Sleepiness and Hypertension in Obstructive Sleep Apnea

doi:10.1378/chest.101.4.903

Chest

Volume 101, Issue 4, April 1992, Pages 903-909

https://doi.org/10.1378/chest.101.4.903 Get rights and content

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.

Section snippets

MATERIALS AND METHODS

Subjects in this study were comprised of the following three groups: 192 patients with OSA; 15 with central sleep apnea (CSA); and 58 with “primary snoring” (PS) but no evidence of sleep apnea. The population as a whole was comprised of 219 men and 46 women, with a mean age of 47 ± 1 yr (±SE). The polygraphic aspect of the diagnosis of sleep apnea syndrome was the presence of more than five disordered breathing events (DBEs) (apneas or hypopneas or both) per hour of sleep. Apneas were defined

General Characteristics

The three groups differed in several features of demographics, sleep, and medical history (Table 1). The mean ages of the three groups ran from 44 to 51 yr and did not differ significantly. Frequent snoring was found in 94 percent of the OSA group, 93 percent of the CSA group, and 82 percent of the PS group (p<0.01). Approximately half of all patients complained of disturbed sleep for two to three nights per week for approximately 3 yr. The presenting chief complaints of the apneic patients are

DISCUSSION

Although sleepiness is a well-recognized aspect of OSA, the specific causes have remained unclear. An intuitive explanation, which is supported by recent interest in the effects of nocturnal sleep disturbance on subjective and objective sleepiness,17, 18, 19 is that the sleepiness results from the frequent brief arousals associated with apneas. Roehrs et al¹⁵ reported that in 466 apneic patients, some measures of arousals associated with DBEs produced a higher correlation with MSLT scores than

REFERENCES (25)

JM Parish et al.
Cardiovascular effects of sleep disorders
Chest
(1990)
JW Shepard et al.
Myocardial stress: exercise versus sleep in patients with COPD
Chest
(1984)
WC Orr et al.
Hypersomnolent and nonhypersomnolent patients with upper airway obstruction during sleep
Chest
(1979)
T Roehrs et al.
Predictors of objective level of daytime sleepiness in patients with sleep-related breathing disorders
Chest
(1989)
C Guilleminault et al.
Snoring: 1. daytime sleepiness in regular heavy snorers
Chest
(1991)
RP Millman et al.
Daytime hypertension in obstructive sleep apnea: prevalence and contributing risk factors
Chest
(1991)
FG Issa et al.
Reversal of central sleep apnea using nasal CPAP Chest
(1986)
P. Lavie
Incidence of sleep apnea in a presumably healthy working population: a significant relationship with excessive daytime sleepiness
Sleep
(1983)
F Cirignotta et al.
Prevalence of every night snoring and obstructive sleep apnoeas among 30-69-year-old men in Bologna, Italy
Acta Neurol Scand
(1989)
JR Stradling et al.
Prevalence of sleep apnea in 1001 men aged years 35-65

RM Coleman et al.

Sleep-wake disorders based on a polysomnographic diagnosis

JAMA

(1982)

WB. Mendelson

The Stony Brook 600: the experience of a sleep disorder center

Ann Clin Psychiatr

(1990)

Cited by (44)

Pro - Sleep fragmentation causes hypersomnolence in sleep apnea: The convergence of rationalism and empiricism
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Intermittent hypoxemia and sleep fragmentation: Associations with daytime alertness in obese sleep apnea patients living at moderate altitude
2016, Sleep Medicine
Citation Excerpt :
Some studies have found an association between measures of intermittent hypoxemia and sleepiness measured with the Multiple Sleep Latency Test (MSLT) [6–9], whereas a fewer number have measured alertness with the Maintenance of Wakefulness Test (MWT) [10–12], a procedure that is often considered to have more face validity than the MSLT. Some of these studies report that measures of nocturnal hypoxemia account for the most variance in daytime measures [6,7], whereas others indicated that measures of sleep fragmentation were more strongly associated with such variables [9,13]. Regardless of whether MSLT or MWT has been used, studies attempting to account for the daytime sleepiness or alertness of the OSA patient have successfully predicted only small amounts of variance with measures derived from polysomnography, typically of the order of 10–15% or less [10–12].
Although obstructive sleep apnea (OSA) has long been associated with daytime sleepiness, far less is known about its association with the ability to remain awake. The aim of this study was to examine the relative importance of inter-correlated measures of OSA severity (eg, various indices of oxygen saturation and sleep fragmentation) in the ability to stay alert as measured objectively by the Maintenance of Wakefulness Test (MWT), defined by a mean sleep latency of ≥12 min.
Seventy-eight obese women and men of similar age and body mass index living at altitude (Mexico City) underwent standard polysomnography, MWT, and completed validated sleep-related questionnaires.
Men had more severe sleep apnea than women (p = 0.002) and were also less alert on MWT (p = 0.022). Logistic regression models indicated that measures of desaturation consistently predicted MWT-defined alertness, whereas varied measures of sleep fragmentation did not. Nearly a third of the variance (r² = 0.304) in MWT-defined alertness was accounted for by the number of desaturations per hour of sleep (p = 0.003), which is considerably higher than other studies have reported in different populations.
The ability to remain awake in obese patients is best accounted for by hypoxemia rather than sleep fragmentation. Whether the size of this effect reflects differences in the population under study (eg, extent of obesity, racial background, residence at moderate altitude) and/or is a function of the measurement of alertness with the MWT remains uncertain.
Comorbidity between sleep apnea and insomnia
2009, Sleep Medicine Reviews
Citation Excerpt :
It is obvious that not all of the factors responsible for excessive somnolence in OSA have been identified. However, there has been speculation about the contribution of intermittent hypoxemia,32,33 the AHI34 and sleep fragmentation.35 Likewise, other factors, such as obesity, diabetes, depression, and subjective estimations of nocturnal sleep loss,36 have also been suggested.
The association between insomnia and sleep apnea has received little attention from health professionals in the past few decades. However, recent studies have shown a high prevalence of insomnia complaints in patients with objectively diagnosed obstructive sleep apnea (OSA) syndrome. In this paper we have reviewed data published on different aspects of this association: the clinical profile of sleep-disordered breathing (SDB)-plus, the nature of the association, the role in the onset of insomnia played by OSA itself and other comorbidity factors such as depression or the restless leg syndrome. Finally, we have reviewed data and hypotheses on the metabolic implications of OSA and insomnia, and we speculate on the role that hypothalamic–pituitary–adrenal axis hyperactivity may play in a hypothetical interrelation between OSA and insomnia. The apparent paradox implied by this clinical association reveals the need for interdisciplinary training for physicians who treat both types of disorders.
Chapter 10 Quantitative analysis of the sleep electroencephalogram
2005, Handbook of Clinical Neurophysiology
This chapter discusses the quantitative analysis of the sleep electroencephalogram (EEG). The standard clinical EEG represents a visual description of brain electrical activity obtained through arrays of electrodes placed across the scalp. Providing excellent temporal resolution for assessing such activity on the order of time frames of neuronal events (e.g., milliseconds), the EEG can rapidly detect acute changes in brain function (such as those which occur at sleep onset and during rapid eye movement (REM) sleep) as well as examine the temporal sequencing of brain processes during brain activation. Recorded electrical activity results from the extracellular flow of current associated with summated excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Although much of the amplitude of brain electrical activity derives from cortical neurons underlying the scalp electrodes, subcortical sites modulate the synchrony of the recorded activity. Specifically, pacemakers in the thalamocortical neuronal circuitry produce rhythmic synchronous activity, which is reduced by arousal and increased with reduced vigilance.
The association of hypertension and secondary cardiovascular disease with sleep-disordered breathing
2003, Chest
Citation Excerpt :
At 75 years of age, the stage is often nonexistent. Tables 1, 2,2A,2B,2C, 2D,345678910111213141516171819202122232425262728293031323334353637383940414243444546474849505152535455565758596061 and 3,3A62636465666768697071727374757677787980 contain the results of all those studies found that met the inclusion criteria described in the “Materials and Methods” section. Overall, the findings are mixed with regards to a definitive direct cause-and-effect relationship between SDB and hypertension, most often due to significant design flaws.
We present a review of the English-language literature from 1972 through 2000 pertaining to systemic high BP in patients with sleep-disordered breathing (SDB). We reviewed studies assessing the relationship between obstructive sleep apnea, central sleep apnea or periodic breathing, and systemic high BP, and present an approach to the management of these patients. Complications of obesity and the role of the sympathetic nervous system are reviewed as well. It is the aim of these reviews to draw qualified conclusions, based on the current literature, with regard to SDB as a causative or contributory factor in systemic hypertension.
Does obstructive sleep apnea confound sleep architecture findings in subjects with depressive symptoms?
2000, Biological Psychiatry
Citation Excerpt :
For example, in a study of 25 male patients with sleep apnea, 40% met criteria for an affective disorder or alcohol abuse (Reynolds et al 1984). Sleep architecture differences in OSA patients contrasted with normal subjects (i.e., compared to Doghramji et al [1997] normative values) have included shorter sleep latency (Fry et al 1989; Hanzel et al 1991; Kass et al 1996; Series et al 1992; Smith et al 1985), increased REML (Mendelson 1992, 1995; Series et al 1992; Stewart et al 1992), decreased REM% (Colt et al 1991; Chervin and Aldrich 1998; Espinoza et al 1987; Hanzel et al 1991; Mendelson 1992, 1995; Oksenberg et al 1997; Roehrs et al 1989; Series et al 1992; Smith et al 1985; Stewart et al 1992), and decreased SWS% (Weitzman et al 1980; White 1992). With the exception of SWS%, these findings are opposite to those observed in depressed patients.
Background: Compared with normal subjects, depressed patients have shorter rapid eye movement sleep latency (REML), increased REM and decreased slow wave sleep as a percentage of total sleep time (REM%, SWS%), and longer sleep latency (SL). Obstructive sleep apnea (OSA) patients experience longer REML, decreased REM% and SWS%, and shorter SL. We examined the interplay of depressive symptoms, OSA, and sleep architecture.
Methods: Subjects (n = 106) were studied with polysomnography. OSA was defined as a Respiratory Disturbance Index ≥15. Subjects were divided into Hi/Lo groups using a Center for Epidemiological Studies—Depression (CES-D) score of 16.
Results: OSA patients had shorter SL than non-OSA patients (14.5 vs. 26.8 min, p < .001); Hi CES-D subjects showed a trend toward longer SL than Lo CES-D subjects (23.7 vs. 17.5 min, p = .079). Significant OSA × CES-D interactions emerged, however, for REM% (p = .040) and SL (p = .002): OSA/Hi CES-D subjects had higher REM% than OSA/Lo CES-D subjects (19.3% vs. 14.3%, p = .021); non–OSA/Hi CES-D subjects had SL (35.3 min) 2–3 times as long as other subjects (p = .002–.012).
Conclusions: Because of the high prevalence of OSA and depression, findings suggest that OSA must be considered in studies of mood and sleep architecture. Conversely, depressive symptoms must be considered in studies of OSA and sleep architecture.

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: Manuscript received March 15; revision accepted August 6.

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Chest

Clinical InvestigationsSleepiness and Hypertension in Obstructive Sleep Apnea

Section snippets

MATERIALS AND METHODS

General Characteristics

DISCUSSION

Chest

Chest

Chest

Chest

Chest

Chest

Reversal of central sleep apnea using nasal CPAP Chest

Incidence of sleep apnea in a presumably healthy working population: a significant relationship with excessive daytime sleepiness

Sleep

Prevalence of every night snoring and obstructive sleep apnoeas among 30-69-year-old men in Bologna, Italy

Acta Neurol Scand

Prevalence of sleep apnea in 1001 men aged years 35-65

Sleep-wake disorders based on a polysomnographic diagnosis

JAMA

The Stony Brook 600: the experience of a sleep disorder center

Ann Clin Psychiatr

Clinical Investigations
Sleepiness and Hypertension in Obstructive Sleep Apnea