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

Patients with heart failure are known to demonstrate periodic respiration during sleep. The mechanism behind periodic respiration is thought to be related to left heart enlargement causing an increased transit time between lung and chemoreceptors leading to an oscillation of the feed back loop controlling respiration. Additionally hyperventilation was shown to play an important role. We report of an 18 year old patient with idiopathic dilated cardiomyopathy (left atrial 52 mm, left ventricular end diastolic diameter 69 mm). Polysomnography revealed prolonged transit time and periodic respiration with impaired sleep. Hypocapnia and hyperventilation was demonstrated. Following successful cardiac transplantation periodic respiration was absent and transit time was normal. There was no hypocapnia or hyperventilation. Hypercapnic ventilatory response did no change. These findings support the model of an oscillation of the feed back loop controlling respiration as the main pathomechanism behind periodic respiration.
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PMID:[Elimination of periodic respiration in heart failure by heart transplantation]. 767 58

The syndrome of chronic heart failure is characterized by exercise intolerance. Exercise is limited by shortness of breath and fatigue, and either symptom occurs in the same patient depending on the type of exercise performed. Exercise capacity correlates poorly with indices of central hemodynamic function, but the increased ventilatory response in chronic heart failure correlates well with exercise capacity. Possible pulmonary causes have been explored, including increased dead space ventilation, abnormal airway function, and abnormal diffusion capacity. However, the finding of hypocapnia and hyperoxemia in arterial blood during exercise in patients with heart failure suggests that blood gas values reflect hyperventilation, and that any abnormality of pulmonary function is secondary to changes elsewhere. Skeletal muscle is abnormal in chronic heart failure, and shows changes in structure, bulk, exercise capacity, blood flow, and intrinsic metabolic activity. The relative importance of these abnormalities is not clearly determined, but the possible presence of an ergo- or metaboloreceptor connection between abnormal exercising muscle and the ventilatory response to exercise suggest a mechanism linking the two cardinal symptoms of chronic heart failure.
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PMID:Mechanisms of exercise intolerance in cardiac failure: abnormalities of skeletal muscle and pulmonary function. 804 88

The aim of this study was to determine what factors beyond age affect post-operative mortality. We included 971 patients (mean age 61 +/- 10 years; 882 men, 89 women). There were 61 patients (6%) 75 years of age and over. Post-operative death rate was 15% in patients 75 and over versus 6% in patients under 75 (p = 0.01). Other variables significantly correlated with post-operative death after univariate analysis were: heart failure, Karnofsky score, VEMS, CV, PaCO2, tumor size, right side resection, pneumonectomy and large exeresis. Multivariate analysis retained 6 independent variables affecting post-operative mortality: age > or = 75 years (p = 0.019), Karnofsky score (p = 0.0001), right side resection (p = 0.0002, pneumonectomy (p = 0.04, large resection (p = 0.029) and hypocapnia (p = 0.01). If these parameters are considered when deciding on surgery, pulmonary exeresis may be proposed in elderly patients.
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PMID:[Pulmonary excisions in patients aged 75 and over. Study of postoperative mortality]. 876 36

Patients suffering from severe heart failure may develop breathing disorders during sleep. Results may be heavy disturbances in sleep architecture, worsening of haemodynamics and of the prognosis of these patients. Causes of breathing disorders are probably instability of breathing regulation caused by hypoxaemia, hypocapnia, and prolonged blood circulation time. This study examined the influence exercised by different concentrations of continuously applied oxygen during night time on breathing disorders, oxygen saturation and sleep architecture in patients with severe heart failure (NYHA III-IV). All patients showed an improvement in sleep architecture. Total sleeping time increased significantly. Fragmentations of sleep by arousal reactions decreased, time of REM-sleep and non-REM-sleep III and IV increased significantly.
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PMID:[Effect of long-term oxygen therapy on sleep architecture in patients with severe dilated cardiomyopathy and Cheyne-Stokes respiration]. 934 Jun 29

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

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

Patients suffering from severe heart failure may develop breathing pattern disorders during sleep, especially in the form of Cheyne-Stokes respiration. Results may be severe disturbances in sleep architecture and worsening of hemodynamics and of prognosis of these patients. Causes of the periodic breathing disorders are probably hypocapnia, hypersensitivity of respiratory control centers, hypoxemia, and prolonged blood circulation time. This study examined the influence of different concentrations of continously administered oxygen during the nighttime on breathing pattern disorders, oxygen saturation, and sleep architecture in 65 patients with severe heart failure (NYHA III-IV). Fifty-two of 65 patients showed an improvement of sleep architecture. Total sleeping time increased significantly (p < 0.01). Fragmentations of sleep by arousals decreased ( p < 0.01); time of random eye movement (REM) sleep and non-REM sleep III and IV increased significantly.
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PMID:Influence of Low-Flow Oxygen Supply on Sleep Architecture in Patients with Severe Heart Failure (NYHA III-IV) and Cheyne-Stokes Respiration. 1186 28

To determine whether sleep quality is influenced by the mode of mechanical ventilation, we performed polysomnography on 11 critically ill patients. Because pressure support predisposes to central apneas in healthy subjects, we examined whether the presence of a backup rate on assist-control ventilation would decrease apnea-related arousals and improve sleep quality. Sleep fragmentation, measured as the number of arousals and awakenings, was greater during pressure support than during assist-control ventilation: 79 +/- 7 versus 54 +/- 7 events per hour (p = 0.02). Central apneas occurred during pressure support in six patients; heart failure was more common in these six patients than in the five patients without apneas: 83 versus 20% (p = 0.04). Among patients with central apneas, adding dead space decreased sleep fragmentation: 44 +/- 6 versus 83 +/- 12 arousals and awakenings per hour (p = 0.02). Changes in sleep-wakefulness state caused greater changes in breath components and end-tidal CO2 during pressure support than during assist-control ventilation. In conclusion, inspiratory assistance from pressure support causes hypocapnia, which combined with the lack of a backup rate and wakefulness drive can lead to central apneas and sleep fragmentation, especially in patients with heart failure.
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PMID:Effect of ventilator mode on sleep quality in critically ill patients. 1460 24

Heart failure is a highly prevalent problem associated with excess morbidity and mortality and economic impact. Because of increased average life span, improved therapy of ischemic coronary artery disease and hypertension, the incidence and prevalence of heart failure will continue to rise into the twenty-first century. Multiple factors may contribute to the progressively declining course of heart failure. One such cause could be the occurrence of repetitive episodes of apnea, hypopnea, and hyperpnea, which frequently occur in patients with heart failure. Episodes of apnea, hypopnea, and hyperpnea cause sleep disruption, arousals, intermittent hypoxemia, hypercapnia, hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on cardiovascular system, and the effects may be most pronounced in the setting of established heart failure and coronary artery disease. Diagnosis and treatment of sleep-related breathing disorders may improve morbidity and mortality of patients with heart failure [34]. Large-scale, carefully executed therapeutic studies are needed to determine if treatment of sleep-related breathing disorders changes the natural history of left ventricular failure.
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PMID:Heart failure and sleep apnea: emphasis on practical therapeutic options. 1280 Jul 79


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