Night apnea

Sleep apnea is a periodic cessation of breathing during sleep lasting more than 10 seconds, combined with constant loud snoring and frequent awakenings, accompanied by severe daytime sleepiness.

Sleep apnea is divided by origin into central, obstructive, and mixed.

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What causes sleep apnea?

Central sleep apnea

Central sleep apnea is characterized by the absence of respiratory movements and air flow through the nasopharynx. This group includes diseases in which sleep apnea is the result of a disorder of the central mechanisms of respiratory regulation: ischemic, inflammatory, alcoholic, atrophic, drug-induced brain damage, organic lesions of the brainstem and posterior cranial fossa; brain damage in Alzheimer-Pick disease; post-ancephalic parkinsonism. This group also includes a rare syndrome of primary alveolar hypoventilation ("Ondine's curse syndrome"), caused by primary insufficiency of the respiratory center. Central sleep apnea is usually observed in children who are cyanotic from birth in the absence of cardiac or pulmonary pathology. In children with this disease, the function of the central chemoreceptors is reduced, and the number of nerve fibers in the medulla oblongata and in the area of the respiratory center is reduced. Central sleep apnea syndrome accounts for about 10% of all cases of apnea.

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Obstructive sleep apnea

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

The main causes of obstructive sleep apnea are:

• obstruction of the upper respiratory tract caused by the collapse of the pharyngeal wall due to a decrease in the tone of the pharyngeal muscles - pharyngeal dilators, abductors of the tongue, pharynx. As a rule, this is observed in people with an 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 bone and cartilaginous formations, but only by the optimal tone of the pharyngeal dilator muscles, mainly the genioglossus muscle, which prevents the tongue from falling back to the back wall of the pharynx. During sleep, there is a decrease in the tone of the muscles of the tongue and oropharynx, which causes obstruction of the respiratory tract.

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

There is also a suggestion that a decrease in the tone of the pharyngeal muscles during sleep causes the development of obstructive sleep apnea only if there is a narrowing of the upper respiratory tract (the reasons for the narrowing are indicated below). This point of view is based on the fact that a decrease in the tone of the pharyngeal muscles is observed during sleep in completely healthy individuals (i.e., under physiological conditions), and obstructive sleep apnea still occurs if there is a narrowing of the lumen of the airways;

• developmental anomalies (micrognathia - small size of the lower jaw, retrognathia, macroglossia, incorrect positioning of the hyoid bone, etc.), leading to a decrease in the diameter of the airways;
• proliferation of pharyngeal lymphoid tissue (adenoids, hypertrophy of the tonsils, lymphoproliferative diseases);
• tumors and cysts in the pharynx area;
• edematous and 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 diseases, kyphoscoliosis, acromegaly (with which macroglossia is observed), taking tranquilizers, alcohol abuse, age over 50, and a burdened heredity.

Mixed sleep apnea

Mixed sleep apnea syndrome develops with a combination of causes from both groups. Mostly, central regulatory mechanisms are disrupted in all types of sleep apnea.

Pathogenesis of sleep apnea

The pathogenesis of the main disorders that occur with sleep apnea consists primarily of hypoxemia and sleep fragmentation.

An episode of apnea lasting more than 10 seconds causes the development of hypoxemia. With a longer apnea, hypoxemia is much more pronounced, and hypercapnia also develops. After reaching a certain threshold level of hypoxemia and hypercapnia, a transition from deep sleep to a more superficial stage occurs, during which the tone of the muscles of the pharynx and mouth increases, and the patency of the pharynx is restored, which is accompanied by loud snoring. Lung ventilation and gas exchange are normalized, and the deep sleep phase begins again before the development of the next episode of apnea and obstruction. According to A. M. Vein et al. (1998), the average duration of apnea periods is 40 sec, but can reach even 200 sec, apnea periods can occur so often that in severe cases they occupy 60% of the total time of night sleep. Thus, frequent and prolonged sleep apnea disrupts sleep, reduces the duration of the superficial and deep phases. This has a huge pathophysiological significance. During the REM phase (rapid eyes movement phase), information received during wakefulness is processed and assimilated, and during deep sleep, energy restoration processes occur in the brain. Violation of the duration of sleep phases leads to a decrease in memory and intelligence. Frequent episodes of apnea lead to hypoxemia, which is accompanied by spasm in the vascular system of the pulmonary circulation, increased pressure in the pulmonary artery, leads to the formation of pulmonary heart disease, arterial hypertension in the systemic circulation, contributes to the development of cardiac arrhythmias, sudden death.

In sleep apnea syndrome, the functional state of the endocrine system undergoes major changes. A decrease in the secretion of somatotropin has been established (Grunstein et al., 1989), which contributes to an increase in the body weight of patients due to a decrease in the lipolytic effect of the somatotropic hormone. Along with this, the nocturnal secretion of catecholamines (Tashiro et al., 1989), atriopeptide increases. Ehlenz et al. (1991) established an increase in the production of endothelin, a powerful vasoconstrictor factor, in patients with sleep apnea syndrome. These changes contribute to the development of arterial hypertension.

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

Symptoms of sleep apnea

Patients suffering from sleep apnea present very characteristic complaints, which make it easy to suspect this disease:

• lack of a feeling of vigor after sleep, a feeling of morning fatigue and exhaustion after waking up;
• constant fatigue and drowsiness during the day;
• increased tendency to fall asleep during breaks at work, while driving a car (patients suffering from sleep apnea are 2-3 times more likely to get into car accidents than other drivers);
• morning headaches and recurring pain in the back of the head and neck during the day;
• increased irritability, emotional lability, decreased memory;
• unpleasant sensations in the legs of an unspecified nature, sometimes perceived as a feeling of aching in the muscles and bones, especially at night (restless legs syndrome);
• decreased sexual desire, sexual weakness;
• characteristic "night complaints" - loud snoring, increased motor activity during sleep, teeth grinding (bruxism), sleep talking, sleep disturbances with frequent episodes of awakening, some patients may have nocturnal enuresis. It should be noted that snoring - one of the leading symptoms of obstructive sleep apnea - differs from common snoring in its periodicity, as well as the onset of silent phases of apnea after periods of intense snoring.

An objective examination of patients may reveal arterial hypertension (in 50% of patients according to Fletcher, 1985), its genesis is not fully known. It is assumed that a decrease in the content and tension of oxygen in organs and tissues stimulates the chemoreceptors of arterial and venous vessels, causing an increase in afferent excitatory influences on the central vegetative neurons, which enhances the vasoconstrictor effect of the sympathetic nerves on the arteries and arterioles (P. A. Zelveyan et al., 1997). A. P. Zilber (1994) emphasizes the importance of increased intracranial pressure in patients with sleep apnea syndrome in the development of arterial hypertension. Nocturnal hypersecretion of catecholamines and increased production of endothelin, which have a vasoconstrictor effect, are also important. A negative effect of hypoxemia on the state of the juxtaglomerular apparatus of the kidneys in patients with sleep apnea cannot be ruled out.

Progression of sleep apnea is often accompanied by disturbances of the heart rhythm. According to Ruhler et al. (1987), the following types of arrhythmia and conduction disturbances are encountered:

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

Tachycardia, ventricular and supraventricular extrasystole during episodes of sleep apnea are more often observed in elderly patients, who usually suffer from cardiovascular diseases. Many patients with sleep apnea develop myocardial infarction, stroke, and sudden death has been described. Sleep apnea reduces the life expectancy of patients.

With the development of pulmonary hypertension, an accentuated second tone is heard on the pulmonary artery during auscultation of the heart.

Most patients with sleep apnea are overweight, usually over 120% of ideal body weight. Some obese patients with sleep apnea syndrome may have Pickwickian syndrome, usually in the obstructive form. Rapaport et al. (1986) provide the following diagnostic criteria for Pickwickian syndrome:

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

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

Diagnosis of sleep apnea

For clinical diagnostics of sleep apnea, it is recommended to use the method of V. I. Rovinsky. It is based on contact with the patient's relatives and their participation in establishing the fact of respiratory arrest during sleep: one of the patient's family members at night, using an ordinary watch with a second hand, determines the duration of episodes of respiratory arrest during sleep, and also calculates the apnea index - the number of episodes of respiratory arrest per 1 hour of sleep.

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Symptoms of Obstructive Sleep Apnea

• loud chronic nocturnal snoring
• periods of shortness of breath or respiratory "flap" during sleep
• severe excessive daytime sleepiness (especially in people driving vehicles)
• accidents at work or on the road caused by daytime sleepiness or daytime fatigue
• individual changes in the patient's character against the background of fatigue or daytime tiredness

Obstructive sleep apnea markers

• weight gain, especially significant weight gain (> 120% of ideal body weight)
• Neck circumference (collar size):
  • men > 43 cm
  • women > 40 cm
• systemic arterial hypertension
• nasopharyngeal stenosis
• pulmonary hypertension (rare marker)
• pulmonary heart (rare marker)

Normally, sleep apnea can also be observed in healthy people, mainly during the REM phase, but its duration does not exceed 10 seconds, while the frequency of apnea episodes is no more than 5 per hour (physiological apnea).

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

The British Lung Society recommends diagnosing sleep apnoea if oxygen desaturation during sleep is greater than 4% at least 15 times in 1 hour, with the patient having a blood oxygen saturation of over 90% while awake (desaturation is a drop in the degree of blood oxygen saturation due to apnoea).

Laboratory data

1. General blood and urine tests are usually without significant changes. Symptomatic erythrocytosis may occur in individuals with Pickwickian syndrome and significant hypoxemia.
2. Blood gas analysis reveals a decrease in the partial pressure of oxygen and an increase in carbon dioxide.

Instrumental research

1. ECG - possible vertical position of the electrical axis of the heart (mainly in people with excess body weight or pulmonary emphysema) and diffuse changes in the form of decreased amplitude of the T wave in many leads. In severe forms of sleep apnea syndrome - various disturbances of the heart rhythm.
2. Spirometry: decreased vital capacity (an inconstant symptom), observed mainly in patients with obesity, Pickwickian syndrome, and pulmonary emphysema.
3. X-ray examination of the lungs - no specific changes, pulmonary emphysema and low position of the diaphragm dome may be observed.
4. Polysomnographic study (performed in specialized research laboratories) - reveals disturbances in sleep phases and their duration.

Sleep Apnea Screening Program

1. General blood tests, urine analysis.
2. ECG.
3. Spirometry.
4. Blood gas analysis.
5. Consultation with a neurologist and otolaryngologist.
6. X-ray examination of the lungs.
7. Counting the number of apnea episodes during 1 hour of night sleep and the duration of apnea (determination of the apnea index).
8. The patient's examination in a specialized sleep research laboratory is a classic polysomnographic study, including the study of sleep phases and their duration, breathing control, ECG, encephalogram and blood gas composition. Electrooculography, registration of air flow near the mouth and nose with a thermistor are also used, chest and anterior abdominal wall excursions are determined during breathing. At the same time, the tension of oxygen and carbon dioxide in the blood and the saturation of hemoglobin in the blood are studied.
9. Monitoring of heart rhythm, conductivity and blood pressure.