Expiration pressure in the pleural cavity. Pressure in the pleural cavity

2

1 Federal State Budgetary Educational Institution of Higher Education "Omsk State Medical University" of the Ministry of Health of the Russian Federation

2 Federal State Budgetary Educational Institution of Higher Education “Omsk State Agrarian University named after P.A. Stolypin"

Adequate drainage of the pleural cavity is, without a doubt, a mandatory, and often the main component of the treatment of most surgical diseases of the chest cavity, and its effectiveness depends on many physical parameters of both the lung and the pleura. Important in the pathophysiology of pleural biomechanics is the formulation of two different, but not mutually exclusive, concepts: an unexpandable lung and an air-leak. An unexpanded lung cannot occupy the entire volume of the pleural cavity even after drainage of fluid and air from the pleural cavity. An incorrectly chosen method for removing pathological contents can not only be of no benefit, but even aggravate the pathological state of the body. At the same time, after and during drainage of the pleural cavity, pneumothorax ex vacuo may develop, which is a persistent pneumothorax without a fistula. Important parameters characterizing the described processes in the pleural cavity are also intrapleural pressure (Ppl), elasticity of the pleural cavity. Normally, at the peak of inspiration, Ppl is up to -80 cm of water. Art., and the end of exhalation: -50 cm of water. Art. The pressure drop in the pleural cavity is below -40 cm of water. Art. when removing pathological contents from the pleural cavity (puncture of the pleural cavity) without the use of additional rarefaction, it is a sign of unexpandable lung. At the moment, it can be firmly considered necessary to monitor changes in intrapleural pressure during therapeutic and diagnostic thoracocentesis, drainage of the pleural cavity in the postoperative period, and any invasive closed interventions in the closed pleural cavity throughout the duration of the drainage or needle in the pleural cavity.

drainage

manometry

armored lung

1. Physiology of breathlessness associated with pleural effusions / T. Rajesh // Pulmonary Medicine. - 2015. - Vol. 21, No. 4. - P. 338-345.

2. Huggins J.T. Pleural manometry / J.T. Huggins, P. Doelken // Clinics in Chest Medicine. - 2006. - Vol. 27, Issue 2. - P. 229-240.

3. Characteristics of Trapped Lung. Pleural Fluid Analysis, Manometry, and Air-Contrast Chest CT / J.T. Huggins // Chest. - 2007. - Vol. 131, Issue 1. - P. 206-213.

4. Pereyra M.F. Unexpandable Lung / M.F. Pereyra, L. Ferreiro, L. Valdes // Arch. bronconeumol. - 2013. - Vol. 49, No. 2. - P. 63-69.

5. Pleural manometry: technique and clinical implications / J.T. Huggins // Chest. - 2004. - Vol. 126, No. 6. - P. 1764–1769.

6. Diagnosis and management of bronchopleural fistula / P. Sarkar // The Indian Journal of Chest Diseases & Allied Sciences. - 2010. - Vol. 52, No. 2. - P. 97-104.

7. Staes W. "Ex Vacuo" pneumothorax / W. Staes, B. Funaki // Seminars in interventional Radiology. - 2009. - Vol. 26, No. 1. - P. 82-85.

8. Comparison of pleural pressure measuring instruments / H.J. Lee // Chest. - 2014. - Vol. 146, No. 4. - P. 1007-1012.

9. Elastance of the pleural space: a predictor for the outcome of pleurodesis in patients with malignant pleural effusion / R.S. Lan // Ann. Intern. Med. - 1997. - Vol. 126, No. 10. - P. 768-774.

10. Intensive care: a guide for doctors / V.D. Malyshev, S.V. Sviridov, I.V. Vedenina and others; ed. V.D. Malysheva, S.V. Sviridov. - 2nd ed., revised. and additional - M.: LLC "Medical Information Agency", 2009. - 712 p.

11. A Pleural Manometry Catheter: pat. US 2016/0263296A1 USA: PCT/GB2014/052871 / Roe E.R. ; applicant and patentee Rocket Medical Plc. – US 15/028, 691; stated 09/22/2014; published on 09/15/2016.

12. Chest drainage systems and methods US: pat. 8992493 B2 USA: US 13/634,116 / James Croteau ; applicant and patentee Atrium Medical Corporation. – PCT/US2011/022985; stated 01/28/2011; published on 03/31/2015.

13. Fessler H.E. Are esophageal pressure measurements important in clinical decision-making? / H.E. Fessler, D.S. Talmor // Respiratory Care. - 2010. - Vol. 55, No. 2. - P. 162-174.

14. Noninvasive method for measuring and monitoring intrapleural pressure in newborns: pat. US 4860766 A USA: A 61 B, 5/00 / Sackner M.A.; applicant and patentee Respitrace Corp. – US 07/008, 062; stated 04/27/1987; published 08/29/1989.

15. Maldonado F. Counterpoint: should pleural manometry be performed routinely during thoracentesis? no. / F. Maldonado, J. Mullon // Chest. - 2012. - Vol. 141, No. 4. - P. 846–848.

Adequate drainage of the pleural cavity, without a doubt, is a mandatory, and often the main component of the treatment of most surgical diseases of the chest cavity. In modern thoracic surgery, there are many methods for draining the pleural cavity, which differ in the localization of the drainage installation, the position of the drainage tube in the pleural cavity, the method of removal and the ability to control the pathological contents of the pleural cavity, the pressure in the pleural cavity and many other parameters. The purpose of drainage of the pleural cavity is to remove the contents from it in order to expand the lung to the entire volume of the pleural cavity, restore the vital capacity of the lung, reduce pain and prevent the generalization of the infectious process. The effectiveness of achieving the goal directly depends on the phenomena occurring in the pleural cavity itself, the biomechanics of the cavity and its contents.

An incorrectly chosen method for removing pathological contents can not only be of no benefit, but even aggravate the pathological state of the body. Complications after thoracocentesis and drainage of the pleural cavity may be damage to the diaphragm, abdominal organs, heart, mediastinal organs, lung root structures. In this review of domestic and, for the most part, foreign literature, we will try to expand on the problem of the dependence of pressure changes in the pleural cavity during drainage on some physical parameters of the chest wall and pleural cavity.

The respiratory mechanics of the pleural cavity is very complex and depends on many factors, including the position of the patient's body, the presence of communication with the environment through the respiratory tract or chest wall, the nature of the pathological contents, the thrust created by the work of the respiratory muscles, the integrity of the bone frame of the chest wall, elasticity the pleura itself.

Pathological contents of the pleural cavity can appear for various reasons. However, from the point of view of the mechanical removal of fluid or air from the pleural cavity, the composition of the pathological contents is more important than the state of the lung and pleura, which determines how the pleural cavity will respond to medical intervention in the future.

Important in the pathophysiology of pleural biomechanics is the formulation of two different, but not mutually exclusive, concepts: an unexpandable lung and an air-leak. These complications do not occur suddenly, however, they significantly complicate the treatment, and their incorrect diagnosis often leads to errors in medical tactics.

An unexpandable lung is called a lung that is unable to occupy the entire volume of the pleural cavity when the pathological contents are removed. In this case, negative pressure is created in the pleural cavity. The following pathological mechanisms can lead to this: endobronchial obstruction, severe fibrotic changes in the lung tissue, and restriction of the visceral pleura. Moreover, such restriction is divided into two categories: Trapped Lung and Lung Entrapment. The first category is similar to what is referred to in the domestic literature by the term "shell lung".

The term "Lung Entrapment" includes a non-expanding lung caused by an active inflammatory or tumor process in the pleura, and is a fibrinous inflammation of the pleura and often precedes the actual "shell lung" (the term Trapped Lung is used in foreign literature). The inability to recover the lung in this state is secondary to the inflammatory process and can often be detected only when air or fluid is removed from the pleural cavity. With the passage of time and the inability to create conditions for the expansion of the lung, it retains a changed shape, that is, it becomes rigid. This occurs due to the activation of not only the connective tissue component in the stroma of the lung due to chronic hypoxia and inflammation, but also the development of fibrosis proper in the visceral pleura. This leads to long-term persistent air and fluid in the pleural cavity, as well as the attachment of an infectious process. When they are removed by aspiration in the absence of a pulmonary fistula, negative pressure remains in the pleural cavity without straightening the lung with pressure values ​​lower than normal. This will increase the pressure gradient between those inside the tracheobronchial tree and the pleural cavity, which will subsequently lead to barotrauma - pressure damage.

The "shell lung" is a modified organ that, even when the contents of the pleural cavity are removed, cannot straighten out, that is, completely occupy the entire hemithorax due to fibrous changes in the visceral pleura, the formation of coarse pleural adhesions between the parietal and visceral pleura due to a chronic inflammatory process in the lung and pleura and asymptomatic pleural effusion. Removal of exudate and air from the pleural cavity through punctures or by installing a drainage tube will not improve the respiratory function of the lung.

In the presence of a (bronchopleural or alveolar-pleural) fistula, the lung also does not straighten out, but due to the fact that atmospheric air constantly persists in the pleural cavity and atmospheric pressure is maintained, and with some types of artificial ventilation even higher. This complication significantly worsens the prognosis, mortality in this category of patients is up to 9.5%. Without drainage of the pleural cavity, this condition cannot be reliably diagnosed. The drainage system, in fact, under the influence of negative pressure, sucks air out of the fistula itself, that is, in fact, from atmospheric air, which is also a factor in additional infection due to the ingress of microorganisms from atmospheric air into the respiratory tract. Clinically, this is manifested by the active discharge of air through the drainage tube on exhalation or during vacuum aspiration. Secondarily, fibrosis of the visceral pleura may develop, which, even if the fistula is eliminated, will not allow the lung to spread to the entire pleural cavity.

It is also important to set off a special term that characterizes an unexpandable lung, pneumothorax ex vacuo - persistent pneumothorax without a fistula and trauma to the hollow organs of the chest cavity. Not only pneumothorax can cause atelectasis, but also atelectasis itself can become a condition for the development of pneumothorax when exudate is removed. Such pneumothorax occurs against the background of a sharp increase in negative pressure in the pleural cavity in combination with bronchial obstruction of 1-2 orders and below and is not associated with damage to the lung or visceral pleura. At the same time, in the pleural cavity, as such, there may not be atmospheric air, or it persists in a small amount. This condition can occur both in spontaneous breathing and in patients with mechanical ventilation, which is associated with airway obstruction in one of the lobes of the lung. Such a “pneumothorax” against the background of the underlying disease may not have its own clinical signs and not be associated with a worsening condition, and radiographically it is represented by separation of the pleura in a limited space in the projection of the upper or lower lobes (Fig. 1). The most important thing in the treatment of this complication in patients is not the installation of pleural drainage, but the elimination of the probable cause of the obstruction, after which the pneumothorax resolves, as a rule, on its own. If there is no data for obstruction of the bronchial tree and there is no pulmonary fistula, then the cause of this condition will be a "shell lung".

Rice. 1. Pneumothorax ex vacuo in a patient with an inflatable lung on a plain chest radiograph

Thus, it can be said that with an unexpandable lung during thoracocentesis and installation of pleural drainage, the likelihood of complications increases significantly, therefore it is so important to focus not only on the indicators of radiological and ultrasound diagnostics, but also to observe pressure processes in the pleural cavity that are not visible on x-ray film and when examining a patient. At the same time, some authors note that thoracocentesis with an unexpandable lung is much more painful due to irritation of the pleura with negative pressure (less than -20 mm of water column). In addition to drainage of the pleural cavity with an unexpandable lung, chemical pleurodesis also becomes impossible due to the persistent divergence of the sheets of the parietal and visceral pleura.

Important parameters characterizing the described processes in the pleural cavity are also intrapleural pressure (Ppl), elasticity of the pleural cavity (Epl). Normally, at the peak of inspiration, Ppl is up to -80 cm of water. Art., and the end of exhalation: -20 cm of water. Art. The drop in the average pressure of the pleural cavity below -40 cm of water. Art. when removing pathological contents from the pleural cavity (puncture of the pleural cavity) without the use of additional rarefaction, it is a sign of unexpandable lung. The elasticity of the pleura implies the ratio of the difference in pressure changes before and after the removal of a certain volume of pathological contents (Pliq1 - Pliq2) in relation to this very volume, which can be represented by the formula: see aq. Art./L With normal expansion of the lung and the presence of exudate of any density in the pleural cavity, the elasticity of the pleural cavity will be about 5.0 cm of water. Art./l, the value of the indicator is more than 14.5 cm of water. Art./L speaks of the unexpandable lung and the formation of a "armoured lung". From the foregoing, it follows that the quantitative measurement of pressure in the pleural cavity is an important diagnostic and prognostic test.

How can intrapleural pressure be measured?

There are direct and indirect methods for measuring this important parameter of respiratory mechanics. Direct is the measurement of pressure directly during thoracocentesis or prolonged drainage of the pleural cavity through a catheter or drainage located in it. A prerequisite is the installation of a catheter or drainage in the lowest position of the existing contents of the pleural cavity. The simplest option in this case is to use a water column, for which a tube from an intravenous system or a sterile column from a glass tube can be used; air must be removed from the system before the procedure. The pressure in the presence of liquid content in this case is determined by the height of the column in the tube relative to the injection site of the needle or the established drainage, which approximately corresponds to the well-known method for measuring central venous pressure using the Waldmann apparatus. The disadvantage of this method is the bulkiness and complexity of creating a stable structure for such measurements, as well as the impossibility of measuring the pressure in a "dry" cavity.

Digital devices are also used to determine and record intrapleural pressure.

Portable digital manometer Compass (Mirador Biomedical, USA) is used to measure pressure in body cavities. The positive side of this portable pressure gauge is its accuracy (high correlation with U-catheter pressure measurement has been proven) and ease of use. Its disadvantages are the possibility of its use only once and the impossibility of recording data on a digital medium, and it is also worth noting the high cost of such a pressure gauge (about $ 40 for one device).

An electronic pleural pressure gauge usually consists of a pleural cavity catheter, a splitter or disconnector, one line of which goes to the exudate removal system, the other to a pressure sensor and an analog-to-digital converter, which in turn allows you to display the image on the screen or record it on a digital medium (Fig. .2). In the studies of J.T. Huggins et al. kits for invasive blood pressure monitoring (Argon, USA), a CD19A analog-to-digital converter (Validyne Engineering, USA) are used; for data recording on a personal computer, the Biobench 1.0 software package (National Instruments, USA) is used. The disconnector may, for example, be the device described by Roe. The advantage of this system over the previously named portable sensor, of course, is the ability to record data on a digital medium, as well as the accuracy of the data obtained and reusability. The disadvantage of this method is the complexity of organizing a workplace for manometry. In addition to the operator himself, who performs the manipulation, additional personnel are needed to turn on and record the data. Also, the highway disconnector in this complex must comply with the requirements of asepsis and antisepsis and, ideally, be disposable.

Rice. 2. Scheme of an electronic pressure gauge for measuring intrapleural pressure

The disadvantages of this method are the pronounced dependence of the data obtained on the sensitivity of the sensor, the state of the adapter-tube (possible occlusion by its solid contents, air ingress), and features of the sensor membrane.

The determination of pressure by such methods occurs indirectly through the drainage tube, since the sensor itself is not located in the pleural cavity. Determination of pressure indicators both at the proximal end of the drain and in the line itself can be of high diagnostic value. The J. Croteau patent describes an aspiration apparatus for draining the pleural cavity with two pre-set levels of vacuum. The first mode - therapeutic, depends on the clinical situation. The second mode, with a higher level of vacuum, is activated when the pressure changes between the distal and proximal sections of the drainage tube, in which two pressure sensors are respectively installed, for example, by more than 20 mm of water. Art. (this setting is configurable). This helps to eliminate obstruction of the drainage and maintain its performance. Also, the described aspirator provides for counting the frequency of respiratory movements and giving a signal (including sound) when it changes. Thus, the principle of vacuum selection is based on measuring the pressure in the drain. The disadvantage is the lack of association of switching levels of rarefaction with physiological fluctuations in pressure in the pleural cavity. The change in pressure in this method serves to eliminate the obstruction of the drainage tube. Such monitoring can predict drainage obstruction and dislocation, which is important for preventing complications and making a quick decision on further treatment tactics.

An indirect method is transesophageal manometry in the thoracic esophagus at a point 40 cm from the incisors or nostrils in an adult. Determination of intraesophageal pressure (Pes) is of limited use for determining optimal positive expiration end pressure (PEEP) in mechanically ventilated patients and tidal ventilation volume when intrapleural pressure cannot be measured directly. Intraesophageal pressure is an average value of pressure in the pleural cavities without the involvement of the pleura in the pathological process and allows you to calculate the transpulmonary pressure gradient (Pl = Palv - Ppl, where Palv is the pressure in the alveoli), but does not provide information about determining Ppl in a particular cavity, especially with an unexpanded lung. The disadvantages of this method are the non-specificity of the measurement in relation to the affected side, as well as the unreliability of the data in the presence of a pathological process in the mediastinum of any kind and dependence on the position of the patient's body (in a horizontal position, the pressure is higher). There may be significant errors with high intra-abdominal pressure, obesity.

In newborns, the possibility of measuring intrapleural pressure by an indirect method is described by determining the movement of the bones of the cranial vault relative to each other and the pressure in the airways. The author proposes this method for the differential diagnosis of apnea in newborns of central origin and obstructive nature. The main disadvantage of this method is the lack of monitoring capabilities due to the fact that to measure the pressure it is necessary to perform the Valsalva maneuver, namely, to block the nostrils with a cannula (newborns, as you know, breathe only through the nostrils) while exhaling through the closed nostrils with a cannula with a pressure sensor. Also, this method does not allow to quantify intrapleural pressure, but is only used to determine the change in pressure during inhalation and exhalation to diagnose airway obstruction.

The methods of pleural manometry, which are more often used in practice, are associated with the creation of a communication between the pleural cavity and the environment through a puncture needle, a catheter, or an existing drainage of the pleural cavity. The determining factor in obtaining reliable data when measuring pressure is the creation of conditions for manometry. Thus, in case of therapeutic and diagnostic puncture of the pleural cavity without the use of active aspiration, the pressure indicator will change as the fluid is removed under the influence of gravity. In this case, it is possible to calculate the elasticity of the pleural cavity and diagnose an "unexpandable lung" (Fig. 3). When using active suction through a drain or catheter, intrapleural pressure monitoring will not be of diagnostic value, since external forces, in addition to gravity, will affect the pressure in the line. Measurement of pressure for a short period of time without removing the contents in order to assess the state of the pleural cavity is also acceptable, but it is less informative due to the impossibility of calculating the elasticity of the pleura.

Rice. 3. Schedule for measuring intrapleural pressure during therapeutic thoracocentesis (removal of exudate)

Still, it is worth noting that at present, even in the leading medical centers of the world, the routine use of pleural manometry is not widespread. The reason for this is the need to deploy additional equipment during pleural puncture (connecting and testing the manometer, connecting it to a needle or catheter that is inserted into the pleural cavity) and the time spent on this, the need for additional training of medical personnel to work with the manometer. F. Maldonado, based on an analysis of studies on measuring intrapleural pressure with an unexpandable lung, argues that at the moment it is impossible to consider the lung unexpandable only on the basis of data on intrapleural pressure and indicate indications for stopping or continuing the removal of pathological discharge from the pleural cavity. In his opinion, it is worth paying attention not only to the elasticity of the pleura, but also to where the “influence point” appears on the intrapleural pressure curve (graph), after which the lung becomes unexpandable and the thoracocentesis procedure should be stopped. However, at the moment there are no studies where such a “point of impact” was considered as a predictor.

Since changes in the indications of the respiratory mechanics of the pleural cavity are a predictor of many complications and outcomes, their monitoring will not only allow avoiding many complications, but also choosing a truly appropriate method of treatment for patients with this pathological condition. Thus, the most important thing in the management of patients with such pathological conditions as an unexpanded lung and prolonged air discharge is the determination of intrapleural pressure and its elasticity in order to select an adequate aspiration regimen and other features of pleural cavity drainage both before radical surgical treatment, and when it is impossible to carry out such . Monitoring of pressure and other parameters should be carried out constantly when the drainage tube is in the pleural cavity, as well as during therapeutic and diagnostic thoracocentesis. This is agreed by such authors who have devoted more than one major clinical study on the study of intrapleural pressure, such as J.T. Huggins, M.F. Pereyra et al. But, unfortunately, there are few simple and affordable means for conducting such studies, which confirms the need to study the issues of intrapleural pressure to increase the diagnostic value, such as pressure fluctuations in different phases of respiration in physiology and in pathological conditions, the relationship of functional tests in diagnostics of respiratory diseases with respiratory mechanics of the pleural cavity.

Bibliographic link

Khasanov A.R., Korzhuk M.S., Eltsova A.A. TO THE QUESTION OF DRAINAGE OF THE PLEURAL CAVITY AND MEASUREMENT OF INTRAPLEURAL PRESSURE. PROBLEMS AND SOLUTIONS // Modern problems of science and education. - 2017. - No. 5.;
URL: http://science-education.ru/ru/article/view?id=26840 (accessed 12.12.2019). We bring to your attention the journals published by the publishing house "Academy of Natural History"

Mechanism of exhalation (expiration) provided through:

Heaviness of the chest.

Elasticity of costal cartilages.

lung elasticity.

The pressure of the abdominal organs on the diaphragm.

At rest, exhalation occurs passively.

In forced breathing, expiratory muscles are taken: internal intercostal muscles (their direction is from above, back, front, down) and auxiliary expiratory muscles: muscles that flex the spine, abdominal muscles (oblique, straight, transverse). When the latter contract, the abdominal organs put pressure on the relaxed diaphragm and it protrudes into the chest cavity.

Breath types. Depending mainly due to which component (raising the ribs or the diaphragm) the volume of the chest increases, 3 types of breathing are distinguished:

- thoracic (costal);

- abdominal;

- mixed.

To a greater extent, the type of breathing depends on age (the mobility of the chest increases), clothing (tight corsets, swaddling), profession (for people engaged in physical labor, the abdominal type of breathing increases). Abdominal breathing is difficult in the last months of pregnancy, and then chest breathing is additionally included.

The most effective abdominal type of breathing:

- deeper lung ventilation;

- facilitates the return of venous blood to the heart.

The abdominal type of breathing prevails among manual workers, climbers, singers, etc. After birth, the child first establishes the abdominal type of breathing, and later - by the age of 7 - chest.

Pressure in the pleural cavity and its change during breathing.

The lungs are covered with a visceral pleura, and the film of the chest cavity is covered with a parietal pleura. Between them contains a serous fluid. They fit tightly to each other (slit 5-10 microns) and slide relative to each other. This sliding is necessary so that the lungs can follow the complex changes in the chest without deforming. With inflammation (pleurisy, adhesions), the ventilation of the corresponding sections 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 exhaling - 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 recoil of the lungs, i.e. the tendency of the lungs to collapse.

When inhaling, an increase in the chest cavity leads to an increase in negative pressure in the pleural cavity, i.e. transpulmonary pressure increases, leading to the expansion of the lungs (demonstration using the Donders apparatus).

When the inspiratory muscles relax, the transpulmonary pressure decreases and the lungs collapse due to elasticity.

If a small amount of air is introduced into the pleural cavity, it will be absorbed, because in the blood of small veins of the pulmonary circulation, the tension of dissolved gases is less than in the atmosphere.

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 cavity can be measured directly (but lung tissue can be damaged). Therefore, it is better to measure it by introducing a 10 cm long canister into the esophagus (into the chest part). The walls of the esophagus are very pliable.

The elastic recoil of the lungs is due to 3 factors:

1. Surface tension of the liquid film covering the inner surface of the alveoli.

2. The elasticity of the tissue of the walls of the alveoli (they contain elastic fibers).

3. The tone of the bronchial muscles.

On any interface between air and liquid, intermolecular cohesion forces act, tending to reduce the size of this surface (surface tension forces). Under the influence of these forces, the alveoli tend to shrink. Surface tension forces create 2/3 of the elastic recoil of the lungs. The surface tension of the alveoli is 10 times less than theoretically calculated for the corresponding water surface.

If the inner surface of the alveolus were covered with an aqueous solution, then the surface tension should have been 5-8 times greater. Under 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 surface tension, i.e., surfactants. Their molecules are strongly attracted to each other, but have a weak relationship with the liquid, as a result of which they gather on the surface and thereby reduce the surface tension.

Such substances are called surface-active substances (surfactants), the role of which in this case is played by the so-called surfactants. They are lipids and proteins. Formed by special cells of the alveoli - type II pneumocytes. The lining has a thickness of 20-100 nm. But lecithin derivatives have the highest surface activity of the components of this mixture.

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 enhances the elastic recoil 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 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 needed to expand the lungs during the first breaths.

2538 0

Basic information

Pleural effusion often presents a difficult diagnostic challenge for the clinician.

A reasoned differential diagnosis can be built on the basis of the clinical picture and the results of a study of the pleural fluid.

In order to maximize the use of data obtained from the study of pleural fluid, the clinician must have a good understanding of the physiological basis for the formation of pleural effusion.

The ability to analyze the results of the study of the cellular and chemical composition of the effusion, along with the data of the anamnesis, physical examination and additional laboratory research methods, makes it possible to make a preliminary or final diagnosis in 90% of patients with pleural effusion.

Nevertheless, it should be noted that, like any laboratory method, the study of pleural fluid often allows you to confirm a preliminary diagnosis, rather than acting as the main diagnostic method.

The final diagnosis based on the results of this research method can only be made if tumor cells, microorganisms or LE cells are found in the pleural fluid.

Anatomy of the pleural cavity

The pleura covers the lungs and lines the inside of the chest. It consists of loose connective tissue, covered with a single layer of mesothelial cells and is divided into the pulmonary (visceral) pleura and parietal (parietal) pleura.

The pulmonary pleura covers the surface of both lungs, and the parietal pleura lines the inner surface of the chest wall, the superior surface of the diaphragm, and the mediastinum. The lung and parietal pleura are connected in the region of the root of the lung (Fig. 136).


Rice. 136. Scheme of the anatomical structure of the lung and pleural cavity.
The visceral pleura covers the lung; The parietal pleura lines the chest wall, diaphragm, and mediastinum. They are connected in the region of the root of the lung.


Despite the similar histological structure, the pulmonary and parietal pleura have two important distinguishing features. Firstly, the parietal pleura is equipped with sensitive nerve receptors, which are not found in the pulmonary pleura, and secondly, the parietal pleura is easily separated from the chest wall, and the pulmonary pleura is tightly soldered to the lung.

Between the pulmonary and parietal pleura there is a closed space - the pleural cavity. Normally, during inhalation, as a result of the multidirectional action of the elastic recoil of the lungs and the elastic recoil of the chest, pressure below atmospheric pressure is created in the pleural cavity.

Typically, the pleural cavity contains 3 to 5 ml of fluid, which acts as a lubricant during inhalation and exhalation. With various diseases, several liters of fluid or air can accumulate in the pleural cavity.

Physiological basis of the formation of pleural fluid

Pathological accumulation of pleural fluid is the result of a violation of the movement of pleural fluid. The movement of pleural fluid into and out of the pleural cavity is regulated by the Starling principle.

This principle describes the following equation:

PZH \u003d K [(GDcap - GDpl) - (KODcap - KODpl)],
where PZh - fluid displacement, K - filtration coefficient for pleural fluid, HDcap - hydrostatic capillary pressure, HDPL - hydrostatic pressure of pleural fluid, CODcap - capillary oncotic pressure, COODpl - oncotic pressure of pleural fluid.

Since the parietal pleura is supplied with branches extending from the intercostal arteries, and the venous outflow of blood into the right atrium is carried out through the azygos vein system, the hydrostatic pressure in the vessels of the parietal pleura is equal to the systemic one.

The hydrostatic pressure in the vessels of the pulmonary pleura is equal to the pressure in the vessels of the lungs, since it is supplied with blood from the branches of the pulmonary artery; venous outflow of blood into the left atrium is carried out through the system of pulmonary veins. Colloidal osmotic pressure in the vessels of both pleural sheets is associated with the serum protein concentration.

In addition, normally a small amount of protein leaving the capillaries of the pleura is captured by the lymphatic system located in it. The permeability of pleural capillaries is regulated by the filtration coefficient (K). With an increase in permeability, the protein content in the pleural fluid increases.

It follows from the Starling equation that the movement of fluid into and out of the pleural cavity is directly regulated by hydrostatic and oncotic pressures. The pleural fluid moves along the pressure gradient from the systemic vessels of the parietal pleura, and then is reabsorbed by the vessels of the pulmonary circulation located in the pulmonary pleura (Fig. 137).



Rice. 137. The scheme of movement of pleural fluid from parietal capillaries to visceral capillaries is normal.
The absorption of the pleural fluid is facilitated by the resulting forces due to pressures in the visceral (10 cm H2O) and parietal pleura (9 cm H2O). The pressure of the moving liquid = K[(GDcap-GDpleur) - (CODcap-CODpleur)], where K is the filtration coefficient.


It is estimated that from 5 to 10 liters of pleural fluid passes through the pleural cavity in 24 hours.

Knowledge of the normal physiology of the movement of the pleural fluid makes it possible to explain some of the provisions associated with the formation of pleural effusion. Since a large amount of pleural fluid is produced and reabsorbed daily under normal conditions, any imbalance in the system increases the likelihood of an abnormal effusion.

There are two known mechanisms leading to pathological accumulation of pleural fluid: a violation of pressure, i.e. changes in hydrostatic and (or) oncotic pressure (congestive heart failure, severe hypoproteinemia) and diseases that affect the surface of the pleura and lead to impaired capillary permeability (pneumonia, tumors) or disrupt the reabsorption of proteins by the lymphatic vessels (mediastinal carcinomatosis).

Based on these pathophysiological mechanisms, pleural effusion can be divided into transudate (resulting from changes in pressure) and exudate (resulting from impaired capillary permeability).

Taylor R.B.

The pressure in the pleural cavity and in the mediastinum is normally always negative. You can verify this by measuring the pressure in the pleural cavity. To do this, a hollow needle connected to a manometer is inserted between two pleura. During a quiet breath, the pressure in the pleural cavity is 1.197 kPa (9 mm Hg) lower than atmospheric, during a quiet exhalation - by 0.798 kPa (6 mm Hg).

Negative intrathoracic pressure and its increase during inspiration is of great physiological importance. Due to the negative pressure, the alveoli are always in a stretched state, which significantly increases the respiratory surface of the lungs, especially during inspiration. Negative intrathoracic pressure plays a significant role in hemodynamics, providing venous return of blood to the heart and improving blood circulation in the pulmonary circle, especially during the inspiratory phase. The suction action of the chest also promotes lymphatic circulation. Finally, negative intrathoracic pressure is a factor contributing to the movement of the food bolus through the esophagus, in the lower part of which the pressure is 0.46 kPa (3.5 mm Hg) below atmospheric pressure.

Pneumothorax. Pneumothorax refers to the presence of air in the pleural cavity. In this case, intrapleural pressure becomes equal to atmospheric pressure, which causes the collapse of the lungs. Under these conditions, it is impossible for the lungs to perform respiratory function.

Pneumothorax can be open or closed. With an open pneumothorax, the pleural cavity communicates with atmospheric air, with a closed pneumothorax, this does not happen. Bilateral open pneumothorax is fatal if artificial respiration is not performed by forcing air through the trachea.

In clinical practice, a closed artificial pneumothorax is used (air is forced into the pleural cavity through a needle) to create functional rest for the affected lung, for example, in pulmonary tuberculosis. After some time, the air from the pleural cavity is sucked in, which leads to the restoration of negative pressure in it, and the lung expands. Therefore, to maintain pneumothorax, it is necessary to re-introduce air into the pleural cavity.

Respiratory cycle

The respiratory cycle consists of inhalation, exhalation and a respiratory pause. Inhalation is usually shorter than exhalation. The duration of inspiration in an adult is from 0.9 to 4.7 s, the duration of exhalation is 1.2-6 s. The duration of inhalation and exhalation depends mainly on the reflex effects coming from the receptors of the lung tissue. Respiratory pause is a non-permanent component of the respiratory cycle. It varies in size and may even be absent.

Respiratory movements are performed with a certain rhythm and frequency, which is determined by the number of chest excursions in 1 minute. In an adult, the frequency of respiratory movements is 12-18 per 1 min. In children, breathing is shallow and therefore more frequent than in adults. So, a newborn breathes about 60 times per minute, a 5-year-old child 25 times per minute. At any age, the frequency of respiratory movements is 4-5 times less than the number of heartbeats.

The depth of respiratory movements is determined by the amplitude of chest excursions and using special methods to explore lung volumes.

Many factors influence the frequency and depth of breathing, in particular, the emotional state, mental load, changes in the chemical composition of the blood, the degree of fitness of the body, the level and intensity of metabolism. The more frequent and deeper the respiratory movements, the more oxygen enters the lungs and, accordingly, more carbon dioxide is excreted.

Rare and shallow breathing can lead to an insufficient supply of oxygen to the cells and tissues of the body. This, in turn, is accompanied by a decrease in their functional activity. To a large extent, the frequency and depth of respiratory movements change in pathological conditions, especially in diseases of the respiratory system.

Inhalation mechanism. Inhalation (inspiration) occurs due to an increase in the volume of the chest in three directions - vertical, sagittal (anteroposterior) and frontal (costal). The change in the size of the chest cavity occurs due to the contraction of the respiratory muscles.

With the contraction of the external intercostal muscles (when inhaling), the ribs take on a more horizontal position, rising upward, while the lower end of the sternum moves forward. Due to the movement of the ribs during inhalation, the dimensions of the chest increase in the transverse and longitudinal directions. As a result of the contraction of the diaphragm, its dome flattens and falls: the abdominal organs are pushed down, to the sides and forward, as a result, the volume of the chest increases in the vertical direction.

Depending on the predominant participation in the act of inhalation of the muscles of the chest and diaphragm, there are thoracic, or costal, and abdominal, or diaphragmatic, types of breathing. In men, the abdominal type of breathing prevails, in women - chest.

In some cases, for example, during physical work, with shortness of breath, the so-called auxiliary muscles, the muscles of the shoulder girdle and neck, can take part in the act of inhalation.

When inhaling, the lungs passively follow the expanding chest. The respiratory surface of the lungs increases, while the pressure in them decreases and becomes 0.26 kPa (2 mm Hg) below atmospheric. This promotes the flow of air through the airways into the lungs. The rapid equalization of pressure in the lungs is prevented by the glottis, since the airways are narrowed in this place. Only at the height of inspiration is the complete filling of the expanded alveoli with air.

exhalation mechanism. Exhalation (expiration) is carried out as a result of relaxation of the external intercostal muscles and raising the dome of the diaphragm. In this case, the chest returns to its original position and the respiratory surface of the lungs decreases. The narrowing of the airways in the glottis causes a slow exit of air from the lungs. At the beginning of the expiratory phase, the pressure in the lungs becomes 0.40-0.53 kPa (3-4 mm Hg) higher than atmospheric pressure, which facilitates the release of air from them into the environment.

Pressure in the pleural cavity (clefts)

The lungs and walls of the chest cavity are covered with a serous membrane - the pleura. Between the sheets of the visceral and parietal pleura there is a narrow (5--10 microns) gap containing serous fluid, similar in composition to lymph. The lungs are constantly in a stretched state.

If a needle connected to a manometer is inserted into the pleural fissure, it can be established that the pressure in it is below atmospheric. Negative pressure in the pleural fissure is due to the elastic traction of the lungs, i.e., the constant desire of the lungs to reduce their volume. At the end of a quiet expiration, when almost all respiratory muscles are relaxed, the pressure in the pleural space (PPl) is approximately 3 mm Hg. Art. The pressure in the alveoli (Pa) at this time is equal to atmospheric. Difference Ra---PPl = 3 mm Hg. Art. is called transpulmonary pressure (P1). Thus, the pressure in the pleural space is lower than the pressure in the alveoli by the amount created by the elastic recoil of the lungs.

During inhalation, due to the contraction of the inspiratory muscles, the volume of the chest cavity increases. The pressure in the pleural space becomes more negative. By the end of a quiet breath, it decreases to -6 mm Hg. Art. As a result of an increase in pulmonary pressure, the lungs expand, their volume increases due to atmospheric air. When the inspiratory muscles relax, the elastic forces of the stretched lungs and abdominal walls reduce the transpulmonary pressure, the volume of the lungs decreases - exhalation occurs.

The mechanism of change in lung volume during respiration can be demonstrated using the Donders model.

With a deep breath, the pressure in the pleural space can decrease to -20 mm Hg. Art.

During active exhalation, this pressure can become positive, yet remain below the pressure in the alveoli by the amount of elastic recoil of the lungs.

There are no gases in the pleural fissure under normal conditions. If you introduce a certain amount of air into the pleural fissure, it will gradually resolve. Absorption of gases from the pleural fissure occurs due to the fact that in the blood of small veins of the pulmonary circulation, the tension of dissolved gases is lower than in the atmosphere. The accumulation of fluid in the pleural fissure is prevented by oncotic pressure: the content of proteins in the pleural fluid is much lower than in the blood plasma. The relatively low hydrostatic pressure in the vessels of the pulmonary circulation is also important.

Elastic properties of the lungs. The elastic recoil of the lungs is due to three factors:

1) surface tension of the liquid film covering the inner surface of the alveoli; 2) the elasticity of the tissue of the walls of the alveoli due to the presence of elastic fibers in them; 3) the tone of the bronchial muscles. The elimination of surface tension forces (filling the lungs with saline) reduces the elastic traction of the lungs by 2/3. If the inner surface of the alveoli were covered with an aqueous solution, the surface

the tension tension should have been 5–8 times greater. Under such conditions, a complete collapse of some alveoli (atelectasis) would be observed with overstretching of others. This does not happen because the inner surface of the alveoli is lined with a substance that has a low surface tension, the so-called surfactant. The lining has a thickness of 20-100 nm. It is made up of lipids and proteins. Surfactant is produced by special cells of the alveoli - type II pneumocytes. The surfactant film has a remarkable property: a decrease in the size of the alveoli is accompanied by a decrease in surface tension; this is important to stabilize the condition of the alveoli. Surfactant formation is enhanced by parasympathetic influences; after transection of the vagus nerves, it slows down.

Quantitatively, the elastic properties of the lungs are usually expressed by the so-called extensibility: where D V1 is the change in the volume of the lungs; DR1 -- change in transpulmonary pressure.

In adults, it is approximately 200 ml / cm of water. Art. In infants, the distensibility of the lungs is much lower - 5-10 ml / cm of water. Art. This indicator changes with lung diseases and is used for diagnostic purposes.

CATEGORIES

POPULAR ARTICLES

2023 "kingad.ru" - ultrasound examination of human organs