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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 most simple definition was given to her by A.P. Zilber (1996): "Respiratory failure (NAM) is a condition of the body in which the ability of the lungs and the ventilation apparatus to ensure the normal gas composition of arterial blood is limited." It should, however, be noted that, as with regard to the terminological definition of respiratory failure, and its classification, the generally accepted point of view has not been developed.

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

The development of respiratory failure extrapulmonary nature lead:

- 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, myostenia, intoxication, use of curare-like drugs, etc.),

- pathology of the muscular system (muscular dystrophy, trauma, collagenosis and other disorders),

- defeat of the chest (pneumothorax, rib valve, pleural effusion, kyphoscoliosis, rheumatoid spondylitis, etc.),

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

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

The predominant lesion of pulmonary mechanisms is caused by:

- circumcision of the central or peripheral airways (foreign bodies, inflammatory diseases, post-intubation laryngeal edema, anaphylaxis, sputum drainage impairment, etc.),

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

- diffuse disorders in case of thickening of the alveolar-capillary membrane (edema, collagenosis, fibrosis, etc.),

- defeat of pulmonary capillaries (capillary toxicosis, microembolism, etc.),

- reduction of pulmonary functioning tissue (resection of the lungs, atelectasis, pneumonia, etc.).

In practical work, the division of bronchopulmonary ADNs into ventilating is widely used, when respiratory mechanics and parenchymal respiration are disturbed, which is caused by a pathological process in the gas exchange zone and the interstitial space of the lungs.

According to the speed of development of clinical symptoms distinguish between acute and chronic forms. Acute respiratory failure (ARF) occurs within a few minutes or days. It can be cured or go into chronic respiratory failure, and that, in turn, in certain situations can suddenly worsen and acquire all the features of acute. The speed of development of failure should not be directly attributed to its severity. ONE does not always turn into inconsistency, and chronic can be no less severe than acute. The transformation of resuscitation into an interdisciplinary specialty led to the fact that patients in the resuscitation and intensive care departments began to receive patients from both one and the other form of insufficiency.

According to the severity of respiratory failure, it is proposed to divide into three forms: a) decompensated, b) compensated, c) hidden (AP 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 ensured even in conditions of rest, despite the inclusion of compensatory mechanisms (hyperventilation and shortness of breath, accelerated blood flow with tachycardia and increased cardiac output, reduced tissue metabolism, etc.). Compensated respiratory failure is characterized by the fact that the compensation mechanisms provide a normal gas composition of arterial blood in conditions of rest, but with a provoking effect (physical exertion, etc.), decompensation may occur. This form, even at rest, is characterized by changes in the ventilation mode, tachycardia with normal blood gas composition. Hidden insufficiency is manifested by low functional reserves of the respiratory system, which are detected during special studies, including with physical stress tests. It is important for the anesthesiologist to know about the presence of such a form of gas exchange disorder in a patient undergoing surgical intervention before the operation, since this can drastically change both the tactics of anesthesia and the management of the early postoperative period.

By the nature of gas exchange disorders, hypoxemic and hypercapnic variants of respiratory failure are distinguished. Violation of carbon dioxide excretion is much easier compensated by increased ventilation than by violation of oxygen absorption. In normal alveolar ventilation, impaired gas exchange leads to hypoxemic respiratory failure, that is, a decrease in PaO2 (due to a reflex increase in ventilation, this is accompanied by a decrease in PaCO2). In contrast, a reduction 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 disturbed (PaO2 <60 mmHg or SaO2 <90%), while generally PCO2 does not exceed 40 mmHg. In the diagnosis of the hypoxemic form of ARF, attention should be paid to the nature of breathing: inspiratory stridor - for violations of the upper respiratory tract, paradoxical breathing - for injuries of the chest, progressive tachypnea, etc. Other clinical signs are not pronounced. At the beginning of the development of ONE, tachycardia with moderate arterial hypertension is often noted, nonspecific neurological manifestations: inadequate thinking, confusion of consciousness and speech, inhibition, etc. Cyanosis is not pronounced, only with the progression of hypoxia, it becomes intense, the consciousness is suddenly disturbed, then a coma (hypoxic) with a lack of reflexes occurs, the blood pressure drops sharply and blood circulation can stop. The duration of hypoxemic ODN can vary from several minutes (during aspiration, asphyxia) to several hours and days (ARDS).

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

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

The discharge of blood from right to left (shunt) can be considered as an extreme degree of irregularity 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 when breathing in pure oxygen, P (A – a) O2 is also increased.

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

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

Low oxygen content in venous blood is associated with anemia, a decrease in cardiac output, and an increased consumption of oxygen by the tissues. Normally, the lungs completely saturate the blood flowing to them with oxygen. However, with a pronounced discharge of blood from right to left, low oxygen content in venous blood may increase hypoxemia.

Hypercapnic respiratory failure (PaCO2> 55 mmHg) is the result of a decrease in alveolar ventilation. Clinical signs of progressive hypercapnia are: respiratory disorders (shortness of breath, a 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 (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, inhibition, coma), cardiovascular disorders (tons, aggression, agitation, lethargy, coma), cardiovascular disorders (t , persistent increase in blood pressure, then decompensation of cardiac activity up to hypoxic cardiac arrest on the background of hypercapnia).

Hypercapnic respiratory failure occurs when the minute volume of respiration decreases and the dead space increases. In both cases, hypercapnia may be promoted by increased production of CO2.

The minute respiratory volume decreases with damage to the central and peripheral nervous system (spinal cord injury, Guillain-Barré syndrome, botulism, myasthenia, amyotrophic lateral sclerosis), muscles (polymyositis, myopathy), chest (scoliosis), overdose of some drugs, hypothyroidism, hypokalemia, and upper airway obstruction. Р (A – a) O2 is normal, except for cases 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 diseases of the lungs such as COPD, bronchial asthma, cystic fibrosis, pneumosclerosis (P (A – a) O2 is usually increased).

Increased CO2 formation occurs, for example, with fever, sepsis, epileptic seizures, and an excess of carbohydrates during parenteral nutrition.

In clinical practice, there is often a mixed respiratory failure, and sometimes it is difficult to determine the leading mechanism of violation of gas exchange. For example, in the postoperative period, blood oxygenation may decrease due to multiple atelectasis, developing primarily as a result of anesthesia (decrease in respiratory volume, impaired cough reflex). Plays the role of limiting the mobility of the diaphragm due to pain or damage to the phrenic nerve and obstruction of the small bronchi due to interstitial edema. Hypoventilation is another consequence of decreased diaphragm mobility. For mixed postoperative respiratory failure are especially predisposed people with existing lung diseases.

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

O2 inhalation is most widely used to ensure sufficient gas exchange with ONE. Various devices are used for this purpose, such as: nasal cannulas, leaky masks, Venturi masks, etc. The disadvantage of nasal catheters and conventional face masks is that the exact FiO2 value remains unknown. For a rough estimate of the O2 concentration when using a nasal catheter, you can use the following rule: 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 ​​(typically 24, 28, 31, 35, 40, or 50%). The venturi mask is often used for hypercapnia: it allows PAO2 to be selected in such a way as to minimize CO2 retention. Non-return breathing masks have valves that prevent mixing of inhaled and exhaled air. Such masks allow you to create FiO2 up to 90%.

Breathing under constant positive pressure starts when, when breathing through a mask without return breathing, PaO2 remains below 60 mm Hg. Art. The method can be applied 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, step by step (by 3-5 cm of water. Art. At a time) is increased until PaO2 reaches 60 mm Hg. Art. (or SaO2 - 90%), but not more than up to 10-15 cm of water. Art. Refusing to breathe under constant positive pressure makes it impossible to eliminate hypoxemia, hemodynamic instability, fear of a closed space, which the patient in a closed mask often experiences, and aerophagy.

The decision on the start of mechanical ventilation is taken taking into account the reversibility of the process that caused respiratory failure and the general condition. A ventilator begins with a marked impairment of gas exchange, a rapid increase in respiratory failure, the ineffectiveness of assisted ventilation and respiratory muscle fatigue due to excessive breathing. The indications for transferring the patient to mechanical ventilation can be formulated as follows:

- respiratory rate> 35 min – 1;

- The maximum vacuum on the inhale 25 cm of water. v .;

- VC <10-15 ml / kg;

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

- RaCO2> 50 mmHg. Art. at pH <7.35;

The criteria presented are more often used for parenchymal damage to the lungs. With hypercapnic ODN, the decision on intubation and mechanical ventilation may be made taking into account the level of consciousness, the preservation of the respiratory pattern, the duration of the underlying disease, etc.
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