Residual effect of nCPAP applied for part of the night in patients with obstructive sleep apnoea

The aim of the present study was to assess whether nasal continuous positive airway pressure (nCPAP) treatment, applied for only a few hours at the beginning of the night, has any residual effect on sleep and breathing during the ensuing hours of unassisted sleep in patients with obstructive sleep apnoea syndrome (OSAS). In 27 patients with newly-diagnosed OSAS, effective nCPAP was applied during the first part of the night and then withdrawn. Polysomnographic parameters after nCPAP withdrawal were compared with those of the corresponding part of the diagnostic polysomnography performed a few days or weeks before and with those of the first part of night on nCPAP. After 255+/-63 (mean+/-SD) min of sleep with normalization of sleep and breathing parameters under nCPAP, there was partial improvement of OSAS severity during the remaining 124+/-56 min of nocturnal sleep without treatment; mean oxygen saturation, desaturation index (equivalent to the apnoea/hypopnoea index) and movement arousal index all improved significantly with respect to the diagnostic night (p=0.001). This improvement was not accounted for by a change in sleep architecture. We conclude that there is an improvement in severity of obstructive sleep apnoea syndrome after only 4 h of nasal continuous positive airway pressure. This carryover effect could explain why a number of patients with obstructive sleep apnoea syndrome apply nasal continuous positive airway pressure for only part of the night or not every night.     

Evaluation of diaphragmatic fatigue in obstructive sleep apnoeas during non-REM sleep

BACKGROUND: Resistive load applied to the airways may induce diaphragmatic fatigue, and hypoxaemia has been shown to predispose to the development of fatigue. Inspiratory muscle fatigue may occur in patients with obstructive sleep apnoea syndrome (OSAS), as these patients repetitively develop both inspiratory loading and hypoxaemia. The results of previous studies on this topic are inconclusive, probably because of the methodological approaches used. METHODS: Six obese patients with OSAS underwent a polysomnographic study. The diaphragmatic pressure time index (PTI) was evaluated as an indicator of diaphragmatic contraction, and the mean frequency of the diaphragmatic electromyogram power spectrum (Fm) and the maximum relaxation rate of transdiaphragmatic pressure (MRR) as indices of a fatiguing diaphragm. A total of 119 randomly selected apnoeas (each including 5-13 occluded efforts) were analysed throughout the night in non-REM sleep to assess possible muscle fatigue due to the high pressure generation in each apnoea. A breath-by-breath within-apnoea analysis was performed on the first three pre-apnoeic breaths, on all the occluded efforts, and on the first three unoccluded breaths following the apnoea interruption. Possible fatigue development due to the cumulative effect of apnoeas over the night was also evaluated. RESULTS: A progressive increase of Fm and MRR was found during the obstructive phase in all the subjects in the within-apnoea analysis. The overnight analysis did not show a reduction in either PTI, Fm, or MRR secondary to recurrent upper airway obstruction during the night. CONCLUSIONS: No evidence of diaphragmatic fatigue or impaired diaphragmatic contraction was found either within each apnoea or throughout the whole night, despite the generation of high PTI values during the apnoeic occluded phases. It is concluded that diaphragmatic fatigue does not occur in OSAS during non-REM sleep.     

Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients

We have investigated pulmonary hemodynamics in a large series of consecutive, unselected patients with obstructive sleep apnea syndrome (OSAS). The aims of this study were to evaluate the frequency of pulmonary artery hypertension (PH) in OSAS and to analyze, as far as possible, its mechanisms. Two hundred twenty patients were included on the basis of a polysomnographic diagnosis of OSAS (apnea+hypopnea index > 20). PH, defined by a resting mean pulmonary artery mean pressure (PAP) of at least 20 mm Hg, was observed in 37 of 220 patients (17%). Patients with PH differed from the others with regard to pulmonary volumes (vital capacity [VC], FEV1) and the FEV1/VC ratio that were significantly lower (p < 0.001); PaO2 (64.4 +/- 9.3 vs 74.7 +/- 10.1 mm Hg; p < 0.001); PaCO2 (43.8 +/- 5.4 vs 37.6 +/- 3.9 mm Hg; p < 0.001), apnea+hypopnea index (100 +/- 33 vs 74 +/- 32; p < 0.001), and mean nocturnal arterial oxygen saturation (SaO2) (88 +/- 6% vs 94 +/- 2%; p < 0.001). Patients with PH were also more overweight (p < 0.001). Multiple regression analysis showed that 50% of the variance of PAP could be predicted by an equation including PaCO2 (accounting for 32% of the variance), FEV1 (12%), airway resistance (4%), and mean nocturnal SaO2 (2%). In conclusion, PH is observed, in agreement with previous studies, in less than 20% of OSAS patients. PH is strongly linked to the presence of an obstructive (rather than restrictive) ventilatory pattern, hypoxemia, and hypercapnia, and is generally accounted for by an associated obstructive airways disease. In this regard, the severity of OSAS plays only a minor role.     

Acoustic analysis of snoring sound in patients with simple snoring and obstructive sleep apnoea

Snoring, a symptom which may indicate the presence of the obstructive sleep apnoea syndrome (OSA), is also common in the general population. Recent studies have suggested that the acoustic characteristics of snoring sound may differ between simple snorers and OSA patients. We have studied a small number of patients with simple snoring and OSA, analysing the acoustic characteristics of the snoring sound. Seventeen male patients, 10 with OSA (apnoea/hypopnoea index (AHI) 26.2 events x h(-1)) and seven simple snorers (AHI 3.8 events x h(-1)), were studied. Full night polysomnography was performed and the snoring sound power spectrum was analysed. Spectral analysis of snoring sound showed the existence of two different patterns. The first pattern was characterized by the presence of a fundamental frequency and several harmonics. The second pattern was characterized by a low frequency peak with the sound energy scattered on a narrower band of frequencies, but without clearly identified harmonics. The seven simple snorers and two of the 10 patients with OSA (AIH 13 and 14 events x h(-1), respectively) showed the first pattern. The rest of the OSA patients showed the second pattern. The peak frequency of snoring was significantly lower in OSA patients, with all but one OSA patient and only one simple snorer showing a peak frequency below 150 Hz. A significant negative correlation was found between AHI and peak and mean frequencies of the snoring power spectrum (p<0.0016 and p<0.0089, respectively). In conclusion, this study demonstrates significant differences in the sound power spectrum of snoring sound between subjects with simple snoring and obstructive sleep apnoea patients.     

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.     

Resolution of obstructive sleep apnoea with growth in the Robin sequence

A 12 year old female with the Robin sequence presented with a one year history of snoring, witnessed apnoeas and daytime sleepiness. Surgery in early childhood had consisted of cleft palate repair, tonsillectomy and adenoidectomy and, later, revision palatoplasty. Overnight polysomnography (PSG) demonstrated severe obstructive sleep apnoea syndrome with an apnoea/hypopnoea index (AHI) of 49 events x h(-1), and repetitive oxygen desaturations below 50%. Nasal continuous positive airway pressure (nCPAP) effectively controlled her sleep abnormalities. After 3 yrs of nCPAP therapy, she requested discontinuation and was fully reassessed. PSG without nCPAP revealed an AHI <5 events x h(-1) with no desaturations below 90% and normal sleep quality. A repeat lateral cephalometrogram showed increased mandibular length and posterior airway space and reduced soft palate length. The patient remains asymptomatic 9 months following nCPAP discontinuation. This case indicates that nasal continuous positive airway pressure is an effective nonsurgical therapy in children with obstructive sleep apnoea syndrome and the Robin sequence. It is likely that mandibular growth, increase in mandibular length and enlargement of the posterior airway space was responsible for the resolution of obstructive sleep apnoea syndrome in this case.     

Simultaneous laboratory-based comparison of ResMed Autoset with polysomnography in the diagnosis of sleep apnoea/hypopnoea syndrome

ResMed Autoset (AS) is a simplified diagnosis system for obstructive sleep apnoea/hypopnoea syndrome (OSAS) based on the respiratory flow/time relationship by pressure variation measured through simple nasal prongs. A multicentre prospective trial was used to compare AS and polysomnography (PSG) for diagnosing 95 patients, with suspected OSAS. Physicians gave a pretest probability of the patient having OSAS. The apnoea/hypopnoea index (AHI) was compared between the two methods of diagnosis for the whole population and for subgroups according to the pretest probability. Twenty-four patients had AHI < 15 events x h(-1) on PSG and 19 AHI 15-30, and 52 patients had AHI > or = 30. Correlation between AHI assessed by AS and PSG was r=0.87 for total sleep time (TST), p<0.0001. A Bland and Altman plot gave an agreement between the two methods of +/-40%. For a threshold of AHI > or = 15 events x h(-1) to diagnose OSAS, AS has a sensitivity of 92%, specificity of 79%, positive predictive value of 93% and negative predictive value of 76%. With a pretest probability > or = 80%, sensitivity and positive predictive value were 98 and 100% respectively. Of six false negative, four had a high pretest probability (> 80%) or Epworth score > or = 10. Using these parameters as a criterion for proceeding to PSG after a negative AS study would mean that two apnoeic patients (AHI 20 and 17 events x h(-1) by PSG) would escape detection. The Autoset is useful for the detection of obstructive sleep apnoea but with high pretest probability and a negative Autoset result polysomnography should be performed.     

Indicator cell lines for detection of primary strains of human and simian immunodeficiency viruses

The pulmonary artery pressure (Ppa) responses to short runs of acute hypoxia at two different levels of end-tidal CO2 were measured in nine normal subjects and in 20 patients with moderate to severe obstructive sleep apnea (OSA). In normal subjects the mean increase in Ppa in response to eucapnic hypoxia was 8 +/- 2 mm Hg (SEM) and was not different from the response to hypercapnic hypoxia (9 +/- 2 mm Hg, p > 0.2). In patients with OSA, the mean increase of Ppa was 8 +/- 1 mm Hg to eucapnic hypoxia, and the response to hypercapnic hypoxia was higher at 10 +/- 1 mm Hg (p = 0.01). Pulmonary pressor response to hypoxia was augmented (> 10 mm Hg) by hypercapnia in four of 20 patients with OSA but in none of the normal subjects. Normoxic hypercapnia alone was a weak stimulus, increasing Ppa by > 5 mm Hg in only two of nine patients with OSA studied. In conclusion, Ppa increases in both normal subjects and patients with OSA exposed to a ramp of acute isocapnic hypoxia. There were clear interindividual differences in pulmonary artery response. Hypercapnia did not produce clinical significant changes in Ppa in either group.     

Anamnestic and polygraphic parameters in obstructive sleep apnea syndrome patients with reduced nasal respiration during the day in comparison with obstructive sleep apnea patients with normal nasal respiration

Nasal obstruction is a predictive factor for snoring and may contribute to the development of an obstructive sleep apnea syndrome (OSAS). The aim of this study was to further evaluate the impact of nasal obstruction in OSAS. Therefore, we investigated 2 groups of OSAS-patients, matched pairs concerning gender, age, and BMI: OSAS-patients with nasal obstruction (N, n = 28), total nasal airflow < 500 ccm/s (referred to 150 pa pressure of difference or unilateral nasal resistance > 1 pa/ccm/s), and 28 OSAS-patients without nasal obstruction (control-group K, total nasal airflow > 700 ccm/s [referred to 150 pa pressure of difference or unilateral nasal resistance > 1 pa/ccm/s]). We performed anterior rhinomanometry, lung-function testing, cardio-respiratory polygraphy, and patients answered a standardized questionnaire. We found the following significant differences: 1) N complained more often (n = 17) about dyspnea at night than K (n = 7, p < 0.05, Chi2-test). 2) N had a higher apnea index (20.4 +/- 19.0/h) than K (9.6 +/- 10.0/h, p < 0.05, Student's t-test). There were, however, no significant differences concerning lung function, number of nocturnal hypopneas, nocturnal SaO2 and heart rate. Our results underline the importance of nasal ventilation in the pathogenesis of OSAS. At least in moderate cases of OSAS a therapy of nasal obstruction might be of success in order to abolish nCPAP-therapy or might reduce nasal problems during nCPAP-therapy and thus ameliorate patient's therapy compliance.     

The obstructive sleep apnoea syndrome--experience of a referral centre

OBJECTIVE: The aims of this study were: (i) to document the presence and severity of obstructive sleep apnoea (OSA) in patients who complained of heavy snoring and other symptoms suggestive of the OSA syndrome; (ii) to examine the correlation between the clinical and polygraphic findings, and (iii) to document the efficacy and compliance of nasal continuous positive airway pressure (CPAP) among these Asian snorers with OSA. METHODS: We analysed our clinical and nocturnal polysomnographic data between January 1986 and December 1995 for physician-referred patients who had complained of snoring and other symptoms suggestive of OSA. RESULTS: A total of 277 diagnostic studies were performed of which 145 (52%) were positive to OSA. For studies performed in the last 2 years (n = 125), 72 of the 125 were positive for OSA. Anthropometric data was not discriminative between the OSA positive snorers and the OSA negative snorers. We found that hypertension and choking were the most significantly related to OSA, conferring a 7 and 4 times relative risk respectively. Nasal CPAP eliminated snoring, apnoeas and oxygen desaturations completely in almost all cases and there were only minor mask-related side effects. CONCLUSION: OSA may not be uncommon among Asian snorers. Of the major traits for OSA risk among our local population, a history of hypertension and reports of nocturnal choking were the most significantly related. We have also shown that nasal CPAP is safe and effective among our local snorers and should be considered a first-line treatment for OSA.     

Forced oscillation technique for the evaluation of severe sleep apnoea/hypopnoea syndrome: a pilot study

The forced oscillation technique (FOT) is a noninvasive method of potential clinical interest for quantitatively assessing airway mechanics during sleep. We investigated the applicability of FOT as a diagnostic tool for noninvasive assessment of airflow obstruction in patients with sleep apnoea/hypopnoea syndrome (SAHS) during sleep. In seven patients previously diagnosed with severe SAHS (mean+/-SD apnoea/ hypopnoea index (AHI) 67+/-14) we performed a full polysomnography (PSG) together with on-line measurement of respiratory impedance (IZI) using FOT. For each patient we determined: 1) number of respiratory events conventionally detected by full PSG, those obtained by FOT and their degree of concordance; and 2) the characteristics and values of IZI during the respiratory events. FOT was well tolerated and easily applied in conjunction with a conventional sleep setup. The mean number of respiratory events x h(-1) detected by PSG and FOT were 55+/-16 and 58+/-17, respectively, with a strong concordance. IZI increased from a baseline of 11+/-4 to 50+/-20 cmH2O x L(-1) x s during apnoea (mean+/-SD). In all but one patient intermittent increases of IZI occurred immediately before each obstructive apnoea. In four patients, the increases of IZI developed at end-expiration whereas in two others occurred during inspiration. During hypopnoea most of the patients showed decreases of IZI during expiration. In conclusion, forced oscillation technique can be used as a noninvasive and complementary tool for the diagnosis of respiratory events and provides an on-line quantitative approach for continuous monitoring of airflow obstruction during sleep in patients with sleep apnoea/hypopnoea syndrome.     

Use of dynamic two-dimensional transesophageal echocardiography for renal cell carcinoma with cavoatrial tumor thrombus

Previous investigations involving continuous blood pressure (BP) monitoring have shown an important alteration of the 24-hour BP profile in patients with obstructive sleep apnea syndrome (OSAS). We investigated the impact of REM sleep on the 24-hour BP cycle in 16 severe OSAS male patients (mean respiratory disturbance index = 66 +/- 16 events/hour of sleep), with hypertension (mean BP 162 +/- 21/105 +/- 11 mmHg World Health Organization (WHO) protocol). Two successive nights of polysomnography were performed, and arterial BP was monitored continuously during the second 24-hour period after brachial artery cannulation. During the daytime, subjects were kept awake and supine. At 3 p.m. BP was continuously monitored during quiet supine wakefulness for 20 minutes. Systolic, diastolic and mean BP and heart rate (HR) were analyzed and tabulated in mean values of 5 minute segments. Sleep/wake information were correlated with cardiovascular variables. Each uninterrupted REM sleep period was identified and comparison between the period of quiet supine wakefulness and REM sleep HR and BP values was performed. 8 OSAS patients presented a normal drop of the mean arterial BP during the nocturnal REM sleep periods compared to quiet supine wakefulness (mean value = -10.8 +/- 7.3 mmHg) ("dippers") while the other 8 subjects ("REM sleep non dippers"), revealed an elevated mean arterial BP during REM sleep (mean value = 18.9 +/- 10.9 mm Hg). The absence of the normal circadian BP dip seen during the nocturnal sleep period is considered as an indication of vascular risk. The REM sleep non dipping may play a role in this risk.     

Respiratory patterns during sleep in Down's syndrome:importance of central apnoeas

Obstructive sleep apnoea episodes have been reported repeatedly in Down's syndrome (DS) patients as a consequence of the presence of predisposing malformations or intercurrent pathology of the upper airways. There are no data on respiratory patterns of uncomplicated Down's syndrome subjects. In order to evaluate the eventual effects of central nervous system (CNS) impairment on respiration in DS, we studied the respiratory patterns during sleep of a group of 10 DS subjects, aged 8.6-32.2 y, without relevant upper airway pathology. In order to control the possible effects of sleep structure and mental retardation on the results obtained, we compared the findings in DS with those obtained from a group formed by subjects affected by fragile X syndrome (six males and one female, aged 10.0-15.42 y) another genetically determined type of mental retardation. Sleep structure was similar in both groups; however, DS subjects showed significantly higher indices of central sleep apnoea and of oxygen desaturation than fragile X patients (P < 0.005). As far as DS individuals were considered, a significant preponderance of central, as opposed to obstructive, sleep apnoeas was found (89.4% vs. 9.4%, respectively; 1.2% were mixed) which showed a significant age-related increase. Central respiratory pauses were mostly preceded by sighs, which occurred more frequently during sleep stages 1 and REM, and were often organized in long sequences of periodic-like breathing. During REM sleep, they were less frequently preceded by sighs and by body movements than during NREM sleep. Obstructive sleep apnoeas occurred more often during REM sleep and were more rarely preceded by sighs or by body movements. Both central and obstructive apnoeas induced significant oxygen desaturation in 50-69.6%. Sleep structure was not significantly modified by apnoeas and oxygen desaturation. We hypothesize that the increase in central sleep apnoeas is related to a dysfunction of the central respiratory control at a brainstem level in DS.     

Nocturnal evolution of respiratory effort in obstructive sleep apnoea syndrome: influence on arousal threshold

It has been recently described that the overnight increase in maximal end-apnoeic oesophageal pressure (P(oes,max)), considered as an index of the arousal threshold to occlusion, mostly contributes to apnoea lengthening during the night. However, the rise in apnoea duration could also be caused by changes in hypoxaemia, chemosensitivity and upper airway resistance. To better define the relative contributions of each of these factors, we examined the recordings of nine patients. Before apnoea, the mean pulmonary resistance at peak inspiratory flow (RPIF) was computed. During apnoea, all swings in oesophageal pressure (P(oes)) were measured to define the P(oes,max), the increase from the minimum to the maximum (deltaP(oes)), the rate of increase in P(oes) (RP(oes)) and the P(oes) at the first occluded breath (P(oes,1)). A gradual and significant increase in apnoea duration (p=0.02), P(oes,max) (p=0.02) and deltaP(oes) (p=0.006) was present across the night without any changes in oxygen saturation, RPIF, and P(oes,1). The slope of increase in P(oes,max), apnoea duration and deltaP(oes) was correlated with the apnoea/hypopnoea index. We conclude that in obstructive sleep apnoea, the nocturnal rise in apnoea duration is attributable more to an increase in the arousal threshold related to apnoea recurrence than to changes in chemosensitivity and upper airway resistance.     

Cerebral hemodynamic changes in sleep apnea syndrome and effect of continuous positive airway pressure treatment

BACKGROUND AND OBJECTIVE: A clear association among snoring, sleep apnea, and increased risk of stroke has been shown by previous studies. However, the possible role played by sleep apnea in the pathogenesis of cerebrovascular disease is subject to debate. To evaluate the influence of hemodynamic changes caused by obstructive sleep apnea syndrome (OSAS), we investigated cerebrovascular reactivity to hypercapnia in patients with OSAS. METHODS: The study was performed at baseline and after 1 night and 1 month of nasal continuous positive airway pressure (n-CPAP) therapy, with patients in the waking state (8:00 to 8:30 AM and 5:30 to 6:00 PM) with transcranial Doppler ultrasonography. Cerebrovascular reactivity was calculated with the breath-holding index (BHI). RESULTS: In the baseline condition, compared with normal subjects, patients with OSAS showed significantly lower BHI values in both the morning (0.57 versus 1.40, p < 0.0001) and the afternoon (1.0 versus 1.51, p < 0.0001). Cerebrovascular reactivity was significantly higher in the afternoon than it was in the morning in both patients (p < 0.0001) and controls (p < 0.05). In patients, the BHI returned to normal values, comparable with those of control subjects, after both 1 night and 1 month of n-CPAP therapy. CONCLUSIONS: These findings suggest an association between OSAS and diminished cerebral vasodilator reserve. This condition may be related to the increased susceptibility to cerebral ischemia in patients with OSAS, particularly evident in the early morning.     

Short-duration nocturnal hypoxemia and persistent pulmonary hypertension

Can daily short-duration hypoxemia (4-8 hours) induce pulmonary hypertension and right ventricular hypertrophy? A clinical model of this type of hypoxemia does exist: isolated nocturnal hypoxemia in patients with obstructive sleep apnea syndrome (OSAS) or chronic obstructive pulmonary disease (COPD). By investigating the pulmonary hemodynamics of these patients, it should be possible to determine whether nocturnal hypoxemia alone can induce pulmonary hypertension. Although nocturnal hypoxemia (in OSAS as well as in COPD) can induce acute episodes of pulmonary hypertension, it would not appear that nocturnal hypoxemia alone would be sufficient to provoke permanent diurnal pulmonary hypertension. This is the conclusion of recent studies concerning diurnal pulmonary hemodynamics in OSAS and COPD patients exhibiting minimal hypoxemia during the day but significant nocturnal desaturation. The therapeutic consequences of these data, particularly in COPD are important: current evidence is insufficient to treat with nocturnal oxygen therapy COPD patients who have minimal diurnal hypoxemia but significant nocturnal desaturation.     

Screening obstructive sleep apnoea syndrome by home videotape recording in children

Overnight polysomnography (PSG) has been used to diagnose and assess the severity of obstructive sleep apnoea syndrome (OSAS) in children. The aim of this study was to determine whether home video-recording of children during sleep may be used for screening OSAS. In 58 children suspected of having OSAS, PSG results were compared with the corresponding analyses of 30 min video-recordings of each child sleeping at home. The video-recordings were evaluated by: 1) overall investigator's clinical judgement; and 2) a scoring system based on noisy breathing, movements, walking episodes, apnoea, chest retractions and mouth breathing. PSG results were highly correlated with the video test results, with agreement in 49 out of 58 (84%). In 36 of the 58 children, the PSG was abnormal compared with 41 out of 58 abnormal video tests. The sensitivity of the overall investigator judgement of video test was 94% (34 out of 36) and the specificity 68% (15 out of 22). Video scores > 10 were highly predictive of OSAS, whilst scores < 5 were associated with normality. Using a stepwise logistic regression analysis, each of the scoring variables was tested against the PSG results and an equation was formulated for predicting PSG by the video test. The equation predicted PSG results in 49 out of 58 (84%) cases. Thirty minutes of home video-recordings during sleep is a reliable screening method for obstructive sleep apnoea syndrome in children. This technique may, thus, improve patient selection for polysomnography.     

Nocturnal pulmonary hypertension in an elderly patient with sleep apnea syndrome

We report a case of sleep apnea syndrome (SAS) with nocturnal pulmonary hypertension (NPH) in a 71-year-old man suffering from dyspnea during sleep. Severe snoring at night and daytime sleepiness were noticed before admission by his wife. Nocturnal oxygen desaturation (NOD) was documented with a pulse oximeter and severe sleep apnea syndrome was diagnosed on the basis of results of respiratory inductive plethysmography, an apnea index (AI) > 20, minimum SpO2 56%. NPH was diagnosed by Swan-Ganz catheter. The levels of NPH were severe. Elevation of systolic pulmonary arterial pressure (PAP) above 40 mmHg was observed 137 episodes at night. Both NPH and NOD were improved by 1 L/min of nasal oxygen therapy. A number of episodes of systolic PAP above 40 mmHg with oxygen therapy was 55 episodes. Peak mean PAP was 36 mmHg in room air vs 33 mmHg in oxygen therapy. Minimum SpO2 with oxygen therapy was improved to 69%. Total time of SpO2 < 90% at night was 153 minutes in room air vs 37 minutes in oxygen therapy. In this case, NPH and NOD due to severe SAS were remarkably improved by oxygen therapy.     

Cephalometric assessment in obstructive sleep apnea

It is reported that some specific craniofacial characteristics are associated with obstructive sleep apnea syndrome (OSAS). To test this finding, the present study developed and assessed the feasibility of a craniofacial index score (CIS) in differentiating patients with OSAS from habitual snorers. Anthropometric measurements and lateral head radiographs were obtained on 24 male and 4 female patients with OSAS who had physician-diagnosed OSAS (respiratory disturbance index (RDI) >20), and 25 male and 5 female habitual snorers (RDI <20). Thirteen cephalometric and four anthropometric measure- ments were used in a discriminant model to construct the CIS. The model was able to correctly classify 82.1% of the OSAS group and 86.7% of the snoring group. In addition, variables that were related to the soft tissues, hyoid bone to mandibular plane, Body Mass Index, and soft palate length had the highest predictive value. These findings indicate that a CIS constructed from cephalometric and anthropometric measurements can be used to identify subjects with and without OSAS.     

Effects of nasal continuous positive airway pressure on breathing pattern and respiratory drive in patients with obstructive sleep apnea syndrome

To examine the influence of continuous positive airway pressure (CPAP) therapy on respiratory center drive in patients with obstructive sleep apnea syndrome (OSAS), 20 normocapnic OSAS patients (group 0) and 20 simple snoring patients were studied. In the first night, diagnostic polysomnography (PSG) was performed. Before and after PSG monitoring, mouth occlusion pressure (P0.1), tidal volume (VT), minute ventilation (VE), respiratory rate (RR), inspiratory time (Ti), expiratory time (Te), total cycle duration (Ttot), inspiratory duty cycle (Ti/Ttot), mean inspiratory flow (VT/Ti) and effective inspiratory impedance (P0.1/VT/Ti, Ieff) were measured while they were breathing room air. In the following night the OSAS patients were treated with nasal CPAP and PSG monitoring and the above mentioned measurements were repeated. The results showed that pre-PSG values of P0.1, RR and P0.1/VT/Ti in the OSAS patients were significantly higher than those in the snoring patients, while VT, Ti, Te and Ttot values were lower. In the first night, the post-PSG P0.1 value in the OSAS patients increased markedly as compared with the pre-PSG. After overnight nasal CPAP therapy, the respiratory disorder index in the OSAS patients decreased markedly, the nadir SaO2 increased markedly, but the post-PSG P0.1 value did not increase significantly. It is concluded that, before sleep, OSAS patients exhibit a higher respiratory drive and a shallow and frequent breathing pattern as compared with simple snoring patients. After nocturnal sleep, the respiratory drive of OSAS patients increases significantly, the breathing pattern becomes more shallow and frequent. Nasal CPAP may effectively relieve the sleep apnea and hypopnea as well as the resulting hypoxemia and therefore correct the changes in breathing pattern and respiratory drive through nocturnal sleep in patients with OSAS.