Obstructive sleep apnea syndrome diagnosis and treatment

Obstructive sleep apnea hypoventilation syndrome refers to the patient’s repeated occurrence of apnea and hypoventilation during sleep. Clinically, it may manifest as snoring with irregular snoring, and the patient feels suffocating, even being repeatedly awakened, often accompanied by a series of syndromes such as increased nocturnal urination, morning headache, dizziness and oropharyngeal dryness. Due to the recurrent nocturnal arousal and wake-up response of the cerebral cortex, the normal sleep structure and rhythm are disrupted, sleep efficiency is significantly reduced, daytime drowsiness, memory loss, cognitive function decline and abnormal behavior in severe cases. Recurrent nocturnal apnea and hypoventilation cause chronic intermittent hypoxia, carbon dioxide retention, elevated sympathetic excitability, increased systemic inflammatory response as well as oxidative stress, and inadequate antioxidant capacity, thus triggering or aggravating cardiovascular and cerebrovascular diseases and metabolic disorders, especially type 2 diabetes and insulin resistance. OSAHS is now widely recognized as a systemic disease and an important cause of sudden death and road traffic accidents, making it a serious social problem. At present, the prevalence of OSAHS in China is about 4%, and the actual prevalence may be higher, and with the increasing number of overweight and obese people, the prevalence of this disease will increase accordingly. Although OSAHS is a common disease in urban and rural grassroots units in China, the diagnosis of this disease requires special equipment CC polysomnography (PSG), and the treatment requires non-invasive ventilation technology, so only tertiary hospitals in large and medium-sized cities or some secondary hospitals can provide standardized diagnosis and treatment of this disease, resulting in a large number of patients not being diagnosed and treated in a timely manner, which has caused great harm to people’s health. As a result, a large number of patients are not diagnosed and treated in time, causing great harm to people’s health. At the same time, because the scientific popularization work in this area has not been done widely and deeply enough for a long time, many people mistakenly think that snoring is not a disease and does not need systematic examination and treatment, and even mistakenly think that snoring is a sign of “healthy and blessed”, and the relevant health management departments also lack correct understanding and necessary attention to this disease. In order to further raise the awareness of the general medical personnel and the public about this disease and improve the diagnosis and treatment level of this disease, especially to improve the diagnosis and treatment level of primary medical units, we organized some domestic respiratory experts and invited some primary care respiratory doctors to discuss and formulate the “Guidelines for the diagnosis and treatment of obstructive sleep apnea and hypoventilation syndrome (2011 revised version)” on the basis of the “Guidelines for the diagnosis and treatment of obstructive sleep apnea and hypoventilation syndrome (2011 revised version)”. OSAHS Diagnosis and Treatment Guidelines for Primary Care. Definition of OSAHS-related terms 1.Sleep apnea (SA): the disappearance or significant weakening (≥90% decrease from baseline amplitude) of oral and nasal airflow during sleep, lasting for ≥10 s. 2.Obstructive sleep apnea (OSA): refers to the disappearance of oral and nasal airflow, with chest and abdominal breathing still present. It is the presence of apnea due to upper airway obstruction, but the central nervous system respiratory drive function is normal and continues to send respiratory motor commands to excite the respiratory muscles, so the thoracoabdominal respiratory movement still exists. 3. Central sleep apnea (CSA): The oral and nasal airflow and thoracoabdominal breathing disappear simultaneously. It is caused by the abnormal regulation of the central respiratory nerve function, the central respiratory nerve cannot send effective instructions, the respiratory movement disappears, and the oral and nasal airflow stops. 4, mixed sleep apnea (MSA): refers to 1 apnea process, the beginning of the oral and nasal airflow and thoracoabdominal breathing disappeared at the same time, a few seconds or tens of seconds after the appearance of thoracoabdominal breathing movement, still no oral and nasal airflow. That is, 1 apnea process, first appear central apnea, and then appear obstructive apnea. 5, hypoventilation (hypopnea): ≥ 30% decrease in oronasal airflow from baseline level during sleep with ≥ 4% decrease in blood oxygen saturation (SpO2) for ≥ 10 s; or ≥ 50% decrease in oronasal airflow from baseline level with ≥ 3% decrease in SpO2 for ≥ 10 s. 6, microarousal: non-rapid eye movement (NREM) during sleep lasting 3 EEG frequency changes of more than 3 s, including theta and alpha wave frequencies >16 Hz (excluding spindle wave). 7.Sleep fragmentation: sleep discontinuity due to repeated awakenings. 8.Apnea hypopnea index (AHI): the sum of the average number of apneas and hypoventilation per hour during sleep. 9, OSAHS: more than 30 repeated episodes of apnea and hypoventilation during 7 h of sleep per night, or AHI ≥ 5 times/h. The apnea event is mainly obstructive, with snoring, sleep apnea, daytime sleepiness and other symptoms. 10, complex sleep apnea syndrome (CompSAS) OSAHS patients with obstructive respiratory events cleared during continuous positive pressure ventilation (CPAP) therapy when optimal treatment levels were achieved, but a central apnea index (CAI) ≥ 5 times/h, or tidal breathing ( CSR) was predominant. Main risk factors 1, obesity: body mass exceeds 20% or more of the standard body mass, i.e., body mass index (BMI) ≥ 28 kg/m2. 2, age: prevalence increases with age in adulthood; prevalence increases in women after menopause, and some data show that the prevalence tends to stabilize after age 70. 3, gender: premenopausal prevalence in women is significantly lower than that in men. 4, upper airway anatomical abnormalities: including nasal obstruction (nasal septum deviation, turbinate hypertrophy, nasal polyps and nasal tumors, etc.), degree II or more tonsillar hypertrophy, soft palate relaxation, excessive length or thickness of the uvula, pharyngeal cavity narrowing, pharyngeal tumors, pharyngeal mucosa hypertrophy, tongue body hypertrophy, tongue root backward, mandibular recession and small jaw deformity, etc. 5, Have a family history of OSAHS. 6, Long-term heavy alcohol consumption and/or sedative, hypnotic or muscle relaxant drugs. 7, Long-term smoking can aggravate OSA. 8, Other related diseases: including hypothyroidism, acromegaly, cardiac insufficiency, stroke, gastroesophageal reflux and neuromuscular diseases. Clinical features: snoring and irregular snoring during nighttime sleep, disturbance of breathing and sleep rhythm, repeated apnea and awakening, or the patient may feel breath-holding, increased nocturnal urination, morning headache, dry mouth, obvious daytime drowsiness, memory loss, and in severe cases, psychological, intellectual and behavioral abnormalities; and may be combined with hypertension, coronary heart disease, arrhythmia (especially slow C-fast arrhythmia), heart failure The patient may have hypertension, coronary heart disease, arrhythmia (especially slow C-fast arrhythmia), heart failure, chronic pulmonary heart disease, stroke, type 2 diabetes mellitus and insulin resistance, renal impairment, and non-alcoholic liver damage, and may have progressive body mass increase. Physical examination and routine examination items 1, height, body mass, BMI. 2, physical examination: including blood pressure (before sleep and after waking up blood pressure), neck circumference, assessment of jaw morphology (focus on the presence of jaw recession, jaw deformity), nasal cavity, pharyngeal examination (pay special attention to the presence of pendulous hypertrophy, tonsillar enlargement and its degree), tongue hypertrophy and adenoid hypertrophy, heart, lung, brain, neurological examination, etc. 3. Routine blood tests: especially red blood cell count, red blood cell pressure (HCT), mean red blood cell volume (MCV), mean hemoglobin concentration (MCHC). 4.Arterial blood gas analysis (if necessary). 5.X-ray cephalometric measurements (including pharyngeal measurements) and X-ray chest radiograph (if necessary). 6.Electrocardiogram. 7.Routine examination of etiology or high-risk factors. 8.The corresponding examination of possible comorbidities. 9.Some patients should have their thyroid function checked. Main laboratory tests 1. PSG monitoring: This test can be performed in units where available. Overnight PSG monitoring is the standard means of diagnosing OSAHS, including: EEG (mostly C4A1, C3A2, 01A2 and 02A1 leads), two-lead electrooculography (EOG), electromyography of the mandibular chin (EMG), ECG, oral and nasal respiratory airflow and thoracoabdominal respiratory movements, arterial oxygen saturation, body position, snoring, anterior tibial EMG, etc. Regular generally need to monitor not less than 7h of sleep throughout the night. 2.Primary portable monitoring (PM) examination: also known as home sleeptesting (HST) or sleep monitoring outside the sleep center, is able to record and analyze a number of sleep physiological data at the same time, and convenient to move to the sleep outdoor (hospital ward, emergency room, patient’s home) for sleep medicine research and The technology for sleep medicine research and sleep disease diagnosis. Compared with the standard PSG in the laboratory, it is a simpler and more practical examination method because it either monitors fewer leads or does not require a technician on duty. 3, the evaluation of the degree of sleepiness: the subjective evaluation of sleepiness mainly has Epworth sleepiness scale (ESS) and Stanford sleepiness scale (SSS), now mostly used ESS sleepiness scale.