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Results for “Sleep Apnea, Obstructive”

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PubMed1998

Platelet activation, epinephrine, and blood pressure in obstructive sleep apnea syndrome.

OBJECTIVE: There is an increased risk of patients with obstructive sleep apnea syndrome (OSAS) to have stroke or cardiac infarcts. Besides hypertension, epinephrine-induced platelet activation could be a further reason for the increased cardiovascular morbidity and mortality in OSAS. METHODS: During a 4-month period (August 1994 to December 1994) we recruited prospectively 76 patients referred for polysomnograms because of a suspected sleep disorder such as OSAS. RESULTS: Fifty patients had no respiratory events during sleep (non-OSAS), 19 patients had more than five but less than 50 obstructive apneas or hypopneas per hour of total sleep time (mild-to-moderate OSAS group), and seven patients had an apnea hypopnea index of more than 50 per hour of total sleep time (severe OSAS group). Blood pressure, plasma epinephrine levels, and P-selectin expression (as a marker for platelet activation) were measured in every patient at 9 PM and 6 AM (before and after the polysomnogram). There was a significant correlation of the apnea hypopnea index with 9 PM and 6 AM systolic and diastolic blood pressure, with 9 PM platelet activation, and with 6 AM epinephrine levels mainly due to high values in the severe OSAS group. CONCLUSIONS: Our results suggest that platelet activation, epinephrine, and high blood pressure play a role in the high prevalence of cerebrovascular and cardiovascular events in patients with OSAS.

Adult↗

PubMed1995

Topical oropharyngeal anesthesia in patients with obstructive sleep apnea.

Topical oropharyngeal anesthesia (TOPA) increases obstructive sleep apnea (OSA) frequency in both normal subjects and loud snorers. The effects of TOPA in established OSA were assessed in six male patients with a mean age (+/- SEM) of 50 +/- 5.3 yr. Following an acclimatization night, each subject underwent two overnight sleep studies, randomly assigned to TOPA (10% lidocaine spray and 0.25% bupivocaine gargle) and control (C) (saline placebo). Patients demonstrated sleep efficiencies of 93 +/- 2.9% (mean +/- SEM) during C and 88 +/- 2.9% during TOPA. Overall apnea-hypopnea (AH) frequency, using inductance plethysmography, showed little change: 21.2 +/- 3.6 on C versus 25.1 +/- 3.5 events/h on TOPA nights (p = 0.12). There was no significant increase in AH duration with TOPA, and oxygen desaturation (> or = 4%) frequency was similar: 21.1 +/- 3.9 per hour during TOPA versus 23.6 +/- 5.9 during C. However, obstructive AHs showed a change in thoracoabdominal motion from C to TOPA nights, with an increase in events with abdominal paradox from 3.1 +/- 1.1 to 10.3 +/- 3.1 per hour (p = 0.03), and a reduction in events with ribcage paradox from 13.1 +/- 1.6 to 8.2 +/- 2.4 per hour (p = 0.08). Central and mixed AHs demonstrated similar frequencies on both nights. These data support an impairment of upper airway (UA) protective reflexes among patients with OSA.

Bupivacaine↗

PubMed1989

[Physiopathology of obstructive sleep apneas].

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.

Airway Resistance↗

PubMed2006

Insulin and obstructive sleep apnea in obese Chinese children.

OBJECTIVE: In adults, obstructive sleep apnea (OSA) is associated with insulin resistance and dyslipidemia. We aimed to establish correlation between OSA, serum lipid profile, and insulin levels in obese snoring children. METHODS: Consecutive obese children with habitual snoring were recruited. They underwent physical examination, overnight polysomnography (PSG), and metabolic studies. OSA was diagnosed if apnea hypopnea index (AHI) > 1.0, and cases were considered to have moderate to severe OSA if AHI > 10. RESULTS: Ninety-four obese subjects with habitual snoring were studied. Seventy-three subjects were male and the median age of the studied group was 12.0 years (IQR 9.7-13.9). None of the subjects had active cardiopulmonary disease, and the BMI values of our subjects were >95th percentile using local reference charts. Sixty subjects had OSA, 47 being mild, and 13 being moderate to severe OSA. Multiple logistic regression analysis revealed that saturation nadir and insulin levels were significantly associated with OSA. CONCLUSION: OSA is prevalent among obese children with habitual snoring and insulin is independently associated with the condition. Its role in the cardiovascular complications of childhood sleep apnea is worthy of further exploration.

Adolescent↗

PubMed2006

[Improvement of cardiopulmonary exercise capacity in patients with obstructive sleep apnea syndrome under CPAP therapy].

BACKGROUND AND PURPOSE: Obstructive sleep apnea syndrome (OSAS) is regarded as a cardiovascular risk factor. Therefore, cardiopulmonary exercise capacity in patients with OSAS before and under treatment with continuous positive airway pressure (CPAP) was investigated. PATIENTS AND METHODS: Cardiopulmonary exercise capacity was investigated in 36 patients with untreated OSAS using spiroergometry. A follow-up after at least 6 months was performed in 17 of these patients being treated with CPAP and in eight CPAP-neglecting patients, who served as controls. RESULTS: Maximum oxygen uptake ( O(2max)) was significantly reduced in all 36 patients with untreated OSAS (17.68 +/- 6.1 ml/min/kg) compared with reference values (30.72 +/- 4.9 ml/min/kg; p < 0.001). After an average of 305.7 +/- 104.8 nights of CPAP therapy, O(2max) rose from 15.33 +/- 4.8 to 18.53 +/- 6.9 ml/min/kg, whereas O(2max) remained unchanged in controls. Further spirometric parameters of exercise capacity as well as arterial blood pressure were also significantly improved under CPAP therapy. CONCLUSION: Cardiopulmonary exercise capacity is markedly reduced in patients with OSAS. Long-term CPAP therapy leads to a significant improvement of reduced cardiopulmonary exercise capacity in these patients.

Adult↗

PubMed2001

[Postoperative management following rhinosurgery interventions in severe obstructive sleep apnea. A pilot study].

BACKGROUND: Patients with severe obstructive sleep apnea (OSA) treated by nasal continuous positive airway pressure (CPAP) often undergo rhinosurgery to improve nasal ventilation and comply with CPAP therapy. The use of nasal packing postoperatively may worsen the severity of their sleep-related breathing disorders, even leading to death. For this reason, postoperative surveillance with CPAP ventilation is recommended. An oral connection piece offers the possibility to continue CPAP therapy. PATIENTS AND METHOD: Five patients with OSA were enrolled in this pilot study. All patients underwent a septorhinoplasty with nasal packing for 2 days. CPAP ventilation was guaranteed postoperatively by using an oral connection piece. The object of the study was to evaluate the feasibility, effectiveness, and acceptance of CPAP ventilation with this oral connection piece in patients with nasal packing. Therefore, the blood oxygenation of the patients was observed by pulse oximetry pre- and postoperatively. RESULTS: None of the patients with nasal packing showed apneas or hypopneas with arterial blood oxygen saturation below 92%. Application of oxygen was not necessary. Cardiorespiratory or neurological complications were not observed. CONCLUSION: The oral connection piece offers a feasible and effective opportunity to continue CPAP ventilation therapy after rhinosurgery in patients with OSA. The acceptance of the method is satisfactory.

Adult↗

PubMed2003

[Why is obstructive sleep apnea (OSA) a cardiovascular risk factor?].

Patients with obstructive sleep apnea (OSA) frequently suffer from cardiovascular diseases. Mechanisms like intrathoracic pressure variations, changes in blood gases (hypoxia), arousals and neurohumeral adaptation mechanisms, combined with breathing disorders are causing these cardiovascular sequelae. In particular repetitive hypoxemia and activation of the sympathetic nervous system have to be considered as stressors for the cardiovascular system. Special clinical findings should take OSA into consideration as a differential diagnosis. A systematic anamnesis with questions to daytime conditions (hypersomnia, decrease of performance), snoring and apneas while sleeping is easy to ascertain, and will lead to the correct diagnosis in more than 90% of cases. The extent and need for therapy should be assessed by three criteria: 1) daytime symptoms, 2) the extent of breathing disorder and 3) cardiovascular comorbidity.

Arousal↗

PubMed2005

Influence of obstructive sleep apnea on heart rate turbulence.

BACKGROUND: Patients with obstructive sleep apnea (OSA) are at increased risk for cardiovascular disease. Increased sympathetic drive is considered as one of the underlying mechanisms. Both heart rate turbulence (HRT) and heart rate variability (HRV) are parameters to describe autonomic regulation. We investigated the influence of sleep-disordered breathing (SDB) on HRT and HRV in patients with OSA. METHODS: Sixty-five patients underwent overnight polysomnography for clinically suspected SDB and simultaneous Holter monitoring (11 p.m.-6 a.m.). Patients with diabetes mellitus, a history of cardiac disease, left ventricular dysfunction, periodic breathing pattern, and those on beta-blockers or theophylline were excluded. According to the apnea-hypopnea index (AHI), the patients were assigned to group A (AHI <20, n = 31) or group B (AHI > or =20, n = 34). HRV (time domain, frequency domain) and HRT (onset, slope) were then related to the severity of SDB. RESULTS: Nighttime turbulence slope (TS) correlated inversely with the AHI (r = -0.45, p = 0.01) and was significantly lower in group B (8.9 +/- 1.6 ms/R-R interval) compared with that in group A (19.8 +/- 4.0 ms/R-R interval, P = 0.01). This relationship remained stable after adjusting TS for the number of ventricular premature contractions. No significant differences in turbulence onset or parameters of nighttime HRV were observed. CONCLUSIONS: Alterations in nighttime HRT correlate with the severity of SDB, indicating abnormalities in cardiac autonomic activity in moderate-to-severe OSA even in the absence of overt cardiac disease. These changes may be associated with the subsequent development of cardiovascular disease.

Adult↗

PubMed2005

The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment.

Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient, and impaired vagal activity plus oxygen radial formation. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA, and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease, which is difficult to control, may reward the curious physician with another treatment avenue.

Continuous Positive Airway Pressure↗

PubMed2006

The link between obstructive sleep apnea and heart failure: underappreciated opportunity for treatment.

Obstructive sleep apnea (OSA) is a newly recognized risk factor for the development of systemic hypertension, ischemic heart disease, and congestive heart failure. Mechanisms responsible for these links include OSA-related hypoxemia and arousal from sleep-induced increased sympathetic activity, large negative intrathoracic pressure-induced increased left ventricular transmural pressure gradient and impaired vagal activity, plus formation of oxygen radicals. Secondary phenomena include increased platelet aggregability, insulin resistance, and endothelial dysfunction with reduced endogenous nitric oxide production. Safe, nonpharmacologic, nonsurgical therapy, namely continuous positive airway pressure, can attenuate OSA and improve cardiac function and quality of life. Searching for signs or symptoms of OSA from the patient (or bed partner), namely loud habitual snoring, apneas, nocturnal choking, orthopnea, paroxysmal nocturnal dyspnea, excessive daytime sleepiness, or cardiovascular disease which is difficult to control, may reward the curious physician with another treatment avenue.

Continuous Positive Airway Pressure↗

PubMed2003

Obstructive sleep apnea in children: an update.

The diagnosis of obstructive sleep apnea in children requires clinical suspicion supplemented with the use of specific diagnostic tests. Polysomnography remains the key to diagnosis, and helps to assess the need for treatment, the risk for perioperative respiratory compromise, and the likelihood of persistent OSAS after treatment. Adenotonsillectomy is the mainstay of treatment, although children with complex medical conditions that affect upper airway anatomy and tone may require additional treatment.

Child↗

PubMed2000

Postoperative treatment of the patient with obstructive sleep apnea.

OBJECTIVE: The postoperative management of patients with obstructive sleep apnea syndrome (OSAS) has been based primarily on the potential loss of the airway. Our hypothesis is that not all patients with OSAS require placement in the intensive care unit after surgery. METHODS: We undertook a prospective, nonrandomized study (N = 38). Data included demographics, polysomnograms, body mass index (BMI), and postoperative course, including any complications within 72 hours. RESULTS: The average respiratory disturbance index was 66, and the average BMI was 29. The average preoperative and postoperative maximal arterial oxygen desaturation values were 82% and 94%, respectively. Patients with BMIs less than 35 did not have desaturation values below 90%. No complications occurred. DISCUSSION: Within the first 72 hours after surgery, no complications were observed in our study groups. Patients with BMIs greater than 35 were at increased risk for postoperative desaturations. The uncomplicated OSAS patient, one without significant comorbid factors, can be treated in a safe and prudent fashion outside of an intensive care unit.

Body Mass Index↗

PubMed2003

Obstructive sleep apnea and depression.

Is there an association between obstructive sleep apnea (OSA) and depression? OSA is a common breathing-related sleep disorder. There have been reports that depressive symptoms can be associated with this sleep disorder. A number of investigations have addressed this issue. Although some have found no correlation, most studies have concluded that there is an association between OSA and depressive symptoms. Other investigations have shown that depressive symptoms improve with treatment of OSA, and that untreated OSA may contribute to treatment resistance in some cases of mood disorders. Within the framework of current psychiatric diagnostic criteria, the depressive symptoms associated with OSA can be viewed as a combination of a mood disorder secondary to a primary medical condition and an adjustment disorder with depressed mood. The question of whether OSA causes depressive symptoms can perhaps be best answered by viewing OSA and depression as having certain symptoms that are common to both disorders.

Adjustment Disorders↗

PubMed2004

[Renal function in hypertensive patients with obstructive sleep apnea].

BACKGROUND: Patients with hypertension often suffer from obstructive sleep apnea (OSA). In addition to hypertension several other risk factors (hypoxemia, hyperlipidemia, and increased sympathic nerve activity) may contribute to progressive renal dysfunction in OSA patients. The aim of this study was to compare renal function in OSA-patients with and without hypertension. METHODS: 81 consecutive patients (50 males, 31 females) were screened for sleep apnea. Parameters of renal function (serum creatinine, creatinine clearance, microalbuminuria), and of lipid and glucose metabolism were correlated to polysomnographic results. RESULTS: OSA (apnea/hypopnea index [AHI] > or = 5) was found in 57 of 81 patients. Mean AHI was 26.7 +/- 26.1. Hypertension (blood pressure > or = 140/90 mmHg or use of antihypertensive drugs) occurred in 63 of 81 patients. Serum creatinine in OSA patients was significantly higher than in patients without OSA (1.11 +/- 0.15 vs. 0.91 +/- 0.12 mg/dl, p < 0.001). Serum creatinine correlated significantly with AHI. Creatinine clearance was associated with age (r = -0.314; p = 0.014) and presence of OSA (r = 0.265; p = 0.093). No correlation was shown between hypertension and serum creatinine or creatinine clearance. Microalbuminuria was not associated with OSA. CONCLUSION: Our results suggest an independent association between OSA and impaired renal function. Further prospective studies will have to be done to elucidate the pathophysiological mechanisms.

Adult↗

PubMed2006

Brain function in obstructive sleep apnea: results from the Brain Resource International Database.

Obstructive sleep apnea (OSA) is expected to impair vigilance and executive functioning, owing to the sensitivity of the prefrontal cortex to the effects of sleep fragmentation and intermittent hypoxia. Studies examining the pattern of cognitive dysfunction show variable results, with the heterogeneity in part due to small sample sizes in current studies and little consistency of the tests used. We examined a group of fifty subjects from the Brain Resource International Database (BRID), predicted to have OSA on the basis of the Multivariable Apnea Prediction Index, and compared them with 200 matched controls. On electrophysiological tests, the OSA group showed reduced eyes closed alpha power, increased auditory oddball N100 and P200 amplitude, but reduced N200 and P300 amplitude. The latency to P300 was not significantly different between groups, but latencies to N200 and P200 were prolonged in the OSA group. Performance testing of the executive function found that verbal interference and the switching of attention were impaired in the OSA group. We have demonstrated that a diagnostic algorithm based on apnea symptoms and demographic factors can be used to select a group with likely OSA manifesting deficits in information processing and executive function.

Acoustic Stimulation↗

PubMed2000

Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy.

Obstructive sleep apnea (OSA) is associated with increased cardiovascular morbidity and mortality. Free oxygen radicals have been implicated in the pathogenesis of cardiovascular disorders. Therefore, we aimed to test the hypothesis that increased oxidative stress constitutes one underlying mechanism for the connection between OSA and cardiovascular disease. In 18 patients with OSA the release of superoxide from polymorphonuclear neutrophils was determined after stimulation with the bacterial tripeptide formylmethionylleucylphenylalanine (fMLP) and the calcium ionophore A23. Superoxide production was measured as superoxide dismutase-inhibitable reduction of cytochrome c. Blood samples were obtained before and after two nights of CPAP therapy and after 4.8 +/- 0.6 mo of follow-up. Ten healthy young volunteers and 10 lung cancer patients without OSA but a similar spectrum of comorbidity served as controls. Before CPAP, neutrophil superoxide generation was markedly enhanced in OSA when compared with both control groups. Effective CPAP therapy led to a rapid and long-lasting decrease of superoxide release in OSA. In conclusion, OSA is linked with a "priming" of neutrophils for enhanced respiratory burst. The increased superoxide generation, which might have major impact on the development of cardiovascular disorders, is virtually fully reversed by effective CPAP therapy.

Adult↗

PubMed2004

Whole genome scan for obstructive sleep apnea and obesity in African-American families.

Obstructive sleep apnea (OSA) is a common, chronic disease associated with obesity. OSA and obesity are both prevalent in African Americans, who are also at increased risk for secondary complications. To identify susceptibility loci for OSA, we undertook a 9-centimorgans genome scan in 59 African-American pedigrees ascertained on the basis of either an affected individual with laboratory-confirmed disease or a proband who was a neighborhood control subject. Variance component linkage analysis was performed for the quantitative phenotypes apnea-hypopnea index (AHI) and body mass index. A candidate region on chromosome 8q (logarithm of odds [LOD] = 1.29, p = 0.006) gave the only evidence for linkage to the AHI. Body mass index was linked to multiple regions, most significantly to markers on chromosome 4q (LOD = 2.63, p = 0.0006) and 8q (LOD = 2.56, p = 0.0007). Evidence of linkage to the AHI was only slightly reduced after adjustment for body mass index. After adjustment for the AHI, some of the primary linkages to body mass index were greatly reduced whereas others remained suggestive. Our results suggest that there are both shared and unshared genetic factors underlying susceptibility to OSA and obesity, and that the genetic determinants of obesity in this population may be modulated by apnea severity.

Adolescent↗

PubMed2004

Occupational screening for obstructive sleep apnea in commercial drivers.

Excluding the presence of obstructive sleep apnea in commercial drivers is valuable, as the syndrome may increase their risk of sleepiness-related accidents. Using polysomnography as the criterion standard, we prospectively compared accuracies of five strategies in excluding the presence of severe sleep apnea and, secondarily, any sleep apnea among 406 commercial drivers. These strategies were as follows: (1) symptoms; (2) body mass index; (3) symptoms plus body mass index; (4) a two-stage approach with symptoms plus body mass index for everyone, followed by oximetry for a subset; and (5) oximetry for all. For excluding severe apnea, the two-stage strategy was highly successful, with 91% sensitivity and specificity, and a negative likelihood ratio of 0.10. This strategy was comparable in accuracy to oximetry, which had a negative likelihood ratio of 0.12, and was 88% sensitive and 95% specific. If we avoided oximetry altogether, then symptoms together with body mass index were 81% sensitive and 73% specific, with a negative likelihood ratio of 0.26. On the other hand, excluding any apnea could not be done with reasonable accuracy unless oximetry was used. We conclude that two-stage screening is likely to be a viable means of excluding severe sleep apnea among commercial drivers.

Adult↗