Sleep-wake response

Introduction Awakening: Refers to a state of alertness, indicating that the individual is mentally and physiologically (mainly in the autonomic nervous system) ready to respond. Inhalation of hypoxia or high CO 2 gas can trigger a sleep wake-up response.

Cause

Sleep can be divided into rapid eye movement (rapid eye-movement REM sleep) and non-rapid eye-sleep (non-rapid-eye-move-ment NREM sleep), which can be further divided into light sleep (I, II) And deep sleep (III, IV).

(1) REM sleep: increased metabolism and brain activity. In addition to the eye muscles and diaphragm muscles, skeletal muscle tensions such as intercostal muscles, inspiratory muscles, and upper airway muscles were significantly inhibited, heart rate and blood pressure were irregular, and ventilatory responses to hypoxia and high CO 2 stimulation were significantly attenuated. The wake-up response was also significantly slow. REM sleep usually lasts 20 to 30 m and repeats every 90 to 120 m.

(2) NREM sleep: metabolism and brain activity are reduced, and electroencephalogram (EEG) shows diffuse slow waves. Heart rate tends to be slow and regular, ventilation is slightly reduced, PaC02 can be increased by 0.27 ~ 0.4kPa (2 ~ 3mmHg). Inhalation of hypoxia or high CO 2 gas can trigger a sleep wake-up response. NREM usually lasts 70 to 100 m, and NREM appears first in normal people's sleep, alternating with REM. REM sleep accounts for about 20% to 25% of total sleep time per night, and NREM accounts for 75% to 80%.

(C) the impact of sleep on the upper airway and thoracic muscle: normal breathing requires a high degree of coordination of respiratory muscle contraction. The upper airway muscle has a certain base tension to keep the airway open. The nerve discharge causes the upper airway muscle to contract before each diaphragm contraction. The contraction of the genioglossus moves the tongue to fix the pharyngeal wall forward, further maintaining the upper airway opening and resisting the trapping effect of the negative pressure in the pharyngeal cavity on the upper airway. Subsequently, the intercostal muscle contraction stabilizes the chest wall, and the diaphragm contraction produces a pleural negative pressure to complete the inhalation.

In the normal NREM sleep phase, the basal tension of the upper airway muscle is reduced, the upper airway diameter is reduced, and the airway resistance is increased, but the discharge phase of the upper airway muscle and the rhythmic contraction of the intercostal muscle remain intact. The base tension of the upper airway muscles, the intercostal muscles, and most of the skeletal muscles is further suppressed during REM sleep. Decreased pharyngeal muscle tone can cause trapping of the upper airway during inhalation. Decreased basal tension of the genioglossus can cause the base of the tongue to shift backwards and the airway to narrow. Decreased intercostal muscle tension can lead to instability of the chest wall during inhalation, resulting in contradictory movements of the chest and abdomen. In the REM sleep phase, the inspiratory phase discharge of the upper airway and intercostal muscle can also be inhibited. When the diaphragm negative pressure increases after the diaphragm contraction, the upper airway trapping tendency and chest wall instability are aggravated.

In addition, REM sleep phase, sleep arousal and external stimuli are mostly inhibited, and more likely to occur ineffective or obstructive ventilation.

an examination

Related inspection

Electrocardiogram polysomnography (PSG) electromyography

The sleep arousal response caused by apnea can occur in all sleep phases, but is usually seen in the NREM light sleep phase II. This is because the wake-up reaction often occurs before deep sleep is reached, resulting in a lack of deep sleep (stages III and IV), and the REM sleep is relatively prolonged. The sleep time after apnea is very short, only 10 to 30 s. Breathing can be normal when sleep wakes up, or it can be snorted due to partial obstruction of the upper airway.

Differential diagnosis

Differential diagnosis of sleep wake-up response:

(1) Obstacle apnea syndrome (OSAS): OSAS is a dominant disease in adult sleep disordered breathing. The diagnosis is based on the presence of no airflow in the upper airway for more than 10 s. Accumulated more than 5 times per h, more than 30 times in 6 hours of sleep per night.

OSAS is mainly found in obese people, and can be associated with congenital and acquired abnormalities of upper airway stenosis caused by hypothyroidism, acromegaly, or tonsils, proliferative gland hypertrophy and small jaw. Most adult OSAS have no obvious anatomical changes, and their pathophysiology has not been fully elucidated. However, it is generally believed that it is associated with decreased airway muscle base tension, loss of upper airway muscle discharge, or discharge and diaphragmatic contraction coordination disorder during sleep time. Abnormal anatomy of the upper airway causes the caliber to be narrowly narrow or the compliance is abnormally increased, and the upper airway is trapped during inhalation, forming OSAS.

The sleep arousal response caused by apnea can occur in all sleep phases, but is usually seen in the NREM light sleep phase II. This is because the wake-up reaction often occurs before deep sleep is reached, resulting in a lack of deep sleep (stages III and IV), and the REM sleep is relatively prolonged. The sleep time after apnea is very short, only 10 to 30 s. Breathing can be normal when sleep wakes up, or it can be snorted due to partial obstruction of the upper airway.

During apnea, although there is no airflow in the upper airway, there is still chest and abdomen breathing exercise, and the chest negative pressure fluctuates greatly, up to 7.8 kPa (80 cmH2O). Due to upper airway trapping, there is little or no external environmental gas entering the alveoli for gas exchange, which can result in severe hypoxemia and C02 retention, progressive bradycardia, and transient tachycardia at the end of the apnea. Occasionally, sinus block, atrioventricular septum, nodular or ventricular escape, hypoxemia-induced acidosis and myocardial ischemia produce atrial and ventricular ectopic rhythm. Severe OSAS patients are accompanied by daytime sleepiness, hypercapnia in waking, and even pulmonary hypertension and right heart failure.

(b) Central sleep apnea syndrome (CSAS): CSAS is defined as the upper airway without airflow for more than 10s, and there is no chest and abdomen breathing exercise. CSAS is less common and can coexist with OSAS. It can occur in any sleep phase, but obvious abnormalities are only seen during NREM sleep. CSAS can exist alone or in conjunction with central nervous system diseases such as brain stem trauma, tumors, infarction, and infection. There have also been reports of CSAS associated with neuromuscular disorders such as polio and myotonic dystrophy. Appropriate ventilation can be maintained when awake, but during sleep, there is an abnormal regulation of the respiratory center, and a central (or obstructive) apnea occurs.

(C) sleep disordered breathing in patients with chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease may be accompanied by significant respiratory and gas exchange deterioration, mainly due to severe arterial oxygen saturation reduction and transient specific respiratory abnormalities such as apnea and hypopnea. The phase of REM sleep is most obvious, and the mechanism is still unclear, which may be related to the abnormal respiratory activity accompanying the sleep. In addition, these patients have a slow chemical ventilatory response when they are awake, and can be further aggravated during sleep to reduce the ventilatory response.

(4) Apnea-like phenomenon

There are two types of apnea-like phenomena that are easily confused with sleep apnea syndrome: 1 mild epilepsy without epileptic seizures may also have apnea. If it occurs during sleep or after a sleep-like episode, the state can be confused with sleep apnea, which can be identified by means of EEG. 2 Chen-Shi's breathing can be seen in patients with reduced cardiac output or prolonged circulation, as well as various neurological diseases affecting the respiratory center and some older people. It is difficult to distinguish from central apnea, and both can coexist. However, the respiratory amplitude of Chen-Shi's breathing changes moderately, from small to large, then becomes smaller to apnea, and the apnea time is shorter. Central apnea tends to occur suddenly, and often combined with wake-up response, apnea time is longer, up to 60s. In addition, Chen-Shi's breathing can continue to be awake, while central apnea does not occur during waking and is often exacerbated during REM sleep.

(5) Irregular breathing during normal sleep

Normal people in the REM sleep phase is usually more regular, and a few minutes of respiratory instability can be seen at the beginning of sleep, and disappear after stable sleep. The apnea seen during this period did not have respiratory movements and was easily mistaken for CSAS. Obstructive sleep apnea can also occur in asymptomatic healthy people, but usually less than 20 times per night, with only mild arterial oxygen saturation. If the REM sleep phase occurs, a significant decrease in arterial oxygen saturation can result from a weakened wake-up response.

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