Exacerbation Of Obstructive Sleep Apnea Research Articles

Management of Psychiatric Disorders in Patients with Respiratory Diseases.

Management of Psychiatric Disorders in Patients with Respiratory Diseases.

Clinical and Polysomnographic Characteristics of Nonobese and Obese Chinese Patients With Obstructive Sleep Apnea.

Obesity is a risk factor associated with the onset and exacerbation of obstructive sleep apnea (OSA). However, the majority of OSA patients in Asian populations are nonobese. To date, there have been insufficient large-scale studies of the differences in the clinical and polysomnographic features of obese and nonobese OSA patients in this population, and few studies have sought to identify predictors of OSA severity in affected obese and nonobese patients. We conducted a case-matched retrospective study, including 652 consecutive Chinese OSA patients (326 nonobese and 326 obese) to assess differences in demographic, clinical, and polysomnographic data between these two groups. Independent predictors of OSA severity were identified through multivariate linear regression analysis. The age and gender distributions of our obese and nonobese OSA patient cohorts did not differ significantly ( P > 0.05), and rates of comorbidities were comparable in these two patient groups ( P > 0.05). Nonobese patients were more likely to report atypical symptoms of OSA, including insomnia ( P < 0.001), irritability ( P < 0.05), and depressive symptoms ( P < 0.01), whereas obese patients were more likely to report typical symptoms of OSA, such as habitual snoring ( P < 0.001), witnessed apnea ( P < 0.05), and daytime sleepiness ( P < 0.001). Relative to nonobese patients, those who were obese exhibited significantly higher apnea-hypopnea index during total sleep time ( P < 0.001), apnea-hypopnea index during nonrapid eye movement sleep ( P < 0.001), and apnea-hypopnea index during rapid eye movement sleep ( P < 0.001), in addition to lower average oxygen saturation ( P < 0.001), minimal oxygen saturation ( P < 0.001), and a higher oxygen desaturation index ( P < 0.001) and arousal index ( P < 0.001). Total sleep time was, on average, shorter for nonobese patients ( P < 0.05), who also exhibited decreased sleep efficiency and more frequent awakening relative to obese patients ( P < 0.05). A multivariate linear regression analysis revealed that neck circumference and waist circumference were independent predictors of OSA severity in obese patients ( P < 0.05). On average, OSA was typically less severe in nonobese patients, who were also more likely to experience atypical OSA symptoms relative to obese patients. These results also suggest that the differential contributions of body fat accumulation and distribution to OSA severity may offer insights into the pathogenesis, clinical manifestations, and optimal management of this condition in nonobese and obese patient populations. It is vital that clinicians consider these differences to properly diagnose and treat this debilitating condition.

Diastolic Blood Pressure Rises with the Exacerbation of Obstructive Sleep Apnea in Males.

To characterize the association pattern between blood pressure (BP), metabolism changes, and obstructive sleep apnea (OSA) severity within male OSA patients. The association between systolic BP (SBP), diastolic BP (DBP), glucose, lipids, apnea-hypopnea index (AHI), oxygen desaturation index (ODI), and arousal index (ArI) was evaluated after adjustment for BMI and waist circumference/hip circumference ratio (WHR) in 1,370 male OSA patients. In the multiple linear regression models using SBP as an independent variable, SBP did not associate with the increase of any OSA indexes. BMI and glucose positively associated with AHI, ODI, and ArI elevation. WHR was also positively associated with increasing AHI and ODI. Total cholesterol levels increased with ODI and ArI increases. Triglyceride was associated with ArI. In the multiple linear regression models using DBP as an independent variable, DBP associated universally with AHI, ODI, and ArI with stable coefficients ranging from 0.19 to 0.20. The remaining independent variables were associated with AHI, ODI, and ArI with a similar trend to the models including SBP as an independent variable. Apnea-hypopnea, hypoxemia, and arousal changed glycometabolism, fat metabolism, and BP profoundly in a particular pattern.

The expression of serum endoplasmic reticulum stress protein-78 in obstructive sleep apnea patients

This study aimed to detect serum level of glucose regulated protein 78(GRP78) in patients with obstructive sleep apnea(OSA) and explore the relationship between endoplasmic reticulum stress and the pathophysiology of OSA. A total of 91 patients with OSA were enrolled in this study, including 30 mild, 28 moderate and 33 severe. The other 27 obese subjects were of age, gender and BMI matched group. Eleven moderate or severe OSA patients were administrated with continuous positive airway pressure (CPAP) treatment for 24 hours. Polysomnography, apnea hypopnea index (AHI), lowest arterial oxygen saturation(SaO2) and percentage of time spent at SaO2 below 90% (SIT90) were measured before and after sleep. Serum GRP78 was measured by ELISA. The expression of GRP78 in mild(3.42±0.97)μg/L, moderate(2.67±1.14)μg/L and severe(2.62±1.11)μg/L OSA groups was significantly higher than in control group(1.75±0.41)μg/L (P<0.05). The GRP78 level in mild OSA group was significantly higher than either moderate or severe OSA group (P<0.05). After 24 h treatment of CPAP, serum GRP78 level decreased significantly [(1.77±0.39)μg/L vs(2.84±0.39)μg/L; P<0.05]. Endoplasmic reticulum stress involves in the pathophysiology of patients with OSA. Higher GRP78 level in mild OSA patients suggests that endoplasmic reticulum related protein GRP 78 might rise then fall during exacerbation of OSA.

Association of Superior Vena Cava Syndrome with Sleep Apnea: Investigation Using an Impulse Oscillometry System

Superior vena cava syndrome (SVCS) patients sometimes show signs of obstructive sleep apnea (OSA). However, the mechanism causing hypoxia during sleep in SVCS patients is still uncertain. The aim of this study was to elucidate 1) the changes in central and peripheral respiratory resistance with SVCS, and 2) interpret the mechanism underlying the development of hypoxia during sleep in patients with SVCS related to OSA. Ten SVCS patients related to a neoplasm were recruited for this study. The degree of apnea hypopnea index (AHI) for OSA was evaluated by portable diagnosing device before and after SVCS treatment. We also analyzed the airway resistance and reactance quantitatively in the supine position by Master Screen impulse oscillometry system (MS-IOS?). After SVCS treatment, mean values of AHI were significantly decreased from 30.9 to 16.9 (/hour) (p = 0.001). Central respiratory resistance (R20) also decreased significantly from 0.40 to 0.33 kPa/L/s (p = 0.025) in the supine position. In contrast, peripheral respiratory resistance (R5-R20) and distal capacitive reactance (X5) did not change significantly. It is thought that the exacerbation of OSA due to SVCS is caused by increasing upper airway resistance related to reversible edema of the upper airway mucous or tissue. In contrast, SVCS may not cause peripheral respiratory tract and lung parenchyma edema.

Exacerbation of Obstructive Sleep Apnea by Oral Indomethacin

Patients with obstructive sleep apnea (OSA) are predisposed to instability in central ventilatory control during sleep. Increased instability, as reflected in an enhanced expired volume in per unit time loop gain, has been associated with a greater predisposition to upper airway collapse. Here, in an otherwise healthy patient with untreated mild OSA, we describe the further exacerbation of OSA after oral indomethacin administration. The subject was a control subject in part of a study to investigate the effects of altering cerebral blood flow (CBF) on ventilatory responses and sleep. He was administered either placebo or 100 mg of indomethacin orally with 20 mL of antacid 2.5 h before sleep on different days. He was studied overnight by polysomnography, arterial blood gases, and transcranial Doppler ultrasound. Administration of 100 mg of oral indomethacin prior to sleep resulted in an almost doubling of the apnea-hypopnea index (14 to 24/h), compared with placebo. This was due to an increase in apneas, rather than hypopneas. Following the indomethacin, changes in arterial blood gases were unremarkable, but both CBF as indexed using transcranial Doppler ultrasound and CBF reactivity to a steady-state change in CO(2) (CBF-CO(2)) reactivity were reduced, and the ventilatory response to CO(2) was elevated. CBF was also further reduced during nonrapid eye movement sleep following the indomethacin when compared with the control night. Indomethacin-induced reductions in CBF and CBF-CO(2) reactivity and related increases in ventilatory instability may lead to a greater predisposition to upper airway collapse and related apnea; these factors may partly explain the exacerbation of OSA.

Severity of Sleep-Disordered Breathing Improves Following Parturition

Changes in sleep-disordered breathing associated with late pregnancy have not previously been systematically investigated; however, a number of case reports indicate exacerbation of obstructive sleep apnea in late pregnancy, often in association with maternal hypertension. We aimed to compare the severity of sleep-disordered breathing and associated maternal blood-pressure responses in late pregnancy with the nonpregnant state. Case-controlled, longitudinal study of sleep-disordered breathing during late pregnancy and postpartum. Ten women referred for suspected sleep-disordered breathing during the third trimester of pregnancy. None. Full overnight polysomnography and continuous systemic blood pressure were measured during the third trimester of pregnancy and 3 months following delivery. Parameters of sleep-disordered breathing, including apnea hypopnea index and minimum overnight arterial oxyhemoglobin saturation, were compared between antenatal and postnatal studies. An improvement in both apnea-hypopnea index and minimum arterial oxyhemoglobin saturation occurred consistently in all subjects postnatally. In non-rapid eye movement sleep, mean apnea-hypopnea index was reduced from 63 +/- 15 per hour antenatally to 18 +/- 4 per hour postnatally (P = .03), and in rapid eye movement sleep, from 64 +/- 11 per hour to 22 +/- 4 per hour (P = .002). Minimum arterial oxyhemoglobin saturation was increased from 86% +/- 2% antenatally to 91% +/- 1% postnatally (P = .01). Arterial blood-pressure responses to apnea peaked at 170 to 180 mm Hg antenatally, while they only peaked at 130 to 140 mm Hg postnatally. This study indicates that late pregnancy may be associated with increased severity of sleep-disordered breathing and associated blood-pressure responses.

Medroxyprogesterone Acetate and Ethanol-induced Exacerbation of Obstructive Sleep Apnea

To determine if medroxyprogesterone acetate (MPA) can block the ethanol-induced worsening of obstructive sleep apnea. Randomized, double-blind, placebo-controlled, crossover trial with 1 week treatment periods. A university-based pulmonary sleep laboratory. Fourteen patients with previously diagnosed obstructive sleep apnea not currently receiving any form of therapy for the disorder. Eight patients completed the entire protocol. Baseline overnight polysomnography was performed. On the second study night, subjects ingested 1 ml/kg body weight 50 percent ethanol prior to repeat overnight polysomnography. If sleep apnea worsened, subjects then received either MPA (20 mg by mouth, three times a day) or placebo for 7 days then underwent repeat polysomnography with the same ethanol dose. A washout period followed, then, the other drug was taken, followed again by polysomnography with antecedent ethanol ingestion. Apnea-hypopnea indices (AHI) increased from 9.6 +/- 5.3 events/h (baseline) to 20.2 +/- 16.0 events/h on the ethanol night (p = 0.03). Low oxygen saturation (SaO2) fell to 79.2 +/- 5.1 percent on the ethanol night compared to baseline, 85.0 +/- 3.7 percent (p < 0.01). MPA improved AHI, nonrapid eye movement AHI, low SaO2, mean saturation nadir, number of desaturations between 80 and 90 percent, and the mean event desaturation when compared with the ethanol alone night. All these parameters were likewise improved when compared with placebo, although only the mean saturation nadir showed statistical significance. These findings were unchanged when also examined for the initial 3 hours of study. In obstructive sleep apnea patients whose disease is made worse by ethanol ingestion, MPA appears to improve oxygenation during obstructive events but not to improve their number or length.

Effect of testosterone administration on upper airway collapsibility during sleep.

Testosterone is thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but the mechanism is unclear. We present a case in which testosterone administration induced or exacerbated OSA in a 13-year-old male. We demonstrated that exacerbation of OSA by testosterone was associated with an increase in upper airway collapsibility during sleep, and that this improved after cessation of hormone administration. Our data strongly suggest that the mechanism by which testosterone administration may induce or exacerbate OSA is through an influence on neuromuscular control of upper airway patency during sleep.

Influence of morphine on respiratory activities of phrenic and hypoglossal nerves in cats

Anesthetic and sedative drugs have been found to diminish the respiratory motor activity of the hypoglossal nerve more than that of the phrenic nerve. This differential depression of motor activity to the upper airway may contribute to the exacerbation of obstructive sleep apnea by sedative drugs. To determine whether morphine has a similar selective action, we recorded phrenic and hypoglossal nerve activities before and after morphine administration in decebrate, vagotomized cats, paralyzed with gallamine. Morphine diminished the activities of both nerves in most animals, but the responses were highly variable, and no consistent pattern of differential depression was apparent. The variability of the results may reflect the complex nature of opiate actions on the control of breathing.

Selective depression by ethanol of upper airway respiratory motor activity in cats.

We studied the effects of systemically administered ethyl alcohol on the respiratory motor activity of the phrenic, hypoglossal and recurrent laryngeal nerves in unanesthetized, decerebrate cats. Some of the cats were studied after carotid sinus nerve section. In addition, parallel studies were done in intact, awake cats with chronic electromyographic electrodes in the diaphragm, genioglossus, and posterior cricoarytenoid (PCA) muscles. In decerebrate animals, alcohol induced a significant reduction of hypoglossal and recurrent laryngeal nerve activities at doses that had little or no effect on the phrenic nerve discharge. Similar changes were observed in chemodenervated cats. In awake animals, genioglossal and PCA muscle activities were depressed by alcohol, whereas diaphragm activity showed no consistent change. Alcohol caused a significant increase in respiratory frequency in awake cats and reduced the responses of genioglossal and PCA muscle activities to hypercapnia and normocapnic hypoxia. We conclude that alcohol induces a selective reduction in upper airway respiratory motor activity by an action that does not require intact suprapontile structures, vagal afferents, or peripheral chemoreceptors. This reduction may contribute to the alcohol-induced exacerbation of obstructive sleep apnea.