Shortness of breath - a violation of the frequency, rhythm or depth of breathing, accompanied, as a rule, a feeling of lack of air.
If the nervous regulation of respiration is not impaired, shortness of breath has a compensatory significance (it is aimed at filling up the lack of oxygen and excreting excess carbon dioxide ). Respiration is a complex reflex act that involves: the cerebral cortex, the respiratory center, spinal nerves, chest muscles, diaphragm, lungs, cardiovascular system, and blood transporting gases. The clinical manifestations of dyspnea depend on the link in which the disorder has developed.
Dyspnea of the central type is associated with a disorder of cortical regulation of respiration or a primary lesion of the respiratory center. With neuroses (most often hysterical), shortness of breath is characterized by very shallow breathing with sharp tachypnea (see) - sometimes up to 50-70 breaths per minute. ("Dog breath"). The task of the paramedic is to calm the patient down, switch his attention, try to make him hold his breath, then breathe deeply and slowly. At the same time, they give sedatives: valerian tincture (1 teaspoon per 30 g of water), Adalin 0.5 g inside, inject Pipolphene 2 ml of a 2.5% solution intramuscularly.
Lesions of the respiratory center, especially in case of poisoning by hypnotics or drugs, usually manifest as respiratory depression (decrease in depth and frequency) and a violation of its rhythm (see Breathing). In these cases, apply the means of stimulating the respiratory center, - Cordiamine 5 ml intravenously, caffeine sodium benzoate 2 ml of a 20% solution subcutaneously or aminophylline 10 ml of a 2.4% solution with 10 ml of 40% glucose solution intravenously.
With a decrease in respiratory volume due to impaired mobility of the diaphragm or chest (meteorism, kyphoscoliosis, chest pain, etc.) or filling the pleural cavity with fluid (for example, hydrothorax), tachypnea rapidly develops during exercise. The signs of the main process (bloated belly, kyphoscoliosis, etc.) help to diagnose. The treatment is aimed at eliminating the cause - the puncture of the pleura with hydrothorax, the venting tube for meteorism, etc.Go
Pulmonary dyspnea may be associated with a decrease in the surface and insufficient elongation (restriction) of the lung tissue, a decrease in bronchial patency (obstruction), or impaired diffusion of gases in the alveoli. Restrictive type of dyspnea (usually with pneumosclerosis ) is characterized by difficulty in breathing (inspiratory dyspnea) and short expiration. Since the vital capacity of the lungs is reduced (see), the boundaries of the lungs are high, the depth of inhalation is limited. In the lungs, wheezing is often heard.
Diffusion insufficiency of the lungs, often combined with a restrictive-acidic process (pneumosclerosis), is characterized by abrupt dyspnea with tachypnea and marked "black" cyanosis (see) of the skin and mucous membranes. Dyspnea and cyanosis significantly increase with the slightest exertion. Treatment should be aimed at eliminating the cause of shortness of breath.
Most often, pulmonary dyspnea is associated with impaired bronchial patency due to spasm of the bronchi, their edema, or obstruction by sputum. Since the degree of bronchial obstruction is changeable, shortness of breath is unequally expressed on different days, sometimes disappears completely, sometimes reaches the degree of suffocation. Characterized by prolonged and difficult exhalation (expiratory dyspnea), swelling on the exhalation of the neck veins (due to increased pressure in the chest cavity) and signs of emphysema (see). Most patients with such shortness of breath, in contrast to patients with cardiac dyspnea, may lie low in bed; limbs are usually warm. In case of bronchial asthma (see), in the lungs, whistling dry rales on the expiration are heard, sometimes audible from a distance.
Treatment - bronchodilators: ephedrine by 0.025 g, or belladonna by 0.015 g orally, or teofedrin 1 / 2-1 tablet orally, or euphyllinum 1 ml of 24% solution intramuscularly (individual selection of medication and dose); with difficult sputum expectoration (see).Go
Cardiac dyspnea develops due to left heart failure, which is manifested either by a small cardiac output, or by congestion of blood in the lungs, or a combination of both. With a small cardiac output, the nutrition of the brain is disturbed; therefore, shortness of breath corresponds to clinically dyspnea of the central type, but increases with physical exertion. Blood stasis in the pulmonary veins violates gas exchange and conditions of ventilation of the lungs. In such cases, the frequency and depth of respiration increase, orthopnea occurs (see). Such shortness of breath may occur at night in a dream (see Cardiac asthma ), but more often after exercise. Cardiac dyspnea is often combined with edema and acrocyanosis (see), the extremities are cold. In the lungs, finely bubbling and medium-bubbling wheezes are often heard, and with the development of pulmonary edema - and large-bubbly. Due to the variety of mechanisms that form cardiac dyspnea, its treatment should be comprehensive, including digitalis , diuretics, prescribed by a doctor. In urgent cases, the paramedic should give the patient a half-sitting position, calm him down, give sedatives (as with dyspnea of the central type), oxygen; slowly inject 0.5 ml of a 0.05% solution of strophanthin with 10 ml of a 40% glucose solution (if the patient has not received digitalis preparations!) slowly, give 50 mg of hypothiazide or 40 mg of lasix orally.
Hematogenous dyspnea due to the effect on the respiratory center of acidic substances during acidosis or metabolic products (for example, kidney or liver failure). Acidosis causes a significant increase in the frequency and depth of breathing (polypnoea). In severe cases (for example, in diabetic coma), breathing becomes noisy (“Kussmaul’s large and noisy breathing”). Treatment — the fight against acidosis (see Restoration of the body ).
Often in patients with heart and lung diseases, the pathogenesis of dyspnea is mixed (for example, cardiac dyspnea may be complicated by a decrease in respiratory excursions due to flatulence, ascites or "respiratory panic" due to brain hypoxia, etc.). Therefore, the treatment should take into account the signs and those types of dyspnea, which in a particular patient are not leading.
Dyspnea (dyspnea; from the Greek. Dyspnoia - difficulty breathing) - a feeling of difficulty breathing, objectively accompanied by a change in its frequency, depth and rhythm.
Dyspnea usually has a compensatory nature and arises in connection with the need to maintain proper gas composition of the blood. In practically healthy people, dyspnea can occur during heavy physical exertion, when inoxidated metabolism accumulates in the blood in excessive amounts and the physiological state of oxygen debt develops. This causes a feeling of fatigue, a feeling of lack of air, rapid breathing. In such cases, shortness of breath becomes an important physiological protective mechanism that prevents overloading the body. The protective role of dyspnea of such origin becomes clear when you consider that breathing is regulated by the central nervous system. The respiratory center reflexively reacts to constantly received exterocene and interoceptive impulses and humoral influences, which are coming to it in connection with one or another state of metabolic processes in the body.
Often, breathing problems are not accompanied by a feeling of lack of air. Such conditions can occur with a rapid rise to height, with a lack of oxygen during work in breathing apparatus, with carbon monoxide poisoning, etc. In such cases, very rapid breathing is observed, however, an unpleasant feeling of lack of air may be absent.
Dyspnea occurs in a number of diseases and, as a clinical symptom, is of great diagnostic and prognostic significance. With some severe diseases, there are special respiratory disorders with a characteristic change in its rhythm - the respiration of Biota and Cheyne - Stokes. With biotovoy breathing separate deep breathing movements are replaced by long pauses. For Cheyne-Stokes breathing, there is a characteristic change of periods of increase in the depth and frequency of respiratory movements with periods of their gradual decrease until a temporary cessation of breathing (apnea), sometimes lasting 10-30 seconds.
Depending on the cause, mechanism of development, and clinical manifestations, cardiac, pulmonary, cardiopulmonary, cerebral, and hematogenous can be distinguished.
Heart Dyspnea . Already at an early stage of circulatory failure, the respiratory center is irritated, pulmonary ventilation increases, and shortness of breath soon appears due to physical exertion and food intake. As heart failure develops (mitral stenosis, cardiosclerosis, etc.), insufficient oxygen saturation of the blood occurs, the partial pressure of O 2 decreases and the CO 2 content in the blood increases, the minute volume of blood decreases, tissue hypoxia occurs. Oxygen indebtedness with circulatory failure reaches a noticeable value only at the far advanced stages of the disease.
Changes in hemodynamics and blood chemistry lead to reflex irritation of the baro-and chemoreceptors in the sinocarotid and aortic zones, vascular pulmonary network, hollow veins, and atria. As a result, a change in the functional state of the respiratory center occurs, shortness of breath occurs. Dyspnea is most often and clearly expressed in patients with mitral stenosis. This is due to increased pressure in the pulmonary artery system and stagnation in the pulmonary circulation.
Pulmonary dyspnea occurs with various disorders of the respiratory system. Severe dyspnea and dyspnea develop when the mucous membrane of the respiratory tract is exposed to irritating gaseous substances (chlorine, ammonia, etc.). In case of poisoning of a delayed-type chemical of phosgene, an early sign of intoxication is a gradually increasing respiration rate, a feeling of lack of air and anxiety. At occurrence of pulmonary edema, the phenomena of disturbance of gas exchange increase, shortness of breath and cyanosis intensify.
Dyspnea is common in acute pneumonia. Shallow and frequent breathing is associated with a decrease in the volume of functioning lung tissue and the irritating effect of the inflammatory process on the afferent endings of the vagus nerve, which causes a decrease in the threshold of the respiratory reflex. Dyspnea in pneumonia also depends on the effect on the respiratory center of toxic products entering the blood from the source of inflammation, fever, etc.
Dyspnea in pleurisy occurs due to changes in mechanical and aerodynamic factors of external respiration. Disturbances of the pulmonary component of the respiratory reflex, shifts in the gas composition of the blood are also important.
Severe dyspnea and asphyxiation in pulmonary embolism are accompanied by a feeling of unconscious fear, pain in the region of the heart with appropriate irradiation and circulatory disorder, sometimes simulating myocardial infarction. The sudden onset of severe dyspnea may be an early differential diagnostic diagnosis of pulmonary artery branch blockage.
Inspiratory dyspnea (difficulty breathing) occurs when the reflex spasm of the glottis. The choking that comes with it is accompanied by a feeling of fear; the breath is noisy, auxiliary muscles are involved in breathing. With swelling of the glottis of a toxico-infectious or allergic nature, severe shortness of breath develops quickly.
When a trachea is crushed by a tumor, shortness of breath develops gradually. The cause of inspiratory dyspnea is mechanical irritation of the proprioceptors of the lungs, intercostal muscles and the diaphragm by forced breathing. With the removal of obstacles (tracheotomy, removal of the tumor) shortness of breath immediately disappears.
Expiratory dyspnea (difficulty breathing out) occurs when the narrowing of the lumen of the small bronchi and bronchioles is due to spasm of the bronchial muscles, inflammatory or allergic edema of the bronchial mucosa. Expiratory dyspnea is usually observed in bronchial asthma. During an attack, the patient assumes a sitting position, resting his hands on the bed, which contributes to the involvement of auxiliary muscles in the breathing act. The phenomena of acute distention of the lungs develop, the lower border of the lungs falls and loses mobility, the intercostal spaces are smoothed out. When percussion is determined pulmonary sound with a timpanic shade.
Cardiopulmonary dyspnea occurs in severe forms of bronchial asthma and pulmonary emphysema. The sclerotic changes in the pulmonary artery that occur in these diseases lead to an increase in pressure in the pulmonary circulation, hypertrophy of the right heart and impaired hemodynamics.
Cerebral dyspnea occurs due to direct irritation of the respiratory center. Dyspnea of this type can occur with organic brain lesions in the region of the respiratory center (head injuries, tumors, parasitic brain lesions, hemorrhages and cerebral thrombosis, inflammatory processes and brain edema). Changes in breathing can be very diverse. Thus, brain abscesses are often accompanied by a significant reduction in respiration, with hemorrhages in the brain stem, periodic breathing may occur (see Pathological breathing). Cerebral dyspnea may occur with functional disorders of the nervous system. Dyspnea with respiratory neurosis, hysteria is characterized by very rapid and shallow breathing.
In infectious diseases, dyspnea is the result of a reflex and direct effect on the respiratory center of toxic products secreted by the causative agent of the disease and high temperature.
In conditions of oxygen starvation, various forms of dyspnea occur. Depending on the degree of hypoxia, the rate of occurrence and the duration of its action, respiratory disorders may be of the most diverse nature. With the gradual development of hypoxia, deep and rapid breathing then becomes shallow and more frequent. In the future, there is a reduction in respiratory movements, periodic forms of breathing appear (wave-like breathing, Cheyne-Stokes, Biota-type breathing), then convulsive atonal breathing movements, alternating respiratory paralysis can occur.
In the pathogenesis of these forms of respiratory disorders, along with direct dysfunctions of the respiratory center, an important role is played by impaired activity of higher educational systems of the brain.
Hematogenous shortness of breath occurs due to changes in the chemism of the blood. Hypercapnia and acidosis usually lead to a significant increase and increase in respiration, accumulation of toxic metabolic products (diabetic coma, uremia, anemia, etc.). In diabetic coma, Kussmaul's “big breath” is observed (deep noisy breaths). Hypoxemia is mainly characterized by increased respiratory movements. With significant hypoxemia, periodic forms of respiration may appear.
Hematogenous dyspnea can conditionally be attributed to dyspnea with exogenous intoxications (poisoning with morphine, alcohol, sleeping pills and drugs, nicotine, etc.). The form of shortness of breath in case of poisoning is determined primarily by the peculiarities of the toxic agent and can vary widely.