SLEEP

Reynolds, Charles, F.;Kupfer, David, J.

doi: 10.1093/sleep/10.3.199pmid: 3306874

Article PDF first page preview Close This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Perez-Padilla,, Rogelio;Conway,, William;Roth,, Tom;Anthonisen,, Nicholas;George,, Charles;Kryger,, Meir

doi: 10.1093/sleep/10.3.216pmid: 3629083

Summary: There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the “pink puffer” (PP) and “blue bloater” (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BE. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 >44 mm Hg) and without (PaCO2 ≤44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaCO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2 low sleep SaO2, and awake-low sleep SaO2, P < 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PP2 was similar in both groups, whereas PaCO2 was different (p < 0.00. Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 de saturation in hypoxemic COPD. Chronic obstructive pulmonary disease, Sleep, Hypercapnia, Hypoxia, Oxygen saturation This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Easton, Paul, A.;West,, Peter;Meatherall, Robert, C.;Brewster, John, F.;Lertzman,, Morley;Kryger, Meir, H.

doi: 10.1093/sleep/10.3.224pmid: 3629084

Summary: The effect of a moderately intoxicating dose of ethanol on sleep was evaluated in five patients with severe emphysematous chronic obstructive pulmonary disease (COPD) (mean FEV, 0.83 L, PaO2 75 mm Hg). Mean serum ethanol before sleep was 129 mg/dl. With alcohol, total sleep time per night decreased from a mean of 293 to 238 min. Relative sleep time per stage also changed; NREM time increased, and REM time decreased >50%. Alcohol caused significant O2 desaturation; group mean sleep arterial oxygen saturation (SaO2) decreased from 90.6 to 87.7% with alcohol. Although the decrease in SaO2 was not uniform across all sleep stages, no individual sleep stage accounted for the desaturation. The fall in Sao2 with alcohol was not explained by increasing apneas or hypopneas. Mean heart rate increased significantly from 71.8 to 77.1 with alcohol, with premature ventricular contractions increasing in two subjects. Excessive alcohol ingestion in severe COPD alters total sleep time and stage distribution, decreases SaO2 without significant change in apneas, and increases heart rate. Prior to sleep, patients with severe COPD should strictly limit ingestion of alcohol. Sleep, Ethanol, Intoxication, Chronic obstructive pulmonary disease This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

George, C., F.;West,, P.;Kryger, M., H.

doi: 10.1093/sleep/10.3.234pmid: 3629085

Summary: Oxygen desaturation in chronic obstructive pulmonary disease (COPD) occurs during sleep and is most marked in REM sleep. REM is not a homogeneous state, consisting of phasic REM (PREM) (REMs, myoclonic twitches) and tonic REM (TREM) (muscle atonia, desynchronized electroencephalogram). In normals, onset of PREM produces transient changes in breathing pattern with a decrease in respiratory amplitude and an increase in frequency, which produce reductions in oxygen saturation (SaO2) Because it is reasonable to expect such breathing pattern changes to cause more desaturation in COPD, and because systematic all-night studies of PREM and TREM have not been reported, we studied 18 patients with severe COPD [Forced expiratory volume in one second (FEV1) = 25.7 ± 3.5 (SEM) % predicted] during sleep and monitored SaO2 and breathing pattern in PREM and TREM. PREM made up 19.7% of total REM (4.6% total sleep time) but was associated with 81.7% of the total REM desaturations of >5% (57.9% of all sleep desaturations of >5%). With PREM onset, breathing pattern changed 72.5% of the time, most often with a transient decrease in amplitude and increase in frequency. Even though 27.5% of PREM was not associated with changes in breathing pattern and many PREM segments were very short, we were still able to show highly significant SaO2 differences between PREM and TREM. Mean TREM Sao2 was 88.0 ± 1.2%; mean PREM SaO2 was 86.6 ± 1.4%, with mean nadir SaO2 for individual PREM segments falling to 84.8 ± 1.5%. Mean awake SaO2 was 89.7 ± 0.8%. We conclude that in COPD the transition from TREM to PREM is associated with breathing pattern changes and oxygen desaturation. Differences in breathing pattern with PREM onset may be related to different effects of PREM processes on respiratory neurons and diaphragm motor neurons. Chronic obstructive pulmonary disease, Phasic REM, Tonic REM This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Cartwright, Rosalind, D.;Knight,, Sara

doi: 10.1093/sleep/10.3.244pmid: 3629086

Summary: The wives of 10 male patients being treated for sleep apnea, obstructive type, were interviewed and given the Social Adjustment Scale (SAS) and Marital Satisfaction Inventory (MSI). The patients also completed an SAS and a Minnesota Multiphasic Personality Inventory (MMPI). These data were compared with those from a sample of divorced patients from the same pool. The married patients were significantly more depressed and socially isolated than were those divorced. Both marital partners showed poor adjustment in the Marital and Social/Leisure areas, and patients also showed poor adjustment in their Parental Role. Marriages do not necessarily represent social support but appear to be an added burden for sleep apneic patients. Apnea, Marital relationship This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Perez-Padilla, J., Rogelio;West,, Peter;Kryger,, Meir

doi: 10.1093/sleep/10.3.249pmid: 3629087

Summary: Six men and three women, asymptomatic light snorers ranging in age from 25–34 years, were studied during sleep to determine the prevalence of snoring in the different sleep stages, the associated changes in oxygen saturation (SaO2), heart rate (HR), and breathing frequency (f), and the associated breathing arrhythmias. Snoring was defined as a 1-minute epoch with more than 80% of the breaths associated with snores. Most of the snuring epochs as well as the apneas and hypopneas occurred during stage 2, mainly because it is the most prolonged sleep stage. The prevalence of snoring, however, normalized for differences in length of sleep stages, was highest in stages 3 and 4 but low in REM, whereas the converse was true for apneas and hypopneas. Snoring caused no change in the mean SaO2, mean HR, or f, as compared with nonsnoring periods in the same sleep stage. Continuous snoring in normal subjects can occur without significant O2 de saturation or breathing arrhythmia. Continuous snoring and breathing arrhythmia tended to occur together in a given subject but were unrelated in time, suggesting a different pathogenesis. Sleep, Respiratory sounds, Snoring This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Greenberg, Glen, D.;Watson, Robert, K.;Deptula,, Dennis

doi: 10.1093/sleep/10.3.254pmid: 3629088

Summary: To evaluate the effect of intermittent hypoxemia on neuropsychological functioning, neuropsychological tests were administered to 14 sleep apnea patients, a control group of 10 patients with other disorders of excessive somnolence, and another control group of 14 healthy volunteers. The sleep disorder groups were matched on two measures of sleepiness. It was found that sleep apnea patients performed significantly worse than both controls on 7 of 14 neuropsychological measures and on a rating of global neuropsychological impairment. The overall level of performance reflected only moderate impairment. Within the sleep apnea group, hypoxemia severity was significantly correlated with deficits on measures of motor and perceptual-organizational ability. Neuropsychological testing, Sleep apnea, Hypoxemia This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

West,, Peter;George, Charles, F.;Kryger, Meir, H.

doi: 10.1093/sleep/10.3.263pmid: 3629089

Summary: Pulse oximeters (Biox III, Nellcor N-100) and a transmittance oximeter [Hewlett-Packard 47201A (HP)] were compared for SaO2 measurement and responsiveness during dynamic changes in arterial oxygen saturation and heart rate. Five sleep apnea syndrome patients were studied because they had large oscillations in SaO2 and heart rate in sleep. During sleep, each patient exhibited a series of rapid (18.0 ± 8.3 s, mean ± SD) oscillations in oxygen saturation (92.1 ± 2.6% to 74.2 ± 7.7%). Oxygen saturation measurements were sampled simultaneously from each oximeter by computer (at 2 Hz). Accuracy was assessed by comparing pulse and transmittance oxygen saturation measurements at the peak and trough of each apnea-related oscillation. Oximeter response was defined in terms of the “delay” or absolute time difference between the pulse oximeters and the transmittance oximeter for the determination of the peak and trough saturations. Linear regression analysis was used to establish accuracy and response relationships between pulse oximeter sensors (reusable ear, reusable digit, disposable digit, and disposable nasal sensors) and the transmittance oximeter sensor (reusable ear sensor). Pulse oximeter response delay was highly correlated with heart rate. Pulse oximeter SaO2 measurement and response characteristics varied considerably with sensor type (disposable, reusable) and sensor location (ear, nose, and digit). One must be aware of these differences in clinical and research application. Pulse and transmittance oximetry, Measurement techniques: Arterial oxygen saturation, Sleep apnea syndrome This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Baruch, Heidi, L.;Kelwala,, Surendra;Kapen,, Sheldon

doi: 10.1093/sleep/10.3.272pmid: 3629090

Summary: Nine narcoleptic and nine control subjects underwent 4 nights of sleep recordings. On nights 3 and 4, they received continuous intravenous infusions of saline. Additionally, on both nights they received 0.2 mg glycopyrrolate at the end of the first REM period (REMl) and 0.5 mg arecoline or placebo in random order 20 min after the end of REM 1. Heart rates were counted for a 40-min period following the end of REMl. There was a significant and similar cardioacceleratory effect after arecoline in both narcoleptic and normal subjects, beginning at 5 min from the start of the infusion and peaking at 9 min. Placebo had no effect. Narcoleptic subjects had consistently higher baseline heart rates than controls on infusion and noninfusion nights, most likely owing to age differences between the two groups. The results suggest that narcoleptic persons do not have increased cholinergic sensitivity, or that the canine model of narcolepsy differs from the human model, or that the muscarinic receptors that play a role in the pathophysiology of narcolepsy differ in sensitivity from those that regulate heart rate. Arecoline, Heart rate, Narcolepsy, Muscarinic receptors, Sleep This content is only available as a PDF. © 1987, Association of Professional Sleep Societies

Fukuda,, Kazuhiko;Miyasita,, Akio;Inugami,, Maki;Ishihara,, Kaneyoshi

doi: 10.1093/sleep/10.3.279pmid: 3629091

Summary: In Japan, a set of experiences called kanashibari is considered identical with isolated sleep paralysis. We investigated this phenomenon by means of a questionnaire administered to 635 college students (390 men and 245 women). Of all subjects, about 40% had experienced at least one episode of kanashibari [subjects of K(+)]. Therefore, isolated sleep paralysis is apparently a more common phenomenon than is usually appreciated. About half of the subjects of K(+) reported that they had been under “physical or psychological stress” or in a “disturbed sleep and wakefulness cycle” immediately before the episode. Many subjects of K(+) experienced the first episode in adolescence. In the distribution of age of first attack, the peak occurred at an earlier age in women subjects than in men subjects. These findings suggest that two factors influence the occurrence of the phenomenon. One is exogenous physical or psychological load and the other is endogenous biological development. Kanashibari attack, Isolated sleep paralysis, Normal human This content is only available as a PDF. © 1987, Association of Professional Sleep Societies