Respiratory Failure: Symptoms

Depending on the clinical picture of the disease, acute and chronic forms of respiratory failure are distinguished, developing according to similar pathogenetic mechanisms. Both forms of respiratory failure differ from each other, primarily by 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, the prognosis and, accordingly, the volume of therapeutic measures. Thus, acute respiratory failure occurs within a few minutes or hours after the onset of the effect of the causative factor. With chronic respiratory failure, hypoxemia and hypercapnia of the arterial blood are formed gradually, in parallel to the progression of the main pathological process in the lungs of other organs and systems), and clinical manifestations of respiratory failure exist, as a rule, for many years.

Nevertheless, it would be incorrect to identify the severity of both forms of respiratory failure only by the rate of development of symptoms: acute respiratory failure can be relatively easy to perform in a number of cases, and chronic respiratory failure, especially at the final stage of the disease, is extremely stinging, and vice versa (A. Zilber). Nevertheless, the slow development of respiratory failure with its chronic form undoubtedly contributes to the formation of numerous compensatory mechanisms in patients, providing, for the time being, relatively small changes in the gas composition of the blood and the acid-base state (at least, the conditions of rest). 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 to the rapid development of its complications. Analysis of the clinical picture of the disease in most cases allows us to reliably detect the fact of the presence of respiratory failure and roughly approximate its degree; at the same time, a more detailed analysis of the gas composition of the blood, changes in pulmonary volumes and capacities, ventilation-perfusion relations, diffusivity of the lungs and other parameters.

Chronic respiratory insufficiency

The most significant clinical signs of chronic respiratory failure are:

• dyspnea;
• central (diffuse) cyanosis;
• strengthening the 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 device can not provide the necessary level of gas exchange, adequate to the metabolic needs of the body (AP Zilber).

Shortness of breath 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 the "overexcitation" of the respiratory center, triggered by hypercapnia, hypoxemia and changes in the pH of the arterial blood.

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 the special chemoreceptors of the carotid body located in the carotid artery bifurcation region, as well as from the chemoreceptors of the ventral region of the medulla oblongata. Glomus cells of the carotid calf susceptible to a decrease in PaO2, PaCO2 and increase the concentration of hydrogen ions (H ⁺ ) and chemoreceptors medulla - only to increased PaCO ₂ 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 accordingly 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 respiration, and the higher the minute volume of respiration and the greater the likelihood of dyspnoea.

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 RaCO ₂ (hypercapnia); stimulation of the respiratory center leads to an increase in the depth and frequency of respiration and to an increase in the minute volume of respiration. It is shown on the diagram that the rate of increase in the minute volume of respiration increases with increasing RCOO ₂ against the background of a simultaneous decrease in the partial pressure of O ₂ in the arterial blood. Conversely, reducing PaCO ₂ below 30-35 mm Hg. Art. (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 respiration. Moreover, the critical fall of RACO ₂ may be accompanied by apnea (temporary respiratory arrest).

The sensitivity of the respiratory center to hypoxemic stimulation of the chemoreceptors of the carotid zone is lower. With normal PACO ₂ in the blood, the minute volume of respiration begins to increase markedly only when the PaO2 decreases to less than 60 mm Hg. Art. With severe respiratory failure. Increasing the volume of breathing during the development of hypoxemia occurs mainly by increasing the frequency of respiratory movements (tachypnea).

It should be added that changes in the pH of the arterial blood affect the respiratory center in the same way as the fluctuations in the values of PaCO ₂ : when the pH is 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 depth and respiration rate caused by changes in the gas composition of the blood, the stretch receptors and irritant receptors of the trachea and bronchial tubes become irritated, reacting to a rapid increase in the volumetric flow of air flow, as well as proprioceptors of respiratory muscles sensitive to an increase in pulmonary resistance. The flow of afferent impulses from these and other receptors reaches not only the respiratory center, but also the cerebral cortex, in connection with which the patient experiences sensations of respiratory discomfort, difficulty breathing, dyspnea.

Depending on the nature of the pathological process in the lungs that caused the development of respiratory failure, external objective manifestations of dyspnea may have a different character Depending on this, the following options for dyspnoea are distinguished:

1. Inspiratory dyspnea with signs of inspiratory difficulty, developing in pathological processes accompanied by compression of the lung and restriction of lung excursions (pleural effusion, pompotorax, fibrotorax, paralysis of the respiratory muscles, pronounced deformity of the thorax, ankylosis of the rib-vertebral articulations, a decrease in the extensibility of the lung tissue in inflammatory or hemodynamic edema of the lungs, etc.). Inspiratory dyspnea is most often observed with a restrictive ventilatory respiratory failure.
2. Expiratory dyspnoea with difficulty exhaling, which most often indicates the presence of respiratory failure by the obstructive type.
3. Mixed shortness of breath, indicating a combination of restrictive and obstructive disorders.
4. Frequent shallow breathing (tachypnea), in which patients can not clearly determine if breathing or exhalation is difficult, and there are no objective signs of such difficulty.

It should be emphasized that the concept of tachypnea (rapidity of breathing) and dyspnoea (dyspnea) is not entirely identical. In principle, tachypnea may not be accompanied by a feeling of respiratory discomfort (for example, in healthy people during exercise). In these cases, the increase in respiration occurs due to irritation of the receptors of the bronchi, the lungs, and also the respiratory muscles that react with the loading increase in metabolism. Nevertheless, with respiratory failure in patients, increased respiration (tachypnea), as a rule, is 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 effectiveness of respiration, since it is accompanied by an increase in the ratio of functional dead space to the respiratory volume (MP / DO). As a result, in order to ensure the same volume of breathing, the respiratory muscles have to perform substantially more work, which sooner or later leads to their fatigue and a progressive decrease in pulmonary ventilation. On the other hand, it enhances the flow of afferent impulses from the proprioceptors of the respiratory muscles, which, when reaching the cerebral cortex, causes a feeling of respiratory discomfort (dyspnoea).

Cyanosis

Cyanosis of the skin and mucous membranes, which appears with respiratory failure, refers to the objective clinical signs of arterial hypoxemia. It appears with a decrease in PaO2 less than 70-80 mm pg. Art. 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. When the gas exchange in the lungs is disturbed by respiratory insufficiency, the blood that is rich in reduced hemoglobin (at a concentration of more than 40 g / l) enters the arterial system of a large circle of circulation from the lungs, in connection with which diffusive (central) cyanosis develops, often giving the skin a peculiar grayish shade. Cyanosis is especially noticeable on the face, on the mucous lips and tongue, on the skin of the upper half of the trunk. If there are no concomitant circulatory disorders, the extremities remain warm.

Central (diffuse, warm) cyanosis is an important objective feature of both ventilation and parenchymal respiratory failure, although the intensity of cyanotic color of the skin and mucous membranes does not always reflect the degree of arterial hypoxemia.

It should be remembered that with pronounced anemia and a decrease in the level of total hemoglobin up to 60-80 g / l, cyanosis is not detected even with significant lung lesions, since for its appearance it is necessary that more than half of all hemoglobin 40 g / l from 60-80 g / l ) was in a restored 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 higher, cyanosis can develop even in the absence of respiratory failure. In such cases, the diagnostic value of this symptom decreases.

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

Finally, with obstructive type of respiratory failure during examination, along with cyanosis, pronounced swelling of the veins of the neck can be detected, due to an increase in intrathoracic pressure and a violation of the flow of blood 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 dyspnoea usually indicate a pronounced respiratory failure according to the obstructive type.

Strengthening the work of the respiratory muscles

Strengthening the work of the respiratory muscles and connecting to the act of respiration of the auxiliary musculature is the most important clinical sign of both forms of respiratory failure. Recall that in addition to the diaphragm (the main respiratory muscle), there are other (auxiliary) muscles of inspiration and exhalation. The outer intercostal muscles, as well as the front internal muscles, refer to the muscles of the inspiration, and the muscles of the anterior abdominal wall - with the muscles of the exhalation. Stair and sternocleidomastoid muscles lift and fix the thorax during inspiration.

Significant pressure of these muscles during the breathing cycle, which is easy to see when you carefully examine the chest, indicates an increase in airway resistance in bronchoobstructive syndrome or the presence of severe restrictive disorders. The intensification of the work of the respiratory muscles is often manifested by the pronounced occlusion of the intercostal spaces, the jugular fossa, the supra- and subclavian areas during inspiration. In severe bronchial obstructive syndrome (for example, during an attack of bronchial asthma), patients usually occupy a forced position, resting their hands on the edge of the table, the bed, on their knees, and fixing the shoulder belt to connect respiratory muscles of the back muscles, shoulder girdle and pectoral muscles.

Intensification of blood circulation

Tachycardia develops at any stage of respiratory failure. At first, it is to a certain extent compensatory in nature and is aimed at preserving the increase in cardiac output and systemic arterial pressure, which is necessary for more adequate supply of tissues with oxygen. In severe disease, despite the "storage and even strengthening of tachycardia, stroke volume, cardiac output, blood pressure may be reduced.

Secondary erythrocytosis

Secondary erythrocytosis, often detected with respiratory failure, is also compensatory. It develops due to stimulation of the bone marrow by hypoxia and is accompanied by an increase in the number of red blood cells and hemoglobin in the peripheral blood. In this case, the skin of patients with respiratory insufficiency looks cyanotic-bard, secondary erythrocytosis in chronic respiratory failure is accompanied by a deterioration in 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 us to identify the main signs of chronic respiratory failure and differentiate the syndrome of bronchial obstruction and restrictive breathing disorders. However, it should be noted that the described clinical signs of respiratory failure are mainly related to the diagnosis of compensated respiratory failure. To identify compensated respiratory failure, in which a number of the mechanisms described above provide, under resting conditions, a normal gas composition of thermal blood, clinical signs must be encapsulated during physical exertion. In practice, for a preliminary assessment of the degree of respiratory failure, and usually focus on the main clinical sign - shortness of breath, taking into account also the conditions of its appearance.

Depending on the severity of dyspnea and other signs of chronic respiratory insufficiency, three degrees of its severity are distinguished:

• I degree - the appearance of dyspnea if necessary to perform physical exertion, exceeding the daily;
• II degree - the occurrence of dyspnea and other signs of respiratory failure in the performance of normal daily loads;
• III degree - the appearance of signs of respiratory failure, even at rest.

It should also be added that in some patients with chronic respiratory failure in clinical follow-up, objective signs of pulmonary arterial hypertension and chronic pulmonary heart can be identified.

Acute respiratory failure

Acute respiratory failure is one of the most serious complications of various diseases of the lungs, chest, neuromuscular breathing apparatus, and the like. 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 emergence of acute respiratory failure requires intensive therapy, since in most cases it poses an immediate threat to the life of the patient (SN 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 impaired lung function and other organs and systems. According to HJ Kim and DH Ingbar (2002), the factors that aggravate the severity of acute respiratory failure and lead to an increase in the frequency of deaths include:

• severe lung damage;
• the need to create a high concentration of oxygen in inhaled air with artificial ventilation (FiO2 is more than 60-80%);
• the need for a ventilatory inspiratory pressure of more than 50 mm of water is created when ventilation. P.
• a long stay on the ventilator;
• presence of multiple organ failure.

The latter factor is crucial in a number of cases, since insufficient provision of O ₂ organs and tissues leads to a sharp disruption of cellular metabolism, and in severe cases to irreversible changes in organs. First of all, the most vital organs of the brain and heart are affected by oxygen deficiency.

The most common acute respiratory failure develops with the following diseases:. Pneumonia;

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

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

• Stage I-at rest, there are no obvious clinical signs of a gas exchange disturbance, but symptoms appear that indicate compensatory activation of respiration and circulation.
• 2 nd stage - at rest there are clinical and laboratory signs of hypercapnia and / or hypoxemia.
• Stage 3 - pronounced decompensation of respiratory functions, respiratory and metabolic acidosis, appear and rapidly progress signs of multiple organ failure.

Dyspnea

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

Sometimes, depending on the etiology of acute respiratory insufficiency, there are objective signs of inhalation or exhalation (inspiratory or expiratory dyspnea). In these cases, a particularly pronounced overexertion of the respiratory muscles, whose work is sharply increased, and a significant portion of oxygen and energy is expended on it. Over time, this overexertion of the respiratory muscles leads to their fatigue reducing the contractility, which is accompanied by an even more pronounced violation of pulmonary ventilation and the increase in hypercapnia and respiratory acidosis.

Weakness of the diaphragm, intercostal and other respiratory muscles is accompanied by a greater tension of the neck muscles, convulsive movements of the larynx during inspiration, which reflects the extreme degree of fatigue of the respiratory muscles. At the same time, it will fail to remember that the inspiratory tension of the respiratory muscles can develop in the late stages of not only restrictive, but also expressed obstructive disorders, indicating a significant increase in airway resistance. In the final stage of acute respiratory failure, desynchronization of the contraction of the respiratory muscles is possible, which is an important sign of a critical violation of the central regulation of respiration. In addition, with severe respiratory failure, three classical "" logical types of breathing can be observed: 1) Cheyne-Stokes respiration; 2) Biota 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 breathing is characterized by a smooth increase in respiratory activity and a similar gradual fading with relatively short periods of apnea. Cheyne-Stokes caused inhibition chemoreceptors ventral part of the brain responding to increasing PaCO ₂ and a concentration of H + ions vice often observed when blood circulation disorders of the respiratory center on a background of increased intracranial pressure, cerebral edema, cardiac, circulatory and respiratory failure, usually at terminal stage disease. Respiration of the Biota is characterized by a periodic cessation of respiratory activity for 10-30 seconds (comparatively long periods of apnea) with a short-term recovery. Breath breathing is observed with deep hypoxia of the brain and respiratory center against the background of brain tumors, craniocerebral trauma, acute disturbance of cerebral circulation, neuroinfection, severe respiratory failure. The breathing of Kussmaul is a deep, noisy, frequent respiration, which usually occurs with the expressed metabolic acidosis and toxic damage of the respiratory center (diabetic ketoacidosis, uremia, severe respiratory or heart failure.

Pallor and diffuse cyanosis

Early stages of development of acute respiratory failure are often characterized by the appearance of pallor of the skin, along with tachycardia and a tendency to increase systemic arterial pressure, indicating a marked centralization of the circulation. The growth of arterial hypoxemia is accompanied by the appearance of diffuse cyanosis, reflecting the rapid increase in the content of reduced (unaturated) hemoglobin in the peripheral blood. In severe cases, with the appearance of signs of pronounced disturbance of microcirculation, cyanosis acquires a peculiar grayish smear ("earthy" skin color). The skin becomes cold, moist, covered with a 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 and IVL: the absence of change indicates the presence of parenchymal respiratory failure, which is based on the formation of pronounced ventilation-perfusion disorders. A positive response to oxygen therapy with a high (up to 100%) O2 content in the inspired air indicates predominance of oxygen diffusion disorders through the alveolar-capillary membrane and the like.

Hemodynamic Disorders

The development of acute respiratory failure in almost all cases is accompanied by tachycardia, which at the initial stages of respiratory failure reflects the compensatory intensification and centralization of the circulation, characteristic of this pathology. However, in severe cases, when neurohumoral regulation of the heart rhythm is disturbed due to severe hypoxia and acidosis, myocardial ischemia and violation of the contractile capacity of the cardiac muscle breaks down, a bradycardia appears that often predicts the development of ventricular extrasystole and ventricular fibrillation in acute respiratory failure.

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 through the centralization of blood circulation). However, late stages are characterized by persistent and progressive reduction in arterial pressure - arterial hypotension due to increasing hypovolemia and a decrease in cardiac output.

Multiple organ failure

Signs of hypoxia of the central nervous system appear in 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 development of coma. During this period, cramps often occur. It is believed that neurological disorders occur when PaO2 is less than 45 mm Hg. Art.

Multiple organ failure occurs in severe acute respiratory failure. In addition to the described violations of the functioning of the central nervous system and the circulatory system may develop:

• decreased diuresis (oligo- and anuria);
• paresis of the intestine;
• acute erosion and ulcers in the stomach and intestines, as well as gastrointestinal bleeding;
• a violation of the liver, kidneys (hepatic-renal failure) and other organs.

Increasing multiorgan failure in acute respiratory failure is a very unfavorable sign, indicating the ineffectiveness of intensive care and accompanied by a high risk of death.

[1], [2], [3], [4], [5], [6]