Obstructive Sleep Apnea and Hypertension

Obstructive Sleep Apnea and Hypertension

  Obstructive sleep apnea or OSA is a life altering and potentially life threatening condition that causes a person to stop breathing repeatedly during sleep. It is defined as the cessation of airflow lasting 10 seconds or greater, during sleep. In Obstructive Sleep Apnea, closure of the upper airway results in the obstruction of airflow despite persistent efforts to breathe. A related event, hypopnea, is characterized by a reduction in airflow associated with a decrease in oxygen saturation.

  The Obstruction occurs in the oropharynx or nasopharynx and is thought to result from a small and floppy airway. The smaller airway is susceptible to reduced neural drive to airway muscles during both non-REM and REM (rapid eye movement) sleep.

  Multiple episodes of sleep apnea and hypopnea can occur repeatedly through the night. Hypoxia and hypercarbia places a strain on the cardiovascular system. The apneas and hypopneas result in desaturations and recurrent micro arousals that terminate the events. Sleep is fragmented and restful sleep is not achieved.

  The predominant signs and symptoms of obstructive sleep apnea are disruptive snoring with pauses in breathing and daytime sleepiness. When the measurement of the apneas and hypopneas is combined with the signs and symptoms, the term obstructive sleep apnea syndrome or OSAS is sometimes used.

  Ultimately, obstructive sleep apnea takes its toll on the individual's quality of life. Obstructive sleep apnea leads to excecessive daytime somnolence or EDS, decreased physical and cognitive performance, increased auto accients and decreased quality of life. Obstructive sleep apnea patients report a diminished functional level on general scales such as SF-36 and validated, sleep-specific, scales like the Functional Outcome of Sleep Questionnaire or FOSQ. Stroke, myocardial infarction, cardiac arrhythmias and systemic hypertension are associated with obstructive sleep apnea syndrome.

  Early recognition of obstructive sleep apnea is important due to its association with cardiovascular sequelea. Proving the casual relationship between OSA and these cardiovascular events has been difficult as they are all impacted by common variables including obesity, age and gender. Ongoing research on the underlying cause of hypertension is starting to focus not only on wakefulness but on what happens in the body during sleep.

Prevalence of Obstructive Sleep Apnea

  A community - based study has shown that 2% of women and 4% of men between 30 and 60 years old are affected by Obstructive Sleep Apnea Syndrome, known as OSAS. This is similar to the incidence of asthma and diabetes mellitus in this age group. The prevalence of Obstructive Sleep Apnea Syndrome is even higher among elderly patients. Overall, an estimated 18 million people are affected. Data has shown the majority of Obstructive Sleep Apnea sufferers are not diagnosed or treated.

Risk Factors of Obstructive Sleep Apnea

  Numerous research studies have confirmed that obesity is the strongest risk factor for the development of obstructice sleep apnea. A body mass index (BMI) more than 28 kg/m² is found in 60-90% of patients diagnosed with sleep apnea. The risk of sleep apnea from obesity, BMI > 29 kg/m², is as high as 10-14 times. Neck circumference, waist-hip ratio and measurements of central fat deposition have been recognized as better indicators of sleep apnea especially in thin individuals.

  Men are also at a higher risk for obstructive sleep apnea than women. The male to female ratio in clinic based populations is as high as 10:1: in community-based samples it is 3:1. The difference may be because women are less likely to report snoring and obstructive sleep apnea may be under-diagnosed in women. The risk for obstructive sleep apnea in females increases with obesity and post-menopausal status.

  Increasing age has been shown to be an independent factor for sleep apnea in the majority of studies. The risk for obstructive sleep apnea has been shown to increase 2-4 times greater in first degree relatives when there is a positive family history for sleep apnea. African Americans, Mexican Americans and Pacific Islanders also have shown increased risk for obstructive sleep apnea. In these populations, co-morbid factors of obesity, hypertension and diabetes are more prevalent than in Caucasians.

  Although less common, jaw or facial attributes such as a recessed chin, over-bite, cross-bite and narrow mandible predispose individuals to the development of obstructive sleep apnea. Facial elongation, enlarged tonsils and adenoids are more common in patients with obstructive sleep apnea. A deviated nasal septum may contribute to increased airway resistance and obstruction.

  Alcohol, especially consumed around bedtime, and sedative medications can worsen obstructive sleep apnea, by impairing uper airway dilator muscle function and blunting the arousal response to the apnea.

Signs and Symptoms of Sleep Apnea

  Tossing and turning is common and bed partners sometimes report excessive body movements. Some patients report a sensation of choking or dyspnea that resolves on awakening. Esophageal reflux is also common. It is believed to result from increased gastric pressure as the sufferer attempts to breathe against the obstruction. Some obstructive sleep apnea sufferers also report frequent trips to the bathroom.

  Excessive sleepiness is the most common daytime symptom of obstructive sleep apnea. Sleepiness can range from feeling drowsy in the afternoon to falling asleep at a meeting or while driving. Some people only complain of fatigue.

  Other daytime symptoms of sleep apnea are the result of fragmented, poor quality sleep. Dull, generalized morning headaches are common. Some sufferers of obstructive sleep apnea report decreased sexual drive or sexual dysfunction. Problems with dexterity, attention, concentration and memory can be detected with physiologic testing. Personality changes may be observed and may place a strain on personal and family relationships.

Diagnosis and Treatment of Obstructive Sleep Apnea

  Continuous positive airway pressure (CPAP) is the most effective noninvasive therapy for obstructive slee apnea. The device consists of a blower unit that attaches to a mask. The mask is typically worn over the nose, however some patients need to wear a mask that covers their nose and mouth. The constant pressure throughout the entire ventilatory cycle acts as a pneumatic splint. Airway patency is maintained during inspiration and expiration.

  CPAP has been shown to be effective in reversing daytime somnolence and improving neurocognitive function. CPAP does prevent desaturations, arousal and acute elevations in systemic blood pressure associated with sleep apnea.

Acute Blood Pressure Changes In Obstructive Sleep Apnea

  The acute cardiovascular effect of Obstructive Sleep Apnea is a moderate to marked increase in systemic blood pressure. Systemic blood pressure crescendos toward the end of the apnea, peaks when air movement is resumed and then returns to baseline. With recurrent sleep apnea, the blood pressure can gradually increase with each successive apnea and it can take minutes to hours to return to baseline.

Epidemiological Studies

  Participants answered a self administered questionnaire on snoring history, obstructive seep apnea awareness and treatment, and sleepiness. During a home visit, baseline physiologic measurements and a history were obtained. Participants were assessed with full unattended polysomnography. Hypertension was defined as a blood pressure of 140/90 and the presence of sleep disordered breathing was assessed using the Apnea Hypopnea Index (AHI) Sleep Apnea was defined as a cessation of airflow and hypopnea as a decrease in airflow.

  The Likelihood of hypertension rose as the AHI increased. The odds ratio for a diagnosis of hypertension started to increase with an AHI of 15. The odds of a person who had an AHI greater than 30 having hypertension were 1.5 times greater than in a person with an AHI of 0. The association between sleep disordered breathing (SDB) and hypertension remained even after the findings were adjusted for the influence of age, sex, BMI, ethnicity, fat distribution, alcohol intake and smoking.

  This is only a snapshot of current associations. The study demonstrates that sleep apnea is associated with systemic hypertension in middle aged and older individuals of different sexes and ethnic backgrounds. No causal relationship can be proven, but those with sleep apnea were more likely to have hypertension independent of the more commonly known risk factors.

  Baseline AHI is a strong predictor of hypertension. The risk of hypertension on follow up was almost three times higher in participants with an AHI of 15 or more versus those with an AHI of 0. An AHI of 5 to 15 increased the odds of developing hypertension at follow up by 2 times. Participants with an AHI of 0.1 to 4.9 were at greater odds of having hypertension at their 4 - year follow up than persons with an AHI of 0. There was no minimal threshold of AHI below which hypertension was not related to sleep apnea.

  The link between sleep apnea and hypertension remained significant even after the analysis was controlled for age, sex, body mass index, neck and waist circumference, alcohol use and smoking status. This research demonstrates a dose - response relationship between sleep apnea at baseline and the presence of hypertension at follo up.

  A study following a cohort of 73,231 US female nurses for 8 years as part of the nationwide nurses health study. Blood pressure and physician - diagnosed hypertension were self - reported through a validated questionnaire. When first asked about their snoring habits, 55,720 nurses did not have hypertension. During the 8 years of follow - up, 7,622 cases of physician diagnosed hypertension were reported. After adjusting for age, body mass index (BMI), waist circumference and lifestyle factors like smoking, women who said they smored regularly were 55% more likely to develop hypertension over the next 8 years than those who reported that they did not snore. Women who said they snored occasionally were 29% more likely to develop hypertension than nurses who reported no snoring.

  The results suggest that snoring itself might be a risk factor for hypertension in women.

  Sleep apnea is begining to appear to be a risk factor for hypertension and its consequences: stroke, angina, and heart failure. In the U.S. population, hypertension is present in 15-35% of men and women aged 40-60 years. Sleep apnea may not be associated with hypertension in all people, and treatment for sleep apnea is not the first line of treatment for hypertension. Nevertheless, because of the link between sleep apnea and hypertension, it is important for physicians and health care practitioners to recognize and diagnose sleep apnea. The clinician should think about sleep apnea in a patient in whom hypertension is hard to control or hypertension is accompanied by symptoms of obstructive sleep apnea.

Blood Pressure Changes with CPAP Therapy

  The research done to date on the impact on blood pressure with the use of nasal CPAP in obstructive sleep apnea has shown mixed results. Approximately half show statistical improvements in systolic and diastolic blood pressure, and half show no statistical change.

  A review of the studies explains potential reasons why the results are mixed.

1. Studies have included normotensive patients with hypertensive patients. This may have diluted the effect of CPAP on blood pressure.
2. In most of the studies the subjects have been on antihypertensive medications. This could minimize the changes in blood pressure with CPAP.
3. Follow up times to determine the effect on blood pressure have been variable.
4. None of the studies looked at the relationship between the onset of hypertension and the onset of obstructive sleep apnea. Hypertension may have begun from another cause and treatment of the obstructive sleep apnea with CPAP may improve management of high blood pressure, but not eliminate it.
5. Compliance with CPAP therapy is also variable.

  The presence of sleep apnea makes blood pressure more difficult to control, and may contribute to the appearance of angina, heart failure, or stroke in hypertensive patients.

  CPAP therapy may lower elevated blood pressure in some patients and make blood pressure easier to manage in other hypertensive patients.

  Ongoing research is helping to build physiologic and epidemiological evidence to support the direct contribution of obstructive sleep apnea to hypertension. Research work is also being conducted on the relationship between sleep apnea, heart disease and dtroke.