Use of heated humidification during nasal CPAP titration in obstructive sleep apnoea syndrome.

Nasal symptoms associated with the use of nasal continuous positive airway pressure (nCPAP) in obstructive sleep apnoea (OSA) can adversely impact on patients' tolerance, acceptance and adherence to nCPAP therapy. Regular use of heated humidification is effective in alleviating these symptoms and improve patient comfort. In a randomised, parallel, double-blinded, controlled study, the present authors examined the use of heated humidification during a single night laboratory nCPAP titration in untreated OSA patients and its effect on nasal symptoms, nasal airway resistance (NAR), effective pressure and treatment tolerability and acceptance. Baseline characteristics of subjects (n=70) receiving placebo and humidification were (mean+/-sem): age 51.2+/-2.2 versus 50.6+/-1.6 yrs; body mass index 33.6+/-0.9 versus 35.2+/-0.9 kg.m-2; Epworth Sleepiness Scale 10.8+/-1.0 versus 11.3+/-0.7; and apnoea-hypopnoea index 43.5+/-4.6 versus 44.4+/-4.1 events.h-1. Total inspiratory NAR, before (0.36+/-0.09 (placebo) versus 0.33+/-0.09 kPa.L-1.s-1) and after nCPAP (0.47+/-0.11 versus 0.29+/-0.04 kPa.L-1.s-1) were not significantly different between the groups. No difference was found in the frequency and severity of nasopharyngeal symptoms, therapeutic pressure and subjective response to nCPAP. In conclusion, heated humidification during the initial nasal continuous positive airway pressure titration offers no additional benefit in nasal physiology, symptoms or subjective response to nasal continuous positive airway pressure, and, therefore, should not be routinely recommended.     

Long-term nasal CPAP does not ameliorate obstructive sleep apnoea

Fifty-seven patients with obstructive sleep apnoea (OSA) were treated for at least six months with nasal continuous positive airway pressure (CPAP). At follow-up, sleep studies were performed in which CPAP was not used for the first half of the night. We compared the severity of OSA at follow-up without CPAP to the severity of OSA during the patient's initial diagnostic study. Apnoea and hypopnoea index (AHI) fell from 41.4 ± 7.5 (mean ±95% CI) to 34.8 ± 7.9 (p= 0.06 by Wilcoxon test) and minimum oxygen saturation rose from 71.6 ± 3.2 to 78.5 ± 2.6 (p<0.001). Some of this change may have been due to reduced REM sleep in the follow-up study (10.5±2.1% Total Sleep Time vs 7.4±2.4% TST, p<0.05). Long-term nasal CPAP was not associated with any reduction of obesity (BMI before CPAP 31.9 ± 1.0, after CPAP 31.7 ± 1.0 (p= 0.39). Systolic arterial pressure fell (before CPAP 143.0 ±4.5 mmHg, after CPAP 136.3 ± 4.6, p < 0.05) but diastolic pressure did not (before CPAP 88.5 ± 3.0 mmHg, after CPAP 85.6 ±2.9 mmHg, p = 0.11). We concluded that the effect of CPAP treatment for six or more months was a small fall in AHI and a small rise in minimum Sa0₂, but that this would be of marginal clinical significance, and may be artefactual. (Aust NZ J Med 1991; 21: 235–238.)     

Objective measurement of compliance with nasal CPAP treatment for obstructive sleep apnoea syndrome

Compliance with nasal continuous positive airway pressure (CPAP) has become a major concern, since this treatment is efficacious, but constraining. In 46 consecutive obstructive sleep apnoea (OSA) patients, we measured compliance with nasal CPAP by establishing a mean rate of use, with a built-in time counter read at three-month intervals, over a mean follow-up period of 232 +/- 27 days. The mean rate of use in the whole group was 5.14 +/- 0.31 hours per day. The acceptance rate was 90.9-93.2%, showing that patient acceptance is not a limitation in the use of nasal CPAP.     

The role of nasal CPAP in obstructive sleep apnoea syndrome due to mandibular hypoplasia

Melnick Needles syndrome (MNS), Treacher Collins syndrome (TCS) and Pierre Robin syndrome (PRS) are congenital abnormalities with characteristic facial appearances that include micrognathia. A 20‐year‐old girl with MNS, a 16‐year‐old boy with TCS and a 12‐year‐old girl with PRS attended the sleep apnoea clinic at our institution at different times. Diagnostic sleep studies were initially performed on all three patients to confirm the diagnosis of obstructive sleep apnoea syndrome (OSAS). They subsequently commenced nasal CPAP (nCPAP) treatment and their progress was followed. A limited sleep study on the patient with MNS demonstrated moderate/severe OSAS with an AHI of 33 events/h. Commencement of nCPAP resulted in symptomatic improvement. Overnight oximetry in the patient with TCS showed repeated desaturation to SpO₂ <90%. Subsequent treatment by nCPAP almost completely abolished the desaturation events. Overnight polysomnography in the patient with PRS demonstrated severe OSAS with an AHI of 49 events/h. After 3 years of nCPAP therapy, this patient requested discontinuation of treatment. Subsequent polysomnography without nCPAP revealed an AHI of <5 events/h. The use of nCPAP in the patients with MNS and TCS resulted in effective control of their sleep abnormalities. Mandibular growth and enlargement of the posterior airway space led to resolution of OSAS in the patient with PRS. There is a definite role for nCPAP therapy in patients with congenital micrognathia and OSAS. The use of nCPAP may obviate the need for more invasive corrective surgery for OSAS and is not necessarily a life‐long requirement.     

Occurrence of breathing disorders during CPAP administration in obstructive sleep apnoea syndrome

The spectrum of breathing events during sleep in patients with obstructive sleep apnoea syndrome (OSAS) after the abolition of obstructive apnoeas has been extensively studied in tracheostomized patients, but has received much less attention in patients submitted to continuous positive airway pressure (CPAP). We analysed the breathing pattern during sleep in forty patients while CPAP was administered. A regular breathing pattern throughout the sleep study was observed in 15 patients. In the remaining 25 subjects, one or more of the following events was observed: central apnoeas, hypopnoeas, periodic breathing, prolonged oxyhaemoglobin desaturations. Central apnoeas during non-rapid eye movement (NREM) sleep appeared almost exclusively after arousals or wakefulness periods; their prevalence did not significantly differ between subjects who showed and who did not show similar events before CPAP. Central apnoeas in rapid eye movement (REM) sleep had a random occurrence. Hypopnoeas were found only in REM sleep, and, like central apnoeas, occurred randomly; in one patient they had a prolonged duration (up to 110 s). Periodic breathing was observed in only two subjects, one of whom had congestive heart failure: it was limited to NREM sleep and was not associated with arousals or shifts in sleep stage. Prolonged oxyhaemoglobin desaturations were found mainly in REM sleep; most subjects with such abnormalities had daytime blood gas alterations. In conclusion, abnormalities of the breathing pattern of patients with OSAS can be observed during CPAP and after tracheostomy, but periodic breathing is less common than is reported after tracheostomy, and is probably caused by different mechanisms.     

The effect of short-term nasal CPAP therapy in cases of obstructive sleep apnea syndrome

Recent studies have shown that nasal CPAP is very effective in the treatment of patients with obstructive sleep apnea syndrome (OSA). To clarify the characteristics of pulmonary function testing and to evaluate the effect of short term nasal CPAP therapy in 13 cases of OSA patients, nasal CPAP was used for 10 to 14 days and polysonography was performed on two consecutive nights without nasal CPAP and at one night with nasal CPAP. Pulmonary function tests and the Uchida-Kraepelin test were performed before the initiation of nasal CPAP therapy and also 7 to 14 days after the nasal CPAP therapy. Apnea index reduced significantly in all cases from 5.10 +/- 19.6 episodes/hour without therapy to 3.1 +/- 3.5 with nasal CPAP (p less than 0.001). Nasal CPAP significantly reduced the frequency of obstructive (p less than 0.001) and mixed apnea (p less than 0.01), but the frequency of central apnea did not change with nasal CPAP. During the nasal CPAP, mean nadir SaO2 rose from 87.3 +/- 2.9% to 92.7 +/- 1.1% (p less than 0.001) and the lowest SaO2 rose from 73.3 +/- 6.4% to 92.0 +/- 2.1% (p less than 0.001). Before the nasal CPAP therapy, daytime PaO2 was 80.6 +/- 6.4 Torr and closing capacity (CC)/FRC ratio was higher when patients were in a supine than in a sitting position. After short term nasal CPAP therapy, daytime PaO2 increased significantly (p less than 0.001), and FRC/TLC in a supine position increased and CC/FRC in a supine position decreased in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial overdrive pacing compared to CPAP in patients with obstructive sleep apnoea syndrome.

AIMS: Obstructive sleep apnoea (OSA) is associated with oxygen desaturation, blood pressure increase, and neurohumoral activation, resulting in possible detrimental effects on the cardiovascular system. Continuous positive airway pressure (CPAP) is the therapy of choice for OSA. In a recent study, nocturnal atrial overdrive pacing (pacing) reduced the severity of sleep apnoea in pacemaker patients. We compared the effects of CPAP with those of pacing in patients with OSA but without pacemaker indication or clinical signs of heart failure. METHODS AND RESULTS: Ten patients with OSA on CPAP therapy were studied for three nights by polysomnography. During the nights that followed a night without any treatment (baseline), the patients were treated with CPAP or pacing in a random order. Pacing was performed with a temporary pacing lead. The pacing frequency was 15 b.p.m. higher than the baseline heart rate. The apnoea-hypopnoea index was 41.0 h(-1) (12.0-66.6) at baseline and was significantly lower during CPAP [2.2 h(-1) (0.3-12.4)] compared with pacing [39.1 h(-1) (8.2-78.5)]. Furthermore, duration and quality of sleep were significantly improved during CPAP when compared with pacing. CONCLUSION: Nocturnal atrial overdrive pacing is no alternative therapeutic strategy to CPAP for the treatment of OSA in patients without clinical signs of heart failure and without conventional indication for anti-bradycardia pacing.     

CPAP treatment for obstructive sleep apnoea in heart failure: expectations unmet.

Heart failure (HF) is an epidemic, increasing in prevalenceas the population ages. The Rotterdam Study shows that personswho live to age 55 have a one in three chance of eventuallydeveloping HF.¹ The staggering prevalence estimate of more thanfive million currently living with HF in the United States mayunderestimate the overall problem, since population-based studiesfind that a substantial proportion of those with systolic dysfunctionare asymptomatic, although still at increased mortality risk.^2,3Despite advances in treatment with drugs, lifestyle modifications,and therapeutic devices, mortality from HF continues to rise,fuelling interest in alternative methods of treatment. One suchtarget of therapy has been obstructive sleep apnoea (OSA). HF and OSA are closely linked by their strong associations withageing and obesity, and frequently     

Impact of CPAP on asthmatic patients with obstructive sleep apnoea.

The impact of continuous positive airway pressure (CPAP) treatment on the airway responsiveness of asthmatic subjects with obstructive sleep apnoea (OSA) has scarcely been studied. A prospective study was performed comparing the changes in airway responsiveness and quality of life in stable asthmatic OSA patients, before and 6 weeks after their nocturnal CPAP treatment. A total of 20 subjects (11 males and nine females) participated in the study. With the nocturnal CPAP treatment, the apnoea/hypopnoea index dropped from 48.1 +/- 23.6 x h(-1) to 2.6 +/- 2.5 x h(-1). There were no significant changes in airway responsiveness after CPAP treatment (provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV(1); PC(20) 2.5 mg x mL(-1) (1.4-4.5)) compared with baseline (PC(20) 2.2 mg x mL(-1) (1.3-3.5)). There was no significant change in FEV(1) either. However, the asthma quality of life of the subjects improved from 5.0 +/- 1.2 at baseline to 5.8 +/- 0.9 at the end of the study. In conclusion, nocturnal continuous positive airway pressure treatment did not alter airway responsiveness or forced expiratory volume in one second in subjects with stable mild-to-moderate asthma and newly diagnosed obstructive sleep apnoea. However, nocturnal continuous positive airway pressure treatment did improve asthma quality of life.     

Hypercapnia in obstructive sleep apnoea syndrome

BACKGROUND: The reports on the prevalence of hypercapnia in Obstructive Sleep Apnoea Syndrome (OSAS) are conflicting. We studied the prevalence of hypercapnia in a population of OSAS patients referred to a Department of Respiratory Medicine and the mechanism of the respiratory failure in OSAS associated with Obesity Hypoventilation Syndrome (OHS) or with Chronic Obstructive Pulmonary Disease (COPD) (Overlap syndrome). METHODS: We studied 219 consecutive OSAS patients during a period of 3 years. We recorded age and anthropomorphic data and performed polysomnography and pulmonary function tests. In relation to the value of PaCO(2), the patients were divided in hypercapnic (PaCO(2)>45 mmHg) patients and normocapnic patients. They were also divided into three groups in relation to the presence of "simple" or "pure" OSAS, to the presence of OSAS associated with COPD, to the presence of OSAS associated with OHS. RESULTS: Seventeen per cent of the patients were hypercapnic. They were significantly heavier, had more severe lung function test abnormalities and more severe nocturnal oxyhemoglobin desaturations than the normocapnic ones, while Forced Expiratory Volume in one second as a percentage of Forced Vital Capacity (FEV1/FVC %) and Apnoea/Hypopnoea Index (AHI) were similar. OHS patients (13%) were significantly younger and heavier, had lower PaO(2) and higher PaCO(2) than "simple" OSAS patients (77%) and Overlap patients (10%) and had more severe restrictive defect. There was no difference in terms of AHI among the three groups, but nocturnal oxyhemoglobin desaturations were more severe in OHS group. In OHS group hypercapnia was correlated to FVC% of predicted and FEV1% of predicted and to the mean nocturnal oxyhemoglobin saturation; in Overlap patients PaCO(2) was correlated to Forced Expiratory Flow rate at low Vital Capacity. CONCLUSION: Seventeen per cent of OSAS patients referred to a Department of Respiratory Medicine were hypercapnic. Hypercapnia in OHS patients correlates to the restrictive ventilatory defect whereas in Overlap patients it seems to correlate to peripheral airways obstruction. The distinction between patients with "simple" or "pure" OSAS and patients affected by OSAS associated with OHS or COPD could be important not only for clinical and prognostic implications, but also for the consequences in terms of ventilatory treatment.     

Nasopharyngeal symptoms in patients with obstructive sleep apnea syndrome. Effect of nasal CPAP treatment

BACKGROUND: Nasal side effects are often reported during nasal continuous positive airway pressure (CPAP) treatment of obstructive sleep apnea syndrome (OSAS) and may make the use of nasal CPAP difficult. OBJECTIVE: The aim of this study was to evaluate the effect of nasal CPAP on nasopharyngeal symptoms in OSAS patients. METHODS: The frequency and severity of nasopharyngeal symptoms and signs were prospectively evaluated in 49 consecutive OSAS patients (37 men, 12 women, mean (SD) age 54 (7) years, body mass index 35 (6) kg/m2) immediately before and after 6 months' treatment with nasal CPAP. RESULTS: Nasopharyngeal symptoms were common already before starting nasal CPAP: 74% of patients reported dryness, 53% sneezing, 51% mucus in the throat, 45% blocked nose, and 37% rhinorrhea. During nasal CPAP treatment, severity and frequency of sneezing (75%) and rhinorrhea (57%) increased. This increase was related to the season when nasal CPAP was applied, and was more profound in winter than in summer. Mild abnormalities on rhinoscopy and paranasal sinus X-rays were common both at baseline and at follow-up with no significant change during treatment. CONCLUSIONS: Nasopharyngeal problems were found to be frequent in patients with OSAS before nasal CPAP treatment, and tended to increase during the treatment.     

CPAP therapy prevents increase in blood pressure after upper airway surgery for obstructive sleep apnoea

Objective

The aim of this study was to investigate the efficacy of continuous positive airway pressure (CPAP) therapy following uvulopalatopharyngoplasty (UPPP) to prevent blood pressure (BP) elevation during sleep.

Methods

Sixteen normotensive patients with OSA were subjected to UPPP with or without septoplasty. These patients were instrumented for 24 h of ambulatory BP recording, polysomnography, nocturnal urinary catecholamine and pain evaluation using a visual analogue scale in the day prior to surgery (D?1), following the surgery (D+1) and 30 days later (D+30). For the D+1, the patients were divided into two groups: the without CPAP therapy group and the with CPAP therapy group.

Results

The apnoea–hypopnoea index (AHI) significantly increased in the patients without CPAP therapy compared with the D?1 (74?±?23 vs. 35?±?6 times/h, p?<?0.05), and in the CPAP group, there was a significant reduction in the average AHI value to 14?±?6 times/h, p?<?0.01. During D+1, we observed an increase in the nocturnal systolic BP (10 %), diastolic BP (12 %) and heart rate (14 %) in the group without CPAP. These metrics were re-established in the CPAP group to values that were similar to those that were observed on the D?1. The absence of nocturnal dipping in the group without CPAP was followed by a significant increase in nocturnal norepinephrine (42?±?12 μg/l/12 h) and epinephrine (8?±?2 μg/l/12 h) levels compared with the D?1 (norepinephrine 17?±?3; epinephrine 2?±?0.3 μg/l/12 h, p?<?0.001). In the patients who used the CPAP treatment, the nocturnal catecholamine levels were similar to D?1. The effectiveness of intravenous analgesic therapy was verified by a significant decrease in the pain scores in patients both with and without CPAP therapy.

Conclusion

These data confirm an increase in the AHI on the night following UPPP with or without septoplasty. This increase promotes an absence of nocturnal dipping and a significant increase in urinary catecholamine levels. CPAP therapy was effective to prevent the transitory increase in BP.     

Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.     

Maxillofacial surgery and nasal CPAP. A comparison of treatment for obstructive sleep apnea syndrome

Nasal continuous positive airway pressure (CPAP) is the primary therapy for obstructive sleep apnea syndrome (OSAS). Recent reports have indicated, however, that there is a small but significant number of failures related to patient compliance. Primary surgical treatment, which has been uvulopalatopharyngoplasty (UPPP), has declined because of poor results. A reviewed of UPPP failures has shown that while UPPP eliminated palatal obstruction, it failed to eliminate base of tongue obstruction. Maxillofacial surgery has been reported as treatment of OSAS by correcting base of tongue obstruction. Thirty patients with severe OSAS were evaluated to compare nasal CPAP and maxillofacial surgery. The goal was to determine if our surgical protocol was as effective as nasal CPAP. All patients initially underwent baseline diagnostic polysomnography to document OSAS. A nasal CPAP study was performed to determine the appropriate positive end-expiratory pressure. The patients in this study were using nasal CPAP, but they found it unacceptable as long-term treatment and elected surgery. Maxillofacial surgery consisted of maxillary, mandibular, and hyoid advancement. Polysomnography was performed six months following surgery and compared with the night 2 CPAP results. The parameters included in the investigation were the respiratory disturbance index (RDI), lowest SaO2, number of SaO2 falls below 90 percent, total sleep time (TST), REM sleep percent, stage 3-4 sleep percent, and wake after sleep onset. The mean RDI before treatment was 72.0 (SD 25.7). After completing therapy, the RDI from surgery and CPAP was 8.8 (SD 6.0) and 8.6 (SD 4.1), respectively. The mean low SaO2 prior to treatment was 61.0 (SD 13.5), and the CPAP results and postsurgical results were 86.2 (SD 5.5) and 86.1 (SD 4.2), respectively. An analysis of variance was used to examine the results, and there was no statistical difference between nasal CPAP and surgery for all respiratory variables.     

Nasal function and CPAP use in patients with obstructive sleep apnoea: a systematic review

Sleep and Breathing - This systematic review was conducted to answer the following 3 questions: ‘Does nasal pathology affect CPAP use?’, ‘What is the effect of CPAP on the...     

Humidified nasal continuous positive airway pressure in obstructive sleep apnoea.

Heated humidification of nasal continuous positive airway pressure (nCPAP) reduces upper airway symptoms and improves initial use in obstructive sleep apnoea syndrome (OSAS). The present study aimed to assess the effect of heated humidification of nCPAP on upper airway symptoms and initial use in obstructive sleep apnoea. This study was of a randomised, crossover design. Subjects with polysomnographically confirmed OSAS were randomised to 3 weeks nCPAP treatment with heated humidification (nCPAP-humid) or placebo humidification (nCPAP pl-humid). Objective and subjective nCPAP use, upper airway symptoms, and treatment satisfaction were compared. Thirty seven of 42 patients completed the protocol. nCPAP-humid reduced the frequency of adverse upper airway symptoms. nCPAP use over 3 weeks was greater with nCPAP-humid compared with nCPAP pl-humid. No difference was found between the treatment arms in terms of subjective treatment satisfaction or alertness. Heated humidification of nasal continuous positive airway pressure reduces upper airway symptoms and is associated with a small increase in initial use but not subjective sleepiness or treatment satisfaction. The results support the use of heated humidification as a strategy to reduce side-effects related to continuous positive airway pressure but not routine initial use.     

Leptin and ghrelin levels in patients with obstructive sleep apnoea: effect of CPAP treatment.

Serum leptin and ghrelin levels were investigated in patients with obstructive sleep apnoea (OSA) syndrome before and during continuous positive airways pressure (CPAP) treatment and compared with body mass index (BMI)-matched controls without OSA. Male patients (n=30) with OSA (apnoea/hypopnoea index=58+/-16, BMI=32.6+/-5.3 kg x m(-2)) underwent CPAP treatment. Fasting leptin and ghrelin were measured at baseline and 2 days, and in the case of leptin 2 months after initiation of treatment. Baseline plasma ghrelin levels were significantly higher in OSA patients than in controls. After 2 days of CPAP treatment, plasma ghrelin decreased in almost all OSA patients (n=9) to levels that were only slightly higher than those of controls (n=9). Leptin levels did not change significantly from baseline after 2 days of CPAP treatment, but were higher than in the control group. After 8 weeks, leptin levels decreased significantly, although the BMI of the patients showed no change. The decrease in leptin levels was more pronounced in patients with a BMI <30 kg x m(-2). These data indicate that the elevated leptin and ghrelin levels are not determined by obesity alone, since they rapidly decreased during continuous positive airways pressure therapy.