Bronchial asthma (BA) is one of the most common diseases in the world. This pathology affects 5% of the world’s population, with two–thirds of patients with AD having night–time bronchospasm attacks, which significantly worsens the quality of sleep and, as a result, increases the severity of the disease . These night–time attacks are commonly referred to as night–time asthma. It is characterized by a significant decrease in the daily rhythm of bronchial permeability during the night’s sleep. Naturally, effective night–time care is very difficult.
The first mention of asthma at night dates back to the 17th century. As early as 1698, Dr. John Floyer, an asthmatic himself, wrote: “I noticed that the attack always occurs at night… At the first waking up, around 1 or 2 a.m., the attack of asthma becomes more obvious, breathing slows down…, the diaphragm seems to be hard and squeezed… It can be very difficult to go down“. Despite such a clear description, it took at least two and a half centuries for asthma to receive more attention at night. There was a dispute between specialists about whether the number of deaths among people with AD increased at night or not. The published joint results of four studies showed that 93 out of 219 deaths occurred between midnight and 8 a.m., which in itself indicates a significant (P< 0.01) increase in the number of deaths at night . Of course, the mortality rate is higher at night than in the rest of the population, but it is only a 5% increase in the number of deaths between midnight and 8 a.m., as opposed to a 28% increase in the same rate among asthmatic patients . Eight out of ten cases of respiratory arrest in asthmatic patients – already in hospital – also occurred in the early morning .
The accelerated volume of exhaled air (forced expiratory volume) in 1 second (PEO) and pycfluometry in asthma patients fall sharply during the night, with the majority of patients more than 50%. Among patients in remission, approximately one third have bronchospasm only at night, and another third have it before bedtime and continue throughout the night. Thus, two thirds of these patients have the lowest bronchial passability between 10 p.m. and 8 a.m..
Most healthy people also experience daily changes in bronchial caliber with night–time bronchospasm. A significant number of studies comparing the daily changes in bronchial permeability in healthy subjects and unstable asthmatic patients showed that, although the changes in asthmatics and healthy subjects are indeed synchronous, the amplitude of the decrease in bronchial permeability in patients with bronchial asthma is significantly higher (50%) than in healthy subjects (8%).
Lack of sleep during the night reduces the degree of nightly narrowing of the respiratory tract. The fact that some narrowing of the airway during the night may persist, even if the patient is awake all night (e.g., during shift work), may be due to changes in the daily rhythms of each individual.
Thus, a night–time bronchospasm in asthma appears to exceed the normal level of daily changes in bronchial caliber. It is a consequence of hypersensitivity to factors causing mild night–time bronchospasm in healthy subjects.
Possible, albeit less likely, causes of airway constriction at night include the position of the body during sleep, interruption of treatment, and the presence of allergens in bedding. On the other hand, the position of the body probably does not affect the width of the bronchial lumen, at least because patients who are in bed around the clock continue to have bronchospasm attacks, mainly at night. The length of time between medication is also not fundamental; regular use of bronchodilators during the day does not lead to the disappearance of night–time bronchospasm, and night–time breathing difficulties are still the subject of complaints from many untreated asthma patients. It is also unlikely that the presence of allergens in bedding is the primary cause of night–time asthma, as their removal, contrary to expectations, does not contribute to the elimination of night–time bronchospasm. However, it is likely that exposure to domestic allergens increases the degree of bronchial reactivity in patients with a corresponding predisposition and may thus lead to night–time bronchospasm.
Bronchospasm in asthma patients may also be caused by cold and dry air. Nighttime asthma is expected to be associated with inhaling cooler air at night or cooling the bronchial wall as a result of a decrease in body surface temperature during the night. It is unlikely that the temperature and humidity of the inhaled air will play a fundamental role, since during the night bronchospasm is persistent even in healthy subjects, when the temperature and humidity of the air are maintained at a constant level during the day. However, one study showed that inhaling warmer and wetter (36–37C, 100% humidity) air during the night compared to room air (23C, 17–24% humidity) resulted in the disappearance of night–time bronchospasm in six of the seven asthma patients who participated in the study. However, this study, firstly, was not numerous, and secondly, it was conducted without polysomnographic control, so it remains unclear how well these patients slept.
The main complaint of patients with night–time asthma attacks is that their sleep is impaired and they often feel tired and sleepy during the day. This type of sleep disturbance has been confirmed by studies conducted in the EEC countries. Nightly bronchospasm attacks are an indicator of the severity of AD, so the diagnosis of such conditions is necessary, for which it is recommended to clarify the daily rhythm of the onset of asphyxiation attacks, the number of wake–ups during the night, the nature and quality of sleep. To this end, patients with AD, especially those with signs of night–time asthma, undergo a polysomnographic study. In the course of this study, in real time, during the night’s sleep of the patient, carry out a one–stage registration of EEG channels (leads C3 / A2 and C4 / A1), EEG of the left and right eyes, EMG from the chin muscles, the sensor of air flow breathing; Sensors of thoracic and abdominal respiratory force; microphone reading (snoring) and body position sensor reading; ECG (precardial leads); pulse and blood oxygen saturation (SaO2) recording. In addition, obstructive sleep apnea syndrome (respiratory arrest with complete cessation of airflow in the respiratory tract for at least 10 seconds) can be detected in patients during a polysomnographic examination, which further aggravates the course of bronchial asthma.
Several groups of researchers have recorded electroencephalogram (EEG) readings of patients with asthma in sleep, with attention paid to the stage of sleep, during which patients woke up with asthma attacks. The largest of these studies revealed that asthma attacks occur at all stages of sleep with a frequency proportional to the sum of time spent in each stage of sleep. This study, conducted using a sleep laboratory, woke up asthmatic patients for two nights during the dreaming phase of sleep (REM–sleep) or during low–wave sleep (NREM–sleep), followed by picfluometry. The results showed that the pycfluometry data were lower when awakened from REM sleep than from NREM sleep. However, the difference between these figures averaged only 200 ml, while the fall of PEEE overnight was about 800 ml. Exhalation time during bronchospasm should have increased, and it was initially thought that asthma patients had asthma that increased during REM sleep. Further studies have shown that there is no change in the mean pycfluometric values between the individual stages of sleep in general, but that the duration of exhalation is noticeably more variable during REM sleep, which corresponds to the general irregularity of frequency and depth of breathing at this stage. As with healthy subjects, asthma patients have reduced ventilation as they move from waking to different stages of sleep; the ventilation level becomes lower during NREM sleep compared to waking and the lowest levels are recorded during REM sleep. In addition, recent studies have shown that nighttime asthma leads to oxygen desaturation during sleep and therefore to chronic hypoxemia.