The Journal for Nurse Practitioners
Volume 4, Issue 6 , Pages 439-444, June 2008

Cardiovascular Effects of Sleep Apnea

  • Katherine J. Dodson

      Affiliations

    • Katherine J. Dodson, RN, MN, FNP-C, works as a Family Nurse Practitioner for Clackamas Community Health in Oregon City, OR.

Article Outline

Abstract 

Obstructive sleep apnea (OSA) is common, yet often undiagnosed. It impacts quality of life and cardiovascular health. Research links OSA to cardiovascular diseases including hypertension, stroke, atherosclerosis, and cardiac arrhythmias. Because 1 in 5 adults are affected by OSA and 75% to 80% of cases that could benefit from treatment remain undiagnosed, it is important that nurse practitioners be aware of its presentation, consequences, and treatment. This article provides an overview of the cardiovascular effects of sleep apnea and its pathophysiology, clinical presentation, screening, and treatment.

Keywords:  Cardiovascular health , CPAP , obstructive sleep apnea , screening , sleep-disordered breathing

 

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Introduction 

Obstructive sleep apnea (OSA) is a common condition that is often unrecognized by primary care providers. It has long been known that sleep apnea increases the risk of automobile accidents, causes daytime sleepiness, and reduces the quality of life. Recent studies have confirmed the link between OSA and cardiovascular diseases including systemic hypertension, stroke, atherosclerosis, and cardiac arrhythmias. To reduce mortality and morbidity associated with sleep-disordered breathing, it is necessary for nurse practitioners (NPs) to be aware of the consequences, presentation, and treatment of OSA. This article is an overview of the cardiovascular effects of OSA and includes discussion about pathophysiology, clinical presentation, screening, and treatment.

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Clinical Presentation of OSA 

OSA is characterized by partial or complete collapse of the upper airway during sleep, leading to frequent apneic or hypoapneic events. This causes repeated arousals with reduction of deep sleep and numerous physical and psychological consequences. Classic symptoms of OSA include disruptive snoring, witnessed apneas (defined as someone observing breathing pauses during sleep), and daytime sleepiness. The snoring and breathing pauses are often reported by the patient's bed partner. The report of daytime sleepiness is essential to the diagnosis.1 Other signs and symptoms include awakening with choking, hypertension, large neck circumference, obesity, resistant hypertension, and atrial fibrillation.2

Pathophysiology 

Apnea is the complete collapse of the upper airway for at least 10 seconds with persistent efforts to breathe. Hypoapnea is the near collapse of the upper airway with a 30% or greater reduction in airflow and a 4% or greater oxygen desaturation.3 The number of apnea and hypoapnea episodes per hour of sleep is referred to as the Apnea-Hypopnea Index (AHI). The AHI is used to define the severity of OSA. Recommended diagnostic criteria for OSA are as follows: AHI of ≥ 5 but < 15 indicates mild OSA; ≥ 15 but < 30, moderate OSA; and ≥ 30 severe OSA.4

The principle pathophysiology of OSA is the abnormal narrowing and collapse of the upper airway, with a loss of tone in the pharyngeal muscles during sleep. Patients make persistent efforts to breath against the occluded upper airway. This leads to repeated arousals and disturbed sleep, with episodes of apnea and hypoapnea. The repetitive cycle of airway collapse leads to acute stressors such as increased sympathetic activity, hypoxemia, hypercapnea, reoxygenation, changes in intrathoracic pressure, vascular endothelial dysfunction, increased oxidative stress, inflammation, increased platelet aggregabitity, and metabolic dysfunction.5 All of these can lead to an increased risk of cardiovascular disease.

Epidemiology 

It is estimated that 1 of every 5 adults has at least mild OSA and 1 of every 15 adults has moderate to severe sleep apnea. Of these, 75% to 80% of cases that could benefit from treatment remain undiagnosed.6 There is a two- to three-fold greater risk for OSA in men than women (Table 1). Women are less likely to be evaluated or diagnosed and have a poorer survival rate, as they are likely to be diagnosed later in the course of the disease and may not be treated as aggressively as men.

Table 1. Risk Factors for OSA
Risk FactorsComments
Obesity (BMI > 30)The combination of these three factors increase the risk for OSA in a nonlinear fashion2
Large neck circumference
Hypertension
Increased BMIPositively associated with OSA when analyzed simultaneously9
Increased waist-to-hip ratio
Increased neck circumference
Pattern of increased intra-abdominal fatLinked to OSA in men10
Morbid Obesity (BMI > 40)Morbid obesity is common in OSA patients
Significant weight increasesThe Wisconsin Sleep Cohort found that a 10% or more increase in weight over 4 years was associated with a 6-fold greater risk of developing OSA9
Loud snoringUsually reported by bed partners. Those with these symptoms have been
Habitual snoringfound to be 3–4 times likely to have an AHI > 1511
Reported breathing pauses
DiabetesA recent study found that 29% of diabetics had OSA12
Genetic predispositionAlteration of upper airway anatomy is the primary cause of OSA, and the size of upper airway structures (ie, lateral pharyngeal walls, tongue, and soft tissue) is inherited13
Current tobacco smokingCurrent smokers are more likely to have sleep-disordered breathing than those who have never smoked and former smokers14
Male genderPossibly related to hormonal differences. Post menopausal women not on
Post-menopausal femaleHRT are 3–4 times more likely to develop OSA than premenopausal women15, 16
Alterations in craniofacial or upper-airway structureMaxillary and mandibular dysmorphisms, narrowed nasal cavities and enlarged tonsils or adenoids all contribute to airway narrowing17
Nasal congestion at nightLinked to OSA and snoring despite cause17

OSA prevalence increases with age with a two- to three-fold higher prevalence in people older than 65 years compared with middle age. The incidence of OSA plateaus at age 65 and this plateau may be due to increased mortality from OSA.6 A few studies suggest that prevalence is higher in African Americans than Caucasians.7, 8

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Consequences of OSA 

The cessations in breathing related to OSA lead to frequent autonomic arousals, repetitive cerebral hypoxemia, and disruptions of sleep architecture. In addition to the various physiological changes, OSA is also linked to impaired daytime functioning, increased automobile accidents, depression, and anxiety.18 Beyond the emotional and cognitive effects, it is important to recognize that sleep apnea causes cardiovascular damage, which leads to a myriad of diseases.

Cardiovascular Responses 

During normal sleep, sympathetic nervous system activity progressively decreases during the deeper states of sleep, leading to decreased heart rate, muscle tone, blood pressure, stroke volume, cardiac output, and systemic vascular resistance.5 For patients with untreated sleep apnea, both daytime and nighttime sympathetic nervous system activity is increased, leading to dramatic increases in blood pressure.3

The cycle of airway collapse followed by efforts to breathe against an occluded airway and arousal with resumption of breathing is repeated hundreds of times per night in those with moderate to severe sleep apnea. Acute hypoxia, carbon-dioxide retention, and negative intrathoracic pressure activate chemoreflexes and lead to systemic vasoconstriction and acute blood pressure increases.3 Baroreceptor resetting may also occur, contributing to increased basal blood pressure.19

Inspiratory effort against a closed airway generates excessive negative intrathoracic pressure that greatly affects cardiac functioning. Left ventricular pressure and afterload may increase and left ventricular relaxation and filling may be impaired. The increased afterload and reduced preload reduces cardiac output, possibly causing cardiac ischemia.5

Chemical Changes 

The cycle of hypoxia, hypercapnia, and pressure surges may serve as stimuli for the release of vasoactive substances that cause endothelial damage and dysfunction, leading to hypertension, hyperlipidemia, and an increased risk of cardiovascular events.3 Platelet aggregation, hematocrit, levels of fibrinogen, and blood viscosity are all increased in OSA.20, 21, 22, 23 These factors combine to contribute to formation of blood clots and atherosclerosis. OSA is also linked to the development of metabolic syndrome, especially in men. Men with OSA, even in the absence of cardiovascular disease, have increased insulin resistance and other metabolic changes, which include higher levels of total and LDL cholesterol, serum leptin, and urinary norepinephrine excretion.24

Cardiac Consequences 

Untreated OSA is correlated with increased fatal and nonfatal cardiovascular events. Men with untreated severe disease have a significantly higher incidence of fatal cardiovascular events than do healthy men, simple snorers, those with mild-moderate disease, and those with severe disease treated with continuous positive airflow pressure (CPAP).25 Fatal events included death from myocardial infarction or stroke. Nonfatal cardiovascular events included nonfatal myocardial infarction, nonfatal stroke, coronary artery bypass surgery, and percutaneous transluminal coronary angiography.

Systemic Hypertension 

OSA is implicated as a causal factor in systemic hypertension although causality has not been proven. One study found that the presence of hypertension 4 years after initial diagnosis of OSA was dependent upon the severity of OSA.26 Another study found that people who had an AHI of 15 or greater were at a 3-fold higher risk of developing hypertension than those with lower AHIs. Further evidence comes from studies that have shown that effective treatment with CPAP can reduce both daytime and nighttime blood pressure in hypertensive adults.27, 28

Heart Failure 

OSA is linked to both diastolic and systolic heart failure. The cumulative effects of hypertension, hypoxemia, increased sympathetic drive, acute surges in blood pressure, and mechanical effects of altered intrathoracic pressure all affect myocardial oxygen demand and can lead to cardiac dysfunction, especially in an already compromised heart.29 Additionally, heart failure may contribute to sleep apnea because patients are predisposed to periodic breathing pauses and upper airway edema, both of which contribute to OSA. In the Sleep Heart Health Study, OSA was found to be an independent risk factor for heart failure as opposed to heart failure contributing to OSA. People who had an AHI of 11 or greater had a 2.38 odds ratio of having heart failure.3

Cardiac Arrhythmias 

Studies have found a link between cardiac arrhythmias and OSA.30, 31 People with severe OSA have a higher rate of atrial fibrillation, nonsustained ventricular tachycardia, and ectopic heart beats. The most significant rhythm disturbances associated with OSA are bradycardia and asystole. It is unclear how this contributes to sudden death and mortality but these arrhythmias are more likely to appear as a result of enhanced vagal tone rather than structural disease.

Cerebral Vascular Accidents 

Many people with OSA have risk factors associated with stroke such as obesity, hypertension, and arrhythmias. Studies do not demonstrate that OSA is the cause of stroke; however, some studies have found an association.29 The combination of hypertension, cardiac arrhythmias, increased blood coagulability, and repeated cerebral hypoxia are the likely mechanisms that lead to an increased risk of thrombus formation and an increased risk of stroke.

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Screening 

The practitioner should follow a step-by-step approach when screening for OSA. The first step is identifying patients who report loud snoring, witnessed apneas, or excessive daytime sleepiness. Daytime sleepiness is a common feature of OSA but may go unnoticed because of its gradual onset and chronicity. Patients may report fatigue or drowsiness during boring, passive, or monotonous situations such as driving, reading, or watching television. Daytime sleepiness should be quantified using a tool such as the Epworth Sleepiness Scale, which screens for subjective daytime sleepiness.1 It is a simple 8-question tool that measures the likelihood to fall asleep during common situations. The tool can be accessed online at: http://www.stanford.edu/∼dement/epworth.html.

As previously discussed, other signs and symptoms of OSA include awakening with choking, hypertension, large neck circumference, being male, obesity, resistant hypertension, and atrial fibrillation. Patients with existing cardiac disease, resistant hypertension, and diabetes also have a high prevalence of OSA.1 Once the clinician suspects OSA, it is necessary to conduct a more in-depth history and clinical assessment. Physical assessment should focus on evaluation for elevated blood pressure, a narrow or crowded airway, truncal obesity, and large neck circumference.32

Patients with suspected OSA should be referred to a sleep specialist for polysomnography. This is usually performed in the sleep laboratory with patients being monitored for electroencephalographic activity, muscle activity, airflow, respiratory effort oximetry, and electrocardiographic activity.3 These laboratories are staffed by trained technicians. Unattended polysomnography is used in some communities with limited resources, but is not the best method for confirming the diagnosis of OSA.

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Treatment 

Positive airway pressure therapy is the mainstay for the treatment of OSA and has been shown to significantly reduce blood pressure. CPAPs are the most common type of devices. They provide noninvasive pressure via a blower and a mask or nasal device and act as a pneumatic splint to keep the airway open.2 Treatment is usually initiated in the sleep laboratory, with pressures titrated for maximum effectiveness. Effective CPAP treatment significantly reduces both daytime and nighttime arterial blood pressures.33 AutoPAPs are available. These devices monitor apneas, hypoapneas, snoring, and inspiratory flow. Rather that providing constant, maximal pressure, as CPAPs do, they adjust to provide the minimal pressure necessary to stabilize the upper airway. Certain patients require BiPAP machines, which provide differing levels of inspiratory and expiratory pressures. These are not first-line therapy but are appropriate for those who have had a treatment failure on CPAP or who require extra respiratory support such as patients with severe pulmonary disease.2

Continuous use of therapy is crucial. Although subtherapeutic therapy has been shown to improve sleep architecture and quality of life, it does not decrease blood pressure and is therefore unlikely to decrease cardiovascular risk.33 Approximately half of the patients who are prescribed CPAP will use it consistently as recommended, averaging about 6 hours of pressure therapy per night. The other half will only use it intermittently.34 There are numerous reasons for failing to use CPAP including inconvenience, lack of understanding of the benefits of treatment, claustrophobia, and side effects of treatment such as nasal congestion, rhinorrhea, eye irritation, dermatological problems, and chest pressure. Frequent contact with the patient, especially during the first few weeks of therapy, is essential to identify and relieve side effects. Methods to reduce side effects include adjusting pressure settings, adding heated humidity to the system, resizing the mask, changing to a different interface, or adding a chin strap. Education and encouragement from health care providers as well as cognitive behavioral therapy, especially for those with claustrophobia, and intensive nursing support have all been shown to improve overall use of therapy.34

Oral appliances are recommended for those who are intolerant of pressure devices. These are specially made by a trained dentist or orthodontist to reposition the mandible or tongue to relieve obstruction. Several surgical procedures are available to treat upper airway obstructions including septoplasty, tonsillectomy, or tracheostomy. It is sometimes necessary to correct anatomical obstructions before pressure devices or oral appliances can be fitted.2

Weight reduction should be encouraged, as it may help relieve symptoms in obese patients. In morbidly obese patients, bariatric surgery may be an effective treatment. Topical nasal steroids may improve nasal patency and be an effective adjunct for those with chronic sinus or nasal congestion. Smoking cessation should also be encouraged. Methods that keep the patient in a nonsupine position, such as positioning pillows, are also indicated as secondary therapy to reduce OSA.35

Effective treatment reduces blood pressure and therefore cardiac risk. Some studies have shown reductions in mean blood pressure of up to 10 mmHg with effective treatment of OSA. A reduction of this magnitude would reduce the risk of coronary heart disease events by 37% and stroke risk by 56%.33

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Summary and Conclusion 

OSA is common and often goes undiagnosed, but causes significant alterations in quality of life and cardiovascular functioning. Every primary care practitioner should be cognizant of the presentation of and treatment for OSA. By screening all patients who have the classic symptoms and risk factors or preexisting cardiovascular disease, the practitioner can be assured that most undiagnosed cases will be detected and treated appropriately. By supporting the patient to engage in continuous treatment the practitioner promotes improved health, cardiovascular health, and a better quality of life for OSA patients.

Although the effects of CPAP and oral appliance therapy have been extensively researched, little research has been conducted regarding other noninvasive methods to reduce apnic events. The effects of weight loss therapy or bariatric surgery have not been adequately pursued. Nonstandard approaches such as positional therapy also have received little attention. As sleep research garners more attention, new studies may provide much needed evidence about the efficacy of treatment and the overall incidence of cardiovascular disease may decrease.

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References 

  1. Kline LR . Clinical presentation and diagnosis of obstructive sleep apnea-hypopnea in adults. UpToDate . Available at: www.uptodate.com March 8, 2007; Accessed July 15, 2007.
  2. Institute for Clinical Systems Improvement [ICSI]. Brief summary: diagnosis and treatment of obstructive sleep apnea in adults. National Guideline Clearinghouse. March 2007. Available at: http://guideline.gov/summary/summary.aspx?doc_id=10809&nbr=005634&string=obstructive+AND+sleep+AND+apnea. Accessed August 31, 2007.
  3. Parrish JM , Somers VK . Obstructive sleep apnea and cardiovascular disease . Mayo Clin Proc . 2004;79(8):1036–1046
  4. Young T , Peppard PE , Gottlieb DJ . Epidemiology of sleep apnea . Am J Respir Crit Care Med . 2002;165:1217–1239
  5. Shamsuzzaman AS , Gersh BJ , Somers VK . Obstructive sleep apnea: implications for cardiac and vascular disease . JAMA . 2003;290(14):1906–1914
  6. Young T , Skatrud J , Peppard PE . Risk factors for obstructive sleep apnea . JAMA . 2004;291(16):2013–2016
  7. Ancoli-Israe S , Klauber M , Stepanowski C , et al.   Sleep-disordered breathing in African-American elderly . Am J Respir Crit Care Med . 1995;152:1946–1949
  8. Redline S . Epidemiology of sleep-disordered breathing . Semin Respir Crit Care Med . 1998;19:113–122
  9. Peppard PE , Young T , Palta M . Longitudinal study of moderate weight change and sleep-disordered breathing . JAMA . 2000;284:3015–3021
  10. Newman AB , Nieto FJ , Guidry U , et al.   Relation of sleep-disordered breathing to cardiovascular risk factors: the Sleep Heart Heath Study . Am J Epidemiol . 2001;154(1):50–59
  11. Young T , Shahar E , Nieto F , et al.   Predictors of sleep-disordered breathing in community-dwelling adults . Arch Intern Med . 2002;162:893–900
  12. Einhorn D , Erman M , Philis-Tsimkas A , et al.   Prevalence and associations of sleep apnea in a population of adults with type 2 Diabetes Mellitus . Diabetes . 2005;54:A582
  13. Schwab RJ , Pasirstein M , Kaplan L , et al.   Family aggregation of upper airway soft tissue structures in normal subjects and patients with sleep apnea . Am J Respir Crit Care Med . 2006;173(4):453–463
  14. Zhang L , Samet J , Caffo B , et al.   Cigarette smoking and nocturnal sleep architecture . Am J Epidemiol . 2006;164(6):529–537
  15. Young T , Finn L , Austin D , et al.   Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study . Am J Respir Crit Care Med . 2003;167:1181–1185
  16. Bixler EO , Vgontzas AN , Have TT . Prevalence of sleep disordered breathing in women: effects of gender . Am J Respir Crit Care Med . 1998;157:144–148
  17. Rappai M , Collop N , Kemp S , et al.   The nose and sleep-disordered breathing: what we know and what we do not know . Chest . 2003;124(6):2039–2054
  18. El-Ad B , Lavie P . Effect of sleep apnea on cognition and mood . Int Rev Psychiatry . 2005;17(4):277–282
  19. Fletcher EC . Sympathetic over activity in the etiology of hypertension of obstuctive sleep apnea . Sleep . 2003;26(1):15–19
  20. Bokinsky G , Miller M , Ault K , et al.   Spontaneous platelet activation and aggregation during obstructive sleep and apnea and its response to therapy with nasal continuous positive airway pressure: a preliminary investigation . Chest . 1995;108:625–630
  21. Hoffstein V , Herridge M , Mateika S , et al.   Hematocrit levels in sleep apnea . Chest . 1994;106:787–791
  22. Chin K , Ohi M , Keta H . Effects of NCPAP therapy on fibrinogen levels in obstructive sleep apnea syndrome . Am J Respir Crit Care Med . 1996;153:1972–1976
  23. Nobili L , Schiavi G , Bonzano E . Morning increase in whole blood viscosity in obstructive sleep apnea syndrome . Clin Hemorheol Microcirculation . 2000;22:21–27
  24. McArdle N , Hillman D , Beilin L , et al.   Metabolic risk factors for vascular disease in obstructive sleep apnea: a matched controlled study . Am J Respir Crit Care Med . 2007;175(2):190–196
  25. Marin JM , Carrizo SJ , Vincente E , et al.   Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopneoea with or without treatment with continuous positive airway pressure: an observational study . Lancet . 2005;365(9464):1046–1053
  26. Peppard PE , Young T , Palta M , et al.   Prospective study of the association between sleep-disordered breathing and hypertension . N Engl J Med . 2000;342:1378–1384
  27. Haentjens P , Van Meerhaeghe A , Moscariello A , et al.   The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea . Arch Intern Med . 2007;167:757–765
  28. Hla KM , Skatrud JB , Finn L , et al.   The effect of correction of sleep-disordered breathing on BP and untreated hypertension . Chest . 2002;122:1125–1132
  29. Caples SM , Garcia-Touchard A , Somers VK . Sleep-disordered breathing and cardiovascular risk . Sleep . 2007;30(3):291–304
  30. Mehra R , Benjamin EJ , Shahar E . Association of nocturnal arrhythmias with sleep disordered breathing: the Sleep Heart Health Study . Am J Respir Crit Care Med . 2006;173:910–916
  31. Alonzo-Fernandez A , Garcia-Rio F , Racionero MA . Cardiac rhythm disturbances and ST-segment depression episodes in patients with obstructive sleep apnea-hypoapnea syndrome and its mechanisms . Chest . 2005;127:15–22
  32. University of Texas, School of Nursing, Family Nurse Practitioner Program. Screening for obstructive sleep apnea in the primary care setting. National Guideline Clearinghouse . Available at: http://guideline.gov/summary/summary.aspx?doc_id=9436&nbr=005057&string=Screening+AND+obstructive+AND+sleep+AND+apnea May 2006; Accessed August 31, 2007.
  33. Becker HF , Jerrentrup A , Ploch T , et al.   Effects of nasal continuous positive airway pressure treatment and blood pressure in patients with obstructive sleep apnea . Circulation . 2003;107:68–73
  34. Weaver T . Compliance with continuous positive airway pressure (CPAP). UptoDate . Available at: http://utdol.com/utd/topic.do?topicKey=sleepdis/6186&view=text 2007; Accessed July 30, 2007.
  35. Morgenthaler TI , Kapen S , Lee-Chiong T , et al.   Practice parameters for the medical therapy of obstructive sleep apnea . Sleep . 2006;29(8):1031–1035

 In conjunction with national ethical standards, the author reports no relationships with business or industry that represent a conflict of interest.

PII: S1555-4155(08)00093-7

doi:10.1016/j.nurpra.2008.02.017

The Journal for Nurse Practitioners
Volume 4, Issue 6 , Pages 439-444, June 2008

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