OSA and hypertension
Apnea = Airflow absent for at least 10 seconds.
OSAS = More than 5 apneas in an hour
Pulmonary hypertension. A potential complication of OSA is pulmonary hypertension, which can lead to cor pulmonale. About 17% of patients with OSA develop permanent (daytime) pulmonary hypertension (mean pulmonary artery pressure, at least 20 mm Hg). Many patients with OSA experience acute rises in pulmonary artery pressure and pulmonary vascular resistance that coincide with sleep-induced apnea and hypoxemia.
Apnea exerts several acute cardiothoracic, neural, and hemodynamic effects, including wide fluctuations in intrathoracic pressure, reduction of blood oxygen saturation, and an increase in carbon dioxide levels. These effects may cause vagal hypertonia and bradycardia, decreased stroke volume, increased afterload, and a surge of sympathetic activity to vascular smooth muscle and perhaps to the adrenal medulla, causing vasoconstriction in certain vascular beds. These repetitive elevations of pulmonary artery pressure during sleep may lead to pulmonary vasculature remodeling and, ultimately, to daytime pulmonary hypertension and hypoxemia. These effects are unrelated to impaired pulmonary function, greater body mass, or a higher prevalence of smoking.[Essential hypertension. Epidemiologic studies suggest a link between sleep apnea and hypertension. At least half of all patients with OSAS are hypertensive. Similarly, studies have shown that about 30% of patients with primary hypertension have sleep apnea. The proposed mechanism for the development of systemic hypertension in patients with OSA is that of repeated sympathomimetic discharge resulting from apneas. Transient BP elevations have been observed during apneic episodes and are thought to be caused by arousals, high negative intrathoracic pressures, nocturnal desaturation, and/or hypercapnia, all of which may stimulate sympathetic activity.
In a population-based study, mean BPs were significantly higher in participants with sleep apnea than in those without it. During sleep, BP also fluctuated to a greater extent in patients with sleep apnea than in control subjects, regardless of the participants' weight, age, or sex. Snoring alone had no effect on BP
Sleep-disordered breathing events are twice as common in males as in females. Approximately 4% of men and 2% of women in the United States have OSAS. The prevalence is higher in nonwhites (16.3%) than in the non-Hispanic white population (2% to 4%, as stated above).
Obesity is also a strong, well-documented risk factor for sleep apnea. An anthropometric finding such as body mass index (BMI; measured as kg/m2) is a major positive predictor. Patients with values greater than 28 kg/m2 (clinically obese) are more likely to develop OSA than are those with lower BMIs. Among patients who are eventually treated for sleep apnea, 40% to 60% have BMIs greater than 28 kg/m2. A neck circumference greater than 17 inches in males or greater than 16 inches in females is also a positive predictor for OSA.
Another risk factor for OSA is age. The prevalence of clinically significant sleep-disordered breathing peaks in middle age, although the number of asymptomatic persons who meet numerical criteria for OSA increases with age. A genetic predisposition may also underlie sleep apnea. Some familial craniofacial features, including a high-arched "ogival" hard palate, may be strong indicators of risk for OSAS. A receding chin is also a risk factor for OSA.
Lifestyle factors also affect the likelihood of developing OSA. Cigarette smoking increases the risk, which appears to resolve with smoking cessation. Alcohol intake and the ingestion of muscle relaxants and respiratory depressants (notably, benzodiazepine hypnotics) can exacerbate sleep-disordered breathing. Also, irritant-related upper airway disorders can aggravate OSA
