A possible mechanism for mixed apnea in obstructive sleep apnea

Hypopneas or pauses in respiratory effort frequently precede episodes of obstructive sleep apnea resulting in mixed apneas. We studied five subjects after chronic tracheostomy for obstructive sleep apnea. During stable non-REM (NREM) sleep, subjects breathed entirely through the tracheostomy. Tracheostomy occlusion caused experimental obstructive apnea which lasted 13.9 +/- 4.7 sec and ended with transient arousal and pharyngeal opening. At the end of the apnea there was marked hyperventilation (inspired minute ventilation rose 21.6 +/- 3.5 L on the first breath) followed by hypocapnia, hypopnea, and pauses in inspiratory effort as the subjects resumed NREM sleep. Hypocapnia was greater before inspiratory pauses lasting at least 5 sec than before shorter pauses (PETco2, 4.2 +/- 1.8 mm Hg below baseline vs 1.2 +/- 2.5 mm Hg below baseline). In three patients, pauses in inspiratory effort following experimental obstructive apnea were prevented by administration of 4 percent CO2 and 40 percent O2 inspired gas. This study suggests that: hyperventilation with hypocapnia occurs at the termination of obstructive apneas, and hypocapnia may be responsible for the attenuation or cessation of respiratory effort initiating the subsequent cycle of obstruction.     

Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction

INTRODUCTION: Hypertension is common in patients with obstructive sleep apnea (OSA). However, the effect of OSA on ventricular function, especially diastolic function, is not clear. Therefore, we have assessed the prevalence of diastolic dysfunction in patients with OSA and the relationship between diastolic parameters and severity of OSA. METHODS: Sixty-eight consecutive patients with OSA confirmed by polysomnography underwent echocardiography. Diastolic function of the left ventricle was determined by transmitral valve pulse-wave Doppler echocardiography. Various baseline characteristics, severity of OSA, and echocardiographic parameters were compared between patients with and without diastolic dysfunction. RESULTS: There were 61 male and 7 female patients with a mean age of 48.1 +/- 11.1 years, body mass index of 28.5 +/- 4.3 kg/m(2), and apnea/hypopnea index (AHI) of 44.3 +/- 23.2/h (mean +/- SD). An abnormal relaxation pattern (ARP) in diastole was noted in 25 patients (36.8%). Older age (52.7 +/- 8.9 years vs 45.1 +/- 11.3 years, p = 0.005), hypertension (56% vs 20%, p = 0.002), and a lower minimum pulse oximetric saturation (SpO(2)) during sleep (70.5 +/- 17.9% vs 78.8 +/- 12.9%, respectively; p = 0.049) were more common in patients with ARP. By multivariate analysis, minimum SpO(2) < 70% was an independent predictor of ARP (odds ratio, 4.34; 95% confidence interval, 1.23 to 15.25; p = 0.02) irrespective of age and hypertension. Patients with AHI > or = 40/h had significantly longer isovolumic relaxation times than those with AHI < 40/h (106 +/- 19 ms vs 93 +/- 17 ms, respectively; p = 0.005). CONCLUSION: Diastolic dysfunction with ARP was common in patients with OSA. More severe sleep apnea was associated with a higher degree of left ventricular diastolic dysfunction in this study.     

Assessment of left ventricular diastolic function by radionuclide ventriculography at rest and exercise in subclinical hypothyroidism,and its response to L-thyroxine therapy

Hypothyroidism is associated with intrinsic myocardial changes reflected by alterations in contractility and relaxation. Diastolic function, however, rather than systolic cardiac function, seems to be mostly impaired by thyroid hormone deprivation. Our aim was to evaluate diastolic function at rest and during maximal exercise by means of radionuclide ventriculography in subclinical hypothyroidism before and after restoration of euthyroidism. Ten subclinical hypothyroid patients (50 +/- 8.7 years) (thyroid-stimulating hormone 11 +/- 4.2 microUI/ml) without cardiac disease were studied before and 6 months after levothyroxine (L-T(4)) replacement (thyroid-stimulating hormone 1.9 +/- 1.1 microUI/ml). We compared the basal and post-therapy cardiac parameters with a control group of 14 euthyroid patients (52.5 +/- 10 years) (thyroid-stimulating hormone 2.5 +/- 1.2 microUI/ml). Multigated equilibrium radionuclide ventriculography was performed to assess systolic and diastolic ventricular function. Student's t and paired Student's t tests were applied for statistical analysis. We found a significant difference between the time to peak filling rate (TPFR) at rest before (0.241 +/- 0.002 ms) and after (0.190 +/- 0.012 ms) treatment with L-T(4). A significant difference that disappeared after restoration of euthyroidism was also observed between the basal TPFR values of the subclinical hypothyroid patients and the control group (0.189 +/- 0.01 ms). The same pattern was observed at maximal exercise. Thus, TPFR, a parameter of left ventricular (LV) diastolic function measured by radionuclide ventriculography, is impaired in subclinical hypothyroid patients both at rest and during exercise and returns to normal values after L-T(4) therapy.     

Inspiratory flow dynamics during phrenic nerve stimulation in awake normals during nasal breathing.

The loss of upper airway (UA) dilators preactivation before inspiratory muscle contraction is an important determinant of the pathophysiology of obstructive sleep apnea. We hypothetized that phrenic nerve stimulation could provide a practical way to explore the effects of the dissociation between UA dilators and inspiratory muscles, and possibly to determine UA critical closing pressure during wakefulness. The pattern of inspiratory airflow was therefore studied in normal awake subjects during diaphragm twitches induced by either electrical phrenic stimulation (ES) or cervical magnetic stimulation (CMS) (n = 9) and with and without a nasal stent during ES (n = 7). End-expiratory stimulations applied during exclusive nasal breathing induced 200 to 300 ms twitch inspiratory flow. The average maximal twitch flow of flow-limited twitches was higher during CMS than ES (1.18 +/- 0.29 L.     

Sleep loss impairs inspiratory muscle endurance

Sleep loss is common in patients with respiratory disorders. To determine whether sleep loss affects respiratory muscle function, we compared respiratory muscle and pulmonary functions after normal sleep with those measured after a 30-h sleepless period in 30 normal male subjects. The respiratory muscle strength was estimated by the maximal static inspiratory and expiratory pressures. Inspiratory muscle endurance was determined by the product of pressure load and the sustained time, i.e., pressure-time index, while the subject breathed against an inspiratory pressure load on a modified Nickerson-Keens device. We found that inspiratory muscle endurance was decremented from 871 +/- 61 to 638 +/- 69 cm H2O.min after sleep deprivation. Twelve-second maximal voluntary ventilation was also significantly reduced after sleep loss. Nevertheless, the respiratory muscle strength, FEV1, and FVC were unaltered. We therefore conclude that inspiratory muscle endurance may deteriorate after a 30-h sleep loss.     

Effects of obstructive sleep apnea syndrome on serum aminotransferase levels in obese patients

PURPOSE: Obesity has been associated with obstructive sleep apnea and hepatic steatosis. We investigated the effects of obstructive sleep apnea and treatment with nasal continuous positive airway pressure (CPAP) on serum aminotransferase levels in obese patients. METHODS: We studied 40 obese men with obstructive sleep apnea syndrome. None had hepatitis B antigen or C antibody, autoimmune disease, or an excessive intake of alcohol. Serum levels of aspartate aminotransferase, alanine aminotransferase, triglyceride, glucose, insulin, and leptin were determined in the afternoon and in the morning immediately after sleep, before and after nasal CPAP treatment. RESULTS: Aminotransferase levels were abnormal in 35% (n = 14) of patients. Before treatment, mean (+/- SD) aspartate aminotransferase levels were higher in the morning than in the previous afternoon (presleep, 34 +/- 20 IU/L; postsleep, 39 +/- 28 IU/L; P = 0.006). The overnight mean increases in aminotransferase levels were less marked after the first night of nasal CPAP treatment (aspartate aminotransferase: from 6 +/- 11 IU/L to 2 +/- 6 IU/L, P = 0.0003; alanine aminotransferase: from 5 +/- 9 IU/L to 2 +/- 6 IU/L, P = 0.006). Leptin levels (n = 23) decreased significantly after treatment (P = 0.0002), whereas insulin resistance (calculated by the homeostasis model assessment method) and triglyceride levels were unchanged. Improvements in aspartate and alanine aminotransferase levels were maintained after 1 and 6 months of nasal CPAP treatment. CONCLUSION: Nasal CPAP therapy may have beneficial effects on serum aminotransferase abnormalities in obese patients who have obstructive sleep apnea.     

Muscle sympathetic nerve activity during wakefulness in heart failure patients with and without sleep apnea

Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction <45%. Of these, 43 had an apnea-hypopnea index > or =15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate. Daytime MSNA was significantly higher in those with sleep apnea (76+/-2 versus 63+/-4 bursts per 100 heartbeats [mean+/-SEM], P=0.005; 58+/-2 versus 50+/-3 bursts/min, P=0.037), irrespective of its etiology (the mean difference for central sleep apnea was 17 bursts per 100 heartbeats; n=14; P=0.006; and for obstructive sleep apnea, 11 bursts per 100 heartbeats; n=29; P=0.032). In a subgroup (n=8), treatment of obstructive sleep apnea lowered MSNA by 12 bursts per 100 heartbeats (P=0.003). Convergence of independent excitatory influences of HF and sleep apnea on central sympathetic neurons results in higher MSNA during wakefulness in HF patients with coexisting sleep apnea. This additional stimulus to central sympathetic outflow may accelerate the progression of HF; its attenuation by treatment of sleep apnea represents a novel nonpharmacological opportunity.     

Improvement in upper airway function after weight loss in patients with obstructive sleep apnea

Overweight patients with obstructive sleep apnea (OSA) are improved by weight reduction, although the underlying mechanisms are not clear. We tested the hypothesis that improvement in OSA after weight loss is associated with improvement in pharyngeal function. Consequently, we measured pharyngeal area at functional residual capacity (AFRC) and at residual volume (ARV), the percent change in pharyngeal area between FRC and RV (delta Aph%) defined as (AFRC - ARV)/AFRC x 100, and lung volume dependence of pharyngeal area (LVD) defined as the difference between AFRC and ARV normalized for the expiratory reserve volume (ERV)--in 12 overweight apneic patients before and after weight loss. We found that after a 26 +/- 18 kg weight loss, there was a significant reduction in the apnea/hypopnea index from 57 +/- 29 to 14 +/- 10 (p less than 0.0005) and increase in the lowest nocturnal oxygen saturation from 54 +/- 20% to 80 +/- 8% (p less than 0.001). This improvement was associated with a significant reduction in delta Aph% from 25 +/- 15% to 9 +/- 18% (p less than 0.05) and a significant decrease in LVD from 1.98 +/- 1.52 cm2/L to 0.16 +/- 0.88 cm2/L (p less than 0.005). There were four patients in whom baseline LVD was low and relatively unchanged after weight loss. Three of these patients exhibited paradoxical inspiratory narrowing of the glottis, which reversed after weight loss; these glottic abnormalities were not present in the rest of the patients with OSA. We conclude that improvement in obstructive sleep apnea after weight loss may be related to improvement in pharyngeal and glottic function.     

阻塞性睡眠呼吸障碍患者频繁觉醒的原因探讨

目的探讨导致睡眠呼吸障碍患者睡眠中频繁发生觉醒的原因。方法对因有白天过度困倦而就诊的25例患者作全晚多导睡眠图(PSG)检查和呼吸模式分析,并与7名健康正常人对照。按国际标准人工判断觉醒。结果上气道阻力综合征(UARS)组10例,呼吸暂停／低呼吸指数(AHI)（2.5±1.4）次/h,动脉血氧饱和度(SaO2)<90%累计时间%(SLT90%)（0.1±0.1）%,觉醒指数(ArI)（30±16）次/h;阻塞性睡眠呼吸暂停综合征(OSAS)组15例,AHI（32.8±19.1）次/h,SLT90%（11.3±16.5）%,ArI（35±17）次/h;正常人组7名,AHI（5.9±4.4）次/h,SLT90%（0.2±0.4）%,ArI（13±5）次/h。OSAS和UARS组的ArI无统计学差异(H=0.49,P=0.48),均高于正常对照组的ArI(H分别为7.36和5.22,P值分别为0.001和0.02),但UARS组AHI、SLT90%明显低于OSAS组(H>5.00,P<0.05),与正常组相近(P>0.05)。结论睡眠时上气道吸气性阻力增高,是导致睡眠频繁觉醒的主要原因。     

Sustained effect of continuous positive airway pressure on baroreflex sensitivity in congestive heart failure patients with obstructive sleep apnea

BACKGROUND: Patients with either heart failure or obstructive sleep apnea have a reduced baroreflex sensitivity for heart rate, a sign of poor prognosis. We previously demonstrated that nocturnal application of continuous positive airway pressure to heart failure patients with obstructive sleep apnea increased baroreflex sensitivity acutely, but it is not known whether these effects persist into wakefulness. OBJECTIVE: To determine whether treating obstructive sleep apnea in heart failure patients with continuous positive airway pressure improves baroreflex sensitivity during wakefulness. METHODS: Spontaneous baroreflex sensitivity was assessed during wakefulness in 33 heart failure patients (left ventricular ejection fraction < or = 45%) with obstructive sleep apnea (apnea-hypopnea index > or = 20). Subsequently, baroreflex sensitivity was reassessed 1 month after patients were randomly allocated to nocturnal continuous positive airway pressure treatment or no treatment (control). RESULTS: Compared with the 14 control patients, the 19 continuous positive airway pressure-treated patients experienced a greater increase in baroreflex sensitivity [median, (25%, 75%)] [from 5.4 (2.2, 8.3) to 7.9 (4.4, 9.4) ms/mmHg; P = 0.01] and left ventricular ejection fraction (P < 0.001). In addition, daytime systolic blood pressure and heart rate decreased more in the continuous positive airway pressure group (from 122 +/- 15 to 113 +/- 12 mmHg; P = 0.02, and from 66 +/- 8 to 62 +/- 8 bpm; P < 0.001, respectively) than in the control group. CONCLUSION: Treatment of coexisting obstructive sleep apnea by continuous positive airway pressure in heart failure patients improves baroreflex sensitivity during wakefulness in addition to improving left ventricular ejection fraction and lowering blood pressure and heart rate. These data indicate that the improved autonomic regulation of heart rate in heart failure patients treated for obstructive sleep apnea during sleep persists into wakefulness.     

Obstructive sleep apnea-dependent and -independent adrenergic activation in obesity

No agreement exists as to the mechanisms responsible for the sympathetic hyperactivity characterizing human obesity, which has been ascribed recently to a chemoreflex stimulation brought about by obstructive sleep apnea rather than to an increase in body weight, per se. In 86 middle-age normotensive subjects classified according to body mass index, waist-to-hip ratio, and apnea/hypopnea index (overnight polysomnographic evaluation) as lean and obese subjects without or with obstructive sleep apnea, we assessed via microneurography muscle sympathetic nerve traffic. The 4 groups were matched for age, gender, and blood pressure values, the 2 obese groups with and without obstructive sleep apnea showing a similar increase in body mass index (32.4 versus 32.0 kg/m2, respectively) and waist-to-hip ratio (0.96 versus 0.95, respectively) compared with the 2 lean groups with or without obstructive sleep apnea (body mass index 24.3 versus 23.8 kg/m2 and waist-to-hip ratio 0.77 versus 0.76, respectively; P<0.01). Compared with the nonobstructive sleep apnea lean group, muscle sympathetic nerve activity showed a similar increase in the obstructive sleep apnea lean group and in the nonobstructive sleep apnea obese group (60.4+/-2.3 and 59.3+/-2.0 versus 40.9+/-1.8 bs/100 hb, respectively; P<0.01), a further increase being detected in obstructive sleep apnea subjects (73.1+/-2.5 bursts/100 heart beats; P<0.01). Our data demonstrate that the sympathetic activation of obesity occurs independently in obstructive sleep apnea. They also show that this condition exerts sympathostimulating effects independent of body weight, and that the obstructive sleep apnea-dependent and -independent sympathostimulation contribute to the overall adrenergic activation of the obese state.     

Pharyngeal compliance in snoring subjects with and without obstructive sleep apnea

Recent studies have demonstrated a reduction in pharyngeal cross-sectional area and in upper airway muscle tone in patients with obstructive sleep apnea. These findings suggest that the pharynx in such patients may be more compliant than normal even in the awake state. We have tested this hypothesis by examining the pressure-area relationship of the pharynx in 13 patients and in 7 control subjects. Measurements were performed during wakefulness, with the subject seated, and at a constant lung volume near functional residual capacity. Pharyngeal area was measured by an acoustic reflection technique. Pharyngeal pressure was varied by having the subject perform gradual inspiratory and expiratory isovolume maneuvers against a distally occluded airway while mouth pressure was recorded. Specific compliance of the pharynx was calculated as the fractional change in pharyngeal area between a pressure of 0 and -10 cm H2O and and between 0 and 10 cm H2O. Specific pharyngeal compliance was 0.036 +/- 0.004 cm H2O-1 (mean +/- SE) in the control group and 0.094 +/- 0.012 cm H2O-1 in patients with OSA (p less than 0.01). These findings indicate that patients with obstructive sleep apnea have increased pharyngeal compliance. This abnormality predisposes to pharyngeal occlusion during sleep when negative transmural pressures are generated in the pharynx.     

Inspiratory muscle activity as a trigger causing the airways to open in obstructive sleep apnea

This report discusses mechanisms causing the airways to open during obstructive sleep apnea (OSAS). In 4 male patients with OSAS, 92 nonrapid eye movement (NERM) sleep apnea episodes and 37 rapid eye movement (REM) sleep apnea episodes were analyzed breath by breath during a one-night study. We calculated the pressure time index of the diaphragm (the product of inspiratory time/cycle duration (Tl/Ttot) and mean transdiaphragmatic pressure swing), evaluated the sleep stages via EEG, and performed frequency spectrum analysis of the EMG of the diaphragm. It was found that with each occluded inspiratory effort the tension time index of the diaphragm (TTdi) increased progressively to reach or slightly exceed the fatigue threshold, 0.15 to 0.18 (during NREM sleep the TTdi of the last occluded breath was 0.195 +/- 0.045 and during REM sleep the TTdi of the last occluded breath was 0.153 +/- 0.037); that a close time relationship was observed as well between the onset of arousal and the opening of the airways. Our data suggest that the airways may be triggered to open by a protective reflex originating in the larynx or the inspiratory muscles upon reaching a certain degree of contraction.     

Breathing during sleep in patients with interstitial lung disease

Patients with interstitial lung disease (ILD) have a rapid shallow breathing pattern while awake that is thought to be due to activation of lung reflexes. We wondered whether sleep would result in changes in respiratory control and thus cause hypoxemia and poor sleep quality. Eleven patients with ILD (5 men and 6 women) and 11 age- and sex-matched control subjects were studied during sleep. Sleep quality was worse in patients with ILD, with more time in Stage 1 (33.7% of total sleep time (TST) versus 13.5%) and less time in REM sleep (11.8 versus 19.9% TST) than found in control subjects, and more fragmentation of sleep (13.7 +/- 3.1 arousals/h and 24.3 +/- 6.0 sleep stage changes/h versus 6.9 +/- 1.0 and 12.7 +/- 1.4, respectively). Patients with ILD with awake SaO2 less than 90% had greater abnormalities in sleep structure than did those with SaO2 greater than 90%. The incidence of apneas and hypopnea periods in patients with ILD was low (apnea plus hypoventilation index of 1.3 +/- 0.45 versus 2.9 +/- 0.82 in control subjects, p = NS). Oxygen saturation dropped during REM sleep in patients, especially in those with more severe awake hypoxemia. Expiratory time (Te), inspiratory time (Ti), and their sum (Ttot) were shorter in the patients, whereas Ti/Ttot was the same as in control subjects. No systematic changes during sleep were seen in these variables. The variability of inspiratory volume index, Ti, Te, and Ti/Ttot was similar to that in control subjects, and was lowest during NREM sleep. The incidence of snoring was comparable in patients and control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of respiratory polysomnographic parameters in matched cohorts of upper airway resistance and obstructive sleep apnea syndrome patients.

OBJECTIVE: To compare respiratory nocturnal polysomnography (NPSG) characteristics between matched cohorts of upper airway resistance syndrome (UARS) and obstructive sleep apnea syndrome (OSAS) patients. METHODS: All patients received 13-channel NPSG, including esophageal pressure (Pes) manometry. By definition, OSAS patients had an apnea-hypopnea index (AHI, number of apneas/hypopneas per hour total sleep time) > or = 15, and UARS patients had an AHI < 5. Respiratory effort-related arousal (RERA) was defined as the absence of apnea/hypopnea with > or = 10 s duration of progressive negative Pes, culminating in an arousal or microarousal. UARS patients, by definition, had > or = 15 RERAs per hour. Fifteen consecutively diagnosed UARS patients were matched with OSAS patients on the basis of body mass index (BMI) and gender. RESULTS: Respiratory disturbance index (sum of the AHI and RERA per hour) was the same for both cohorts: UARS, 36+/-4; OSAS, 42+/-6 (p = 0.34). There were no differences between cohorts for mean inspiratory Pes nadirs for each 30-s epoch of sleep compared for each sleep stage over an entire night. For randomly selected breaths from supine stage 2 sleep, the mean inspiratory Pes nadir was the same for the cohorts: UARS, -16.6+/-2 cm H2O; OSAS, -16.1+/-3 cm H2O (p = 0.30). Differences between cohorts for each parameter fell within respective 95% confidence intervals. CONCLUSION: With the exception of AHI, respiratory NPSG parameters were the same for UARS and OSAS patients when BMI and gender were controlled for.     

Uvulopalatopharyngoplasty in snorers with sleep apneas: predictive value of presurgical polysomnography

To determine its predictive value, polysomnography was performed on 14 snorers with sleep apnea syndrome (SAS) before and 3 months after uvulopalatopharyngoplasty (UPPP). In the 8 patients considered as cured (less than 10 apneas per hour after UPPP), total apnea index (TAI) decreased from 29.7 +/- 22.6 to 4.9 +/- 3.5. Rapid eye movement sleep (REM) increased from 10.9 +/- 3.6 to 14 +/- 5.7% of the total sleep period (TSP). In the 6 uncured patients, TAI decreased from 59.7 +/- 15.7 to 32 +/- 15.7 and REM increased from 7.7 +/- 5.6 to 15.8 +/- 7.2% of TSP. Snoring and drowsiness decreased in both cured and uncured patients. A presurgical apnea index less than 40 seems to be a reliable predictor of successful UPPP. The association of obstructive apnea with either central apnea or mixed apnea was not a factor of poor prognosis. Better sleeping could explain in part the clinical improvement in both cured and uncured patients, but postoperative polysomnography is needed to detect asymptomatic SAS.     

Comparison of autonomic withdrawal in men with obstructive sleep apnea syndrome, systemic hypertension, and neither condition

Obstructive sleep apnea syndrome is characterized by obesity, nocturnal breathing abnormalities, arterial hypertension, and an increased number of cardiovascular events. Sympathetic activity is increased during nocturnal apneic episodes, which may mediate the cardiovascular complications of sleep apnea. We studied 15 male subjects with obstructive sleep apnea syndrome and associated hypertension, 54 subjects with mild to moderate essential hypertension, and 25 healthy normotensive men. Cardiovascular autonomic control was assessed using frequency domain measures of heart rate variability (HRV) during a controlled breathing test and during orthostatic maneuver. Compared with normotensive and hypertensive groups, total power and low- and high-frequency components of HRV during controlled breathing were significantly (analysis of variance, p<0.0001) lower in the obstructive sleep apnea syndrome. During the orthostatic maneuver, the change in total power of HRV was different between the 3 groups (analysis of variance, p = 0.004). The total power of HRV tended to increase in the normotensive (4.11+/-12.29 ms2) and in hypertensive (2.31+/-12.65 ms2) groups, but decreased (1.13+/-1.23 ms2) in the hypertensive group with obstructive sleep apnea syndrome. According to multivariate regression analysis, age and sleep apnea were the major independent determinants of HRV. This study found that an abnormal response to autonomic nervous tests characterizes hypertension in overweight subjects with obstructive sleep apnea syndrome. This could be due to autonomic withdrawal or supersaturation of the end-organ receptors by excessive and prolonged sympathetic stimulation. Our results also show the reduced response of orthostatic maneuver and controlled breathing in the hypertensive group compared with the normotensive group.     

Respiratory muscle function during obstructive sleep apnea

Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep. Inspiratory muscles may be subjected to potentially fatiguing loads during an obstructive apnea and this may be related to the termination of obstructive apnea. We have measured transdiaphragmatic pressure (Pdi) and breathing patterns in six male patients with OSA during sleep to characterize respiratory muscle function in OSA and determine whether apnea termination is consistently related to a pressure time index of the diaphragm (PTI) associated with respiratory muscle fatigue. There was a large intersubject variability in Pdi generation during apnea. No consistent level of PTI was associated with apnea termination. During prolonged apneas, the respiratory duty cycle plateaued, which is suggestive of an inhibitory reflex possibly mediated by chest wall afferents. There were intersubject differences in both inspiratory and expiratory muscle recruitment during apnea. In the majority of patients, the diaphragm appeared to be the primary inspiratory muscle during apnea, but in some it appeared to be the intercostal/accessory muscles. The majority of patients demonstrated an increase in gastric pressure and inward abdominal movement during the expiratory phases of an apnea, consistent with abdominal muscle recruitment stimulated by increased ventilatory drive.     

Sleep apnea and hypothyroidism: mechanisms and management

PURPOSE: There is a high incidence of sleep apnea in patients with untreated hypothyroidism. Thyroxine treatment is said to significantly reduce the apnea index and length and sleep apnea symptoms. We undertook a review of 10 consecutive hypothyroid patients with sleep apnea to investigate mechanisms and management of these two disorders. PATIENTS AND METHODS: Polysomnograms were obtained in 10 consecutive hypothyroid patients referred to our sleep disorders unit. All patients were studied while hypothyroid. Eight patients were restudied later when euthyroid. Lung function, blood gas values, and awake supraglottic resistance were also assessed in each patient. RESULTS: All 10 patients had sleep apnea and were treated with thyroxine. In one patient, hypothyroid myopathy involving the upper airway was demonstrated to be a potential mechanism of sleep apnea in hypothyroidism. Nocturnal angina and ventricular arrhythmias developed in two patients, despite the use of low thyroxine doses. Nasal continuous positive airways pressure (CPAP) was begun in eight patients. Initiation of CPAP prevented further angina or arrythmia in the patients with these cardiac complications. Six of the eight patients who were available for follow-up studies had persistent sleep apnea despite an euthyroid status (apnea index before thyroxine, 51 +/- 6; apnea index after thyroxine, 45 +/- 8), and CPAP therapy was continued in these patients. CONCLUSION: Our experience suggests that the apnea index does not decrease significantly in all patients with hypothyroidism and sleep apnea when euthyroidism is achieved. Treatment of hypothyroidism in the presence of sleep apnea is potentially hazardous and may lead to cardiovascular complications. Management by a combination of CPAP and low-dose thyroxine is helpful in this situation.     

Possibility of close relationship between sleep disorder breathing and acute coronary syndrome

OBJECTIVES: Sleep apnea syndrome and acute coronary syndrome (ACS) are related, but any further association with congestive heart failure (CHF) remains unclear. METHODS: Sixty-five patients with ACS (ACS group) and 48 patients with CHF (CHF group)underwent Holter electrocardiography and respiratory monitoring to identify sleep apnea. RESULTS: There were significant differences in age, sex, frequency of smoking, and ejection fraction between the two groups. The apnea hypopnea index showed similar high values in both ACS group (21.7 +/- 17.0/hr) and CHF group (19.4 +/- 17.9/hr). In the ACS group, 24 patients (37%) had central sleep apnea syndrome and 29 patients (45%) had obstructive sleep apnea syndrome. There were no significant differences in the incidences of central and obstructive sleep apnea syndromes between the two groups. Sympathetic nerve activity was significantly higher in ACS group than in CHF group (low/high frequency power ratio in overall study, 2.64 +/- 2.43 vs 1.24 +/- 1.05, p = 0.0003; in asleep study, 2.64 +/- 2.35 vs 1.23 +/- 1.04, p = 0.0002; in awake study, 2.73 +/- 2.36 vs 1.50 +/- 1.46, p = 0.002). CONCLUSIONS: Sleep apnea was observed at the same frequency in the ACS group and the CHF group including higher sympathetic nerve activity, and there was no significant difference in frequency of desaturation. This study suggested that sleep disorder breathing is frequently and similarly associated with both CHF and ACS.