Arterial oxygenation during sleep in patients with right-to-left cardiac or intrapulmonary shunts.

We have studied arterial oxygen saturation (SaO2), breathing patterns, and electroencephalographic (EEG) sleep stage during nocturnal sleep in six patients with right-to-left cardiac or intrapulmonary shunts and six patients with chronic bronchitis and emphysema, chosen because they were equally hypoxaemic when awake (SaO2 during wakefulness: bronchitis 74-90%, mean 83%; shunt 77-89%, mean 83%). The patients with bronchitis had far greater falls in SaO2 when asleep than those with shunts (maximum fall in SaO2 during sleep: bronchitis 14-47%, mean 29%; shunt 5-10%, mean 8%; p less than 0.01). Significant episodes of hypoxaemia (defined as SaO2 falls greater than 10%) occurred in all six bronchitic patients, from once to seven times per night, but in none of the patients with shunts (p less than 0.05). Twenty-four of the 27 episodes of hypoxaemia occurred in rapid-eye-movement (REM) sleep and 24 were associated with hypopnoea. The two groups of patients had similar EEG sleep patterns and the same amount of hypopnoea during sleep. Thus the level of arterial oxygenation when the patient is awake is not the sole determinant of the degree of nocturnal hypoxaemia; the pathological process is also important.     

Respiration during sleep in normal man.

Respiratory volumes and timing have been measured in 19 healthy adults during wakefulness and sleep. Minute ventilation was significantly less (p less than 0.05) in all stages of sleep than when the subject was awake (7.66 +/- 0.34(SEM) 1/min), the level in rapid-eye-movement (REM) sleep (6.46 +/- 0.29 1/min) being significantly lower than in non-REM sleep (7.18 +/- 0.39 1/min). The breathing pattern during all stages of sleep was significantly more rapid and shallow than during wakefulness, tidal volume in REM sleep being reduced to 73% of the level during wakefulness. Mean inspiratory flow rate (VT/Ti), an index of inspiratory drive, was significantly lower in REM sleep than during wakefulness or non-REM sleep. Thus ventilation falls during sleep, the greatest reduction occurring during REM sleep, when there is a parallel reduction in inspiratory drive. Similar changes in ventilation may contribute to the REM-associated hypoxaemia observed in normal subjects and in patients with chronic obstructive pulmonary disease.     

Effects of protriptyline on sleep related disturbances of breathing in restrictive chest wall disease.

The effects of protriptyline on sleep stage distribution and gas exchange have been assessed in eight patients with nocturnal hypoventilation secondary to restrictive chest wall disease. At a dose of 10-20 mg taken when they retired the total sleeping time was unaltered but the proportion of rapid eye movement (REM) sleep fell from 22% to 12% (p less than 0.05). The total time spent at an arterial oxygen saturation of less than 80% decreased (p less than 0.01) and the magnitude of the fall correlated with the reduction in REM sleep (r = 0.67, p less than 0.05). There was also a reduction in the maximum carbon dioxide tension reached during the night (p less than 0.01). The arterial oxygen tension measured diurnally increased (p less than 0.05) from a median of 8.0 kPa (60 mm Hg) to 9.0 kPa (67.5 mm Hg), but the carbon dioxide tension and base excess were unchanged. Anticholinergic side effects were experienced by most patients but did not limit treatment.     

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.     

Effect of sleep deprivation on overnight bronchoconstriction in nocturnal asthma.

Nocturnal cough and wheeze are common in asthma. The cause of nocturnal asthma is unknown and there is conflicting evidence on whether sleep is a factor. Twelve adult asthmatic subjects with nocturnal wheeze were studied on two occasions: on one night subjects were allowed to sleep and on the other they were kept awake all night, wakefulness being confirmed by electroencephalogram. Every patient developed bronchoconstriction overnight both on the asleep night, when peak expiratory flow (PEF) fell from a mean (SE) of 418 (40) 1 min-1 at 10 pm to 270 (46) 1 min-1 in the morning, and on the awake night (PEF 10 pm 465 (43), morning 371 (43) 1 min-1). The morning values of PEF were, however, higher (p less than 0.1) after the awake night and both the absolute and the percentage overnight falls in PEF were greater when the patients slept (asleep night 38% (6%), awake night 20% (4%); p less than 0.01). This study suggests that sleep is an important factor in determining overnight bronchoconstriction in patients with nocturnal asthma.     

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.     

Control of nocturnal hypoventilation by nasal intermittent positive pressure ventilation.

Ten patients with respiratory failure and nocturnal hypoventilation were treated for three to nine months by nasal intermittent positive pressure ventilation. Four patients had chronic obstructive lung disease (median FEV1 19% predicted) and six restrictive chest wall disorders (median FVC 25% predicted); eight of the patients also had cardiac failure. The median daytime arterial oxygen tension, measured before and after at least three months' treatment, increased from 6.2 (range 5.4-9.6) to 9.1 (7.1-9.8) kPa in those with restrictive disease (p less than 0.05), and from 6.0 (5.7-6.5) to 7.1 (6.3-7.7) kPa in the four with airflow limitation (NS). Median values for arterial carbon dioxide tension over the same time fell from 8.2 (range 6.7-9.8) to 6.5 (6.0-6.9) kPa in the group with restrictive disease (p less than 0.05) and from 8.2 (7.0-9.2) to 7.1 (4.9-7.7) kPa in those with airflow limitation (p less than 0.02). Total sleep time while patients were using nasal positive pressure ventilation varied from 155 to 379 (median 341) minutes, and included 4-26% rapid eye movement sleep (median 14%). The percentage of monitored time during the night in which the arterial oxygen saturation was less than 80% fell from a median (range) of 96 (3-100) to 4 (0-9) in the six patients with restrictive disease and from 100 (98-100) to 40 (2-51) in those with airflow limitation. There were no changes in spirometric values but exercise tolerance improved in all patients. The technique may prove an acceptable alternative to long term domiciliary oxygen therapy in selected patients.     

Sleep after laparoscopic cholecystectomy

The sleep pattern and oxygenation of 10 patients undergoing laparoscopic cholecystectomy were studied on the night before operation and the first night after operation. Operations were performed during general anaesthesia and postoperative analgesia was achieved without the administration of opioids. There were no significant changes in the total time awake or the number of arousals on the postoperative night compared with the night before operation. During the postoperative night, we found a decrease (P = 0.02) in slow wave sleep (SWS) with a corresponding increase in stage 2 sleep (P = 0.01). SWS was absent in four of the patients after operation, whereas in six patients it was within the normal range (5-20% of the night). The proportion of rapid eye movement (REM) sleep was not significantly changed after operation. There were no changes in arterial oxygen saturation on the postoperative compared with the preoperative night. Comparison of our results with previous studies on SWS and REM sleep disturbances after open laparotomy, suggests that the magnitude of surgery or administration of opioids, or both, may be important factors in the development of postoperative sleep disturbances.      

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.     

Effect of Non-Carbonic Acidosis on Total Splanchnic Perfusion and Cardiac Output During Anaesthesia with O2-N2O-Barbiturate-Relaxant

Seven dogs were anaesthetized using mebumal natrium-O2-N2O-gallamonijdidum. The PaCO2 was kept at a constant level by means of mechanical ventilation, and non-carbonic acidosis was induced with HCl infusion (0.3 normal). The arterial pH varied from 7.45 to 6.88. During this acidosis, a rising arterio-venous oxygen difference was observed, with an unchanged total oxygen consumption. The pulse fell, but the mean pressures in the right atrium and aorta were unchanged. The peripheral resistance rose by 50%, whereas the fall in cardiac output of 20% was non-significant (0.10 greater than P greater than 0.05). The total splanchnic perfusion fell by 28%, and the change in flow was correlated to the change in pH. Total splanchnic perfusion (ml min-1) = -4078+655x pH (N = 42, r = 0.67, P less than 0.001). Total splanchnic perfusion as a fraction of the cardiac output remained unchanged. The resistance in the splanchnic area rose by 50%. The oxygen saturation in the portal vein and mixed venous blood changed in parallel. It is concluded that contraction of the blood vessels is the most important effect on the circulation resulting from non-carbonic acidosis during the anaesthesia employed here.     

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.     

Branched-chain amino acid in chronic renal failure patients: respiratory and sleep effects.

Sleep disorders, including a high incidence of sleep apnea, have been recognized as a significant problem in chronic renal failure (CRF) patients. In a preliminary study, we examined CRF patients on maintenance hemodialysis for three nights; one control night, and thereafter randomized to infusion of saline (placebo) for one night and 4% branch-chain amino acid (BCAA) solution for one night. Polysomnographic and respiratory data [respiratory rate, oxygen saturation and end-tidal CO2 (ETCO2)] was recorded continuously throughout the nights and data from each hour compared with baseline (awake) values. The patients studied were characterized by reduced sleep quality and decreased amount of rapid eye movement (REM) sleep. The BCAA infusion was associated with a return of REM sleep to normal and a significant decrease in ETCO2 during both REM and non-REM sleep (P less than 0.05). Our findings demonstrate respiratory stimulation during sleep with infusion of BCAA; this stimulatory effect on respiration (in contrast to many respiratory stimulants) is associated with an increased amount of REM sleep.     

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.     

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.     

Sleep hypoxia in myotonic dystrophy and its correlation with awake respiratory function.

BACKGROUND--Tiredness and daytime respiratory failure occur frequently in myotonic dystrophy. Sleep hypoxaemia was studied in 12 patients with myotonic dystrophy and correlations were sought with their daytime lung and respiratory muscle function. METHODS--All patients underwent overnight sleep studies, clinical assessment, measurement of flow-volume loops and carbon monoxide transfer factor, arterial blood gas analysis, and physiological assessment of both thoracic muscle function and upper airways obstruction. RESULTS--The mean nadir of oxygen saturation during sleep was 75% (95% confidence interval 69% to 81%). A mean of 3.4% of total sleep duration was spent at an oxygen saturation level below 85%. Five of the 12 patients had an apnoea index of > 5, the group mean apnoea/hypopnoea index being 15.8 events/sleep hour. The mean awake arterial oxygen tension (PaO2) was 10.7 kPa. There was a trend to hypercapnoea with a mean awake arterial carbon dioxide tension of 6.1 kPa; carbon dioxide retention worsened during sleep. Respiratory muscle dysfunction was mainly evident as a low maximum expiratory mouth pressure. Upper airway obstruction assessed by physiological criteria was found in four of the 12 patients. The proportion of total sleep duration with oxygen saturation levels below 85% was directly related to body mass index (weight/height2) and inversely related to the awake PaO2. Body mass index was inversely related to the overnight nadir of oxygen saturation. CONCLUSIONS--Patients with myotonic dystrophy are often hypoxic during sleep and the subgroup that are obese, or have symptoms of sleep apnoea, or both, are particularly at risk. Sleep studies should be considered in this subgroup of patients with myotonic dystrophy.     

Minimum oxygen requirements during anaesthesia with the Triservice anaesthetic apparatus A study of drawover anaesthesia in the young adult

Thirty-six servicemen were anaesthetised using the Triservice anaesthetic apparatus. They were allocated randomly into one of two groups, to breathe spontaneously or to receive artificial ventilation, and into subgroups who were given air alone, or air supplemented with 1 or 4 litres/minute of oxygen. A further 12 subjects were studied subsequently using 0.5 litres/minute of added oxygen. Intra-operative blood gases were compared with those of awake premedicated controls. Artificial ventilation was associated with an unchanged arterial oxygen tension with air alone; in the other subgroups arterial oxygen tension was higher than with spontaneous respiration when related to inspired oxygen fraction (p less than 0.05). Air anaesthesia caused significant hypoxaemia with spontaneous ventilation (p less than 0.05), and 50% of the subjects required assisted ventilation. There was also a significant respiratory acidosis (p less than 0.05). Intermittent positive pressure ventilation is the method of choice for field anaesthesia when oxygen is unavailable. Spontaneous respiration must be supplemented with at least 0.5 litres minute of oxygen.     

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.     

Oxygen desaturation during sleep and exercise in patients with interstitial lung disease.

The relations between mean and maximum fall in arterial oxygen saturation (SaO2) during sleep, hypoxaemia during moderate and maximum exercise, and lung mechanics were studied in 16 patients with interstitial lung disease. Mean and minimum SaO2 during sleep were significantly related to each other and to daytime oxygenation but not to lung mechanics. Although the maximum fall in SaO2 during sleep was similar to the fall during maximum exercise (a level seldom achieved during normal daily activities), profound hypoxaemic episodes during sleep were rare and brief and therefore contributed little to the mean SaO2. The fall in mean SaO2 during sleep was not significant and was considerably less than during moderate exercise (average 0.5 v an estimated 4.5%, p less than 0.05). It is therefore concluded that in patients with interstitial lung disease oxygen desaturation during sleep is mild and less severe than hypoxaemia during exercise.     

Prediction of oxygenation during sleep in patients with chronic obstructive lung disease.

The accuracy of a prediction equation for assessing the lowest arterial oxygen saturation (SaO2) during sleep was determined in 24 consecutive patients with chronic obstructive lung disease referred for assessment for home oxygen therapy. Subjects had a mean (SD) FEV1 of 0.81 (0.31) litre and an FEV1/FVC of 37% (12%). There was reasonable agreement between predicted and measured values (mean difference [predicted-measured] = -2.5%) but the prediction was not precise as the 95% confidence interval for the difference was +8% to -13%. The duration of arterial oxygen desaturation, defined as the percentage of total sleep time spent below a given SaO2, was not predicted accurately. It is concluded that nocturnal arterial oxygen desaturation in individual patients with chronic obstructive lung disease cannot be predicted from "awake" measurements with sufficient accuracy to be clinically useful.     

Ketotifen and nocturnal asthma.

Patients with asthma often wheeze at night and they also become hypoxic during sleep. To determine whether ketotifen, a drug with sedative properties, is safe for use at night in patients with asthma, we performed a double blind crossover study comparing the effects of a single 1 mg dose of ketotifen and of placebo on arterial oxygen saturation (SaO2), breathing patterns, electroencephalographic (EEG) sleep stage, and overnight change in FEV1 in 10 patients with stable asthma. After taking ketotifen, the patients slept longer and their sleep was less disturbed than after taking placebo, true sleep occupying 387 (SEM 8) minutes after ketotifen and 336 (19) minutes after placebo (p less than 0.02). On ketotifen nights the patients had less wakefulness and drowsiness (EEG sleep stages 0 and 1) and more non-rapid eye movement (non-REM) sleep than on placebo nights, but the duration of REM sleep was similar on the two occasions. Nocturnal changes in SaO2, the duration of irregular breathing, and overnight change in FEV1 were unaffected by ketotifen.