Sleep apnea

Nocturnal apnea is a periodically occurring respiratory arrest in a dream lasting more than 10 seconds in combination with constant strong snoring and frequent awakenings, accompanied by pronounced daytime drowsiness.

The night apnea is divided by origin into central, obstructive, mixed.

[1], [2], [3], [4], [5], [6], [7], [8]

What causes sleep apnea?

Central night apnea

The central form of nocturnal apnea is characterized by the absence of respiratory movements and air flow through the nasopharynx. This group includes diseases in which nocturnal apnea is the result of a violation of the central mechanisms of the regulation of breathing: ischemic, inflammatory, alcoholic, atrophic, medicamentous brain lesions, organic lesions of the brainstem and posterior cranial fossa; brain damage in Alzheimer's disease; poststansephalic parkinsonism. The same group includes a rare syndrome of primary alveolar hypoventilation ("Undine's Curse Syndrome") due to the primary insufficiency of the respiratory center. Central nocturnal sleep apnea is usually seen in children who are cyanotic with birth in the absence of cardiac or pulmonary pathology. In children with this disease, the function of the central chemoreceptors is reduced, and in the medulla oblongata and in the region of the respiratory center the number of nerve fibers is reduced. The syndrome of central sleep apnea is about 10% of all cases of apnea.

[9], [10], [11], [12], [13]

Obstructive nocturnal apnea

In obstructive nocturnal apnea, the airflow periodically stops completely, while the respiratory excursions of the anterior abdominal wall and thorax are preserved.

The main causes of obstructive sleep apnea are as follows:

• violation of patency of the upper respiratory tract due to collapse of the pharyngeal wall due to a decrease in the tone of the pharyngeal muscles - dilators of the pharynx, abductors of the tongue, pharynx. As a rule, this is observed in persons with initially narrowed oropharynx. Obstruction occurs at the level of the root of the tongue, since in this part of the pharynx, its lumen is supported not by bony and cartilaginous formations, but only by the optimal tone of the pharyngeal dilator muscles, mainly the chin-lingual muscle, which prevents the tongue from sinking to the posterior wall of the pharynx. During sleep, there comes a decrease in the tone of the muscles of the tongue and the oropharynx, which causes obstruction of the airways.

It is assumed that there is a defect in controlling the tone of the pharyngeal muscles by specialized structures of the brainstem.

There is also the assumption that a decrease in the tone of the pharynx muscles during sleep causes the development of obstructive sleep apnea only if there is a narrowing of the lumen of the upper respiratory tract (the causes of narrowing are indicated below). This view is based on the fact that a decrease in the tone of the pharynx muscles is observed during sleep in completely healthy persons (ie under physiological conditions), and obstructive nocturnal sleep apnea nevertheless occurs if there is narrowing of the lumen of the airways;

• developmental anomalies (micrognathia - small size of the lower jaw, retrognathia, macroglossia, wrong position of the hyoid bone, etc.), leading to a decrease in the diameter of the airways;
• proliferation of pharyngeal lymphoid tissue (adenoids, tonsillar hypertrophy, lymphoproliferative diseases);
• tumors and cysts in the pharynx;
• edematous inflammatory changes in the soft tissues of the neck; pronounced hyperplasia of the submucosal layer of the upper respiratory tract.

Important predisposing factors for the development of obstructive sleep apnea are obesity, chronic obstructive pulmonary disease, kyphoscoliosis, acromegaly (with it there is macroglossia), tranquilizers, alcohol abuse, age over 50 years, weighed weights.

Mixed sleep apnea

The syndrome of mixed sleep apnea develops when the causes of both groups are combined. For the most part, the central mechanisms of regulation are violated in all types of sleep apnea.

The pathogenesis of nocturnal sleep apnea

The pathogenesis of the main disorders that occur during nocturnal sleep apnea is primarily in hypoxemia and sleep fragmentation.

The episode of apnea lasting more than 10 seconds causes the development of hypoxemia. With more prolonged apnea, hypoxemia is much more pronounced, and also hypercapnia develops. After reaching a certain threshold level of hypoxemia and hypercapnia, there is a transition from deep sleep to a more superficial stage, at which the tone of the muscles of the pharynx and mouth rises, and the patency of the pharynx is restored, which is accompanied by strong snoring. Ventilation of the lungs and gas exchange are normalized, again the deep sleep phase begins until the next episode of apnea and obstruction develops. According to AM Wein et al. (1998), the average duration of apnea periods is 40 s, but can reach even 200 s, periods of apnea can occur so often that in severe cases occupy 60% of the total time of night sleep. Thus, nighttime apnea, which often occurs and lasts for a long time, disturbs sleep, reduces the duration of the surface and deep phases. This has a huge pathophysiological significance. During the REM-phase (the rapid eye movement phase), processing and assimilation of information obtained during the waking period occurs, and during the deep sleep, the processes of energy recovery in the brain occur. Violation of the duration of the phases of sleep leads to a decrease in memory, intelligence. Frequent episodes of apnea lead to hypoxemia, which is accompanied by spasm in the system of small blood vessels, increased pressure in the pulmonary artery, leads to the formation of the pulmonary heart, arterial hypertension in a large circle, contributes to the development of cardiac arrhythmias, sudden death.

With the syndrome of sleep apnea, the functional state of the endocrine system undergoes great changes. A decrease in the secretion of somatotropin (Grunstein et al., 1989) has been established, which contributes to an increase in the body weight of patients due to a decrease in the lipolytic effect of growth hormone. Along with this, there is an increase in the night secretion of catecholamines (Tashiro et al., 1989), atriopeptide. Ehlenz et al. (1991) found an increase in endothelin production - a potent vasoconstrictor factor in patients with sleep apnea syndrome. These changes contribute to the development of hypertension.

In patients with sleep apnea syndrome, testosterone secretion is significantly reduced, which causes the development of sexual weakness in men.

Symptoms of nocturnal apnea

Patients suffering from nocturnal apnea present very characteristic complaints that make it easy to suspect this disease:

• lack of a sense of vivacity after sleep, a feeling of morning fatigue and weakness after waking up;
• constant fatigue and drowsiness throughout the day;
• increased inclination to fall asleep during a break in work, while driving a car (patients suffering from nocturnal apnea are 2-3 times more likely to get into car accidents than other drivers);
• morning headaches and relapsing during the day, pain in the neck, neck;
• increased irritability, emotional lability, decreased memory;
• unpleasant sensations in the legs of an indeterminate nature, sometimes perceived as a feeling of aching in the muscles, bones, especially at night (restless legs syndrome);
• decreased sexual desire, sexual weakness;
• characteristic "night complaints" - strong snoring, increased motor activity in the dream, gnashing of teeth (bruxism), conversation in a dream, disturbances in a night's sleep with frequent episodes of awakening, some patients may have bedwetting (enuresis). It should be noted that snoring - one of the leading symptoms of sleepy obstructive sleep apnea - differs from banal snoring by its frequency, and also by the onset of periods of intense snoring of silent phases of apnea.

In an objective study of patients, arterial hypertension can be detected (in 50% of patients according to Fletcher, 1985), its genesis is not completely known. It is assumed that the decrease in oxygen content and tension in organs and tissues stimulates the chemoreceptors of arterial and venous vessels, causing an increase in afferent stimulatory effects on central vegetative neurons, which enhances the vasoconstrictor effect of sympathetic nerves on arteries and arterioles (PA Zelveyan et al., 1997). ). AP Zilber (1994) emphasizes the importance of increasing intracranial pressure in patients with sleep apnea syndrome in the development of arterial hypertension. Nighttime hypersecretion of catecholamines and an increase in endothelin production, which have a vasoconstrictive effect, also play a role. The negative effect of hypoxemia on the state of the juxtaglomerular apparatus of the kidneys in patients with nocturnal apnea is also possible.

Progression of nocturnal apnea is often accompanied by heart rhythm disturbances. According to the data of Ribieri co-author. (1987), there are the following types of arrhythmias and conduction disorders:

• sinus arrhythmia - in 78-100% of patients (many researchers consider sinus arrhythmia as a screening parameter in the diagnosis of sleep apnea syndrome);
• sinus bradycardia with a heart rate of up to 30-40 per minute - in 10-40% of patients;
• sinoauricular and atrioventricular blockade - in 10-36% of patients

Tachycardia, ventricular and supraventricular extrasystole during episodes of nocturnal apnea are more common in elderly patients suffering, as a rule, diseases of the cardiovascular system. Many patients with nocturnal apnea develop myocardial infarction, stroke, and describe the possibility of sudden death. Nighttime apnea reduces the life expectancy of patients.

With the development of pulmonary hypertension in the auscultation of the heart, the accent of tone II on the pulmonary artery is heard.

Most patients with nocturnal sleep apnea are overweight, often more than 120% of the ideal. In some patients with obesity and sleep apnea syndrome, Pickwick's syndrome can be identified, with the definition, as a rule, of the obstructive form of the syndrome. Rapaport et al. (1986) cite the following diagnostic criteria for Pickwick's syndrome:

• day hypoxemia and hypercapnia;
• arterial hypertension;
• polycythemia;
• pulmonary heart;
• hypothalamic obesity.

In obese people, one of the causes of obstructive sleep apnea is the narrowing of airways due to the deposition of "fat cushions." The increase in neck size in men and women is a significant risk factor for the development of sleep apnea syndrome. According to Davies and Stradling (1990), men with a neck circumference of 43 cm and more, and women - 40 cm or more have the highest risk of developing sleep apnea.

Diagnosis of nocturnal sleep apnea

For the clinical diagnosis of nocturnal apnea, it is recommended to use the method of VI Rovinsky. It is based on contact with the patient's relatives and on their participation in establishing the fact of stopping breathing in a dream: one of the family members of the patient at night using a standard clock with a second hand determines the duration of episodes of stopping breathing in a dream, and calculate the apnea index - the number of episodes of respiratory arrest for 1 hour of sleep.

[14], [15], [16], [17], [18], [19], [20], [21], [22]

Symptoms of obstructive nocturnal sleep apnea

• loud night snore
• periods of interception of respiration or respiratory "shutter" during sleep
• marked excessive daytime sleepiness (especially in persons driving a vehicle)
• Accidents at work or road accidents caused by daytime sleepiness or daytime fatigue
• individual changes in the character of the patient on the background of fatigue or day fatigue

Markers of obstructive nocturnal sleep apnea

• an increase in body weight, in particular a significant (> 120% of ideal body weight)
• neck circumference (collar size):
  • men> 43 cm
  • women> 40 cm
• systemic arterial hypertension
• nasopharyngeal narrowing
• pulmonary hypertension (rare marker)
• pulmonary heart (rare marker)

Normally, stopping breathing in a dream can also be observed in healthy people, mainly during the REM phase, but its duration does not exceed 10 s, with the frequency of apnea episodes not more than 5 per hour (physiological apnea).

Pathognomonic for sleep apnea is a condition where apnea lasting more than 10 s occurs at least 30 times during 7 hours of sleep or the apnea index is greater than 5, or the index of respiratory disorders (the number of episodes of apnea and hypopnea per 1 hour of sleep) is greater than 10.

The British Pulmonary Society recommends the diagnosis of "nocturnal sleep apnea" if during sleep at least 15 times during 1 hour oxygen desaturation is more than 4% if the patient has more than 90% oxygen saturation during wakefulness (desaturation - a drop in the degree of oxygen saturation of the blood due to apnea).

Laboratory data

1. General tests of blood and urine - usually without significant changes. In persons with Pickwick syndrome, as well as with significant hypoxemia, symptomatic erythrocytosis may occur.
2. Investigation of the gas composition of blood - a decrease in the partial pressure of oxygen and an increase in carbon dioxide.

Instrumental research

1. ECG - the vertical position of the electric axis of the heart is possible (mainly in individuals who have excess body weight or pulmonary emphysema) and diffuse changes in the form of a decrease in the amplitude of the T wave in many leads. In severe forms of sleep apnea syndrome - various violations of the heart rate.
2. Spirography: a decrease in vital capacity (a non-permanent symptom), is observed mainly in patients with obesity, Pickwick's syndrome, emphysema.
3. X-ray examination of the lungs - there are no specific changes, lung emphysema, low diaphragm dome standing can be observed.
4. Polysomnographic research (performed in specialized research laboratories) reveals a violation of the phases of sleep and their duration.

The program of examination for nocturnal sleep apnea

1. General blood tests, urinalysis.
2. ECG.
3. Spirography.
4. Investigation of the gas composition of blood.
5. Consultation of a neurologist and otolaryngologist.
6. X-ray examination of the lungs.
7. Counting the number of episodes of apnea within 1 hour of night sleep and the duration of apnea (definition of apnea index).
8. A study of a patient in a specialized sleep research laboratory is a classical polysomnographic study that includes the study of sleep phases and their duration, breath control, ECG, encephalogram and gas composition of blood. Electrooculography is also used, recording of air flow near the mouth and nose with a thermistor, excursions of the chest and anterior abdominal wall during respiration are determined. At the same time, the tension in the blood of oxygen and carbon dioxide and the saturation of hemoglobin of the blood are investigated.
9. Monitor the control of cardiac rhythm and conduction and blood pressure.