Sleep apnea hypoventilation syndrome (SAHS) Sleep apnea hypoventilation syndrome is a clinical syndrome in which various causes lead to recurrent apnea and/or hypoventilation, hypercapnia, and sleep disruption during the sleep state, resulting in a series of pathophysiological changes in the organism.
Definition and classification.
(A) Definition: Sleep apnea hypoventilation syndrome is defined as recurrent episodes of apnea more than 30 times per night during sleep or sleep apnea hypoventilation index (AHI)” = 5 times/hour and accompanied by clinical symptoms such as drowsiness. Apnea is defined as the complete cessation of nasal and oral airflow for more than 10 seconds during sleep; hypoventilation is defined as a decrease in the intensity (amplitude) of respiratory airflow by more than 50% compared to the basal level during sleep, accompanied by a decrease in oxygen saturation by 4% compared to the basal level or micro-awakening;
Sleep apnea hypoventilation index refers to the number of apnea plus hypoventilation per hour of sleep time.
(II) Classification: Central (CSAS) Obstructive (OSAS) Mixed (MSAS)
Epidemiology.
In OSAHS, for example, in people over 40 years of age, the prevalence is 2%-4% in the United States, with more men than women and a higher prevalence 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.
(A) Central sleep apnea syndrome (CSAS)
CSAS alone is less common and generally does not exceed 10% of apnea patients, and only 4% has been reported. The ventilation can be further divided into two categories: hypercapnia and normocapnia. It can coexist with obstructive sleep apnea ventilation syndrome and most have neurological or motor system lesions. The pathogenesis may be related to the following factors: reduced responsiveness of the respiratory center to different stimuli during sleep; instability of the respiratory feedback regulation of the central nervous system to hypoxemia, especially due to changes in CO2 concentration; abnormal expiratory and inspiratory conversion mechanisms, etc.
(B) Obstructive sleep apnea hypoventilation syndrome (OSAHS)
OSAHS accounts for the majority of SAHS, with family clustering and genetic factors, and most of them have pathological basis of narrowing of the upper airway, especially the nasal and pharyngeal areas, such as obesity, allergic rhinitis, nasal polyps, tonsillar hypertrophy, soft palate relaxation, excessive length and thickness of the palatal lobe, tongue hypertrophy, tongue root backward, 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, the reduced responsiveness of the upper airway muscles to the stimulation of low oxygen and carbon dioxide during sleep, and, in addition, the combined effect of neurological, humoral and endocrine factors.
Clinical manifestations.
(a) Daytime clinical manifestations.
1, drowsiness: the most common symptom, the milder manifestations of 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 apnea and hypoxemia at night, the sleep continuity is interrupted, the number of awakenings increases, and the quality of sleep decreases, often with mildly different dizziness, fatigue and 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, hypogonadism: about 10% of patients may have hypogonadism 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-panting-snoring, generally the time of airflow interruption is 20-30 seconds, individually up to 2 minutes or more, at which time the patient may appear obvious cyanosis.
2.Apnea: 75% of the co-sleepers in the same room or bed found that the patient had apnea and often pushed the patient awake for fear that the breathing could not be restored. apnea mostly terminated with gasping, holding awake or loud snoring. patients with OSAHS had obvious thoraco-abdominal contradictory breathing.
3.Wake up with suffocation: sudden wake up with suffocation after apnea, often accompanied by turning over, involuntary movement of 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 rotate more frequently at night.
5, hyperhidrosis: sweating is more frequent, obvious in the neck and upper chest, related to hypercapnia caused by respiratory effort and apnea after airway obstruction.
6.Nocturia: Some patients complained of more frequent urination at night, and individual urine loss.
7, abnormal sleep behavior: manifested as fear, shrieking, murmuring, nocturnal wandering, hallucinations, etc.
(C) Manifestations of systemic organ damage.
OSAHS 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.
2, coronary heart disease: manifested as various types of arrhythmias, nocturnal angina pectoris and myocardial infarction. It is caused by endothelial damage of coronary arteries caused by hypoxia, lipid deposition in the intima, and increased blood viscosity due to erythrocyte increase.
3, Various types of arrhythmias.
4.Pulmonary heart disease and respiratory failure
5, Ischemic or hemorrhagic cerebrovascular disease
6, mental abnormalities: such as manic psychosis or depression
7, diabetes mellitus
(iv) Signs: CSAS may have corresponding signs of the primary disease, and patients with OSAHS may have obesity, nasal turbinate hypertrophy, etc.
Laboratory and other tests.
(i) Blood tests: In prolonged illness and severe hypoxemia, there may be varying degrees of increase in blood red blood cell count and hemoglobin.
(I) Blood tests: In those with prolonged illness and severe hypoxemia, hemoglobin and hemoglobin may be increased to varying degrees.
(B) Arterial blood gas analysis: In severe disease or combined with pulmonary heart disease and respiratory failure, there may be hypoxemia, hypercarbia and respiratory acidosis.
(C) 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.
(iv) Pulmonary function tests: In severe cases with pulmonary heart disease and respiratory failure, there are different degrees of ventilation dysfunction.
(v) Electrocardiogram: In the presence of hypertension, coronary artery disease, there are changes such as ventricular hypertrophy, myocardial ischemia or arrhythmia.
Diagnosis.
Based on typical clinical symptoms and signs, it is not difficult to diagnose SAHS. To confirm the diagnosis and to understand the severity and type of the disease, corresponding examinations are required.
(I) Clinical diagnosis: The preliminary clinical diagnosis can be made based on the patient’s snoring during sleep with apnea, daytime drowsiness, body obesity, thick neck circumference and other clinical symptoms.
(ii) Polysomnography: PSG monitoring is the gold standard for confirming the diagnosis of SAHS, and can determine its type and severity.
(iii) Etiological diagnosis: Ear, nose and throat and oral examination are routinely performed for confirmed SAHS to understand the presence of local anatomical and developmental abnormalities, hyperplasia and tumors. Head and neck radiographs, CT and MRI to determine the cross-sectional area of the oropharynx can be used for localization of stenosis. Determination of the endocrine system can be performed in some patients.
Differential diagnosis.
(A) Simple snoring: there is obvious snoring, PSG examination is not consistent with the diagnosis of upper airway resistance syndrome, there is no apnea and hypoventilation, and there is no hypoxemia.
(I) Simple snoring: there is obvious snoring, PSG examination is not consistent with the diagnosis of upper airway resistance syndrome, there is no apnea and hypoventilation, and there is no hypoxemia.
(ii) Upper airway resistance syndrome: increased airway resistance.
(iii) Episodic sleeping sickness: excessive daytime sleepiness with sudden collapse during episodes. There is a family history.
Treatment.
(i) Treatment of central sleep apnea syndrome.
1, treatment of the original disease: such as neurological diseases, treatment of congestive heart failure, etc.
2, respiratory excitatory drugs: mainly to increase the driving force of the respiratory center and improve apnea and hypoxemia. Medication: amitriptyline (50mg, 2-3 times/day), acetazolamide (125-250mg, 3-4 times/minute or 250mg at bedtime) and theophylline (100-200mg, 2-3 times/day)
3.Oxygen therapy: It can correct hypoxemia, reduce the number of apnea and hypoventilation in patients with secondary congestive heart failure, and may aggravate hypercapnia in neuromuscular diseases, but may aggravate obstructive apnea if combined with OSAHS.
4, adjuvant ventilation therapy: for severe patients, the application of mechanical ventilation can enhance spontaneous breathing, 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 change: sleep in lateral position, 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
4.Surgical treatment.
(1)Nasal surgery
(2)Soft palatopharyngoplasty of palatal lobe
(3)Laser-assisted pharyngoplasty
(4)Cryogenic radiofrequency ablation
(5)Orthognathic surgery