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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 (CSR) during sleep is common in patients with severe congestive heart failure induces repetitive oxygen desaturation with arousals, and impairs sleep. This causes daytime symptoms and likely an increase in sympathetic activity. It has, therefore, been suggested that CSR is independently related to mortality. The major mechanisms behind CSR include reduced body stores of oxygen, a low apneic threshold for carbon dioxide, prolonged circulation time between the lung and the carotid body, and disturbance of respiratory control due to arousals. It is apparent that the main task in treating CSR is the therapy of congestive heart failure. Indeed, diuretics to treat pulmonary congestion as well as ACE-inhibitors reduce CSR. Recently, theophylline (an antagonist of the ventilatory depressant adenosine) was shown to reduce CSR and oxygen-desaturation. Continuous positive airway pressure did improve CSR but not sleep and may reduce cardiac output in a subgroup of patients with heart failure. Nocturnal oxygen reduces CSR and improves exercise tolerance as well as sleep. This and its apparent safety makes oxygen an appropriate treatment for nocturnal CSR. Whether successful treatment of nocturnal CSR has any impact on the natural course of heart failure needs to be determined in further studies.
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PMID:[Cheyne-Stokes respiration in patients with congestive heart failure]. 953 95

Sleep-related breathing disorders, including obstructive sleep apnea (OSA) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA), commonly occur in patients with congestive heart failure (CHF). In this setting they can have adverse pathophysiologic effects on the cardiovascular system. OSA may lead to development or progression of left ventricular (LV) dysfunction by increasing LV afterload through the combined effects of elevations in systemic blood pressure and a generation of exaggerated negative intrathoracic pressure, and by activating the sympathetic nervous system through the influence of hypoxia and arousals from sleep. Abolition of OSA by continuous positive airway pressure (CPAP) can improve cardiac function in patients with CHF. In contrast to OSA, CSR-CSA is likely a consequence rather than a cause of CHF. Here, pulmonary congestion causes hyperventilation by stimulating pulmonary irritant receptors. This leads to reductions in PaCO2 below the apneic threshold during sleep, precipitating posthyperventilatory central apneas. CSR-CSA is associated with increased mortality in CHF, probably because of sympathetic nervous system activation caused by recurrent apnea-induced hypoxia and arousals from sleep. Treatment of CSR-CSA by supplemental O2, theophylline, and CPAP can alleviate central apneas. Of these treatments, however, only CPAP has been shown to improve cardiac function and symptoms of heart failure. We conclude that effective treatments of OSA and CSR-CSA may prove to be useful adjuncts to the standard pharmacologic therapy of patients with CHF.
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PMID:Sleep apnea in congestive heart failure. 955 21

Patients with congestive heart failure and Cheyne-Stokes respiration have a low arterial oxygen saturation, especially during sleep, which can be increased by breathing oxygen. Chronic alterations in blood gases are known to modulate the hypercapnic ventilatory response (HCVR). We therefore evaluated whether the HCVR is influenced by nocturnal nasal oxygen in patients with heart failure and Cheyne-Stokes respiration. Twenty patients with chronic congestive heart failure and a left ventricular ejection fraction < or = 35% (mean 18.3% +/- SD 6.0%) as well as 25 healthy control subjects were studied. The patients were assigned to 1 week each of nocturnal nasal oxygen and room air with a flow of 41 min-1 in a randomized cross-over fashion. After each week resting ventilation and HCVR were evaluated by the rebreathing technique. Breathing oxygen during the night for 1 week increased the basal nocturnal oxygen saturation from 92.5% +/- 1.6% to 96.5% +/- 0.9% (P < 0.000,01) and reduced Cheyne-Stokes respiration. HCVR was 1.22 +/- 0.90 l min-1 mmHg-1 after nocturnal room air and did not differ from that in the control subjects (1.31 +/- 0.62 l min-1 mmHg-1). In the patients HCVR decreased to 0.91 +/- 0.52 l min-1 mmHg-1 after nocturnal oxygen (P = 0.019). There were no significant changes with nocturnal oxygen in resting minute ventilation, respiratory rate or end-tidal PCO2. We conclude that nocturnal nasal oxygen reduces HCVR in patients with congestive heart failure and Cheyne-Stokes respiration.
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PMID:Nocturnal oxygen and hypercapnic ventilatory response in patients with congestive heart failure. 969

The purpose of our study was to determine the prevalence of sleep related breathing disorders (SRBD) in patients with an implantable cardioverter-defibrillator (ICD) and to evaluate prospectively the possible influence of SRBD on arrhythmia recurrence and circadian arrhythmia variation as well as on cardiac mortality during long-term follow-up. Forty consecutive ICD recipients with cardiac disease and a documented history of spontaneous, life-threatening, ventricular tachyarrhythmias underwent full-night polysomnography and were followed for 2 years. In 16 of 40 patients (40%), SRBD were diagnosed (Apnea/Hypopnea Index (AHI) > 10); in 9 of these 16 patients (56%) central sleep apneas (CSA) occurred (in 8 of these 9 patients in combination with Cheyne-Stokes respiration). Seven of the 16 patients with SRBD (44%) revealed obstructive sleep apneas (OSA). AHI was 32 +/- 15 (12-60) in patients with CSA and 32 +/- 27 (11-86) in patients with OSA. Patients with and without SRBD were comparable concerning left ventricular ejection fraction, NYHA classification, cardiac disease, ICD indication, and concomitant medication. ICD registered ventricular tachyarrhythmias occurred in 10 of 24 patients (42%) without SRBD, in 4 of 9 patients (44%) with CSA, and in 3 of 7 patients (44%) with OSA. The numbers and circadian variation of episodes registered during follow-up in patients without SRBD, with OSA or CSA were comparable (14 +/- 25, median 4 vs 15 +/- 15, median 7 vs 4 +/- 5, median 2.5). The 2-year cardiac mortality was highest in patients with CSA (4/9 (44%) vs. 0/7 patients (0%) with OSA vs 3/24 patients (12.5%) without SRBD. Thus, the prevalence of SRBD in patients with chronic heart failure and a history of malignant ventricular tachyarrhythmias is high (40%) and the occurrence of CSA seems to be predictive for cardiac mortality in these patients. An influence of moderate SRBD on arrhythmia recurrence and circadian variation of spontaneous sustained tachyarrhythmic events could not be demonstrated.
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PMID:[Clinical significance of sleep apnea disorders after implantation of a cardioverter-defibrillator in patients with cardiac disease and sustained ventricular tachyarrhythmia]. 985 58

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
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PMID:[Sleep-related cardiac insufficiency and respiratory disorders. Prevalence, physiopathology, and treatment]. 1033 59

Chronic heart failure (CHF) patients frequently show sleep-disordered breathing consisting of periodic breathing (PB) and Cheyne-Stokes respiration (CSR) with central sleep apnoea (CSA). Since the diagnosis of sleep-disordered breathing, in CHF patients, can be made only by means of full polysomnography, the aim of the present study was to evaluate whether or not daytime respiratory function can identify patients at risk of nocturnal PB and/or CSR/CSA. Twenty-seven patients (mean age 54 +/- 8.5 yrs), eight New York Heart Association Functional Class (NYHAFC) II, 17 NYHAFC III and two NYHAFC IV, with severe cardiac failure (cardiac output 2.0 +/- 0.66 L.min-1, ejection fraction 22.5 +/- 5.77%, pulmonary capillary wedge/pressure 23 +/- 9.05 mmHg). Mouth occlusion pressure (P0.1)/maximal inspiratory pressure (MIP) was significantly higher in patients with nocturnal CSR/CSA (5.04 +/- 1.49 versus 3.24 +/- 2.13%, analysis of variance (ANOVA) 0.03), whereas their arterial carbon dioxide tension (Pa,CO2) was significantly lower (4.15 +/- 0.56 (31.2 +/- 4.23 mmHg) versus 4.67 +/- 0.53 kPa (35.1 +/- 4 mmHg), ANOVA 0.02). Logistic regression analysis demonstrated that CSR/CSA occurrence may be predicted by daytime measurement of P0.1/MIP and Pa,CO2 (p = 0.04 and 0.01 respectively; odds ratio 1.93 and 0.76 respectively). The sensitivity was 70%, specificity 76.5%, false positive rate 36.4%, false negative rate 18.8%, positive predictive value 71.4% and negative predictive value 85%. This model seems useful for predicting respiratory pattern changes in chronic heart failure patients and the authors suggest that polysomnography be performed only in high-risk patients, saving costs and the resources of sleep laboratories.
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PMID:Identification of chronic heart failure patients at risk of Cheyne-Stokes respiration. 1054 73

Little is known about how arousal develops during the ventilatory phase of Cheyne-Stokes breathing. This study employs neural network analysis of electroencephalograms (EEGs) to describe these changes and relate them to changes in systolic blood pressure, which is probably a subcortical marker of arousal. Six patients with Cheyne-Stokes respiration (apnoea/hypopnoea index 32-69 h(-1)) caused by stable chronic heart failure underwent polysomnography including arterial beat-to-beat systolic blood pressure determination. Periods of 15 sequential apnoeas during nonrapid eye movement sleep were identified for each subject. For each apnoea, the EEG was examined second-by-second using neural net analysis from 28 s before to 28 s after apnoea termination (first return of oronasal airflow), and this was compared with the systolic blood pressure pattern. During the apnoeic phase, sleep deepened progressively. Arousal started to develop at or just before apnoea termination and progresses through the breathing phase. The rise and fall in the systolic blood pressure closely followed the rise and fall in electroencephalographic sleep depth. In conclusion, during Cheyne-Stokes breathing, cortical electroencephalographic arousal begins at or just before the resumption of breathing. Cortical electroencephalographic sleep depth changes are closely mirrored by changes in arterial systolic blood pressure, suggesting that the state changes in the cortical and basal brain structures may be synchronous.
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PMID:Second by second patterns in cortical electroencephalograph and systolic blood pressure during Cheyne-Stokes. 1057 46

Central sleep apnea with Cheyne-Stokes respiration (CSR) during sleep affects about 40 % of patients with chronic heart failure (CHF). During CSR simultaneous periodic fluctuations in wakefulness and respiration with accompanying changes in blood pressure and heart rate are observed. CSR can be described as an oscillation of the ventilatory feedback loop controlling respiration. The major synergistically acting mechanisms causing this oscillation include reduced body stores of oxygen and carbon dioxide, hyperventilation with concomitant hypocapnia, prolonged circulation time, and a relatively high hypercapnic ventilatory response. The repetitive desaturations and arousals following CSR cause daytime symptoms and an increase in sympathetic activity. In CHF chronically increased sympathetic activity has negative effects on left ventricular function and is associated with reduced exercise tolerance and poor prognosis. Therefore CSR is expected to have an unfavorable influence on the course of CHF. Whether successful treatment of nocturnal CSR has any impact on the high mortality of CHF needs to be resolved in controlled studies with sufficient sample size.
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PMID:Central sleep apnea and chronic heart failure. 1089 7

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
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PMID:[Heart failure and sleep respiratory disorders. Prevalence, physiopathology and treatment]. 1093 1

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.
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PMID:Adaptive pressure support servo-ventilation: a novel treatment for Cheyne-Stokes respiration in heart failure. 1152 Jul 25


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