Respiratory depression from drugs, symptoms, treatment. Acute poisoning: respiratory disorders. Treatment of respiratory disorders

Respiratory failure- this is a pathological condition of the body, in which the maintenance of a normal gas composition is not ensured arterial blood or it is achieved due to such work of the external respiration apparatus, which reduces the functional capabilities of the organism. The term "respiratory failure" is synonymous with "lack of external respiration". The term "respiratory failure" is physiologically more justified, since it covers the occurrence of secondary pathological and compensatory changes in the respiratory system in case of damage to the pulmonary link. From the same point of view, it is inappropriate to equate the concepts of "respiratory failure" and "pulmonary failure". Lung failure is caused by a pathological process in them and is characterized not only by the occurrence of respiratory failure, but also by a violation of other functions - immunity, acid-base balance, water-salt metabolism, prostaglandin synthesis, metabolite release, homeostasis regulation, etc.

Respiratory failure can occur with various pathological processes in the body, and in pulmonary pathology it is the main clinical and pathophysiological syndrome.

Pathogenesis respiratory failure in lung disease is most often caused by a violation of the function of the external respiration apparatus. The main pathophysiological mechanisms for the development of respiratory failure are: a) violations of the processes of ventilation of the alveoli, b) changes in the diffusion of molecular oxygen and carbon dioxide through the alveolocapillary membrane, c) impaired perfusion, i.e. blood flow through the pulmonary capillaries.

Violations of ventilation of the alveoli can be caused by disorders in the function of individual links of the external respiration apparatus - centrogenous (respiratory center of the brain), neuromuscular (motor neurons of the spinal cord, peripheral motor and sensory nerves, respiratory muscles), thoraco-diaphragmatic (thorax, diaphragm and pleura) and bronchopulmonary (lungs and airways).

Function respiratory center may be impaired due to direct action on the central nervous system of various pathogenic factors or reflexively. Pathogenic factors that cause depression of the respiratory center are drugs and barbiturates, metabolic products that linger in the blood (for example, carbon dioxide or underoxidized organic acids), stroke or any other vascular catastrophe in the brain, neurological diseases or increased intracranial pressure. With violations of the functions of the respiratory center, respiratory failure develops due to a decrease in the depth and frequency of breathing, disorders of its rhythm ( different kinds periodic respiration - Cheyne - Stokes respiration, Biot).

Motor neuron function spinal cord, innervating the respiratory muscles, can be disrupted with the development of a tumor in the spinal cord, with poliomyelitis. The nature and degree of disturbance of external respiration in this case depend on the site of damage to the spinal cord (for example, if the pathological process affects the cervical part of the spinal cord, the work of the diaphragm is disrupted) and on the number of affected motor neurons.

Violation of ventilation can occur when the nerves innervating the respiratory muscles are damaged (inflammation, beriberi, trauma), with partial or complete paralysis of the muscles (as a result of the use of relaxants, tetanus, botulism, hypokalemia, poisoning with curare-like poisons, etc.), with a violation of the function of the muscles themselves respiratory muscles (myositis, dystrophy).

The function of the thoraco-diaphragmatic link of the external respiration apparatus can be impaired in the following cases: 1) due to pathology chest(congenital or acquired deformation of the ribs and spinal column, for example, fracture of the ribs, kyphoscoliosis, Bechterew's disease, ossification of the costal cartilage, etc.), 2) with a high standing diaphragm (paresis of the stomach and intestines, flatulence, ascites, obesity), 3) with the presence of pleural adhesions, 4) compression of the lung with effusion, as well as blood and air in hemo- and pneumothorax. Excursions of the chest can be limited to sharp pains that occur during breathing, for example, with intercostal neuralgia, inflammation of the pleura, etc.

Violations of the function of the bronchopulmonary link of the external respiration apparatus are caused by various pathological processes in the airways and lungs.

Alveolar ventilation disorders, depending on the mechanisms that cause these disorders, are divided into obstructive, restrictive and mixed.

Obstructive insufficiency of ventilation of the alveoli occurs due to narrowing of the airways lat., obstructio - an obstacle) and increase the resistance to air movement. With difficulty in the passage of air in the airways, not only the ventilation of the lungs is disturbed, but also the mechanics of breathing. Due to the difficulty of exhalation, the work of the respiratory muscles sharply increases. Decreased VC, FVC and MVL.

Obstructive disorders of alveolar ventilation are usually caused by bronchial spasm or their local damage (tumor in the bronchi, cicatricial stenosis, inflammatory or congestive swelling of the bronchial mucosa, hypersecretion of bronchial glands, etc.).

Restrictive type of violation of ventilation of the alveoli due to a decrease in the respiratory surface of the lungs or their extensibility (from lat., restrictio - restriction, reduction). The latter limits the ability of the lungs to expand. To compensate for this and achieve the desired change in lung volume, more than usual transpulmonary pressure must be generated during inspiration. This, in turn, increases the work done by the respiratory muscles. Breathing becomes difficult, especially during physical exertion, VC and MVL decrease.

A decrease in lung volume, manifested by a restrictive type of ventilation insufficiency, is observed in acute and chronic massive inflammatory processes and congestion in the lungs, with tuberculosis, pneumonia, chronic heart failure, exudative pleurisy, spontaneous pneumothorax, pulmonary emphysema, massive obstructions to chest expansion (kyphoscoliosis), thickening of the interstitial tissue (pneumosclerosis), etc. Restrictive insufficiency of external respiration can lead to destruction of large areas of lung tissue by a tuberculous process, removal of a segment, lobe of the lung or the whole lung, atelectasis.

The development of restrictive ventilation disorders is also facilitated by a change in the activity of the lung surfactant as a factor that reduces the surface tension of the fluid lining the inner surface of the alveoli. Insufficient activity of the surfactant leads to the collapse of the alveoli and the development of atelectasis, hindering the diffusion of oxygen.

Mixed type of violation of ventilation of the alveoli characterized by the presence of signs of both obstructive and restrictive ventilation disorders.

Violation of lung ventilation can be caused by uneven air flow into individual zones of the lung. In diseases, their healthy areas are filled faster than the affected ones. Gas is also removed from them faster during exhalation, therefore, with a subsequent inhalation, gas from the dead space of pathologically altered zones of the lungs can enter healthy areas.

A certain role in the pathogenesis of respiratory failure is played by the state of capillary blood flow in the pulmonary artery. Respiratory failure due to a decrease in lung perfusion (the flow of an appropriate amount of blood through the pulmonary capillaries) can lead to left and right ventricular heart failure (myocardial infarction, myocarditis, cardiosclerosis, exudative pericarditis, etc.), some congenital and acquired heart defects ( pulmonary stenosis, stenosis of the right atrioventricular orifice), vascular insufficiency, embolism pulmonary artery. Since, under these conditions, the minute volume of blood decreases and its movement in the vessels of the systemic circulation slows down, the tissues experience oxygen starvation, and there is a lack of oxygen and an excess of carbon dioxide in the blood.

Respiratory insufficiency is divided according to etiology into primary and secondary; according to the rate of formation of clinical and pathophysiological manifestations - into acute and chronic; by changes in the gas composition of the blood - into latent, partial and global.

Primary respiratory failure due to damage directly to the external respiratory apparatus, and secondary- pathology of other parts of the respiratory system (circulatory organs, blood, tissue respiration).

Acute respiratory failure- This special form violation of gas exchange, in which the supply of oxygen to the blood and the removal of carbon dioxide from the blood cease, which often ends in asphyxia (cessation of breathing). In the development of acute respiratory failure, three stages are distinguished - initial, deep hypoxia and hypercapnic coma.

In the initial stage, carbon dioxide, rapidly accumulating in the body, excites the respiratory center, bringing the depth and frequency of breathing to the maximum possible values. In addition, respiration is reflexively stimulated by a decrease in molecular oxygen in the blood.

In the stage of deep hypoxia, the phenomena of hypoxia and hypercapnia increase. The heart rate increases, blood pressure rises. With a further increase in carbon dioxide in the blood, its narcotic effect begins to manifest itself (the stage of hypercapnic coma), blood pH decreases to 6.8 - 6.5. increased hypoxemia and, accordingly, hypoxia of the brain. This, in turn, depresses breathing, lowers blood pressure. The result is respiratory paralysis and cardiac arrest.

The causes causing acute respiratory failure can be severe mechanical damage, compression syndrome, foreign body aspiration, obstruction of the upper respiratory tract, sudden bronchospasm (for example, a severe choking attack or an asthmatic condition in bronchial asthma), extensive atelectasis, inflammation, or pulmonary edema.

Chronic respiratory failure It is characterized by a gradual increase in gas exchange disorders and the tension of compensatory processes, which are manifested by hyperventilation and increased blood flow in the unaffected lung tissue. The timing of the development of chronic respiratory failure (months or years) and its stages depend, respectively, on the rate of aggravation and the degree of violations of alveolar ventilation, gas diffusion and perfusion. As chronic respiratory failure worsens, the work of the respiratory muscles at rest increases more and more, the volumetric blood flow rate and redistributive vascular reactions increase, aimed at increasing the amount of oxygen transported by arterial blood. Increases metabolism and the body's need for oxygen. As a result, there comes a moment when, even at rest, maintaining a normal blood gas composition becomes impossible. Then, with a decrease in the compensatory capabilities of the cardiovascular system and the blood system, tissue hypoxia, hypercapnia and gaseous acidosis develop.

In the development of chronic respiratory failure, three stages or degrees are distinguished: 1 - latent, latent, or compensated, 2 - pronounced, or subcompensated, and 3 - pulmonary-cardiac decompensation, or decompensated.

Depending on changes in the gas composition of the blood, latent, partial and global respiratory failure are distinguished. Latent respiratory failure is not accompanied by disturbance of the blood gas composition at rest, but compensation mechanisms are strained in patients. With partial respiratory failure, arterial hypoxemia or venous hypercapnia is noted. Global respiratory failure is characterized by arterial hypoxemia and venous hypercapnia.

Main clinical manifestations of respiratory insufficiency are shortness of breath and cyanosis, additional - anxiety, euphoria, sometimes drowsiness, lethargy, in severe cases - lack of consciousness, convulsions.

Shortness of breath (dyspnea) - a feeling of lack of air and the associated need to increase breathing. Objectively, shortness of breath is accompanied by a change in its frequency, depth and rhythm, as well as the ratio of the duration of inhalation and exhalation. The presence of a painful feeling of lack of air, which causes the patient not only involuntarily, but also consciously to increase the activity of respiratory movements, is the most significant difference between dyspnea and other types of respiratory dysregulation - polypnea, hyperpnea, etc.

Shortness of breath is caused by excitation of the inhalation center, which extends not only to the periphery to the respiratory muscles, but also to the overlying parts of the central nervous system, so it is often accompanied by a feeling of fear and anxiety, from which patients sometimes suffer more than shortness of breath itself.

Subjective sensations do not always coincide with its objective signs. So, in some cases, patients complain of a feeling of lack of air in the absence of objective signs of shortness of breath, i.e. there is a false sensation of shortness of breath. On the other hand, there are cases when, in the presence of constant shortness of breath, the patient gets used to it and ceases to feel it, although there are all external manifestations of shortness of breath (the patient suffocates, often takes a breath when talking) and significant disturbances in the function of external respiration.

Inspiratory dyspnea, which is characterized by difficulty in inhaling, occurs when the lumen of the upper respiratory tract narrows (diphtheritic croup, laryngeal swelling, tracheal compression). With expiratory shortness of breath, exhalation is difficult, which can be observed during an attack of bronchial asthma. Mixed dyspnea is characterized by difficulty in both the inspiratory and expiratory phases and occurs in lung diseases accompanied by a decrease in the respiratory surface.

The second important clinical sign respiratory failure is cyanosis - a bluish coloration of the skin and mucous membranes, due to the high content of reduced hemoglobin in the blood. Cyanosis is detected clinically only when the circulating blood contains more than 50 g / l of reduced hemoglobin (the norm is up to 30 g / l). In acute respiratory failure, cyanosis may develop within seconds or minutes; in chronic respiratory failure, cyanosis develops gradually. Cyanosis is more noticeable on the lips, face, fingers, and nails.

It is customary to distinguish between central and peripheral cyanosis. Respiratory failure is characterized by central cyanosis, which is characterized by diffuseness and an ash-gray skin tone. Due to increased blood flow, the skin is warm to the touch (“warm cyanosis”). Peripheral cyanosis is caused by a slowdown in blood flow in the tissues and is observed in diseases of the heart - vascular system. This cyanosis has the character of acrocyanosis - expressed on the hands and feet, on the earlobes, often has a reddish tint, the skin is cold to the touch ("cold cyanosis"). If, after 5 to 10 minutes of inhalation of pure oxygen, cyanosis disappears, this confirms the presence of peripheral cyanosis.

Breathing is a set of physiological processes that provide oxygen to human tissues and organs. Also, in the process of breathing, oxygen is oxidized and excreted from the body in the process of metabolism of carbon dioxide and partially water. The respiratory system includes: nasal cavity, larynx, bronchi, lungs. Breathing consists of them stages:

• external respiration (provides gas exchange between the lungs and external environment);
• gas exchange between alveolar air and venous blood;
• transport of gases through the blood;
• gas exchange between arterial blood and tissues;
• tissue respiration.

Disturbances in these processes may occur due to diseases. Serious breathing disorders can be caused by such diseases:

• Bronchial asthma;
• lung disease;
• diabetes;
• poisoning;

External signs of respiratory failure make it possible to roughly assess the severity of the patient's condition, determine the prognosis of the disease, as well as the localization of damage.

Causes and symptoms of respiratory failure

Breathing problems can be caused by a variety of factors. The first thing to pay attention to is breathing rate. Excessively rapid or slow breathing indicates problems in the system. Also important is breathing rhythm. Rhythm disturbances lead to the fact that the time intervals between inhalations and exhalations are different. Also, sometimes breathing can stop for a few seconds or minutes, and then it appears again. Lack of consciousness may also be associated with problems in the airways. Doctors are guided by the following indicators:

• Noisy breathing;
• apnea (stop breathing);
• violation of the rhythm / depth;
• Biot's breath;
• Cheyne-Stokes breathing;
• Kussmaul breathing;
• tychipnea.

Consider the above factors of respiratory failure in more detail. noisy breathing This is a disorder in which breath sounds can be heard from a distance. There are violations due to a decrease in airway patency. It can be caused by diseases, external factors, rhythm and depth disturbances. Noisy breathing occurs in the following cases:

• Damage to the upper respiratory tract (inspiratory dyspnea);
• swelling or inflammation in the upper airways (stiff breathing);
• bronchial asthma (wheezing, expiratory dyspnea).

When breathing stops, disturbances are caused by hyperventilation of the lungs during deep breathing. Apnea causes a decrease in the level of carbon dioxide in the blood, disrupting the balance of carbon dioxide and oxygen. As a result, the airways narrow, the movement of air becomes difficult. IN severe cases observed:

• tachycardia;
• decline blood pressure;
• loss of consciousness;
• fibrillation.

IN critical cases cardiac arrest is possible, since respiratory arrest is always fatal to the body. Doctors also pay attention when examining depth And rhythm breathing. These disorders can be caused by:

• metabolic products (slags, toxins);
• oxygen starvation;
• craniocerebral injuries;
• bleeding in the brain (stroke);
• viral infections.

Damage to the central nervous system causes Biot's breath. Damage to the nervous system is associated with stress, poisoning, impaired cerebral circulation. May be caused by encephalomyelitis of viral origin (tuberculous meningitis). Biot's breathing is characterized by the alternation of long pauses in breathing and normal uniform respiratory movements without rhythm disturbance.

An excess of carbon dioxide in the blood and a decrease in the work of the respiratory center causes Cheyne-Stokes breathing. With this form of breathing, the respiratory movements gradually increase in frequency and deepen to a maximum, and then pass to more superficial breathing with a pause at the end of the "wave". Such "wave" breathing is repeated in cycles and can be caused by the following disorders:

• vasospasm;
• strokes;
• hemorrhage in the brain;
• diabetic coma;
• intoxication of the body;
• atherosclerosis;
• exacerbation of bronchial asthma (attacks of suffocation).

In younger children school age these disorders are more common and usually resolve with age. Also among the causes may be traumatic brain injury and heart failure.

The pathological form of breathing with rare rhythmic breaths is called Kussmaul breath. Doctors diagnose this type of breathing in patients with impaired consciousness. Also similar symptom causes dehydration.

Type of shortness of breath tachypnea causes insufficient ventilation of the lungs and is characterized by an accelerated rhythm. It is observed in people with a strong nervous tension and after heavy physical work. Usually passes quickly, but may be one of the symptoms of the disease.

Treatment

Depending on the nature of the disorder, it makes sense to contact the appropriate specialist. Since respiratory disorders can be associated with many diseases, if you suspect a manifestation asthma contact an allergist. Helps with intoxication toxicologist.

Neurologist help restore normal rhythm breath after shock states And severe stress. With past infections, it makes sense to contact an infectious disease specialist. For a general consultation with mild breathing problems, a traumatologist, endocrinologist, okncologist, and somnologist can help. In case of severe respiratory disorders, it is necessary to call an ambulance without delay.

Oppression of the central origin. It is known that all general anesthetics can lead to respiratory depression and death due to central respiratory failure. This effect is probably due almost entirely to their narcotic effect on the central nervous system, although diethyl ether and some other anesthetics also disrupt neuromuscular transmission of impulses (weak curare-like action). Inhalation of ether at concentrations up to 20%, however, does not cause complete neuromuscular block of the diaphragm, so respiratory depression at low concentrations of ether is due in large part to its central effect on respiratory neurons. A number of inhalation anesthetics are also characterized by some irritating or stimulating effects. For example, ether directly depresses the respiratory center, but at the same time causes excitatory reflexes, emanating mainly from the lower respiratory tract and pulmonary stretch receptors. These reflexes are responsible for the hyperventilation observed at the onset of ether anesthesia. With shallow anesthesia, this reflex stimulation can maintain breathing for over normal level, despite the fact that the respiratory center is depressed by the anesthetic. Diethyl ether stimulates respiration during shallow anesthesia and through metabolic acidosis, release of catecholamines and increased activity sympathetic nerve. With a higher dose of anesthetic, an increasingly strong depression of the respiratory center occurs, and it is more and more difficult to excite the reflexes indicated above. With sufficiently strong respiratory depression, the onset of hypoxia stimulates carotid hemoreceptors, and then breathing is maintained only in this way. In the end, however, this mechanism also falls out. There is also a reflex emanating from the upper respiratory tract. It is caused by the irritant effect of the ether (in high concentration) on the mucous membrane of the larynx and pharynx and leads to transient apnea at the very beginning of anesthesia. Ether stimulates the secretion salivary glands and bronchial glands and thus hinders its penetration into the body. Such stimulating effects, with the exception of late laryngospasm, are absent with intravenous administration of anesthetics (thiopental, hexobarbital). Barbiturates and urethane, on the other hand, inhibit expiratory and inspiratory vagal respiratory reflexes.

Narcotic analgesics(morphine, etc.) depress breathing in proportion to their analgesic power. They cause a stronger and longer lasting respiratory depression when combined with other anesthetics, barbiturates, and psychopharmacological agents, so that treatment dose, which does not depress breathing or depresses it slightly, in combination with the above agents can cause life-threatening respiratory failure. This effect is observed both in healthy people and in patients with respiratory failure (pulmonary emphysema, bronchial asthma, etc.). As is known, in chronic respiratory failure (pulmonary emphysema), the respiratory center damaged by hypercapnia can be completely paralyzed by small doses of opiates and from inhalation. high concentrations oxygen, and patients do not experience shortness of breath. The great sensitivity of children to opiates is well known. Less known sensitivity to these analgesics in patients with hypothyroidism. They, like the sick lung diseases, they can only be used in extreme cases, and then very carefully.

We observed one patient, a 25-year-old man, in the final stage of chronic myelosis, who, due to very painful priapism, had to undergo blockade of nn for several hours. pudendalis with novocaine, give butaliton (baytinal) at a dose of 1 g, intramuscularly inject analgin at a dose of 5 ml, 0.5 mg of atropine, 100 ml of idol intramuscularly and irradiate the penis with x-rays. But all this did not work. Only about 3 hours after the intramuscular injection of 25 ml of chlorpromazine and 0.02 ml of pantopon under the skin, the patient calmed down a little, but died two hours later. The presence of a connection between death and the medications used, in particular chlorpromazine and pantopon, can neither be proved nor discarded, since the patient had other causes that explain the onset of death, including hemorrhagic diathesis with massive gastric hemorrhage. Regardless, this case is very instructive.

In the end, it must be pointed out that in old people there is a suspicion of a tendency to drug-induced respiratory depression under the influence of opiates, etc. It is interesting to observe that under the influence of morphine disappear (even at doses that do not cause strong ventilation depression) physiological deep respiratory movements, normal frequency which reaches 30-35 per hour. It is assumed that there is a connection between this effect and postoperative pulmonary atelectasis. Synthetic opiate substitutes - dextromoramide (palfium), pethidine (lidol, etc.), short-acting fentanyl also cause depression of the respiratory center in varying degrees. In equianalgesic doses, fentanyl depresses respiration to the same extent as pethidine (lidol) and morphine. Respiratory depression under the influence combined drugs fentanyl with droperidol (thalamonal, etc.) is due to fentanyl. Various respiratory disorders are also described in combined application monoamine oxidase and pethidine inhibitors - shallow breathing, wheezing, etc.

With regard to the morphine antagonist, nalorphine, it must be emphasized that in this case we are not talking about real antagonism, but only about the competitive removal of morphine from the cells of the central nervous system under the influence of nalorphine. The latter is also an analgesic, like morphine, but it depresses a person's breathing almost twice as weakly and has twice as strong an affinity for the respiratory center as does morphine. This explains the conflicting data on stimulation, inhibition or lack of effect on respiration in the initial period of its use in morphine poisoning. The unequal results are due to the use of different doses of both agents. So, with strong respiratory depression with high doses of morphine, nalorphine, displacing morphine and exerting a less strong inhibitory effect on breathing, improves it. On the contrary, when mild degree morphine poisoning, it is not recommended to use nalorphine, as it can increase respiratory depression. In such cases, xanthines (caffeine, etc.) are more suitable. And, finally, nalorfin does not have a practical effect in respiratory depression with other depressants of the central nervous system (barbiturates, etc.). In such cases, nalorphine, like levallorphan tartrate (lorphan), similar to it, can increase respiratory depression. In very high doses ah nalorphine depresses respiration, including morphine poisoning, to the same extent as morphine, or stronger than it. Pentazocin (fortral), which has recently been used as an analgesic in the treatment of patients with myocardial infarction, has a similar effect. Its analgesic effect is approximately the same as that of pethidine (lidol), but it is believed that it causes less severe respiratory depression than the latter and morphine. However, as a narcotic antagonist, it has a very weak effect.

Sleeping and sedative medications can also cause respiratory depression.(barbiturates, chloral hydrate, etc.), magnesium sulfate (for parenteral administration), psychopharmacological agents, diphenylhydantone, etc. For example, benzodiazepines, in particular diazepam (Valium, Relanium, etc.) can cause acute respiratory failure when administered intravenously or intramuscular injection during intratracheal anesthesia or during intravenous administration, before which barbiturates were injected (or not injected) into a vein. The apnea that occurred in such cases necessitated controlled breathing. According to newer data, sleep apnea is not as frequent occurrence. Somers et al., administering intravenous diazepam to patients with cardioversion, observed transient apnea, which in only two cases did not necessitate controlled breathing. Respiratory depression with cyanosis and coma was also observed after the use of higher doses of chlordiazepoxide (Librium, Disepin), for example, after taking 30 mg in a patient with "asthma". Triethylperazine (Torecan), like other phenothiazine derivatives, can cause apnea and cyanosis preceded by extrapyramidal symptoms and episodes of hyperventilation. In respiratory depression caused by phenothiazines, other factors usually play a role, such as the treatment of convulsions with electricity. After intravenous administration of diphenylhydantoin, used as an antiarrhythmic agent, are known, in addition to cases of fatal ventricular fibrillation, and sleep apnea. When injected rapidly into a vein, apnea occurs before the heart stops. In severe poisoning with diphenylhydantoin, breathing also slows down, becomes superficial, irregular.

Local anesthetics, especially in overdose or hypoxia, can also depress breathing to varying degrees. It is believed that inalidic acid (Nelidix, Negro) can cause respiratory depression in patients with impaired respiratory function and advanced respiratory infections. Respiratory depression is also observed in quinidine-induced syncope, in imipramine poisoning, in the so-called "gray syndrome" (gray syndrome) of chloramphenicol, as in many other poisonings. In some cases, for example, with atropine poisoning, tachypnea or tachydispnea (adrenaline poisoning) is first observed, which then turn into apnea. And, finally, we should not forget the possibility of severe inhibition of the fetal respiratory center when a pregnant woman takes barbiturates, phenothiazines, opiates, etc. immediately before or during childbirth. Children born as drug addicts have miosis and withdrawal symptoms, including changes in breathing ( tachypnea).

Neuromuscular blockade. Respiratory failure that occurs after the use of curare and its substitutes has a completely different mechanism of occurrence. It is caused by the neuromuscular blockade provoked by these agents. The effect of these drugs (curare, procaine administered intraspinally) may initially be masked by increased signals to the respiratory center and caused by an increase in PCO2 and a decrease in PO2 in arterial blood. In other words, more powerful stimuli come out of the respiratory center to the respiratory muscles, which overcome their still incomplete paralysis. different muscles respond differently to curare-like agents, and furthermore, there are individual differences within each species, as well as between different types. In this regard, in particular, the unequal reactions of the muscles of rats and humans are emphasized. As you know, the last, as a rule, are affected and the first to recover are the intercostal muscles, then the diaphragm. This allows you to use with therapeutic purpose curare-like drugs and in cases where they do not special measures to maintain breathing. When the body is depleted of potassium due to the use of diuretics, the effect of muscle relaxants is enhanced - curarization is longer and does not respond to the action of prostigmine. That is why before their use it is necessary to ensure a sufficiently high potassium level or not to prescribe diuretics according to at least within 4 days before the operation, however, even in such cases, it may be necessary to introduce new portions of potassium. It is also emphasized that respiratory acidosis causes high plasma levels of tubocurarine and respiratory neuromuscular blockade, while respiratory alkalosis causes the opposite effects. It should also be noted that the inhalation anesthetic methoxyfluran potentiates the action of non-depolarizing muscle relaxants. Their action is enhanced by kidney failure, as well as under the influence of some antibiotics (streptomycin, etc.).

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Each drug has its own contraindications and can lead to various side effects. Therefore, when treating with any medication, it is necessary to carefully study the instructions, consult a doctor, adhere to the recommended dosage and control your well-being. In some cases, the use medicines may lead to the development respiratory disorders. Let's talk a little more about such a problem as respiratory depression from drugs, the symptoms and what is happening, let's look at a little more detail.

The term "respiratory depression" means insufficiency of pulmonary ventilation or respiratory failure. With such a violation in the blood of a person, the amount of oxygen is significantly reduced and / or the volume of carbon dioxide increases by an order of magnitude.

What drugs can cause respiratory depression?

Respiratory depression can be provoked by the use of many drugs. It is worth recognizing that most often such a violation of health occurs with an overdose of medicines and with their insufficiently correct use. Also, respiratory failure can be explained by individual intolerance to drugs.

Respiratory depressant effect narcotic analgesics represented by opiates. Also, such a negative effect is possible with the use of sleeping pills and sedatives. In some cases, respiratory failure develops against the background of the use of local anesthetics, especially when they are overdosed. Another similar violation can be triggered by drugs that cause neuromuscular blockade (procaine, etc.), some antibiotics and other drugs.

About how respiratory depression manifests itself, what are the symptoms due to the action of drugs

Severe respiratory depression can be manifested by quite serious symptoms, including increased respiration and heart rate. The victim may experience loss of consciousness, and a decrease in blood pressure is also quite often observed. TO possible symptoms also include the appearance of shortness of breath, paradoxical movements of the chest and cough. Respiratory depression may be manifested by the participation of auxiliary muscles - to facilitate the performance of respiratory movements. The victim's neck veins swell. Of course, the appearance of problems of this kind provokes a strong fear. There is also a noticeable bluing skin, occurrence pain in the chest. Respiratory arrest may also occur.

If drugs cause a slow development of respiratory failure, there is an increase in pressure inside blood vessels. The patient develops a so-called pulmonary hypertension. Lack of adequate correction causes damage to blood vessels, as a result of which the supply of oxygen to the blood is reduced even more, which leads to an increase in the load on the heart and to the development of heart failure.

About how respiratory depression is corrected, which one is effective

If you suspect the development of respiratory failure, doctors take measures to identify the causes of such a violation. Of course, it is necessary to exclude the use of drugs that caused such symptoms. Might have to pick them up adequate replacement.

With respiratory depression, the patient is primarily shown oxygen. If the patient does not have chronic form respiratory failure, the volume of oxygen must be significant. Breathing during such therapy should slow down.

With a particularly severe form of respiratory depression, artificial ventilation of the lungs is performed. A special plastic tube is inserted through the nose or mouth into the trachea, then it must be connected to a device that pumps air into the lungs. Exhalation is carried out passively - since the lungs have elastic traction. Focusing on the degree of violation and existing diseases, they select a special mode of operation of the device artificial respiration. In the event that the lungs cannot work normally, additional oxygen is also introduced through the breathing apparatus. Mechanical ventilation helps to save a life if the patient simply cannot breathe on his own.

In order to optimize the functioning of the heart and lungs, it is extremely important to normalize water-salt balance in organism. Doctors are also taking measures to optimize blood acidity, for example, using sedatives. Such compounds help reduce the body's need for oxygen and improve lung function.

In some cases, therapy for respiratory depression involves the use of corticosteroids. Similar hormonal preparations will help patients whose lung tissue has been severely damaged due to long-term disorders.

Patients who have been diagnosed with respiratory depression, which we continue to talk about on this page / site /, need to be observed by a doctor for a long time. Such patients should regularly perform different breathing exercises selected by a qualified professional. In some cases, the means of physiotherapy are also selected.

Respiratory depression caused by taking medications requires very close attention and timely correction. It is worth noting that in some cases such a symptom is an indication for immediate first aid.

Respiratory failure occurs when poisoned a wide variety of substances and is one of the most common causes death of patients. It is usually combined and leads to lethal outcome before it is possible to remove the poison from the body or neutralize it with antidotes. The use of modern methods of dealing with respiratory disorders allows you to gain time to neutralize and remove the poison from the body. Acute poisoning can also lead to disruption of gas exchange at each stage.

Airway patency violated by poisoning with various poisons. If the patient is in a precomatous or comatose state, this is facilitated by the retraction of the tongue, mandible, epiglottis, regurgitation of gastric contents and its aspiration, aspiration of saliva and mucus from the oral cavity, nose and pharynx. In case of poisoning with organophosphorus substances (thiophos, chlorophos, karbofos, etc.) due to hypersecretion of the bronchial glands and impaired drainage function of the tracheobronchial tree, respiratory disorders will be associated with airway obstruction. In case of poisoning with acids and alkalis, a violation of the airway can occur due to a sharp edema of the larynx and vocal cords. Finally, pulmonary edema and foam obturation of the respiratory tract are observed in case of poisoning with chemical warfare agents (phosgene, diphosgene, vapors of mustard gas, lewisite, chlorine). In addition, poisoning (by barbiturates, opiates) is accompanied by depression of the respiratory center, paralysis of the respiratory muscles (curare-like, organophosphorus substances). Oxygen transport and hemoglobin (carbon monoxide, hemolytic poisons), respiratory enzymes (cyanide poisoning) can be blocked. For successful treatment it is necessary to know in detail the mechanism of development of respiratory insufficiency. However general rules resuscitation should be observed for various respiratory disorders.

First necessary condition is maintaining airway patency. To solve this challenging task there is a wide arsenal of means from a sharp tilting of the head of the victim with the extension of the lower jaw to the imposition of a tracheostomy with aspiration of bronchial secretions. When the cache-left reflex is depressed, the drainage function bronchi. In order to artificially induce a cough, isotonic sodium chloride solution (3-5 ml) is injected into the trachea through a puncture of the larynx between the thyroid and cricoid cartilages. If necessary, such punctures are repeated 3-4 times. If more prolonged cough stimulation is required, microtracheostomy is effective.

Under local anesthesia between the cricoid and thyroid cartilage the trachea is punctured with a thick needle, through which a polyethylene catheter is passed to the level of the tracheal bifurcation. The needle is removed, and the catheter is fixed to the skin with one suture. Antibiotics, proteolytic enzymes, isotonic solution sodium chloride. If the cough reflex is completely suppressed, maintaining bronchial drainage is carried out using the IKAR-2 artificial cough apparatus, toilet bronchoscopy, suction of the contents of the respiratory tract through an endotracheal tube, as well as a thin catheter passed into the trachea through the glottis. To thin the bronchial secretion and facilitate its suction, it is advisable to use alkaline inhalation, aerosols of proteolytic enzymes (chymopsin), antibiotic solutions.

Retraction of the tongue, lower jaw, epiglottis indicates oppression of the laryngeal and pharyngeal reflexes. Therefore, there is a risk of aspiration of the contents of the mouth, nose, pharynx and stomach into the lower respiratory tract with a violation of their patency. In these cases, it is necessary to introduce a gastric tube, preferably a Sengstein and Blakemore tube with two inflatable cuffs obturating the lower part of the esophagus and the entrance to the stomach. In cases of severe violation of swallowing and patency of the upper respiratory tract, if necessary, prolonged artificial ventilation of the lungs, tracheal intubation or tracheostomy is indicated. Due to greater simplicity and fewer complications, endotracheal intubation has recently replaced tracheostomy. The endotracheal tube can be in the trachea without causing complications for 2-3 days.

A special type of violation of the transport of gases is pulmonary edema, which can develop as a result of poisoning with gases and vapors of toxic substances. Since the disruption of gas exchange is caused by the foamy liquid, inhalation of antifoam agents is effective. For this purpose, oxygen is passed through a humidifier filled with ethyl alcohol. For unconscious persons, inhalations of oxygen passed through 20-30% are used. ethanol, using a mask. If the patient is conscious, use 96% ethyl alcohol and nasal catheters. Every 30-40 minutes make 10-15 minute breaks. At the same time, edematous fluid is aspirated to restore tracheobronchial patency. good effect with pulmonary edema, inhalation of oxygen under high blood pressure- 3-6 kPa (30-60 mm of water column) through the mask. An increase in intraalveolar pressure contributes to a decrease in blood filling of the lungs and prevents the filtration of edematous fluid through the alveolo-capillary membrane. With pulmonary edema caused by poisoning, important role increases the permeability of the pulmonary capillaries.

To combat pathological capillary permeability, it is necessary to use calcium chloride, vitamins of the P complex and ascorbic acid, amide nicotinic acid, glucocorticosteroid drugs. To reduce the blood filling of the lungs with elevated and normal blood pressure, it is advisable to use ganglionic blockers. For the purpose of dehydration, diuretics are prescribed (eufillin, mannitol, etc.). In severe cases, pulmonary intubation or tracheostomy is indicated with artificial ventilation under high pressure - up to 4 kPa (40 mm of water column).

In cases where poisoning leads to depression of the respiratory center(barbiturates, opiates), paralysis of the respiratory muscles (curare-like and organophosphorus substances), tonic and clonic convulsions of the respiratory muscles (dikain), maintaining airway patency by itself cannot ensure normal gas exchange. In this case, it is necessary to observe the second mandatory condition of resuscitation - to maintain adequate pulmonary ventilation, the effectiveness of which is judged by blood saturation with oxygen and carbon dioxide. These data can be most easily obtained by oximetry and the study of the acid-base state using the Microastrup apparatus. The need for constant control determinations in the treatment of severe poisoning is beyond doubt. However, on examination, it can be determined whether it is necessary to carry out artificial ventilation lungs. Cyanosis of the skin and mucous membranes, frequent and shallow breathing with the participation of additional respiratory muscles, restlessness, skin sweating, tachycardia and increased blood pressure indicate a respiratory disorder requiring mechanical ventilation.

When sudden cessation of breathing in the absence of the necessary equipment and equipment, artificial ventilation of the lungs can be carried out according to the "mouth to mouth" or "mouth to nose" method. These methods can support the life of the victim for a long time.

For first aid manual devices are used. For multi-day artificial lung ventilation in stationary conditions devices are used that operate from an electric drive and regulate the main parameters of ventilation - tidal volume, respiratory rate, inhalation / exhalation ratio. The usefulness of ventilation should be monitored by arterial blood gas analysis.

The use of mechanical ventilation through an endotracheal tube or tracheostomy has significantly improved the results of the treatment of acute poisoning.

Artificial lung ventilation is effective in case of poisoning carbon monoxide blocking hemoglobin. This is explained by the fact that the rate of release of hemoglobin from the compound with carbon monoxide depends on the content of oxygen and carbon dioxide in the inhaled mixture. At the same time, the decrease in the concentration of carboxyhemoglobin to acceptable numbers is accelerated by 4 times. In this regard, significant success has been achieved with the use of pressure chambers. If, when breathing clean air, the concentration of carboxyhemoglobin decreases from 70 to 10% (permissible limit) in 2 hours, then in a pressure chamber with a pressure of 202 kPa (2 atm), inhalation of 100% oxygen reduces this period to 12 minutes. In violation of tissue respiration in patients with severe carbon monoxide poisoning clinical effect can be achieved intravenous administration 15-60 mg of cytochrome C. This drug also has an effect in cases of histotoxic tissue damage in case of cyanide poisoning, sleeping pills.

So, the main points of resuscitation in case of poisoning are:

1) ensuring the patency of the respiratory tract, without which gas exchange between blood and alveolar air is impossible;

2) maintaining the required volume of ventilation through the use of artificial ventilation. Monitoring the effectiveness of the latter is carried out by gas analysis of arterial blood, the main parameters of the acid-base state;

3) some parameters of artificial ventilation are determined by the specific situation. So, if poisoning is accompanied by pulmonary edema, artificial ventilation should be carried out under high pressure. With cerebral edema, it is carried out with negative expiratory pressure. IN normal conditions long-term ventilation is carried out with mixtures containing no more than 60% oxygen due to its toxicity. At the same time, in case of carbon monoxide poisoning, artificial ventilation with 100% oxygen is indicated;

4) respiratory analeptics should be used only with complete patency of the respiratory tract, if poisoning is accompanied by depression of the respiratory center and mainly in cases where it is necessary to briefly support external respiration and there is no way to provide artificial ventilation. The main method of dealing with respiratory failure in case of poisoning is artificial ventilation.

Treatment of acute poisoning, 1982