Respiratory failure - Symptoms.

Depending on the clinical picture of the disease, acute and chronic forms of respiratory failure are distinguished, developing by similar pathogenetic mechanisms. Both forms of respiratory failure differ from each other, first of all, in the rate of change in the gas composition of the blood and the possibility of forming mechanisms for compensating these disorders. This determines the nature and severity of clinical manifestations, prognosis and, accordingly, the scope of therapeutic measures. Thus, acute respiratory failure occurs within a few minutes or hours after the onset of the action of the factor causing it. In chronic respiratory failure, hypoxemia and hypercapnia of arterial blood develop gradually, in parallel with the progression of the main pathological process in the lungs or other organs and systems), and clinical manifestations of respiratory failure usually exist for many years.

However, it would be wrong to identify the severity of both forms of respiratory failure only by the rate of development of symptoms: acute respiratory failure in some cases can proceed relatively easily, while chronic respiratory failure, especially at the final stage of the disease, is extremely difficult, and vice versa (A.P. Zilber). Nevertheless, the slow development of respiratory failure in its chronic form undoubtedly contributes to the formation of numerous compensatory mechanisms in patients, which provide, for the time being, relatively small changes in the gas composition of the blood and acid-base balance (at least under resting conditions). In acute respiratory failure, many compensatory mechanisms do not have time to form, which in most cases leads to the development of severe clinical manifestations of respiratory failure and the rapid development of its complications. In most cases, the analysis of the clinical picture of the disease allows us to fairly reliably identify the very fact of the presence of respiratory failure and roughly estimate its degree; at the same time, to study the specific mechanisms and forms of respiratory failure, a more detailed analysis of the gas composition of the blood, changes in lung volumes and capacities, ventilation-perfusion relationships, diffusion capacity of the lungs and other parameters is necessary.

Chronic respiratory failure

The most significant clinical signs of chronic respiratory failure are:

• dyspnea;
• central (diffuse) cyanosis;
• increased work of the respiratory muscles;
• intensification of blood circulation (tachycardia, increased cardiac output, etc.);
• secondary erythrocytosis.

Dyspnea

Shortness of breath (dyspnea) is the most constant clinical symptom of respiratory failure. It occurs when the ventilation apparatus cannot provide the necessary level of gas exchange adequate to the metabolic needs of the body (A.P. Zilber).

Dyspnea is a subjective painful sensation of lack of air, respiratory discomfort, which is often accompanied by a change in the frequency, depth and rhythm of respiratory movements. The main cause of dyspnea in patients with chronic respiratory failure is "overexcitation" of the respiratory center, initiated by hypercapnia, hypoxemia and changes in arterial blood pH.

As is known, the change in the functional activity of the respiratory center occurs under the influence of the flow of afferent impulses emanating from special chemoreceptors of the carotid body located in the bifurcation area of the carotid artery, as well as from the chemoreceptors of the ventral part of the medulla oblongata. The glomus cells of the carotid body are sensitive to a decrease in PaO2, an increase in PaCO2 and the concentration of hydrogen ions (H ⁺ ), and the chemoreceptors of the medulla oblongata are sensitive only to an increase in PaCO2 _and the concentration of hydrogen ions (H ⁺ ).

The respiratory center, perceiving afferent impulses from these chemoreceptors, constantly monitors the presence (or absence) of hypoxemia and hypercapnia, and in accordance with this regulates the intensity of the flow of efferent impulses directed to the respiratory muscles. The more pronounced hypercapnia, hypoxemia and changes in blood pH, the greater the depth and frequency of breathing, the higher the minute volume of breathing and the greater the likelihood of dyspnea.

It is known that the main stimulus of the respiratory center, reacting to changes in the gas composition of the blood, is an increase in PaCO ₂ (hypercapnia); stimulation of the respiratory center leads to an increase in the depth and frequency of breathing and to an increase in the minute volume of breathing. The diagram shows that the rate of increase in the minute volume of breathing with an increase in PaCO ₂ increases significantly against the background of a simultaneous decrease in the partial pressure of O ₂ in arterial blood. Conversely, a decrease in PaCO ₂ below 30-35 mm Hg (hypocapnia) leads to a decrease in afferent impulses, a decrease in the activity of the respiratory center and a decrease in the minute volume of breathing. Moreover, a critical drop in PaCO ₂ can be accompanied by apnea (temporary cessation of breathing).

The sensitivity of the respiratory center to hypoxemic stimulation of the carotid zone chemoreceptors is lower. With normal PaCO2 _in the blood, the minute volume of respiration begins to increase noticeably only when PaO2 decreases to a level below 60 mm Hg, i.e. with severe respiratory failure. The increase in respiratory volume during the development of hypoxemia occurs mainly through an increase in the frequency of respiratory movements (tachypnea).

It should be added that changes in the pH of arterial blood affect the respiratory center in a similar way to fluctuations in PaCO2 values _: when the pH decreases to less than 7.35 (respiratory or metabolic acidosis), hyperventilation of the lungs occurs and the minute volume of respiration increases.

As a result of the increase in the depth and frequency of breathing caused by the change in the gas composition of the blood, the stretch receptors and irritant receptors of the trachea and bronchi, which react to the rapid increase in the volumetric speed of the air flow, as well as the proprioceptors of the respiratory muscles, sensitive to the increase in pulmonary resistance, are irritated. The flow of afferent impulses from these and other receptors reaches not only the respiratory center, but also the cerebral cortex, as a result of which the patient experiences sensations of respiratory discomfort, difficulty breathing, and shortness of breath.

Depending on the nature of the pathological process in the lungs that caused the development of respiratory failure, external objective manifestations of dyspnea may be of different nature. Depending on this, the following types of dyspnea are distinguished:

1. Inspiratory dyspnea with signs of difficulty in inhalation, developing in pathological processes accompanied by compression of the lung and limitation of pulmonary excursion (pleural effusion, pneumothorax, fibrothorax, paralysis of the respiratory muscles, severe deformation of the chest, ankylosis of the costovertebral joints, decreased extensibility of the lung tissue in inflammatory or hemodynamic pulmonary edema, etc.). Inspiratory dyspnea is more often observed in restrictive type of ventilation respiratory failure.
2. Expiratory dyspnea with difficulty exhaling, which most often indicates the presence of obstructive respiratory failure.
3. Mixed dyspnea indicating a combination of restrictive and obstructive disorders.
4. Frequent shallow breathing (tachypnea), in which patients cannot clearly determine whether inhalation or exhalation is difficult, and there are no objective signs of such difficulty.

It should be emphasized that the concepts of tachypnea (increased respiratory rate) and dyspnea (shortness of breath) are not entirely identical. In principle, tachypnea may not be accompanied by a feeling of respiratory discomfort (for example, in healthy people during physical exertion). In these cases, increased respiratory rate occurs due to irritation of the receptors of the bronchi, lungs, and respiratory muscles that respond to the increased metabolic rate. However, in patients with respiratory failure, increased respiratory rate (tachypnea) is usually accompanied by respiratory discomfort (a painful feeling of lack of air). It should be remembered that an increase in the frequency of respiratory movements leads to a decrease in the efficiency of breathing, since it is accompanied by an increase in the ratio of the functional dead space to the tidal volume (FDS/TV). As a result, to ensure the same volume of breathing, the respiratory muscles have to do significantly more work, which sooner or later leads to their fatigue and a progressive decrease in pulmonary ventilation. On the other hand, this increases the flow of afferent impulses from the proprioceptors of the respiratory muscles, which, reaching the cerebral cortex, causes a feeling of respiratory discomfort (dyspnea).

Cyanosis

Cyanosis of the skin and mucous membranes, which appears with respiratory failure, is an objective clinical sign of arterial hypoxemia. It appears when PaO2 decreases below 70-80 mm Hg. Cyanosis is associated with impaired blood oxygenation in the lungs and with an increase in the content of reduced hemoglobin in capillary blood.

It is known that in a healthy person the level of reduced hemoglobin in the blood flowing from the lungs never exceeds 40 g/l; the skin has a normal pinkish color. In case of gas exchange disorders in the lungs during respiratory failure, blood rich in reduced hemoglobin (in a concentration of more than 40 g/l) enters the arterial system of the systemic circulation from the lungs, which causes diffuse (central) cyanosis, which often gives the skin a peculiar grayish tint. Cyanosis is especially noticeable on the face, on the mucous membrane of the lips and tongue, on the skin of the upper half of the body. If there are no accompanying circulatory disorders, the extremities remain warm.

Central (diffuse, warm) cyanosis is an important objective sign of both ventilatory and parenchymal respiratory failure, although the intensity of the bluish coloration of the skin and mucous membranes does not always reflect the degree of arterial hypoxemia.

It should be remembered that with severe anemia and a decrease in the level of total hemoglobin to 60-80 g / l, cyanosis is not detected even with significant lung damage, since for its appearance it is necessary that more than half of the total hemoglobin (40 g / l from 60-80 g / l) is in the reduced form, which is incompatible with life. On the contrary, in the presence of erythrocytosis and an increase in the level of total hemoglobin in the blood to 180 g / l and above, cyanosis can develop even in the absence of respiratory failure. In such cases, the diagnostic value of this symptom is reduced.

Sometimes, with ventilatory respiratory failure with severe hypercapnia, examination reveals a painless blush on the cheeks, caused by the dilation of peripheral vessels.

Finally, in the case of obstructive respiratory failure, during examination, along with cyanosis, it is possible to detect pronounced swelling of the veins of the neck, caused by increased intrathoracic pressure and impaired blood outflow through the veins into the right atrium, leading to an increase in central venous pressure (CVP). Swelling of the veins of the neck together with central cyanosis and expiratory dyspnea, as a rule, indicate severe respiratory failure of the obstructive type.

Strengthening the work of the respiratory muscles

Increased work of the respiratory muscles and involvement of accessory muscles in the act of breathing is the most important clinical sign of both forms of respiratory failure. Let us recall that in addition to the diaphragm (the main respiratory muscle), there are other (auxiliary) muscles of inhalation and exhalation. The external intercostal muscles, as well as the anterior internal muscles, are related to the muscles of inhalation, and the muscles of the anterior abdominal wall are related to the muscles of exhalation. The scalene and sternocleidomastoid muscles lift and fix the chest during inhalation.

Significant pressure of these muscles during the respiratory cycle, which can be easily noticed with careful examination of the chest, indicates an increase in airway resistance in broncho-obstructive syndrome or the presence of severe restrictive disorders. Increased work of the respiratory muscles is often manifested by a pronounced depression of the intercostal spaces, jugular fossa, supra- and subclavian regions during inhalation. In severe broncho-obstructive syndrome (for example, during an attack of bronchial asthma), patients usually take a forced position, resting their hands on the edge of a table, bed, knees, and thus fixing the shoulder girdle to involve the auxiliary muscles of the back, shoulder girdle and chest muscles in breathing.

Intensification of blood circulation

Tachycardia develops at any stage of respiratory failure. At first, it has a compensatory nature to a certain extent and is aimed at maintaining an increase in cardiac output and systemic arterial pressure, which is necessary for a more adequate supply of tissues with oxygen. In severe cases of the disease, despite the maintenance and even increase in tachycardia, stroke volume, cardiac output, and arterial pressure may decrease.

Secondary erythrocytosis

Secondary erythrocytosis, often detected in respiratory failure, is also compensatory. It develops due to irritation of the bone marrow by hypoxia and is accompanied by an increase in the number of erythrocytes and hemoglobin content in the peripheral blood. In this case, the skin of patients with respiratory failure looks bluish-burgundy, secondary erythrocytosis in chronic respiratory failure is accompanied by deterioration of the rheological properties of the blood, which contributes to the progression of pulmonary arterial hypertension.

Thus, clinical examination of the patient in most cases allows to identify the main signs of chronic respiratory failure and differentiate bronchial obstruction syndrome and restrictive respiratory disorders. However, it should be noted that the described clinical signs of respiratory failure relate mainly to the diagnosis of compensated respiratory failure. To identify compensated respiratory failure, in which a number of the above mechanisms provide a normal gas composition of the thermal blood under resting conditions, clinical signs must be assessed during physical activity. In practice, for a preliminary assessment of the degree of respiratory failure, they usually focus on the main clinical sign - dyspnea, also taking into account the conditions of its occurrence.

Depending on the severity of shortness of breath and other signs of chronic respiratory failure, three degrees of its severity are distinguished:

• Stage I - the appearance of shortness of breath when it is necessary to perform physical activity that exceeds daily activity;
• Stage II - the occurrence of shortness of breath and other signs of respiratory failure when performing normal daily activities;
• Stage III - the appearance of signs of respiratory failure even at rest.

It should also be added that in some patients with chronic respiratory failure, clinical examination can reveal objective signs of pulmonary arterial hypertension and chronic pulmonary heart disease.

Acute respiratory failure

Acute respiratory failure is one of the most severe complications of various diseases of the lungs, chest, neuromuscular respiratory system, etc. Acute respiratory failure is undoubtedly one of the main indicators of the severity of pneumonia and many other lung diseases. It can develop in the first few hours or days of the disease. The occurrence of acute respiratory failure requires intensive care, since in most cases it poses an immediate threat to the patient's life (S.N. Avdeev).

Mortality in acute respiratory failure reaches 40-49% and depends on the nature of the disease that caused acute respiratory failure, the severity of the dysfunction of the lungs and other organs and systems. According to HJ Kim and DH Ingbar (2002), factors that aggravate the severity of acute respiratory failure and lead to an increase in the frequency of fatal outcomes include:

• severe lung damage;
• the need to create a high concentration of oxygen in the inhaled air during mechanical ventilation (FiO2 greater than 60-80%);
• the need to create a peak inspiratory pressure greater than 50 mm H2O during mechanical ventilation;
• prolonged stay on mechanical ventilation;
• the presence of multiple organ failure.

The latter factor is of decisive importance in a number of cases, since insufficient supply of organs and tissues with O2 _leads to a sharp disruption of cellular metabolism, and in severe cases - to irreversible changes in the organs. The most sensitive to oxygen deficiency vital organs - the brain and heart - suffer first.

Most often, acute respiratory failure develops with the following diseases: pneumonia;

• pulmonary edema (hemodipamic, inflammatory, toxic);
• airway obstruction in bronchial asthma, asthmatic status, COPD, aspiration of gastric contents, etc.;
• pleural effusion;
• pneumothorax;
• pulmonary atelectasis;
• neuromuscular diseases that limit the function of the respiratory muscles;
• overdose of drugs (narcotic analgesics, sedatives, barbiturates);
• breathing disorders during sleep and others.

The clinical picture of acute respiratory failure is characterized by a rapid increase in symptoms and involvement of vital organs in the pathological process, primarily the central nervous system, heart, kidneys, gastrointestinal tract, liver and the lungs themselves. In acute respiratory failure, three pathogenetic stages are usually distinguished:

• Stage 1 - at rest, there are no obvious clinical signs of gas exchange disorders, but symptoms already appear indicating compensatory activation of respiration and circulation.
• Stage 2 - clinical and laboratory signs of hypercapnia and/or hypoxemia appear at rest.
• Stage 3 - severe decompensation of respiratory function, respiratory and metabolic acidosis develop, signs of multiple organ failure appear and progress rapidly.

Dyspnea

Shortness of breath is one of the first clinical signs of acute respiratory failure. Most often, breathing becomes more frequent (tachypnea), which is usually accompanied by a rapidly progressing sensation of respiratory discomfort (dyspnea). The number of respiratory movements usually exceeds 24 per minute.

Sometimes, depending on the etiology of acute respiratory failure, objective signs of difficulty in inhaling or exhaling (inspiratory or expiratory dyspnea) appear. In these cases, the pronounced overstrain of the respiratory muscles is especially noticeable; their work is sharply increased, and a significant portion of oxygen and energy is spent on it. Over time, such overstrain of the respiratory muscles leads to their fatigue and decreased contractility, which is accompanied by an even more pronounced impairment of pulmonary ventilation and an increase in hypercapnia and respiratory acidosis.

Weakness of the diaphragm, intercostal and other respiratory muscles is accompanied by high tension of the neck muscles, convulsive movements of the larynx during inspiration, which reflects the extreme degree of fatigue of the respiratory muscles. It should be remembered that inspiratory tension of the respiratory muscles can develop in the late stages of not only restrictive, but also severe obstructive disorders, indicating a significant increase in airway resistance. In the final stage of acute respiratory failure, desynchronization of respiratory muscle contraction is possible, which is an important sign of a critical disorder of the central regulation of breathing. In addition, with severe respiratory failure, three classic "logical" types of breathing can be observed: 1) Cheyne-Stokes breathing, 2) Biot breathing and 3) Kussmaul breathing. These types of breathing are somehow associated with severe, including hypoxic, damage to the brain and respiratory center, but are not specific for respiratory failure. Cheyne-Stokes respiration is characterized by a smooth increase in respiratory activity and its gradual fading with relatively short periods of apnea. Cheyne-Stokes respiration is caused by the suppression of chemoreceptors of the ventral part of the brain, which respond to an increase in PaCO2 _and the concentration of H+ ions. Vice versa, it is observed in case of disturbances in the blood supply to the respiratory center against the background of increased intracranial pressure, cerebral edema, cardiac, vascular and respiratory failure, usually at the terminal stage of the disease. Biot's respiration is characterized by periodic cessation of respiratory activity for 10-30 s (comparatively long periods of apnea) with its short-term recovery. Biot's respiration is observed in case of deep hypoxia of the brain and respiratory center against the background of brain tumors, traumatic brain injury, acute cerebrovascular accident, neuroinfection, severe respiratory failure. Kussmaul breathing is a deep, noisy, rapid breathing that usually occurs with severe metabolic acidosis and toxic damage to the respiratory center (diabetic ketoacidosis, uremia, severe respiratory or heart failure.

Pallor and diffuse cyanosis

The early stages of acute respiratory failure are often characterized by the appearance of pale skin, along with tachycardia and a tendency to increase systemic arterial pressure, indicating pronounced centralization of blood circulation. The increase in arterial hypoxemia is accompanied by the appearance of diffuse cyanosis, reflecting a rapid increase in the content of reduced (unsaturated) hemoglobin in the peripheral blood. In severe cases, with the appearance of signs of severe microcirculation disorder, cyanosis takes on a peculiar grayish honey fungus ("earthy" skin color). The skin becomes cold, damp, covered with sticky cold sweat.

In acute respiratory failure, it is important to assess not only the severity and prevalence of cyanosis, but also its change under the influence of oxygen therapy and artificial ventilation: the absence of change indicates the presence of parenchymatous respiratory failure, which is based on the formation of severe ventilation-perfusion disorders. A positive reaction to oxygen therapy with a high (up to 100%) O2 content in the inhaled air indicates the prevalence of oxygen diffusion disorders through the alveolar-capillary membrane, etc.

Hemodynamic disorders

The development of acute respiratory failure is accompanied by tachycardia in almost all cases, which at the initial stages of respiratory failure reflects the compensatory intensification and centralization of blood circulation characteristic of this pathology. However, in severe cases, when neurohumoral regulation of the heart rhythm is disrupted due to severe hypoxia and acidosis, myocardial ischemia and impaired contractility of the heart muscle occur, bradycardia appears, which in acute respiratory failure often heralds the development of ventricular extrasystole and ventricular fibrillation.

The dynamics of systemic arterial pressure has a two-phase character. In the initial stages of acute respiratory failure, as a rule, arterial hypertension develops (including due to the centralization of blood circulation). However, the late stages are characterized by a persistent and progressive decrease in arterial pressure - arterial hypotension, caused by increasing hypovolemia and a decrease in cardiac output.

Multiple organ failure

Signs of CNS hypoxia appear with severe acute respiratory failure. Patients become restless, excited, sometimes euphoric. Further progression of acute respiratory failure is accompanied by a gradual fading of consciousness and the development of coma. Convulsions often occur during this period. It is believed that neurological disorders appear with PaO2 less than 45 mm Hg.

Multiple organ failure develops in severe acute respiratory failure. In addition to the described disorders of the central nervous system and circulatory system, the following may develop:

• decreased diuresis (oligo- and anuria);
• intestinal paresis;
• acute erosions and ulcers in the stomach and intestines, as well as gastrointestinal bleeding;
• dysfunction of the liver, kidneys (hepatorenal failure) and other organs.

Progressive multiple organ failure in acute respiratory failure is a very unfavorable sign, indicating the ineffectiveness of intensive therapy and accompanied by a high risk of death.

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