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Purpose of Review

This paper reviews treatment options for sleep disordered breathing (SDB) in patients with heart failure. We sought to identify therapies for SDB with the best evidence for long-term use in patients with heart failure and to minimize uncertainties in clinical practice by examining frequently discussed questions: what is the role of continuous positive airway pressure (CPAP) in patients with heart failure? Is adaptive servo-ventilation (ASV) safe in patients with heart failure? To what extent is SDB a modifiable risk factor?

Recent Findings

Consistent evidence has demonstrated that the development of SDB in patients with heart failure is a poor prognostic indicator and a risk factor for cardiovascular mortality. However, despite numerous available interventions for obstructive sleep apnea and central sleep apnea, it remains unclear what effect these therapies have on patients with heart failure. To date, all major randomized clinical trials have failed to demonstrate a survival benefit with SDB therapy and one major study investigating the use of adaptive servo-ventilation demonstrated harm.

Summary

Significant questions persist regarding the management of SDB in patients with heart failure. Until appropriately powered trials identify a treatment modality that increases cardiovascular survival in patients with SDB and heart failure, a patient’s heart failure management should remain the priority of medical care.
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The intersecting relationships of sleep disordered breathing (SDB), arrhythmogenic risk and chronic heart failure (HF) are complex and most likely multi-directional and synergistic. Autonomic dysfunction is a common pathophysiological feature of each of these entities. Intermittent hypoxia, hypercapnia, mechanical cardiac influences due to upper airway obstruction and rostral fluid shifts are SDB-specific mechanisms which may trigger, perpetuate and exacerbate HF and arrhythmogenesis. Specific pathophysiological mechanisms will vary according to the predominance of central as compared to obstructive sleep apnea. The risk of cardiac arrhythmias and HF attributable to SDB may be considerable given the high prevalence of SDB and its likely physiologic burden. The current review focuses on the data, which have accrued elucidating the specific contributory mechanisms of SDB in cardiac arrhythmias and HF, highlighting the clinical relevance and effects of standard SDB treatment on these outcomes, and describing the role of novel therapeutics.  相似文献   

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《COPD》2013,10(2):243-252
Sleep-related disordered breathing (SDB) and its influence on desaturation were examined in stable COPD patients with waking SpO2 > 90%. With respiratory inductance plethysmography, thoracic-abdominal respiratory movements for all events with more than 4% desaturation were analyzed in 26 patients. Types of SDB were confirmed by full polysomnography. Irregular breathing induced desaturation, while stable respiration continued during some desaturation events. Three types of altered ventilation were observed: hypoventilation, paradoxical movement and periodic breathing. An unusual type of paradoxical movement, with normal airflow despite progressive desaturation, was observed in REM sleep. Patients were divided into desaturation (15 patients) and non-desaturation (11 patients) groups. Daytime arterial blood gas, lung function values, and 6-min walking distance did not differ. Awake, mode, maximum and minimum nocturnal SpO2 were lower in the desaturation group. SDB-induced desaturation events in the desaturation group were more frequent (9.2 ± 3.5 vs. 1.8 ± 2.2 times), a greater SpO2 decrease (11.4 ± 7.1% vs. 5.2 ± 2.1%) and longer duration (73.2 ± 34.8 vs. 18.8 ± 39.0 min). Patterns of SDB in the desaturation group were hypoventilation (74.4 ± 23.4%), paradoxical movement (10.2 ± 14.5%), periodic breathing (12.1 ± 18.3%) and unclassified (5.8 ± 11.2%). These results reveal that lower SpO2 and SDB influence nocturnal desaturation in stable COPD patients.  相似文献   

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This issue of Sleep and Breathing presents a section on sleep in COPD, a widespread disease consuming many health resources which is often diagnosed so late that little chance of reversibility remains. The early detection of the warning clinical signs can include sleep studies, mainly in the presence of arterial carbon dioxide levels higher than expected from pulmonary function tests. Two of the articles deal with hypercapnia and nocturnal hypoventilation in COPD; the third underlines the impact of tobacco smoking on snoring and on oxygen availability to tissues, showing a poor reliability of pulse oximetry in subjects with heavy smoking habits.  相似文献   

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近年来,睡眠呼吸暂停综合征逐渐受到重视,其目的是阐述慢性充血性心力衰竭合并中枢性睡眠呼吸暂停综合征机制及治疗进展。  相似文献   

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Definition: Cheyne-Stokes respiration is a breathing disorder characterized by recurrent central sleep apneas, mainly during sleep, alternating with a crescendo-decrescendo pattern of tidal volume. Pathophysiology and Prognosis: The pathophysiology of Cheyne-Stokes respiration, involving the cardiovascular, pulmonary and sympathetic nervous system, is still not well understood. Although 50% of moderate to severe congestive heart failure patients suffer from significant Cheyne-Stokes respiration, studies been undertaken to determine the prevalence of this phenomenon and its implications regarding patients' life expectancy and quality of life were conducted only in recent years. Other studies suggest that Cheyne-Stokes respiration has a negative prognostic value upon congestive heart failure patients. Treatment: Novel therapeutic approaches have been attempted in order to treat Cheyne-Stokes respiration; they include oxygen delivery, various pharmaceutical treatments aimed to stabilize the ventilatory system and other pharmaceutical treatments aimed to improve the left ventricular ejection fraction. However, none of them was effective. Objectives: This review summarizes some of the current knowledge regarding Cheyne-Stokes respiration pathophysiology, prevalence, prognostic implication and available treatments. Definition: Das Cheyne-Stokes-Atemmuster wurde erstmalig zu Beginn des 19. Jahrhunderts beschrieben und kennzeichnet eine Atemstörung, bei der vor allem während des Schlafs Atempausen (Apnoephasen) auftreten. Diese Apnoephasen wechseln mit einem Atemmuster mit Kreszendo/Dekreszendo-Charakter ab. Pathophysiologie und Prognose: Die Pathophysiologie der Cheyne-Stokes-Atmung, die kardiovaskuläre, pulmonale und zentralvenöse Aspekte umfasst, ist noch weitgehend unklar. Obwohl nahezu 50% der Patienten mit schwerer Herzinsuffizienz eine Cheyne-Stokes-Atmung aufweisen, wurden erst in den letzten Jahren die Prävalenz dieser Begleiterkrankung und die möglichen Auswirkungen auf die Lebenserwartung und die Lebensqualität charakterisiert. Erste Studien lassen vermuten, dass Patienten mit Cheyne-Stokes-Atmung eine deutlich schlechtere Prognose als Patienten mit Herzinsuffizienz ohne Cheyne-Stokes-Atmung aufweisen. Behandlung: Ziel der bisher eingesetzten Therapie ist es, das Atemsystem zu stabilisieren und die kardiovaskuläre Funktion zu optimieren, um dadurch das Leben der Patienten zu verlängern. Doch weder die Verabreichung von Sauerstoff noch der Einsatz verschiedener pharmakotherapeutischer Konzepte zeigten bisher einen nachhaltigen Erfolg. Gegenstand: In dieser Übersicht werden wichtige Aspekte der Pathophysiologie der Cheyne Stokes Atmung, seine prognostische Bedeutung sowie vorhandene Therapiekonzepte besprochen und kritisch bewertet.  相似文献   

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It is increasingly recognized that sleep-disordered breathing (SDB) is a common modifiable risk factor for cardiovascular disease with significant impact on morbidity and potentially mortality. SDB is highly prevalent in patients with systolic or diastolic heart failure. A high index of suspicion is necessary to diagnose SDB in patients with heart failure because the vast majority of affected patients do not report daytime symptoms. Recent clinical trials have demonstrated improvement in heart function, exercise tolerance, and quality of life after treatment of SDB in patients with heart failure. Accumulating evidence suggests that treatment of SDB should complement the established pharmacologic therapy for chronic heart failure. However, mortality benefit has yet to be demonstrated.  相似文献   

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