Depending on the severity of OSAHS, clinicians should choose different treatment methods.
The first is based on lifestyle improvement (e.g., weight loss, smoking, alcohol, tea, coffee, sedative-hypnotic drugs, lateral sleep, etc.); mild patients can use oral orthodontic appliances; moderate to severe patients can be treated with continuous positive airway pressure ventilation.
Clinical diagnosis: according to the degree of the disease is divided into three levels
The diagnosis of obstructive sleep apnea hypoventilation syndrome (OSAHS) is based on history, signs and polysomnography (PSG) results. OSAHS can be classified as mild, moderate or severe according to the apnea hypoventilation index (AHI) and nocturnal arterial oxygen saturation (SaO2) (Table 1). The AHI was used as the main judgment criterion, and the nocturnal minimum SaO2 was used as the reference criterion.
Comprehensive assessment: laboratory and sleep monitoring
Routine examination
The physical examination of patients included blood pressure, neck circumference, jaw morphology, nasopharyngeal and laryngeal examination, and heart, lung, brain and nervous system examination. Laboratory tests include routine blood work, arterial blood gas analysis, lipids, glucose and thyroid function. x-ray cephalometry can show the plane of upper airway obstruction. Pulmonary function tests are performed to assess ventilation dysfunction in the setting of concurrent pulmonary heart disease and respiratory failure. Electrocardiogram and echocardiogram may reveal abnormalities such as ventricular hypertrophy, myocardial ischemia or arrhythmias.
Evaluation of the degree of drowsiness
First, the Epworth Sleepiness Scale is mostly used for subjective evaluation.
Second, objective evaluation should be performed with the PSG to objectively assess daytime sleepiness in suspected patients. Multiple sleep latency test: To objectively determine the degree of somnolence by having the patient take a series of naps during the day. The frequency of the test is once every 2 h, and the duration of each sleep is about 30 min. The average latency of sleep and the number of abnormal fast-acting phase sleeps are calculated, and sleep latency <5 min is considered narcolepsy; 5-10 min is considered suspected; >10 min is considered normal.
Initial screening diagnostic instrument examination
Most of them are portable, such as simple oxygen saturation monitoring, oral and nasal airflow + oxygen saturation, oral and nasal airflow + snoring + oxygen saturation + chest and abdominal movements, etc. They are suitable for patients with mild disease who lack PSG monitoring conditions at the primary level or cannot be examined in the sleep monitoring room due to changes in sleep environment or too many leads, and are used for OSAHS initial screening, efficacy evaluation and follow-up.
Polysomnography
Polysomnography is the standard method for diagnosing OSAHS and is used in patients with clinical suspicion of OSAHS, such as unexplained daytime hypoxemia or erythrocytosis, unexplained nocturnal arrhythmias, nocturnal angina, early morning hypertension; it is also used to diagnose other sleep disorders and to monitor the degree of hypoxia during nighttime sleep to evaluate the efficacy of OSAHS.
Nocturnal segmental monitoring is performed during the first 2–4 h of the same night with PSG monitoring, followed by 2–4 h of continuous positive airway pressure (CPAP) pressure adjustment. It is recommended in cases of AHI >20 breaths/h, recurrent prolonged sleep apnea or hypoventilation with severe hypoxemia;
CPAP pressure tuning for >3 h due to increased FTI sleep in late sleep; CPAP pressure completely eliminates all apnea, hypoventilation and snoring in FTI and non-FTI sleep when the patient is in the flat position. If these conditions are not met, PSG monitoring should be performed overnight and CPAP pressure should be adjusted overnight.
Afternoon nap monitoring can be used in patients with significant daytime sleepiness and usually requires 2–4 h of sleep to meet the diagnostic requirements; this method has a certain failure rate and false positive results.
Multisystem damage in OSAHS
Hypertension
The Seventh Report on Hypertension in the United States lists OSAHS as the leading cause of secondary hypertension. Data from 20 hospitals in China showed that the prevalence of hypertension in OSAHS patients was 49.3%, and that the prevalence of hypertension increased with increasing AHI.
Intermittent hypoxia in OSAHS patients stimulates carotid chemoreceptors and causes post-apnea sympathetic nervous system excitation, leading to blood pressure fluctuations. Intermittent hypoxia also directly damages the vascular endothelium, activates the renin-angiotensin-aldosterone system, initiates inflammation and oxidative stress, and accelerates target organ functional damage and apoptosis.
The rapid increase in negative intrathoracic pressure during apnea increases the transmural gradient in the atria, ventricles, and aorta, and causes a rapid increase in return blood volume and elevated blood pressure. Long-term chronic effects can cause hypertrophy of vascular smooth muscle, resulting in increased blood pressure during sleep and after waking at night. 24-h non-arytenoid and anti-arytenoid blood pressure changes and nocturnal hypertension are common in patients with OSAHS.
Coronary heart disease
The risk of coronary heart disease is 1.2- to 6.9-fold higher in patients with OSAHS than in the normal population, and moderately severe (AHI ≥ 20 beats/h) OSAHS is an independent risk factor for coronary heart disease, and AHI is an independent predictor of death from coronary heart disease. The 5-year mortality rate was 24.6% higher in patients with coronary artery disease combined with OSAHS than in the control group. CPAP treatment for patients with OSAHS can help reduce the morbidity and mortality of patients with coronary heart disease and improve the prognosis.
Possible mechanisms of OSAHS-induced coronary heart disease.
(1) Onset of hypoxia and hypercapnia;
(2) Intermittent hypoxia and ischemia-reperfusion induced oxidative stress;
(3) Decrease in SaO2 stimulates renal secretion of erythropoietin and causes an increase in blood viscosity;
(4) OSAHS patients are in a pre-thrombotic state;
(5) Increase in endothelin-1, a blood vasoconstrictor, and decrease in nitric oxide, a vasodilator;
(6) Activation of inflammatory factors affects lipid metabolism.
Cardiac arrhythmias
Almost all types of arrhythmias can be observed in patients with OSAHS, especially the incidence of slow arrhythmias and sudden cardiac death is significantly higher. Arrhythmias tend to occur at night and correlate with the severity of OSAHS. It is believed that autonomic disorders, inflammatory responses and oxidative damage, which affect sinus node and atrioventricular conduction function, are the main causes of bradyarrhythmias in OSAHS patients. Slow arrhythmias increase blood viscosity and slow blood flow, which predispose to cardiac emergencies.
Studies suggest that patients with atrial fibrillation combined with OSAHS have a recurrence rate more than two times higher after ablation than patients without sleep apnea. In addition, persistent hypoxemia, hypercapnia, sympathetic hyperexcitability and left atrial traction may create new lesions and lead to AF recurrence. OSAHS is an independent predictor of AF recurrence, and treatment with CPAP may reduce the risk of AF recurrence.
Chronic heart failure
In patients with chronic heart failure, sleep apnea is highly prevalent and can precipitate and exacerbate chronic heart failure. Central sleep apnea is most often seen in patients with chronic heart failure.
The mechanism by which OSAHS and central sleep apnea affect chronic heart failure: increased negative intrathoracic pressure increases left ventricular transmural pressure and increases left ventricular afterload; increased venous return blood volume increases right ventricular internal diameter, leftward septal shift prevents left ventricular filling and decreases left ventricular compliance, resulting in reduced preload; decreased cardiac output per beat, decreased oxygen supply, and increased myocardial ischemia, which can trigger or worsen chronic heart failure in the long term. chronic heart failure.
The increased sympathetic excitability and peripheral vasoconstriction in sleep apnea patients; and the increase in cardiac output after the termination of apnea increases the peripheral vascular resistance, causing a sudden rise in blood pressure and an increase in heart rate, which increases the burden on the heart and increases myocardial oxygen consumption. The sustained sympathetic excitation promotes the release of catecholamines, accelerating myocardial remodeling and inducing arrhythmias.
Stroke
OSAHS is an independent risk factor for stroke, and the detection rate of central sleep apnea in stroke patients is about 7%. The study showed that patients with OSAHS had 4.33 times more ischemic strokes and 1.98 times more deaths than controls; the proportion of stroke patients with OSAHS was also significantly higher and increased the severity of OSAHS. Follow-up of 106 elderly patients with moderate-to-severe OSAHS found that the use of CPAP for sleep apnea in conjunction with treatment of the underlying disease in this group reduced the risk of cardiovascular and cerebrovascular events, thereby improving prognosis.
Respiratory system
There is a lack of large-scale epidemiological studies on the incidence of pulmonary hypertension in patients with OSAHS, but a 2009 study found that the incidence of pulmonary hypertension in patients with mild to moderate OSAHS combined with moderate airflow limitation was 70%, with approximately 33% of these patients having severe pulmonary hypertension, and that mortality was significantly higher in patients with OSAHS with combined pulmonary hypertension.
Pulmonary hypertension in OSAHS may be associated with intermittent hypoxia, obesity, high endothelin-1 expression, endothelial dysfunction, mechanical effects of forceful breathing, and the constrictor reflex due to repeated nocturnal awakenings. Treatment of OSAHS can improve patients’ clinical symptoms and effectively reduce pulmonary artery pressure and pulmonary vascular resistance.
The prevalence of asthma in patients with OSAHS is 35.1%, while 37% of asthmatic patients have habitual snoring and 40% have high OSAHS possibility, and their OSAHS incidence is related to the severity of asthma. disorders of coagulation mechanism and vascular endothelial damage in OSAHS patients lead to increased occurrence of pulmonary embolism. Patients with OSAHS in combination with COPD have more severe hypoxemia and hypercapnia, predispose to pulmonary hypertension, increased inflammatory status, and increased morbidity and mortality.
Metabolic abnormalities
The incidence of OSAHS is significantly higher in patients with metabolic syndrome, and the incidence of increased fasting glucose, insulin resistance and diabetes is much higher in patients with OSAHS than in the healthy population. Studies have shown that OSAHS is independently associated with insulin resistance. Dyslipidemia is prevalent in the OSAHS population. Studies have confirmed that hyperlipidemia in OSAHS patients is associated with AHI, duration of apnea, nocturnal SaO2, and the degree and duration of reduction.
Digestive
Surveys have shown that 50 -76% of OSAHS patients have gastroesophageal reflux and that reflux symptoms are significantly reduced in OSAHS patients treated with CPAP. Also, OSAHS can cause hypoxic liver damage.