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

A case of paraneoplastic encephalomyelitis and subacute pandysautonomia associated with an occult atypical carcinoid tumour of the lung is described. The main clinical features were lethargy, impaired memory, constipation, and orthostatic hypotension. Neurological investigation was unremarkable except for mononuclear pleocytosis and increased protein level in the cerebrospinal fluid (CSF). Tests of autonomic function revealed a low plasma norepinephrine level, a marked drop of blood pressure (BP) to vertical tilt and Valsalva maneuver, and a marked rise of BP to dilute norepinephrine infusion. A few days prior to death, the patient became hypothermic and had repeated episodes of respiratory arrest associated with transient atrioventricular block on the electrocardiogram (ECG). A polysomnographic study confirmed a sleep apnea syndrome. Autopsy revealed an atypical carcinoid tumour in one tracheobronchial lymph node, widespread lymphocytic infiltrates and loss of neurons in the cerebral, cerebellar and brainstem grey matter, the spinal cord and roots, and the paravertebral sympathetic ganglia as well as microglial and astrocytic proliferation in the central nervous system.
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PMID:Paraneoplastic encephalomyelitis and subacute dysautonomia due to an occult atypical carcinoid tumour of the lung. 220 90

Nocturnal oxygen administered to patients with disordered breathing ameliorates hypoxemia. As a result, an important chemical stimulus to arousal is diminished. This could cause prolongation of disordered breathing events, worsen respiratory acidosis, and induce potentially harmful cardiac arrhythmias. The presence of chronic obstructive pulmonary disease (COPD) could further aggravate the situation since such patients may have depressed hypercarbic responses. To test this hypothesis, 20 obese men with sleep apnea and COPD were studied polysomnographically on two nights receiving air on one or oxygen at 4 L/min on the other. Supplemental oxygen increased mean DOB event duration from 25.7 to 31.4 seconds (p less than 0.001), increased end apneic PCO2 from 52.8 to 62.3 mm Hg (p less than 0.025), and decreased mean end apneic pH from 7.34 to 7.28 (p less than 0.001). At the same time, it improved mean sleeping and end-apneic oxygen saturation. The number of ventricular extra-systoles (PVCs) per minute of sleep showed small increases in three subjects while breathing oxygen. Complex ventricular arrhythmias were unaffected by oxygen in five subjects. Oxygen eliminated atrioventricular block in two subjects. We conclude that nocturnal supplemental oxygen does not increase ventricular arrhythmias in the majority of patients with COPD and coexisting disordered breathing events. While the clinical significance of an oxygen associated increase in ventricular extrasystoles in three subjects is unclear, nocturnal monitoring by telemetry or ambulatory recorder should be sufficient to detect such patients.
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PMID:Acute oxygen in patients with sleep apnea and COPD. 307 93

The results of 24-hour continuous electrocardiographic monitoring of 23 patients with documented sleep apnea syndrome were reviewed to evaluate the prevelance of cardiac arrhythmias and conduction disturbances in this disorder. During sleep, marked sinus arrhythmia (more than 30 beats/min variation) was found in 18 patients. Extreme sinus bradycardia (heart rate less than 30 beats/min) and sinus pauses (more than 1.8 sec) were found in only two patients. First-degree and type I second-degree atrioventricular block were found in another patient. There was a decrease in grade of ventricular ectopy from wakefulness to sleep. These data suggest that the prevalence of serious arrhythmias and conduction disturbances during sleep in patients with the sleep apnea syndrome is much lower than previously reported.
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PMID:Cardiac arrhythmias and conduction disturbances in the sleep apnea syndrome. Prevalence and significance. 712 58

Many nocturnal cardiac arrhythmias and conduction defects have been reported in the adult sleep apnoea syndrome. The most original is the great variability of the heart rate which is cyclical and related to the apnoeic episodes, and easily differentiated from simple respiratory sinus arrhythmia. It is characterised by an initial bradycardia followed by rebound tachycardia. The bradycardia is vagally dependent (inhibited by atropine) probably secondary to carotid chemoreceptor stimulation by the hypoxaemia. The tachycardia is mainly attributed to the cessation of vagal hypertonicity although catecholamine stimulation has been suggested. The origin of these changes is purely functional, regressing with treatment of apnoea (waking, tracheotomy), the maintenance of arterial oxygen concentrations with oxygen therapy and parasympathetic blockade (atropine). The intensity of the phenomenon is related to the degree of arterial desaturation, which is itself related to basal arterial saturation (SaO2) and the duration of the apnoeas. Prolonged systole due to paroxysmal sino-atrial or atrioventricular block may be observed at night in these patients. The influence of vagal overactivity is confirmed (suppression of vagotomy) with no organic pathology (diurnal absence, tracheotomy, normal electrophysiological testing) in favour of a relationship with apnoea. Though less common than conduction abnormalities, atrial arrhythmias (extrasystoles, flutter, fibrillation) are also possible complications of sleep apnoea. The absence of an organic substrate is indicated by their regression post-tracheotomy and the efficacy of atropine (again in favour of a vagally-induced mechanism). Finally, nocturnal ventricular hyper-excitabilty is sometimes observed, the probable mechanism being the association of severe hypoxaemias (SaO2 < 60%) and the increased sympathetic tone at the end of the apnoea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arrhythmia and syndrome of obstructive sleep apnea in adults]. 802 77

To determine if there was a relationship between cardiac arrhythmias and sleep apnea, we studied the prevalence of arrhythmias in a consecutive series of patients referred to our clinic for assessment of this disorder. Two hundred of 263 physician-referred patients were eligible for the study and, of these, 173 (86.5%) had complete investigations. All patients underwent a full night of polysomnography and Holter monitoring. Sleep apnea was diagnosed if patients had more than 10 apneas and hypopneas per hour (AHI). In 76 patients (43.9%) sleep apnea was diagnosed (median AHI = 33). The prevalence of arrhythmias in patients with sleep apnea versus those without was, respectively: complex ventricular ectopy (including ventricular tachycardia), 1.3% (95% CI, 0.4 to 6.9) versus 4.1% (CI, 1.6 to 10.1); frequent ventricular premature beats (> 30/h), 2.6% (CI, 0.8 to 8.9) versus 6.2% (CI, 2.9 to 12.8); second-degree atrioventricular block, 1.3% (CI, 0.4 to 6.9) versus 4.1% (CI, 1.6 to 10.1); sinus arrest, 5.2% (CI, 2.2 to 12.6) versus 1.0% (CI, 0.2 to 5.6). None of these differences was statistically significant. We conclude that the prevalence of cardiac arrhythmias is low in patients without serious cardiac or respiratory comorbidity who are referred for assessment of sleep apnea. Furthermore, the presence or absence of arrhythmias in this group is unrelated to sleep apnea severity.
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PMID:Sleep apnea and cardiac arrhythmias. Is there a relationship? 836 32

Sleep apnea is associated with many adverse cardiovascular sequelae, including hypertension, nocturnal angina, decreased cardiac output, and bradyarrhythmias. The purpose of this study was to determine if patients referred for pacemaker therapy with asymptomatic bradyarrhythmias have underlying sleep apnea as the etiology of their bradyarrhythmias. This study included eight patients (7 males, 1 female) referred to a cardiac electrophysiology practice for pacemaker therapy. Patients included had asymptomatic bradyarrhythmias that consisted of severe sinus bradycardia, second-degree atrioventricular block, and complete heart block. In 7 of 8 patients, the bradyarrhythmias occurred at night or during the day while asleep. No patients were conditioned athletes. Symptoms often associated with bradyarrhythmias, such as lightheadedness and syncope, were not present. However, seven patients had at least one symptom suggestive of sleep apnea, such as excessive daytime fatigue, snoring, cessation of breathing during sleep (apnea), or frequent night-time awakenings. Overnight polysomnography studies were obtained on patients who had one or more symptoms suggestive of sleep apnea. In this study 7 of 8 patients (88%) referred for pacemaker therapy with asymptomatic bradyarrhythmias were documented by polysomnography to have sleep apnea. When treated with either sleep position modification, nasal continuous positive airway pressure (nasal CPAP), or tracheostomy, all seven patients had improvement in sleep apnea symptoms and remained asymptomatic from their bradyarrhythmias without pacemaker therapy over an average follow-up period of 22 months. One patient without symptoms suggestive of sleep apnea declined pacemaker therapy and remained asymptomatic. From these results, we concluded that asymptomatic transient bradyarrhythmias may suggest a diagnosis of sleep apnea. The evaluation of a patient referred for pacemaker therapy with asymptomatic bradyarrhythmias should include questions related to sleep apnea symptoms. Establishing the diagnosis of sleep apnea may reduce the need for pacemaker therapy and permit appropriate treatment of the underlying cause of these bradyarrhythmias.
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PMID:Asymptomatic bradyarrhythmias as a marker for sleep apnea: appropriate recognition and treatment may reduce the need for pacemaker therapy. 877 19

The relationship between pacing mode and sleep is not yet known, and therefore polysomnography was used to evaluate the effect. A total of 16 patients (8 men and 8 women; mean age, 72 +/- 9 years) with DDD pacemakers made up the study population. Of these 16 patients, 8 patients had complete AV block and 8 patients had sick sinus syndrome. The recording was done twice in VVI and DDD modes. Between VVI mode and DDD mode, sleep latency time (VVI mode: 38 +/- 25, DDD mode 23 +/- 27 min), frequency of temporary waking (8.3 +/- 6.7, 3.7 +/- 2.9 times), the number of episodes of apnea (59 +/- 84, 36 +/- 55 times, the apnea-hypopnea index (AHI) (15 +/- 18, 10 +/- 13), and efficacy of sleep (72% +/- 10%, 81% +/- 11%) were significantly different. Also, the apnea index improved significantly in DDD mode. There was no significant difference in total sleep time and in total duration of temporary waking between the two groups. From the study results, a reduction in sleep disturbance was achieved when DDD pacing mode was chosen, rather than VVI mode. Furthermore, efficacy of sleep also improved significantly compared with VVI mode. Interestingly, sleep apnea syndrome in four patients with AHI > or = 15 notably ameliorated when DDD mode was chosen; however, the mechanism involved in amelioration is still ambiguous and needs further assessment.
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PMID:Effect of pacing mode on sleep disturbance. 1459 11

We report a case of a patient with an implantable cardioverter defibrillator and no prior history of heart block with managed ventricular pacing (MVP) programmed who had frequent recurrent episodes of polymorphic ventricular tachycardia. All of the episodes were initiated by transient atrioventricular block which resulted in short-long-short sequences permitted by MVP. This case illustrates that MVP should be used with caution not only in patients with complete heart block, but also in patients at risk for brief heart block due to such states as hypervagatonia due to sleep apnea.
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PMID:Frequent recurrent polymorphic ventricular tachycardia during sleep due to managed ventricular pacing. 2002 16

While the left bundle branch block frequently reflects underlying cardiac disease, conductive disorders occurring at three levels (sinus node, atrioventricular node, and branches of the bundle of His), are usually part of the aging heart. In addition, AV nodal block and sinus node dysfunction are readily compounded with drugs, often indispensable (beta-blockers, calcium-blockers, digoxin, antiarrhythmic), and very common among the elderly. Indications for permanent pacing are accurately described and come in four classes: I, recommended (mandatory) - IIa, raisonable - IIb, possible - III, contraindicated. In 2009, 24H ECG Holter and electrophysiological study are generally disappointing in the positive diagnosis of syncope, so the clinical characteristics of syncope are essential in the decision of device implantation. Indeed, in the absence of ECG recorded at the time of the syncope, the diagnosis of BAV or BSA cannot be certain, and on the contrary, vague symptoms should not be attributed to a patent bradycardia of sinus or AV block origin without any precaution. Finally, the relationship between sinus dysfunction and carotid sinus syndrome remain poorly understood, dysautonomia is common among the elderly, and the existence of conduction disorders associated with syndrome of sleep apnea should not be ignored.
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PMID:[Cardiac conduction disorders in the elderly]. 2005 60

Central sleep apnea is an important but frequently missed clinical diagnosis. The purpose of this clinical case series is to demonstrate that in a subset of patients with central sleep apnea, inpatient telemetry ECG recordings may reveal a consistent relationship between changes in sinus rate, AV conduction, and the presence and rate of respiratory artifact that should raise the clinical suspicion of central sleep apnea. In the three presented cases, marked sinus bradycardia or AV block was followed by the simultaneous occurrence of abrupt acceleration of heart rate and the appearance of rapid micro-oscillations consistent with respiratory artifact. These changes suggested central sleep apnea characterized by bradycardia during the apneic spells followed by awakening of the breathing center and postvagal tachycardia. In each case, central sleep apnea was confirmed by visual observation of the patient, documentation of arterial desaturations during episodes of bradycardia, and in two, by a subsequent sleep study. Physicians should be aware of the potential and significance of these electrocardiographic disturbances in patients with central sleep apnea.
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PMID:"Awakenings": electrocardiographic findings in central sleep apnea. 2094 62


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