Sleep Apnea Syndrome in the Elderly
Introduction
Introduction to sleep apnea syndrome in the elderly Sleep apnea syndrome (SAS) is the second largest sleep disorder after insomnia, causing severe hypoxemia and sleep disorders, and hypertension, arrhythmia, cardiovascular and cerebrovascular diseases and respiratory failure. The occurrence of the disease is closely related. A small number of patients can be killed at night. In addition, due to daytime sleepiness, impaired memory and responsiveness, the patient's ability to work decreases, and the incidence of accidents increases. For this reason, SAS has become an emerging edge discipline - an important part of sleep medicine, and has received increasing attention from the medical community at home and abroad. In recent years, with the wide application of non-invasive ventilation technology, the treatment of SAS has also made breakthrough progress. basic knowledge The proportion of illness: 1% - 4% (the prevalence rate of the elderly over 60 years old is about 1% - 4%, mostly due to obesity) Susceptible people: the elderly Mode of infection: non-infectious Complications: Hypertension, Arrhythmia
Cause
The cause of sleep apnea syndrome in the elderly
Central sleep apnea syndrome (30%):
Intrinsic is mainly caused by abnormalities in respiratory regulation disorders. Respiratory regulation abnormalities can occur in the following diseases: cerebrovascular accident, neurological lesions, anterior spinal cordectomy, vascular embolism or degenerative lesions caused by bilateral spinal cord lesions, familial Autonomic abnormalities, insulin-related diabetes, encephalitis, other diseases such as muscles, occipital macropore developmental malformations, poliomyelitis, congestive heart failure, etc.
Obstructive sleep apnea syndrome (30%):
The main causes are upper airway stenosis during sleep, active upper airway contraction stenosis caused by abnormal reflex, etc. Obesity is often narrowed in the upper airway, and upper airway lesions associated with obstructive sleep apnea are also nasal structures. Abnormalities, hypertrophy of the pharyngeal wall, tonsil hypertrophy, acromegaly, giant tongue, congenital small jaw deformity, abnormal structure of the pharynx and larynx.
Anatomical stenosis of the upper respiratory tract (15%):
Due to the anatomical narrowing of the upper respiratory tract, the muscles are relaxed during sleep, and the negative pressure of the chest is increased during inhalation, and the lingual wall of the tongue is attached to the pharyngeal wall to occlude the upper respiratory tract.
Upper respiratory diastolic muscle group is less excitatory due to sleep (10%):
Regardless of the intrapleural pressure during inhalation, airway occlusion caused by decreased excitability during sleep in the upper respiratory diastolic muscle group.
Coordination of coordination between upper respiratory diastolic muscle groups (10%):
Airway occlusion is caused by uncoordinated coordination between the upper respiratory diastolic muscle groups.
Pathogenesis
1. The predisposing factors and mechanism of obstructive sleep apnea
Sleep apnea is not an independent disease, but a common pathological manifestation of multiple lesions. Its occurrence is the result of a combination of factors (Table 1). A comprehensive understanding of these predisposing factors can help guide further treatment. For example, for some patients with upper airway anatomical stenosis (Table 2), surgical treatment may be effective.
The key to the occurrence of OSA is the collapse of the pharyngeal airway during sleep. The obstruction of the airway can be in the nasopharynx, oropharynx or throat, and more than 80% of the patients have a joint obstruction of the oropharynx and the throat and throat. The causes of occlusion are both anatomical and functional, and they all play a role by increasing the collapsibility of the pharyngeal airway and affecting the strength of its opening and closing.
The pharyngeal airway lacks the support of bony or cartilage structure. It is a soft tube composed of muscles and has collapsibility. OSA patients have anatomical and functional defects due to the pharyngeal airway itself, combined with obesity and edema. The collapse is further increased, and the main force causing the pharyngeal airway to close is the negative pressure in the pharyngeal airway, which is caused by the contraction movement of the diaphragm and other respiratory muscles during inhalation; the activity of the pharyngeal dilator muscle, which is dominated by the genioglossus, is against the pharynx. Negative pressure in the lumen maintains the main force of upper airway opening. After falling asleep, the respiratory center is driven to decrease, the activity of the pharyngeal dilator muscle is weakened, and the upper airway resistance is increased. When the respiratory drive drops to a certain level, the diaphragm muscle and other inspiratory muscles are produced. The negative pressure of the pharyngeal cavity predominates. When the critical pressure of the pharyngeal airway wall can be exceeded, the balance of the force that maintains the opening and closing of the airway is broken, the airway collapses, and the OSA occurs, during the OSA. The blood oxygen gradually decreases, the CO2 gradually increases, and the negative pressure in the pharynx increases. They all cause the brainstem activation system by stimulating the corresponding chemical and baroreceptors. Temporary awakening, air recovery, the end of OSA, such as sensitivity to chemical receptors decreased baroreceptor reflex inhibition, respiratory muscle dysfunction and alcohol, narcotics, sedative hypnotics can be caused by the awakening of the ability to reduce and prolong the duration of OSA.
2. The etiology and mechanism of central sleep apnea
When central sleep apnea occurs, the central respiratory drive is temporarily lost, the airflow and respiratory movements of the chest and abdomen are all disappeared, the intrathoracic pressure is zero, and the relationship between CSA and respiratory control dysfunction is clear.
Cheyne-Stokes respiration and periodic breathing are common types of CSA, mostly in NREM sleep I, II stage, seen in patients with cardiac insufficiency and early entry into the plateau, and high CO2 response in the respiratory center after falling asleep. Sexual decline, that is, the response threshold increased, PaCO2 was not enough to stimulate breathing, CSA appeared; PaCO2 gradually increased with the prolongation of SA time, after the response threshold was reached, the patient experienced a brief awakening, respiratory recovery, and the central high CO2 response threshold As a result, higher PaCO2 levels cause hyperventilation, PaCO2 drops to a lower level, and after re-sleeping, CSA reoccurs, recurring, and repeated cycles (Figure 2), which shows that the respiratory center is high CO2 during sleep. The worse the sensitivity of hypoxia, that is, the higher the reaction threshold, the more likely CSA occurs; the more awakening after falling asleep, the more unstable the respiratory control function, the more likely CSA occurs; in NREM sleep I, II, due to shallow sleep It is prone to wakefulness, so CSA is prone to occur; as sleep deepens, it enters NREM III, IV sleep period. The number of awakenings decreases, respiratory regulation tends to be stable, CSA times decrease, and REM sleeps. Period, adjustable function still plays a role in breathing dependence on chemical regulation relief, CSA also a decreasing trend.
3. Pathophysiology
Frequent SA can cause severe blood gas abnormalities and sleep disorders, which affect the various systems of the body. In recent years, the damage caused by SA caused by autonomic nervous system dysfunction has also attracted extensive attention.
Prevention
Elderly sleep apnea syndrome prevention
Change sleep, eating habits: take the side to sleep, dinner should not be full, quit smoking, alcohol, weight loss, avoid taking sedatives.
Complication
Complications of sleep apnea syndrome in the elderly Complications, hypertension, arrhythmia
Complications such as hypertension, right heart dilatation, bradycardia, arrhythmia, polycythemia, and sexual dysfunction.
Symptom
Symptoms of sleep apnea syndrome in the elderly Common symptoms Sleepiness, sleep, apnea, snoring, snoring, shortness, sleepiness, insomnia, depression, libido, lack of deep sleep
The clinical symptoms of SAS patients are complex and diverse, and the severity is different. Many patients have no discomfort during the day. In addition to the clinical symptoms directly related to SA itself, multiple systemic damage caused by SA can also cause corresponding clinical symptoms.
The most important clinical symptoms are sleep snoring, frequent respiratory arrest and daytime sleepiness. Snoring is one of the most typical symptoms of SAS. The patient's snoring is loud and irregular, intermittent and intermittent, and the sound is high and low. As a "resuscitative snoring", frequent sleep apnea is often found by the patient's spouse. This phenomenon is more than 90% accurate for moderate to severe patients, regardless of time, location, irresistible Falling asleep is a manifestation of severe SAS and is one of the main reasons for patients to see a doctor.
Sleep apnea has a wide-ranging effect on the cardiovascular system. SAS is a risk factor for hypertension other than obesity, age, etc. It is an important cause of secondary hypertension. Arrhythmia is very common in SAS patients. The main causes of such patients are prone to sudden death, the most common are sinus arrhythmia (including sinus bradycardia, tachycardia, sinus block and sinus arrest), followed by room, ventricular premature contraction, once ~ Second degree atrioventricular block and ventricular tachycardia, the prevalence of ischemic heart disease in SAS patients increased, and with the severity of SAS, often caused myocardial deficiency in known or potential ischemic heart disease Increased blood, angina pectoris, myocardial infarction, malignant arrhythmia or deterioration of heart function, 10% to 20% of patients with SAS have pulmonary hypertension, with chronic obstructive pulmonary disease, the performance is more obvious, and even right heart failure , SA is also an independent risk factor for cerebrovascular disease.
Long-term sleep apnea, shortness of breath during daytime activities may be a manifestation of insufficient alveolar ventilation. Loss of libido and impotence are not uncommon in male patients with severe SAS; SA can cause sleep disturbance and decrease in growth hormone secretion. The performance is particularly obvious, which can seriously affect the growth and development of children. The near memory of patients with severe SAS is decreased, attention, concentration, understanding, personality and behavioral abnormalities are not uncommon. These seriously affect the work, study and life of patients. In addition to affecting their own health, they will also cause certain harm to families and society due to traffic accidents and work injuries.
The incidence of SA in neonates, especially premature infants is very high. Pathological SA may be related to sudden infant death syndrome (SIDS). The causes of SAS patients are mostly sleepy, poor academic performance, and excitement. Irritability, abnormal behavior during the day, snoring, abnormal nighttime sleep movements and enuresis are also common, growth retardation is very prominent in severely ill children, elderly SAS patients with increased insomnia as the main complaints, due to more combined with other diseases, SAS symptoms are often atypical.
CSA can also cause repeated hypoxia and sleep disorders. The pathophysiological changes are the same as OSAS, but CSAS is less obese, snoring, daytime sleepiness and sexual dysfunction are light, insomnia is easy to wake up, and there may be depressive symptoms.
Examine
Examination of sleep apnea syndrome in the elderly
Those who are suspected of insufficient ventilation during the day or who have difficulty breathing may have blood tests and blood gas analysis.
Head X-ray examination
The degree of abnormalities of the maxillofacial region can be quantitatively understood. Nasopharyngoscopy can help to evaluate the degree of anatomical abnormalities of the upper airway. It is helpful for considering the surgical treatment. The thyroid hormone level can be determined by suspected hypothyroidism. In patients with respiratory failure, blood stasis, blood gas analysis and pulmonary function tests, dynamic electrocardiogram findings, sleep arrhythmia or heart rate fluctuations in sleep state, often suggest the possibility of SAS.
2. Sleep respiration monitoring
With the help of your spouse and your family, you can get a basic understanding of the patient's sleep and breathing by carefully asking about your medical history and systematic examination. Provide a diagnosis clue about SAS, suggest possible causes and complications, and initially determine the severity, but finally To establish or exclude the diagnosis, a polysomnograph (PSG) should be used in the sleep center for sleep breathing monitoring. The monitoring signals include the following three aspects:
1 sleep conditions: EEG, eye movements and genioglossus EMG.
2 Respiratory conditions: nose and mouth airflow, chest and abdomen respiratory movements and dynamic SpO2 monitoring.
3 ECG, if necessary, can simultaneously monitor ambulatory blood pressure, esophageal pressure, snoring, leg movement and body position changes. In recent years, traditional paper records have been gradually replaced by computerized data collection, storage and analysis systems, family, disease The simple primary screening device at the bedside has also been applied even through remote center working system remote monitoring. Because PSG is expensive, and some patients have difficulty sleeping in different places, nighttime SaO2 dynamic monitoring can be used as a screening.
Diagnosis
Diagnosis and diagnosis of sleep apnea syndrome in the elderly
Diagnostic criteria
1. Diagnostic criteria
SAS can be diagnosed with SA for more than 30 times or more than 5 times per hour with 7 hours of sleep all night, and the corresponding clinical symptoms can be improved with SA reduction after non-invasive ventilation treatment. Establish a diagnosis.
2. Diagnosis method
In addition to routine physical examination, SAS patients should pay attention to the following aspects. Obesity is one of the predisposing factors of SA. The risk is 4 times of gender and 2 times of age. The neck circumference reflects the upper airway caliber during sleep. And the indicators with strong functional specificity, upper airway anatomy and stenosis accompanied by poor sleep and daytime sleepiness, often suggesting the presence of SA, and the possibility of surgery, combined with the presence of cardiopulmonary disease can cause hypoxemia and respiratory regulation Unstable, induced SA, lip cyanosis, lower extremity edema can be seen in concurrent alveolar ventilatory during the day, measuring blood pressure before and after waking, help to understand the relationship between hypertension and SAS, such as signs of hypothyroidism in physical examination, need further an examination.
Differential diagnosis
SAS can affect various systems of the whole body. The clinical manifestations during the day are complex and diverse, lacking specificity, and easily misdiagnosed as diseases of other systems, such as neurosis, heart disease, and avoiding misdiagnosis. The key to missed diagnosis is to strengthen sleep-disordered breathing disorders. The understanding that daytime sleepiness is one of the most prominent symptoms of SAS, and it is also the main reason for patients to see a doctor, should be identified.
