid was available from all subjects, and lung tissue from 21 subjects. To assess the variability, 10 sputum positive subjects collected subsequent sputum on days 2, 7, 14, 30 and 90. ABs were determined by light microscopy after membrane filtration of specimen digests. The mean sputum AB content was highest in Group 1 (2.4 +/- 5.5 AB.mL-1), lower in Group 2 (0.2 +/- 0.3 AB.mL-1) and lowest in Group 3 (0.1 +/- 0.1 AB.mL-1) suggesting a correlation with cumulative exposure. However, many negative sputum samples were noted, when BAL specimens were positive. The AB content of sputum and BAL specimens did not correlate. ABs were found in sputum of all subjects with a tissue content of > 1,000 AB-cm-3, but in none with contents of < 1,000 AB-cm-3. Substantial variability of ABs was found in the five sequentially collected sputa of 10 initially positive patients (coefficient of variation 28-93%), but only two false negatives were found in these 50 samples. Thus, sputum analysis for asbestos bodies is an insensitive method for assessing the lung asbestos burden, much less sensitive than bronchoalveolar lavage fluid analysis. However, a sputum sample positive for asbestos bodies is suggestive of a high lung asbestos burden.

The aim of this study was to investigate the relationship between release of tumor necrosis factor-alpha (TNF-alpha) by alveolar macrophages (AM) and the phenotypic characteristics of bronchoalveolar lavage (BAL) cells in sarcoidosis. We studied the spontaneous release of TNF-alpha by AM in vitro and the phenotypic characteristics of freshly recovered BAL T-cells and AM in 31 individuals (13 with active sarcoidosis, nine with inactive sarcoidosis, and nine normal controls). TNF-alpha was measured by enzyme-linked immunosorbent assay (ELISA) in supernatants from unstimulated AM after 24 h culture. Phenotypic markers of BAL cells were determined by an immunocytochemical assay. AM of patients with active sarcoidosis released more TNF-alpha (1,355 +/- 133 pg/ml/ 10(6) AM/24 h) than those of the inactive group (651 +/- 142 pg/ml/10(6) AM/24 h) or the normal controls (425 +/- 121 pg/ml/10(6) AM/24 h), with p0.001 for both comparisons. The amount of TNF-alpha released correlated positively with the percentage expression of CD4 (r = 0.72) and CD25 (r = 0.70) by lymphocytes, and of CD14 (r = 0.63), VLA-4 (r = 0.59), FRD1 (r = 0.67) and 27E10 (r = 0.67) by AM, with p0.001 for all correlations. In conclusion, this relationship suggests that these antigens may be considered as cellular activation markers, and that some of these AM antigens may indirectly characterize the AM phenotype that is capable of producing TNF-alpha.

Hintergrund: Ziel dieser Analyse ist es, die Koexistenz zentraler Schlafapnoe (CSA) und periodischer Atmungsmuster bei Patienten mit Herzinsuffizienz (HI) und obstruktiver Schlafapnoe (OSA), genauer zu charakterisieren. Signifikante Anteile zentraler Apnoen/Hypopnoen und das Vorliegen eines periodischen Atmungsmusters werden als Indikatoren fur eine beeintrachtigte Atmungsregulation bei Patienten mit HI vermutet. Im Rahmen dieser Analyse werden neben der Pravalenz auch mogliche Risikofaktoren solcher Indikatoren untersucht. Patienten und Methoden: In das SCHLA-HF Register wurden aus 138 deutschen Zentren (91 kardiologische Praxen und 47 kardiologische Kliniken) 10.490 Patienten mit chronischer HI und HF-REF eingeschlossen. Anschliesend erfolgte ein Schlafapnoe-Screening mit Hilfe des 2-Kanal Screeningsystems ApneaLink. Patienten mit einem AHI≥15/h und/oder klinischem Verdacht auf das Vorliegen einer Schlafbezogenen Atmungsstorung (SBAS), wurden in eine der kooperierenden Schlafkliniken uberwiesen. Dort erhielten sie zur Diagnosesicherung eine Polysomnographie (PSG). Von den 10.490 Patienten wurden 1.394 in die abschliesende Analyse einbezogen. Ergebnisse/Fazit: Die Pravalenz signifikanter Anteile von CSA und objektiv gemessenem periodischen Atmungsmuster bei Patienten mit HI und OSA ist hoch. Je hoher der Anteil zentraler Atemereignisse ist, desto haufiger besteht ein periodisches Atmungsmuster. Die Risikofaktoren fur signifikante Anteile zentraler Apnoen/Hypopnoen sind weitestgehend identisch mit denen fur das Vorliegen eines periodischen Atmungsmusters. Diese Indikatoren fur eine Instabilitat der Atmungsregulation konnten dazu dienen, klinische Risikoprofile zu erstellen, anhand derer bereits im Vorfeld Therapieentscheidungen getroffen werden konnten

Background: The presence of altered ventilator control instability in congestive heart failure (CHF) patients with obstructive sleep apnea (OSA) may have significant therapeutic implications. Indicators for ventilator control instability can be significant proportions of central sleep apnea (CSA) and/or a periodic breathing (PB) pattern. The aim of the present study was to determine the prevalence of such indicators in CHF patients with OSA. Patients and Methods: The ongoing German multi-center SchlaHF registry prospectively included 7007 stable CHF patients (NYHA class ≥II and LVEF ≤45%) from cardiology practices and cardiology departments of hospitals. Patients were studied with a two-channel screening device (nasal airflow, pulse oximetry; ApneaLink, ResMed, Sydney, Australia) that detects PB patterns based on an algorithm using pattern recognition. Patients with suspected SDB received polysomnography (PSG) with certified scoring. Results: Of the 2183 PSG-patients 1583 (73%) had an AHI ≥15/h, of whom 49% had OSA (≥50% of apneas and hypopneas were obstructive). In such CHF patients with OSA the prevalence of a significant proportion of central apneas and hypopneas (20-49%) was 35%. The prevalence of objectively assessed PB was 44% in OSA patients. 350 (59%) heart failure patients with OSA presented with either a significant proportion of CSA and/or a PB pattern. Conclusions: The high prevalence of a significant proportion of CSA and objectively assessed PB pattern in CHF patients with OSA suggests ventilator control instability that may have an impact on the appropriate modality of positive airway pressure therapy to suppress apneas and hypopneas.

Background: Conventional pulmonary rehabilitation programs improve exercise tolerance but have no effect on pulmonary function in patients with chronic obstructive pulmonary disease (COPD). The role of controlled breathing using respiratory biofeedback during rehabilitation of patients with COPD remains unclear. Objectives: To compare the effects of a conventional 4-week pulmonary rehabilitation program with those of rehabilitation plus controlled breathing interventions. Methods: A randomized controlled trial was performed. Pulmonary function (FEV1), exercise capacity (6-min walking distance, 6MWD), health-related quality of life (chronic respiratory questionnaire, CRQ) and cardiac autonomic function (rMSSD) were evaluated. Results: Forty COPD patients (mean ± SD age 66.1 ± 6.4, FEV1 45.9 ± 17.4% predicted) were randomized to rehabilitation (n = 20) or rehabilitation plus controlled breathing (n = 20). There were no statistically significant differences between the two groups regarding the change in FEV1 (mean difference –0.8% predicted, 95% CI –4.4 to 2.9% predicted, p = 0.33), 6MWD (mean difference 12.2 m, 95% CI –37.4 to 12.2 m, p = 0.16), CRQ (mean difference in total score 0.2, 95% CI –0.1 to 0.4, p = 0.11) and rMSSD (mean difference 2.2 ms, 95% CI –20.8 to 25.1 ms, p = 0.51). Conclusions: In patients with COPD undergoing a pulmonary rehabilitation program, controlled breathing using respiratory biofeedback has no effect on exercise capacity, pulmonary function, quality of life or cardiac autonomic function.

Chronic obstructive pulmonary disease (COPD) is associated with impaired exercise tolerance, but it has not been established to what extent cardiac autonomic function impacts on exercise capacity.To evaluate whether there is an association between airflow limitation and cardiac autonomic function and whether cardiac autonomic function plays a role in exercise intolerance and daily physical activity (PA) in patients with COPD.Univariate and multivariate analyses were performed to evaluate the association between both 6-minute walking test (6MWT) and PA (steps per day) and pulmonary function, cardiac autonomic function (HR at rest, HRR and heart rate variability, HRV) in patients with COPD.In 154 COPD patients (87 females, mean [SD]: age 62.5 [10.7] years, FEV(1) %predicted (43.0 [19.2]%), mean HR at rest was elevated (86.4 [16.4] beats/min) and HRV was reduced (33.69 [28.96] ms) compared to published control data. There was a significant correlation between FEV(1) and HR at rest (r = -0.32, p0.001), between HR at rest and 6MWD (r = -0.26, p = 0.001) and between HR at rest and PA (r = -0.29, p = 0.010). No correlation was found between HRV and 6MWD (r = 0.089, p = 0.262) and PA (r = 0.075, p = 0.322). In multivariate analysis both HR and FEV(1) were independent predictors of exercise capacity in patients with COPD.In patients with COPD the degree of airflow limitation is associated with HR at rest. The degree of airflow limitation and cardiac autonomic function, as quantified by HR at rest, are independently associated with exercise capacity in patients with COPD.