Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 57-year-old man was admitted with dyspnea. Clinical evaluation revealed atrial fibrillation and congestive heart failure (CHF). Standard medical therapy of CHF failed to completely improve the dyspnea and polysomnography revealed Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). He was equipped with noninvasive positive pressure ventilation (NPPV) with bilevel positive airway pressure (BiPAP). The combined therapy of medical treatment of the CHF and administration of NPPV with BiPAP reduced the CSR-CSA. This regimen resulted in marked improvement of cardiac function, evaluated by echocardiography, and reduction of plasma concentration of brain natriuretic peptide. After the patient recovered from CHF and was discharged from hospital, he continued to use NPPV with BiPAP at home. In patients with CHF, it is important to be aware of sleep-related breathing disorders because treatment will not only improve the hypoxemia, but also the cardiac dysfunction.
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PMID:Improvement of cheyne-stokes respiration, central sleep apnea and congestive heart failure by noninvasive bilevel positive pressure and medical treatment. 1532 13

Five adult patients with congestive heart failure (CHF) due to dilated cardiomyopathy complicated by Cheyne-Stokes respiration/central sleep apnea (CSR/CSA) were treated with continuous positive airway pressure (CPAP) with an initial pressure of 5 cm H2O. Four patients were followed up for 12 months with CPAP of 5 cm H2O. The rest, a 93-year-old patient, was followed up for 30 months, and the CPAP was reset at 8 cm H2O due to worsened cardiac function after 6 months and it was reset at 6 cm H2O due to dryness of the nose after 23 months. For all the patients with nightly CPAP use for 6.0+/-1.4 h per day for a year, frequency of CSR/CSA was significantly reduced after 3 and 12 months with CPAP (p<0.05). Moreover, their symptoms, cardiac function and sleep quality were significantly improved after 3 months (p<0.05), and were maintained above the pre-CPAP levels after 12 months, except for the oldest patient whose cardiac function tended to deteriorate. The results suggest that CSR/CSA in CHF can be treated with CPAP set at a lower pressure than the conventional method, and that CPAP at 5-8 cm H2O is often effective in eliminating CSR/CSA, improving sleep quality, and presumably maintaining cardiac function.
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PMID:Cheyne-Stokes respiration in congestive heart failure: continuous positive airway pressure of 5-8 cm H2O for 1 year in five cases. 1726 69

In subjects with sinus rhythm, respiration has a profound effect on heart rate variability (HRV) at high frequencies (HF). Because this HF respiratory arrhythmia is lost in atrial fibrillation (AF), it has been assumed that respiration does not influence the ventricular response. However, previous investigations have not considered the possibility that respiration might influence HRV at lower frequencies. We hypothesized that Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would entrain HRV at very low frequency (VLF) in AF by modulating atrioventricular (AV) nodal refractory period and concealed conduction. Power spectral analysis of R-wave-to-R-wave (R-R) intervals and respiration during sleep were performed in 13 subjects with AF and CSR-CSA. As anticipated, no modulation of HRV was detected at HF during regular breathing. In contrast, VLF HRV was entrained by CSR-CSA [coherence between respiration and HRV of 0.69 (SD 0.22) at VLF during CSR-CSA vs. 0.20 (SD 0.19) at HF during regular breathing, P < 0.001]. Comparison of R-R intervals during CSR-CSA demonstrated a shorter AV node refractory period during hyperpnea than apnea [minimum R-R of 684 (SD 126) vs. 735 ms (SD 147), P < 0.001] and a lesser degree of concealed conduction [scatter of 178 (SD 56) vs. 246 ms (SD 72), P = 0.001]. We conclude that CSR-CSA entrains the ventricular response to AF, even in the absence of HF respiratory arrhythmia, by inducing rhythmic oscillations in AV node refractoriness and the degree of concealed conduction that may be a function of autonomic modulation of the AV node.
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PMID:Influence of Cheyne-Stokes respiration on ventricular response to atrial fibrillation in heart failure. 1599 46

In patients with obstructive sleep apnoea (OSA), the very low frequency power spectral density index (VLFI) derived from analysis of heart rate correlates with the severity of obstructive apnoeas. VLFI is also associated with Cheyne-Stokes respiration/central sleep apnoea (CSR/CSA) in congestive heart failure (CHF). The present authors have tested the hypothesis that per cent VLFI, derived from a standard Holter ECG recording, can be used to detect the presence of OSA and CSR/CSA in patients with mild-to-moderate CHF. In total, 60 CHF patients underwent polysomnography with monitoring of heart rate. Data from 33 patients were analysed for per cent VLFI. Of the 60 patients, 27 were excluded due to atrial fibrillation, extensive pacing or frequent ventricular extra systoles. Receiver operator characteristic curves were constructed to establish the per cent VLFI that would optimally identify the presence or absence of sleep-disordered breathing. Using an apnoea-hypopnoea index>20 events.h-1 and setting the per cent VLFI at 2.23% yielded a sensitivity of 85%, specificity of 65%, positive predictive value of 61% and a negative predictive value of 87%. The latter increased to 100% when using an apnoea-hypopnoea cut-off of 30 events.h-1. In conclusion, these results suggest that spectral analysis of heart rate may be useful as a "rule-out test" for sleep-disordered breathing in patients with mild-to-moderate congestive heart failure.
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PMID:Can heart rate variation rule out sleep-disordered breathing in heart failure? 1688 Mar 76

Use of extended electrocardiography (ECG) for detection of sleep disordered breathing SDB when obstructive sleep apneas and Cheyne-Stokes breathing are simultaneously present is explored. A multi-tier algorithm is designed that uses quantitative changes in the morphology of the QRS complex of Lead 1 and V4 due of SDB events and combines those changes with variations in heart rate to detect each type of SDB. For this purpose, ECG signals are divided into 15 minute epochs. These epochs are then subjected to baseline wander removal and R peak detection. An envelope of R peaks is computed to derive R Wave Attenuation (RWA). Concurrently, the heart rate variability (HRV) is also computed. Various biomarkers derived from these trends are combined to develop an algorithm to classify Normal, OSA and CSR epochs. One hundred and five (105) data clips from 15 subjects were used to test the proposed algorithm. It produced detection rates of 93.75%, 100% and 83.3% for Normal, OSA and CSR epochs respectively in case of training set (66 clips). Detection rates of 75%, 85.71% and 70.5% for Normal, OSA and CSR epochs respectively were obtained in case of test set (39 clips).
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PMID:ECG biomarkers for simultaneous detection of obstructive sleep apnea and Cheyne-Stokes breathing. 1800 40

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

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

There are different treatment options for obstructive sleep apnea, which are selectively used based on severity of sleep apnea, physical structure of the upper airway, and other medical aspects including co-morbidities. Weight loss as well as avoidance of alcohol and other CNS depressants is generally recommended. Positional training, oral appliances and surgery of the upper airways are used in selected cases. CPAP is the most effective method for treating obstructive sleep apnea irrespective of disease severity. In patients with central sleep apnea or Cheyne-Stokes respiration (CSA/CSR) diagnosis and treatment of the underlying cause is mandatory. Adaptive servo-ventilation appears to be an effective treatment modality for patients with complex sleep apnea and with CSA/CSR that is resistant to CPAP.
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PMID:[Modern therapy of sleep apnea]. 1903 17

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

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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