Respiratory failure and sleep in neuromuscular disease.

Sleep hypoxaemia in non-rapid eye movement (non-REM) and rapid eye movement (REM) sleep was examined in 20 patients with various neuromuscular disorders with reference to the relation between oxygen desaturation during sleep and daytime lung and respiratory muscle function. All the patients had all night sleep studies performed and maximum inspiratory and expiratory mouth pressures (PI and Pemax), lung volumes, single breath transfer coefficient for carbon monoxide (KCO), and daytime arterial oxygen (PaO2) and carbon dioxide tensions (PaCO2) determined. Vital capacity in the erect and supine posture was measured in 14 patients. Mean (SD) PI max at RV was low at 33 (19) cm H2O (32% predicted). Mean PE max at TLC was also low at 53 (24) cm H2O (28% predicted). Mean daytime PaO2 was 67 (16) mm Hg and PaCO2 52 (13) mm Hg (8.9 (2.1) and 6.9 (1.7) kPa). The mean lowest arterial oxygen saturation (SaO2) was 83% (12%) during non-REM and 60% (23%) during REM sleep. Detailed electromyographic evidence in one patient with poliomyelitis showed that SaO2% during non-REM sleep was maintained by accessory respiratory muscle activity. There was a direct relation between the lowest SaO2 value during REM sleep and vital capacity, daytime PaO2, PaCO2, and percentage fall in vital capacity from the erect to the supine position (an index of diaphragm weakness). The simple measurement of vital capacity in the erect and supine positions and arterial blood gas tensions when the patient is awake provide a useful initial guide to the degree of respiratory failure occurring during sleep in patients with neuromuscular disorders. A sleep study is required to assess the extent of sleep induced respiratory failure accurately.     

Oxygen treatment of sleep hypoxaemia in Duchenne muscular dystrophy.

Patients with Duchenne muscular dystrophy develop progressive ventilatory muscle weakness and often die of respiratory complications. Recurrent, often profound, hypoxaemia has been shown in a previous study by this group to occur during rapid eye movement (REM) sleep in these patients before they develop sleep symptoms. In this study the efficacy and physiological effects of nocturnal oxygen in such patients have been assessed. Seven patients with Duchenne muscular dystrophy (age range 16-22 years; mean vital capacity 1.37 litres) with normal arterial blood gas tensions when awake were investigated by standard overnight polysomnography on an acclimatization night followed by two successive nights on which they received room air and nasal oxygen (2 litres/min) respectively in random order. Total sleep time, proportion of REM and non-REM sleep, and frequency and duration of arousals were similar on the two nights. When breathing air six of the seven subjects developed oxygen desaturation of more than 5% during REM sleep. With oxygen only one subject showed any oxygen desaturation exceeding 2.5%. Oxygen desaturation was associated with periods of hypopnoea or cessation of respiratory effort. The mean duration of episodes of hypopnoea and apnoea was prolonged during oxygen breathing by 19% and the mean duration of episodes during REM sleep by 33% (the proportion of REM sleep associated with hypopnoea and apnoea increased in all subjects). Heart rate in non-REM sleep fell by 9.3%; heart rate variation in REM and non-REM sleep was unchanged. These acute studies show that oxygen reduces the sleep hypoxaemia associated with respiratory muscle weakness; whether long term treatment will be possible or desirable is not clear as oxygen potentiates the underlying ventilatory disturbance.     

Effects of acetazolamide in patients with the sleep apnoea syndrome.

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.     

Pulmonary arterial hypertension in patients with sleep apnoea syndrome

BACKGROUND: Pulmonary arterial hypertension (PAH) in patients with sleep apnoea syndrome (SAS) is classically ascribed to associated chronic obstructive pulmonary disease (COPD). The aim of this retrospective study was to evaluate the possible occurrence of PAH as a complication of SAS in patients without COPD. METHODS: Right heart catheterisation was performed in 44 patients with SAS and without COPD confirmed by polysomnography (apnoea index >5/h) admitted for the administration of nasal continuous positive airway pressure (CPAP). RESULTS: Precapillary PAH, defined as mean pulmonary arterial pressure of >20 mm Hg with pulmonary capillary wedge pressure <15 mm Hg, was observed in 12/44 (27%) patients with SAS. There were no significant differences in apnoea index between patients with (PAH+) and those without PAH (PAH-) (42.6 (26.3) versus 35.8 (21.7) apnoeas/h). The PAH+ group differed significantly from the PAH- group in the following respects: lower daytime arterial oxygen tension (PaO(2)) (9.6 (1.1) versus 11.3 (1.5) kPa, p=0.0006); higher daytime arterial carbon dioxide tension (PaCO(2)) (5.8 (0.5) versus 5.3 (0.5) kPa, p=0.002); more severe nocturnal hypoxaemia with a higher percentage of total sleep time spent at SaO(2) <80% (32.2 (28.5)% versus 10.7 (18.8)%, p=0.005); and higher body mass index (BMI) (37.4 (6) versus 30.3 (6.7) kg/m(2), p=0.002). The PAH+ patients had significantly lower values of vital capacity (VC) (87 (14)% predicted versus 105 (20)% predicted, p=0.005), forced expiratory volume in one second (FEV(1)) (82 (14)% predicted versus 101 (17)% predicted, p=0.001), expiratory reserve volume (40 (16)% predicted versus 77 (41)% predicted, p=0.003), and total lung capacity (87 (13)% predicted versus 98 (18)% predicted, p=0.04). Stepwise multiple regression analysis showed that mean pulmonary artery pressure (PAPm) was positively correlated with BMI and negatively with PaO(2). CONCLUSION: Pulmonary arterial hypertension is frequently observed in patients with SAS, even when COPD is absent, and appears to be related to the severity of obesity and its respiratory mechanical consequences.     

Ventilation and gas exchange during sleep in patients with interstitial lung disease.

Ventilation and gas exchange during overnight sleep was studied in a group of seven patients with severe interstitial lung disease (mean vital capacity 50%, mean diffusing capacity 46% predicted), to see whether clinically significant oxygen desaturation occurred. Patients with a history of loud snoring or clinically significant airflow obstruction were excluded. Sleep was fragmented in these patients, but all achieved rapid eye movement (REM) sleep. All patients showed episodes of oxygen desaturation during sleep--mean (SEM) awake arterial oxygen saturation (SaO2) was 92.9% (0.3%) compared with a mean minimum SaO2 during sleep of 83.2% (2.1%) (p less than 0.01). These episodes were, however, transient, and mean SaO2 showed only a slight fall between wakefulness and sleep (non-REM 91.5%, REM 90.4%; NS). Furthermore, SaO2 during non-REM sleep correlated well (p less than 0.001) with SaO2 during wakefulness. Respiratory frequency showed a significant fall between wakefulness and sleep--21.1 (1.8) versus 17.3 (1.5) breaths per minute (p less than 0.02). Our data suggest that nocturnal oxygen treatment need not be considered in patients with interstitial lung disease unless the level of oxygenation while they are awake indicates the need for such treatment.     

Nocturnal hypoxaemia and quality of sleep in patients with chronic obstructive lung disease.

Fifty patients with chronic obstructive lung disease were questioned about their sleep quality and their responses were compared with those of 40 similarly aged patients without symptomatic lung disease. Patients with chronic obstructive lung disease reported more difficulty in getting to sleep and staying asleep and more daytime sleepiness than the control group. More than twice as many patients (28%) as controls (10%) reported regular use of hypnotics. In a subgroup of 16 patients with chronic obstructive lung disease (mean FEV1 0.88 (SD 0.44) sleep, breathing, and oxygenation were measured to examine the relationship between night time hypoxaemia and sleep quality. Sleep architecture was disturbed in most patients, arousals occurring from three to 46 times an hour (mean 15 (SD 14)/h). Arterial hypoxaemia during sleep was common and frequently severe. The mean (SD) arterial oxygen saturation (SaO2) at the onset of sleep was 91% (7%). Nine patients spent at least 40% of cumulative sleeping time at an SaO2 of less than 90% and six of these patients spent 90% of sleeping time below this level. Only four of 15 patients did not develop arterial desaturation during sleep. The mean minimum SaO2 during episodes of desaturation was less in rapid eye movement (REM) sleep (72% (17%)) than in non-REM sleep (78% (10%), p less than 0.05). The predominant breathing abnormality associated with desaturation was hypoventilation; only one patient had obstructive sleep apnoea. Arousals were related to oxygenation during sleep such that the poorer a patient's arterial oxygenation throughout the night the more disturbed his sleep (arousals/h v SaO2 at or below which 40% of the total sleep time was spent: r = 0.71, p less than 0.01). Hypoxaemia during sleep was related to waking values of SaO2 and PaCO2 but not to other daytime measures of lung function.     

Nocturnal saturation and respiratory muscle function in patients with chronic obstructive pulmonary disease.

BACKGROUND--Nocturnal desaturations, mainly caused by hypoventilation, occur frequently in patients with chronic obstructive pulmonary disease (COPD). Daytime arterial oxygen and carbon dioxide tensions (PaO2 and PaCO2) appear to predict which patients will desaturate at night. It is unknown if respiratory muscle strength, which may be decreased in these patients, plays an additional part. METHODS--Polysomnography, maximal respiratory pressures, lung function, and arterial blood gas tensions were measured in 34 patients with COPD (mean (SD) forced expiratory volume in one second (FEV1) 41.7 (19.9)% pred). RESULTS--Significant correlations were found between the mean nocturnal arterial oxygen saturation and maximal inspiratory mouth pressure (r = 0.65), maximal inspiratory transdiaphragmatic pressure (r = 0.53), FEV1 (r = 0.61), transfer coefficient (KCO) (r = 0.38), arterial oxygen saturation (SaO2) (r = 0.75), and PaCO2 (r = -0.44). Multiple regression analysis showed that 75% of the variance in nocturnal SaO2 (70%) and FEV1 (5%). CONCLUSION--Inspiratory muscle strength and nocturnal saturation data are correlated, but daytime SaO2 and FEV1 remain the most important predictors of nocturnal saturation.     

Changes in day and night time oxygenation with protriptyline in patients with chronic obstructive lung disease.

The effect of protriptyline, a tricyclic antidepressant, on sleep architecture, nocturnal arterial oxygen desaturation, pulmonary function, and diurnal arterial blood gases was investigated in an open study of 14 patients with stable chronic obstructive lung disease. Daytime and overnight measurements were made before and 2 and 10 weeks after they started protriptyline (20 mg daily at bedtime). Two patients had to be excluded before the second visit and one before the third visit because of changes in treatment for their chest disease. Protriptyline caused mouth dryness in all patients and dysuria in six men. With protriptyline there were no significant changes in total sleep time, sleep period time, or the percentages of total sleep time occupied by stage I-II and stage III-IV sleep. The mean (SEM) percentage of total sleep time spent in rapid eye movement (REM) sleep decreased from 11.1 (1.7) to 4.6 (0.7) at two weeks and to 4.2 (1.0) at 10 weeks. After protriptyline the time spent during sleep with an arterial oxygen saturation (SaO2) below each 5% increment above 65% was less than the baseline time; the lowest SaO2 (%) reached during sleep increased from 64.5 (1.7) to 72.7 (2.1) at 2 weeks and to 77.4 (2.1) at 10 weeks. Lung volumes and expiratory flows were unchanged during the study. Daytime arterial oxygen tension (PaO2) increased from 57 (1.4) mm Hg before treatment to 62 (1.9) mm Hg at 2 weeks and to 66 (1.9) mm Hg at 10 weeks (7.6 (0.2), 8.3 (0.3), 8.8 (0.3) kPa). Carbon dioxide tension fell from 52 (2.3) mm Hg to 49 (1.4) mm Hg at 2 weeks and to 48 (2.0) mm Hg at 10 weeks (6.9 (0.3), 6.5 (0.2), 6.4 (0.3) kPa), but these changes were not significant. These results suggest that protriptyline may benefit patients with chronic obstructive lung disease by reducing the sleep induced falls in SaO2 and improving diurnal PaO2; a controlled trial is now required.     

Self reported snoring and daytime sleepiness in men aged 35-65 years.

BACKGROUND: It has been suggested that snoring alone, without conventional sleep apnoea or hypopnoea, may disrupt sleep and produce substantial daytime hypersomnolence. This study addresses this potential relationship. METHOD: Eight hundred and fifty men, aged 35-65 years, drawn from one general practice were visited at home and asked a range of questions potentially related to sleepiness, snoring, and sleep apnoea; these included inquiries about alcohol and cigarette consumption, nasal stuffiness, shift work, hypnotic or other drug use, and medical diagnoses. In addition, measurements of height, weight, and overnight arterial oxygen saturation were made. The relation between snoring and sleepiness, with allowance made for potentially confounding variables, including sleep apnoea, was assessed by multiple logistic regression. RESULTS: Positive answers to all questions about sleepiness were correlated significantly with self reported snoring. After potentially confounding variables and any sleep apnoea had been controlled for, positive answers to four questions about inappropriate drowsiness or sleepiness were independently related to snoring. For example, the odds ratio of admitting to "having almost had two or more car accidents while driving due to sleepiness" was 5.8 (95% confidence intervals: 2.7-12.5) in an "often" snorer. CONCLUSIONS: Although epidemiological associations such as this do not prove a causal relation, the study suggests that snoring (without classical sleep apnoea) may sometimes reduce sleep quality sufficiently to produce substantial daytime drowsiness.     

Supplemental oxygen and quality of sleep in patients with chronic obstructive lung disease.

The hypothesis that supplemental oxygen could improve the quality of sleep was tested in 23 consecutive patients (14 male, nine female; age 42-74 years) with chronic obstructive lung disease (mean (SD) FEV1 0.81 (0.32) litre, FEV1/FVC 37% (12%). Patients breathed compressed air or supplemental oxygen via nasal cannulas on consecutive nights in a randomised, double blind, crossover trial. Quality of sleep was assessed by questionnaire and by electroencephalographic sleep staging. The study had a power of 80% to detect, at the 0.05 level, a 20% improvement in total sleep time. Seventeen patients slept for two nights in the laboratory. Oxygenation during sleep was improved by oxygen administration, but there was no improvement in quality of sleep. There was an acclimatisation effect with better sleep on the second night. Six patients spent an additional acclimatisation night in the laboratory as well as the two study nights. There was no difference in sleep quality between the second and third nights or between the compressed air and the oxygen nights in these patients. Subgroups of patients with an arterial carbon dioxide tension of over 43 mm Hg (5.7 kPa) (n = 12) and arterial oxygen saturation of less than 90% (n = 11) while awake did not show any improvement in quality of sleep on the oxygen night. It is concluded that supplemental oxygen improves nocturnal oxygenation but does not immediately improve the quality of sleep in the laboratory in patients with chronic obstructive lung disease.     

Role of hypoxia on increased blood pressure in patients with obstructive sleep apnoea.

BACKGROUND--Cyclical changes in systemic blood pressure occur during apnoeic episodes in patients with obstructive sleep apnoea (OSA). Although several factors including arterial hypoxaemia, intrathoracic pressure changes, and disruption of sleep architecture have been reported to be responsible for these changes in blood pressure, the relative importance of each factor remains unclear. This study assessed the role of hypoxaemia on the increase in blood pressure during apnoeic episodes. METHODS--The blood pressure in apnoeic episodes during sleep and the blood pressure response to isocapnic intermittent hypoxia whilst awake were measured in 10 men with OSA. While asleep the blood pressure was measured non-invasively using a Finapres blood pressure monitor with polysomnography. The response of the blood pressure to hypoxia whilst awake was also measured while the subjects intermittently breathed a hypoxic (5% or 7% oxygen) gas mixture. Each hypoxic gas exposure was continued until a nadir arterial oxygen saturation (nSaO2) of less than 75% was reached, or for a period of 100 seconds. The exposure was repeated five times in succession with five interposed breaths of room air in each run. RESULTS--The mean (SD) increase in blood pressure (delta MBP) during apnoeic episodes was 42.1 (17.3) mm Hg during rapid eye movement (REM) sleep and 31.9 (12.5) mm Hg during non-REM sleep. The delta MBP during apnoeic episodes showed a correlation with the decrease of nSaO2 (delta SaO2) (r2 = 0.30). The change in blood pressure in response to intermittent hypoxia whilst awake was cyclical and qualitatively similar to that during apnoeic episodes. Averaged delta MBP at an SaO2 of 7% and 5% oxygen was 12.6 (5.7) and 13.4 (3.6) mm Hg, respectively, whereas the averaged delta MBP at the same delta SaO2 during apnoeic episodes was 38.4 (15.5) and 45.2 (20.5) mm Hg, respectively. CONCLUSIONS--The blood pressure response to desaturation whilst awake was about one third of that during apnoeic episodes. These results suggest that factors other than hypoxia may play an important part in raising the blood pressure during obstructive sleep apnoea.     

Sleep apnoea in Scheie''s syndrome

An 18-year-old student presented with a two-year history of daytime sleepiness and noisy breathing during sleep. Both he and his brother, aged 25 years, had Scheie's syndrome, a mucopolysaccharidosis characterised by small stature, micrognathia, corneal clouding, hepatosplenomegaly, raised urinary mucopolysaccharides, and undetectable levels of alpha-L-iduronidase assayed in cultured fibroblasts. Both brothers had sleep apnoea (apnoea index, 59 and 35 respectively) during which there was a significant fall in heart rate and arterial oxygen saturation. One brother had EEG changes suggestive of cerebral hypoxia and the other had ventricular extrasystoles at the end of several episodes. Tracheostomy in the younger brother produced a dramatic symptomatic improvement and reduced the number and severity of apnoeic episodes (post-tracheostomy apnoea index 2.4).     

Value of nocturnal oxygen saturation as a screening test for sleep apnoea

The sensitivity and specificity of overnight recording of arterial oxygen saturation (SaO2) in routine clinical practice was evaluated in 41 subjects who were being investigated for possible sleep apnoea-hypopnoea syndrome. SaO2 was measured with an ear probe oximeter (Biox IIa) and chart recorder during an "acclimatisation" night immediately before a detailed polysomnographic study. The recordings were classified by two observers as positive, negative, or uninterpretable. Twelve of the 41 patients had the obstructive sleep apnoea syndrome when defined in terms of an apnoea-hypopnoea index greater than 15 events an hour on the second night. The sensitivity of nocturnal SaO2 on the acclimatisation night when the diagnostic criterion was an apnoea-hypopnoea index of greater than 5, greater than 15, and greater than 25/h was 60%, 75%, and 100% respectively. Corresponding values for specificity were 95%, 86%, and 80%. Oximetry alone therefore allowed recognition of a moderate or severe sleep apnoea syndrome. In routine practice an appreciable number of equivocal results is likely and repeat oximetry or more detailed polysomnography will then be required if clinical suspicion is high.     

Randomised controlled trial of non-invasive ventilation (NIV) for nocturnal hypoventilation in neuromuscular and chest wall disease patients with daytime normocapnia

BACKGROUND: Long term non-invasive ventilation (NIV) reduces morbidity and mortality in patients with neuromuscular and chest wall disease with hypercapnic ventilatory failure, but preventive use has not produced benefit in normocapnic patients with Duchenne muscular dystrophy. Individuals with nocturnal hypercapnia but daytime normocapnia were randomised to a control group or nocturnal NIV to examine whether nocturnal hypoventilation is a valid indication for NIV. METHODS: Forty eight patients with congenital neuromuscular or chest wall disease aged 7-51 years and vital capacity<50% predicted underwent overnight respiratory monitoring. Twenty six with daytime normocapnia and nocturnal hypercapnia were randomised to either nocturnal NIV or to a control group without ventilatory support. NIV was started in the control group if patients fulfilled preset safety criteria. RESULTS: Peak nocturnal transcutaneous carbon dioxide tension (Tcco2) did not differ between the groups, but the mean (SD) percentage of the night during which Tcco2 was >6.5 kPa decreased in the NIV group (-57.7 (26.1)%) but not in controls (-11.75 (46.1)%; p=0.049, 95% CI -91.5 to -0.35). Mean (SD) arterial oxygen saturation increased in the NIV group (+2.97 (2.57)%) but not in controls (-1.12 (2.02)%; p=0.024, 95% CI 0.69 to 7.5). Nine of the 10 controls failed non-intervention by fulfilling criteria to initiate NIV after a mean (SD) of 8.3 (7.3) months. CONCLUSION: Patients with neuromuscular disease with nocturnal hypoventilation are likely to deteriorate with the development of daytime hypercapnia and/or progressive symptoms within 2 years and may benefit from the introduction of nocturnal NIV before daytime hypercapnia ensues.     

The predictors of central and obstructive sleep apnoea in haemodialysis patients.

BACKGROUND: Sleep apnoea (SA) is often observed in haemodialysis patients, but there have been few studies on types of SA and their predictors. We therefore investigated the prevalence and types of SA and the associations between types of SA and clinical factors in haemodialysis patients. METHODS: We initially examined nocturnal oxygen desaturation index (ODI) (desaturation of >4%/events per hour) in 119 haemodialysis patients (68 males, mean age of 61.4 years). Patients with ODI of more than five were diagnosed as having SA. Then, 30 patients underwent polysomnography and we measured Apnoea-hypopnoea index (AHI), which was calculated as the number of apnoeas plus hypopnoeas per hour of sleep. Clinical characteristics were examined in all patients. RESULTS: Forty-one (34.5%) of the 119 patients had SA. Twenty-seven (22.7%) of the 119 patients had SA with subjective symptoms such as daytime somnolence and snoring. There was a significant difference between body mass index (BMI) in patients with SA and that in patients without SA (22.5 vs 19.8 kg/m2, P<0.001). There were significantly higher prevalences of hypertension (85.4 vs 66.7%, P<0.05) and diabetes mellitus (36.6 vs 10.3%, P<0.01) in patients with SA than those in patients without SA. Multivariable analysis showed that BMI was independently associated with the occurrence of SA (OR 1.20, 95% CI 1.05-1.38). Mean AHI of 30 patients who underwent polysomnography was 53.2+/-28.9 [central apnoea, 4.1+/-5.6 (8%); obstructive apnoea, 21.7+/-21.5 (42%); mixed apnoea, 4.9+/-8.0 (9%); hypopnoea, 21.4+/-15.5 (41%)]. The number of obstructive apnoea events per hour was significantly correlated with BUN (r=0.490, P<0.01), Cr (r=0.418, P<0.05) and BMI (r=0.489, P<0.01) and was inversely correlated with serum bicarbonate (r=-0.646, P<0.01) and brain natriuretic peptide (BNP) (r=-0.481, P<0.01). The number of central apnoea events per hour was correlated inversely with PaO2 (r=-0.393, P<0.05) and PaCO2 (r=-0.388, P<0.05) and tended to be correlated with cardiothoracic ratio (CTR) (r=0.347, P=0.060). CONCLUSIONS: There is a high prevalence of SA in haemodialysis patients. The dominant type of SA in haemodialysis patients is obstructive sleep apnoea (OSA). Uraemia (BUN, Cr), metabolic acidosis (serum bicarbonate) and BMI are good predictors of OSA. PaO2, PaCO2 and CTR are good predictors of central sleep apnoea (CSA). Good management of these factors might improve SA in haemodialysis patients.     

Changes in ventilation and its components in normal subjects during sleep.

Non-invasive measurements were made of ventilation, its derivatives, the contributions of abdomen and rib cage and arterial oxygen saturation in six healthy normal men whilst awake and during sleep. Minute ventilation fell significantly during slow wave (SW) sleep and rapid eye movement (REM) sleep (awake = 6.3 1 min-1, SW sleep = 5.7 1 min-1, REM sleep = 5.4 1 min-1; p less than 0.04). Mean inspiratory flow also fell significantly but timing was unchanged. The abdominal (diaphragmatic) contribution to ventilation fell very significantly during SW sleep but returned to awake levels during REM sleep (awake 54%, SW sleep 38%, REM sleep 56%; p less than 0.007). There were also significant falls in arterial oxygen saturation during SW and REM sleep (awake 97.3%, SW sleep 96.5%, REM sleep 96.2%; p less than 0.002). These falls represent reductions in arterial oxygen tension similar to those seen in patients with chronic airways obstruction and can be accounted for entirely by the associated reduction in ventilation.     

Sleep apnoea in patients with quadriplegia.

BACKGROUND--This study was undertaken to establish the prevalence of, and the factors contributing towards, sleep disordered breathing in patients with quadriplegia. METHODS--Forty representative quadriplegic patients (time since injury > 6 months, injury level C8 and above, Frankel category A, B, or C; mean (SE) age 35.0 (1.7) years) had home sleep studies in which EEG, EOG, submental EMG, body movement, nasal airflow, respiratory effort, and pulse oximetry (SpO2) were measured. Patients reporting post traumatic amnesia of > 24 hours, drug or alcohol abuse or other major medical illness were excluded from the study. A questionnaire on medications and sleep was administered and supine blood pressure, awake SpO2, spirometric values, height, and neck circumference were measured. RESULTS--A pattern of sustained hypoventilation was not observed in any of the patients. Sleep apnoeas and hypopnoeas were, however, common. Eleven patients (27.5%) had a respiratory disturbance index (RDI, apnoeas plus hypopnoeas per hour of sleep) of > or = 15, with nadir SpO2 ranging from 49% to 95%. Twelve of the 40 (30%) had an apnoea index (AI) of > or = 5 and, of these, nine (75%) had predominantly obstructive apnoeas-that is, > 80% of apnoeas were obstructive or mixed. This represents a prevalence of sleep disordered breathing more than twice that observed in normal populations. For the study population RDI correlated with systolic and diastolic blood pressure and neck circumference. RDI was higher in patients who slept supine compared with those in other postures. Daytime sleepiness was a common complaint in the study population and sleep architecture was considerably disturbed with decreased REM sleep and increased stage 1 non-REM sleep. CONCLUSIONS--Sleep disordered breathing is common in quadriplegic patients and sleep disturbance is significant. The predominant type of apnoea is obstructive. As with non-quadriplegic patients with sleep apnoea, sleep disordered breathing in quadriplegics is associated with increased neck circumference and the supine sleep posture.     

Comparison of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep in patients with chronic obstructive lung disease.

The effects of almitrine bismesylate and medroxyprogesterone acetate on oxygenation during wakefulness and sleep were compared in six patients with chronic obstructive lung disease and carbon dioxide retention. Patients received 1.5 mg/kg almitrine (a peripheral chemoreceptor stimulant), 100 mg of medroxyprogesterone (a central respiratory stimulant), or matched placebo daily for 15 days in random order in a crossover trial. When subjects were awake almitrine increased the ventilatory response to hypoxia and increased arterial oxygen tension (PaO2) to a greater extent than medroxyprogesterone, whereas medroxyprogesterone augmented the ventilatory response to hypercapnia and decreased arterial carbon dioxide tension (PaCO2) to a greater extent than almitrine. Neither drug influenced sleep architecture significantly, except that medroxyprogesterone increased the number of arousals. Almitrine had a more favourable effect than placebo on oxygenation as estimated from arterial oxygen saturation (SaO2) during the different stages of sleep, the number of episodes of hypoxaemia, and the amount of time that SaO2 was below 80%. The only change with medroxyprogesterone by comparison with placebo was a decrease in the number of hypoxaemic episodes. It is concluded that both active drugs improved blood gases during wakefulness, but that 1.5 mg/kg of almitrine is superior to 100 mg of medroxyprogesterone in improving SaO2 during sleep.     

Habitual snoring with and without obstructive sleep apnoea: the importance of cephalometric variables.

BACKGROUND: The obstructive sleep apnoea syndrome is characterised by an increased apnoea-hypopnoea index and a reduction in the minimal arterial oxygen saturation (SaO2) values during sleep. The extent to which these variables can be predicted by cephalometric and otorhinolaryngological variables was tested. METHODS: One hundred consecutive habitual snorers (84% male), with a mean (SD) age of 50.1 (10.1) years, were studied. The 45 patients with less severe sleep apnoea, with an apnoea-hypopnoea index of 10 or less (group A), were compared with the 55 with an index above 10 (group B). RESULTS: Body mass index, some cephalometric variables, and some otorhinolaryngological variables differed significantly between group A and group B, in particular the soft tissue measures PNS-P (posterior nasal spine to palate), MP-H (mandibular plane to hyoid bone), degree of oropharynx stenosis, and tongue size. In a multiple regression correlation analysis MP-H, SNB (angle from sella to nasion to subspinale point), SNA (angle from sella to nasion to supramentale point), PAS (posterior airway space), tongue size, and body mass index contributed significantly to the equation explaining the severity of sleep apnoea. Nevertheless, these variables together explained only 33% of the variance of the apnoea-hypopnoea index in the total sample; they were more important for patients with moderate to severe stages of the disease. CONCLUSION: The lack of association between cephalometric variables and mild sleep apnoea suggests that the differences in these variables (soft tissue measures) may be the consequence rather than the cause of habitual snoring and the obstructive sleep apnoea syndrome.