Termination of prolonged artificial ventilation of the lungs. Literature review. Complications of prolonged IVL Why is it connected to the device after the operation?

V modern medicine widely used apparatuses artificial ventilation lungs to force air (sometimes with the addition of other gases, such as oxygen) into the lungs and remove carbon dioxide from them.

Usually, such a device is connected to a breathing (endotracheal) tube inserted into the trachea (windpipe) of the patient. After the tube is inserted into a special balloon located on it, air is pumped, the balloon inflates and blocks the trachea (air can enter or leave the lungs only through the endotracheal tube). This tube is double and the inner part can be removed for cleaning, sterilization or replacement.

In the process of artificial ventilation of the lungs, air is injected into them, then the pressure decreases, and the air leaves the lungs, pushed out by the spontaneous contraction of their elastic tissues. This process is called intermittent positive pressure ventilation (the most commonly used ventilation pattern).

Used in the past, artificial respiration apparatus forced air into the lungs and removed it forcibly (ventilation with negative pressure), nowadays such a scheme is practiced much less often.

The use of artificial lung ventilation devices

Most often, artificial lung ventilation devices are used during surgical operations when respiratory arrest is possible. These are usually organ surgeries. chest or abdominal cavity, during which the respiratory muscles can be relaxed with special medications.

Artificial ventilation devices are also used to restore normal breathing of patients in the postoperative period and to maintain the life of people with disabilities. respiratory system, for example, as a result of an accident.

The decision to use mechanical ventilation is made based on an assessment of the patient's ability to breathe independently. To do this, measure the volume of air entering and leaving the lungs over a period (usually one minute), and the level of oxygen in the blood.

Connecting and disconnecting artificial lung ventilation devices

Patients with ventilators connected are almost always in the intensive care unit (or in the operating room). The hospital staff of the department has special training on the use of these devices.

In the past, intubation (insertion of an endotracheal tube) often irritated the trachea and especially the larynx, so it could not be used for more than a few days. The endotracheal tube made of modern materials gives the patient much less inconvenience. However, if mechanical ventilation is needed for a long time, a tracheostomy, an operation in which an endotracheal tube is inserted through an opening in the trachea, must be performed.

In case of impaired lung function, additional oxygen is supplied to the patient's lungs through artificial ventilation devices. Normal atmospheric air contains 21% oxygen, but some patients are ventilated lungs with air, which contains up to 50% of this gas.

Artificial respiration can be abandoned if, with the improvement of the patient's condition, his strength is restored to such an extent that he can breathe on his own. At the same time, it is important to ensure a gradual transition to spontaneous breathing. When the patient's condition makes it possible to lower the oxygen content in the supplied air to the atmospheric level, then at the same time the intensity of the supply of the respiratory mixture is also reduced.

One of the most common techniques is to set the machine for a small number of breaths, allowing the patient to breathe independently in between. This usually happens a few days after connecting to a ventilator.

Pathways

Nose - the first changes in the incoming air occur in the nose, where it is cleansed, warmed and moisturized. This is facilitated by the hair filter, vestibule and nasal concha. Intensive blood supply to the mucous membrane and cavernous plexuses of the shells provides rapid warming or cooling of the air to body temperature. Water evaporating from the mucous membrane humidifies the air by 75-80%. Long-term inhalation of air of low humidity leads to drying of the mucous membrane, the ingress of dry air into the lungs, the development of atelectasis, pneumonia and an increase in resistance in the airways.


Pharynx separates food from air, regulates pressure in the middle ear area.


Larynx provides vocal function by preventing aspiration by means of the epiglottis, and the closure of the vocal cords is one of the main components of cough.

Trachea - the main air duct, the air is heated and humidified in it. The cells of the mucous membrane capture foreign substances, and the cilia propel the mucus up the trachea.

Bronchi (lobar and segmental) end with terminal bronchioles.


The larynx, trachea and bronchi are also involved in cleansing, warming, and humidifying the air.


Conductive wall structure airways(VP) differs from structure respiratory tract gas exchange zone. The wall of the conducting airways consists of a mucous membrane, a layer of smooth muscles, submucosa, connective and cartilaginous membranes. The epithelial cells of the airways are equipped with cilia, which, rhythmically oscillating, advance the protective layer of mucus in the direction of the nasopharynx. The VP mucosa and lung tissue contain macrophages that phagocytose and digest mineral and bacterial particles. Normally, mucus from the airways and alveoli is constantly removed. The mucous membrane of the EP is represented by ciliated pseudo-stratified epithelium, as well as secretory cells secreting mucus, immunoglobulins, complement, lysozyme, inhibitors, interferon and other substances. The cilia contain many mitochondria, which provide energy for their high locomotor activity(about 1000 movements per minute), which allows you to transport phlegm at a speed of up to 1 cm / min in the bronchi and up to 3 cm / min in the trachea. In a day, about 100 ml of sputum is normally evacuated from the trachea and bronchi, and in pathological conditions up to 100 ml / hour.


The cilia function in a double layer of mucus. The lower one contains biologically active substances, enzymes, immunoglobulins, the concentration of which is 10 times higher than in the blood. This determines the biological protective function mucus. Upper layer it mechanically protects the cilia from damage. Thickening or reduction of the upper layer of mucus during inflammation or toxic effects inevitably disrupts the drainage function of the ciliated epithelium, irritates the respiratory tract and reflexively causes a cough. Sneezing and coughing protect the lungs from the penetration of mineral and bacterial particles.


Alveoli


In the alveoli, gas exchange occurs between the blood of the pulmonary capillaries and air. The total number of alveoli is approximately 300 million, and their total surface area is approximately 80 m 2. The diameter of the alveoli is 0.2-0.3 mm. Gas exchange between alveolar air and blood is carried out by diffusion. The blood of the pulmonary capillaries is separated from the alveolar space only by a thin layer of tissue - the so-called alveolar-capillary membrane formed by the alveolar epithelium, the narrow interstitial space and the capillary endothelium. The total thickness of this membrane does not exceed 1 micron. The entire alveolar surface of the lungs is covered with a thin film called surfactant.

Surfactant reduces surface tension at the interface between liquid and air at the end of expiration, when the volume of the lung is minimal, increases elasticity lungs and plays the role of a decongestant factor(does not let water vapor from the alveolar air), as a result of which the alveoli remain dry. It reduces surface tension when the volume of the alveoli decreases during exhalation and prevents its collapse; reduces shunting, which improves oxygenation of arterial blood at lower pressures and minimal O 2 in the inhaled mixture.


The surfactant layer consists of:

1) the surfactant itself (microfilms of phospholipid or polyprotein molecular complexes at the border with the air environment);

2) hypophase (deep-lying hydrophilic layer of proteins, electrolytes, bound water, phospholipids and polysaccharides);

3) the cellular component, represented by alveolocytes and alveolar macrophages.


The main chemical constituents of surfactant are lipids, proteins and carbohydrates. Phospholipids (lecithin, palmitic acid, heparin) make up 80-90% of its mass. Surfactant covers bronchioles with a continuous layer, lowers breathing resistance, maintains filling

At low stretching pressure, it reduces the action of the forces that cause the accumulation of fluid in the tissues. In addition, the surfactant cleans the inhaled gases, filters and traps the inhaled particles, regulates the exchange of water between the blood and the air of the alveoli, accelerates the diffusion of CO2, and has a pronounced antioxidant effect. The surfactant is very sensitive to various endogenous and exogenous factors: circulatory disorders, ventilation and metabolism, changes in PO 2 in the inhaled air, and its pollution. With surfactant deficiency, atelectasis and RDS of newborns occur. Approximately 90-95% of the alveolar surfactant is recycled, purified, accumulated and re-secreted. The half-life of surfactant components from the lumen of the alveoli of healthy lungs is about 20 hours.

Pulmonary volumes

Ventilation of the lungs depends on the depth of breathing and the frequency of respiratory movements. Both of these parameters can vary depending on the needs of the body. There are a number of volumetric indicators that characterize the condition of the lungs. Normal adult averages are as follows:


1. Respiratory volume(DO-VT- Tidal Volume)- the volume of inhaled and exhaled air with calm breathing. Normal values ​​are 7-9 ml / kg.


2. Inspiratory reserve volume (ROVD -IRV - Inspiratory Reserve Volume) - the volume that can be additionally received after a calm inhalation, i.e. the difference between normal and maximum ventilation. Normal value: 2-2.5 liters (about 2/3 VC).

3. Expiratory reserve volume (ROVid - ERV - Expiratory Reserve Volume) - the volume that can be additionally exhaled after a calm exhalation, i.e. the difference between normal and maximum exhalation. Normal value: 1.0-1.5 l (about 1/3 VC).


4.Residual volume (RO - RV - Residal Volume) - the volume remaining in the lungs after maximum exhalation. About 1.5-2.0 liters.


5. Lung vital capacity (VC - VT - Vital Capacity) - the amount of air that can be exhaled to the maximum after the maximum inhalation. VC is an indicator of the mobility of the lungs and chest. VC depends on age, sex, size and position of the body, degree of fitness. Normal values ​​of VC are 60-70 ml / kg - 3.5-5.5 liters.


6. Inspiratory reserve (RV) -Inspiratory capacity (Evd - IC - Inspiritory Capacity) - maximum amount air that can enter the lungs after a calm exhalation. Equal to the sum of DO and ROVD.

7.Total lung capacity (OEL - TLC - Total lung capacity) or maximum lung capacity - the amount of air contained in the lungs at the height of maximum inspiration. Consists of VC and OO and is calculated as the sum of VC and OO. The normal value is about 6.0 liters.
The study of the structure of the OEL is decisive in elucidating the ways of increasing or decreasing VC, which can be of significant practical importance. An increase in VC can be regarded positively only if the VC does not change or increases, but less than VC, which occurs with an increase in VC due to a decrease in OO. If, simultaneously with the increase in VC, there is still greater magnification OEL, then this cannot be considered a positive factor. When VC is below 70% VC, the function external respiration deeply disturbed. Usually, in pathological conditions, VC and VC change in the same way, with the exception of obstructive pulmonary emphysema, when VC, as a rule, decreases, RO increases, and VC may remain normal or be higher than normal.


8.Functional residual capacity (FRC - FRC - Functional residual volume) - the amount of air that remains in the lungs after a calm exhalation. Normal values ​​in adults are from 3 to 3.5 liters. FOE = OO + Rowyd. By definition, FRU is the volume of gas that remains in the lungs during calm exhalation and can be a measure of the area of ​​gas exchange. It is formed as a result of a balance between the oppositely directed elastic forces of the lungs and the chest. Physiological significance FRU consists in the partial renewal of the alveolar air volume during inspiration (ventilated volume) and indicates the volume of alveolar air constantly in the lungs. The decrease in FRU is associated with the development of atelectasis, the closure of small airways, a decrease in lung compliance, an increase in the alveolar-arterial difference in O 2 as a result of perfusion in the atelectasized areas of the lungs, and a decrease in the ventilation-perfusion ratio. Obstructive ventilation disorders lead to an increase in FRU, restrictive disorders - to a decrease in FRU.


Anatomical and functional dead space


Anatomical dead space called the volume of the airways in which gas exchange does not occur. This space includes the nasal and oral cavity, pharynx, larynx, trachea, bronchi and bronchioles. The amount of dead space depends on the height and position of the body. It can be roughly assumed that a seated person has the volume of dead space (in milliliters) equal to twice the body weight (in kilograms). Thus, in adults, it is equal to about 150-200 ml (2 ml / kg of body weight).


Under functional (physiological) dead space understand all those parts of the respiratory system in which gas exchange does not occur due to reduced or absent blood flow. The functional dead space, in contrast to the anatomical, includes not only the airways, but also those alveoli that are ventilated but not perfused with blood.


Alveolar ventilation and dead space ventilation

The part of the minute volume of respiration that reaches the alveoli is called alveolar ventilation, the rest of it is ventilation of the dead space. Alveolar ventilation is a measure of overall respiratory efficiency. It is on this value that the gas composition maintained in the alveolar space depends. As for the minute volume, it only to a small extent reflects the efficiency of ventilation of the lungs. So, if the minute volume of respiration is normal (7 l / min), but breathing is frequent and shallow (DO-0.2 l, RR-35 / min), then ventilate

Will be the main way dead the space into which air enters earlier than into the alveolar; in this case, the inhaled air will hardly reach the alveoli. Insofar as the volume of the dead space is constant, the alveolar ventilation is the greater, the deeper breathing and less frequency.


Elongation (compliance) lung tissue
Lung compliance is a measure of the elastic traction as well as the elastic resistance of the lung tissue that is overcome during inhalation. In other words, extensibility is a measure of the elasticity of the lung tissue, that is, its compliance. Mathematically, extensibility is expressed as a quotient from a change in lung volume and a corresponding change in intrapulmonary pressure.

Extensibility can be measured separately for the lungs and the chest. WITH clinical point vision (especially during mechanical ventilation) of greatest interest is precisely the compliance of the lung tissue itself, reflecting the degree of restrictive pulmonary pathology... In modern literature, lung compliance is usually denoted by the term "compliance" (from english word"Compliance", abbreviated - C).


Lung compliance decreases:

With age (in patients over 50);

In the supine position (due to the pressure of the abdominal organs on the diaphragm);

During laparoscopic surgical interventions in connection with carboxyperitoneum;

In acute restrictive pathology (acute polysegmental pneumonia, RDS, pulmonary edema, atelectasis, aspiration, etc.);

With chronic restrictive pathology (chronic pneumonia, pulmonary fibrosis, collagenosis, silicosis, etc.);

With the pathology of the organs that surround the lungs (pneumo- or hydrothorax, high standing of the dome of the diaphragm with intestinal paresis, etc.).


The worse the compliance of the lungs, the greater the elastic resistance of the lung tissue must be overcome in order to achieve the tidal volume as with normal compliance. Consequently, in the case of deteriorating lung compliance, when the same tidal volume is reached, the pressure in the airways increases significantly.

This position is very important for understanding: with volumetric ventilation, when a forced tidal volume is supplied to a patient with poor lung compliance (without high airway resistance), a significant increase in peak airway pressure and intrapulmonary pressure significantly increases the risk of barotrauma.


Airway resistance


The flow of the respiratory mixture in the lungs must overcome not only the elastic resistance of the tissue itself, but also the airway resistance Raw (abbreviation of the English word "resistance"). Since the tracheobronchial tree is a system of tubes of various lengths and widths, the resistance to gas flow in the lungs can be determined according to known physical laws. In general, the resistance to flow depends on the pressure gradient at the beginning and at the end of the tube, as well as on the magnitude of the flow itself.


Gas flow in the lungs can be laminar, turbulent, and transient. A laminar flow is characterized by a layer-by-layer translational gas movement with

Variable speed: the flow rate is highest in the center and gradually decreases towards the walls. Laminar gas flow prevails at relatively low speeds and is described by Poiseuille's law, according to which the resistance to gas flow is most dependent on the radius of the tube (bronchi). Reducing the radius by 2 times leads to an increase in resistance by 16 times. In this regard, the importance of choosing the widest possible endotracheal (tracheostomy) tube and maintaining the patency of the tracheobronchial tree during mechanical ventilation is understandable.
The resistance of the airways to the gas flow increases significantly with bronchiolospasm, edema of the bronchial mucosa, accumulation of mucus and inflammatory secretions due to narrowing of the lumen of the bronchial tree. The resistance is also influenced by the flow rate and the length of the tube (bronchi). WITH

By increasing the flow rate (forcing inspiration or expiration), airway resistance increases.

The main reasons for the increase in airway resistance are:

Bronchiolospasm;

Edema of the bronchial mucosa (exacerbation of bronchial asthma, bronchitis, subglottic laryngitis);

Foreign body, aspiration, neoplasms;

Accumulation of sputum and inflammatory secretions;

Emphysema (dynamic compression of the airways).


Turbulent flow is characterized by the chaotic movement of gas molecules along the tube (bronchi). It prevails at high volumetric flow rates. In the case of turbulent flow, the airway resistance increases, since it is even more dependent on the flow rate and the radius of the bronchi. Turbulent movement occurs at high flows, sharp changes in the flow rate, in the places of bends and branches of the bronchi, with a sharp change in the diameter of the bronchi. That is why turbulent flow is typical for patients with COPD, when, even in remission, there is an increased airway resistance. The same applies to patients with bronchial asthma.


The airway resistance is unevenly distributed in the lungs. The greatest resistance is created by the bronchi of medium caliber (up to the 5-7th generation), since the resistance of large bronchi is low due to their large diameter, and of small bronchi - due to a significant total cross-sectional area.


Airway resistance also depends on the volume of the lungs. With a large volume, the parenchyma has a greater "stretching" effect on the airways, and their resistance decreases. The use of PEEP increases lung volume and therefore decreases airway resistance.

Airway resistance is normally:

In adults - 3-10 mm water column / l / s;

In children - 15-20 mm water column / l / s;

In infants under 1 year old - 20-30 mm water column / l / s;

In newborns - 30-50 mm water column / l / s.


On expiration, the airway resistance is 2-4 mm H2O / L / s greater than on inspiration. This is due to the passive nature of exhalation, when the state of the airway wall affects the gas flow to a greater extent than during active inhalation. Therefore, full exhalation requires 2-3 times longer than inhalation. Normally, the ratio of time inhalation / exhalation (I: E) is about 1: 1.5-2 for adults. The completeness of exhalation in a patient during mechanical ventilation can be assessed by monitoring the expiratory time constant.


Breath work


The work of breathing is performed mainly by the inspiratory muscles during inhalation; exhalation is almost always passive. At the same time, in the case of, for example, acute bronchospasm or edema of the mucous membrane of the respiratory tract, exhalation also becomes active, which significantly increases common work external ventilation.


During inhalation, the work of breathing is mainly spent on overcoming the elastic resistance of the lung tissue and the resistance of the airways, while about 50% of the energy expended is accumulated in the elastic structures of the lungs. During exhalation, this accumulated potential energy is released, which allows the expiratory resistance of the airways to be overcome.

The increase in resistance to inhalation or exhalation is compensated for by additional work of the respiratory muscles. The work of breathing increases with a decrease in lung compliance (restrictive pathology), an increase in airway resistance (obstructive pathology), tachypnea (due to ventilation of the dead space).


Normally, only 2-3% of the total oxygen consumed by the body is spent on the work of the respiratory muscles. This is the so-called "cost of breathing". At physical work the cost of breathing can reach 10-15%. And with pathology (especially restrictive), more than 30-40% of the total oxygen absorbed by the body can be spent on the work of the respiratory muscles. In severe diffusional respiratory failure, the cost of breathing increases up to 90%. At some point, all the additional oxygen obtained by increasing ventilation goes to cover the corresponding increase in the work of the respiratory muscles. That is why, at a certain stage, a significant increase in the work of breathing is a direct indication for the start of mechanical ventilation, at which the cost of breathing decreases to almost zero.


The work of breathing, which is required to overcome the elastic resistance (compliance of the lungs), increases as the tidal volume increases. The work required to overcome airway resistance increases with increasing respiratory rate. The patient seeks to reduce the work of breathing, changing the respiratory rate and tidal volume, depending on the prevailing pathology. For each situation, there is an optimal respiratory rate and tidal volume at which the work of breathing is minimal. So, for patients with reduced compliance, from the point of view of minimizing the work of breathing, more frequent and shallow breathing is suitable (low-compliant lungs are difficult to expand). On the other hand, with increased airway resistance, deep and slow breathing is optimal. This is understandable: an increase in the tidal volume allows you to "stretch", expand the bronchi, reduce their resistance to gas flow; for the same purpose, patients with obstructive pathology during exhalation compress their lips, creating their own "PEEP" (PEEP). Slow and slow breathing contributes to the elongation of exhalation, which is important for more complete removal expired gas mixture in conditions of increased expiratory airway resistance.


Respiration regulation

The breathing process is regulated by the central and peripheral nervous system. The reticular formation of the brain contains the respiratory center, which consists of the centers of inhalation, exhalation and pneumotaxis.


Central chemoreceptors are located in the medulla oblongata and are excited with an increase in the concentration of H + and PCO 2 in cerebrospinal fluid... Normally, the pH of the latter is 7.32, PCO 2 is 50 mm Hg, and the content of HCO 3 is 24.5 mmol / l. Even a slight decrease in pH and an increase in PCO 2 increase lung ventilation. These receptors respond to hypercapnia and acidosis more slowly than peripheral ones, since additional time is required to measure the values ​​of CO 2, H + and HCO 3 due to overcoming the blood-brain barrier. The contraction of the respiratory muscles controls the central respiratory mechanism, which consists of a group of cells medulla oblongata, bridge, and pneumotaxic centers... They tone the respiratory center and, by impulses from the mechanoreceptors, determine the excitation threshold at which inhalation stops. Pneumotaxic cells also switch inhalation and exhalation.


Peripheral chemoreceptors located on the inner membranes of the carotid sinus, aortic arch, left atrium, control humoral parameters (PO 2, PCO 2 in arterial blood and cerebrospinal fluid) and immediately respond to changes internal environment organism, changing the mode of spontaneous breathing and, thus, correcting pH, PO 2 and PCO 2 in arterial blood and cerebrospinal fluid. Pulses from chemoreceptors regulate the amount of ventilation required to maintain a certain metabolic rate. In optimizing the ventilation mode, i.e. the establishment of the frequency and depth of breathing, the duration of inhalation and exhalation, the force of contraction of the respiratory muscles at a given level of ventilation, mechanoreceptors are also involved. Ventilation of the lungs is determined by the level of metabolism, the effect of metabolic products and O2 on chemoreceptors, which transform them into afferent impulses of the nervous structures of the central respiratory mechanism. The main function of arterial chemoreceptors is the immediate correction of respiration in response to changes in the blood gas composition.


Peripheral mechanoreceptors, localized in the walls of the alveoli, intercostal muscles and the diaphragm, respond to stretching of the structures in which they are located, to information about mechanical phenomena. Main role mechanoreceptors of the lungs play. Inhaled air enters the airway to the alveoli and participates in gas exchange at the level of the alveolar-capillary membrane. As the walls of the alveoli stretch during inhalation, mechanoreceptors are excited and send an afferent signal to the respiratory center, which inhibits inhalation (Hering-Breuer reflex).


During normal breathing, the intercostal-diaphragmatic mechanoreceptors are not excited and are of secondary importance.

The regulatory system ends with neurons that integrate impulses that come to them from chemoreceptors and send excitation impulses to the respiratory motor neurons. The cells of the bulbar respiratory center send both excitatory and inhibitory impulses to the respiratory muscles. Coordinated excitation of the respiratory motoneurons leads to synchronous contraction of the respiratory muscles.

Respiratory movements that create air flow occur due to the coordinated work of all respiratory muscles. Motor nerve cells

The neurons of the respiratory muscles are located in the anterior horns of the gray matter spinal cord(cervical and thoracic segments).


In humans, the cortex also participates in the regulation of respiration. large brain within the limits allowed by chemoreceptor regulation of respiration. For example, volitional breath holding is limited by the time during which PaO 2 in the cerebrospinal fluid rises to levels that excite arterial and medullary receptors.


Respiratory biomechanics


Ventilation of the lungs occurs due to periodic changes in the work of the respiratory muscles, the volume of the chest cavity and lungs. The main muscles of inspiration are the diaphragm and the external intercostal muscles. During their contraction, the dome of the diaphragm is flattened and the ribs are raised upward, as a result, the volume of the chest increases, and the negative intrapleural pressure (Ppl) increases. Before inspiration (at the end of expiration), Ppl is approximately minus 3-5 cm H2O. Alveolar pressure (Palv) is taken as 0 (i.e. equal to atmospheric pressure), it also reflects airway pressure and correlates with intrathoracic pressure.


The gradient between alveolar and intrapleural pressure is called transpulmonary pressure (Ptp). At the end of exhalation, it is 3-5 cm H2O. During spontaneous inspiration, an increase in negative Ppl (up to minus 6-10 cm of water column) causes a decrease in pressure in the alveoli and airways below atmospheric. In the alveoli, the pressure drops to minus 3-5 cm of water column. Due to the pressure difference, air enters (is sucked in) from the external environment into the lungs. The ribcage and diaphragm act as a piston pump, drawing air into the lungs. This "suction" effect of the chest is important not only for ventilation, but also for blood circulation. During spontaneous inspiration, additional "suction" of blood to the heart (maintenance of preload) and activation of pulmonary blood flow from the right ventricle through the pulmonary artery system occur. At the end of inspiration, when gas movement stops, alveolar pressure returns to zero, but intrapleural pressure remains reduced to minus 6-10 cm H2O.

Exhalation is normally a passive process. After relaxation of the respiratory muscles, the elastic traction forces of the chest and lungs cause the elimination (squeezing) of gas from the lungs and restoration of the original lung volume. In the event of a violation of the patency of the tracheobronchial tree (inflammatory secretion, edema of the mucous membrane, bronchospasm), the exhalation process is difficult, and the exhalation muscles (internal intercostal muscles, pectoral muscles, muscles abdominal etc.). With depletion of the expiratory muscles, the exhalation process becomes even more difficult, the exhaled mixture is delayed and the lungs are dynamically inflated.


Non-respiratory lung function

Lung function is not limited to gas diffusion. They contain 50% of all endothelial cells of the body, which line the capillary surface of the membrane and are involved in the metabolism and inactivation of biologically active substances passing through the lungs.


1. The lungs control the general hemodynamics by different filling of their own vascular bed and the effect on biologically active substances that regulate vascular tone(serotonin, histamine, bradykinin, catecholamines), the conversion of angiotensin I to angiotensin II, participation in the metabolism of prostaglandins.


2. The lungs regulate blood coagulation by secreting prostacyclin, an inhibitor of platelet aggregation, and removing thromboplastin, fibrin and its degradation products from the bloodstream. As a result, the blood flowing from the lungs has a higher fibrinolytic activity.


3. The lungs are involved in protein, carbohydrate and fat metabolism, synthesizing phospholipids (phosphatidylcholine and phosphatidylglycerol - the main components of the surfactant).

4. The lungs produce and eliminate heat, maintaining the body's energy balance.


5. Lungs cleanse blood from mechanical impurities. Cell aggregates, microthrombi, bacteria, air bubbles, fat droplets are retained by the lungs and are subject to destruction and metabolism.


Types of ventilation and types of ventilation disorders


A physiologically clear classification of ventilation types has been developed, which is based on the partial pressures of gases in the alveoli. In accordance with this classification, the following types of ventilation are distinguished:


1. Normal ventilation - normal ventilation, in which the partial pressure of CO2 in the alveoli is maintained at about 40 mm Hg.


2. Hyperventilation - increased ventilation that exceeds the metabolic needs of the body (PaCO2<40 мм.рт.ст.).


3. Hypoventilation - decreased ventilation compared to the metabolic needs of the body (PaCO2> 40 mm Hg).


4. Increased ventilation - any increase in alveolar ventilation compared to the level of rest, regardless of the partial pressure of gases in the alveoli (for example, during muscular work).

5.Eupnea - normal ventilation at rest, accompanied by a subjective feeling of comfort.


6. Hyperpnea - an increase in the depth of breathing, regardless of whether the frequency of respiratory movements is increased or not.


7. Tachypnea - increased breathing rate.


8. Bradypnea - decreased breathing rate.


9.Apnea - cessation of breathing, mainly due to the lack of physiological stimulation of the respiratory center (decrease in CO2 tension in arterial blood).


10.Dyspnea (shortness of breath) is an unpleasant subjective feeling of shortness of breath or shortness of breath.


11. Orthopnea - severe shortness of breath associated with stagnation of blood in the pulmonary capillaries as a result of left heart failure. In a horizontal position, this condition is aggravated, and therefore it is difficult for such patients to lie.


12. Asphyxia - cessation or depression of breathing, associated mainly with paralysis of the respiratory centers or closure of the airways. At the same time, gas exchange is sharply disrupted (hypoxia and hypercapnia are observed).

For diagnostic purposes, it is advisable to distinguish between two types of ventilation disorders - restrictive and obstructive.


The restrictive type of ventilation disorders includes all pathological conditions in which respiratory excursion and the ability of the lungs to expand, i.e. their extensibility decreases. Such disorders are observed, for example, with lesions of the pulmonary parenchyma (pneumonia, pulmonary edema, pulmonary fibrosis) or with pleural adhesions.


The obstructive type of ventilation disorders is caused by the narrowing of the airways, i.e. increasing their aerodynamic resistance. Similar conditions occur, for example, with the accumulation of mucus in the respiratory tract, swelling of their mucous membrane or spasm of bronchial muscles (allergic bronchiolospasm, bronchial asthma, asthmoid bronchitis, etc.). In such patients, the resistance to inhalation and exhalation is increased, and therefore, over time, the airiness of the lungs and FRU increase in them. A pathological condition characterized by an excessive decrease in the number of elastic fibers (disappearance of alveolar septa, unification of the capillary network) is called pulmonary emphysema.

This information is intended for healthcare and pharmaceutical professionals. Patients should not use this information as medical advice or guidance.

Types of artificial lung ventilation

1. What is artificial lung ventilation?

Artificial lung ventilation (ALV) is a form of ventilation designed to solve the task that the respiratory muscles normally perform. The task includes providing oxygenation and ventilation (removal of carbon dioxide) to the patient. There are two main types of ventilation: positive pressure ventilation and negative pressure ventilation. Positive pressure ventilation can be invasive (through an endotracheal tube) or non-invasive (through a face mask). Ventilation with volume and pressure phase change is also possible (see question 4). The many different modes of ventilation include controlled ventilation (CMV in the English abbreviation - ed.), Assisted ventilation (VIVL, ACV in the English abbreviation), intermittent mandatory (mandator) ventilation (IMV in the English abbreviation), synchronized intermittent mandatory ventilation (SIMV ), Pressure Controlled Ventilation (PCV), Pressure Support Ventilation (PSV), Inverted Inspiratory Ratio Ventilation (IVL, IRV), Pressure Relief Ventilation (PRV in English), and high frequency modes.

It is important to distinguish between endotracheal intubation and mechanical ventilation, as one does not necessarily imply the other. For example, a patient may need endotracheal intubation to maintain airway patency, but still be able to independently maintain ventilation through the endotracheal tube, without the help of mechanical ventilation.

2. What are the indications for mechanical ventilation?

Mechanical ventilation is indicated for many disorders. At the same time, in many cases the indications are not strictly delineated. The main reasons for the use of mechanical ventilation include the inability to provide sufficient oxygenation and the loss of adequate alveolar ventilation, which can be associated either with primary parenchymal lung damage (for example, with pneumonia or pulmonary edema), or with systemic processes that indirectly affect lung function (as occurs in sepsis or dysfunction of the central nervous system). In addition to this, holding general anesthesia often implies mechanical ventilation, because many drugs have a depressing effect on breathing, and muscle relaxants cause paralysis of the respiratory muscles. The main task of mechanical ventilation in conditions of respiratory failure is to maintain gas exchange until the pathological process that caused this failure is eliminated.

3. What is non-invasive ventilation and what are the indications for it?

Non-invasive ventilation can be performed in either negative or positive pressure mode. Negative pressure ventilation (usually with a tank - "iron lung" - or cuirass respirator) is rarely used in patients with neuromuscular disorders or chronic fatigue of the diaphragm due to chronic obstructive pulmonary disease (COPD). The shell of the respirator wraps around the torso below the neck, and the negative pressure created under the shell leads to a pressure gradient and gas flow from the upper respiratory tract to the lungs. The exhalation is passive. This ventilation mode eliminates the need for tracheal intubation and the associated problems. The upper airways should be free, but this makes them vulnerable to aspiration. Due to stagnation of blood during internal organs hypotension may occur.

Non-invasive positive pressure ventilation (NIPPV in English - Ed.) Can be performed in several modes, including continuous positive pressure mask ventilation (NPP, CPAP in English abbreviation), bi-level positive pressure (BiPAP), pressure-assisted mask ventilation, or a combination of these ventilation methods. This type of ventilation can be used in those patients who do not want tracheal intubation - patients with terminal stage disease or with some types of respiratory failure (for example, exacerbation of COPD with hypercapnia). In end-stage patients with respiratory distress, NIPPV is a reliable, effective and more comfortable means of supporting ventilation compared to other methods. The method is not so complicated and allows the patient to maintain independence and verbal contact; ending non-invasive ventilation, when indicated, is associated with less stress.

4. Describe the most common ventilation modes: CMV, ACV, IMV.

These three modes with conventional volume switching are essentially three different ways respirator response. With CMV, the patient's ventilation is entirely controlled by a preset tidal volume (tidal volume) and a target respiratory rate (RR). CMV is used in patients who have completely lost the ability to make attempts to breathe, which, in particular, is observed during general anesthesia with central respiratory depression or muscle paralysis caused by muscle relaxants. The ACV mode allows the patient to induce an artificial breath (which is why it contains the word "auxiliary"), after which the set tidal volume is delivered. If for some reason bradypnea or apnea develops, the respirator switches to a backup controlled ventilation mode. The IMV mode, originally proposed as a means of weaning from a respirator, allows the patient to breathe spontaneously through the breathing circuit of the apparatus. The respirator carries out mechanical ventilation with the established DO and RR. SIMV mode eliminates hardware breaths during ongoing spontaneous breaths.

The debate over the advantages and disadvantages of ACV and IMV continues to be heated. In theory, since not every breath is positive pressure, IMV can lower the mean airway pressure (Paw) and thus reduce the likelihood of barotrauma. In addition, with IMV the patient is easier to synchronize with the respirator. It is possible that ACV is more likely to cause respiratory alkalosis, since the patient, even with tachypnea, receives the entire DO with each breath. Any type of ventilation requires some breathing work from the patient (usually more with IMV). In patients with acute respiratory failure (ARF), the work of breathing at the initial stage and until the pathological process underlying the respiratory disorder begins to regress, it is advisable to minimize it. Usually in such cases it is necessary to provide sedation, occasionally - muscle relaxation and CMV.

5. What are the initial respirator settings for ARF? What tasks are solved using these settings?

Most patients with ARF require complete replacement ventilation. The main tasks in this case are to ensure the saturation of arterial blood with oxygen and to prevent complications associated with artificial ventilation. Complications can arise from increased airway pressure or prolonged exposure increased concentration inspiratory oxygen (FiO2) (see below).

Most often they start with the regime VIVL guaranteeing the arrival of a given volume. However, press-cyclic modes are becoming more and more popular.

You must choose FiO2... Usually start at 1.0, slowly decreasing to the minimum concentration tolerated by the patient. Long-term exposure to high FiO2 values ​​(> 60-70%) may result in oxygen toxicity.

Respiratory volume is selected taking into account body weight and pathophysiological mechanisms of lung damage. At present, a volume setting in the range of 10–12 ml / kg body weight is considered acceptable. However, in conditions such as acute respiratory distress syndrome (ARDS), lung volume decreases. Insofar as high values pressures and volumes can worsen the course of the underlying disease; smaller volumes are used - in the range of 6-10 ml / kg.

Breathing rate(RR) is usually set in the range of 10 - 20 breaths per minute. For patients requiring a large volume of minute ventilation, a respiratory rate of 20 to 30 breaths per minute may be required. At a frequency> 25, carbon dioxide (CO2) removal is not significantly improved, and a respiration rate> 30 predisposes to gas trap due to a shortened expiratory time.

Positive end-expiratory pressure (PEEP; see question 6) is usually set low initially (eg, 5 cm H2O) and can be gradually increased to improve oxygenation. Small values ​​of PEEP in most cases of acute lung injury help to maintain the airiness of the alveoli, which are prone to collapse. Modern data indicate that a low PEEP makes it possible to avoid the effect of oppositely directed forces that arise during the re-opening and collapse of the alveoli. The effects of such a force can exacerbate lung damage.

The inspiratory volumetric velocity, the shape of the inflation curve, and the inspiratory-expiratory ratio (I / E) are often set by the respiratory therapist, but the meaning of these settings should also be understood by the intensive care physician. The peak inspiratory flow rate determines the maximum inflation rate of the respirator during the inspiratory phase. At the initial stage, a flow of 50–80 l / min is usually considered satisfactory. The I / E ratio depends on the set minute volume and flow. At the same time, if the inhalation time is determined by the flow and DO, then the expiration time is determined by the flow and breathing frequency. In most situations, an I: E ratio of 1/2 to 1/3 is justified. However, COPD patients may need even longer expiratory times for adequate expiration.

Decreases in I: E can be achieved by increasing the airflow speed. However, a high inspiratory rate can increase airway pressure and sometimes impair gas distribution. At a slower flow, it is possible to reduce airway pressure and improve gas distribution due to an increase in I: E. An increased (or "inverse", as will be mentioned below) ratio I: E increases Paw, and also increases side effects from the cardiovascular system. Shortened expiratory time is poorly tolerated in obstructive airways disease. Among other things, the type or shape of the airflow curve has little effect on ventilation. Constant flow (rectangular shape of the curve) provides inflating at a set volumetric velocity. Choosing a descending or ascending inflation curve can result in improved gas distribution as airway pressure rises. Inspiratory pause, expiration retardation, and intermittent double-in-breaths are all configurable as well.

6. Explain what PEEP is. How to choose the optimal level of PEEP?

PEEP is additionally set for many types and modes of ventilation. In this case, the pressure in the airways at the end of the expiration remains above atmospheric. PEEP is aimed at preventing the collapse of the alveoli, as well as restoring the lumen of the alveoli that have collapsed in a state of acute damage. The functional residual capacity (FRC) and oxygenation increase in this case. Initially, PEEP is set at approximately 5 cm H2O, and increased to maximum values ​​- 15–20 cm H2O - in small portions. High levels of PEEP can negatively affect cardiac output (see question 8). Optimal PEEP provides the best arterial oxygenation with the least reduction in cardiac output and acceptable airway pressure. The optimal PEEP also corresponds to the level of the best expansion of the collapsed alveoli, which can be quickly established at the patient's bed, increasing the PEEP to the degree of pneumatization of the lungs, when their extensibility (see question 14) begins to fall.

It is not difficult to monitor airway pressure after each increase in PEEP. The airway pressure should rise only in proportion to the established PEEP. If the pressure in the airways begins to rise faster than the set values ​​of PEEP, this will indicate an overstretching of the alveoli and an excess of the level of optimal opening of the collapsed alveoli. Continuous positive pressure (CPP) is a form of PEEP delivered by a breathing circuit when the patient is breathing spontaneously.

7. What is intrinsic or auto-PEEP?

First described by Pepe and Marini in 1982, the internal PEEP (PEEPVn) means the occurrence of positive pressure and gas movement inside the alveoli at the end of expiration in the absence of an artificially created external PEEP (PEEPVn). Normally, the volume of the lungs at the end of expiration (FOE) depends on the result of the opposition of the elastic traction of the lungs and the elasticity of the chest wall. Balancing these forces under normal conditions results in no pressure gradient or end-expiratory airflow. PEEPvn occurs due to two main reasons. If the respiratory rate is too high or the expiratory time is too short, with mechanical ventilation, there is not enough time for healthy lungs to complete an exhalation before the start of the next respiratory cycle. This leads to the accumulation of air in the lungs and the appearance of positive pressure at the end of expiration. Therefore, patients ventilated with a large minute volume (for example, with sepsis, trauma) or with a high I / E ratio are at risk of developing PEEPVn. A small diameter endotracheal tube can also obstruct exhalation, contributing to PEEPI. Another main mechanism development of PDKVvn is associated with damage to the lungs themselves.

Patients with increased airway resistance and lung compliance (eg, asthma, COPD) have a high risk of PEEP. Due to airway obstruction and the associated difficulty in exhaling, these patients tend to experience PEEP in both spontaneous breathing and mechanical ventilation. PDKVn has the same side effects as PDKVn, but requires more vigilance in relation to itself. If the respirator, as is usually the case, has an outlet open to the atmosphere, then the only way to detect and measure PEEPin is to close the exhalation outlet while monitoring the airway pressure. This procedure should become routine, especially for high-risk patients. The therapeutic approach is based on etiology. Altering the respirator parameters (such as lowering the respiratory rate or increasing the inflation rate with decreasing I / E) can create conditions for complete exhalation. In addition, therapy of the underlying pathological process (for example, with the help of bronchodilators) can help. In patients with limited expiratory flow in obstructive airways positive effect was achieved by using the PDKVn, which ensured a decrease in the gas trap. In theory, PEEPn could act as an airway strut allowing full exhalation. However, since PEEP is added to PEEPvn, severe hemodynamic and gas exchange disorders can occur.

8. What are side effects PDKVn and PDKVvn?

Barotrauma - due to overstretching of the alveoli.
Decreased cardiac output, which may be due to several mechanisms. PEEP increases intrathoracic pressure, causing an increase in transmural pressure in the right atrium and a decrease in venous return. In addition, PEEP leads to a rise in pressure in pulmonary artery, which makes it difficult to eject blood from the right ventricle. The consequence of dilatation of the right ventricle may be the prolapse of the interventricular septum into the cavity of the left ventricle, which prevents filling of the latter and contributes to a decrease in cardiac output. All this will manifest itself as hypotension, especially severe in patients with hypovolemia.

In routine practice, emergency endotracheal intubation is performed in patients with COPD and respiratory distress. Such patients are in a serious condition, as a rule, for several days, during which they are poorly nourished and do not replace fluid losses. After intubation, patients' lungs are vigorously inflated to improve oxygenation and ventilation. Auto-PEEP rapidly increases, and severe hypotension occurs in conditions of hypovolemia. Treatment (if preventive measures are unsuccessful) includes intensive infusion, provision of conditions for a longer expiration, and elimination of bronchospasm.
During PEEP, an erroneous assessment of cardiac filling parameters (in particular, central venous pressure or pulmonary artery occlusion pressure) is also possible. The pressure transmitted from the alveoli to the pulmonary vessels can lead to a false increase in these indicators. The more flexible the lungs are, the more pressure is transmitted. The correction can be made using a rule of thumb: from the measured value of the pulmonary capillary wedge pressure (LCP), one must subtract half of the PEEP value exceeding 5 cm H2O.
The overstretching of the alveoli with excess PEEP reduces blood flow in these alveoli, increasing the dead space (MP / DO).
PEEP can increase the work of breathing (with triggered ventilation modes or with spontaneous breathing through the respirator circuit), since the patient will have to create more negative pressure to turn on the respirator.
To others side effects include increased intracranial pressure (ICP) and fluid retention.

9. Describe the types of pressure limited ventilation.

The ability to conduct pressure-limited ventilation - in trigger mode (pressure-assisted ventilation) or forced mode (pressure-controlled ventilation) - appeared on most respirators for adults only in last years... For neonatal ventilation, the use of pressure-limited modes is routine. In pressure-supporting ventilation (PSV), the patient begins to inhale, which causes the respirator to deliver gas to a predetermined - designed to increase the BW - pressure. Artificial inspiration ends when the inspiratory flow falls below a preset level, usually below 25% of the maximum value. Note that the pressure is maintained until the flow is at its minimum. These flow characteristics are well suited to the patient's external respiration requirements, with the result that the regimen is tolerated with greater comfort. This mode of spontaneous ventilation can be used in patients who are in a terminal state to reduce the work of breathing spent on overcoming the resistance of the breathing circuit and increasing the DO. Pressure support can be used in conjunction with the IMV mode or alone, with or without PEEP or NPP. In addition, PSV has been shown to accelerate the recovery of spontaneous breathing after mechanical ventilation.

In Pressure Controlled Ventilation (PCV), the inspiratory phase is terminated when the setpoint is reached. maximum pressure... Tidal volume depends on airway resistance and lung compliance. PCV can be used alone or in combination with other modes such as IVL (IRV) (see question 10). The characteristic flow of PCV (high initial flow followed by a fall) is likely to have properties that improve lung compliance and gas distribution. It has been suggested that PCV can be used as a safe and patient-friendly initial mode ventilation of patients with acute hypoxic respiratory failure. Respirators are now entering the market that provide the minimum guaranteed volume in controlled pressure mode.

10. Does the inverse ratio of inspiration and expiration matter when ventilating a patient?

The type of ventilation, denoted by the acronym IVL (IRV), has been used with some success in patients with SALS. The mode itself is perceived ambiguously, since it involves an extension of the inspiratory time above the usual maximum - 50% of the respiratory cycle time with pressocyclic or volumetric ventilation. As the inspiratory time increases, the I / E ratio becomes inverted (eg 1/1, 1.5 / 1, 2/1, 3/1). Most intensive care physicians do not recommend exceeding the 2/1 ratio due to the possible deterioration of hemodynamics and the risk of barotrauma. Although oxygenation has been shown to improve with prolonged inspiratory time, no prospective randomized trial has been performed on this topic. The improvement in oxygenation can be explained by several factors: an increase in the average Paw (without an increase in peak Paw), opening - as a result of a slowdown in the inspiratory flow and the development of PEEPVn - of additional alveoli with a larger inspiratory time constant.

A slower inspiratory flow can reduce the likelihood of baro- and volotrauma. However, in patients with airway obstruction (eg, COPD or asthma), due to increased PEEP, this regimen may have a negative effect. Given that patients with IVL often experience discomfort, deep sedation or muscle relaxation may be required. Ultimately, despite the lack of irrefutably proven advantages of the method, it should be recognized that IVL can be of independent importance in the treatment of advanced forms of SALS.

11. Does mechanical ventilation have an effect on various body systems, except for the cardiovascular system?

Yes. Increased intrathoracic pressure can cause or contribute to an increase in ICP. As a result of prolonged nasotracheal intubation, sinusitis may develop. A constant threat to patients on artificial ventilation lies in the possibility of developing hospital-acquired pneumonia. Quite common are gastrointestinal bleeding from stress ulcers that require preventive therapy... Increased production of vasopressin and decreased levels of natriuretic hormone can lead to water and salt retention. Patients lying motionless and in critical condition are at constant risk of thromboembolic complications, therefore it is quite appropriate here preventive measures... Many patients require sedation and, in some cases, muscle relaxation (see question 17).

12. What is controlled hypoventilation with acceptable hypercapnia?

Guided hypoventilation is a technique that has found application in patients requiring mechanical ventilation that could prevent overstretching of the alveoli and possible damage to the alveolar-capillary membrane. Current evidence suggests that high volumes and pressures can cause or predispose to lung damage due to overstretching of the alveoli. Controlled hypoventilation (or tolerable hypercapnia) implements a strategy of safe, pressure-limited ventilation that prioritizes inflation pressure over pCO2. Conducted in this regard, studies of patients with SALP and status asthmaticus showed a decrease in the frequency of barotrauma, the number of days requiring intensive therapy, and mortality. To maintain the peak Paw below 35–40 cm of water column, and the static Paw below 30 cm of water column, the DO is set approximately in the range of 6–10 ml / kg. A small DO is justified in SALP - when the lungs are affected inhomogeneously and only a small volume of them is able to be ventilated. Gattioni et al. Described three areas in the affected lungs: the area of ​​the atelectasized pathological process alveoli, the area of ​​collapsed, but still able to open alveoli and a small area (25–30% of the volume of healthy lungs) capable of ventilating the alveoli. The traditionally prescribed DO, which significantly exceeds the volume of the lungs available for ventilation, can cause hyperextension of healthy alveoli and thereby aggravate acute lung damage. The term "child's lungs" was proposed precisely because only a small part of the lung volume is able to ventilate. A gradual rise in pCO2 to a level of 80–100 mm Hg is quite admissible. A decrease in pH below 7.20–7.25 can be eliminated by introducing buffer solutions. Another option is to wait until the normally functioning kidneys compensate for the hypercapnia with bicarbonate retention. Tolerable hypercapnia is generally well tolerated. Possible adverse effects include expansion cerebral vessels increasing ICP. Indeed, intracranial hypertension is the only absolute contraindication for tolerable hypercapnia. In addition, with permissible hypercapnia, an increased sympathetic tone, pulmonary vasoconstriction and cardiac arrhythmias, although all rarely become dangerous. In patients with an initial dysfunction of the ventricles, suppression of cardiac contractility can be of serious importance.

13. What other methods are used to control pCO2?

There are several alternative methods pCO2 control. Reduced CO2 production can be achieved by deep sedation, muscle relaxation, cooling (naturally, avoiding hypothermia) and reducing the amount of carbohydrates consumed. A simple method to increase CO2 clearance is tracheal gas insufflation (TIG). In this case, a small (as for suction) catheter is inserted through the endotracheal tube, passing it to the level of the tracheal bifurcation. A mixture of oxygen and nitrogen is fed through this catheter at a rate of 4–6 l / min. This leads to leaching of the dead space gas with constant minute ventilation and airway pressure. The average decrease in pCO2 is 15%. This method is well suited to those patients with head trauma who can benefit from controlled hypoventilation. In rare cases, an extracorporeal CO2 removal method is used.

14. What is lung compliance? How to define it?

Compliance is a measure of extensibility. It is expressed through the dependence of the change in volume on a given change in pressure and for the lungs is calculated by the formula: DO / (Paw - PEEP). Static elongation is 70–100 ml / cm H2O. With SALP, it is less than 40–50 ml / cm water column. Compliance is an integral indicator that does not reflect regional differences in SALS - a condition in which affected areas alternate with relatively healthy ones. The nature of changes in lung compliance serves as a useful guide in determining the dynamics of ARF in a particular patient.

15. Is prone ventilation the method of choice in patients with persistent hypoxia?

Studies have shown that in the prone position, oxygenation is significantly improved in most patients with SALP. Perhaps this is due to an improvement in ventilation-perfusion relations in the lungs. However, due to the increasing complexity of nursing care, prone ventilation has not become a common practice.

16. What approach is required by patients "fighting with a respirator"?

Agitation, respiratory distress, or “fighting the respirator” must be taken seriously as a number of causes are life-threatening. In order to avoid irreversible deterioration of the patient's condition, it is necessary to quickly determine the diagnosis. To do this, first separately analyze the possible causes associated with the respirator (apparatus, circuit and endotracheal tube), and the reasons related to the patient's condition. Causes associated with the patient's condition include hypoxemia, airway obstruction with sputum or mucus, pneumothorax, bronchospasm, infectious processes like pneumonia or sepsis, pulmonary embolism, myocardial ischemia, gastrointestinal bleeding, increasing PEEP and anxiety.

Respirator-related causes include leaking or leaking circuit, inadequate ventilation or insufficient FiO2, endotracheal tube problems including extubation, tube obstruction, cuff rupture or deformation, incorrect trigger sensitivity or inspiratory flow rate settings. Until the situation is fully understood, it is necessary to manually ventilate the patient with 100% oxygen. Auscultate the lungs and check vital signs (including pulse oximetry and end-expiratory CO2) without delay. Arterial blood gas analysis and chest x-ray should be done if time permits.

To control the patency of the endotracheal tube and remove sputum and mucous plugs, it is permissible to quickly guide the catheter for suction through the tube. If a pneumothorax with hemodynamic disorders is suspected, decompression should be performed immediately, without waiting for a chest x-ray. In the case of adequate oxygenation and ventilation of the patient, as well as stable hemodynamics, a more thorough analysis of the situation is possible, and, if necessary, sedation of the patient.

17. Should muscle relaxation be used to improve ventilation conditions?

Muscle relaxation is widely used to facilitate mechanical ventilation. This promotes moderate improvement in oxygenation, reduces peak Paw, and provides better patient-respirator matching. And in specific situations such as intracranial hypertension or ventilation in unusual modes (for example, IVL or extracorporeal method), muscle relaxation can be even more beneficial. The disadvantages of muscle relaxation are the loss of the possibility of neurological examination, loss of cough, the possibility of unintentional muscle relaxation of the patient in consciousness, numerous problems associated with the interaction of drugs and electrolytes, and the possibility of prolonged block.

Also, no scientific evidence that muscle relaxation improves the outcomes of critically ill patients. The use of muscle relaxants should be well considered. Until adequate sedation of the patient is performed, muscle relaxation should be excluded. If muscle relaxation seems to be absolutely shown, it should be carried out only after the final weighing of all the pros and cons. To avoid prolonged block, the use of muscle relaxation, if possible, should be limited to 24–48 hours.

18. Is there really a benefit from separate ventilation?

Separate ventilation of the lungs (RIVL) is an independent ventilation of each lung, usually using a double-lumen tube and two respirators. Originally developed to improve the conditions for thoracic surgeries, RIVL has been extended to some cases in intensive care practice. Here, patients with unilateral lung involvement can become candidates for separate ventilation. It has been shown that this type of ventilation improves oxygenation in patients with unilateral pneumonia, pulmonary edema and contusions.

Protecting a healthy lung from the contents of the affected lung, achieved by isolating each of them, can be life-saving for patients with massive bleeding or lung abscess. In addition, RIVL may be useful in patients with bronchopleural fistula. For each lung, individual rotation parameters can be set, including values ​​for TO, flow rate, PEEP and NPP. There is no need to synchronize the work of two respirators, since, as practice shows, hemodynamic stability is better achieved when they work asynchronously.

Apparatus ventilation is used mainly for the treatment of ventilation failure, pulmonary congestion and edema, and the syndrome of "small cardiac output".

Ventilation failure. There are three main groups of patients with ventilation failure requiring mechanical ventilation. The first group consists of patients with relatively normal lungs, but with depression of the respiratory center. The range of this group is quite wide: from patients with postoperative depression of the respiratory center (caused by medicinal substances) who need mechanical ventilation for several hours, to patients in whom the defeat of the respiratory center is caused by embolism, an episode of hypoxia or cardiac arrest, and requiring mechanical ventilation during many days. The best indicator that determines the need for artificial ventilation is the level of arterial pCO 2 above 55-60 mm Hg. Art., although other factors may influence the solution of this issue. For example, many patients after cardiopulmonary bypass develop metabolic alkalosis associated with preoperative use of diuretics ( causing loss potassium) and disposal of large quantities of canned blood citrate. With pronounced metabolic alkalosis, respiratory depression occurs, which leads to a normalization of pH. Under these conditions (for example, with BE + 10 meq / L and pCO 2 60 mm Hg), it would be an obvious mistake to resort to artificial ventilation of the patient.

The second group, related to ventilation failure, includes elderly and middle-aged patients with chronic pulmonary diseases. They often have increased physiological dead space, venous mixing, and airway resistance. Treatment of such patients presents a certain problem, since the use of uncontrolled oxygen therapy can lead to hypercapnia, and controlled oxygen therapy does not always completely normalize the lowered arterial pCO 2. The use of isoprenaline * and other bronchodilators increases the risk of hypercapnia and hypoxemia (Fordham, Resnekoy, 1968). Therefore, it may be necessary to transfer the patient to artificial ventilation earlier than in patients without concomitant diseases lungs. In such cases, the decision on the use of mechanical ventilation should be based on a thorough analysis of the functions of the heart and respiration.

Assessment of the condition of patients of the third group also encounters certain difficulties. These patients usually show clear signs of respiratory distress, however, changes in blood gases are much less pronounced than one would expect, judging by clinical condition sick. This is explained by the fact that big number factors. The formation of a significant amount of secretion, scattered areas of atelectasis, congestion in the lungs, pleural effusion and a large heart - all this leads to a significant increase in the work of breathing. At the same time, decreased cerebral blood flow, hypoxemia, sedatives and toxemia can cause depression of the respiratory center. Eventually, a moment comes when the breathing resistance exceeds the patient's ability to provide adequate ventilation - ventilation failure occurs. Therefore, the setting of indications for apparatus ventilation in such patients is determined mainly by clinical signs and largely depends on the presence of external manifestations breathing disorders. These signs include an increase in respiration rate (over 30-35 per minute in an adult and over 40-45 per minute in children), acquiring a "grunting" difficulty with the use of accessory muscles. The patient looks emaciated, can hardly pronounce no more than a few words, loses interest in the environment. An increase in heart rate (over 100-120 beats per minute in adults and over 130 beats per minute in children) and a certain darkening of consciousness indicate the need for urgent measures. Blood gases in these cases often do not reflect the severity of the patient's condition. Arterial pCO 2 rarely exceeds 50-55 mm Hg. Art. Occasionally, however, a low arterial pO 2 indicates a marked increase in right-to-left shunting and possibly a drop in cardiac output. The latter can usually be determined by the low pO 2 of mixed venous blood.

When establishing indications for mechanical ventilation, it is necessary to take into account the history, the nature of the operation performed, the general course of the postoperative period and the presence of respiratory disorders. In general, mechanical ventilation is resorted to earlier in patients with previous lung diseases and a complex nature of the defect, especially if there are doubts about the radical nature of the operation. The occurrence of pulmonary edema is also an indication for more early start treatment. Thus, mechanical ventilation should be applied earlier in a patient who underwent radical correction of Fallot's tetrad than in a patient operated on for a simple ventricular septal defect. Similarly, tracheostomy and mechanical ventilation can be used prophylactically at the end of the operation in a patient with a pronounced increase in pressure in the left atrium and chronic disease history of lungs undergoing replacement surgery mitral valve... It should be borne in mind that the emerging respiratory disorders in the future can progress extremely quickly.

Pulmonary edema... Detection of congestion in the lungs or their edema during X-ray examination cannot be considered a sufficient indication for mechanical ventilation. The situation should be assessed taking into account the history, changes in pressure in the left atrium and A - apo 2. In a patient with a long-term increase in pressure in the left atrium, edema develops relatively rarely. However, an increase in pressure in the left atrium above the initial level can be considered as the most important indicator in favor of the beginning of equipment ventilation. Very useful information also gives the value of А ​​- аpO2 during respiration pure oxygen... This indicator should be used to assess the effectiveness of treatment. If A - apO 2 while breathing 100% oxygen, despite all the measures taken, continues to grow, or if under the same conditions arterial pO 2 falls below 100-200 mm Hg. Art., of course, you should resort to artificial ventilation.

Syndromes of "small cardiac output" and "postperfusion lungs". Since the correct selection of patients for surgery and surgical technique have improved significantly in recent years, the first of these syndromes is less common. A patient with low cardiac output has cyanosis, peripheral vasoconstriction, and low blood pressure in combination with high venous pressure. Urinary flow is reduced or absent. Metabolic acidosis is common. A darkening of consciousness gradually sets in. The pO2 of mixed venous blood is usually low. Sometimes peripheral circulation is so limited that perfusion of most peripheral tissues is absent. In this case, the pO 2 of the mixed venous blood may be normal despite the low cardiac output. These patients, as a rule, have completely clean lungs and there are no indications for mechanical ventilation ** except for the possibility of a decrease in the work of breathing. Since its increase in this kind of patients is unlikely, the need for artificial ventilation is highly questionable.

On the other hand, data have been obtained that make it possible to consider mechanical ventilation as undoubtedly advisable in “postperfusion pulmonary syndrome”. As already mentioned, a characteristic feature of this syndrome is a pronounced increase in venous mixing and intrapulmonary shunting from right to left. Similar phenomena occur in all patients operated on under cardiopulmonary bypass, but their severity varies significantly in different patients. To a large extent, shunting is due to the presence of exudate in the alveoli, which determines a rather slow rate of normalization. However, there is always another component associated with the onset of atelectasis. In this case, vigorous physiotherapy and prolonged mechanical ventilation can help. The effect of the remaining shunts can be mitigated by using 100% oxygen. Since it is known that the work of breathing is increased in this condition, its decrease will lead to a further improvement in arterial oxygenation. This increases the saturation of the mixed venous blood and thus mitigates the effect of shunting on arterial oxygenation. Thus, it can be concluded that although mechanical ventilation is able to reduce cardiac output (Grenvik, 1966), a decrease in the work of breathing and total venous mixing usually more than compensates for this shift. As a result general state the patient improves significantly.

* β-Stimulant. The drug is also known under other names: izuprel, isoproterenol, izadrin, novodrin (approx. Transl.).

** The point of view of the authors seems to us at least controversial, since both our experience and the observations of other authors (V.I.Burakovsky et al., 1971) indicate the undoubted benefits of artificial ventilation in the syndrome of "small cardiac output", naturally in combination with other therapeutic interventions(approx. transl.).

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