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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) is a form of periodic breathing, commonly observed in patients with heart failure (HF), in which central apneas alternate with hyperpneas that have a waxing-waning pattern of tidal volume. Uniform criteria by which to diagnose a clinically significant degree of CSR-CSA have yet to be established. CSR-CSA is caused by respiratory control system instability characterized by a tendency to hyperventilate. Central apnea occurs when Pa(CO(2)) falls below the threshold for apnea during sleep due to ventilatory overshoot. Patients with CSR-CSA are generally hypocapnic, with a Pa(CO(2)) closer than normal to the apneic threshold such that even slight augmentation in ventilation drives Pa(CO(2)) below threshold and triggers apnea. Factors contributing to hyperventilation in HF include stimulation of pulmonary irritant receptors by pulmonary congestion, increased chemoreceptor sensitivity, reduced cerebrovascular blood flow, and recurrent arousals from sleep. Controversy remains as to whether CSR-CSA is simply a reflection of HF severity, or whether it exerts unique adverse effects on prognosis. The main adverse influence of CSR-CSA on cardiovascular function appears to be excessive sympathetic nervous system activity due to apnea-related hypoxia and arousals from sleep. A number of studies have examined the potential relationship between CSR-CSA and mortality in HF. Most reported that CSR-CSA was associated with an increased risk for mortality, but these studies were small. Further research is therefore needed to elucidate mechanisms which contribute to the pathogenesis of CSR-CSA, and to determine whether its treatment can reduce morbidity and mortality in patients with HF.
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PMID:Central sleep apnea and Cheyne-Stokes respiration. 1825 Feb 16

Sleep-disordered breathing (SDB) has a higher prevalence in patients with heart failure than in the general middle-aged population. Obstructive sleep apnea (OSA), one of the forms of SBD, promotes poorly controlled hypertension, coronary events, and atrial fibrillation events that can lead to acutely decompensated heart failure (ADHF), and evidence suggests that untreated OSA increases mortality in patients with heart failure. Cheyne-Stokes respiration and central sleep apnea (CSA) have long been associated with heart failure and, in many patients, can coexist with OSA. In this article, we propose a systematic approach to diagnose and treat OSA in patients with ADHF based on current evidence.
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PMID:Sleep-disordered breathing in patients with decompensated heart failure. 1875 44

There are three major types of sleep-disordered breathing (SDB) with respect to prevalence and health consequences, i.e. obstructive sleep apnoea syndrome (OSAS), Cheyne-Stokes respiration and central sleep apnoea (CSR-CSA) in chronic heart failure, and obesity hypoventilation syndrome (OHS). In all three conditions, hypoxia appears to affect body functioning in different ways. Most of the molecular and cellular mechanisms that occur in response to SDB-related hypoxia remain unknown. In OSAS, an inflammatory cascade mainly dependent upon intermittent hypoxia has been described. There is a strong interaction between haemodynamic and inflammatory changes in promoting vascular remodelling. Moreover, during OSAS, most organ, tissue or functional impairment is related to the severity of nocturnal hypoxia. CSR-CSA occurring during heart failure is primarily a consequence of cardiac impairment. CSR-CSA has deleterious consequences for cardiac prognosis and mortality since it favours sympathetic activation, ventricular ectopy and atrial fibrillation. Although correction of CSR-CSA seems to be critical, there is a need to establish therapy guidelines in large randomised controlled trials. Finally, OHS is a growing health concern, owing to the worldwide obesity epidemic and OHS morbidities. The pathophysiology of OHS remains largely unknown. However, resistance to leptin, obesity and severe nocturnal hypoxia lead to insulin resistance and endothelial dysfunction. In addition, several adipokines may be triggered by hypoxia and explain, at least in part, OHS morbidity and mortality. Overall, chronic intermittent hypoxia appears to have specific genomic effects that differ notably from continuous hypoxia. Further research is required to fully elucidate the molecular and cellular mechanisms.
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PMID:Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives. 1882 54

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

Non-invasive mechanical ventilation (NIV) has been employed alternatively to invasive mechanical ventilation (IMV) in acute treatment as well as in long-term domiciliary use. In hypercapnic acute respiratory failure (ARF), NIV significantly reduces intubation and mortality rates and should thus be preferred to IMV whenever possible and as quick as possible. On the other hand, NIV is not generally recommended in hypoxemic ARF. Strong evidence supports the use of domiciliary NIV in chronic respiratory failure caused by neuromuscular diseases or by thoracic restrictions. In contrast, its influence on long time survival in COPD patients is not clearly proven. Prescription of home NIV in COPD should therefore be confined to severe degrees of chronic respiratory failure. Adaptive servo ventilation is another ventilatory mode that is increasingly used in patients with chronic heart failure and Cheyne-Stokes respiration.
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PMID:[Non-invasive ventilation in the treatment of acute respiratory and chronic ventilatory failure]. 1925 12

The awareness of Cheyne-Stokes respiration (CSR) and of the co-existence of the obstructive sleep apnoea syndrome and central breathing disturbances has rapidly grown in recent years. CSR is defined by a waxing and waning pattern of the breathing amplitude. Sleep related breathing disorders in patients with heart failure are associated with impaired clinical outcome and survival. While continuous positive airway pressure treatment (CPAP) is widely used to treat CSR, it has failed to improve overall survival of heart failure patients. Nevertheless, it has been shown that CPAP reduces mortality if breathing disturbances were sufficiently eliminated. Therefore, optimal suppression of CSR is critical. While CPAP reduces CSR by 50% on average, adaptive servoventilation (ASV) normalises CSR in most patients. ASV devices apply different levels of pressure support: during periods of hypoventilation the inspiratory pressure is increased while it is reduced to the lowest possible level during hyperventilation. The devices deliver an expiratory pressure to overcome upper airways obstruction. Pressure support is defined by the difference between expiratory and inspiratory pressure. Thus, while pressure support is fixed in bilevel devices, it varies under ASV. However, the hypothesis that ASV might improve survival in CSR patients has to be proved in prospective studies in CPAP nonresponders. There is a lack of evidence on the use of bilevel devices in CSR. However, ASV has proven both to effectively treat CSR and to be superior to CPAP in respiratory and sleep parameters in short term and medium term studies. Nevertheless, data on the long term use and the influence on cardiac parameters are necessary.
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PMID:Therapeutical options for the treatment of Cheyne-Stokes respiration. 1968 53

Due to its high prevalence in patients with heart failure and its negative predictive value concerning morbidity and mortality, Cheyne-Stokes respiration (CSR) is a sleep disorders of major interest. CSR correlates with the degree of heart failure and is characterised by a typical crescendo/decrescendo breathing pattern combined with phases of central sleep apnoea, caused by pulmonary oedema and oscillation of ventilatory control. Thus, CSR is a marker of the severity of heart failure. Treatment of CSR first involves optimisation of heart failure therapy by cardiologists and then application of non-invasive means of ventilatory support. Treatment of patients with severe heart failure with non-invasive positive pressure ventilatory support leads to a significant reduction of CSR, sympathetic activity, and daytime sleepiness and improves cardiac output and 6-minute walking distance. At present, a prospective randomised, controlled intervention-study (Serve-HF study) is being conducted in order to show if therapy of CSR can improve patient survival. This review describes the pathophysiology, epidemiology, and therapeutic options of CSR with a special focus on the elevated cardiovascular risk of patients with CSR.
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PMID:[Cheyne-Stokes respiration and cardiovascular risk]. 1959 Oct 86

It seems that the causes of the insomnia are dyspnea and an orthopnea in the heart failure patient. But, only such a fit is not the cause of the insomnia because it complains about the insomnia even if heart failure is slight. An obstructive sleep apnea (OSA) is the risk of the heart failure. A heart failure patient often complicates a central sleep apnea (CSA) and a Cheyne-Stokes respiration (CSR), and has much sleep fragmentation and difficulty maintaining sleep. And sleep disorders are sometimes started by the medications such as the cardiovascular system agent thing; beta blocker and the statins. Sleep disorders represent a major challenge in terms of differential diagnosis in heart failure patients. This is particularly relevant to insomnia and sleep disordered breathing (SDB) such as OSA, CSA and CSR. Thus, expending the knowledge on both insomnia and SDB may contribute to improve medical quality among physician.
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PMID:[Heart failure]. 1976 33

Sleep disorder specialists manage 90% of patients suffering from obstructive sleep apnoea, which affects 10% of the general population. From another perspective, cardiovascular disease specialists are particularly challenged by sleep apnoea, since it affects a large proportion of their patients and its complications are largely cardiovascular. At least 50% of patients with chronic heart failure (HF) suffer from sleep apnoea, predominantly central and/or Cheyne-Stokes respiration as opposed to obstructive sleep apnoea. While its effect on survival remains uncertain, sleep apnoea promotes the progression of chronic HF and is a predictor of poor prognosis. After screening by cardiologists, patients presenting with chronic HF and sleep apnoea should be referred to a sleep disorder specialist for diagnostic confirmation and treatment. In Part I of this review, we describe the diagnostic steps recommended when sleep apnoea is suspected in patients with chronic HF. We also review the definitions of abnormal sleep-related respiratory events and the prevalence, pathophysiology and haemodynamic consequences of sleep apnoea in this patient population.
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PMID:Sleep apnoea in patients with heart failure. Part I: diagnosis, definitions, prevalence, pathophysiology and haemodynamic consequences. 1978 69

Nasal continuous positive airway pressure (CPAP) is generally recommended for the treatment of obstructive sleep apnoea. CPAP lowers the cardiovascular morbidity and mortality associated with severe obstructive sleep apnoea. At least 50% of patients presenting with chronic heart failure (HF) have sleep apnoea; a subset of these patients may have obstructive sleep apnoea and may derive a survival benefit from CPAP. However, this population is also prone to developing central sleep apnoea, Cheyne-Stokes respiration or both (CSA/CSR), for which CPAP lowers the apnoea-hypopnoea index only partially and for which the overall effect of CPAP on survival remains to be determined, particularly as it has been observed to increase the mortality rate in subsets of patients. Other treatments may prove effective in patients with chronic HF and CSA/CSR, although none, thus far, has been found to confer a survival benefit. New ventilatory modes include bi-level positive airway pressure and automated adaptive servoventilation, the latter being most effective against CSA/CSR. Measures that can alleviate CSA/CSR indirectly include beta-adrenergic blockers and renin-angiotensin-aldosterone system inhibitors, nocturnal supplemental oxygen and cardiac resynchronization therapy (CRT). The effects of theophylline, acetazolamide and nocturnal CO(2) have also been studied. The second part of this review describes the applications and effects of therapies that are available for sleep apnoea in patients with chronic HF.
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PMID:Sleep apnoea in patients with heart failure: part II: therapy. 1991 72


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