Close Server: KOPWWW05 | Not logged in

From Our Print Archives

Much More Than a Nuisance

Health Consequences of Sleep Disorders

Vol. 17 • Issue 9 • Page 57

Between 50 million and 70 million U.S. residents experience sleep-related problems.1These difficulties affect all age groups.2,3The Sleep in America Poll determined in 2008 that 44% of adults had experienced a sleep problem every night or almost every night of the prior month.4lthough sleep disorders are common, less than 50% of adults say their healthcare providers ask them about their sleep.4,5

More than 90 sleep disorders have been identified. This article discuss­es evidence for medical consequences associated with obstructive sleep apnea (OSA) and sleep deprivation.

Obstructive Sleep Apnea

OSA is the most prevalent disorder of breathing in sleep. OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) collapse of the upper airway despite continued effort to breathe. These episodes cause a sequence of changes starting with hypercapnia and hypoxemia, which stimulate an increased effort to breathe against a closed airway. This results in sympathetic activation and terminates in a brief arousal from sleep. Activation of the sympathetic nervous system causes an increased heart rate, constriction of peripheral blood vessels (leading to increased blood pressure), increased mental activity, increased respiratory rate and effort, and increased release of glucose into the bloodstream. Over time, these repeated surges strain the cardiovascular system. Repeated arousals and sleep fragmentation cause excessive sleepiness and fatigue during the day.3

Common signs and symptoms of OSA in adults include excessive sleepiness, unrefreshing sleep, fatigue, snoring, gasping or choking, pauses in breathing, frequent brief awakenings and nocturia. In children, signs and symptoms are different: hyperactivity, irritability, aggressive behavior, excessive sleepiness, snoring, arousals, unusual sleep positions and nocturnal enuresis.6

OSA in Children

Obstructive sleep apnea occurs in up to 3% of children.2Altered neurobehavioral function and learning has been reported in children with OSA. A meta-analysis of 61 studies of the relationship between sleep-disordered breathing (SDB) and neurobehavioral functioning found strong evidence of deficits in behavior and emotion regulation, scholastic performance, sustained attention, selection attention and alertness.7Findings were associated with impulsivity, hyperactivity and aggressive behavior, which are common in attention deficit-hyperactivity disorder (ADHD). Similarity in signs and symptoms should prompt the inclusion of OSA in the differential diagnosis list for possible ADHD.

End-organ injury in children with untreated OSA is believed to be due to episodic hypoxemia, hypercapnia and sleep fragmentation. Delay in treatment may result in irreversible morbidity. Untreated OSA in childhood may be an antecedent to adult disease, especially in those that are genetically predisposed.8

Adenotonsillectomy is often the treatment of choice for children with OSA, but it may not be as efficacious as previously thought. The frequency of mild OSA after adenotonsillectomy has been estimated at 45% to 50%; an additional 20% to 25% of patients have moderate to severe disease.8Continuous positive airway pressure (CPAP) is reserved for children with craniofacial abnormalities, obesity or residual OSA after adenotonsillectomy. As evidence about the effectiveness of adenotonsillectomy evolves, treatment practices may change.

OSA and Hypertension

The proposed mechanisms for OSA influencing the development of hypertension include hypoxia (known to stimulate endothelial growth), hypercapnia and increased sympathetic tone. One study found that SDB was independently associated with hypertension in a dose response relationship.9In another study, patients with SDB were more likely to have hypertension.10The odds started to increase with an apnea hypopnea index (AHI) of 15 per hour. Patients with an AHI of more than 30 per hour were 1.5 times more likely to develop hypertension. A prospective study determined that OSA acutely increased nocturnal blood pressure and sustained daytime hypertension with a threefold increased risk of new onset hypertension in patients with an AHI of 15 or more per hour.11

Multiple observational studies have identified improvement in daytime blood pressure control with effective CPAP use. One study documented a 2.5 mm Hg reduction in blood pressure after 4 weeks of therapeutic CPAP therapy and larger reductions in patients with severe OSA.12In a separate study, researchers followed patients for more than 60 days and found dramatic reductions in mean blood pressure (9.9 mm Hg ± 11.4 mm Hg) in a small cohort with severe OSA.13

These findings strengthen the belief that OSA is likely a causal factor in hypertension. The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7) recommends sleep apnea screening for all patients who are newly diagnosed with refractory hypertension.14

OSA and Heart Failure

Hypoxemia from OSA may play a critical role in decreased myocardial contractility through neurohormonal mechanisms. Cross-sectional data support a significant association between SDB and heart failure.15Another study found that CPAP produced an average 35% relative increase in left ventricular ejection fraction.16In addition to OSA, patients with heart failure often have central sleep apnea.

OSA and Cardiac Dysrhythmias

Several studies have identified an association between OSA and nocturnal dysrhythmias. The most common include premature ventricular contractions, nonsustained ventricular tachycardia, sinus arrest, second-degree atrioventricular conduction block and bradycardia.17The Sleep Heart Health Study documented a twofold to fourfold increased risk of nocturnal dysrhythmias such as atrial fibrillation, nonsustained ventricular tachycardia and ectopic ventricular beats in patients with severe OSA (30 or more AHI per hour).18Atrial fibrillation is often triggered between 8 p.m. and 8 a.m.3Another study found that within 12 months of successful cardioversion, patients with untreated OSA had a recurrence rate double that of patients treated with CPAP.19

OSA and Myocardial Ischemia

The hearts of patients with OSA are constantly challenged by the repetitive insults of hypoxemia, surges in blood pressure and heart rate, increased negative intrathoracic pressure and increased sympathetic tone. A release of inflammatory mediators such as cytokines and C-reactive protein also occurs. These events contribute to endothelial dysfunction, atherosclerosis and coronary artery disease.3The Wisconsin Sleep Cohort also identified significant cardiac mortality in patients with OSA.20In another study, patients with atherosclerosis and OSA faced a 50% or greater risk of sudden cardiac death between 10 p.m. and 6 a.m.21Another study found that among patients with OSA, the odds of experiencing an acute myocardial infarction between midnight and 6 a.m. was six times higher than during the rest of the day.22

In another study, researchers compared CPAP treatment in controls, snorers, and patients with mild, moderate and severe OSA.23After 10 years, patients with severe untreated OSA had a 2.5 times higher likelihood of a fatal cardiovascular event and were 2.68 times more likely to experience a nonfatal cardiovascular event. Patients who were effectively treated with CPAP significantly reduced their cardiovascular risks to slightly higher than normal controls and snorers. This evidence gives significant weight to the benefits of treating OSA with CPAP.


OSA is a risk factor for stroke, and it can be caused by a stroke.3 atients with OSA had an increased risk of stroke or death from any cause, and this risk persisted after adjustment for age, sex, race, smoking, alcohol use, body mass index, diabetes, hypertension, hyperlipidemia or atrial fibrillation.24Even patients with mild OSA may have a higher prevalence of stroke.25

OSA and Diabetes

Obstructive sleep apnea is associated with glucose intolerance and insulin resistance and may predispose patients to type 2 diabetes independent of obesity.3Researchers documented a 2.8% rate of type 2 diabetes in patients with an AHI of 5 or below and a 14.7% rate of diabetes in patients with an AHI of 15 or above.26This relationship is independent of other risk factors, but whether OSA is causal is unclear. In another study of 25 patients with type 2 diabetes and OSA treated with CPAP, researchers documented a significant reduction in hemoglobin A1cin patients who used CPAP for more than 4 hours per night.26The evidence was sufficient for the International Diabetes Federation to recommend that all patients with type 2 diabetes be screened for OSA and that all OSA patients be screened for type 2 diabetes.27

OSA and Mortality

Two large studies provide important evidence of the association between OSA and death. In the Wisconsin Sleep Cohort study, an 18-year follow-up of 1,522 subjects found a significantly high mortality risk with untreated SDB, independent of age, sex, BMI and other confounders. Patients with severe SDB had a threefold greater risk of all-cause mortality.20

In the Busselton Health Study, moderate to severe OSA was associated with 33% mortality over 14 years compared with 6.5% mortality in patients with mild OSA and 7.7% in patients with no sleep apnea.28This remained significant after adjustment for age, gender, mean arterial pressure, total cholesterol, high-density lipoprotein cholesterol, BMI, diabetes, angina and smoking.

Sleep Deprivation

There is clear evidence that sleeplessness worsens reaction time and impairs concentration, performance, attention and vigilance. The most common consequence of sleep deprivation, excessive somnolence, endangers the patient as well as the population. Recently, studies have examined the relationship between sleep deprivation and obesity, diabetes and mortality.

Sleep Deprivation in Children

Multiple studies in children have found a strong association between short sleep duration and obesity. These sequelae begin as early as infancy. In a study of 915 infants, researchers found that infants who slept less than 12 hours per day had a higher BMI.29Another team found that children who had problems sleeping between ages 2 and 4 years were 1.9 times more likely to be obese at age 21.30Another researcher observed a negative linear association between habitual sleep duration and body weight.31

A link may exist between inadequate, poor-quality sleep and prehypertension in adolescents without sleep apnea. A study evaluated 238 13- to 16-year-olds to measure sleep quality, sleep quantity and blood pressures.32The researchers found that patients who slept 6.5 hours or less had increased odds of developing prehypertension (defined as ≥ 90thpercentile for age, sex and height). This association continued after adjustment for contributing factors, and these adolescents had a systolic blood pressure elevation of 4 mm Hg compared with other children (p < 0.01). These studies demonstrate that adequate sleep may be a powerful tool for preventing obesity and hypertension and supporting strong neurobehavioral functioning.

Sleep Deprivation and Obesity

Several studies of adults have investigated the relationship between sleep duration and obesity. Typically, the relationship is a U-shaped curve, with lower risk in patients who sleep 7 to 8 hours per night and increased risk in shorter and longer sleepers. Some experts suggest that the hormones that control appetite, leptin and ghrelin, are influenced by sleep deprivation. Lack of sleep reduces leptin and increases ghrelin. Others believe that sleep deprivation has an impact on glucose homeostasis, cortisol levels, growth hormone secretion, circulating catecholamine levels or inflammatory responses.33

In the Whitehall II Study, short sleep duration was significantly associated with obesity risk.34Researchers found a significant inverse association between hours of sleep and waist circumference. Patients who slept 5 hours or less had a 65% increased risk for obesity compared with those who slept 7 hours. The researchers found no prospective association.

A study of 68,183 women who self-reported weight and sleep duration of less than 7 hours had a modest increase in weight over a mean follow-up of 16 years.35 ompared with patients who slept 7 hours, those who slept 5 hours had a relative obesity risk of 1.15, and women who slept 6 hours had a relative risk of 1.06.

Sleep Deprivation and Diabetes

In a multivariate, longitudinal analysis of 8,992 adults, patients who reported 5 or fewer hours of sleep and 9 or more hours of sleep were significantly more likely to have diabetes after controlling for obesity, history of hypertension and other covariates.36The association between short sleep duration and diabetes is consistent in experimental sleep restriction studies, but the mechanisms for an association between long sleep duration and diabetes is unknown.

Sleep Deprivation and Mortality

The Whitehall II study investigated the associations of sleep duration and change in sleep duration with all-cause, cardiovascular and noncardiovascular mortality.34The findings suggest that decreased sleep duration affects all-cause mortality via an increase in cardiovascular deaths, while excessive sleep duration affects overall mortality via an increase in noncardiovascular deaths.

Putting It Into Practice

Sleep is a basic human function, and it is foundational to good health. NPs should evaluate the quality and quantity of each patient's sleep. Pay particular attention to patients at highest risk due to the following: neurobehavioral dysfunction including suspected ADHD; hypertension; heart failure; cardiac dysrhythmias; myocardial ischemia; stroke; type 2 diabetes; and obesity.

Include three general sleep questions in history taking:

• How many hours do you sleep on most nights? If it is less than normal for age, ask whether the patient has difficulty falling asleep or staying asleep.

• Do you feel sleepy or fatigued during the day, or do you feel your sleep is unrefreshing? In children, ask about hyperactivity, irritability and aggressive behaviors. Ask about snoring, breathing difficulties in sleep and restless sleep.

• Do you display any unusual behaviors during sleep? If yes, obtain detailed information about the activity, and consider referral to a sleep specialist.

A polysomnogram is the gold standard diagnostic tool for OSA. When sleep deprivation is a matter of lifestyle, counsel about the potential risks and provide suggestions for change. When sleep deprivation results from a sleep disorder, evaluation and treatment are imperative.

Teresa Valerio is a family nurse practitioner at Illinois Neurological Institute Sleep Center in Morton and Peoria, Ill. She is a member of the speaker bureau for Philips Respironics.


1. National Heart Lung and Blood Institute. 2003 National Sleep Disorders Research Plan. Available at: Accessed June 16, 2009.

2. Sheldon SH, et al. Principles and Practice of Sleep Medicine. 1sted. Philadelphia, Pa.: Elsevier Saunders; 2005.

3. Kryger MH, et al. Principles and Practice of Sleep Medicine. 4thed. Philadelphia, Pa.: Elsevier Saunders; 2005.

4. National Sleep Foundation. 2008 Sleep in America Poll. Available at Accessed June 16, 2009.

5. National Sleep Foundation. 2004 Sleep in America Poll. Available at: Accessed June 16, 2009.

6. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 2ndi> ed.: Diagnostic and Coding Manual. Westchester, Ill.: American Academy of Sleep Medicine; 2005.

7. Beebe DW. Neurobehavioral morbidity associated with disordered breathing during sleep in children: a comprehensive review. Sleep. 2006;29(9):1115-1134.

8. Gozal D, Kheirandish-Gozal L. The multiple challenges of obstructive sleep apnea in children: morbidity and treatment. Curr Opin Pediatr. 2008;20(6):654-658.

9. Bixler EO, et al. Association of hypertension and sleep-disordered breathing. Arch Intern Med. 2000;160(15):2289-2295.

10. Nieto FJ, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;283(14):1829-1836.

11. Peppard PE, et al. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378-1384.

12. Pepperell JC, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomized parallel trial. Lancet. 2002;359(9302):204-210.

13. Becker HF, et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation. 2003;107(1):68-73.

14. Chobanian AV, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood pressure. Hypertension. 2003;42(6):1206-1252.

15. Shahar E, et al. Sleep-disordered breathing and cardiovascular disease; cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19-25.

16. Kaneko Y, et al. Cardiovascular effects of continuous positive airway pressure in patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;348(13):1233-1241.

17. Bhadriraju D, et al. Sleep apnea syndrome: implications on cardiovascular disease. Crit Pathw Cardiol. 2008;7(4):248-253.

18. Mehra R, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: The Sleep Heart Health Study. Am J Respir Crit Care Med. 2006;173(8):910-916.

19. Kanagala R, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589-2594.

20. Young T, et al. Sleep disordered breathing: eighteen-year follow-up of the Wisconsin sleep cohort. Sleep. 2008;31(8):1071-1078.

21. Gami AS, et al. Day-night pattern of sudden death in obstructive sleep apnea. N Eng J Med. 2005;352(12):1206-1214.

22. Kuniyoshi FH, et al. Day-night variation of acute myocardial infarction in obstructive sleep apnea. J Am Coll Cardiol. 2008;52(5):343-346.

23. Marin JM, et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365(9464):1046-1053.

24. Yaggi HK, et al. Obstructive sleep apnea as a risk factor for stroke and death. N Engl Jour Med. 2005;353(19):2034-2041.

25. Reichmuth A, et al. Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med. 2005;172(12):1590-1595.

26. Babu AR, et al. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med. 2005;165(4):447-452.

27. Shaw JE, et al. Sleep-disordered breathing and type 2 diabetes: a report from the International Diabetes Federation Taskforce on Epidemiology and Prevention. Diabetes Res Clin Pract. 2008;81(1):2-12.

28. Marshall MS, et al. Sleep apnea as an independent risk factor for all-cause mortality: The Busselton Health Study. Sleep. 2008;31(8):1079-1085.

29. Taveras EM, et al. Short sleep duration in infancy and risk of childhood overweight. Arch Pedriatr Adolesc Med. 2008;162(4):305-311.

30. Mamun AA, et al. Do childhood sleeping problems predict obesity in young adulthood? Evidence from a prospective birth cohort study. Am J Epidemiol. 2007;166(12):1368-1373.

31. Marshall NS, et al. Is sleep duration related to obesity? A critical review of the epidemiological evidence. Sleep Med Rev. 2008;12(4):289-298.

32. Javaheri S, et al. Sleep quality and elevated blood pressure in adolescents. Circulation. 2008;118(10):1034-1040.

33. Stranges S, et al. Cross-sectional versus prospective associations of sleep duration with changes in relative weight and body fat distribution: the Whitehall II Study. Am J Epidemiol. 2008;167(3):321-329.

34. Ferrie JE, et al. A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort. Sleep. 2007;30(12):1659-1666.

35. Patel SR, et al. Association between reduced sleep and weight gain in women. Am J Epidemiol. 2006;164(10):947-954.

36. Gangwisch JE, et al. Sleep duration as a risk factor for diabetes incidence in a large scale US sample. Sleep. 2007;30(12):1667-1673.


Email: *

Email, first name, comment and security code are required fields; all other fields are optional. With the exception of email, any information you provide will be displayed with your comment.

First * Last
Title Field Facility
City State

Comments: *
To prevent comment spam, please type the code you see below into the code field before submitting your comment. If you cannot read the numbers in the below image, reload the page to generate a new one.

Enter the security code below: *

Fields marked with an * are required.


Back to Top

© 2017 Merion Matters

660 American Avenue Suite 300, King of Prussia PA 19406