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Respiratory failure

Despite the fact that respiratory disorders can occur at any stage of gas exchange, the development of respiratory failure as a clinical syndrome is associated exclusively with the pathology of external respiration. The simplest definition was given to her by A.P. Zilber (1996): “Respiratory failure (DN) is a condition of the body in which the ability of the lungs and ventilation apparatus to provide normal gas composition of arterial blood is limited.” However, it should be noted that, as with respect to the terminological definition of respiratory failure, its classification of the generally accepted point of view has not been developed.

According to the pathogenesis, respiratory failure is usually divided into two main groups: 1) with a primary lesion of extrapulmonary mechanisms, 2) with a primary lesion of the pulmonary mechanisms.

Extrapulmonary respiratory failure is caused by:

- violation of the central regulation of respiration (damage to the brain and spinal cord of traumatic, metabolic, circulatory, toxic, neuroinfectious etiology, etc., e

- violation of neuromuscular transmission (poliomyelitis, polyradiculoneuritis, myosthenia, intoxication, the use of curariform drugs, etc.),

- pathology of the muscle apparatus (myodystrophy, trauma, collagenosis and other disorders),

- damage to the chest (pneumothorax, costal valve, pleural effusion, kyphoscoliosis, rheumatoid spondylitis, etc.),

- diseases of the blood system, accompanied by a decrease in the amount of hemoglobin,

- circulatory pathology leading to impaired perfusion in the lungs (blood loss, heart failure, etc.).

Predominant damage to the pulmonary mechanisms is caused by:

- the formation of the central or peripheral respiratory tract (foreign bodies, inflammatory diseases, post-intubation laryngeal edema, anaphylaxis, impaired sputum drainage, etc.),

- restriction of alveolar tissue (interstitial edema, pneumofibrosis, etc.),

- diffuse disorders with thickening of the alveolo-capillary membrane (edema, collagenosis, fibrosis, etc.),

- damage to the pulmonary capillaries (capillarotoxicosis, microembolism, etc.),

- reduction of functioning lung tissue (lung resection, atelectasis, pneumonia, etc.).

In practical work, the division of bronchopulmonary ONE into ventilation is widely used, when the mechanics of respiration and parenchymal are disturbed, which is due to the pathological process in the gas exchange zone and interstitial space of the lungs.

According to the rate of development of clinical symptoms, acute and chronic forms are distinguished. Acute respiratory failure (ARF) occurs within minutes or days. It can be cured or go into chronic respiratory failure, and she, in turn, in certain situations can suddenly worsen and acquire all the features of acute. The speed of failure should not be directly related to its severity. ONE does not always turn into insolvency, and chronic can be no less severe than acute. The transformation of resuscitation into an interdisciplinary specialty led to the fact that patients with one or the other form of insufficiency began to enter the intensive care and intensive care units.

According to the severity of the course, respiratory failure is proposed to be divided into three forms: a) decompensated, b) compensated, c) hidden (A.P. Zilber, 1996).

For the practice of intensive care, the first two forms are most important. With decompensated respiratory failure, the normal gas composition of arterial blood is not provided even at rest, despite the inclusion of compensatory mechanisms (hyperventilation and shortness of breath, accelerated blood flow with tachycardia and increased cardiac output, decreased tissue metabolism, etc.). Compensated respiratory failure is characterized by the fact that compensation mechanisms provide the normal gas composition of arterial blood at rest, but decompensation can occur with a provoking effect (physical activity, etc.). For this form, even at rest, changes in the ventilation regimen, tachycardia with normal gas composition of the blood are characteristic. Latent insufficiency is manifested by low functional reserves of the respiratory system, which are detected during special studies, including physical exercise tests. It is important for an anesthesiologist to find out about the presence of this form of gas exchange disturbance in a patient undergoing surgery, since this can dramatically change both the tactics of anesthesia and the management of the early postoperative period.

By the nature of gas exchange disorders, hypoxemic and hypercapnic versions of respiratory failure are distinguished. Violation of the removal of carbon dioxide is much more easily compensated by increased ventilation than a violation of oxygen absorption. Under normal alveolar ventilation, gas exchange disorders lead to hypoxemic respiratory failure, that is, to a decrease in PaO2 (due to a reflex increase in ventilation, this is accompanied by a decrease in PaCO2). On the contrary, a decrease in alveolar ventilation leads to a simultaneous decrease in PaO2 and an increase in PaCO2, which is called hypercapnic respiratory failure. An important consequence of hypercapnia is respiratory acidosis.

Hypoxemic respiratory failure is determined when oxygenation is predominantly impaired (PaO2 <60 mm Hg or SaO2 <90%), while, as a rule, PCO2 does not exceed 40 mm Hg. In the diagnosis of the hypoxemic form of ARF, attention should be paid to the nature of breathing: an inspiratory stridor for impaired upper airways, paradoxical breathing for chest injuries, progressive tachypnea, etc. Other clinical signs are not pronounced. At the beginning of the development of ODN, tachycardia with moderate arterial hypertension, nonspecific neurological manifestations: inadequate thinking, confusion and speech, inhibition, etc., are often noted. Cyanosis is not expressed, only with the progression of hypoxia it becomes intense, consciousness is suddenly impaired, then a coma (hypoxic) occurs with the absence of reflexes, blood pressure decreases sharply and blood circulation may stop. The duration of hypoxemic ONE can range from several minutes (with aspiration, asphyxiation) to several hours and days (RDSV).

There are several main reasons for the development of hypoxemic respiratory failure: 1) the unevenness of the ventilation-perfusion relationship; 2) blood discharge "from right to left"; 3) low partial pressure of oxygen in the inhaled air; 4) violation of the diffusion of gases through the alveolar-capillary membrane; 5) increased oxygen demand.

The unevenness of the ventilation-perfusion relationship occurs with many diseases, for example, with pneumonia, bronchial asthma, sarcoidosis, etc. This is the most common cause of hypoxemic respiratory failure. From areas where blood flow prevails over ventilation, blood undersaturated with oxygen flows out, which is not compensated by normal or increased blood oxygenation in areas where ventilation prevails over blood flow. Hypoxemia is usually eliminated by breathing with a mixture of high oxygen concentration. P (A – a) O2 is increased.

The discharge of blood from right to left (shunt) can be considered as an extreme degree of unevenness of the ventilation-perfusion relationship, when a significant part of the blood flows through unventilated areas of the lungs.
This condition develops, for example, with ARDS and cardiogenic pulmonary edema. With a discharge of more than 30%, hypoxemia is not eliminated by breathing pure oxygen, P (A – a) O2 is also increased.

The low partial pressure of oxygen in the inhaled air is a rare cause of respiratory failure. It occurs at high altitudes (for example, in the mountains) and in the presence of a large amount of foreign gases in the air (for example, as a result of an industrial accident); P (A – a) O2 is normal.

Violation of gas diffusion through the alveolar-capillary membrane is quite common, for example, with interstitial lung diseases, but it rarely leads to hypoxemia and is usually detected only with the help of stress tests. The removal of carbon dioxide is not disturbed, since it diffuses much faster than oxygen; P (A – a) O2 can be increased.

A low oxygen content in venous blood occurs with anemia, a decrease in cardiac output, and increased tissue oxygen consumption. Normally, the lungs completely saturate with oxygen the blood entering them. However, with a pronounced discharge of blood from right to left, a low oxygen content in the venous blood can increase hypoxemia.

Hypercapnic respiratory failure (PaCO2> 55 mmHg) is the result of decreased alveolar ventilation. Clinical signs of progressive hypercapnia are respiratory disorders (shortness of breath, gradual decrease in respiratory and minute respiratory volumes, bronchial hypersecretion, unexpressed cyanosis or facial hyperemia), increasing neurological symptoms (indifference, aggressiveness, agitation, inhibition, coma), cardiovascular disorders (tachycardia , persistent increase in blood pressure, then decompensation of cardiac activity up to hypoxic cardiac arrest on the background of hypercapnia).

Hypercapnic respiratory failure occurs with a decrease in minute volume of breathing and an increase in dead space. In both cases, hypercapnia may contribute to increased CO2 production.

A decrease in the minute volume of breathing occurs in case of damage to the central and peripheral nervous system (spinal cord injury, Guillain-Barré syndrome, botulism, myasthenia gravis, amyotrophic lateral sclerosis), muscles (polymyositis, myopathy), chest (scoliosis), with an overdose of some drugs, hypothyroidism, hypokalemia, and upper respiratory tract obstruction. P (A – a) O2 is normal, except when there are concomitant lung diseases.

The increase in dead space occurs due to areas that are normally ventilated, but poorly supplied with blood. This mechanism is responsible for respiratory failure in lung diseases such as COPD, bronchial asthma, cystic fibrosis, pneumosclerosis (P (A – a) O2 is usually increased).

Increased CO2 production occurs, for example, with fever, sepsis, epileptic seizures, and excess carbohydrates with parenteral nutrition.

In clinical practice, mixed respiratory failure is often observed, and sometimes it is difficult to determine the leading mechanism of gas exchange disorders. For example, in the postoperative period, blood oxygenation may decrease due to multiple atelectases, developing primarily as a result of anesthesia (decreased tidal volume, impaired cough reflex). The restriction of diaphragm mobility due to pain or damage to the phrenic nerve and obstruction of the small bronchi due to interstitial edema also play a role. Hypoventilation is another consequence of reduced diaphragm mobility. Mixed postoperative respiratory failure is particularly prone to people with existing lung diseases.

Therapy of respiratory failure is largely determined by the reasons that led to its development, as well as severity. It consists of many areas focused on improving lung ventilation, gas exchange at the level of the alveolo-capillary membrane, pulmonary circulation, microcirculation, blood flow, suppression of infection, etc. A common element in the treatment tactics of such patients is the rapid diagnosis, cause-effect relationship and the adoption of urgent emergency measures to eliminate hypoxemia or hypercapnia. The main therapeutic measures in this direction include ensuring free airway, oxygen and drug therapy, inhalation, the use of respiratory support in case of inconsistent spontaneous breathing of the patient. The most important aspect of intensive care is also the provision of adequate monitoring of gas exchange and other vital functions.

O2 inhalation is most widely used to ensure sufficient gas exchange during ODN. For this purpose, various devices are used, such as: nasal cannulas, leaky masks, Venturi masks, etc. The disadvantage of nasal catheters and conventional face masks is that the exact value of FiO2 remains unknown. For a rough estimate of O2 concentration using a nasal catheter, the following rule can be used: at a flow rate of 1 l / min FiO2 is 24%; an increase in speed of 1 l / min increases FiO2 by 4%. The flow rate should not exceed 5 l / min. The venturi mask provides accurate FiO2 values ​​(usually 24, 28, 31, 35, 40, or 50%). The Venturi mask is often used for hypercapnia: it allows you to choose PaO2 in such a way as to minimize CO2 retention. Masks without breathing have valves that prevent the mixing of inhaled and exhaled air. Such masks allow you to create FiO2 up to 90%.

Respiration under constant positive pressure begins if, when breathing through the mask without breathing, the PaO2 remains below 60 mm Hg. Art. The method can be used if the patient is conscious, the cough reflex is preserved, hemodynamics is stable. Use a tight-fitting mask with a safety valve. First, a constant positive pressure is 3-5 cm of water. Art. Then it is increased stepwise (by 3-5 cm of water. Art. At a time) until RaO2 reaches 60 mm Hg. Art. (or SaO2 - 90%), but not more than 10-15 cm of water. Art. Refusal of breathing under constant positive pressure makes it impossible to eliminate hypoxemia, instability of hemodynamics, fear of a confined space, which is often experienced by a patient in a closed mask, and aerophagy.

The decision to start mechanical ventilation is made taking into account the reversibility of the process that caused respiratory failure, and the general condition. Mechanical ventilation begins with a pronounced violation of gas exchange, a rapid increase in respiratory failure, ineffective ventilation and respiratory muscle fatigue due to excessive work of breathing. Indications for transferring the patient to mechanical ventilation can be formulated as follows:

- respiratory rate> 35 min – 1;

- maximum inspiratory depression of 25 cm of water. st .;

- YELLOW <10-15 ml / kg;

- PaO2 <60 mm Hg. Art. with FiO2> 60%;

- PaCO2> 50 mmHg. Art. at pH <7.35;

The presented criteria are more often used for parenchymal lung damage. With hypercapnic ONE, the decision on intubation and mechanical ventilation can be made taking into account the level of consciousness, the safety of the respiratory pattern, the duration of the underlying disease, etc.
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Respiratory failure

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