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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because apnea length during periodic breathing varies according to the preceding increase in ventilation and reduction in PaCO 2, differences in the cycle length of periodic breathing among patients with normal and impaired cardiac function might be explained by the influence of lung-to-carotid body circulatory delay, as reflected by lung-to-ear circulation time (LECT), on hyperpnea length rather than on apnea length. It was therefore hypothesized that circulatory delay is an important determinant of periodic-breathing hyperpnea length but not apnea length. To test this hypothesis, LECT, periodic-breathing cycle length, apnea length, and hyperpnea length were compared in 10 patients with idiopathic central sleep apnea (ICSA), whose cardiac function was normal, as opposed to 10 with Cheyne-Stokes respiration and central sleep apnea (CSR-CSA) in association with congestive heart failure (CHF). As compared with ICSA patients, cycle length was significantly longer in patients with CSR-CSA (37.3 +/- 3.0 s versus 59.0 +/- 4.9 s, p < 0.005). This difference was due to significantly longer hyperpnea length in the CSR-CSA patients (16.7 +/- 2.8 s versus 36.7 +/- 3.4 s, p < 0.001), since apnea length was similar in the two groups. In addition, LECT was longer in the CSR-CSA patients (24.3 +/- 2.0 s versus 10.3 +/- 1.0 s, p < 0.001), and correlated strongly with cycle length (r = 0.88, p < 0.001) and hyperpnea length (r = 0.90, p < 0.001) but not with apnea length. LECT correlated inversely with cardiac output (r = -0.72, p < 0.006), indicating that LECT is a valid measure of circulatory delay. Thus, circulatory delay is an important determinant of hyperpnea length but not of apnea length in patients with ICSA and CSR-CSA.
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PMID:Cycle length of periodic breathing in patients with and without heart failure. 875 9

A central sleep apnea is the absence of respiratory effect, and, thus, the absence of airflow during sleep. Central hypopnea, a related disorder, is also discussed. The sensory component of central sleep apnea; defects involving the integrative and executive neurons; non-neurologic causes of central sleep apneas, including chronic obstructive pulmonary disease and congestive heart failure; diagnosis; treatment; and other topics are reviewed in detail.
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PMID:Central sleep apnea. 887 79

Obstructive and central sleep apnea are common in patients with congestive heart failure (CHF). These sleep-related breathing disorders are characterized by two pathophysiologic features that could have important implications for disease progression in CHF: sympathetic nervous system activation, and adverse changes in cardiac loading conditions. In patients with obstructive sleep apnea, blood pressure is frequently elevated as a result of excessive sympathetic nervous system activity elicited by the combination of apnea, hypoxia, and arousals from sleep. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular afterload, reduces cardiac output, and may promote the progression of pump failure. Increased afterload and hypoxia can also predispose such patients to myocardial ischemia and arrhythmias. In patients with CHF, abolition of coexisting obstructive sleep apnea by nasal continuous positive airway pressure improves left ventricular function. Central sleep apnea (i.e., Cheyne-Stokes respiration) is also characterized by apnea, hypoxia, and increased sympathetic nervous system activity and, when present in CHF, is associated with increased risk of death. Recent medium-term trials involving small numbers of patients have demonstrated that nocturnally applied continuous positive airway pressure in patients with CHF and central sleep apnea alleviates central sleep apnea, improves left ventricular function, reduces sympathetic nervous system activity and improves symptoms of CHF. These studies emphasize the importance of considering obstructive and central sleep apnea in the differential diagnosis of conditions that could contribute to the development or progression of CHF. They also suggest that continuous positive airway pressure is a promising nonpharmacologic adjunctive therapy for patients with CHF and coexisting sleep-related breathing disturbances that warrants further investigation.
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PMID:Pathophysiologic and therapeutic implications of sleep apnea in congestive heart failure. 889 61

A central apnea is a disorder characterized by apneic events during sleep with no associated ventilatory effort. Central sleep apnea syndrome is characterized by repeated apneas during sleep resulting from loss of respiratory effort. Although the etiology of central apnea remains obscure in most cases, current investigations into breathing control system during sleep and association with certain diseases have pointed out possible mechanisms. Ventilation during sleep is highly dependent on the nonbehavioral control system. As a result, any diseases affecting this control system could influence the breathing patterns while the patient is asleep. As our results show, most patients with central sleep apnea and without congestive heart failure had quantifiable abnormalities like diminished carbon dioxide response curves. Neurological diseases affecting the brainstem are able to produce breathing pattern disorders in sleep. Well-known neurological diseases such as arteriosclerosis in the elderly, infarctions, tumors, hemorrhage, accidents with damage of this region, encephalitis, poliomyelitis or other infectious diseases may cause central apnea during sleep, even if in wakefulness no abnormalities of breathing patterns are present. Apneas cause hypoxemia, hypercapnia and increased sympathicotonia. This may result in development of pulmonary artery hypertension or systemic hypertension. Published results demonstrate that medical treatment is ineffective in these patients. Implantation of a diaphragm pacing device is an invasive measure, the efficacy of the diaphragm pacing has not been proven by long-term trials, however. Mechanical ventilation was shown to be the most efficient treatment. A therapeutic procedure using a timed n-BiPAP device is able to normalize blood gases during sleep. The n-BiPAP prevented the development of severe pulmonary artery hypertension during sleep.
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PMID:Central sleep apnea. 904 68

Despite advances in medical therapy of congestive heart failure (CHF), morbidity and mortality for this disorder remain high. One factor that could contribute to the poor prognosis of CHF is Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). This breathing disorder is a frequent complication of CHF, where it is associated with increased mortality. One reason for this higher mortality may be that apnea-related hypoxia and arousals from sleep can increase sympathetic nervous system activity (SNA), as manifested by increases in overnight urinary and daytime plasma norepinephrine concentrations ([UNE] and [PNE], respectively). Recently published randomized trials have demonstrated that nasal continuous positive airway pressure (CPAP), if applied nightly at high enough levels over periods of at least 1-3 months, can alleviate CSR-CSA in patients with CHF in association with hemodynamic improvement, as evidenced by increased left ventricular ejection fraction (LVEF) and inhibition of SNA, as manifest by reductions in [UNE] and [PNE]. These findings indicate a role for CPAP as a non-pharmacologic adjunctive therapy for CHF complicated by CSR-CSA. Longer-term trials of CPAP are needed to determine whether this intervention can provide long-lasting clinical benefit to patients with CHF and CSR-CSA.
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PMID:Hemodynamic and sympathoinhibitory effects of nasal CPAP in congestive heart failure. 908 19

A number of novel and important observations have recently arisen that emphasize the interaction between sleep apnea and cardiovascular function. New evidence of a role for obstructive sleep apnea as an independent factor in the genesis of hypertension and nocturnal myocardial ischemia has been described. Advances have been made in the understanding of the acute impact of sleep-disordered breathing on hemodynamic function, and a better understanding of the interaction between sleep-disordered breathing and congestive heart failure is now emerging. There is now strong evidence that reversal of sleep-related breathing disorders by nasal continuous positive airway pressure leads to improvements in markers of cardiovascular outcome in selected patients with congestive heart failure. These findings augur well for the development of new diagnostic approaches and treatment strategies for patients with sleep apnea and coexisting cardiovascular disease.
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PMID:Cardiovascular disease and sleep apnea. 936 91

In patients with congestive heart failure (CHF), elevated, left ventricular (LV) volume might lead to pulmonary congestion and hypocapnia, which would create a predisposition to the development of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In addition, because LV volume affects cardiac output, it should influence the lengths of hyperpneas. We therefore evaluated LV volumes and transcutaneous PCO2 (PtcCO2) during wakefulness and stage 2 sleep in 16 patients with CHF due to nonischemic dilated cardiomyopathy (NIDC). Data were then compared between those with (n = 7) and those without CSR-CSA (n = 9). LV end-diastolic volume (LVEDV) was significantly higher in patients with than those without CSR-CSA (585 +/- 118 versus 312 +/- 41 ml, p < 0.05). Compared with patients without CSR-CSA, those with CSR-CSA had lower mean stage 2 sleep PtcCO2 (36.3 +/- 2.2 versus 41.2 +/- 1.2 mm Hg, p < 0.05) and a lesser change in PtcCO2 from wakefulness to stage 2 sleep (-0.4 +/- 0.3 versus 2.0 +/- 0.4 mm Hg, p < 0.001). Among patients with CSR-CSA, hyperpnea length was inversely related to LVEDV (R = 0.769, p = 0.043) owing to the direct relationship of cardiac output to LVEDV (R = 0.791, p = 0.034). We conclude that CSR-CSA in patients with CHF due to NIDC is associated with increased LV volumes possibly through the direct or indirect influence of LV volume on PaCO2 and cardiac output.
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PMID:Left ventricular volume in patients with heart failure and Cheyne-Stokes respiration during sleep. 937 74

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

Stimulating cardiac beta 1-adrenoceptors with oxyfedrine causes dilatation of coronary vessels and positive inotropic effects on the myocardium. beta 1-adrenergic agonists increase coronary blood flow in nonstenotic and stenotic vessels. The main indication for the use of the phosphodiesterase inhibitors pamrinone, mirinone, enoximone and piroximone is acute treatment of severe congestive heart failure. Theophylline is indicated for the treatment of asthma, chronic obstructive pulmonary disease, apnea in preterm infants ans sleep apnea syndrome. Severe arterial occlusive disease associated with atherosclerosis can be beneficially affected by elcosanoids. These drugs must be administered parenterally and have a half-life of only a few minutes. Sublingual or buccal preparations of nitrates are the only prompt method (within 1 or 2 min) of terminating anginal pain, except for biting nifedipine capsules. The short half-life (about 2.5 min) of nitroglycerin (glyceryl trinitrate) makes long term therapy impossible. Tolerance is a problem encountered with longer-acting nitric oxide donors. Knowledge of the pharmacokinetic properties of vasodilating drugs can prevent a too sudden and severe blood pressure decrease in patients with chronic hypertension. In considering the administration of a second dose, or another drug, the time necessary for the initially administered drug to reach maximal efficacy should be taken into account. In hypertensive emergencies urapidil, sodium nitroprusside, nitroglycerin, hydralazine and phentolamine are the drugs of choice, with the addition of beta-blockers during catecholamine crisis or dissecting aortic aneurysm. Childhood hypertension is most often treated with angiotensin-converting enzyme (ACE) inhibitors or calcium antagonists, primarily nifedipine. Because of the teratogenic risk involved with ACE inhibitors, extreme caution must be exercised when prescribing for adolescent females. The propagation of health benefits to breast-fed infants, combined with more women delaying pregnancy until their fourth decade, has entailed an increase in the need for hypertension management during lactation. Low dose hydrochlorothiazide, propranolol, nifedipine and enalapril or captopril do not pose enough of a risk of preclude breastfeeding in this group. The most frequently used antihypertensive agents during pregnancy are methyldopa, labetalol and calcium channel antagonists. Methyldopa and beta-blockers are the drugs of choice for treating mild to moderate hypertension. Prazosin and hydralazine are used to treat moderate to severe hypertension and hydralazine, urapidil or labetalol are used to treat hypertensive emergencies. The use of overly aggressive antihypertensive therapy during pregnancy should be avoided so that adequate uteroplacental blood flow is maintained. Methyldopa is the only drug accepted for use during the first trimester of pregnancy.
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PMID:Clinical pharmacokinetics of vasodilators. Part II. 967 32

Nonhypercapnic central sleep apnoea is a disorder of respiratory control characterized by hyperventilation previously attributed to the stimulation of either pulmonary vagal afferent nerve fibres or respiratory chemoreceptors. This report describes central sleep apnoea in a patient with congestive heart failure following bilateral lung transplant in whom pulmonary vagal afferent nerve activity was absent.
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PMID:Central sleep apnoea in congestive heart failure despite vagal denervation after bilateral lung transplantation. 972 8


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