What is the best position to sleep in if you have asthma? Nocturnal asthma

It can easily be considered one of the most common diseases in the world. About five percent of residents suffer from this disease. Some constantly experience attacks of suffocation, difficulty breathing, incomplete inhalation, difficulty breathing, etc.

Many patients are well aware that attacks usually make themselves felt most often at night or in the early morning hours. They affect the patient’s general condition, the quality of sleep deteriorates, and the quality of life decreases. The patient, instead of sleeping, struggles with bronchial obstruction. Bronchial patency may decrease between 10 pm and 8 am.

This is how nocturnal asthma manifests itself, which is characterized by a decrease in bronchial patency during night sleep. When we sleep, we are all unconscious and quickly help ourselves.

This type of asthma was first discussed at the end of the 17th century. John Floyer, suffering from the disease, noticed that the attacks made themselves known precisely at night, with the first occurring approximately in the first or second hour. According to the patient's descriptions, the sensations in the diaphragm area were especially unpleasant.

It took approximately 250 years for the disease to come under the close attention of medical scientists. The reason for this was the increased mortality of patients. During the research, it turned out that death overtook patients precisely at night, when they were sleeping. Studies have established that 8 out of 10 people with asthma died at night in a hospital setting. This indicator is very significant, and therefore it was impossible not to pay attention to the statistics. It is worth noting that in general, at that time, 5% of patients in the world died from the disease.

Many people with nocturnal asthma experience a serious decrease in peak flow measurements. Expiratory (exhalation) volume may drop by 50% overnight. During the remission stage, spasms may occur at night; a third of patients experience them before bedtime. Interestingly, some healthy people can sometimes suffer from nocturnal bronchospasms caused by changes in the caliber of the bronchial tract.

Cause of narrowing of the airways

One of the theories explaining the narrowing in the bronchi is incorrect posture during sleep. The theory of allergens that may be present in bedding remains highly probable. The first assumption, however, is often refuted, since asthma patients undergoing medical examination can lie all day long, changing position, which does not affect the condition in any way. Severe attacks occur at night.

Some scientists see the cause of the problem in irregular medication use, but the facts prove that there is no fundamental difference in the intervals. Even with constant and timely use of medications, significant improvements are not observed. The theory about allergens is also questioned, since their removal did not bring results. It is possible that they may be the root cause, but there is no evidence that it is allergens that contribute to the development of nocturnal asthma.

The spasm can be caused by inhaling cold or dry air. There is a simple explanation for this: when inhaling cooled air, a patient with asthma exhibits the effect of bronchial hyperreactivity, which leads to bronchospasm. The temperature drops towards evening, hence this assumption. However, they have already managed to refute it, proving that temperature does not have a significant effect, keeping it at a certain level during the day. This did not help avoid attacks. However, it seems that it is the change in the air temperature gradient at night or during the day that provokes bronchospasm.

Another study found that at a temperature of 36°C and 100% humidity, patients felt better. Asthma did not manifest itself. However, the number of participants was too small.

Symptoms and complaints

Complaints of asthma patients, characterized by the occurrence of attacks at night, can be reduced to sleep disturbances, the appearance of excessive daytime sleepiness, these are the indications given by patients during examinations in Europe.

An indicator of the severity of bronchial asthma is the occurrence of nighttime asthma attacks and their daily occurrence. A spastic night cough can also be considered an equivalent, with the cough variant of bronchial asthma. In some cases, patients may be diagnosed obstructive sleep apnea syndrome in a dream, which manifests itself in cessation of breathing lasting 10 seconds or more. The presence of such a syndrome further aggravates the course of asthma.

Quite often, patients experience a reduction in ventilation volumes depending on the various stages of dreams. During so-called NREM sleep, the lowest level of ventilation is observed. Recent studies have established that the presence of asthma leads to chronic hypoxia. Nocturnal hypoxia in an asthmatic can be measured by overnight pulse oximetry.

Nocturnal asthma provokes changes in the bronchi in accordance with a specific daily rhythm.
In Delhi, India, a large-scale study was conducted at a local university to determine the relationship and nature of sleep dysfunction in patients with bronchial asthma. The control group consisted of 30 young people with various forms of the disease. The results of the study revealed problems with sleep and breathing during sleep in 90% of the subjects. In parallel, studies were conducted in the USA, which made it possible to establish the negative impact of sleep problems from asthma on a person’s performance, physical and mental activity.

Nocturnal asthma is a serious disease that affects quality of life and is difficult to treat. The medical community did not distinguish it as an independent nosological unit because nevertheless, this is an inflammatory disease, but indeed with certain modalities and the nature of the course. The presence of nocturnal bronchospasms indicates insufficient or poor quality asthma treatment. In this case, it is necessary to urgently begin treatment of the patient and constantly monitor his condition. Therapy in this case is carried out using inhaled long-acting β-agonists in combination with inhaled glucocorticosteroids. Taking this drug can reduce the symptoms of this disease and improve sleep during nighttime asthma.

With the right choice of medications and adequate treatment, it is possible to completely eliminate sleep disturbances and the existing symptoms of the disease. If treatment of the acute form of the disease does not produce an effect, this leads to chronic sleep disturbance. It will be necessary to correctly identify the therapy that has a positive effect on respiratory function. If nocturnal asthma is accompanied apnea attacks, it is necessary to use special therapy, which involves increasing pressure on the upper respiratory tract. A similar treatment technology has received name of CPAP therapy and is performed using special equipment.

Nocturnal bronchial asthma is a serious medical problem, the solution of which and the search for new treatment technologies will improve the quality of life of many people in different countries of the world.

Can nocturnal asthma disrupt your sleep? Nocturnal asthma, with its symptoms such as chest tightness, shortness of breath, coughing and wheezing, can prevent you from sleeping at all. Symptoms of nocturnal asthma can disrupt your sleep and prevent you from getting a good rest, leaving you feeling tired and sluggish throughout the next day. Nocturnal asthma should not be ignored. This is very serious and requires an accurate diagnosis and effective treatment.

Nocturnal asthma and sleep disorders

Asthma symptoms are 100 times more severe when they worsen during sleep. Nighttime wheezing, coughing and breathing problems are common but also potentially life-threatening symptoms. Most people underestimate the seriousness of nocturnal asthma.

Studies have shown that most deaths due to asthma occur at night. Asthma attacks at night can cause serious sleep problems, resulting in sleep deprivation, drowsiness, fatigue and irritability during the day. These problems can affect your overall life and make it difficult to control your symptoms during the day.

Causes of nocturnal asthma

The exact reasons why asthma symptoms worsen during sleep are unknown. But there are still many hypotheses explaining what can cause an exacerbation of the disease. These include close contact with allergens during sleep, severe cooling of the respiratory tract, horizontal body position, or hormonal secretions that disrupt the circodian rhythm. Even sleep itself changes the performance of the lungs and airways. Reasons also include:

Excessive mucus production or sinusitis

During sleep, the airways become very narrow and mucus blocks them. This can cause coughing during sleep, which can further constrict the airways. Increased sinus congestion can also trigger an asthma attack in hypersensitive airways. Sinusitis is very common in asthma.

Internal pathogens

Asthma exacerbation can only occur during sleep, regardless of what time of day sleep occurs. For example, asthmatics who work night shifts may suffer from asthma symptoms during the day while they sleep. Most researchers suggest that lung function declines 4 to 6 hours after sleep. This shows that there are internal triggers that trigger asthma during sleep.

Horizontal body position

Horizontal body position can provoke exacerbation of asthma. This can be caused by a variety of factors, such as a buildup of secretions in the airways (sinus drip or postnasal drip), increased volume of circulating blood in the lungs, decreased lung capacity, and increased airway unresponsiveness.

Air conditioned

Cold air from an air conditioner can cause severe hypothermia in the respiratory tract. The airways become cooler and drier, which is a major cause of exacerbation of tension-type asthma. And it also aggravates nighttime asthma.

GERB (Gastroesophageal reflux disease)

If you often suffer from heartburn, acid reflux from the stomach into the esophagus and larynx can cause a reflex called bronchospasm. Reflux gets worse when you lie down or, if you take certain asthma medications, that weaken the valve between your esophagus and stomach. Sometimes stomach acid irritates the lower part of the esophagus and activates the vagus nerve, which sends signals to the bronchial tubes, thereby causing bronchoconstriction (narrowing of the bronchial tube). If gastric juice constantly rises up the esophagus to the larynx and a few drops of it enter the trachea, bronchi and lungs, then the body’s reaction will be very serious. This can result in severe irritation of the airways, increased mucus production and bronchoconstriction. If you start treating GERD and asthma correctly and on time, you can stop attacks of nocturnal asthma.

Delayed reaction of the body

After close contact with an allergen or asthma trigger, the airways become severely narrowed or allergic asthma worsens. But sometimes this happens with some delay. This exacerbation of the disease can last about an hour. About 50% of those who experience a sudden exacerbation of asthma experience a second phase of airway narrowing three to eight hours after exposure to the allergen. This phase is called the delayed reaction of the body. A delayed reaction is characterized by an increase in the sensitivity of the airways, the development of inflammatory processes in the bronchi and a longer blockage of the airways.

Most studies have shown that if contact with an allergen occurs in the evening, rather than, say, in the morning, then the body's reaction is more likely to be delayed, and an asthma attack can be very serious.

Hormones

Hormones circulating in the blood have characteristic circodian rhythms that differ in people who suffer from asthma. Epinephrine is one such hormonal substance that has an important effect on the bronchi. This hormone helps keep the muscle tissue surrounding the airways relaxed so that the airways remain wide enough. In addition, epinephrine inhibits the action of other substances, such as histamine, which causes mucus formation and bronchospasms. The level of epinephrine in the body and the maximum volumetric expiratory flow rate decrease by 4 am, and the level of histamine, on the contrary, increases. A decrease in epinephrine levels leads to an exacerbation of nocturnal asthma symptoms during sleep.

How to treat nocturnal asthma?

For quotation: Babak S.L., Chuchalin A.G. NIGHT ASTHMA // Breast cancer. 1998. No. 17. S. 3

“... Nocturnal respiratory disorders in patients with bronchial asthma are usually combined under the term “nocturnal asthma.” However, simply combining all types of nocturnal respiratory disorders in asthma patients into the concept of nocturnal asthma is not valid, since the factors causing this condition are often of a different nature. The modern approaches being developed in the correction of this painful condition largely depend on knowledge about the nature, nature and mechanisms of occurrence of this respiratory phenomenon, which determines the close attention of scientists from different countries to this problem...”

“...Overnight respiratory disorders in patients with bronchial asthma (BA) are agreed to be subsumed under the heading of nocturnal asthma. Nevertheless, the straightforward integration of all types of overnight respiratory disorders in patients with BA into the term “nocturnal asthma” is not reasonable since the factors predisposing to this condition are of different nature. The developed current approaches to correcting this abnormality largely depend on knowledge of the nature, pattern and mechanisms of the occurrence of this respiratory phenomenon, which draws the fixed attention of scientists from different countries to this problem...”

S. L. Babak, Candidate of Medical Sciences, Head. sleep laboratory research institute

Pulmonology, Ministry of Health of the Russian Federation, Moscow
A.G. Chuchalin - academician, director of the Research Institute of Pulmonology of the Ministry of Health, Moscow
S.L. Babak – Candidate of Medical Sciences, Head, Laboratory of Sleep, Research Institute of Pulmonology, Ministry of Health of the Russian Federation, Moscow
A.G. Chuchalin — Academician, Director, Research Institute of Pulmonology, Ministry of Health of the Russian Federation, Moscow

P As clinical and experimental data accumulate, views and ideas on some features of the course of bronchial asthma (BA) have led to the advisability of identifying some of its forms. Currently, close attention is paid to the so-called nocturnal asthma(NA), which as a criterion of severity was introduced into the modern consensus on the treatment and diagnosis of bronchial asthma, adopted at the V National Congress on Respiratory Diseases (Moscow, 1995), and is characterized by awakening from respiratory discomfort at night. On the other hand, there are established ideas about the “overlap syndrome” (OVERLAP), which is defined as a combination of the phenomena of respiratory arrest during sleep (obstructive sleep apnea-hypopnea syndrome) with existing chronic obstructive pulmonary disease, a variant of which is bronchial asthma. Thus, knowledge is currently being accumulated about the nature, nature and mechanisms of development of such a phenomenon as nocturnal respiratory disorders in asthma patients, which explains the close attention of scientists from different countries to this problem.

Relevance

In recent years, there has been a significant increase in patients with AD (R. Barnes, 1989) and the percentage of patients with AD among them is quite high. According to Turner - Warwick (1987), one third of asthma patients suffer from nocturnal asthma attacks at least every night. The clinical importance is also confirmed by modern studies of sudden deaths and respiratory arrest (apnea), developing in asthmatics at night against the background of nocturnal bronchial obstruction. Restless sleep with severe hypoxemia, as a rule, is of utmost importance in reducing the mental and physical performance of patients. However, despite numerous studies, questions of pathogenetic mechanisms and treatments for this manifestation of asthma are controversial and not fully understood. An important part in understanding AN is the development of the inflammatory process at night. However, it would not be entirely correct to explain nocturnal bronchoconstriction only by bronchoalveolar cellular infiltration observed in patients with AN, since it has a great affinity with circardian physiological rhythms. The urgent need to study the peculiarities of the occurrence of clinical manifestations of pathological conditions occurring during sleep served as an impetus for the formation of a new direction in medicine - sleep medicine and opened a new page in the study of the pathogenesis of AD (Vein, 1992).

Potential mechanisms of bronchial obstruction in AN

It is known that in most healthy individuals the airways are subject to circadian fluctuations. (N. Lewinsohn et al., 1960; N. Kerr, 1973; M. Hetzel et al., 1977). Thus, when comparing the circadian rhythms of bronchial patency based on the results of peak flowmetry of healthy individuals and patients with asthma, the authors showed that there is a synchronous drop in forced expiratory volume in 1 s (FEV 1 ) and peak expiratory flow (PEF). However, the magnitude of the fall amplitude in healthy individuals was 8%, and in patients with asthma - 50% (in some patients it exceeded 50%). Patients with this level of decrease in nocturnal bronchial patency are called “morning dippers.” (N. Lewinsohn et al., 1960; A. Reinberg, 1972; S. Soutar, J. Costello, O. Ljaduolo, 1975; T. Clark, 1977). In the studies of T. Clark (1977), C. Gaulter (197 7), P. Barnes (1982) showed that the greatest number of awakenings associated with the phenomena of bronchospasm occurs from the middle of the night to the early morning (2 - 6 hours). V. Bellia (1989), studying the reaction of the PEP at different times of the day, considers this indicator diagnostic criterion for nocturnal deterioration of bronchial patency. This study revealed a significant decrease in FEV 1 at night, which indicates increased obstruction and the likelihood of an attack of AN. When studying respiratory parameters, M. Hetsel (1977) revealed that in patients with exacerbations of asthma at night, FEV significantly decreases 1 and PEP, the residual lung volume increases. The patency of the middle and small bronchi is impaired when examining the function of external respiration. The discussion about the potential mechanisms for the development of attacks of nocturnal difficulty breathing has been going on for a long time and, despite numerous attempts to explain this phenomenon, it still remains relevant. The found provoking and predisposing factors are subject to new revision every year, and the approach to them is very ambiguous. Among them, the following should be highlighted and discussed:

Contact with allergen

A significant role in the occurrence of nocturnal attacks of suffocation, according to some authors, is played by allergens inhaled by patients in bed (fluff, dust and feathers) (A. Reinberg et al., 1972; M. Sherr et al., 1977). This hypothesis was confirmed by experimental work in which patients with atopic asthma were given dust inhalations for several days, which caused a nighttime deterioration of bronchial obstruction and the induction of AN attacks (R. Davis et al., 1976). At the same time, the assumption about the role of allergens in the occurrence of AN is questioned by studies by T. Clark and M. Hetzel (1977), showing that attacks of AN occur in the absence of an allergen.
An interesting study is one that traces the connection between reagin IgE antibodies involved in an allergic reaction and other mediators and biogenic amines. Thus, it was revealed that the acrophase of IgE antibodies occurs in the period from 5 to 6 hours, and it is in the pre-morning hours that the process of activation and release of inflammatory mediators (histamine) occurs, inducing an asthmatic response.

Esophageal reflux and aspiration

The appearance of asthma attacks at night, according to M. Martin et al. (1982), a factor such as gastroesophageal reflux also influences. In a horizontal position, aspiration or reflux of gastric contents occurs, which can cause stimulation of the vagal receptors located in the lower parts of the esophagus, inducing a bronchoconstrictor effect in patients with AN. This rather common mechanism in patients with asthma was further confirmed by a number of studies (R. Davis et al., 1983; M. Perpina, 1985). Identification of this mechanism allows, when prescribing appropriate treatment, to eliminate this provoking moment (R. Goodall et al., 1981).

Body position

The issue of body position during sleep and its connection with the occurrence of attacks of suffocation at night are debated in the literature. It has been suggested that the increase in obstruction during sleep depends on the patient's body position. N. Douglas et al. (1983) believe that body position does not cause prolonged bronchospasm in patients suffering from asthma attacks at night. Studies of PEP and functional residual capacity (FRC) in 31 pediatric patients aged from 2.8 to 8.3 years, 10 of whom had frequent nocturnal attacks, and 11 were completely absent, in the sitting and lying position revealed a significant drop in PEP in the position lying down in all asthmatics, and the percentage reduction in patients with AN and without nocturnal attacks was the same. FRC also tended to decrease. The level of decrease in FRC was significant in patients with asthma without nocturnal attacks and in the control group. The authors tried to show that the sleep position of patients with AN contributes to the development of various pulmonary function disorders. (Greenough et al, 1991). The results of this study are consistent with the studies of Mossberg (1956), who showed that in a horizontal position during sleep, mucociliary clearance worsens and the cough reflex decreases, which contributes to the disruption of the removal of secretions from the bronchi and can lead to obstruction of their lumen; this the mechanism is absent in patients with a small amount of sputum (T. Clark et al., 1977). Thus, the question of the role of body position in the occurrence of nocturnal attacks is ambiguous and controversial.

Characteristics of the sleep process

The role of sleep in the pathogenesis of AN has also attracted much attention. The fact that patients with nocturnal attacks suffer from sleep disturbances is indisputable. Studying the influence of sleep on the development of asthma attacks is a difficult task both because of the technical implementation and because of the specific attitude of patients to this kind of research. All this together is the reason for the small number of works devoted to this problem, despite the enormous interest in it. There are works in the literature that attempt to study such a complex process as sleep and its role in the occurrence of AN. J. Lopes et al. (1983) measured total airway resistance and inspiratory muscle activity during sleep. In healthy individuals, during sleep with slow eye movements, the total resistance of the upper respiratory tract increased by an average of 20 - 30% of the value during wakefulness. The researchers concluded that the change in overall airway resistance is likely due to an increase in airway muscle tone, which leads to an increase in the work of breathing during sleep. When these changes occur in patients with asthma, obstruction increases many times. Studies with night sleep deprivation in patients with AN have shown a decrease in the degree of nocturnal bronchial obstruction as measured by peak flow measurements (J. Catterall, 1985). These results, although they confirm the role of night sleep in the genesis of the disease, do not clarify the mechanisms of its influence. Interruption of sleep prevents the development of bronchial obstruction (M. Hetsel et al., 1987). It is believed that, despite the altered circadian rhythm of bronchial resistance in patients with asthma, sleep itself does not cause attacks of difficulty breathing (T. Clark et al., 1989). When trying to study the connection between sleep stages and asthmatic attacks, it was revealed that the number of attacks is “scattered” throughout the entire sleep period (S. Connoly et al., 1979) and it seems unclear today the role of any stage in the occurrence of asthmatic attacks. Of interest is the paradoxical stage of sleep, received this name due to the discrepancy between complete muscle relaxation and the active EEG pattern, otherwise REM sleep (“rapid eays movement”). When examining tracheal muscle tone in dogs during the REM stage, a marked variability in tone from bronchoconstriction to bronchodilation was revealed. (S. Soutar et al., 1975). Intrathoracic esophageal monitoring to measure airway resistance revealed its increase during NREM sleep in healthy individuals, and upon transition to REM sleep its values reached the level during wakefulness. (J. Lopes et al., 1983) However, in subsequent similar studies this pattern was not revealed in healthy individuals. (R. Brown, 1977) . Thus, determining airway resistance and the level of bronchial patency in various stages of sleep is technically intractable today. The existing work that addresses aspects of sleep in the occurrence of AN is generally insufficient and requires more careful attention, and the solution to such issues faces a number of objective and subjective problems.

Sleep apnea

The role of obstructive sleep apnea-hypopnea syndrome in patients with AN is unclear. Thus, in the work of Shu Chan (1987), it was shown that apnea is part of the “trigger” mechanism for the occurrence of nocturnal attacks of suffocation in asthma due to developing occlusion of the upper respiratory tract.

Hypothermia of the respiratory tract

The development of bronchial obstruction when inhaling dry and cold air is well known and proven experimentally (E. Deal et al., 1979). When maintaining a constant temperature and humidity of inhaled air for 24 hours a day, the level of nocturnal bronchoconstriction when measured in healthy individuals did not decrease and remained within acceptable limits (N. Kerr, 1973). When asthmatics were placed in a room overnight at a temperature of 36-37 °C with 100% oxygen saturation in the inspired air, falls during the night were eliminated in 6 out of 7 asthmatics (W. Chen et al., 1982).

Airway inflammation

Inflammation of the airways is considered by some authors to be a fundamental factor in the occurrence of nocturnal asthma attacks. A study of bronchoalveolar lavage performed in 7 patients with AN and 7 without nocturnal attacks showed a statistically significant increase in the number of leukocytes, neutrophils and eosinophils at night, in particular at 4 a.m. in a patient with AN. There was a correlation between the increase in inflammatory cells and the decrease in PEP during these hours. During the daytime, this pattern did not tend to increase. All this allowed M. Martin et al. (1991) suggest that the inflammatory mechanism in combination with epithelial damage is a fundamental factor in the occurrence of nocturnal deterioration in breathing. This opinion does not contradict the results of S. Szefler et al. (1991)

Changes in physiological circadian rhythms

It is known that in AD there is internal desynchronosis - disorganization of the circadian rhythms of many functions of the human body (Amoff, Wiener, 1984). Ind et al. (1989) distinguish among the endogenous circadian rhythms the following, possibly influencing AN: physiological, biochemical, inflammatory. Of great interest is the connection between nocturnal deterioration of breathing and circadian changes in hormones. A. Reinberg et al. (1963) suggested a connection between nocturnal bronchospasm and low levels of urinary excretion of 17-hydroxycorticosteroids. In 1969, A. Reinberg et al. confirmed the opinion that the level of circulating catecholamines decreases at night. S. Connoly (1979), S. Soutar (1977) revealed a connection between nocturnal deterioration of PEFR and the level of circulating steroids. Other studies have shown not only a synchronicity in the fall of PERF and circulating catecholamines, but also a connection with a decrease in the level of histamine and cyclic nucleotides (R. Barnes et al., 1989). The results obtained by A. Reinberg in 1972 are interesting, when the following patterns were determined when administering ACTH to healthy individuals: the maximum increase in cortisol and MOS was observed with the administration of ACTH at 7 o’clock, the minimum at 21 o’clock. However, earlier M. Hetsel (1980 ), T. Clark (1980) showed that fluctuations in MOS persisted even against the background of constant administration of glucocorticoids, which is quite consistent with the assumption made earlier by A. Reinberg (1972) about the existence of cortisol-resistant effector cells of the bronchi in some patients. Most likely, patients with asthma may combine different circadian rhythms of bronchial patency and urinary catecholamine excretion. Based on these works, which are quite interesting and contradictory, it can be assumed that glucocorticoid adrenal insufficiency in patients with asthma may contribute to the occurrence of nocturnal attacks, without being the only pathogenetic mechanism.
The patterns of changes in the circadian rhythm of mediators and the receptor apparatus of the cell in combination with the study of hormone levels in patients with AN can be traced in the work of S. Szefler (1991). The plasma levels of histamine, adrenaline, cortisol, cAMP and b-adrenergic receptors on peripheral blood lymphocytes were studied in 7 patients with AN, 10 healthy individuals and 10 asthmatics without night attacks at 4 a.m. and at 4 p.m. There was a 2-fold increase in the concentration of histamine in the blood at 4 p.m. in all studied individuals, as well as the content of adrenaline and cortisol in the peripheral blood. The level of their decrease at night was different in the study groups and prevailed in patients with AN. The connection between changes in bronchial patency and the content of adrenaline has been most studied. It can be considered firmly established that the decrease in the level of circulating adrenaline, which occurs at 3-4 am, correlates with a deterioration in bronchial patency, which leads to attacks of suffocation (M. Hetsel, 1981). Nocturnal deterioration of bronchial patency, coinciding with a decrease in the level of adrenaline in the blood, allowed us to suggest that the weakening of endogenous β-stimulation at night can cause a deterioration in bronchial patency both due to spasm of smooth muscles and due to degranulation of mast cells, causing an increase in histamine level. In healthy people, despite similar circadian changes in adrenaline levels, no increase in histamine levels is observed. This is most likely explained by the fact that unsensitized mast cells are more resistant, and a lower level of adrenergic stimulation is sufficient for their normal functioning (G. Ryan, 1982). T. Clark et al. (1984) when administering adrenaline at night, they obtained a positive result in reducing the level of histamine in the blood. Taking b-stimulants reduced the degree of nocturnal drop in bronchial bronchial patency in patients with asthma, i.e., the circadian rhythm of bronchial patency depends not only on the functioning of the sympathetic-adrenal system, but also on other regulatory systems.
It is known that at night the bronchoconstrictor tone of the vagus nerve increases. This position was confirmed in an experiment with vagotomy and the resulting significant decrease in the tone of the bronchial tract during REM sleep in dogs (Sullivan et al., 1979). In clinical studies of patients with AN (blind, placebo-controlled studies), atropine administered intravenously at a dose of 30 mg and ipratropium bromide administered via a nebulizer at a dose of 1 mg were shown to cause an increase in bronchial obstruction. At the same time, it is noted that the mechanisms and interpretation of the data obtained are difficult. Thus, it was found that the level of cGMP decreases at night, when the tone of the n.vagus increases, but the mechanism of the connection between them is not clear and requires clarification (Reinchardt et al., 1980). It was also indicated that vagal blocks do not affect the concentration of epinephrine in the blood plasma. Inhibition of bronchial sensitivity to histamine is also indicated.

Non-adrenergic - non-cholinergic innervation (NANCHI)

NANHI occupies an important place in the regulation of bronchial patency. The activity of the NANC system, including inhibitory and excitatory components, is currently being intensively studied in the clinic of internal diseases. NANC fibers are perhaps the only ones that have an inhibitory effect on human bronchial smooth muscle. Disruption of bronchodilator vasointestinal non-adrenergic innervation in asthma may explain complete bronchoconstriction (Ollerenshaw et al., 1989). Sensory neuropeptides, including substance P, neurokinins and calcitonin, can be released from C-fiber endings with possible involvement in the axon reflex mechanism (R. Barnes, 1986). Bronchial hyperresponsiveness is also subject to circadian fluctuations. The fact that the bronchial response increases during inhalation of histamine and allergens during the night has been shown in a number of studies (De Vries, 1962; Gervais, 1972). Increased bronchomotor tone and mucosal permeability, as well as the state of the receptors, play a role in bronchial hyperreactivity at night. Thus, despite quite extensive research, the mechanisms of occurrence of nocturnal attacks are not clear enough today. It is extremely difficult to identify a separate pathogenetic factor.
Nocturnal asthma can be defined as a fairly common, complex clinical, morphological and pathophysiological condition, which is based on bronchial hypersensitivity. This is due to various mechanisms, including both an increase in the activity of various physiological circadian rhythms (rhythmic changes in the lumen of the respiratory tract, changes in the sympathetic, parasympathetic, NANHI), and a decrease in the level of circulation of cortisol and adrenaline, which have an anti-inflammatory effect. This whole complex range of phenomena leads to the development of spasm of the smooth muscles of the bronchi, increased capillary permeability, the development of edema of the mucous membrane of the respiratory tract and, as a consequence, to bronchial obstruction at night.

Treatment of nocturnal asthma

Modern studies of the nature of AN, which have revealed the heterogeneity and diversity of the causes of nocturnal bronchoconstriction, have prompted us to reconsider the approaches to the treatment of this pathology that existed before the early 90s. It is necessary to point out that the very existence of AN in patients implies a loss of control over the patient’s condition, and therefore requires an increase in the activity of the therapy (Reinhardt et al., 1980; Van Aalderan et al., 1988). Quite controversial can be considered the established opinion that the first step is to prescribe adequate doses of inhaled steroids (Horn, 1984; T. Clark et al., 1984) or an oral short course of tableted hormonal drugs in combination with b 2 therapy -long-acting agonists, leading to a significant decrease in bronchial hyperreactivity and a decrease in inflammation of the mucous membrane of the bronchial tree (Kraan et al., 1985). It was believed that oral b 2 -agonists, when taken once in the evening, will prevent nocturnal bronchoconstriction through a direct relaxing effect on bronchial smooth muscle and an indirect effect on mast cells, which are the main cells involved in the inflammatory process.
Unfortunately, AN has proven resistant to conventional anti-asthma therapy, and nocturnal deterioration in breathing in many cases is the body's response to an increase in the dose of b2-agonists in therapy (Gastello et al., 1983), although bronchoconstriction is always quickly relieved by the use of a bronchodilator (Pedersen , 1985; Rhind et al., 1985). Recent work on the effects of prolonged forms of b 2 -agonists on mast cells during long-term use has shown a possible decrease in their effectiveness associated with a change in the number of receptors exposed on the outer surface of the plasma membrane of inflammatory cells and smooth muscle cells of the tracheobronchial tree (Neuenkirchen et al. .,1990). Inhaled forms of these drugs, most often used in medical practice, contribute to frequent awakenings of patients and, as a result, disrupt sleep and destabilize normal physiological rhythms. Therefore, the combination of prolonged forms of b 2 can be considered quite justified -agonists with membrane-stabilizing drugs, interest in which has increased many times and therefore they are becoming increasingly important in the treatment of patients with asthma (Stiles et al., 1990). Dwelling further on drugs of various groups, I would like to emphasize the importance of long-acting drugs with controlled drug release, which are perhaps the only option for drug treatment of nocturnal asthma. The use of high technology in the creation of such drugs, ease of use for the patient, a high degree of purification of the filler and a minimal risk of adverse reactions - these are the few undeniable qualities that put such drugs in first place when choosing drug therapy.
Theophyllines(TF) are the main drugs used in the treatment of asthma. Prolonged (“retard”) forms have opened a new page in the treatment and prevention of nocturnal asthma attacks (M. Martin et al., 1984).
The pharmacological effect of TF is based on inhibition of phosphodiesterase and increased accumulation of cyclic adenosine monophosphate in tissues, which reduces the contractile activity of smooth muscles of the bronchi, brain vessels, skin, kidneys, and also inhibits platelet aggregation and has a stimulating effect on the respiratory center. When taken orally, TFs are well absorbed from the gastrointestinal tract. The maximum concentration of the drug is achieved after 0.5 - 2 hours. The nature of food can affect the bioavailability and level of TF in plasma, which, in particular, decrease with a protein diet (Fedoseev et al., 1987). At therapeutic levels of concentration in the plasma of healthy people, 60% of TF is in free form. The total clearance of TF during intravenous infusion is 63.4 ml/min with a half-life of 6.7 hours (Fedoseev, 1987). No significant differences were found in the half-life of enteral and intravenous administration of TF (6.6 and 6.1 hours, respectively). Individual fluctuations in the half-life range from 3 to 13 hours (Jonkman, 1985). In addition, theophylline metabolism is subject to circadian changes (Busse, 1985), and administration of a daily dose in the evening (Jonston et al., 1986) produced the highest plasma concentrations in the early morning hours, when the risk of respiratory distress was highest, which is beneficial influenced bronchial patency (Chuchalin, Kalmanova, 1992). When prescribing the drug with a traditional 2-fold dose (extended 12-hour forms) to patients with asthma, there is insufficient control of difficulty breathing in the morning, since at night the absorption of TF worsens and a concentration is created significantly lower than in the daytime, especially in the elderly age (Schlueter, 1986). In studies by Govard (1986), the drug was administered once in the evening at the maximum daily dose. A single maximum dose did not cause an increase in side effects, and this dosage regimen is most optimal in patients with AN. An analysis of the effect of TF on the nature and degree of sleep disturbance in patients with nocturnal asthma was carried out by Madaeva et al. (1993). Studies have shown that the use of the drug Teopek in a dose of 450 mg once in the evening (before bedtime) significantly reduced asthma attacks in the early morning hours. Nocturnal passage through the bronchial tree also significantly improved, although the breathing pattern had a tendency toward hypoventilation. Significant improvement was also observed in the group of patients combining sleep apnea and AN; the number of apnea attacks sharply decreased during Teopec therapy. However, as studies have shown, TFs do not contribute to improving the structure of sleep itself, but in many cases worsen qualitative and quantitative indicators that were significantly changed initially, which is typical for the course of AN.
Thus, although it has a number of undeniable advantages, TF monotherapy nevertheless has a number of significant disadvantages that sharply limit its use. That is why in recent years a number of researchers (Pedersen, 1985; Rhind, 1985; Vyse, 1989) have proposed combination therapy that combines a single daily dose of TF with a therapeutic dose of a cyclopyrrolone drug (zopiclone). Cyclopyrrolone drugs have a high degree of binding to the GABA receptor complex in the central nervous system, thereby shortening the period of falling asleep, reducing the number of night awakenings, while maintaining a normal sleep structure (without reducing the proportion of REM sleep in it and improving sleep cycles). The recommended dose is 7.5 mg (1 tablet) for a single dose before bedtime for a course of 2 - 4 weeks. The following dosage regimen is recommended theophylline :
1. The first week of treatment begins with a single dose of 500 mg before bedtime:
. patients weighing less than 40 kg begin taking a single dose of 250 mg;
. for smokers, the dose of the drug is 14 mg/kg body weight, dividing the indicated dose into 2 doses: 2/3 in the evening before bed, 1/3 in the morning upon awakening;
. for patients with diseases of the cardiovascular system and liver dysfunction, the dose of the drug is 8 mg/kg body weight.
2. After 1 week, switch to taking a constant single dose:
. for body weight less than 70 kg - 450 mg at bedtime;
. with body weight more than 70 kg - 600 mg before bedtime.

Membrane stabilizing drugs

Of this group of drugs, the most interesting is sodium cromoglycate, the action of which is based on the inhibition of the release of mediators of the allergic reaction from “sitized cells” (in the lungs, inhibition of the mediator response prevents the development of both the early and late stages of the asthmatic reaction in response to immunological and other stimuli). A special feature of the drug is its reversible binding to plasma proteins (about 65%) and its non-susceptibility to metabolic breakdown, and therefore it is excreted unchanged from the body in urine and bile in approximately equal quantities. The second drug with a membrane-stabilizing effect is nedocromil sodium, the action of which is based on preventing the release of histamine, leukotriene C 4 , prostaglandin D 2 and other biologically active substances from the population of mast cells (mast cells) and other cells involved in the inflammatory response of the bronchi. Long-term use of the drug reduces bronchial hyperreactivity, improves respiratory function, reduces the intensity and frequency of asthma attacks and the severity of cough (Calhoun, 1992). Modern forms of the drug in the form of fine powder and dosed aerosol allow only 5% of the dose to be absorbed from the respiratory tract into the systemic bloodstream. The remaining 95% is removed from the lungs with a current of exhaled air or deposited on the walls of the oropharynx, then swallowed and excreted from the body through the digestive tract. It should be emphasized that, despite the fact that sodium cromoglycate is a fine powder, it is ineffective when the capsule is swallowed, and the effect of the drug develops only upon direct contact with the mucous membrane of the respiratory tract. According to the work of Fisher, Julyas (1985), the condition of patients with AN significantly improved in 85% of cases with its regular use. Apparently, sodium cromoglycate is the drug that underlies the preventive treatment of patients with AN.
Glucocorticosteroid drugs are widely used in the form of inhalation forms for the treatment of severe forms of asthma. Acting locally on the bronchial mucosa and having anti-inflammatory, anti-allergic and anti-exudative effects, restoring the patient’s response to bronchodilators, they, however, have not found their widespread use in patients with AN. The issue of their prescription is controversial, since when they are used in the maximum daily dose in the morning, there is an increase in the frequency and severity of asthma attacks at night (Givern, 1984). The use of inhaled forms of steroid drugs is controversial in nocturnal attacks of suffocation in patients with mild and moderate forms of asthma and is indicated in patients with severe forms of asthma as basic maintenance therapy.
Sympathomimetics are powerful bronchodilators. Selectively acting b 2 -agonists have the greatest effect. These drugs are resistant to the action of catechol-O-methyltransferase, preventing the release of histamine, a slow-reacting substance from mast cells and neutrophil chemotaxis factors (leukotrienes and prostaglandin D2). The creation of prolonged forms of these drugs was a new page in the prevention of nocturnal asthma attacks. Two types of drugs deserve the main attention: 1) prolonged 12-hour forms based on the hydroxynaphthoic acid salt of salmeterol; 2) drugs with controlled release of oral medicinal substances based on salbutamol sulfate. The ability to control the release of the drug allows for the creation of optimal therapeutic concentrations at night, which accordingly raises the question of the dosage regimen to obtain a lasting effect. In the work of Heins (1988), when comparing sympathomimetics and long-acting theophyllines, side effects (tachycardia and tremor) predominated in b 2 -agonists. Similar data were obtained in the work of Scott (1987). Arnaud et al. (1991) tried to show the effect of using prolonged forms of sympathomimetics in patients with AN in comparison with slow-release TF in 49 patients with nocturnal asthma attacks. The study revealed a greater severity of side effects when using TF than sympathomimetics (tremor, tachycardia). The number of awakenings from asthmatic attacks significantly decreased with a single dose of drugs from both groups in the evening, and the effectiveness of sympathomimetics was significantly higher, despite the lower concentration. Indicators of bronchial patency improved equally with the use of both TF and sympathomimetics. Based on this, it was concluded that sympathomimetics are preferable in patients with AN for reliable control of attacks of nocturnal breathlessness. The work of Dahl and Harving (1988) showed that when 12-hour aerosolized forms of sympathomimetics were prescribed in the evening hours, bronchial obstruction indicators significantly improved in patients with AN. When using 12-hour tablet forms (Koeter, Postma, 1985) - 2/3 of the daily dose in the evening and 1/3 of the daily dose in the morning - a similar dependence was noted. In a comparative study of sympathomimetics and glucocorticosteroids (Dahl, Pederson, 1989), preference was given to sympathomimetics, although in some cases effectiveness was shown only with their combined use. A comparative analysis of sympathomimetics and anticholinergic drugs did not show a significant difference when measuring patency rates (Wolstenholme, Shettar, 1988). The inconsistency of the data obtained in different years may be explained by both the imperfection of the technological process of preparing the drug (depending on the excipient, the size of the active particles and the form of preparation), and the lack of analysis of the effect of the drug on the nature, depth, cyclicity of night sleep and changes in circadian rhythms in patients with NA, since the latter are subject to significant variability and pathological variability under the influence of various pharmacological substances (Dahl, Pederson, 1990).
Assessment of the influence of sympathomimetics, TF and their combination on night indicators

Asthma attacks at night, or suffocation, are the last, pronounced degree of shortness of breath. This means that at such moments a person acutely feels a lack of air for normal breathing, and fear for his life appears due to a sudden attack. Choking in a person can develop for several reasons. These are foreign bodies entering the respiratory tract, a tumor in the bronchi or larynx, bronchial asthma, lung cancer, pneumonia, pneumothorax. Nocturnal asthma attacks are possible due to diseases of the cardiovascular system: myocardial infarction, heart disease, pericarditis.

The very phenomenon of suffocation is explained by the fact that at the time of an attack, oxygen stops flowing into the blood and obstruction of the airways occurs. At the same time, during the day a person may not be bothered by shortness of breath during any physical activity. So, attacks of suffocation and night cough can occur for the following reasons:

bronchial asthma, which causes obstruction of bronchial obstruction in the lungs;
, which disrupts the structure of the bronchial tree and, like myocardial disease, causes blood stagnation in the pulmonary circulation;
asthma with heart failure, which is also caused by stagnation in the pulmonary circulation.

Bronchial asthma at night

Asthma attacks at night can be caused by several factors. For example, the lungs may fill with an excessive amount of blood, which causes a decrease in the tone of the nervous system. Also, the cause of an attack can be a change in the person’s position in bed. Most people who face this problem find it very difficult to endure nighttime suffocation. In this state, the patient constantly tries to catch more air in his mouth, the skin becomes covered with cold sweat, and there are frequent cases of tachycardia.

When diagnosing, the doctor will clearly hear strong wheezing and crepitus above the base of the lungs. And in the next stages it will be wheezing over the entire surface of the respiratory organs.

More than half of cases of nocturnal asthma occur due to increased venous pressure in the patient. This can even be noticed visually: the veins in the neck swell more than usual. With this diagnosis, not only the lungs are damaged, the liver may enlarge, the subcutaneous tissue swells, and other signs of heart failure appear.

Attacks of suffocation at night also occur with left ventricular failure. However, you will most likely confuse this symptom with a regular cough.

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Bronchial asthma attack at night: what to do?

Nighttime panic associated with a sudden attack can be very frightening not only for the patient himself, but also for those around him. In such a situation, it is very important to have a balanced, confident and calm person nearby to help. He must be able to provide first aid and relieve the symptoms of bronchial asthma.

First, the patient must be rid of all tight clothing that can compress the body and interfere with proper breathing. Next, provide a constant flow of fresh air in the room and help during an attack to choose a comfortable position that will make it easier to breathe and cough. The optimal and correct option is considered to be the following: sit the patient astride a chair, while tilting him towards the back of the chair so that he transfers his weight to his arms.

There is a method using hot water, the temperature of which should be about 40 °C. You need to put either your arms or your legs in it. In this case, you can bend your arms at the elbow joints, and if you put your legs in the water, the easiest way to achieve muscle relaxation is to bend your knees and simply steam them. With this procedure, you can use mustard plasters. They are placed on the feet and hands.

The main thing is to know for sure that mustard will not cause allergic reactions in humans. If the cause of the attack is not bronchial asthma, but heart failure, then you can rub the heart area and chest with a cloth soaked in a solution of vinegar, water and salt. But for pulmonary diseases such compresses are contraindicated. In the case when you do not know the exact cause of the attack, it is better not to experiment and let the patient catch his breath.

If you see that in the evening symptoms of an upcoming attack of bronchial asthma have appeared, then an onion compress will help prevent it. To do this, you need to grate 2 onions and put the resulting mass on the area between the shoulder blades. Cover the area with paper, a cloth on top and wrap the patient in a woolen scarf. This compress must be kept for 3 hours, after which it must be kept warm.

In the event that suffocation does occur, you can use this technique to alleviate it. Place the patient on his back and, using two palms, press his chest 10 times as he exhales. This will help allow more air to enter the lungs when you inhale.

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Treatment of asthma attacks

An asthma attack at night is not just a cough, but the likelihood of complications and even the risk of death. The body will not be able to withstand for a long time without a normal supply of oxygen. Therefore, the patient must be constantly monitored by his attending physician.

Each patient suffering from suffocation needs an individual treatment plan, a course of medications and constant monitoring.

The treatment itself, depending on the development of the disease, may change. If this is your first time experiencing asthma attacks at night and you don’t know who to turn to, you need emergency medical help. And the diagnosis must be established after examination by a cardiologist, allergist, pulmonologist or psychotherapist.

Not everyone knows, but today asthma is one of the most common diseases on the planet. The scale of the problem is as follows: at least 5% of people on the globe suffer from bronchial asthma, and in some countries it is 10 or even 15% of the population, and their number continues to increase. Patients with bronchial asthma often experience breathing disorders during sleep. Moreover, in addition to the nocturnal asthmatic symptoms and attacks typical for this disease, a number of patients also experience obstructive sleep apnea. However, with apnea, in most cases a person does not subjectively feel suffocation and, as it seems to him, does not wake up. Objectively, such pauses in breathing lead to oxygen starvation of the body during sleep.

Relationship between bronchial asthma and obstructive sleep apnea

The combination of bronchial asthma and sleep apnea is a common occurrence. And the point is not only that both diseases are common, which means that the presence of two problems in one patient is simply possible according to the theory of probability. According to recent clinical studies of domestic and foreign specialists, on average, 25% of patients with bronchial asthma have obstructive apnea syndrome, which significantly exceeds the usual prevalence of sleep apnea among the general population. Moreover, the more severe a patient’s asthma, the higher the likelihood that he suffers from sleep apnea.

Why the combination of sleep apnea and bronchial asthma is so often not fully understood. It has been suggested that one of the reasons for this may be concomitant allergic rhinitis and swelling of the upper respiratory tract. Difficulty in nasal breathing leads to the fact that a person is forced to breathe predominantly through the mouth during sleep. Such “wrong” breathing contributes to increased vibrations of the walls of the pharynx, their vibration appears as the sounds of snoring.

A completely safe and highly effective hardware method for treating obstructive sleep apnea. And in patients suffering from bronchial asthma, eliminating sleep apnea makes an additional contribution to achieving optimal control over the course of their underlying disease.