What to do with nighttime asthma attacks. Nocturnal asthma. Factors contributing to the development of the disease

Last article updated: April, 2019

Choking at night- This is a very alarming complaint that may be a manifestation of heart or lung disease. Patients endure this symptom very painfully, since it takes them by surprise during sleep, and in some cases there is no one nearby to help or hold, which further worsens the situation, horrifying the person and giving a feeling of helplessness and defenselessness.

It is not always possible to fall asleep after such an attack, as the patient is afraid of a second attack. But nighttime suffocation is not always a sign of illness; often patients with an overexcited nervous system experience exactly the same symptoms, while there is no real danger to their life. Therefore, in this article I would like to draw a line between dangerous and non-dangerous suffocation.

Please note that here we will not talk about suffocation that occurs for the first time, but only about suffocation that recurs from time to time over a long period of time. Since sudden suffocation that occurs for the first time (even during the daytime) may be a sign of an acute disease requiring emergency treatment (heart attack, thromboembolism, pulmonary edema, status asthmaticus, etc.).

So, to begin with, it should be said that in the vast majority of cases, the cause of a sudden attack of suffocation at night is a disease of the heart, lungs, or instability of the nervous system, including mental illness. Let's look at all possible states in order and discuss their distinctive features.

Nocturnal suffocation is a very common symptom for people suffering from heart failure. As a rule, patients complain that it is difficult for them to breathe air (there is a lack of air). Often this condition is accompanied by coughing and sweating.

Shortness of breath decreases when sitting and after taking diuretics; there may also be a positive effect after taking nitroglycerin. Such patients necessarily have some kind of chronic heart disease - hypertension or coronary artery disease, problems with valves, etc.

Heart failure does not occur out of the blue, therefore, in people suffering from attacks of night suffocation due to heart failure, changes in the heart are necessarily detected during examination. That is, it cannot be that a person suffers from heart failure at night, but during the day he has absolutely no complaints and all indicators, including ECG, ultrasound and chest x-ray are normal.

Angina is, first of all, a pressing or burning pain that usually occurs behind the sternum. But sometimes angina pectoris manifests itself not in the form of pain, but in the form of suffocation, the mechanism of which is associated with the development of acute, but short-term, heart failure. Such suffocation is difficult to distinguish from suffocation in chronic heart failure described earlier.

As a rule, patients suffering from attacks of suffocation at night due to angina pectoris have similar symptoms during the day, especially during physical exertion, while patients with heart failure do not experience suffocation during the day, but only shortness of breath.

An additional examination helps to identify angina (coronary heart disease) - a stress test (VEM, Treadmill, Stress ECHO) or radioisotope scanning (used routinely abroad).

Bronchial asthma

Asthma is a lung disease that is expressed in a sudden spasm of the bronchi (airways), which leads to a sharp decrease in ventilation of the lungs and, as a result, a lack of oxygen in the blood.

Nocturnal asthma attacks are quite common and, unlike “heart attacks,” they are accompanied by a feeling of incomplete exhalation (it’s hard to exhale air, not inhale!). Patients have the feeling that some kind of valve is working in the lungs, letting air in, but not letting it out.

Nitroglycerin and diuretics do not alleviate the patient’s condition in any way; only inhalers, for example, salbutamol, or intravenous administration of steroids (hormones) help.

Asthma is diagnosed based on complaints, family history (history) and spirometric examination of the lungs; alternatively, salbutomol is prescribed during an attack; if this brings relief, then the cause of such night suffocation becomes more obvious.

Many young people with unstable functioning of the nervous system (the so-called NCD or VSD) sometimes develop a feeling of suffocation at night. This, as a rule, is not even suffocation, but a feeling of lack of air.

This condition is accompanied by very vivid emotional experiences, and if patients with asthma and heart failure describe the attack in two or three words, then patients suffering from NCD, in addition to the suffocation itself, feel dozens of additional complaints: dizziness, nausea, palpitations, vague pain in the chest, fear , panic, trembling in the body, chills, sweating, etc. Of course, patients with heart and lung disease can also experience these symptoms, but suffocation is what bothers them 100 times more than all other accompanying “little things.”

In patients with NCD, everything interferes simultaneously and equally strongly. These studies do not reveal any deviations from the norm, and the age of such patients usually does not exceed 30-40 years. Most of them undergo examinations many times, go to different specialists, believing that they are terminally ill, but the doctors do not understand this. In this group of patients, a good effect is achieved with the help of sedatives, tranquilizers, antipsychotics, and even better - psychotraining.

From all of the above, we can say that when assessing chronic nocturnal suffocation, one must be guided by the principle “there is no smoke without fire.” And if during the day the patient is completely “healthy” according to the examination and consultation with specialized specialists, then you should not “get hung up”, but should try to solve this problem with a psychotherapist or psychiatrist, especially since there will definitely be no harm from this.

In conclusion, it should be noted that although this article was written for patients, it is not a guide for diagnosis; the decision is always made by the doctor.

S. L. Babak
Candidate of Medical Sciences, employee of the sleep laboratory, Research Institute of Pulmonology, Ministry of Health of the Russian Federation, Moscow

With the accumulation of clinical and experimental data, views and ideas on some features of the course of bronchial asthma (BA) led to the advisability of isolating and studying 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 5th National Congress on Respiratory Diseases (Moscow, 1995), and characterized by awakening from respiratory discomfort at night. On the other hand, there are distorted ideas about “overlap syndrome” (OVERLAP), which is defined as a combination of the phenomena of breathing pauses during sleep (obstructive sleep apnea-hypopnea syndrome) with existing chronic obstructive pulmonary disease, a variant of which is. Thus, knowledge is currently being accumulated about the nature, nature and mechanisms of development of such a phenomenon as nocturnal respiratory disorders in patients with asthma, which determines 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 (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, the issues of pathogenetic mechanisms and treatment of this manifestation of AD 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 asthma (Vein, 1992).

Potential mechanisms of bronchial obstruction in AN.

It is known that in most healthy individuals the airways are subject to circadian fluctuations. (Lewinsohn et al., 1960; Kerr 1973; 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 decline in FEV 1 and PEF. However, the magnitude of the fall amplitude in healthy people was 8%, and in patients with asthma - 50% (in some patients it exceeded 50%). Patients with this level of drop in nocturnal bronchial patency are called “morning dippers.” (Lewinsohn et al., 1960; Reinberg, 1972; Soutar, Costello, Ljaduolo, 1975; Clark 1977). Studies by Clark (1977), Gaulter (1977), Barnes (1982) show that the greatest number of awakenings associated with bronchospasm occur from the middle of the night to the early morning (from 02.00 to 06.00). Bellia and Visconti (1989), studying the PEF reaction at different times of the day, consider this indicator a diagnostic criterion for nighttime 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, Hetsel (1977) found that in patients with exacerbations of asthma at night, FEV 1 and PEF significantly decrease, and 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 an 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). (Reinberg et al., 1972; Gervais 1972; Sherr et al., 1977). This hypothesis was confirmed by experimental work in which patients with atopic asthma underwent dust inhalation for several days, which caused a night-time deterioration of bronchial obstruction and the induction of attacks of AN (Davies et al., 1976). At the same time, the assumption about the role of allergens in the occurrence of AN is questioned by studies by Clark and Hetzel (1977), showing that attacks of AN occur in the absence of an allergen.

An interesting study traced the relationship between reagin IgE antibodies involved in an allergic reaction with other mediators and biogenic amines. Thus, it was revealed that the acrophase of IgE antibodies occurs in the period from 05.00-06.00 hours, that is, it is in the pre-morning hours that the process of activation and release of inflammatory mediators (IgE and histamine) inducing an asthmatic response occurs.

Esophageal reflux and aspiration.

According to Martin et al. (1982), the appearance of asthma attacks at night is also influenced by such a factor as gastroesophageal reflux. In a horizontal position, aspiration or reflux of 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 subsequently confirmed by a number of studies. (Davis et al., 1983; Hughes et al. 1983; Riulin 1983; Waters et al., 1984; Perpina 1985; Pellicer et al., 1985). Identification of this mechanism allows, when prescribing appropriate treatment, to eliminate the above-described provoking moment (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 is debated in the literature. It has been suggested that the increase in obstruction during sleep depends on the patient's body position. Whyte, Douglas, (1983), believe that the patient’s position does not cause prolonged bronchospasm in patients suffering from asthma attacks at night. Conducted studies of PEF and FRC in 31 pediatric patients from 2.8 to 8.3 years, ten of whom had frequent nocturnal attacks, and eleven were completely absent, in the sitting and lying position revealed a significant drop in PEF in the supine position for all tics , and the percentage of reduction in patients with AN and without nocturnal attacks was the same. FRC also showed a decreasing trend. The level of FRC reduction 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 mechanism is absent in patients with a small amount of sputum (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 eNA has also received considerable 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 technically 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. Lopes et al. (1983) measured total airway resistance and inspiratory muscle activity during sleep. In healthy people, 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 associated with an increase in airway muscle tone, which leads to an increase in the work of breathing during sleep and, as a result, a reduction in breathing difficulty. 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 with a halving of peak flow measurements (Catterall 1985; Rhind et al., 1986). These results, although they confirm the role of night sleep in the genesis of the disease, do not clarify the mechanisms of its influence. Sleep interruption prevents the development of bronchial obstruction (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 (Clark et al., 1989). When trying to study the connection between sleep stages and tic attacks, it was revealed that the number of attacks is “scattered” throughout the entire sleep period (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, which 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. (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. (Lopes et al.,1983). However, in subsequent similar studies, this pattern was not revealed in healthy individuals. (Brown 1977; Ingram et al., 1977). Thus, the determination of airway resistance and the level of bronchial patency in various stages of sleep is technically intractable today. The existing work addressing 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, the work of Shu Chan (1987) showed that apnea is part of the “trigger” mechanism for the occurrence of nocturnal asthma attacks 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 (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. (Kerr,1973). When asthmatics were placed in a room overnight at a temperature of 36 o -37 o C with 100% oxygen saturation in the inspired air, falls during the night were eliminated in 6 out of 7 tics (Chen et al., 1982).

Inflammation of the respiratory tract.

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. all (1989) distinguish among the endogenous circadian rhythms the following possibly influencing NA: physiological, biochemical, inflammatory. Of great interest is the connection between nocturnal deterioration of breathing and circadian changes in hormones. Reinberg et al. (1963) suggested a connection between nocturnal bronchospasm and low levels of urinary excretion of 17-hydroxycorticosteroids. In 1969 Reinberg et al. confirmed the opinion that the level of circulating catecholamines decreases at night. Connoly (1979), Soutar (1977) identified a relationship 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 an association with a decrease in histamine and cyclic nucleotide levels (Barnes et al., 1980; Reinhardt et al., 1980). The results obtained by Reinberg in 1972 are interesting, when the following patterns were determined when ACTH was administered to healthy individuals: the maximum increase in cortisol and MOS was observed when ACTH was administered at 7.00, the minimum at 21.00. However, earlier Hetsel (1980) and Clark (1980) showed that fluctuations in MOS persisted even against the background of constant administration of glucocorticoids, which is quite consistent with the earlier assumption made by 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 secretion from the adrenal glands 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 Szefler (1991), Ando et al. (1991). The content of histamine in plasma, adrenaline, cortisol, cAMP and b - adrenergic receptors on peripheral blood lymphocytes were studied in 7 patients with AN, 10 healthy individuals and 10 tics without night attacks at 04.00 in the morning and at 16.00. There was a 2-fold increase in the concentration of histamine in the blood at 16.00 in all studied individuals, as well as the content of adrenaline and cortisol on peripheral blood lymphocytes. 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 that occurs at 3-4 am correlates with a deterioration in bronchial patency, which leads to attacks of suffocation (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 b-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 non-sensitized mast cells are more resistant, and a lower level of adrenergic stimulation is sufficient for their normal functioning (Ryan et al., 1982). Horn (1984), Clark et al. (1984) with the administration of adrenaline at night 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, that is, 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 (Baustw, Bohnert, 1969). 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 in patients with AN (blind, placebo-controlled studies), atropine administered intravenously at a dose of 30 mg and ipratropium bromide administered by 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).

Non-adrenergic - non-cholinergic innervation (NANC) occupies an important place in the regulation of nocturnal 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 gene-inducing peptide, can be released from C-fiber terminals with possible involvement in the axon reflex mechanism (Barnes, 1986). Bronchial hyperresponsiveness is also subject to circadian fluctuations. The fact that the bronchial response increases when histamine and allergens are inhaled overnight 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.

Thus, nocturnal 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 sympathetic, parasympathetic, non-adrenergic, non-cholinergic innervation), 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 NIGHT 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 is the established view that the first step is the administration of adequate doses of inhaled steroids (Horn 1984; Clark et al., 1984) or a short course of oral hormonal tablets in combination with therapy b