The pathophysiological basis of sleep apnea is characterized by frequent short breathing pauses, decreased blood oxygen saturation, and disturbed sleep structure during sleep. Sleep apnea syndrome can indeed cause hypertension.
This is because sleep apnea can cause patients to experience repeated hypoventilation or apnea during sleep, causing the body to experience intermittent hypoxia and reoxygenation. This process can stimulate oxidative stress and inflammatory responses, leading to damaged vascular endothelial function and imbalance of the autonomic nervous system, which may eventually cause hypertension.
Studies have found that about 50% of patients with sleep apnea have hypertension, while 30%-40% of patients with hypertension also have sleep apnea. This association mainly leads to increased blood pressure through mechanisms such as repeated hypoxia, sympathetic nerve excitement, and inflammatory response.
1. Sleep Apnea And Hypertension
Epidemiological studies have found that the incidence of OSAS in the general population is 2%~10%, while the incidence of OSAS in people with hypertension is about 30%. The incidence of hypertension in the general population is 10%~19%, and the incidence of hypertension in OSAS patients is 45%~48%.
In OSAS patients, regardless of whether they have hypertension or not, abnormal changes in blood pressure occur during sleep. Blood pressure is lowest at the beginning of apnea, rises near the end of apnea, and reaches the highest level after apnea, generally 25% higher than before apnea.
Some scholars prospectively observed two groups of OSAS patients, one group received relevant intervention treatment, and the other group served as the control group. After 4 years of follow-up, the incidence of hypertension in the treatment group was significantly reduced compared with the control group, and there was a quantitative correlation between the degree of hypertension and the number of shallow breaths or no breathing per hour of sleep.
In a large longitudinal study, snoring, a basic symptom of OSAS, significantly increased the risk of hypertension. The study found that an additional apnea event per hour of sleep would increase the risk of hypertension by 1%, while every 10% decrease in nighttime blood oxygen would increase this risk by 13%.
2. How Does Sleep Apnea Cause Hypertension
Sleep apnea is an independent risk factor for hypertension, independent of age, gender, obesity, smoking, alcoholism, life stress, and heart and kidney diseases.
At present, the exact mechanism of sleep apnea causing high blood pressure has not been fully elucidated. The most significant pathophysiological changes of sleep apnea are intermittent hypoxemia and hypercapnia, accompanied by awakening during sleep and changes in sleep structure.
(1) Sleep Fragmentation And Sympathetic Overactivity
Frequent apnea interrupts sleep and causes sleep structure disorders. This fragmented sleep continuously activates the sympathetic nervous system, putting the body in a “stress state” and causing blood pressure to rise significantly at night and in the morning.
Sleep apnea patients suffer from repeated episodes of apnea during sleep, accompanied by hypoxemia and hypercapnia, which affect the brainstem and cardiovascular centers through a feedback mechanism, increasing sympathetic nerve tone and leading to increased blood pressure.
Studies have shown that sleep apnea can cause an increase in endothelin and adrenaline levels and an increase in sympathetic nerve activity. Compared with patients without sleep apnea, patients with sleep apnea have increased muscle sympathetic activity, and continuous positive airway pressure (CPAP) can reduce this high level of nerve activity.
Studies have shown that patients with sleep apnea have increased sympathetic tone not only during the night but also during the day. Some experiments that simulate chronic intermittent hypoxia to produce systemic hypertension also suggest that sleep apnea causes increased blood pressure, which is attributed to sympathetic nervous system activation, and anatomical studies strongly suggest that this activation is extensive and involves the cortex and brainstem of the sympathetic nervous system.
Studies have shown that severe sleep apnea means more awakenings, resulting in more frequent and intermittent sympathetic nerve stimulation, while normal sleep is disrupted by repeated awakenings and awakening reactions, forming multiple sleep fragments, reducing the total effective sleep time, and causing varying degrees of sleep deprivation. All of these can produce higher levels of sympathetic nerve activity, which in turn leads to the occurrence and development of hypertension.
(2) Chronic Inflammation And Oxidative Stress
Repeated hypoxia-reoxygenation process can trigger systemic inflammatory response and oxidative stress, damage vascular endothelial function, promote arteriosclerosis, and thus aggravate hypertension.
(3) Chemoreflex Disorder
Chemoreflex is an important regulator of sympathetic nerve excitability. Peripheral chemoreceptors located in the carotid body respond to hypoxia, and central chemoreceptors located in the brainstem respond to hypercapnia. The stimulation of both hypoxic and hypercapnic chemoreflexes can cause hyperventilation and sympathetic nerve excitation.
It has been demonstrated that patients with sleep apnea have increased peripheral chemoreflex sensitivity, and the tonic activity of the chemoreflex helps explain the high levels of sympathetic excitability seen in patients with sleep apnea even during daytime wakefulness in the absence of hypoxia.
Sleep apnea patients have abnormal chemoreceptive reflex function. When hypoxemia occurs, ventilation, sympathetic nerve activity, heart rate, and blood pressure responses are all enhanced in sleep apnea patients. Therefore, abnormal chemoreflex function may be one of the potential mechanisms for the formation of hypertension in sleep apnea patients.
(4) Intermittent Hypoxia
When sleep apnea occurs, the blood oxygen level of patients drops sharply. In response to the lack of oxygen, the body releases a large amount of catecholamines (such as adrenaline), which causes vasoconstriction and increased heart rate. Long-term effects can cause high blood pressure. In addition, hypoxia can also activate the renin-angiotensin-aldosterone system (RAAS), further promoting water and sodium retention and increased vascular resistance.
The relationship between sleep apnea and RAAS is very complex and still unclear. Animal studies have shown that acute hypercapnia and hypoxia can increase plasma aldosterone concentration and plasma renin activity, respectively. Moreover, the simultaneous presence of the two can further increase plasma aldosterone concentration and plasma renin activity.
Single nighttime continuous positive airway pressure therapy for patients with severe sleep apnea can reduce nocturnal plasma renin activity and aldosterone concentrations. Further studies have shown that CPAP treatment of 11 sleep apnea patients with poorly controlled blood pressure had a significant decrease in plasma aldosterone concentrations after 3 months.
The study found that compared with the group without sleep apnea, the group of patients with sleep apnea had a higher body mass index and 24-hour urine aldosterone levels, accompanied by low renin levels. For hypertensive patients with sleep apnea, aldosterone secretion can be stimulated without renin and angiotensin.
In summary, sleep apnea is closely related to hypertension, and there are many mechanisms involved in the formation of hypertension in patients with sleep apnea.
3. Sleep Apnea And Hypertension: Their Interaction
Abnormal nocturnal blood pressure pattern: Patients with sleep apnea often show a rise in blood pressure at night (non-dipper hypertension), and this pattern is significantly associated with the risk of cardiovascular and cerebrovascular events.
Refractory hypertension: If the patient’s hypertension is difficult to control with medication, be alert to the possibility of concurrent sleep apnea. Studies have shown that about 80% of patients with refractory hypertension have moderate to severe OSA.
Vicious cycle: High blood pressure itself may also worsen sleep apnea. For example, the reduced heart function caused by high blood pressure may exacerbate nighttime breathing disorders.
4. Diagnosis And Treatment
(1) Identification Of High-risk Groups
If there are conditions such as snoring, daytime sleepiness, obesity (BMI ≥ 30), thick neck circumference (male ＞ 43cm, female ＞ 40cm), etc., polysomnography (PSG) is recommended to confirm the diagnosis.
(2) Targeted treatment
Continuous positive airway pressure (CPAP): It is the first-line treatment for OSA and can effectively improve hypoxia and sleep structure and lower blood pressure. Studies have shown that regular use of CPAP can reduce systolic blood pressure by an average of 2-3 mmHg and diastolic blood pressure by 1.5-2 mmHg.
Lifestyle intervention: weight loss, smoking cessation, alcohol restriction, side-lying sleeping, etc.
Lose weight: Studies have shown that losing 5-10% of your body weight can significantly improve apnea symptoms and lower blood pressure.
Improve sleeping posture: Sleeping on the side is usually more helpful in reducing the incidence of apnea than lying on the back.
Avoid alcohol and sedatives: These substances can worsen apnea and high blood pressure.
(3) Drug Combination Therapy
For patients with hypertension, RAAS inhibitors (such as prils or sartans) or calcium channel blockers are preferred.
5. Prevention And Long-term Management
Regular screening: Hypertensive patients should proactively screen for sleep apnea, especially young people or those with refractory hypertension.
Multidisciplinary collaboration: Joint diagnosis and treatment between the cardiovascular and respiratory departments can improve blood pressure control rate and reduce the risk of complications such as heart failure and arrhythmia.
Long-term follow-up: Even if blood pressure is stable, the severity of sleep apnea should be assessed regularly to avoid recurrence of the disease.
