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[The effects of transcutaneous electrical stimulation during sleep on obstructive sleep apnea].

OBJECTIVE: To study the effects of transcutaneous electrical stimulation during sleep on obstructive sleep apnea syndrom (OSAS). METHOD: Sixteen patients with OSAS were studied by polysomnography during all-night sleep with and without submental transcutaneous electrical stimulation (TES) of the genioglossus. RESULT: Fourteen of the 16 patients (87%) who accepted the TES were treated successfully (reduction of Al > 50%). The average apnea index showed a decrease of 29 events per hour when the TES were performed (P < 0.001). The average apnea time decreased from 22 to 7 sec (P < 0.001). The apnea time/TST decreased from 27% +/- 11% to 7% +/- 3%. The lowest SaO2 increased from 71% to 87% (P < 0.001). TES did not cause arousal. The sleep stages of SWS, and REM sleep effect (SE) increased significantly. CONCLUSION: TES is a conservative but effective treatment in patients with obstructive sleep apnea syndrome, although it failed to improve central sleep apnea.

Aged↗

Surgical management for snoring and sleep apnea.

Obstructive sleep apnea is a serious medical problem producing both physical and behavioral derangement. It is essential to provide a thorough workup and evaluation of all patients seeking care for snoring or OSA. Polysomnography is the standard for evaluation and assessment of the severity of OSA in every patient. The evaluation and workup for surgical intervention should include a thorough history, complete head and neck evaluation, nasopharyngeal laryngoscopy with a flexible fiberoptic endoscope, and appropriate imaging (e.g., cephalometrics). This workup allows pathologic entities of the upper airway (e.g., neoplasia, cysts) to be ruled out and regions of disproportionate anatomy (e.g., large soft palate, uvula, base of tongue, and a hypoplastic mandible) to be documented. Treatment of site-specific based on the finding of the evaluation. Treatment of snoring is often addressed by more conservative palatal procedures such as LAUP, RVTR, or electrocautery of the soft palate. The more aggressive palatal procedures such as UPPP are generally reserved for OSA. Nasal airway reconstruction may aid in the treatment of OSA, because increased nasal resistance and obstruction may significantly increase the negative pressure of the upper airway, leading to collapse of the velopharyngeal, base-of-tongue, and hypopharyngeal regions. Children with OSA usually respond well to adenotonsillectomy. Occasionally, uvulopalatopharyngeal procedures may be necessary. Craniofacial anomalies and significant skeletal anomalies such as severe mandibular hypoplasia have historically been problematic. Tracheostomies were at one time the only way to secure the airway in these patients. New developments in distraction osteogenesis have enabled mandibular lengthening and airway improvement, leading to earlier decannulation of these patients. The combined phase I and phase II treatment has a success rate of greater than 90%. Phase I treatment may include nasal reconstruction, uvulopalatopharyngeal, base-of-tongue, and hypopharyngeal surgery. Phase I surgery has a documented success rate of about 70% to 80%. Phase II surgery (MMA) has a success rate approaching 100%. In certain cases, MMA may be used as the primary treatment of OSA.

Adenoidectomy↗

ST-segment depression during sleep in obstructive sleep apnea.

It was hypothesized that obstructive sleep apnea may precipitate myocardial ischemia, reflected by ST-segment depression, in some patients during sleep. Overnight sleep studies and simultaneous 3-channel Holter monitoring were performed on 23 consecutive patients with obstructive sleep apnea without a history of coronary artery disease. Each patient was randomly assigned to nasal continuous positive airway pressure for the first half of the night. An episode of significant ST depression was defined as > 1 mm from baseline for > 1 minute. The total duration (minutes) of ST depression was indexed to the total sleep time (minutes per hour of sleep). Seven patients (30%) had ST depression during sleep. In all 7 patients the duration of ST depression decreased during nasal continuous positive airway pressure (30 +/- 18 vs 11 +/- 13 minutes per hour of sleep) in association with a reduction in the apnea-hypopnea index (65 +/- 35 vs 7 +/- 6/hour), arousal index (49 +/- 14 vs 6 +/- 4/hour) and the duration that oxygen saturation was < 90% (44 +/- 27 vs 12 +/- 23% total sleep time). When patients were not on nasal continuous positive airway pressure, the apnea-hypopnea and arousal indexes were higher during periods of ST depression than when ST segments were isoelectric, whereas oxygen saturation was not different. These 7 patients underwent exercise testing, which was positive for inducible myocardial ischemia in 1 patient. It is concluded that ST depression is relatively common in patients with obstructive apnea during sleep and that the duration of ST depression is significantly reduced by nasal continuous positive airway pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential.

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a prevalent disorder associated with substantial cardiovascular and neurobehavioral morbidity. Yet this is a disorder for which there are no widely effective pharmacotherapies. The pathophysiology of obstructive sleep apnea namely, normal respiration in waking with disordered breathing only in sleep, suggests that this disorder should be readily amenable to drug therapy. Over the past 10 years, we have gained tremendous insight into the neurochemical mechanisms involved in state-dependent control of respiration. It is apparent from this work that there are many potential avenues for pharmacotherapies, including several seemingly conflicting directions for serotonergic therapies. Serotonin delivery is reduced to upper airway dilator motor neurons in sleep, and this contributes, at least in part, to sleep-related reductions in dilator muscle activity and upper airway obstruction. The dilator motor neuron post-synaptic serotonin receptors are 5-HT(2A) and 5-HT(2C) subtypes, and in adults the presynaptic 5-HT receptor in motor nuclei is 5-HT(1B), an inhibitory receptor. Serotonin receptors are also found within central respiratory neuronal groups, and these receptor subtypes include 5-HT(1A) (inhibitory) and 5-HT(2) receptors. Peripherally, stimulation of 5-HT(2A), 5-HT(2C) and 5-HT(3) receptor subtypes have an inhibitory effect on respiration via action at the nodose ganglion. Many of these receptor subtypes and their signal transduction pathways may be affected by oxidative stress in obstructive sleep apnea. These alterations will make finding drug therapies for sleep apnea more challenging, but not insurmountable. Future directions are suggested for elucidating safe, well-tolerated serotonergic drugs for this disorder. Tryptophan was one of the first serotonergic drugs tested for OSAHS. This drug was withdrawn from the market as a result of reports linking tryptophan use with eosinophilic myalgia syndrome and life-threatening pulmonary hypertension. Newer drugs with serotonergic activity tested in persons with sleep-disordered breathing include buspirone, fluoxetine and paroxetine. Trials are presently being conducted to evaluate the effects of 5-HT(2A) and 5-HT(3) antagonists on OSAHS. Many of the drugs tested have not shown significant improvement in sleep apnea. However, with continued effort to elucidate the pharmacology of neurochemical control of state-dependent changes in respiratory control, the availability of pharmacological therapy for this disorder is not too far away.

Cardiovascular System↗

Hemodynamic consequences of obstructive sleep apnea.

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.

Adult↗

Circulating vascular endothelial growth factor levels in patients with obstructive sleep apnea.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is associated with intermittent hypoxia during sleep. Vascular endothelial growth factor (VEGF) has detectable levels in the circulation and its expression is highly regulated by oxygen tension. We therefore hypothesized that serum VEGF levels will be elevated in patients with OSA. DESIGN: Blood samples were collected at random times during the day from 68 adults and 41 children who were clinically suspected for the presence of OSA, and who underwent overnight polysomnography. SETTING: University hospital sleep laboratory. PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: For both children and adults, serum VEGF levels were significantly higher in polysomnographically confirmed OSA (AHI>15 and AI>5 in adults and children respectively) when compared to those with mild or no disease (p<0.0001). Furthermore, significant correlations were found between VEGF concentrations and respiratory disturbance index and sleep time spent at SpO2 <90%. In addition, VEGF levels in children were higher for any given duration of hypoxia during sleep (p<0.0001). No differences in VEGF emerged between evening and morning samples. However, temporal delays in blood sample processing were associated with spuriously increased VEGF concentrations. Exploratory analysis of the data revealed that serum VEGF concentrations of >150 pg/ml in adults and >100 pg/ml in children were predictive of OSA, when an apnea-hypopnea index >30 and an apnea index >5 were used as disease criteria in adults and children, respectively. CONCLUSIONS: We conclude that circulating VEGF levels are frequently elevated in OSA patients, and may play a role in the regulation of tissue oxygen delivery.

Body Mass Index↗

Genioglossus activity during sleep in normal control subjects and children with obstructive sleep apnea.

Children with obstructive sleep apnea syndrome (OSAS) have more collapsible airways compared with normal subjects, yet sustain stable breathing during wakefulness and part of sleep. This indicates successful neuromuscular compensation. Using a custom intraoral surface electrode to record pharyngeal dilator muscle activity (the genioglossus [EMGgg] normalized to the wakeful baseline), we performed overnight polysomnograms in three groups of children: (1) patients with OSAS without continuous positive airway pressure (CPAP) (n = 13); (2) patients with OSAS with CPAP (n = 5); and (3) control subjects without CPAP (n = 13). Our objective was to evaluate the EMGgg as a function of sleep state and during disordered breathing, compared with stable sleep and wakefulness. In control subjects, the EMGgg decreased from wakefulness to Stage 2 (mean +/- SD, 65 +/- 6%), and further during REM (51 +/- 9%) (p < 0.05). In patients with OSAS, the EMGgg for apneic breaths during REM (37 +/- 9%) was lower than during stable breathing (83 +/- 17%) (p < 0.05) and wakefulness (p < 0.05). CPAP lowered the EMGgg in patients with OSAS during all sleep states. These data indicate that (1) EMGgg compensatory mechanisms remain active during sleep in patients with severe OSAS; (2) EMGgg reductions are temporally associated with sleep apnea events; and (3) REM sleep is associated with the lowest and most variable EMGgg.

Adolescent↗

Determination of obstructive site in obstructive sleep apnea.

Patients with obstructive sleep apnea syndrome (OSAS) may have airway obstruction at various levels, including the uvula-soft palate complex, base of tongue, and/or possibly other sites. For patients with tongue base and/or laryngeal obstruction, uvulopalatopharyngoplasty (UPPP, ppp) will not alleviate the obstruction. Prior authors have proposed that the hyoid bone position as determined by cephalometric x-rays can predict which patients have obstruction at a lower site than the soft palate. In this study, patients with obstructive sleep apnea syndrome were evaluated with polysomnographic testing, fiberoptic endoscopy, and cine-CT scans (Imatron Scanner with multiple level rapid sequence scans) in an attempt to determine precisely the site of airway obstruction. Measurements of airway size taken at the time of fiberoptic pharyngoscopy were compared with those determined by the cine-CT studies. Initial results revealed that fiberoptic pharyngoscopy in the sitting and supine positions was helpful in confirming pharyngeal airway sites with smaller diameters in awake patients. However, the cine-CT exam performed in both sleeping and awake states provided more direct data regarding the airway during sleep. We feel that with more clinical experience the cine-CT technique will prove to be the most helpful study for identification of the obstructive airway site in obstructive sleep apnea syndrome.

Airway Obstruction↗

[Snoring and obstructive sleep apnea].

Snoring and obstructive sleep apnea are similar disorders in etiology, with differences in clinical presentation and treatment. 5-20% of young and 40-50% of older population are affected by either of these disorders. Etiology of snoring should be sought in the anatomic irregularities of commencing portions of the upper respiratory and gastrointestinal tracts, obesity, alcohol abuse, use of some medications as well as in the sleep architecture disturbance. Treatment success depends on correctly established diagnosis and precise localisation of anatomic irregularity implicated in snoring. A wide array of diagnostic tests exist some of which are mandatory while the others are used on a case-by-case basis. Treatment is either conservative or surgical. The success rate is 30-90% depending on the type and the management of disorder. An algorithm for diagnosis and treatment of snoring and obstructive sleep apnea is shown at the end of the paper.

Humans↗

Association of elevated levels of vascular endothelial growth factor in obstructive sleep apnea syndrome with patient age rather than with obstructive sleep apnea syndrome severity.

BACKGROUND: Although certain studies report high levels of vascular endothelial growth factor (VEGF) in obstructive sleep apnea syndrome (OSAS), the effect of systemic hypoxia on circulating VEGF remains controversial. OBJECTIVES: To study the association of serum VEGF and OSAS in a large group of patients. METHODS: One hundred patients with OSAS (mean age 58.1+/-12.4 years, mean body mass index 30.6+/-5.4 kg/m2) were tested for serum VEGF levels, and the findings were correlated with the severity of OSAS, as determined by the apnea-hypopnea index (AHI) on the basis of polysomnography and background data. RESULTS: The mean AHI was 40.0+/-21.2 (range 10-106). Mean minimal oxygen saturation was 80.6+/-11.7% (range 43-98%) and mean time of oxygen saturation under 90% was 50.0+/-75.0 min (range 0-300 min). The mean VEGF level was 445.2+/-289.8 pg/ml in the study group (vs. 280 pg/ml reported in normal controls). The mean platelet count was 233.8+/-64.4 10(3)/ml and the mean VEGF/platelet ratio was 1.95+/-1.40 pg/10(6). There was no association of VEGF or VEGF/platelets with the severity of OSAS. However, both factors showed a significant correlation with patient age (r=0.224, p=0.01 and r=0.425, p=0.01, respectively). Age was the only parameter to significantly predict VEGF and VEGF/platelets on multivariate analysis (R2=0.713, p=0.001 and R2=0.844, p=0.001, respectively). CONCLUSION: The elevation of serum VEGF in OSAS is not associated with the severity of the disease, but it is associated with patient age. VEGF might be involved in the long-term adaptive mechanism in OSAS, and its age-dependent increase might partly explain the reduced mortality in elderly OSAS patients.

Adult↗

Recent weight gain in patients with newly diagnosed obstructive sleep apnea.

OBJECTIVE: Patients with obstructive sleep apnea are often obese. Obesity may contribute to both sleep apnea itself and to the cardiovascular risk associated with sleep apnea. Weight loss in obese patients with sleep apnea may alleviate symptoms and decrease the severity of sleep apnea. Whether patients with obstructive sleep apnea are indeed predisposed to recent weight gain, as compared with similarly obese subjects without sleep apnea, is not known. PATIENTS AND METHODS: We compared 1-year weight histories in 53 male and female patients newly diagnosed with obstructive sleep apnea, compared with 24 controls matched for gender, age, body mass index, and percent body fat. Sleep apnea patients had never been treated. Control subjects were proven to be free of sleep-disordered breathing by overnight polysomnography. RESULTS: Patients with obstructive sleep apnea (n = 53) had a significant recent weight gain of 7.4 +/- 1.5 kg compared with a weight loss of 0.5 +/- 1.7 kg (P = 0.001) in similarly obese controls (n = 24). Male patients with obstructive sleep apnea (n = 28) had a history of significant weight gain (6.8 +/- 2.3 kg) over the year preceding the study compared with male control subjects (n = 13), in whom average weight fell by 0.58 +/- 2.4 kg (P = 0.03). Female patients (n = 25) with obstructive sleep apnea had an 8.0 +/- 1.9 kg weight gain compared with female controls (n = 11) who had a history of weight loss of 0.46 +/- 2.6 kg (P = 0.02). CONCLUSION: These findings support the concept that patients with obstructive sleep apnea may be susceptible to increasing obesity in the period preceding the diagnosis of obstructive sleep apnea.

Adipose Tissue↗

Right and left ventricular functional impairment and sleep apnea.

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.

Cheyne-Stokes Respiration↗

Pharmacotherapies for obstructive sleep apnea: how close are we?

Obstructive sleep apnea is a prevalent disorder associated with significant neurobehavioral and cardiovascular morbidities. At present, however, there are no widely effective, well-tolerated pharmacotherapies for obstructive sleep apnea. The pathogenesis of this disorder predicts that sleep apnea should respond to drug therapies. Specifically, respiration during waking in persons with sleep apnea is normal, while collapse of the upper airway occurs exclusively in sleep. This state-dependency in upper airway patency suggests state-dependent changes in neurochemical control of the upper airway dilator motoneurons, and this, in turn, suggests that appropriate medications would maintain upper airway dilator function in sleep and prevent sleep related collapse of the upper airway. The past few years have brought significant insight into the neural mechanisms governing upper airway dilator muscle function. This article provides updates on neurochemical mechanisms, emphasizing a role for serotonergic control, and reviews recent drug therapy trials for sleep apnea. We are currently well poised to develop effective pharmacotherapies for obstructive sleep apnea, with opportunities to target several regions involved in respiratory control.

Animals↗

Baroreflex control of sympathetic nerve activity and heart rate in obstructive sleep apnea.

-Patients with obstructive sleep apnea are at increased risk for hypertension. The mechanisms underlying this increased risk are not known. We tested the hypothesis that obstructive sleep apnea, independent of factors such as hypertension, obesity, and age, is characterized by impairment of baroreflex sensitivity. We measured muscle sympathetic nerve activity (MSNA) and heart rate responses to activation and deactivation of baroreceptors in newly diagnosed, never treated, normotensive patients with obstructive sleep apnea. These responses were compared with those obtained in healthy control subjects closely matched for age, body mass index, and blood pressure. Heart rate and MSNA changes during infusion of phenylephrine (baroreceptor activation) were similar in the control subjects and patients with sleep apnea. Infusion of nitroprusside (baroreceptor deactivation) elicited similar decreases in mean arterial pressure (MAP) but lesser MSNA increases in patients with sleep apnea than in control subjects. Calculation of DeltaMSNA/DeltaMAP ratio revealed that baroreflex regulation of sympathetic activity for similar blood pressure changes was diminished in patients with sleep apnea in comparison to normal control subjects (P=0.01). However, increases in heart rate during nitroprusside infusion were comparable in both groups. Sympathetic, blood pressure and heart rate responses to the cold pressor test were also similar in the 2 groups. Our results indicate that normotensive patients with sleep apnea have a selective impairment of the sympathetic response to baroreceptor deactivation but not to baroreceptor activation or to the cold pressor test. The impairment of baroreflex sympathetic modulation in patients with sleep apnea is not accompanied by any impairment of baroreflex control of heart rate.

Airway Obstruction↗

Oropharyngeal collapse predicts treatment response with oral appliance therapy in obstructive sleep apnea.

STUDY OBJECTIVES: To examine whether primary oropharyngeal collapse of the upper airway during sleep predicts treatment success with oral appliance therapy in patients with obstructive sleep apnea. DESIGN: Prospective physiologic study. SETTING: Multidisciplinary sleep disorders clinic in a university teaching hospital. PATIENTS: Twelve treatment-naïve adult patients with obstructive sleep apnea (apnea-hypopnea index > or = 10/h and at least 2 of the following symptoms: snoring, fragmented sleep, witnessed apneas, or daytime sleepiness). INTERVENTION: Custom-made mandibular advancement splint (MAS). MEASUREMENTS AND RESULTS: A baseline diagnostic polysomnogram confirmed AHI > or = 10 per hour. During the following acclimatization period, a custom-made adjustable MAS was incrementally advanced until maximum comfortable mandibular protrusion was reached. A second polysomnogram with MAS in situ determined efficacy. Following a 1-week washout period, a final sleep study was performed using multisensor catheters (with and without MAS, in random order during the same night) to determine upper-airway closing pressures and the site or sites of upper-airway collapse. MAS resulted in significant improvements, mean +/- SEM, in AHI (22.0 +/- 2.6 vs 9.2 +/- 1.9/h, p < .01) and upper-airway closing pressures during stage 2 non-rapid eye movement sleep (-1.1 +/- 0.3 vs -2.8 +/- 0.5 cm H2O, p < .01). All 4 patients with primary oropharyngeal collapse achieved an AHI < 5 per hour. Only 1 of the 8 patients with primary velopharyngeal collapse achieved an AHI < 5 per hour. Oropharyngeal collapse, compared with velopharyngeal collapse, predicted treatment success with MAS (p < .02). CONCLUSIONS: These preliminary data suggest that primary oropharyngeal collapse of the upper airway during sleep is an important predictor of treatment outcome with MAS therapy.

Adult↗

Cephalometric airway analysis in obstructive sleep apnea syndrome.

In obstructive sleep apnea syndrome, polysomnograms characterize the nature and severity of the disorder but, rarely, its specific site. Therefore, 90 patients with documented obstructive sleep apnea were evaluated by cephalometric technique, with special attention paid to the size and position of the soft palate and uvula, volume and position of the tongue, mandibulo-maxillary relationship, hyoid position, and size of the pharyngeal airway space. Results showed major differences between control patients and patients with obstructive sleep apnea in over 50% (30/52) of the objectively measured indices of the cephalometric airway. Further, many changes in the cephalograms of these patients can be correlated with disease severity.

Adult↗

Relationship of ventricular ectopy to oxyhemoglobin desaturation in patients with obstructive sleep apnea.

Patients with obstructive sleep apnea are considered to be at increased risk of sudden, presumably arrhythmia-related death during sleep. The present study was undertaken to determine the relationship between ventricular ectopy and the severity of oxyhemoglobin desaturation in these patients. Thirty-one male patients with obstructive sleep apnea (mean age, 55 +/- 11 years) underwent overnight polysomnography. Arterial oxyhemoglobin saturation (SaO2) was monitored by ear oximetry, and premature ventricular complexes (PVC) were detected using electrocardiographic leads CC5 and CM5. The data were recorded on electromagnetic tape for subsequent computer-assisted analysis to obtain PVC frequency as a function of decile levels of SaO2. Total sleep time averaged 333 +/- 75 minutes, the apnea index was 44 +/- 26 per hour, and the hypopnea index was 18 +/- 24 per hour. Premature ventricular complexes were observed in 23 (74 percent) of the subjects. By analysis of variance, no significant relationship was found between PVC frequency and decile levels of SaO2 for saturations greater than 60 percent; however, in the 16 subjects with SaO2 below 60 percent, a significant increase in PVC frequency was detected with decreasing SaO2 (p less than 0.01). Ventricular bigeminy was observed with SaO2 below 60 percent in three of these 16 subjects. From these results, we conclude that patients with obstructive sleep apnea are at relatively low risk of developing ventricular arrhythmias provided SaO2 remains greater than 60 percent, while those with SaO2 below 60 percent are at increased risk and should be managed accordingly.

Adult↗

Obstructive sleep apnea in children.

Obstructive sleep-disordered breathing is common in children. From 3 percent to 12 percent of children snore, while obstructive sleep apnea syndrome affects 1 percent to 10 percent of children. The majority of these children have mild symptoms, and many outgrow the condition. Consequences of untreated obstructive sleep apnea include failure to thrive, enuresis, attention-deficit disorder, behavior problems, poor academic performance, and cardiopulmonary disease. The most common etiology of obstructive sleep apnea is adenotonsillar hypertrophy. Clinical diagnosis of obstructive sleep apnea is reliable; however, the gold standard evaluation is overnight polysomnography. Treatment includes the use of continuous positive airway pressure and weight loss in obese children. These alternatives are tolerated poorly in children and rarely are considered primary therapy. Adenotonsillectomy is curative in most patients. Children with craniofacial syndromes, neuromuscular diseases, medical comorbidities, or severe obstructive sleep apnea, and those younger than three years are at increased risk of developing postoperative complications and should be monitored overnight in the hospital.

Child↗