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

1.26 of 340 patients with chronic heart failure (aortic-valve or mitral-valve disease, congestive cardiomyopathy) showed Cheyne-Stokes respiration in supine position. 2. The incidence of Cheyne-Stokes respiration in males is more than twice as high as in females with similar hemodynamic conditions. 3. Lung volumes and airway resistance did not appreciably deviate from the predicted values and are therefore of no etiologic significance. 4. Delay of the feedback between changes in the alveolar gas tensions and respiratory center caused by a prolonged circulation time (decreased cardiac index and increased central blood volume) is the predominant cause of Cheyne-Stokes breathing in patients with chronic heart failure. 5. Metabolic alkalosis (e.g. after diuretics) favors Cheyne-Stokes respiration in patients with congestive heart failure and low cardiac output, by lessening respiratory changes in pH of blood and cerebrospinal fluid.
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PMID:[Cheyne-Stokes respiration in chronic heart insufficiency]. 87 30

Although the apnea/hypopnea index is the most widely used measure of breathing pattern abnormality during sleep, this index gives no information about the strength of the oscillation in the breathing pattern, its periodicity or its regularity. Such information may be required in research studies involving breathing patterns and how they are affected by interventions. We are exploring spectral analytic methods to determine two normalized indices, the periodicity index and the modified modulation index, to examine periodic breathing for all-night sleep studies. These methods are automatic and require no user interaction. Data were obtained from 11 heart failure patients who slept for a total of 21 nights in the sleep laboratory. Because individual patients had a marked regularity of their Cheyne-Stokes respiration during sleep, one would expect an extremely high correlation between the traditional measures of breathing pattern abnormality and these spectral analytic techniques. Indeed we found that there was an extremely high correlation between the periodicity index and the modulation index and the traditional measures of apnea/hypopnea index and the proportion of the night with periodic breathing (p less than 0.02 in all cases). When the breathing pattern was irregular but still with many apneas there was a discrepancy between the apnea index and the indices of periodicity. These techniques are still preliminary and future studies will determine their limitations in other patient populations and where the pattern is unstable.
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PMID:Short technical note: quantification of periodic breathing: preliminary studies. 151 13

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
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PMID:Right and left ventricular functional impairment and sleep apnea. 152 13

This report describes a case of Cheyne-Stokes respiration linked to heart failure, with periodic disturbances of atrioventricular conduction during the augmentation phase of the tidal volume. The circulatory retardation caused by heart failure induced a phase lag of the negative retroaction system and secondarily an oscillation in the respiratory command. The conduction disturbances resulted from vagal stimulation of multifactorial origin. The atrioventricular conduction disturbances were analogous to those seen in other periodic respiratory diseases.
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PMID:[Conduction disorders in Cheyne-Stokes respiration caused by cardiac insufficiency]. 233 Nov 33

We studied five patients with chronic stable congestive heart failure (CHF), all of whom demonstrated recurrent apneas in association with Cheyne-Stokes respiration (CSR) during sleep. All five patients had symptoms consistent with a sleep apnea syndrome. Nasal continuous positive airway pressure (NCPAP) was administered at 8 to 12.5 cm H2O to all patients during sleep. The number of apneas fell from (mean +/- SE) 60 +/- 12/h of sleep on the control night to 9 +/- 7/h of sleep (p less than 0.01) on the NCPAP night, whereas mean nocturnal SaO2 rose from 88 +/- 2% on the control night to 92 +/- 2% (p less than 0.025) while on NCPAP. This was associated with resolution of symptoms of sleep apnea. In addition, resting left ventricular ejection fraction (LVEF) as measured by radionuclide angiography (RNA) rose from 31 +/- 8% while off NCPAP to 38 +/- 10% (p less than 0.05) while on NCPAP. Furthermore, all five patients experienced marked improvement in symptoms of heart failure from functional classes III and IV (New York Heart Association Classification) prior to NCPAP therapy to class II after NCPAP therapy was instituted. We conclude that, in certain patients, CSR during sleep associated with chronic CHF constitutes a sleep apnea syndrome, which can be alleviated by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function.
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PMID:Effect of nasal continuous positive airway pressure on sleep apnea in congestive heart failure. 269 Jul 5

For the purpose of elucidating the mechanisms and/or effects of the cardiovascular changes occurring during Cheyne-Stokes respiration, we utilized Doppler echocardiography to determine intracardiac flow velocity profiles during the changing phases. Left ventricular inflow (LVI) and outflow (LVO) were examined in ten patients, nine with heart failure and one with a cerebrovascular accident. The mean LVI, peak early (E) and late diastolic (A) and LVO velocities were measured at the end of both the hyperpneic and apneic phases. The phasic hemodynamic changes observed during Cheyne-Stokes respiration by Doppler profile could be explained by the development of LV diastolic dysfunction and a decrease in LV stroke volume during the apneic phase of Cheyne-Stokes respiration. Alternatively, an increase in PCO2 during the apneic phase may increase pulmonary vascular resistance lowering preload and stroke volume, whereas during the hyperpneic phase, pulmonary vascular resistance is reduced with resultant increase in left ventricular preload and increase in stroke volume. Both theories are speculative and the precise hemodynamic changes associated with Cheyne-Stokes respiration requires further investigation.
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PMID:Doppler evaluation of changing cardiac dynamics during Cheyne-Stokes respiration. 230 87

A patient with symptoms of sleep apnea syndrome had signs of congestive cardiac failure. A sleep study fulfilled the criteria for sleep apnea. Features of Cheyne-Stokes respiration coexisted. Management of the cardiac failure by weight loss principally due to diuretic use eliminated the symptoms of sleep apnea.
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PMID:Cardiac failure presenting as sleep apnea. Elimination of apnea following medical management of cardiac failure. 319 74

Fifteen patients with left ventricular heart failure (LVF) without known breathing disorders during sleep had full-night recordings of sleep and breathing to study the incidence and impact of the apnea of Cheyne-Stokes breathing. This group showed a marked degree of sleep-related breathing abnormalities, 40% demonstrating Cheyne-Stokes breathing with five or more central apneas per hour of sleep. Cheyne-Stokes breathing during sleep in patients with LVF predicted an increased short-term mortality rate. All six patients with LVF and Cheyne-Stokes breathing with more than five apneas per hour of sleep were dead within six months, while only three of nine patients without recurrent apnea died within six months, a significant difference (P less than .05) even in this small group. Among seven patients with LVF studied with the polysomnogram, there were statistically significant differences between the Cheyne-Stokes and non-apnea groups in total sleep time, awakening per hour, and the number of arterial desaturations. Although sleep disturbances have been anecdotally described in patients with LVF, no previous investigation has determined the incidence and impact of Cheyne-Stokes breathing during sleep in LVF. Our findings that Cheyne-Stokes breathing predicts an adverse short-term mortality rate confirm the clinical impression that Cheyne-Stokes breathing is a poor prognostic sign in LVF.
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PMID:Cheyne-Stokes breathing during sleep in patients with left ventricular heart failure. 396 65

A previous uncontrolled study suggested that nasal continuous positive airway positive airway pressure (NCPAP) may improve left ventricular ejection fraction (LVEF) in patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In order to more critically evaluate the effects of NCPAP on cardiac function, we undertook a randomized, controlled trial of NCPAP in 29 patients with heart failure and CSR-CSA over a 3-mo period, with LVEF as the primary outcome measure. Patients with CHF and associated CSR-CSA who were receiving optimal medical therapy were randomly assigned to a control group (n = 15) or a group receiving nightly NCPAP (n = 14). Twelve patients in each group completed the study. There was a greater improvement of LVEF in the NCPAP group than in the control group during the study (mean +/- SEM = 7.7 +/- 2.5 versus - 0.5 +/- 1.5%, p = 0.019). In addition, there was a significantly greater reduction in the number of apneas and hypopneas (-28.5 +/- 3.9 versus -6.1 +/- 7.0 per hour of sleep, p = 0.012) in the NCPAP group than in the control group. Significantly greater improvements in symptoms of fatigue (5.6 +/- 1.2 versus 0.8 +/- 0.7, p = 0.005) and disease mastery (3.6 +/- 1.1 versus -0.7 +/- 0.7, p = 0.031) were also observed in the NCPAP group. We conclude that in patients with chronic heart failure and CSR-CSA, nightly administration of NCPAP can attenuate CSR-CSA, improve cardiac function, and alleviate symptoms of heart failure.
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PMID:Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure. 781 79

Two patients with heart failure and Cheyne-Stokes breathing are presented. We have discussed the possible physiopathological mechanism of Cheyne-Stokes breathing and clinical, instrumental and laboratory data for a correct diagnostic evaluation.
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PMID:[Periodic Cheyne-Stokes respiration caused by increased circulation time. Report of 2 clinical cases]. 793 60


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