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Identification and treatment of sleep apnea in patients with chronic headache.

This study investigates the relationship between nocturnal or morning headache and obstructive sleep apnea syndrome (sleep apnea). It is not known if headache of any type is more common in patients with sleep apnea than in other patients, but morning headache is a symptom of sleep apnea. A method is needed for identifying patients with chronic headache who might benefit from evaluation and treatment of sleep apnea. We performed a retrospective assessment of frequency of morning headache in patients grouped according to final diagnosis: sleep apnea (n = 72), periodic leg movements of sleep (n = 28), and psychophysiologic insomnia (n = 42). Prospective overnight sleep studies were obtained in a different group of 19 patients who presented for evaluation of headache. We selected certain patient characteristics as possibly indicative of sleep apnea-related headache. The retrospective study showed that 24% of patients with sleep apnea had frequent morning headache, which was not different from the other groups. In the separate group of 19 patients with chronic headache and suspected sleep disorder, 17 had sleep apnea. Nasal continuous positive airway pressure was prescribed to 14 patients. Marked improvement in headache occurred and persisted in 4 patients and moderate improvement in 3. Responders to therapy were more likely to have vascular headaches than mixed or tension headaches, more severe sleep apnea, and a nocturnal or morning timing to their headaches. However, there was large overlap in severity of sleep apnea and likelihood of response. We conclude that morning headache is not more common in sleep apnea than in other sleep disorders. However, over 30% of patients with chronic headache and other symptoms of sleep apnea have significant improvement in headache after treatment of sleep apnea.

Adult↗

Role of chemosensitivity in intrathoracic pressure changes during obstructive sleep apnea.

We tested the hypothesis that the awake ventilatory response to hypoxia and hypercapnia may contribute to the variability of respiratory effort developed in response to upper airway obstruction in obstructive sleep apnea syndrome. The polygraphic recordings of 38 patients diagnosed as having obstructive sleep apnea on the basis of an apnea+hypopnea index greater than 10 were examined. All subjects received hypoxic and hypercapnic ventilatory tests the day before the nocturnal polysomnography. Thirty apneas during non-rapid eye movement (NREM) sleep and at least 10 apneas during rapid eye movement sleep were analyzed. For each considered apnea, we measured esophageal pressure (Pes) swings during the first three breaths preceding apnea and during the first three and last three occluded efforts occurring during the apnea. We considered as indices of respiratory effort the overall increase from the minimum to the maximum Pes (delta Pes), the rate of increase of Pes during apnea (RPes), and the maximal respiratory effort at the end of apnea (Pes max fin). In NREM sleep, all three indices of respiratory effort were correlated positively with the awake ventilatory response to hypoxia or hypercapnia and with the apnea index. No correlation was found between the indices of respiratory effort and body mass index, age, pulmonary function tests, awake blood gases, apnea duration, and apnea desaturation. In rapid eye movement sleep, none of the considered variables predicted the degree of respiratory effort. In conclusion, our results suggest that the degree of ventilatory response to upper airway occlusion in obstructive sleep apnea may be influenced by the sensitivity of central neural drive to chemical stimuli.

Adult↗

Apnea is not prolonged by acid gastroesophageal reflux in preterm infants.

OBJECTIVE: To examine the temporal relationship between apnea and gastroesophageal reflux (GER) and to assess the effect of GER on apnea duration. METHODS: A total of 119 preterm infants underwent 12-hour cardiorespiratory monitoring studies using respiratory inductance plethysmography, heart rate, oxygen saturation (SaO2), and esophageal pH. The studies were scored for GER (pH <4 for > or =5 seconds) and apnea > or =15 seconds or > or =10 seconds that occurred within 30 seconds of GER. Apnea > or =10 seconds was used to assess whether GER would prolong apnea duration. RESULTS: There were 6255 episodes of GER. Only 1% of GER episodes were associated with apnea > or =15 seconds, and there was no difference in apnea rate before, during, or after GER. There was also no difference in rate of apnea > or =10 seconds before versus during GER; however, there was a decrease in apnea rate immediately after GER. The presence of GER during apnea did not prolong apnea duration, and GER had no effect on the lowest SaO2 or heart rate during apnea. CONCLUSION: There is no evidence of a temporal relationship between acid-based GER and apnea in preterm infants. In addition, GER does not prolong apnea duration and does not exacerbate the resultant decrease in heart rate and SaO2.

Apnea↗

Influence of sex and age on duration and frequency of sleep apnea events.

OBJECTIVES: Differences between men and women potentially provide insight into the regulation sleep apnea events. This study, therefore, examined how apnea frequency and duration varied according to age, sex, and sleep stage in a clinical population. DESIGN: NA SETTING: NA PATIENTS: Patients were 215 women and 215 men referred to a sleep disorders center with symptoms of obstructive sleep apnea and matched for BMI. Apnea events were compared across three age groups (18-39, 40-59, and 60-88 years) in stage 2 and in REM sleep. INTERVENTIONS: NA RESULTS: In stage 2 sleep, young and middle aged women were similar averaging 15 and 13 apnea events per hour respectively. Men had significantly more events averaging 27 and 30 events per hour for the corresponding age groups. The apnea frequency doubled from middle age to older women, and the sex difference narrowed between the older males and females to a non significant difference (26 events per hour for women versus 34 events per hour for men). Apnea duration was significantly longer in men than in women. Stage 2 apnea duration increased significantly with age for men (20.1, 21.5, 23.8 s) and women (16.7, 18.3, 20.6 s) across the three age groups. This also occurred in REM sleep in for men (22.8, 26.5, 29.8 s) and women (19.3, 22.4, 26.6 s). CONCLUSIONS: Duration did not demonstrate the marked "menopausal effect" that there was for apnea frequency. Female gender and younger age conferred benefit primarily by preventing airway collapse (reduced apnea frequency) with less of an effect on apnea duration, i.e., the ability to end the apnea. Compared to stage 2 sleep, REM sleep reduced the differences between men and women in apnea frequency. One explanation may be that differences in muscle tone of the upper airway account for the sex differences in apnea frequency.

Adolescent↗

[Effects of sleep stage on blood pressure and heart rate in patients with obstructive sleep apnea syndrome].

OBJECTIVE: To determine the effects of sleep stage on blood pressure(BP) and heart rate(HR) and to explore the relationship between BP and HR in patients with obstructive sleep apnea syndrome (OSAS). METHODS: Manometric tube was retained in the radial artery, and whole-night polysomnography (PSG) was done synchronously in 13 patients with OSAS. RESULTS: (1) The increase in BP during apnea was higher in REM sleep than in NREM sleep, but the difference was not significant (P > 0.05). When BP in awake state was regared as baseline, the increases in SBP pre-apnea and post-apnea and the increases in DBP post-apnea were significantly higher in REM sleep(-1.9 +/- 11.9 mm Hg, 32.6 +/- 20.6 mm Hg, 18.2 +/- 11.6 mm Hg, respectively) than in NREM sleep (-8.4 +/- 8.0 mm Hg, 20.4 +/- 6.9 mm Hg, 13.2 +/- 5.8 mm Hg, P < 0.05, respectively). (2) In different sleep stages, HR was markedly higher at the end of apnea than before apnea(NREM: 76 +/- 8 bpm vs 70 +/- 8 bpm, P < 0.05; REM: 85 +/- 11 bpm vs 71 +/- 8 bpm, P < 0.01). HR in post-apnea (P < 0.01) and the increase in HR during apnea (NREM: 6.9 +/- 2.2 bpm, REM: 14.1 +/- 10.1 bpm, P < 0.05) were remarkably higher in REM sleep than in NREM sleep, but not for pre-apneic HR. (3) In NREM sleep, HR in pre-apnea was significantly correlated with the increase in SBP and DBP during apnea(r = -0.699, P < 0.01; r = -0.602, P < 0.05, respectively); The increase in SBP during apnea in NREM sleep was also correlated with post-apnea HR (r = -0.669, P < 0.01). CONCLUSION: Sleep stage has effects on BP and HR and the changes in BP are correlated with the changes in HR during apnea in patients with OSAS.

Adult↗

Arterial stiffness increases during obstructive sleep apneas.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.

Adult↗

[Clinical characteristics of obstructive sleep apnea syndrome in children].

OBJECTIVE: To explore the clinical features and diagnosis of obstructive sleep apnea syndrome (OSAS) in children. METHODS: Sixty children with OSAS were reviewed, every patient was monitored with polysomnography (PSG) for 7 hours at night for 11 parameters, including the longest apnea time (LAT), apnea and hypopnea index (AHI), the lowest oxygen saturation (SaO(2)), and snore index etc., the parameters of the 2 groups were compared. Meanwhile, tonsillectomy and adenoidectomy were performed for 40 cases of OSAS, and the parameters obtained before and after operation were analyzed. RESULTS: Adenotonsillar hypertrophy and the loud snoring during sleep were found in all cases. The mean values of the PSG parameters were as follows: the longest apnea time was 53 (8-178) seconds (s); the total time of apnea was 310.5 (26-5,260) s; the time of apnea was 26 (3-240) s; the longest hypopnea time was 41 (5-94) s; the total times of hypopnea was 170 (5-2,860) s; the time of hypopnea was 10 (1-85); the apnea index was 4.1 (0.5-25.9); the hypopnea index was 1.4 (0-16.1); the apnea and hypopnea index (AHI) was 6.8 (0.5-38.2); the snore index was 81.7 (1.3-414.8); the lowest saturation of oxygen was 0.78 (0.25-0.93). There was not statistically significant difference in the parameters between 2-7 year group and over 7 year group (P > 0.05). The parameters of postoperation group: the mean value of the longest apnea time was 15.5 (0-60) s; the total time of apnea was 56.4 (60-205) s; the time of apnea was 10.33 (0-40); the longest hypopnea time was 13.25 (0-30) s; the total times of hypopnea was 44.6 (0-73); the hypopnea time was 4.32 (0 - 30) s; the apnea index was 0.6 (0-12); the hypopnea index was 0.62 (0-4); the apnea and hypopnea index (AHI) was 1.25 (0.1-12); the snore index was 30.08 (1.8-102); the lowest oxygen saturation was 93.5% (64%-97%). Compared with preoperation groups there was a statistically significant difference (P < 0.01). Clinically effective rate of the surgeries was over 90%. CONCLUSION: Adenotonsillar hypertrophy seemed to be an important cause of OSAS in children. Snoring, dyspnea, apnea and low ventilation are the major clinical characteristics of OSAS in children. Confirmed diagnosis of the syndrome in children requires PSG recordings.

Child↗

[The status of arterial and mixed venous blood gases in the initial phase of intubation apnea. Studies on the Christiansen-Douglas-Haldane effect].

The Christiansen-Douglas-Haldane effect describes the reduced CO2 binding capacity of oxygenated as compared to deoxygenated hemoglobin on the basis of its increased acidity. This study describes the development of the above effect during the first 2 min of hyperoxic intubation apnea. METHODS. After institutional approval 12 patients (NYHA III, ASA IV) scheduled for coronary-artery bypass grafting were studied after written informed consent. Routine monitoring measures included invasive arterial and pulmonary-arterial pressure monitoring. Pulse oximetry (Nellcor N 101) was also used during intubation apnea. Premedication consisted of flunitrazepam 2.0 mg p.o. the evening before operation and another 2.0 mg p.o. 90-120 min before induction of anesthesia. Following standardized preoxygenation induction of anesthesia was performed with 20-25 micrograms/kg fentanyl and 0.1 mg/kg pancuronium. After cessation of spontaneous respiration, controlled ventilation was continued with 100% oxygen until intubation. Thirteen arterial (a) and mixed-venous (v) blood samples were drawn sequentially immediately before and during the first 2 min of apnea and analyzed using Corning 150 pH/blood gas analyzer and a Corning 2500 CO-oximeter. RESULTS. As shown in Table 1 and Fig. 1, paO2 decreased from 485 +/- 100 mmHg before apnea to 376 +/- 68 mmHg after 2 min of apnea while pvO2 remained constant at 47-50 mmHg. Arterial oxygen saturation (saO2) showed stable values greater than 97% while svO2 slightly increased from 81.9% to 82.4% until the end of apnea. A biphasic increase was observed in paCO2 from 41.2 +/- 3.4 mmHg before to 54.5 +/- 3.9 mmHg at the end of apnea. An increase in pvO2 during apnea was linear from 45.7 +/- 3.9 mmHg to 51.9 +/- 4.0 mmHg. After 28.5 s of apnea paCO2 exceeded pvCO2 due to the Haldane effect ("pCO2 reversal"). During apnea, pHa decreased biphasically from 7.40 +/- 0.03 to 7.31 +/- 0.02. The speed of decrease was 0.106 pH units/min (5-35 s) in the 1st and 0.023 pH units/min in the 2nd min of apnea; pHv decreased almost linearly from 7.37 +/- 0.03 mmHg (5s) to 7.33 +/- 0.02 mmHg (115s). After 20.66 s of apnea pHa exceeded pHv ("pH reversal"); pH-reversal occurred earlier than pCO2 reversal (p less than = 0.05). CONCLUSIONS. During early hyperoxic apnea, venoarterial pH and pCO2 reversal can be observed due to the Christiansen-Douglas-Haldane effect. pH reversal starts earlier than pCO2 reversal. Reversal time is dependent on arterial-mixed-venous pCO2 difference (avDpCO2) before apnea, arterial-mixed-venous O2 saturation difference (avDsO2) and cardiac output. The amount of reversal is dependent on avDsO2, i.e. the pH difference of arterial and m

Aged↗

The gender bias in sleep apnea diagnosis. Are women missed because they have different symptoms?

BACKGROUND: Population-based studies have shown that sleep apnea is underdiagnosed in women, relative to men. One hypothesis for this gender bias is that women with sleep apnea are missed because clinical guidelines for the evaluation and diagnosis of sleep apnea, established primarily on men, are not valid for women. In this investigation, data from the Wisconsin Sleep Cohort Study, a community-based study of the natural history of sleep apnea, were used to determine whether women with sleep apnea have unique symptoms or complaints. METHODS: The sample comprised 551 men and 388 women, none of whom had ever been given a diagnosis of sleep apnea. Data on typical sleep apnea symptoms and other factors were obtained by interview and survey. Sleep apnea status was determined from the frequency of apneic and hypopneic events during sleep as recorded by in-laboratory, whole-night polysomnography. The sensitivity and relative predictive power of each symptom or factor for sleep apnea at different severity levels were calculated and compared by gender. RESULTS: Regardless of severity level, women with sleep apnea did not report symptoms that differed significantly from those of men with the same level of sleep apnea. For men and women, snoring was the most sensitive and strongest predictor of sleep apnea. CONCLUSIONS: Current clinical indications for sleep apnea evaluation are as appropriate for women as they are for men. Other reasons for the gender disparity in sleep apnea diagnosis, including the possibility that health care providers disregard typical symptoms in women, should be pursued.

Diagnosis, Differential↗

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.

Cardiac Output, Low↗

Rate of oxyhemoglobin desaturation in obstructive versus nonobstructive apnea.

Preapneic thoracic gas volume (Vtg), arterial saturation (SaO2), and mixed venous oxygen saturation (SvO2), have been shown to influence the rate of SaO2 fall (dSaO2/dt) during apnea. We asked the following question: does tissue oxygen consumption (tVO2) affect the dSaO2/dt during apnea? We attempted to answer this question by comparing dSaO2/dt during obstructive apneas (high tVO2) with dSaO2/dt during nonobstructive apneas (low tVO2) in six adult baboons. Fiberoptic central venous and arterial catheters were used for continuous monitoring of SvO2, SaO2, and cardiac output. A sapphire-bearing turbine monitored minute ventilation and airflow cessation. A Respitrace and esophageal pressures were used to assess relative differences in Vtg. Obstructive apneas (30, 45, and 60-s) were created by clamping an indwelling cuffed endotracheal tube at end-expiration. Nonobstructive apneas were created by paralyzing the animals with atracurium and interrupting ventilation for periods equivalent to those of the obstructed apneas. The ventilator was adjusted to duplicate the respiratory rate, tidal volume, and relative Vtg of the spontaneously breathing animal. Mean tVO2 during spontaneous breathing was 110 ml/min (Fick method) and decreased to 90 ml/min during paralysis (p less than 0.05). The dSaO2/dt for the three apnea durations (mean, all animals), obstructive versus nonobstructed were: 0.85 and 0.74%/s (n = 6), 0.87 and 0.75%/s (n = 6), and 0.60 and 0.48%/s (n = 4), respectively. The dSaO2/dt was significantly lower during the nonobstructive apneas. We conclude that differences in VO2 during apnea may affect the dSaO2/dt and that for the same duration apnea, central apneas may show less desaturation than obstructive apneas where vigorous muscular efforts at overcoming obstruction are common.

Animals↗

The association of the severity of obstructive sleep apnea with plasma leptin levels.

OBJECTIVE: To examine whether circulating leptin levels correlate with the severity of disease in patients with obstructive sleep apnea. DESIGN: Prospective nonrandomized study. SETTING: Referral sleep laboratory for patients with sleep-disordered breathing and biochemistry laboratory. Patients Thirty-two subjects (mean +/- SD age, 47 +/- 12 years) who were referred for suspected sleep apnea underwent an overnight sleep study and fasting morning venous blood sampling. Patients were divided into 3 groups with respect to apnea-hypopnea index: (1) severe sleep apnea (n = 8), apnea-hypopnea index greater than 20; (2) mild sleep apnea (n = 12), apnea-hypopnea index between 5 and 20; and (3) nonapneic control (n = 12), apnea-hypopnea index less than 5. RESULTS: Leptin levels (mean +/- SD) were 21.2 +/- 8.6, 16.2 +/- 5.2, and 10.6 +/- 7.5 ng/mL (P =.005) in patients with severe and mild obstructive sleep apnea and nonapneic controls, respectively. Plasma leptin levels correlated positively with the degree of sleep-disordered breathing as recorded by the apnea-hypopnea index (r = 0.54, P =.001) and percentage of sleep time spent with oxygen saturation below 90% (r = 0.39, P =.02). CONCLUSIONS: Circulating leptin concentrations in patients with obstructive sleep apnea, independent of body mass index and age, are significantly higher than levels in nonapneic controls and there is a positive relationship between leptin concentrations and the severity of sleep apnea. Hyperleptinemia may be a prognostic marker of obstructive sleep apnea syndrome.

Adult↗

The incidence of obstructive apneas in preterm infants with and without bronchopulmonary dysplasia.

We tested the hypotheses that (1) preterm infants with bronchopulmonary dysplasia (BPD) have an increased incidence of obstructive apneas as compared to those without BPD (control) and (2) the respiratory pattern during obstructive apneas may be associated with more pronounced hypoventilation. Ventilation was measured with a flow-through system. We examined 2929 total apneas in 12 infants with BPD and 4366 apneas in 12 control infants matched for study weight (1.51 +/- 0.11 kg in the BPD group and 1.62 +/- 0.12 kg in the control group, P = 0.6) and for postconceptional age (33.3 +/- 0.8 weeks in the BPD group compared with 33.4 +/- 0.7 weeks in the control group, P = 0.6). The incidence of central apneas predominated in the BPD group (2551/2929, 87%) and in the control group (4188/4366, 96%). Obstructive apneas were more frequent in the BPD group (378/2929, 13%) than in the control group (178/4366, 4%, P = 0.004). The increased incidence of obstructive apneas in infants with BPD was observed in Quiet sleep (9.1 vs. 1.6%, P = 0.03) and in REM sleep (14.2 vs. 3.6%, P = 0.009). This increased incidence of obstructive apneas was applicable to short apneas (< 10 s, 10.9 vs. 2.7%, P = 0.003) and long apneas (> 10 s, 27.5 vs. 16.4%, P = 0.01). There were no significant changes in ventilatory pattern that could be uniquely attributed to one type of apnea. The findings suggest: (1) the great variability in the incidence of obstructive apneas reported in the literature relates, at least in part, to the clinical status of the infants and (2) ventilatory pattern is not a useful predictor of either type of apnea.

Apnea↗

Sleep apnea in heart transplant recipients: type, symptoms, risk factors, and response to nasal continuous positive airway pressure.

BACKGROUND: We determined the type, symptoms, and risk factors for sleep apnea in heart transplant recipients and the response to nasal continuous positive airway pressure. METHODS: A retrospective study on heart transplant recipients with sleep apnea was conducted in a tertiary care medical center with follow-up telephone interviews. Between February 1988 and August 1998, 147 patients underwent orthotopic heart transplantation at our institution. Seventeen patients (11.6%) who were suspected of having sleep apnea underwent polysomnography at a mean interval of 17.5 months after transplantation. RESULTS: All were diagnosed with sleep apnea: 13 had obstructive sleep apnea and 4 had mixed sleep apnea. Mean age at polysomnography was 50.8 years (range, 24-67 years). The patients presented with snoring (100%), excessive daytime somnolence (65%), witnessed apneas (53%), and morning fatigue (53%). Sixteen (94%) had a mean weight gain of 10.4 kg after transplantation, and 1 patient lost 14.6 kg. In the 11 patients with obstructive sleep apnea who underwent nasal continuous positive airway pressure titration, significant improvements occurred in the apnea-hypopnea index (decreased from 37.6 to 10.4; p = 0.01) and mean arousal index (decreased from 44.5 to 19.4; p = 0.01). Only 2 of the 8 patients with sleep apnea for whom nasal continuous positive airway pressure was recommended continued to use it at the time of telephone follow-up. CONCLUSIONS: Sleep apnea, especially obstructive sleep apnea, occurs frequently in heart transplant recipients. Obstructive sleep apnea appears to present in the typical manner, and although a positive response to nasal continuous positive airway pressure can be documented by polysomnography, long-term use of nasal continuous positive airway pressure may be low.

Adult↗

Sleep apnea, delirium, depressed mood, cognition, and ADL ability after stroke.

OBJECTIVES: The incidence of sleep apnea and stroke increases with age. The aim of this study was to investigate the presence of sleep apnea after stroke and its relationship to delirium, depressed mood, cognitive functioning, ability to perform activities of daily living (ADLs), and psychiatric and behavior symptoms. DESIGN: Cross-sectional study. SETTING: Geriatric stroke rehabilitation unit. PARTICIPANTS: 133 patients (78 women and 55 men, mean age 77.1 +/- 7.7 years) consecutively admitted to a geriatric stroke rehabilitation unit. MEASUREMENTS: All patients underwent overnight respiratory sleep recordings at 23 +/- 7 days (range 11 to 41 days) after suffering a stroke. The patients were assessed using the Organic Brain Syndrome Scale, Montgomery-Asberg-Depression-Rating Scale, Mini-Mental State Examination (MMSE), and Barthel-ADL Index. Sleep apnea was defined as an apnea-hypopnea index (AHI) of 10 or more. RESULTS: The median of the AHI for the studied sample (N = 133) was 13 (range 0-79; interquartile range 6-28). Fifty-nine percent fulfilled the criteria for sleep apnea; 52% with first-ever stroke had sleep apnea. More patients with sleep apnea than without were delirious, depressed, or more ADL-dependent. Sleep apnea patients also had a higher frequency of ischemic heart disease and had more often suffered from an earlier cerebral infarction. Multivariate analysis showed that obesity, low ADL scores, ischemic heart disease, and depressed mood were independently associated with sleep apnea. Low ADL scores, apnea-related hypoxemia, body mass index < or = 27, and impaired vision were independently associated with delirium. The presence of sleep apnea was not associated with any specific type of stroke or location of the brain lesion. CONCLUSIONS: Sleep apnea is common in stroke patients and is associated with delirium, depressed mood, latency in reaction and in response to verbal stimuli, and impaired ADL ability. We suggest a trial investigating whether delirium, depressed mood, and ADL ability improve with nasal continuous positive airway pressure treatment of sleep apnea in stroke patients.

Activities of Daily Living↗

Prolonged apnea in the preterm infant is not a random event.

We tested the hypothesis that in preterm infants, prolonged apneas (apneas > or = 20 sec) are not random events but are preceded by frequent and progressively longer respiratory pauses associated with changes in ventilatory variables. We studied 36 preterm infants with apnea [birth weight 1190 +/- 60 g (mean +/- SEM), study weight 1300 +/- 60 g, gestational age 28 +/- 1 weeks, and postnatal age 23 +/- 2 days]. A nosepiece with a flow-through system was used to measure ventilation and alveolar gases. Throughout the monitoring period for each infant we established 10-min moving "window of observation" followed by a 1-min interval examined for the detection of a prolonged apnea. Within the 10-min window, three variables were defined: the number of apneic episodes, the maximum length of a single apneic episode, and the total duration of apneic time. During the following minute (eleventh) the presence or absence of a prolonged apnea was determined. Chi-square test for a linear-trend in the rate of prolonged apnea and multiple logistic regression analysis showed that the relative risk of a prolonged apnea increases significantly from preceding periods without apnea to preceding periods containing the potential predictors of prolonged apnea. The strongest predictor was total duration of apneic time in the previous 10 min. When the 1 min before prolonged apnea was compared with the 1 min of similar sleep state not having prolonged apnea, minute ventilation decreased, primarily due to a decrease in respiratory frequency. Oxygen saturation decreased and alveolar PCO2 did not change. These findings suggest that prolonged apnea is not a random event but is preceded by a disturbance of the respiratory control system characterized by (1) frequent apneas of progressive duration, (2) decrease in respiratory minute volume and frequency, and (3) decreased O2 saturation.

Apnea↗

Transition times to oral feeding in premature infants with and without apnea.

OBJECTIVE: To determine whether a significant relationship exists between the presence of apnea and the number of days it takes a premature infant to attain full oral feeding. DESIGN: A two-way analysis of variance factorial design (apnea x aminophylline) was used with infants grouped according to presence or absence of apnea and whether they were receiving aminophylline. SETTING: Neonatal intensive-care and step-down nurseries of a level III teaching hospital. PATIENTS/PARTICIPANTS: Eligibility criteria for this study included gestational age of 28-34 weeks, less than 48 hours of mechanical ventilation, and absence of congenital anomalies. Infants were classified into one of four groups: Group 1 (NN) consisted of infants who had no recorded apnea and were not receiving aminophylline (n = 27); group 2 (AA) consisted of infants receiving aminophylline who continued to experience apnea during the transition time to oral feeding, (n = 20); group 3 (NA) consisted of infants receiving aminophylline who did not experience apnea during the transition time to oral feeding (n = 12); and group 4 (AN) were infants who experienced some apnea but never received aminophylline (n = 6). All 65 enrolled subjects completed the study. PROCEDURES: Review of medical records and daily nursing notes to record apnea instances and oral feeding status for each 24-hour period. MAIN OUTCOME MEASURES: The number of days between the first attempted oral feeding and full oral feeding was recorded, as well as number of apnea instances occurring during the transition time. RESULTS: An analysis of variance procedure showed that groups who did not experience apnea had a significantly (F[1, 61] = 10.19, p < .01) shorter transition time (NN = 6.6 days, NA = 5.4 days) than groups who did (AA = 11.3 days, AN = 10.3 days). Apnea was found to be correlated strongly with transition time (R = .42, p < .001). A multiple linear regression forward selection procedure showed apnea to make the greatest contribution to variance in transition time in days with a partial R2 of .18 (p < .001). CONCLUSION: Apnea appears to be a factor that influences the length of time it takes a premature infant to begin receiving full oral feedings.

Aminophylline↗

Effect of induced transient arousal on obstructive apnea duration.

Six untreated male patients (age 19-55 yr) with obstructive sleep apnea underwent nocturnal polysomnography with acoustic stimulation to determine the effect of transient arousal on obstructive apneas during sleep. Binaural tone bursts (25-95 dB) were delivered in late expiration during the second obstructive apnea of a cycle consisting of four consecutive apneas. For the group, stimulated apneas were significantly shorter (P < 0.05, Fisher's protected least significant difference test) than were the unstimulated apneas when transient electrocortical arousal was elicited in both non-rapid-eye-movement (non-REM) sleep [mean 17 +/- 7 (SD) vs. 26 +/- 9, 23 +/- 10, and 26 +/- 12 s for 2nd vs. 1st, 3rd, and 4th apnea, respectively, of each cycle] and REM sleep (mean 19 +/- 10 vs. 35 +/- 15, 45 +/- 18, and 39 +/- 20 s). Without electrocortical arousal, the stimulated apnea was significantly shortened in non-REM (23 +/- 9 vs. 25 +/- 7, 24 +/- 8, and 26 +/- 8 s) but not in REM (32 +/- 16 vs. 37 +/- 12, 32 +/- 15, and 30 +/- 16 s). Tones delivered relatively early and late in the apnea were equally likely to be associated with resolution of the apnea. The nadir of arterial oxygen saturation of hemoglobin was inversely proportional to apnea length, with higher saturation nadirs associated with the stimulated apneas. These data indicate that transient arousal, induced by nonrespiratory stimulation, influences the resolution of obstructive apneas during sleep.

Acoustic Stimulation↗