What is the minute volume of breathing at rest? Breath volumes

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Common to all living cells is the process of breaking down organic molecules through a successive series of enzymatic reactions, resulting in the release of energy. Almost any process in which the oxidation of organic substances leads to the release of chemical energy is called breathing. If it requires oxygen, then breathing is calledaerobic, and if reactions occur in the absence of oxygen - anaerobic breathing. For all tissues of vertebrate animals and humans, the main source of energy is the processes of aerobic oxidation, which occur in the mitochondria of cells adapted to convert the energy of oxidation into the energy of reserve high-energy compounds such as ATP. The sequence of reactions by which the cells of the human body use the energy of the bonds of organic molecules is called internal, tissue or cellular breathing.

The respiration of higher animals and humans is understood as a set of processes that ensure the supply of oxygen to the internal environment of the body and its use for oxidation organic matter and removal of carbon dioxide from the body.

The function of breathing in humans is realized by:

1) external, or pulmonary, respiration, which carries out gas exchange between the external and internal environment of the body (between air and blood);
2) blood circulation, which ensures the transport of gases to and from tissues;
3) blood as a specific gas transport medium;
4) internal, or tissue, respiration, which carries out the direct process of cellular oxidation;
5) means of neurohumoral regulation of breathing.

The result of the activity of the external respiration system is the enrichment of the blood with oxygen and the release of excess carbon dioxide.

Changes in the gas composition of blood in the lungs are ensured by three processes:

1) continuous ventilation of the alveoli to maintain the normal gas composition of the alveolar air;
2) diffusion of gases through the alveolar-capillary membrane in a volume sufficient to achieve equilibrium in the pressure of oxygen and carbon dioxide in the alveolar air and blood;
3) continuous blood flow in the capillaries of the lungs in accordance with the volume of their ventilation

Lung capacity

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Total capacity. The amount of air in the lungs after maximum inspiration is the total lung capacity, the value of which in an adult is 4100-6000 ml (Fig. 8.1).
It consists of the vital capacity of the lungs, which is the amount of air (3000-4800 ml) that comes out of the lungs during the deepest exhalation after the deepest inhalation, and
residual air (1100-1200 ml), which still remains in the lungs after maximum exhalation.

Total capacity = Vital capacity+ Residual volume

Vital capacity makes up three lung volumes:

1) tidal volume , representing the volume (400-500 ml) of air inhaled and exhaled during each respiratory cycle;
2) reserve volumeinhalation (additional air), i.e. the volume (1900-3300 ml) of air that can be inhaled during a maximum inhalation after a normal inhalation;
3) expiratory reserve volume (reserve air), i.e. volume (700-1000 ml) that can be exhaled at maximum exhalation after normal exhalation.

Vital capacity = Inspiratory reserve volume + Tidal volume + Expiratory reserve volume

functional residual capacity. During quiet breathing, after exhalation, an expiratory reserve volume and residual volume remain in the lungs. The sum of these volumes is called functional residual capacity, as well as normal lung capacity, resting capacity, equilibrium capacity, buffer air.

functional residual capacity = Expiratory reserve volume + Residual volume

Fig.8.1. Lung volumes and capacities.

Ventilator! If you understand it, it is equivalent to the appearance, as in the films, of a superhero (doctor) super weapons(if the doctor understands the intricacies of mechanical ventilation) against the death of the patient.

To understand mechanical ventilation you need basic knowledge: physiology = pathophysiology (obstruction or restriction) of breathing; main parts, structure of the ventilator; provision of gases (oxygen, atmospheric air, compressed gas) and dosing of gases; adsorbers; elimination of gases; breathing valves; breathing hoses; breathing bag; humidification system; breathing circuit (semi-closed, closed, semi-open, open), etc.

All ventilators provide ventilation by volume or pressure (no matter what they are called; depending on what mode the doctor has set). Basically, the doctor sets the mechanical ventilation regimen for obstructive pulmonary diseases (or during anesthesia) by volume, during restriction by pressure.

The main types of ventilation are designated as follows:

CMV (Continuous mandatory ventilation) - Controlled (artificial) ventilation

VCV (Volume controlled ventilation) - volume controlled ventilation

PCV (Pressure controlled ventilation) - pressure controlled ventilation

IPPV (Intermittent positive pressure ventilation) - mechanical ventilation with intermittent positive pressure during inspiration

ZEEP (Zero endexpiratory pressure) - ventilation with pressure at the end of expiration equal to atmospheric

PEEP (Positive endexpiratory pressure) - Positive end expiratory pressure (PEEP)

CPPV (Continuous positive pressure ventilation) - ventilation with PDKV

IRV (Inversed ratio ventilation) - mechanical ventilation with a reverse (inverted) inhalation:exhalation ratio (from 2:1 to 4:1)

SIMV (Synchronized intermittent mandatory ventilation) - Synchronized intermittent mandatory ventilation = A combination of spontaneous and mechanical breathing, when, when the frequency of spontaneous breathing decreases to a certain value, with continued attempts to inhale, overcoming the level of the established trigger, mechanical breathing is synchronously activated

You always need to look at the letters ..P.. or ..V.. If P (Pressure) means by distance, if V (Volume) by volume.

1. Vt – tidal volume,
2. f – respiratory rate, MV – minute ventilation
3. PEEP – PEEP = positive end expiratory pressure
4. Tinsp – inspiratory time;
5. Pmax - inspiratory pressure or maximum airway pressure.
6. Gas flow of oxygen and air.

1. Tidal volume(Vt, DO) set from 5 ml to 10 ml/kg (depending on the pathology, normal 7-8 ml per kg) = how much volume the patient should inhale at a time. But to do this, you need to find out the ideal (proper, predicted) body weight of a given patient using the formula (NB! remember):

Men: BMI (kg)=50+0.91 (height, cm – 152.4)

Women: BMI (kg)=45.5+0.91·(height, cm – 152.4).

Example: a man weighs 150 kg. This does not mean that we should set the tidal volume to 150kg·10ml= 1500 ml. First, we calculate BMI=50+0.91·(165cm-152.4)=50+0.91·12.6=50+11.466= 61,466 kg our patient should weigh. Imagine, oh allai deseishi! For a man weighing 150 kg and height 165 cm, we must set the tidal volume (TI) from 5 ml/kg (61.466·5=307.33 ml) to 10 ml/kg (61.466·10=614.66 ml) depending on pathology and extensibility of the lungs.

2. The second parameter that the doctor must set is breathing rate(f). The normal respiratory rate is 12 to 18 per minute at rest. And we don't know what frequency to set: 12 or 15, 18 or 13? To do this we must calculate due MOD (MV). Synonyms for minute breathing volume (MVR) = minute ventilation (MVL), maybe something else... This means how much air the patient needs (ml, l) per minute.

MOD=BMI kg:10+1

according to the Darbinyan formula (outdated formula, often leads to hyperventilation).

Or modern calculation: MOD=BMIkg·100.

(100%, or 120%-150% depending on the patient’s body temperature..., from the basal metabolism in short).

Example: The patient is a woman, weighs 82 kg, height is 176 cm. BMI = 45.5 + 0.91 (height, cm - 152.4) = 45.5 + 0.91 (176 cm - 152.4) = 45.5+0.91 23.6=45.5+21.476= 66,976 kg should weigh. MOD = 67 (rounded up immediately) 100 = 6700 ml or 6,7 liters per minute. Now only after these calculations can we find out the breathing frequency. f=MOD:UP TO=6700 ml: 536 ml=12.5 times per minute, which means 12 or 13 once.

3. Install REER. Normally (previously) 3-5 mbar. Now you can 8-10 mbar in patients with normal lungs.

4. The inhalation time in seconds is determined by the ratio of inhalation to exhalation: I: E=1:1,5-2 . In this parameter, knowledge about the respiratory cycle, ventilation-perfusion ratio, etc. will be useful.

5. Pmax, Pinsp peak pressure is set so as not to cause barotrauma or rupture the lungs. Normally I think 16-25 mbar, depending on the elasticity of the lungs, the patient’s weight, and extensibility chest etc. In my knowledge, lungs can rupture when Pinsp is more than 35-45 mbar.

6. The fraction of inhaled oxygen (FiO 2) should be no more than 55% in the inhaled breathing mixture.

All calculations and knowledge are needed so that the patient has the following indicators: PaO 2 = 80-100 mm Hg; PaCO 2 =35-40 mm Hg. Just, oh allai deseishi!

To assess the quality of lung function, it examines tidal volumes (using special devices - spirometers).

Tidal volume (TV) is the amount of air that a person inhales and exhales during quiet breathing in one cycle. Normal = 400-500 ml.

Minute respiration volume (MRV) is the volume of air passing through the lungs in 1 minute (MRV = DO x RR). Normal = 8-9 liters per minute; about 500 l per hour; 12000-13000 liters per day. When increasing physical activity MOD increases.

Not all inhaled air participates in alveolar ventilation (gas exchange), because some of it does not reach the acini and remains in the respiratory tract, where there is no opportunity for diffusion. The volume of such airways is called “respiratory dead space”. Normally for an adult = 140-150 ml, i.e. 1/3 TO.

Inspiratory reserve volume (IRV) is the amount of air that a person can inhale during the strongest maximum inhalation after a quiet inhalation, i.e. over DO. Normal = 1500-3000 ml.

Expiratory reserve volume (ERV) is the amount of air that a person can additionally exhale after a quiet exhalation. Normal = 700-1000 ml.

Vital capacity of the lungs (VC) is the amount of air that a person can maximally exhale after the deepest inhalation (VC=DO+ROVd+ROVd = 3500-4500 ml).

Residual lung volume (RLV) is the amount of air remaining in the lungs after maximum exhalation. Normal = 100-1500 ml.

Total lung capacity (TLC) is the maximum amount of air that can be held in the lungs. TEL=VEL+TOL = 4500-6000 ml.

DIFFUSION OF GASES

Composition of inhaled air: oxygen - 21%, carbon dioxide - 0.03%.

Composition of exhaled air: oxygen - 17%, carbon dioxide - 4%.

The composition of the air contained in the alveoli: oxygen - 14%, carbon dioxide -5.6%.

As you exhale, the alveolar air is mixed with the air in the respiratory tract (in the “dead space”), which causes the indicated difference in air composition.

The transition of gases through the air-hematic barrier is due to the difference in concentrations on both sides of the membrane.

Partial pressure is that part of the pressure that falls on a given gas. At atmospheric pressure 760 mmHg, oxygen partial pressure is 160 mmHg. (i.e. 21% of 760), in the alveolar air the partial pressure of oxygen is 100 mm Hg, and carbon dioxide is 40 mm Hg.

Gas voltage is the partial pressure in a liquid. Oxygen tension in venous blood is 40 mm Hg. Due to the pressure gradient between alveolar air and blood - 60 mm Hg. (100 mm Hg and 40 mm Hg), oxygen diffuses into the blood, where it binds to hemoglobin, converting it into oxyhemoglobin. Blood containing a large amount of oxyhemoglobin is called arterial. In 100 ml arterial blood contains 20 ml of oxygen, 100 ml of venous blood contains 13-15 ml of oxygen. Also, along the pressure gradient, carbon dioxide enters the blood (since it is contained in large quantities in the tissues) and carbhemoglobin is formed. In addition, carbon dioxide reacts with water, forming carbonic acid (the reaction catalyst is the enzyme carbonic anhydrase, found in red blood cells), which breaks down into a hydrogen proton and bicarbonate ion. CO 2 tension in venous blood is 46 mm Hg; in alveolar air – 40 mm Hg. (pressure gradient = 6 mm Hg). Diffusion of CO 2 occurs from the blood into the external environment.

One of the main characteristics of external respiration is the minute volume of respiration (MVR). Ventilation is determined by the volume of air inhaled or exhaled per unit of time. MVR is the product of tidal volume and the frequency of respiratory cycles. Normally, at rest, DO is 500 ml, the frequency of respiratory cycles is 12 - 16 per minute, hence the MOD is 6 - 7 l/min. Maximum ventilation is the volume of air that passes through the lungs in 1 minute during maximum frequency and depth.

breathing movements

Alveolar ventilation So, external breathing, or ventilation of the lungs, ensures that approximately 500 ml of air enters the lungs during each inspiration (BEFORE). Saturation of blood with oxygen and removal of carbon dioxide occurs when contact of the blood of the pulmonary capillaries with the air contained in the alveoli.

Alveolar air is the internal gas environment of the body of mammals and humans. Its parameters - oxygen and carbon dioxide content - are constant. The amount of alveolar air approximately corresponds to the functional residual capacity of the lungs - the amount of air that remains in the lungs after a quiet exhalation, and is normally equal to 2500 ml. It is this alveolar air that is renewed by atmospheric air entering through the respiratory tract. It should be borne in mind that not all of the inhaled air participates in pulmonary gas exchange, but only that part of it that reaches the alveoli. Therefore, to assess the effectiveness of pulmonary gas exchange, it is not so much pulmonary ventilation that is important, but alveolar ventilation.

In addition, there are alveoli, which are currently ventilated, but not supplied with blood. This part of the alveoli is the alveolar dead space. The sum of anatomical and alveolar dead space is called functional or physiological dead space. Approximately 1/3 of the tidal volume is due to the ventilation of dead space filled with air that is not directly involved in gas exchange and only moves in the lumen of the airways during inhalation and exhalation. Therefore, ventilation of the alveolar spaces—alveolar ventilation—is pulmonary ventilation minus dead space ventilation. Normally, alveolar ventilation is 70 - 75% of the MOD value.

Calculation of alveolar ventilation is carried out according to the formula: MAV = (DO - MP)  RR, where MAV is minute alveolar ventilation, DO - tidal volume, MP - dead space volume, RR - respiratory rate.

Figure 6. Ratio of MOR and alveolar ventilation

We use these data to calculate another value characterizing alveolar ventilation - alveolar ventilation coefficient . This coefficient shows how much of the alveolar air is renewed with each breath. By the end of a quiet exhalation, there is about 2500 ml of air (FRC) in the alveoli; during inhalation, 350 ml of air enters the alveoli, therefore, only 1/7 of the alveolar air is renewed (2500/350 = 7/1).

Pathways

Nose - the first changes in the incoming air occur in the nose, where it is cleaned, warmed and moistened. This is facilitated by the hair filter, vestibule and turbinates. Intensive blood supply to the mucous membrane and cavernous plexuses of the shells ensures rapid warming or cooling of the air to body temperature. Water evaporating from the mucous membrane humidifies the air by 75-80%. Prolonged inhalation of air with low humidity leads to drying of the mucous membrane, entry of dry air into the lungs, development of atelectasis, pneumonia and increased resistance in the airways.

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

Larynx provides vocal function by using the epiglottis to prevent aspiration, and the closure of the vocal cords is one of the main components of cough.

Trachea - the main air duct, in which the air is warmed and humidified. Mucosal cells capture foreign substances, and cilia move mucus up the trachea.

Bronchi (lobar and segmental) end in terminal bronchioles.

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

The structure of the wall of the conducting airways (AP) differs from the structure of the airways of the gas exchange zone. The wall of the conducting airways consists of the mucous membrane, a layer of smooth muscle, submucosal connective and cartilaginous membranes. Epithelial cells The airways are equipped with cilia, which, oscillating rhythmically, push the protective layer of mucus towards the nasopharynx. The mucous membrane of the EP and lung tissue contain macrophages that phagocytize and digest mineral and bacterial particles. Normally, mucus is constantly removed from the respiratory tract and alveoli. The mucous membrane of the EP is represented by ciliated pseudostratified 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 motor activity (about 1000 movements per minute), which allows them to transport sputum at a speed of up to 1 cm/min in the bronchi and up to 3 cm/min in the trachea. During the day, about 100 ml of sputum is normally evacuated from the trachea and bronchi, and in pathological conditions up to 100 ml/hour.

Cilia function in a double layer of mucus. At the bottom are biologically active substances, enzymes, immunoglobulins, the concentration of which is 10 times higher than in the blood. This causes biological protective function mucus. Upper layer it mechanically protects the eyelashes from damage. Thickening or reduction of the upper layer of mucus due to inflammation or toxic effects inevitably disrupts the drainage function of the ciliated epithelium, irritates the respiratory tract and reflexively causes coughing. Sneezing and coughing protect the lungs from mineral and bacterial particles.

Alveoli

In the alveoli, gas exchange occurs between the blood of the pulmonary capillaries and the air. The total number of alveoli is approximately 300 million, and their total surface area is approximately 80 m2. The diameter of the alveoli is 0.2-0.3 mm. Gas exchange between alveolar air and blood occurs 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, a narrow interstitial space and the endothelium of the capillary. 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 boundary between liquid and air at the end of exhalation, when the volume of the lung is minimal, increases elasticity lungs and plays the role of an anti-edematous factor(does not allow water vapor from the alveolar air to pass through), 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 pressure and minimal O 2 content 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);

2) hypophase (the underlying hydrophilic layer of proteins, electrolytes, bound water, phospholipids and polysaccharides);

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

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

At low tensile pressure, it reduces the forces that cause fluid accumulation in tissues. In addition, surfactant purifies inhaled gases, filters and traps inhaled particles, regulates the exchange of water between the blood and the alveolar air, accelerates the diffusion of CO 2, and has a pronounced antioxidant effect. Surfactant is very sensitive to various endo- and exogenous factors: circulatory disorders, ventilation and metabolism, changes in PO 2 in the inhaled air, and air pollution. With surfactant deficiency, atelectasis and RDS of newborns occur. Approximately 90-95% of alveolar surfactant is recycled, cleared, accumulated and resecreted. Half-life of surfactant components from the alveolar lumen healthy lungs is about 20 hours.

Lung 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 volume indicators that characterize the condition of the lungs. Normal average values ​​for an adult are as follows:

1. Tidal volume(DO-VT- Tidal Volume)- volume of inhaled and exhaled air during quiet breathing. Normal values- 7-9ml/kg.

2. Inspiratory reserve volume (IRV) -IRV - Inspiratory Reserve Volume) - the volume that can additionally arrive after a quiet inhalation, i.e. difference between normal and maximum ventilation. Normal value: 2-2.5 l (about 2/3 vital capacity).

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

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

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

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

7.Total lung capacity (TLC) - Total lung capacity) or maximum capacity lungs - 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 l.
Studying the structure of TLC is crucial in elucidating ways to increase or decrease vital capacity, which can have significant practical significance. An increase in vital capacity can be assessed positively only in cases where the vital capacity does not change or increases, but less than the vital capacity, which occurs when the vital capacity increases due to a decrease in the volume. If, simultaneously with an increase in VC, an even greater increase in TLC occurs, then this cannot be considered a positive factor. When VC is below 70% TLC, the function of external respiration is deeply impaired. Usually, in pathological conditions, TLC and vital capacity change in the same way, with the exception of obstructive pulmonary emphysema, when vital capacity, as a rule, decreases, VT increases, and TLC 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 quiet exhalation. Normal values ​​for adults are from 3 to 3.5 liters. FFU = OO + ROvyd. By definition, FRC is the volume of gas that remains in the lungs during a quiet exhalation and can be a measure of the area of ​​gas exchange. It is formed as a result of the balance between the oppositely directed elastic forces of the lungs and chest. Physiological significance FRC consists of a partial renewal of the alveolar air volume during inspiration (ventilated volume) and indicates the volume of alveolar air constantly present in the lungs. A decrease in FRC is associated with the development of atelectasis, closure of small airways, a decrease in lung compliance, an increase in the alveolar-arterial difference in O2 as a result of perfusion in atelectasis areas of the lungs, and a decrease in the ventilation-perfusion ratio. Obstructive ventilation disorders lead to an increase in FRC, restrictive disorders lead to a decrease in FRC.

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 approximately assumed that in a sitting person the volume of dead space (in milliliters) is equal to twice the body weight (in kilograms). Thus, in adults it is about 150-200 ml (2 ml/kg body weight).

Under functional (physiological) dead space understand all those areas 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 one, includes not only the airways, but also those alveoli that are ventilated but not perfused with blood.

Alveolar 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 dead space ventilation. Alveolar ventilation serves as an indicator of the efficiency of breathing in general. The gas composition maintained in the alveolar space depends on this value. As for minute volume, it only to a small extent reflects the effectiveness of ventilation. So, if the minute volume of breathing is normal (7 l/min), but breathing is frequent and shallow (UP to 0.2 l, RR-35/min), then ventilate

There will be mainly dead space, into which air enters before the alveolar; in this case, the inhaled air will hardly reach the alveoli. Because the the volume of dead space is constant, alveolar ventilation is greater, the deeper the breathing and the lower the frequency.

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

Compliance can be measured separately for the lungs and the chest. From a clinical point of view (especially during mechanical ventilation), the compliance of the lung tissue itself, which reflects the degree of restrictive pulmonary pathology, is of greatest interest. In modern literature, lung compliance is usually referred to as “compliance” (from English word“compliance”, abbreviated as C).

Lung compliance decreases:

With age (in patients over 50 years old);

In a lying position (due to pressure from organs abdominal cavity to the diaphragm);

During laparoscopic surgical interventions due to carboxyperitoneum;

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

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

With 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 same tidal volume as with normal compliance. Consequently, in the case of deteriorating lung compliance, when the same tidal volume is achieved, the pressure in the airways increases significantly.

This point is very important to understand: 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 resistive resistance of the airways Raw (an abbreviation for the English word “resistance”). Since the tracheobronchial tree is a system of tubes of varying lengths and widths, the resistance to gas flow in the lungs can be determined from the known physical laws. In general, flow resistance depends on the pressure gradient at the beginning and end of the tube, as well as on the magnitude of the flow itself.

Gas flow in the lungs can be laminar, turbulent, or transient. Laminar flow is characterized by layer-by-layer translational movement of gas with

Varying speed: the flow speed is highest in the center and gradually decreases towards the walls. Laminar gas flow predominates at relatively low speeds and is described by Poiseuille’s law, according to which the resistance to gas flow depends to the greatest extent 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 tracheal patency is clear. bronchial tree during mechanical ventilation.
The resistance of the respiratory tract to gas flow increases significantly with bronchiolospasm, swelling of the bronchial mucosa, accumulation of mucus and inflammatory secretions due to narrowing of the lumen of the bronchial tree. Resistance is also affected by flow rate and length of the tube(s). WITH

By increasing the flow rate (forcing inhalation or exhalation), airway resistance increases.

The main reasons for increased airway resistance are:

Bronchiolospasm;

Swelling 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 predominates at high volumetric flow rates. In the case of turbulent flow, airway resistance increases, since it depends to an even greater extent on the flow speed and the radius of the bronchi. Turbulent movement occurs at high flows, sudden changes in flow speed, in places of bends and branches of the bronchi, and with a sharp change in the diameter of the bronchi. This is why turbulent flow is characteristic of patients with COPD, when even in remission there is increased resistance respiratory tract. The same applies to patients with bronchial asthma.

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

Airway resistance also depends on lung volume. With a large volume, the parenchyma has a greater “stretching” effect on the airways, and their resistance decreases. The use of PEEP helps to increase lung volume and, consequently, reduce airway resistance.

Normal airway resistance is:

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

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

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

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

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

Work of breathing

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

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

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

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. For severe diffusion 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 starting mechanical ventilation, at which the cost of breathing is reduced to almost 0.

The work of breathing required to overcome elastic resistance (lung compliance) increases as tidal volume increases. The work required to overcome airway resistance increases with increasing respiratory rate. The patient seeks to reduce the work of breathing by changing the respiratory rate and tidal volume depending on the prevailing pathology. For each situation, there are optimal respiratory rates and tidal volumes at which the work of breathing is minimal. Thus, for patients with reduced compliance, from the point of view of minimizing the work of breathing, more frequent and shallow breathing is suitable (hard lungs are difficult to straighten). On the other hand, when airway resistance is increased, deep and slow breathing is optimal. This is understandable: an increase in tidal volume allows you to “stretch”, expand the bronchi, and reduce their resistance to gas flow; for the same purpose, patients with obstructive pathology compress their lips during exhalation, creating their own “PEEP”. Slow and infrequent breathing helps lengthen exhalation, which is important for more complete removal exhaled gas mixture under conditions of increased expiratory resistance of the respiratory tract.

Breathing regulation

The breathing process is regulated by the central and peripheral nervous system. In the reticular formation of the brain there is a respiratory center, consisting of the centers of inhalation, exhalation and pneumotaxis.

Central chemoreceptors are located in the medulla oblongata and are excited when the concentration of H+ and PCO 2 in the cerebrospinal fluid. Normally, the pH of the latter is 7.32, PCO 2 is 50 mmHg, and the HCO 3 content is 24.5 mmol/l. Even a slight decrease in pH and an increase in PCO 2 increase 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. Contractions of the respiratory muscles are controlled by the central respiratory mechanism, consisting of a group of cells in the medulla oblongata, pons, and pneumotaxic centers. They tone the respiratory center and, based on impulses from mechanoreceptors, determine the threshold of excitation at which inhalation stops. Pneumotaxic cells also switch inspiration to expiration.

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 body, changing the regime spontaneous breathing and thus correcting pH, PO 2 and PCO 2 in arterial blood and cerebrospinal fluid. Impulses from chemoreceptors regulate the amount of ventilation required to maintain a certain metabolic level. In optimizing the ventilation mode, i.e. Mechanoreceptors are also involved in establishing the frequency and depth of breathing, the duration of inhalation and exhalation, and the force of contraction of the respiratory muscles at a given level of ventilation. 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 nerve structures central respiratory mechanism. The main function of arterial chemoreceptors is the immediate correction of breathing in response to changes in blood gas composition.

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

During normal breathing, intercostal-diaphragmatic mechanoreceptors are not excited and have an auxiliary value.

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

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

Respiratory muscle neurons are located in the anterior horns of the gray matter spinal cord(cervical and thoracic segments).

In humans, the cerebral cortex also takes part in the regulation of breathing within the limits allowed by the chemoreceptor regulation of breathing. 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.

Biomechanics of breathing

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 of which the volume of the chest increases and the negative intrapleural pressure (Ppl) increases. Before the start of inhalation (at the end of exhalation) Ppl is approximately minus 3-5 cm water column. Alveolar pressure (Palv) is taken as 0 (i.e. equal to atmospheric pressure), it also reflects the pressure in the airways 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 of water column. During spontaneous inspiration, an increase in negative Ppl (up to minus 6-10 cm water column) causes a decrease in pressure in the alveoli and respiratory tract below atmospheric pressure. In the alveoli, the pressure drops to minus 3-5 cm of water column. Due to the pressure difference, air enters (sucks in) from external environment into the lungs. The chest and diaphragm act as a piston pump, drawing air into the lungs. This “suction” action of the chest is important not only for ventilation, but also for blood circulation. During spontaneous inspiration, additional “suction” of blood to the heart occurs (maintaining preload) and activation of pulmonary blood flow from the right ventricle through the system pulmonary artery. At the end of inspiration, when gas movement stops, alveolar pressure returns to zero, but intrapleural pressure remains reduced to minus 6-10 cm water column.

Exhalation is normally a passive process. After relaxation of the respiratory muscles, the forces of elastic traction of the chest and lungs cause the removal (squeezing out) of gas from the lungs and restoration of the original volume of the lungs. If the patency of the tracheobronchial tree is impaired (inflammatory secretion, swelling of the mucous membrane, bronchospasm), the exhalation process is difficult, and the exhalation muscles (internal intercostal muscles, pectoral muscles, abdominal muscles, etc.). When the expiratory muscles are exhausted, the exhalation process becomes even more difficult, the exhaled mixture is retained and the lungs become dynamically overinflated.

Non-respiratory lung functions

The functions of the lungs are not limited to the diffusion of gases. They contain 50% of all endothelial cells in the body, which line the capillary surface of the membrane and participate in the metabolism and inactivation of biologically active substances passing through the lungs.

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

2. The lungs regulate blood clotting 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 higher fibrinolytic activity.

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

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

5. The lungs cleanse the blood of mechanical impurities. Cell aggregates, microthrombi, bacteria, air bubbles, and 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, based on the partial pressures of gases in the alveoli. In accordance with this classification, the following types of ventilation are distinguished:

1.Normoventilation - normal ventilation, in which the partial pressure of CO2 in the alveoli is maintained at about 40 mmHg.

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

3. Hypoventilation - reduced ventilation compared to the metabolic needs of the body (PaCO2>40 mmHg).

4. Increased ventilation - any increase in alveolar ventilation compared to the resting level, 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 - increase in respiratory rate.

8.Bradypnea - decreased respiratory rate.

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

10.Dyspnea (shortness of breath) - unpleasant subjective feeling shortness of breath or difficulty breathing.

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

12. Asphyxia - cessation or depression of breathing, associated mainly with paralysis of the respiratory centers or closure of the airways. Gas exchange is sharply impaired (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 the respiratory excursion and the ability of the lungs to expand are reduced, 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 a narrowing of the airways, i.e. increasing their aerodynamic resistance. Similar conditions occur, for example, when mucus accumulates in the respiratory tract, swelling of their mucous membrane or spasm of the bronchial muscles (allergic bronchiolospasm, bronchial asthma, asthmatic bronchitis, etc.). In such patients, the resistance to inhalation and exhalation is increased, and therefore, over time, the airiness of the lungs and their FRC increase. 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.