I. Definition
Sleep apnea hypoventilation syndrome is defined as 30 or more recurrent episodes of sleep apnea or sleep apnea hypoventilation index (AHI) ≥5 times/hour during sleep each night with clinical symptoms such as drowsiness. Apnea is the complete cessation of oral and nasal whistling airflow for more than 10 seconds during sleep; hypoventilation is the reduction of whistling airflow intensity (amplitude) by more than 50% compared with the basal level during sleep, and is accompanied by a decrease in oxygen saturation by ≥4% compared with the basal level or micro-awakening; sleep apnea hypoventilation index is the number of apnea plus hypoventilation per hour of sleep time.
II. Classification
1.Central type (CSAS)
2.Obstructive type (OSAS)
3.Mixed type (MSAS)
Epidemiology
In OSAHS, for example, the prevalence is 2%-4% in the United States, more males than females, and higher in the elderly, up to 6.5% in Australia, 4.1% in Hong Kong, 3.62% in Shanghai, and 4.81% in Changchun, China.
Etiology and pathogenesis
Central whistling sleep apnea syndrome (CSAS)
CSAS alone is less common, generally not exceeding 10% of patients with whistling apnea, and only 4% has been reported. The patency can be further divided into two main categories: hypercapnia and normocapnia. It can coexist with obstructive sleep apnea syndrome and most have neurological or motor system pathology. The pathogenesis may be related to the following factors.
1. reduced responsiveness of the whistling center to different stimuli during sleep.
2, instability of the feedback regulation of the central nervous system to whistling caused by hypoxemia and especially by changes in CO2 concentration.
3, abnormalities in the mechanism of whistling and inspiration conversion, etc.
Obstructive whistling sleep apnea hypoventilation syndrome (OSAHS)
The majority of SAHS, with family clustering and genetic factors, most have a pathological basis in the narrowing of the upper whistle tract, especially the nasal and pharyngeal areas, such as obesity, allergic rhinitis, nasal polyps, tonsillar hypertrophy, soft palate relaxation, palatal lobe too long and too thick, tongue hypertrophy, tongue root back, mandibular recession, temporomandibular joint dysfunction and small jaw deformity. Some endocrine diseases can also be combined with the disease. The pathogenesis may be related to the increased collapse of the soft tissues and muscles of the upper airway in the sleep state and the reduced responsiveness of the upper airway muscles to the stimulation of low oxygen and carbon dioxide during sleep, in addition to the combined effect of neurological, humoral and endocrine factors.
III. Clinical manifestations
(A) Daytime clinical manifestations
1, drowsiness: the most common symptom, the lighter the daytime work or study time sleepy, drowsy, serious meal, talk with people can fall asleep, and even serious consequences, such as dozing off while driving lead to traffic accidents.
2, dizziness and weakness: due to repeated whistling pauses at night, hypoxemia, so that the sleep continuity is interrupted, the number of awakenings increases, the quality of sleep decreases, often with mildly different dizziness, fatigue, weakness.
3. Mental behavior abnormalities: inattention, decreased ability to perform fine operations, decreased memory and judgment, inability to perform work when symptoms are severe, and dementia may be manifested in the elderly. The damage of nocturnal hypoxemia to the brain and the change of sleep structure, especially the reduction of deep sleep phase, are the main reasons.
4.Headache: It often appears in the early morning or at night, vague pain is common, not severe, can last 1-2 hours, sometimes need to take painkillers to relieve, related to elevated blood pressure, intracranial pressure and changes in cerebral blood flow.
5, personality changes: irritability, agitation, anxiety, etc., family and social life are affected to a certain extent, due to the gradual emotional distancing from family members and friends, depression may occur.
6.Decreased sexual function: about 10% of patients may have decreased sexual desire or even impotence.
(II) Clinical manifestations at night
1.Snoring: It is the main symptom, the snoring is irregular and of different heights, often alternating snoring – airflow stopping – gasping – snoring, generally the time of airflow interruption is 20-30 seconds, individual up to 2 minutes or more, at this time the patient may appear obvious cyanosis.
2.Pause in inspiration: 75% of the co-sleepers in the same room or bed found that the patient had a pause in inspiration, often fearing that the inspiration could not be restored and pushed the patient awake, the pause in inspiration is mostly terminated with gasping, holding awake or loud snoring. patients with OSAHS have obvious thoraco-abdominal contradictory whistling.
3, suffocating awakening: sudden suffocating awakening after a whistling pause, often accompanied by turning over, involuntary movement of the limbs or even convulsions, or suddenly doing up, feeling panic, chest tightness or discomfort in the precordial area.
4, hyperactivity: due to hypoxemia, patients turn over and turn more frequently at night.
5, hyperhidrosis: sweating is more frequent, evident in the neck and upper chest, and is associated with hypercapnia caused by whistling force and whistling pause after airway obstruction.
6, nocturia: some patients complained of increased urination at night, and individual urine loss.
7, abnormal sleep behavior: manifested as fear, shrieking, murmuring, nocturnal wandering, hallucinations, etc.
(iii) Manifestations of systemic organ damage
Patients often have abnormal manifestations of the cardiovascular system as the first signs and symptoms, which can be an independent risk factor for hypertension and coronary heart disease. 1, hypertension: the incidence of hypertension in patients with OSAHS is 45%, and the treatment effect of antihypertensive drugs is poor.
1, coronary heart disease: manifested as various types of arrhythmias, nocturnal angina and myocardial infarction. The twenty due to hypoxia-induced coronary artery endothelial damage, lipid deposition in the intima, and increased blood viscosity due to increased red blood cells.
2, Various types of arrhythmias.
3, Pulmonary heart disease and whistle failure.
4, Ischemic or hemorrhagic cerebrovascular disease.
5, mental abnormalities: such as manic psychosis or depression.
6, diabetes mellitus.
(D) Physical signs
There may be corresponding signs of the primary disease, and patients with OSAHS may have obesity, nasal turbinate hypertrophy, etc.
V. Laboratory and other tests
1.Blood test: If the condition is prolonged and the hypoxemia is severe, the blood red blood cell count and hemoglobin may be increased to different degrees.
2, arterial blood gas analysis: severe disease or combined with pulmonary heart disease, whistle failure, may have hypoxemia, hypercarbia and whistle acidosis.
3. Chest X-ray examination: In case of complicated pulmonary hypertension, hypertension and coronary artery disease, there may be corresponding symptoms such as enlarged heart shadow and prominent pulmonary artery segment.
4, pulmonary function tests: in severe cases with pulmonary heart disease, whooping failure, there are different degrees of ventilation dysfunction.
5. Electrocardiogram: In case of hypertension and coronary artery disease, there are changes such as ventricular hypertrophy, myocardial ischemia or arrhythmia.
VI. Diagnosis
According to the typical clinical symptoms and signs, it is not difficult to diagnose SAHS, but to confirm the diagnosis and understand the severity and type of the disease, the corresponding examination is required.
1.Clinical diagnosis: The preliminary clinical diagnosis can be made based on the patient’s snoring with inhalation pause during sleep, daytime sleepiness, body obesity, thick neck circumference and other clinical symptoms.
2. Polysomnography: PSG monitoring is the gold standard for confirming the diagnosis of SAHS and can determine the type and severity of the disease.
3. Etiological diagnosis: Ear, nose and throat and oral examination are routinely performed for diagnosed SAHS to understand whether there are local anatomical and developmental abnormalities, hyperplasia and tumor, etc. Head and neck radiographs, CT and MRI to determine the cross-sectional area of the oropharynx can be used to determine the localization of stenosis. Measurement of the endocrine system can be performed in some patients.
VII. Differential diagnosis
1 .Simple snoring: there is obvious snoring, PSG examination is not consistent with the diagnosis of upper airway resistance syndrome, there is no whistling pause and hypoventilation, and there is no hypoxemia.
2 . Upper airway resistance syndrome: increased airway resistance.
3, Episodic sleeping sickness: excessive daytime sleepiness and sudden collapse during episodes. There is a family history.
Treatment
(A) Treatment of central sleep apnea syndrome.
1, treatment of the primary cause: such as neurological diseases, treatment of congestive heart failure, etc.
2, whistling excitatory drugs: mainly to increase the drive of the whistling center, improve the apnea and hypoxemia. Medication: amitraz (50mg, 2-3 times / day), acetazolamide (125-250mg, 3-4 times / min or 250mg at bedtime) and theophylline (100-200mg, 2-3 times / day).
3, oxygen therapy: can correct hypoxemia, in patients secondary to congestive heart failure, can reduce the number of whistling pauses and hypoventilation, for neuromuscular disease may aggravate hypercapnia, but if combined with OSAHS may aggravate obstructive whistling pauses.
4, adjuvant ventilation therapy: in severe patients, the application of mechanical ventilation can enhance voluntary whistling, non-invasive positive pressure ventilation and invasive mechanical ventilation can be used.
(B) treatment of obstructive sleep apnea hypoventilation syndrome
1, general treatment.
(1) weight loss: diet control, drugs and surgery.
(2) sleep position changes: lateral sleep, elevate the head of the bed.
(3) Quit smoking and alcohol, avoid sedatives.
(2) Drug treatment: the effect is not sure. Acetazolamide can be tried. Modafinil has a certain effect on improving daytime sleepiness, and is applied to patients whose sleepiness symptoms do not improve significantly after receiving CPAP treatment.
3.Device treatment.
(1), transnasal continuous positive airway pressure ventilation (CPAP)
Indications.
(1) Patients with AHI ≥ 15 times/hour.
(2) Patients with AHI <15 times/hour, but with obvious symptoms such as daytime drowsiness.
③Patients with failed surgical treatment or recurrence.
④Patients who cannot tolerate other treatment methods.
Contraindications: Coma, pulmonary maculopathy, hemoptysis, pneumothorax and unstable blood pressure.
(2).Bilevel positive airway pressure (BIPAP) treatment.
(3), automatic pressure regulation intelligent (Auto-CPAP) whistler treatment (4) oral appliance (oral appliance, OA) treatment.
Indications.
(1) Simple snoring.
②Patients with mild or moderate OSAHS.
(3) Those who cannot tolerate other treatment methods.
Contraindications: Those who have temporomandibular arthritis or dysfunction should not be taken.
1.Surgical treatment.
(1) Nasal surgery
(2) Soft palate pharyngoplasty with palatal lobe
(3) Laser-assisted pharyngoplasty
(4) Cryogenic radiofrequency ablation
(5) Orthognathic surgery.
Prevention methods
1.Enhance physical exercise and maintain good living habits.
2, avoid smoking and alcohol addiction, because smoking can cause increased symptoms of the whistling tract, drinking alcohol aggravates snoring, nocturnal whistling disorders and hypoxemia. Especially drinking alcohol before bedtime.
3, for obese people, we should actively reduce weight and strengthen exercise. Our experience is to reduce the weight by more than 5-10%.
4.Snoring patients mostly have decreased blood oxygen content, so they are often accompanied by hypertension, heart rhythm disorder, increased blood viscosity and increased heart burden, which may easily lead to the occurrence of cardiovascular and cerebrovascular diseases, so we should pay attention to the monitoring of blood pressure and take antihypertensive substances on time.
5, bedtime sedation, sleeping matter is prohibited, so as not to aggravate the inhibition of the central regulation of the whistle.
6, to take a lateral sleep position, especially the right lateral position is appropriate to avoid the tongue, soft palate, uvula relaxation back during sleep, aggravating the upper airway blockage. A small leather ball can be pasted on the back during sleep, which helps to keep the lateral sleep position mandatory.
7.Patients after surgery should eat mainly soft food, do not eat too hot food. Avoid strenuous activities.