Respiratory Failure: An Overview of Information

Syndrome of respiratory failure can complicate the course of most acute and chronic respiratory diseases and is one of the main reasons for repeated hospitalizations, disability, physical activity in everyday life and premature death of patients. At the same time it should be borne in mind that respiratory failure is often found in the practice of anesthesiologists, resuscitators, neuropathologists, traumatologists, surgeons and doctors of other specialties, which is explained by the variety of its causes, which are far from always associated with the pathology of the respiratory system.

Respiratory failure is a condition of the body in which either maintenance of the normal blood gas composition is not ensured, or this is achieved by abnormal operation of the external respiration apparatus, which leads to a decrease in the functional capabilities of the organism.

The normal function of respiration is provided by: central regulation by the center of respiration (carbon dioxide stimulus); state of the conductor system of impulses along the anterior spines of the spinal cord; the state of conduction at the level of the neuromuscular synapse and muscle mediators; condition and function of the ribbed frame; changes in the functional state of the pleural cavity, diaphragm, lungs, airway patency; state of the inhaled gas mixture. Great importance in the development of respiratory failure belongs to the state of cardiac activity and blood flow in a small circle of blood circulation.

In pathological conditions at these levels, the normal gas composition of the blood can be maintained for a long time by the voltage of the compensatory mechanisms: an increase in the frequency and depth of breathing, increased heart rate and blood flow velocity, increased kidney function for excretion of acid metabolic products, an increase in the oxygen capacity of blood others with the formation of a latent respiratory insufficiency. When decompensation develops a pronounced picture of respiratory failure with the development of hypoxic syndrome.

Respiratory failure is classified by many systems, but there is no single international one yet.

From a practical point of view, the classification of B.E. Votchala (1972). The genesis is different: centrogenic respiratory failure (with the defeat of the center of breathing); neuromuscular (with lesion of the conductor pathways, and muscles); thoracodiaphragmatic (in case of damage to the costal framework or disturbance, diaphragm function); bronchopulmonary - obstructive respiratory failure due to violation of the patency of the airways (bronchospasm, inflammation, foreign bodies, tumors, asphyxia, etc.), restrictive, pathological alveoli (inflammation, alveolar edema or swelling, etc.) or compression of the lung, pleural effusion, Diffusion, developing in the pathology of microcirculation in the lungs or destruction of the surfactant. In the course of the course, respiratory failure may be acute (ODN) and chronic (HDN). By gravity, it can be compensated, with a decrease in the partial pressure of oxygen in the arterial blood to 80 mm Hg. P. Subcompensated - up to 60 mm Hg. P. Decompensated with a decrease in PaO2 below 60 mm Hg. Art. And the development of hypoxic syndrome.

Chronic respiratory failure by therapists is diagnosed if the cause is not surgical thoracic pathology, usually benign or malignant tumors. Sometimes the surgeon has to determine the severity of the disease. According to B.E. Votchala distinguish 4 degrees:

• I - dyspnoea with running and fast climbing stairs;
• II - shortness of breath with normal loads in daily life (moderate walking, cleaning, etc.);
• III - shortness of breath at low loads (dressing, washing);
• IV - dyspnea at rest.

Many pulmonologists and therapists use the so-called "household" classification of the severity of chronic respiratory failure - the appearance of dyspnea with a moderate rise in the stairs:

• I degree - shortness of breath at the level of the third floor;
• II degree - at the level of the second floor;
• III degree - at the level of the first floor.

Acute respiratory failure of various genesis can occur in the practice of any surgeon. Centrogenic acute respiratory failure is noted in cases of craniocerebral trauma, a syndrome of brain compression, inflammation, poisoning. The neuromuscular form is more common with cervical spine injuries and spinal cord injuries, rarely with myasthenia gravis, syringomyelia, botulism, tetanus. Thoracic diaphragmatic (parietal) acute respiratory failure is characteristic for fractures of the ribs, especially with violation of the thoracic cage, diaphragmatic hernia, diaphragm relaxation, compression of the diaphragm with swollen bowel loops.

Bronchopulmonary acute respiratory failure is the most frequent in the practice of surgeons. Restrictive form is most often observed with pneumothorax, pleurisy, hemothorax, alveolar cancer, pneumonia, abscesses and gangrene of the lungs and other diseases of the parenchymal part of the pulmonary cloak. In addition to the clinical picture of acute respiratory failure, lung radiography is used to identify the cause. Other studies are conducted according to indications already by thoracic surgeons.

Obstructive respiratory failure can occur with bronchospasm, tongue lancing, developmental defects of the bronchial tree (diverticula, tracheal prolapse), bronchial tumors, fibrinous-ulcerative and adhesive bronchitis. Rarely, but asphyxia occurs. Outdoor; Asphyxia develops with suffocation. In surgical practice, there may be a regurgitation (Mendelsohn syndrome) due to entry into the airways of emetics, blood (hemoaspiration) or copious secretion of the bronchial secretion that closes the lumen of the bronchi (atelectasis). There may be foreign bodies and burns, but this is very rare, since the lungs are protected by reflex spasm of the vocal cords. Acute obstruction develops suddenly: breathing is greatly hampered, superficial, often arrhythmic, auscultation is not performed or cacophony with a bronchial component is listened to. Emergency radiography and bronchoscopy not only allow you to put a topical diagnosis. X-ray obstruction is manifested by atelectasis of the lung (homogeneous intense darkening with a shift of the mediastinum towards the dimming).

As a separate issue it is necessary to consider asphyxiation from drowning. There are three types of drowning:

1. A true drowning with water ingress into the airways is found in 75-95% of cases when, after a brief stoppage of breathing, a reflex spasm is removed from the vocal cords and, with involuntary inhalation, a large amount of water enters the bronchi and alveoli. It is accompanied by pronounced cyanosis of violet color, swelling of the veins of the neck and extremities, discharge of foamy pink liquid from the mouth.
2. Asphyxic drowning, which occurs in 5-20% of cases, when there is a sharp reflex laryngospasm with a small but sudden flow of water into the pharynx or nose. At the same time, water does not enter the lungs, but goes into the stomach, overflowing it. Sometimes there can be vomiting with regurgitation, then this kind of drowning becomes true. In asphyxiated cyanosis blue color, from the mouth and nose comes a white or slightly pink "fluffy" foam.
3. "Syncopal" drowning is observed in 5-10% of cases. Occurs when the heart reflex stops and breathes when suddenly immersed in cold water. This can also be with emotional shock, the introduction of a cold solution into a vein, the introduction of a cold solution into the ear; nose or throat ("laryngopharyngeal shock").

Respiratory failure is a life-threatening violation of O2 consumption and CO2 emissions. It can include a gas exchange disturbance, a reduction in ventilation, or both. Common manifestations may be shortness of breath, respiratory involvement of additional muscles, tachycardia, increased sweating, cyanosis and impaired consciousness. The diagnosis is made on the basis of clinical and laboratory data, studies of gases in the arterial blood and X-ray study. Treatment is carried out in the intensive care unit, includes correction of the causes of respiratory failure, inhalation of O2, removal of sputum, respiratory support, if necessary.

When breathing occurs oxygenation of arterial blood and elimination of CO ₂ from venous blood. Therefore, respiratory failure is divided as a result of inadequate oxygenation or inadequate ventilation, although both disorders are often present.

Artificial ventilation (IVL) can be non-invasive and invasive. The choice of the method of treatment is based on the knowledge of the mechanisms of breathing.

Respiratory failure is a condition in which the lungs are unable to provide a normal gas composition of the arterial blood, resulting in hypercapnia and / or hypoxemia. According to another commonly used definition proposed by E. Campbell, respiratory failure is a condition in which, under resting conditions in the arterial blood, the oxygen partial pressure (PaO2) is below 60 mmHg. Art. And / or the partial pressure of carbon dioxide (PaCO2) above 49 mm Hg. Art.

Both definitions, in fact, refer to the most severe cases of decompensated respiratory failure, manifested at rest. However, from the clinical point of view, respiratory failure is important to be determined at the earliest possible stages of development, when diagnostic changes in the arterial blood gas composition are not detected at rest, but only with an increase in the activity of the respiratory system, for example, under physical exertion. In this respect, we are impressed by the definition of respiratory failure, proposed more than half a century ago (1947) at the 15th All-Union Congress of Physicians: "Respiratory failure is a condition in which either the maintenance of normal arterial blood gas is not maintained, or the latter is achieved through abnormal operation of the external respiration apparatus , leading to a decrease in functionality. " According to this definition, we can distinguish two stages of the development of the respiratory insufficiency syndrome: compensated and decompensated.

[1], [2], [3], [4], [5], [6], [7]

Methods and modes of mechanical ventilation

Ventilators monitor the pressure or volume of inspiration, or both. There is a certain relationship between pressure and volume: a certain volume corresponds to a certain pressure and vice versa. The parameters displayed on the device differ in different modes, but they are based on the respiratory rate, total ventilation volume, flow rate, waveform and the ratio of the duration of inspiration and expiration (b / vd).

Volume-controlled ventilation. With this ventilation mode, the patient is given a predetermined volume of air, the pressure in the airways can be different. This type of ventilation is used with auxiliary ventilation (assist-control - A / C) and synchronized intermittent mandatory ventilation (SIMV).

A / C is the simplest and most effective way of mechanical ventilation. Each attempt at inspiration is captured by a trigger, and the apparatus delivers a predetermined volume of air. In the absence of independent attempts of inspiration, the device carries out forced ventilation with a specified frequency of inspiration.

SIMV provides a predetermined number and volume of breaths synchronized with the patient. Unlike A / C, independent inspiration attempts are not supported, but an inspiratory valve opens and allows an independent inhalation. This regime remains popular, although it does not support breathing and is not effective in excommunicating a patient from mechanical ventilation.

Pressure-cycled ventilation. This mode includes pressure-controlled ventilation (PCV), pressure-assisted ventilation (PSV), and several non-invasive options using a tight-fitting facial mask. In all cases, the fan supplies a certain inspiratory pressure, while the volume may vary. Changes in the mechanics of the respiratory system can lead to unrecognized changes in minute ventilation. Since under this regime the pressure under which the lungs stretch is limited, it can theoretically be useful for RD-CB; although clinically it is not proven its advantages in comparison with A / C.

PCV resembles A / C; Each inspiration attempt that exceeds the established trigger sensitivity limit is maintained by pressure for a certain time, in addition, the minimum breathing rate is maintained.

With PSV, the minimum inspiratory frequency is not specified; All inhalations are initiated by the patient. The supply pressure is normally turned off when the inspiratory attempt is completed. Thus, the longer or longer the inspiration attempt, the more the amount of inspiration will be. This mode is usually used when the patient is excommunicated from mechanical ventilation. A similar regime is ventilation with a constant positive air pressure (CPPP), in which a constant pressure is maintained throughout the entire breathing cycle. In contrast to the PSV, in which different pressures on inhalation and exhalation are possible, CPAP maintains the same pressure.

Noninvasive positive pressure ventilation (NIPPV) is the supply of positive pressure during ventilation through a tightly fitting mask to the nose or nose and mouth. It is used as an option for PSV in patients with spontaneous breathing. The doctor sets a positive inspiratory positive airway (IPAP) and positive expiratory airway pressure (EPAP) pressure. Since the respiratory tract is not protected, it is possible to carry out such ventilation in patients with preserved protective reflexes and in full consciousness to avoid aspiration. NIPPV should be avoided in patients with unstable hemodynamics and with congestion in the stomach. In addition, IPAP should be set below the opening pressure of the esophagus (20 cm H2O) to avoid air ingress into the stomach.

Fan settings. The fan parameters are set depending on the situation. Respiratory volume and respiratory rate determine minute ventilation. Typically, the tidal volume is 8-9 ml / kg of ideal body weight, although in some patients, especially with neuromuscular diseases, it is better to use a larger tidal volume to prevent atelectasis. Certain disorders (eg, ARDS) require a reduction in the respiratory volume.

The sensitivity of the trigger is set so that it can capture independent inspiration attempts. Usually, the sensitivity is set at -2 cm of water. Art. If you set a very high limit, weakened patients will not be able to initiate a breath. If you set the sensitivity too low, this will lead to hyperventilation.

The breathing / exhalation ratio for normal breathing mechanics is set to 1: 3. In patients with asthma or COPD in the acute stage, the ratio should be 1: 4 and above.

The flow rate is usually set at about 60 l / min, but it can be increased to 120 l / min in patients with obstructions to air flow.

PEEP increases lung volume at the end of exhalation and does not allow the lungs to close at the end of exhalation. PEEP is usually set at 5 cm of water. Which avoids atelectasis, which can occur after intubation or with a prolonged position on the back. A higher value improves oxygenation in patients with violations of alveolar ventilation, for example, in cardiogenic pulmonary edema and ARDS, leading to redistribution of fluid from the alveoli to the interstitium and opening the collapsed alveoli. PEEP can reduce FiO with adequate arterial oxygenation, which in turn reduces the likelihood of lung damage to oxygen if prolonged ventilation with a high FiO (> 0.6) is required. PEEP increases the intrathoracic pressure by preventing venous return, which can cause hypotension in hypovolemia.

Complications of artificial ventilation

Complications can be associated with intubation of the trachea or ventilation. In the first case, sinusitis, ventilator-associated pneumonia, stenosis of the trachea, damage to the vocal cords, the formation of tracheal-esophageal or tracheal-vascular fistulas may occur. Complications of ventilation are pneumothorax, hypotension and fan-associated lung damage (VAPL), the latter associated with airway disease or lung parenchyma as a result of cyclic closure and opening of airspace, excessive lung stretching or both.

If acute hypotension occurs in a patient with mechanical ventilation, first of all, strain pneumothorax should be excluded. Hypotension is most often the result of a decrease in venous return with increased intrathoracic pressure when a high PEEP is used or the patient has a high internal PEEP with asthma / COPD; especially often it occurs with hypovolemia. Hypotension can also be the result of the sympatholytic action of sedatives used for intubation and ventilation. After exclusion of intense pneumothorax and causes of hypotension associated with the ventilator, it is necessary to disconnect the patient from the device and carry out manual ventilation of the lungs with a bag of 2-3 breaths per minute with 100% oxygen on the background of correction of hypovolemia (500-1000 ml of saline in adults, 20 ml / kg in children). With the rapid improvement of the condition, it is assumed that the clinical problem is associated with the ventilation and that the ventilation parameters need to be corrected.

Like all patients in critical condition, it is necessary to prevent deep vein thrombosis and gastrointestinal bleeding. In the first case, prophylaxis is carried out with heparin at a dose of 5,000 units subcutaneously twice a day, or compression devices (bandages, stockings, etc.) are used. To prevent gastrointestinal bleeding appoint H2 blockers (for example, famotidine 20 mg orally or intravenously twice a day) or sucralfate (1 g inside 4 times a day). Proton pump inhibitors should be used in patients with active bleeding or if they have already been prescribed.

The most effective way to reduce the likelihood of complications is to reduce the duration of mechanical ventilation.

[8], [9], [10], [11], [12], [13]

The mechanism of breathing

Normally, during inspiration, a negative pressure is created in the pleural cavity, a pressure gradient between atmospheric air and lungs creates a flow of air. In case of ventilation, the pressure gradient is created by the apparatus.

Peak pressure is measured by opening the airway (PaO2) and is created by the ventilator. It represents the total pressure necessary to overcome the resistance of the inspired flow (resistance pressure), the elastic thrust of the lungs and chest (elastic pressure) and the pressure in the alveoli at the beginning of the inspiration (positive end-expiratory pressure of PEEP). In this way:

Resistance pressure is the derivative of the resistance of conductive paths and airflow. With mechanical ventilation, the air flow must overcome the resistance of the respiratory circuit, the endotracheal tube and, most importantly, the patient's airways. Even when these factors are constant, increasing the air flow increases the pressure of the resistance.

Elastic pressure is a derivative of the elasticity of the lung tissue, the walls of the chest and the volume of insufflation gas. With a constant volume, the elastic pressure increases with decreasing lung extensibility (as in fibrosis) or restricting a chest or diaphragm excursion (as with intense ascites).

The pressure at the end of the exhalation in the alveoli is normally at atmospheric. However, if the air does not completely exit from the alveoli with airway obstruction, with resistance to air flow or shortening of the exhalation time, the end-expiratory pressure will exceed atmospheric pressure. This pressure is called internal or auto PEEP to distinguish it from the external (therapeutic) PEEP created by the ventilator.

At any increase in peak pressure (for example, above 25 cm H2O), it is necessary to estimate the relative contribution of the pressure of resistance and elastic pressure by measuring the plateau pressure. For this purpose, the exhalation valve remains closed for an additional 0.3-0.5 s after inhalation, delaying the exhalation. During this period, the pressure in the airway decreases, as the flow of air stops. As a result of this method, the pressure at the end of the inspiration is an elastic pressure (assuming that the patient does not attempt to breathe in or out). The difference between the peak and the plateau pressure is the pressure of the resistance.

Increased resistance pressure (for example, above 10 cm H2O) indicates a violation of patency of the endotracheal tube due to increased secretion, the formation of clots or bronchospasm. Increased elastic pressure (more than 10 cm H2O) indicates a decrease in the extensibility of the lungs due to edema, fibrosis or lung atelectasis; exudative pleurisy of large volume or fibrotorax, as well as extrapulmonary causes: shingles or chest deformation, ascites, pregnancy or severe obesity.

The internal PEEP can be measured in a patient without spontaneous ventilation with an end-of-expiration delay. Immediately before inhalation, the exhalation valve closes for 2 seconds. The flow decreases, the pressure of resistance is eliminated; The resulting pressure reflects the pressure in the alveoli at the end of the exhalation (internal PEEP). A non-quantitative method for estimating the internal PEEP is based on the determination of the traces of the expiratory flow. If the expiratory flow continues until the next inspiration begins, or the patient's chest does not take its original position, it means that there is an internal PEEP. The consequences of increased internal PEEP are an increase in the inspiratory work of the respiratory system and a decrease in venous return.

The detection of internal PEEP should prompt a search for the cause of airway obstruction, although a high minute ventilation (> 20 l / min) alone can cause an internal PEEP without airflow obstructions. If the reason for the restriction of flow, then it is possible to reduce the inspiratory time or respiratory rate, thereby increasing the expiratory fraction in the respiratory cycle.