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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocapnia contributes to the genesis of Cheyne-Stokes respiration and central sleep apnoea in patients with congestive heart failure (CHF) and is associated with increased mortality. However, the cause of hypocapnia in patients with chronic stable CHF is unknown. Since pulmonary congestion can induce hyperventilation via stimulation of pulmonary vagal afferents, the present study tested the hypothesis that in patients with CHF (carbon dioxide tension in arterial blood (Pa,CO2)) is inversely related to pulmonary capillary wedge pressure (PCWP), and that alterations in PCWP would cause inverse changes in Pa,CO2. In 11 CHF patients undergoing diagnostic cardiac catheterization, haemodynamic variables and arterial blood gas tensions were measured simultaneously at baseline. In three patients, these measurements were repeated after coronary angiographic dye infusion and nitroglycerine infusion. At baseline, Pa,CO2 correlated inversely with PCWP (r=-0.80, p=0.003). In the three patients in whom multiple measurements were made, acute alterations in PCWP caused inversely proportional changes in Pa,CO2. The present study concludes that in patients with congestive heart failure, pulmonary capillary wedge pressure is an important determinant of carbon dioxide tension in arterial blood. These findings imply that hypocapnia in patients with chronic stable congestive heart failure is a respiratory manifestation of elevated left ventricular filling pressures.
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PMID:Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure. 1184 25

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

Cheyne-Stokes respiration is frequently observed in congestive heart failure. Among other factors, prolongation of circulation time, hypocapnia and hypoxia are thought to underlie this sleep-related breathing disorder. Primary pulmonary hypertension (PPH) is also characterized by reduced cardiac output and blood gas alterations. Therefore, the aim of the present study was to determine whether a nocturnal periodic breathing (PB) occurs in PPH. A total of 20 consecutive patients with PPH who had been admitted for pharmacological investigation of pulmonary vasoreactivity were investigated by lung function testing, right heart catheterization and full-night attended polysomnography. PB was detected in six patients (30%) (mean +/- SEM: apnoea/hypopnoea index 37 +/- 5 h(-1); arterial oxygen saturation was <90% during 56 +/- 6.5% of total sleep time). The patients with PB had more severe haemodynamic impairment than those without. They also had a more marked reduction in the pulmonary diffusion capacity and greater arterial hypoxia. PB was markedly improved or even eradicated by nasal oxygen during the night. Periodic breathing occurs in patients with advanced primary pulmonary hypertension and can be reversed by nocturnal nasal oxygen. The clinical and prognostic significance of periodic breathing in primary pulmonary hypertension needs to be determined by further studies.
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PMID:Nocturnal periodic breathing in primary pulmonary hypertension. 1199 95

Nocturnal periodic breathing (PB) closely resembling Cheyne-Stokes respiration in congestive heart failure has been reported to occur in end-stage primary pulmonary hypertension (PPH). We herein describe the clinical course of a 56-year-old female patient with PPH and severe hypoxemia, hypocapnia, and right ventricular compromise in whom sleep-disordered breathing (SDB) resolved after successful double-lung transplantation. This case illustrates the crucial roles of blood gas alterations and hemodynamic impairment in the emergence of PB in PPH, and is in favor of a genuine association between advanced right heart failure and the development of SDB.
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PMID:Reversal of nocturnal periodic breathing in primary pulmonary hypertension after lung transplantation. 1471 66

The effect of standard cardiac resynchronisation therapy (CRT) on the severity of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure was studied. It was hypothesised that CRT, through its known beneficial effects on cardiac function, would stabilise the control of breathing and reduce CSR. Twenty-eight patients who were eligible for CRT and receiving optimised medical treatment for congestive heart failure were referred for overnight polysomnography, including monitoring of thoracic and abdominal movements to identify CSR and obstructive sleep apnoea events. Patients underwent repeat polysomnography after 6 months of CRT to re-evaluate sleep quality and sleep-disordered breathing. Twelve of the 28 patients had significant CSR (43%); 10 patients had a successful implantation and underwent repeat polysomnography a mean+/-SD 27+/-7 weeks after continuous biventricular pacing. Six of the 10 patients experienced a significant decrease in CSR severity following CRT, associated with correction of congestive heart failure-related hyperventilation and hypocapnia. Circulation time, oxygen saturation, frequency of obstructive apnoeas and sleep quality did not change. In conclusion, cardiac resynchronisation therapy is associated with a reduction in Cheyne-Stokes respiration, which may contribute to improved clinical outcome in patients treated with cardiac resynchronisation therapy.
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PMID:Improvement in Cheyne-Stokes respiration following cardiac resynchronisation therapy. 1638 57

Cheyne-Stokes respiration (CSR) is a form of central sleep-disordered breathing (SDB) in which there are cyclical fluctuations in breathing that lead to periods of central apneas/hypopnea, which alternate with periods of hyperpnea. The crescendo-decrescendo pattern of respiration in CSR is a compensation for the changing levels of blood oxygen and carbon dioxide. Severe congestive heart failure seems to be the most important risk factor for the development of CSR. A number of pathophysiologic changes, such as sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure have harmful effects on the cardiovascular system, and the presence of CSR is associated with increased mortality and morbidity in subjects with variable degrees of heart failure. The management of CSR involves optimal control of underlying heart failure, oxygen therapy, and positive airway pressure support. In this review, we initially define and describe the epidemiology of central sleep apnea (CSA) and CSR, its pathogenesis, clinical presentation, diagnostic methods, and then discuss the recent developments in the management in patients with heart failure.
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PMID:Cheyne-stokes respiration in patients with heart failure. 1995 65

Sleep-disordered breathing is one of the important factors contributing to the development and/or progression of heart failure (HF). This condition is related to recurring attacks of apnea, hypopnea, and hyperpnea, sleep disruptions, arousals, intermittent hypoxemia, hypocapnia, and hypercapnia, and intrathoracic pressure changes. Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction (apnea and hypopnea), increased breathing effort against totally or partially occluded upper airway, and sleep disruptions. Cardiovascular consequences are the most serious complications of OSA and include acute myocardial infarction, heart failure, left/right ventricular dysfunction, arrhythmias, stroke, and systemic and pulmonary hypertension. Cheyne-Stokes respiration and central apneas may also occur in patients with HF. This article reviews the most recent information on the physiopathology, diagnosis, and treatment modalities of obstructive and central apneas in patients with HF.
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PMID:[Heart failure and sleep apnea]. 2047 19

Heart failure (HF) and sleep apnoea are common disorders which frequently coexist. Two main types of apnoea occur: one is obstructive which, through recurring episodes of snoring, hypoxaemia, large negative intra-thoracic pressures and arousals from sleep leading to downstream inflammatory and autonomic nervous system changes, is thought to be a causative factor to the development of systemic hypertension and HF. The other type of apnoea, Cheyne-Stokes respiration with central sleep apnoea (CSR-CSA), is characterized by an oscillatory pattern of ventilation with a prevailing hyperventilation-induced hypocapnia, often in the absence of significant hypoxaemia and snoring, and is thought to be a consequence of advanced HF-related low cardiac output, high sympathetic nervous system activation and pulmonary congestion. CSR-CSA may be a compensatory response to advanced HF. Rostral fluid shift during sleep may play an important role in the pathogenesis of both obstructive sleep apnoea (OSA) and CSA. Studies of positive airway pressure (PAP) treatment of OSA and CSA in HF have shown short-term improvements in cardiac and autonomic function; however, there is no evidence of improved survival. Loop gain may provide useful marker of continuous PAP (CPAP) responsiveness in patients with central apnoea. A greater understanding of the pathophysiology of the interaction between obstructive and central apnoea and the various types of HF, and the mechanisms of therapies, such as PAP, is required to develop new strategies to overcome the disabling symptoms, and perhaps improve the mortality, that accompany HF with sleep apnoea.
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PMID:Sleep apnoea in heart failure: To treat or not to treat? 2799 40

Central sleep apnea and Cheyne-Stokes respiration are commonly observed breathing patterns during sleep in patients with congestive heart failure. Common risk factors are male gender, older age, presence of atrial fibrillation, and daytime hypocapnia. Proposed mechanisms include augmented peripheral and central chemoreceptor sensitivity, which increase ventilator instability during both wakefulness and sleep; diminished cerebrovascular reactivity and increased circulation time, which impair the normal buffering of Paco2 and hydrogen ions and delay the detection of changes in Paco2 during sleep; and rostral fluid shifts that predispose to hypocapnia.
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PMID:Central Sleep Apnea in Patients with Congestive Heart Failure. 2847 76


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