Pleural pressure. mechanism of its occurrence
Pleura, pleura, which is the serous membrane of the lung, is divided into visceral (pulmonary) pleura and parietal (parietal). Each lung is covered with pleura (pulmonary), which, along the root surface, passes into the parietal pleura, which lines the chest cavity walls adjacent to the lung and limits the mediastinum from the sides.
The pleural cavity (cavitas pleurаlis) is located between the parietal and visceral pleura in the form of a narrow slit, it contains a small amount of serous fluid that moisturizes the pleural sheets, which helps to reduce friction of the visceral and parietal pleura sheets against each other during respiratory movements of the lungs.
The pressure in the pleural cavity is below atmospheric pressure, which is defined as negative pressure. It is due to the elastic traction of the lungs, i.e. the constant desire of the lungs to reduce their volume. The pressure in the pleural cavity is lower than the alveolar pressure by the amount created by the elastic traction of the lungs: Ppl \u003d Ralv - Re.t.l .. elastic traction of the lungs is due to three factors:
The surface tension of the liquid film covering the inner surface of the alveoli is a surfactant.
2) The elasticity of the tissue of the walls of the alveoli, which have elastic fibers in the wall.
3) Toned bronchial muscles
The accumulation of air or gases in the pleural cavity.
Spontaneous pneumothorax occurs when the pulmonary alveoli rupture (with tuberculosis, pulmonary emphysema); traumatic - with damage to the chest.
Tense pneumothorax occurs when air enters the pleural cavity and the inability to remove it on its own. This leads to an increase in pressure, compression of the mediastinal structures, impaired venous flow, shock and possible death.
What are the lung volumes and capacities, what methods do you know for determining them?
In the process of pulmonary ventilation, the gas composition of the alveolar air is continuously renewed. The amount of pulmonary ventilation is determined by the depth of breathing, or tidal volume, and the frequency of respiratory movements. During breathing movements, the lungs of a person are filled with inhaled air, the volume of which is part of the total volume of the lungs. For a quantitative description of pulmonary ventilation, the total lung capacity was divided into several components or volumes. In this case, the lung capacity is the sum of two or more volumes.
Pulmonary volumes are subdivided into static and dynamic. Static lung volumes are measured with completed respiratory movements without limiting their speed. Dynamic lung volumes are measured during respiratory movements with a time limit for their implementation.
Pulmonary volumes. The volume of air in the lungs and respiratory tract depends on the following indicators: 1) anthropometric individual characteristics of a person and the respiratory system; 2) the properties of the lung tissue; 3) the surface tension of the alveoli; 4) the strength developed by the respiratory muscles.
Lung containers. Vital lung capacity (VC) includes tidal volume, inspiratory reserve volume, expiratory reserve volume. In middle-aged men, VC varies within 3.5-5.0 liters and more. For women, lower values \u200b\u200bare typical (3.0-4.0 liters). Depending on the method of measuring VC, the inhalation VC is distinguished, when after a full exhalation, the deepest inhalation is made and the exhalation VC, when the maximum exhalation is made after a full inhalation.
Methods for measuring lung volumes
1. Spirometry - measurement of lung volumes. Allows you to define VC, DO, ROVD, ROVD.
2. Spirography - registration of lung volumes. Allows you to document the VC, DO, ROVD, ROVD, as well as the respiratory rate.
Determination of residual volume
With the help of a closed-loop spirograph using helium / according to the degree of dilution of helium /.
General body plethysmography / bodyplethysmography /.
What is pulmonary and alveolar ventilation? What are the methods for determining the MOU?
What is dead space, what is its meaning?
When does maximum ventilation occur? What is breathing reserve, how to calculate it?
What is the name of the structural-functional unit of the lungs?
What is the composition of atmospheric, exhaled and alveolar air? Definition and comparison.
What regularities provide for the diffusion of gases from one medium to another?
How is gas exchange in the lungs? What is the partial pressure of gases in the alveolar air and the tension of gases in the blood?
How is oxygen transported by blood? What is the oxygen capacity of blood, what is it normal?
How is carbon dioxide transported by blood? What is the role of carbonic anhydrase in this process?
Where is the respiratory center? What structures does it consist of?
What does the functional system that ensures the constancy of the blood gas composition includes?
What is mechanical ventilation?
In what cases is artificial lung ventilation used?
What methods are used for mechanical ventilation?
What is artificial respiration?
What methods are used for artificial respiration?
What is the general characteristic of body fluids? What are intracellular and extracellular fluids?
What is included in the blood system?
What are the functions of blood?
What organs perform the function of a blood depot, what is the significance of a blood depot?
What is the composition of the blood?
What is plasma and what is its composition?
The lungs and the walls of the chest cavity are covered with a serous membrane - the pleura, consisting of visceral and parietal sheets. Between the layers of the pleura there is a closed slit space containing serous fluid - the pleural cavity.
Atmospheric pressure, acting on the inner walls of the alveoli through the airways, stretches the lung tissue and presses the visceral leaf against the parietal leaf, i.e. the lungs are constantly stretched. With an increase in the volume of the chest as a result of contraction of the inspiratory muscles, the parietal leaf will follow the chest, this will lead to a decrease in pressure in the pleural fissure, therefore the visceral leaf, and with it the lungs, will follow the parietal leaf. The pressure in the lungs will become lower than atmospheric, and air will enter the lungs - inhalation occurs.
The pressure in the pleural cavity is lower than atmospheric pressure, therefore pleural pressure is called negative, conventionally taking atmospheric pressure as zero. The more the lungs stretch, the higher their elastic traction becomes and the lower the pressure in the pleural cavity drops. The magnitude of the negative pressure in the pleural cavity is equal to: by the end of a quiet breath - 5-7 mm Hg. By the end of maximum inspiration - 15-20 mm Hg, by the end of a calm exhalation - 2-3 mm Hg, by the end of maximum expiration - 1-2 mm Hg.
Negative pressure in the pleural cavity is due to the so-called elastic traction of the lungs - the force with which the lungs constantly strive to reduce their volume.
The elastic traction of the lungs is due to three factors:
1) the presence of a large number of elastic fibers in the walls of the alveoli;
2) bronchial muscle tone;
3) the surface tension of the liquid film covering the walls of the alveoli.
The substance that covers the inner surface of the alveoli is called a surfactant (Figure 5).
Figure: 5. Surfactant. A slice of the alveolar septum with an accumulation of surfactant.
Surfactant - This is a surfactant (a film that consists of phospholipids (90-95%), four proteins specific to it, as well as a small amount of carbon hydrate), is formed by special cells of type II alveolo-pneumocytes. Its half-life is 12-16 hours.
Surfactant functions:
· When inhaling, it protects the alveoli from overstretching due to the fact that the surfactant molecules are located far from each other, which is accompanied by an increase in the surface tension;
· During exhalation, protects the alveoli from collapse: surfactant molecules are located close to each other, as a result of which the surface tension decreases;
· Creates the possibility of expansion of the lungs at the first inhalation of the newborn;
· Affects the rate of diffusion of gases between alveolar air and blood;
· Regulates the intensity of water evaporation from the alveolar surface;
· Possesses bacteriostatic activity;
· Has a decongestant (reduces the sweating of fluid from the blood into the alveoli) and antioxidant effect (protects the walls of the alveoli from the damaging effects of oxidants and peroxides).
Study of the mechanism of changes in lung volume using the Donders model
Physiological experiment
The change in lung volume occurs passively, due to changes in the volume of the chest cavity and pressure fluctuations in the pleural fissure and inside the lungs. The mechanism of changes in lung volume during breathing can be demonstrated using the Donders model (Fig. 6), which is a glass reservoir with a rubber bottom. The upper opening of the tank is closed with a stopper through which a glass tube is passed. At the end of the tube, placed inside the reservoir, the lungs are strengthened behind the trachea. Through the outer end of the tube, the lung cavity communicates with atmospheric air. Pulling the rubber bottom down will increase the volume of the reservoir, and the pressure in the reservoir becomes below atmospheric, which leads to an increase in lung volume.
The lungs are covered by the visceral, and the film of the chest cavity is covered by the parietal pleura. Serous fluid is contained between them. They fit tightly to each other (5-10 microns gap) and slide relative to each other. This sliding is necessary so that the lungs can follow the complex changes of the chest without deforming. With inflammation (pleurisy, adhesions), ventilation of the corresponding parts of the lungs decreases.
If you insert a needle into the pleural cavity and connect it to a water pressure gauge, it turns out that the pressure in it:
when inhaling - by 6-8 cm H 2 O
when you exhale - 3-5 cm H 2 O below atmospheric.
This difference between intrapleural and atmospheric pressure is commonly referred to as pleural pressure.
Negative pressure in the pleural cavity is due to the elastic traction of the lungs, i.e. the desire of the lungs to subside.
When inhaling, an increase in the chest cavity leads to an increase in negative pressure in the pleural cavity, i.e. transpulmonary pressure increases, causing the lungs to expand.
fall off - exhale.
Donders' apparatus.
If you introduce a small amount of air into the pleural cavity, then it will dissolve, because in the blood of small veins of the pulmonary circulation tension solution. gases less than in the atmosphere. When the inspiratory muscles relax, transpulmonary pressure decreases and the lungs collapse due to elasticity.
The accumulation of fluid in the pleural cavity is prevented by the lower oncotic pressure of the pleural fluid (less proteins) than in plasma. The decrease in hydrostatic pressure in the pulmonary circulation is also important.
The change in pressure in the pleural space can be measured directly (but lung tissue can be damaged). But it is better to measure it by introducing a balloon l \u003d 10 cm into the esophagus (the overweight part of the esophagus). The walls of the esophagus are malleable.
The elastic traction of the lungs is due to 3 factors:
The surface tension of the liquid film covering the inner surface of the alveoli.
The elasticity of the tissue of the walls of the alveoli (contain elastic fibers).
Bronchial muscle tone.
At any interface between air and liquid, intermolecular cohesion forces act to reduce the size of this surface (surface tension forces). Under the influence of these forces, the alveoli tend to contract. Surface tension forces create 2/3 of the elastic traction of the lungs. The surface tension of the alveoli is 10 times less than the theoretically calculated for the corresponding water surface.
If the inner surface of the alveoli was covered with an aqueous solution, then the surface tension should have been 5-8 times greater. In these conditions, there would be a collapse of the alveoli (atelectasis). But that doesn't happen.
This means that in the alveolar fluid on the inner surface of the alveoli there are substances that reduce the surface tension, i.e. surfactants. Their molecules are strongly attracted to each other, but have a weak agent with a liquid, as a result of which they collect on the surface and thereby reduce the surface tension.
Such substances are called surfactants, and in this case, surfactants. They are lipids and proteins. Formed by special cells of the alveoli - type II pneumocytes. The lining is 20-100 nm thick. But the greatest surface activity of the components of this mixture is possessed by lecithin derivatives.
With a decrease in the size of the alveoli. surfactant molecules approach each other, their density per unit surface is greater and the surface tension decreases - the alveolus does not collapse.
With an increase (expansion) of the alveoli, their surface tension increases, since the density of the surfactant per unit surface decreases. This increases the elastic traction of the lungs.
In the process of breathing, the strengthening of the respiratory muscles is spent on overcoming not only the elastic resistance of the lungs and chest tissues, but also on overcoming the inelastic resistance to the gas flow in the airways, which depends on their lumen.
Violation of the formation of surfactants leads to the collapse of a large number of alveoli - atelectasis - lack of ventilation of large areas of the lungs.
In newborns, surfactants are necessary to expand the lungs during the first breaths.
There is a disease of newborns, in which the surface of the alveoli is covered with fibrin precipitate (gealine membranes), which reduces the activity of surfactants - it is reduced. This leads to incomplete expansion of the lungs and severe disruption of gas exchange.
Pneumothorax is the entry of air into the pleural cavity (through a damaged chest wall or lungs).
Due to the elasticity of the lungs, they fall down, pressing against the piston, occupying 1/3 of their volume.
When unilaterally, the lung on the intact side can provide sufficient oxygen saturation of the blood and removal of CO 2 (at rest).
Bilateral - if artificial ventilation of the lungs is not performed, or sealing of the pleural cavity - to death.
Unilateral pneumothorax is sometimes used for therapeutic purposes: the introduction of air into the pleural cavity for the treatment of tuberculosis (cavities).
In the pleural cavity there are three separate serous sacs - one of them contains the heart, and the other two contain the lungs. The serous membrane of the lung is called the pleura. It consists of two sheets:
Visceral, - the visceral (pulmonary) pleura tightly covers the lung, goes into its grooves, thus separating the lobes of the lung from each other,
Parietal, - the parietal (parietal) pleura lines the inside of the chest cavity wall.
In the area of \u200b\u200bthe lung root, the visceral pleura passes into the parietal pleura, thus forming a closed slit-like space - the pleural cavity. The inner surface of the pleura is covered with mesothelium and moistened with a small amount of serous fluid, thereby reducing friction between the pleural sheets during respiratory movements. The pressure in the pleural cavity is lower than atmospheric pressure (taken as zero) by 4-9 mm Hg. Art., therefore it is called negative. (With calm breathing, intrapleural pressure is 6-9 mm Hg in the inspiratory phase, and 4-5 mm Hg in the expiratory phase; with a deep breath, the pressure can drop to 3 mm Hg). Intrapleural pressure arises and is maintained as a result of the interaction of the chest with the lung tissue due to their elastic traction. At the same time, the elastic traction of the lungs develops an effort that always seeks to reduce the volume of the chest. In addition, atmospheric air produces unilateral (internally) pressure on the lungs through the airways. The chest is resistant to the transfer of air pressure from the outside to the lungs, therefore atmospheric air, stretching the lungs, presses them against the parietal pleura and chest wall. The formation of the final value of intrapleural pressure also involves the active forces developed by the respiratory muscles during respiratory movements. Also, the maintenance of intrapleural pressure is influenced by the processes of filtration and absorption of pleural fluid (due to the activity of mesothelial cells, which also have the ability to absorb air from the pleural cavity).
Due to the fact that the pressure in the pleural cavity is lowered, when the wall of the chest cavity is injured with damage to the parietal pleura, ambient air enters it. This phenomenon is called pneumothorax. In this case, the intrapleural and atmospheric pressures equalize, the lung collapses and its respiratory function is disturbed (since ventilation of the lung in the presence of respiratory movements of the chest and diaphragm becomes impossible)
There are the following types of pneumothorax: closed, - occurs when the visceral (for example, with spontaneous pneumothorax) or visceral and parietal pleura (for example, when a lung is injured by a fragment of a rib) without penetrating damage to the chest wall, - while air enters the pleural cavity from the lung,
Open, - occurs when a penetrating wound of the chest, - while air can enter the pleural cavity both from the lung and from the environment,
Tense. - is an extreme manifestation of closed pneumothorax, with spontaneous pneumothorax occurs rarely, - while air enters the pleural cavity, but, due to the valve mechanism, does not come back, but accumulates in it, which may be accompanied by a displacement of the mediastinum and severe hemodynamic disorders.
By etiology, they are distinguished: spontaneous (spontaneous), - occurs when the pulmonary alveoli rupture (tuberculosis, pulmonary emphysema);
Traumatic - occurs when the chest is damaged,
Artificial - the introduction of air or gas into the pleural cavity with a special needle, which causes compression of the lung, - is used to treat tuberculosis (causes the cavity to collapse due to compression of the lung).
Mechanism of occurrence negative pressure in the pleural cavitycan be clarified by means of a modified .
If you choose a bottle of such a size that corresponds to the size of the animal's chest, and, placing its lungs in this bottle, suck the air out of it, then the lungs will occupy almost all of its volume. In this case, the pressure in the slit-like space between the wall of the bottle and the lungs will become somewhat lower than atmospheric. This is because the stretched elastic tissue of the lungs tends to shrink. The force in which the elastic tissue of the lung is compressed - the so-called elastic traction of the lung tissue - counteracts the atmospheric pressure.
The phenomena that occur in the described version of the Donders model exactly correspond to those that exist under normal physiological conditions during inhalation and exhalation. The lungs in the chest are always stretched, and the stretching of the lung tissue increases during inhalation and decreases during exhalation. This is the reason negative pressure in the pleural cavityand its increase on inspiration and decrease on expiration. The fact that the lungs are really constantly stretched can be seen if the chest cavity is opened: the lungs will immediately collapse due to elastic traction and occupy about only ⅓ of the chest cavity.
The stretching of the lung tissue depends on the fact that atmospheric pressure acts on the lungs only from the inside through the airways and does not act on them from the outside due to the stubbornness of the chest wall. Therefore, the lungs are in the chest cavity under unilateral pressure, which, by stretching them, tightly presses against the chest wall so that they fill the entire pleural cavity, the traces of which remain only in the form of a narrow pleural fissure containing a thin layer of serous fluid.
The force of atmospheric pressure is expended to some extent in overcoming the elastic traction of the lungs. Therefore, the surface of the lungs is pressed against the chest wall with less force than the value of atmospheric pressure. As a result, the pressure in the pleural fissure, even during exhalation, is less than atmospheric by the amount of elastic traction of the lungs, that is, by about 6 mm Hg. Art.
The elastic traction of the lungs is due to two factors:
the presence of a large number of elastic fibers in the wall of the alveoli,
surface tension of the alveolar wall.
Neyergard back in 1929 showed that about ⅔, the elastic traction of the lungs depends on the surface tension of the alveolar wall. This is consistent with new data showing that the lungs retain their elastic properties after the destruction of their elastic tissue by the enzyme elastin.
Since the forces of surface tension may not be the same in different alveoli, it is possible for some of them to collapse and stick together during exhalation due to the fact that other alveoli remain stretched. This, however, does not happen due to the fact that the inner surface of the alveoli is covered with a water-insoluble, thin monomolecular film of a substance called surfactan (from the English word surface). Surfactan has a low surface tension and prevents the complete collapse of the alveoli, stabilizing their size. If the newborn is absent, the lungs do not expand (atelectasis). Surfactan is alpha lecithin. It is assumed that it is formed in the mitochondria of the cells of the alveolar epithelium. After cutting both vagus nerves, its production is inhibited.
Measurement of intrapleural pressure in a newborn shows that during exhalation it is equal to atmospheric pressure and becomes negative only during inhalation.
The appearance of negative pressure in the pleural fissure is explained by the fact that the chest of a newborn grows faster than the lungs, due to which the lung tissue is subjected to constant (even in the exhalation position) stretching. In the creation of negative pressure in the pleural fissure, it is also important that the pleural sheets have a high absorption capacity. Therefore, the gas introduced into the pleural cavity is absorbed after a while and negative pressure is restored in the pleural cavity. Thus, there is a mechanism that actively maintains negative pressure in the pleural fissure.
The negative pressure in the chest cavity is of great importance for the movement of blood through the veins. The walls of large veins located in the chest cavity are easily stretchable, and therefore negative pressure in the pleural cavity is transmitted to them. The negative pressure in the vena cava is an auxiliary mechanism that facilitates the return of blood to the right heart. It is clear that with an increase in negative pressure during inhalation, the flow of blood to the heart also increases. On the contrary, when straining and coughing, intrathoracic pressure rises so much that venous blood return can sharply decrease.