Reasons for the development of respiratory failure. Respiratory failure: acute, chronic, help, treatment. Alveolar disorders

For the diagnosis of respiratory failure, a number of modern research methods are used, which allow to get an idea of the specific causes, mechanisms and severity of the course of respiratory failure, concomitant functional and organic changes. internal organs, hemodynamic state, acid-base state, etc. For this purpose, the function of external respiration, blood gas composition, respiratory and minute ventilation volumes, hemoglobin and hematocrit levels, blood oxygen saturation, arterial and central venous pressure, heart rate, ECG, if necessary, pulmonary artery wedge pressure (PWLA) are determined, echocardiography is performed. and others (A.P. Zilber).

Assessment of respiratory function

The most important method for diagnosing respiratory failure is the assessment of the respiratory function of the respiratory function), the main tasks of which can be formulated as follows:

Diagnosis of violations of the function of external respiration and an objective assessment of the severity of respiratory failure.
Differential Diagnosis obstructive and restrictive disorders of pulmonary ventilation.
Substantiation of pathogenetic therapy of respiratory failure.
Evaluation of the effectiveness of the treatment.

These tasks are solved using a number of instrumental and laboratory methods: pyrometry, spirography, pneumotachometry, tests for the diffusion capacity of the lungs, impaired ventilation-perfusion relations, etc. The volume of examinations is determined by many factors, including the severity of the patient's condition and the possibility (and expediency!) a full and comprehensive study of FVD.

The most common methods for studying the function of external respiration are spirometry and spirography. Spirography provides not only a measurement, but a graphical recording of the main indicators of ventilation during calm and shaped breathing, physical activity, and pharmacological tests. AT last years The use of computer spirographic systems greatly simplified and accelerated the examination and, most importantly, made it possible to measure the volumetric velocity of inspiratory and expiratory air flows as a function of lung volume, i.e. analyze the flow-volume loop. Such computer systems include, for example, spirographs manufactured by Fukuda (Japan) and Erich Eger (Germany) and others.

Research methodology. The simplest spirograph consists of a double cylinder filled with air, immersed in a container of water and connected to a device to be registered (for example, a drum calibrated and rotating at a certain speed, on which the readings of the spirograph are recorded). The patient in a sitting position breathes through a tube connected to an air cylinder. Changes in lung volume during respiration are recorded by a change in the volume of a cylinder connected to a rotating drum. The study is usually carried out in two modes:

In the conditions of the main exchange - in the early morning hours, on an empty stomach, after a 1-hour rest in the supine position; 12-24 hours before the study, medication should be stopped.
In conditions of relative rest - in the morning or afternoon, on an empty stomach or not earlier than 2 hours after light breakfast; before the study, rest for 15 minutes in a sitting position is necessary.

The study is carried out in a separate dimly lit room with an air temperature of 18-24 C, after familiarizing the patient with the procedure. When conducting a study, it is important to achieve full contact with the patient, since his negative attitude towards the procedure and the lack of necessary skills can significantly change the results and lead to an inadequate assessment of the data obtained.

The main indicators of pulmonary ventilation

Classical spirography allows you to determine:

the value of most lung volumes and capacities,
main indicators of pulmonary ventilation,
oxygen consumption by the body and ventilation efficiency.

There are 4 primary lung volumes and 4 containers. The latter include two or more primary volumes.

lung volumes

Tidal volume (TO, or VT - tidal volume) is the volume of gas inhaled and exhaled during quiet breathing.
Inspiratory reserve volume (RO vd, or IRV - inspiratory reserve volume) - the maximum amount of gas that can be additionally inhaled after a quiet breath.
Expiratory reserve volume (RO vyd, or ERV - expiratory reserve volume) - the maximum amount of gas that can be additionally exhaled after a quiet exhalation.
Residual lung volume (OOJI, or RV - residual volume) - the volume of reptile remaining in the lungs after maximum exhalation.

lung capacity

The vital capacity of the lungs (VC, or VC - vital capacity) is the sum of TO, RO vd and RO vyd, i.e. maximum volume of gas that can be exhaled after maximum deep breath.
Inspiratory capacity (Evd, or 1C - inspiratory capacity) is the sum of TO and RO vd, i.e. the maximum volume of gas that can be inhaled after a quiet exhalation. This capacity characterizes the ability of lung tissue to stretch.
Functional residual capacity (FRC, or FRC - functional residual capacity) is the sum of OOL and PO vyd i.e. the amount of gas remaining in the lungs after a quiet exhalation.
The total lung capacity (TLC, or TLC - total lung capacity) is the total amount of gas contained in the lungs after a maximum breath.

Conventional spirographs, widely used in clinical practice, allow you to determine only 5 lung volumes and capacities: TO, RO vd, RO vyd. VC, Evd (or, respectively, VT, IRV, ERV, VC and 1C). To find the most important indicator of lung ventilation - functional residual capacity (FRC, or FRC) and calculate the residual lung volume (ROL, or RV) and total lung capacity (TLC, or TLC), it is necessary to apply special techniques, in particular, helium dilution methods, flushing nitrogen or whole body plethysmography (see below).

The main indicator in the traditional method of spirography is the vital capacity of the lungs (VC, or VC). To measure VC, the patient, after a period of quiet breathing (TO), first takes a maximum breath, and then, possibly, a full exhalation. In this case, it is advisable to evaluate not only the integral value of VC) and inspiratory and expiratory vital capacity (VCin, VCex, respectively), i.e. the maximum volume of air that can be inhaled or exhaled.

The second obligatory method used in traditional spirography is a test with the determination of forced (expiratory) vital capacity of the lungs OGEL, or FVC - forced vital capacity expiratory), which allows you to determine the most (formative speed indicators of pulmonary ventilation during forced exhalation, characterizing, in particular, the degree Intrapulmonary airway obstruction As with the VC test, the patient inhales as deeply as possible, and then, in contrast to the VC determination, exhales the air as fast as possible (forced expiration), which registers a gradually flattening exponential curve. Evaluating the spirogram of this expiratory maneuver, several indicators are calculated:

Forced expiratory volume in one second (FEV1, or FEV1 - forced expiratory volume after 1 second) - the amount of air removed from the lungs in the first second of exhalation. This indicator decreases both with airway obstruction (due to an increase in bronchial resistance) and with restrictive disorders (due to a decrease in all lung volumes).
Tiffno index (FEV1 / FVC,%) - the ratio of forced expiratory volume in the first second (FEV1 or FEV1) to forced vital capacity (FVC, or FVC). This is the main indicator of the expiratory maneuver with forced exhalation. It decreases significantly in broncho-obstructive syndrome, since the slowing of exhalation due to bronchial obstruction is accompanied by a decrease in forced expiratory volume in 1 s (FEV1 or FEV1) in the absence or slight decrease general meaning FZhEL (FVC). With restrictive disorders, the Tiffno index practically does not change, since FEV1 (FEV1) and FVC (FVC) decrease almost to the same extent.
Maximum expiratory flow rate at 25%, 50% and 75% of forced vital capacity . These indicators are calculated by dividing the corresponding forced expiratory volumes (in liters) (at the level of 25%, 50% and 75% of total FVC) by the time to reach these volumes during forced exhalation (in seconds).
Mean expiratory flow rate at 25~75% of FVC (COC25-75% or FEF25-75). This indicator is less dependent on the patient's voluntary effort and more objectively reflects bronchial patency.
Peak volumetric forced expiratory flow rate (POS vyd, or PEF - peak expiratory flow) - the maximum volumetric forced expiratory flow rate.

Based on the results of the spirographic study, the following are also calculated:

the number of respiratory movements during quiet breathing (RR, or BF - breathing freguency) and
minute volume of breathing (MOD, or MV - minute volume) - the amount of total ventilation of the lungs per minute with calm breathing.

Investigation of the flow-volume relationship

Computer spirography

Modern computer spirographic systems allow you to automatically analyze not only the above spirographic indicators, but also the flow-volume ratio, i.e. dependence of the volume flow rate of air during inhalation and exhalation on the value of lung volume. Automatic computer analysis of the inspiratory and expiratory flow-volume loop is the most promising method for quantifying pulmonary ventilation disorders. Although the flow-volume loop itself contains much of the same information as a simple spirogram, the visibility of the relationship between volumetric airflow rate and lung volume allows a more detailed study of the functional characteristics of both the upper and lower airways.

The main element of all modern spirographic computer systems is a pneumotachographic sensor that registers the volumetric air flow rate. The sensor is a wide tube through which the patient breathes freely. In this case, as a result of a small, previously known, aerodynamic resistance of the tube between its beginning and end, a certain pressure difference is created, which is directly proportional to the volumetric air flow rate. Thus, it is possible to register changes in the volumetric flow rate of air during inhalation and exhalation - pneumotachogram.

Automatic integration of this signal also makes it possible to obtain traditional spirographic indicators - lung volume values in liters. Thus, at each moment of time, information about the volumetric air flow rate and the volume of the lungs in this moment time. This allows a flow-volume curve to be plotted on the monitor screen. A significant advantage of this method is that the device operates in an open system, i.e. the subject breathes through the tube along an open circuit, without experiencing additional resistance to breathing, as in conventional spirography.

The procedure for performing breathing maneuvers when registering a flow-volume curve is similar to writing a normal coroutine. After a period of compound breathing, the patient delivers a maximum breath, resulting in the inspiratory portion of the flow-volume curve being recorded. The volume of the lung at point "3" corresponds to the total lung capacity (TLC, or TLC). Following this, the patient performs a forced expiration, and the expiratory part of the flow-volume curve (“3-4-5-1” curve) is recorded on the monitor screen. reaching a peak (peak volumetric velocity - POS vyd, or PEF), and then decreases linearly until the end of the forced exhalation, when the forced exhalation curve returns to its original position.

At healthy person the shape of the inspiratory and expiratory parts of the flow-volume curve differ significantly from each other: the maximum volumetric flow rate during inspiration is reached at about 50% VC (MOS50%inspiratory > or MIF50), while during forced exhalation the peak expiratory flow (PEF or PEF ) occurs very early. The maximum inspiratory flow (MOS50% of inspiration, or MIF50) is about 1.5 times the maximum expiratory flow at mid-vital capacity (Vmax50%).

The described flow-volume curve test is carried out several times until a concurrence of results is obtained. In most modern instruments, the procedure for collecting the best curve for further processing of the material is carried out automatically. The flow-volume curve is printed along with multiple pulmonary ventilation measurements.

Using a pneumotochographic sensor, the curve of the volumetric air flow rate is recorded. Automatic integration of this curve makes it possible to obtain a tidal volume curve.

Evaluation of the results of the study

Most lung volumes and capacities, both in healthy patients and in patients with lung disease, depend on a number of factors, including age, sex, chest size, body position, fitness level, and the like. For example, the vital capacity of the lungs (VC, or VC) in healthy people decreases with age, while the residual volume of the lungs (ROL, or RV) increases, and the total lung capacity (TLC, or TLC) practically does not change. VC is proportional to the size of the chest and, accordingly, the height of the patient. In women, VC is on average 25% lower than in men.

Therefore, from a practical point of view, it is not advisable to compare the values of lung volumes and capacities obtained during a spirographic study: with single “standards”, the fluctuations in the values \u200b\u200bof which due to the influence of the above and other factors are very significant (for example, VC normally can range from 3 to 6 l) .

The most acceptable way to evaluate the spirographic indicators obtained during the study is to compare them with the so-called due values, which were obtained when examining large groups of healthy people, taking into account their age, sex and height.

Proper values of ventilation indicators are determined by special formulas or tables. In modern computer spirographs, they are calculated automatically. For each indicator, the boundaries of normal values in percentage are given in relation to the calculated due value. For example, VC (VC) or FVC (FVC) is considered reduced if its actual value is less than 85% of the calculated proper value. A decrease in FEV1 (FEV1) is stated if the actual value of this indicator is less than 75% of the due value, and a decrease in FEV1 / FVC (FEV1 / FVC) - if the actual value is less than 65% of the due value.

Limits of normal values of the main spirographic indicators (as a percentage in relation to the calculated proper value).

Indicators	Conditional norm	Deviations
		Moderate	Significant


FEV1/FVC

In addition, when evaluating the results of spirography, it is necessary to take into account some additional conditions under which the study was carried out: the levels of atmospheric pressure, temperature and humidity of the surrounding air. Indeed, the volume of air exhaled by the patient usually turns out to be somewhat less than that which the same air occupied in the lungs, since its temperature and humidity, as a rule, are higher than those of the surrounding air. To exclude differences in the measured values associated with the conditions of the study, all lung volumes, both due (calculated) and actual (measured in this patient), are given for conditions corresponding to their values at a body temperature of 37 ° C and full saturation with water. in pairs (BTPS system - Body Temperature, Pressure, Saturated). In modern computer spirographs, such a correction and recalculation of lung volumes in the BTPS system are performed automatically.

Interpretation of results

A practitioner should have a good idea of the true possibilities of the spirographic research method, which are usually limited by the lack of information about the values of the residual lung volume (RLV), functional residual capacity (FRC) and total lung capacity (TLC), which does not allow a full analysis of the RL structure. At the same time, spirography makes it possible to get a general idea of the state of external respiration, in particular:

identify a decrease in lung capacity (VC);
identify violations of tracheobronchial patency, and using modern computer analysis of the flow-volume loop - at the earliest stages of the development of obstructive syndrome;
identify the presence of restrictive disorders of pulmonary ventilation in cases where they are not combined with impaired bronchial patency.

Modern computer spirography allows obtaining reliable and complete information about the presence of broncho-obstructive syndrome. More or less reliable detection of restrictive ventilation disorders using the spirographic method (without the use of gas-analytical methods for assessing the structure of the TEL) is possible only in relatively simple, classic cases of impaired lung compliance, when they are not combined with impaired bronchial patency.

Diagnosis of obstructive syndrome

The main spirographic sign of obstructive syndrome is the slowing down of forced exhalation due to an increase in airway resistance. When registering a classic spirogram, the forced expiratory curve becomes stretched, such indicators as FEV1 and the Tiffno index (FEV1 / FVC, or FEV, / FVC) decrease. VC (VC) at the same time either does not change, or slightly decreases.

A more reliable sign of broncho-obstructive syndrome is a decrease in the Tiffno index (FEV1 / FVC, or FEV1 / FVC), since absolute value FEV1 (FEV1) can decrease not only with bronchial obstruction, but also with restrictive disorders due to a proportional decrease in all lung volumes and capacities, including FEV1 (FEV1) and FVC (FVC).

Already in the early stages of the development of an obstructive syndrome, the calculated indicator of the average volumetric velocity decreases at the level of 25-75% of FVC (SOS25-75%) - O "is the most sensitive spirographic indicator, indicating an increase in airway resistance earlier than others. However, its calculation requires sufficient accurate manual measurements of the descending knee of the FVC curve, which is not always possible according to the classical spirogram.

More accurate and more accurate data can be obtained by analyzing the flow-volume loop using modern computerized spirographic systems. Obstructive disorders are accompanied by changes predominantly in the expiratory part of the flow-volume loop. If in most healthy people this part of the loop resembles a triangle with an almost linear decrease in the volumetric air flow rate during exhalation, then in patients with impaired bronchial patency, a kind of “sagging” of the expiratory part of the loop and a decrease in the volumetric air flow rate are observed at all values of lung volume. Often, due to an increase in lung volume, the expiratory part of the loop is shifted to the left.

Reduced spirographic indicators such as FEV1 (FEV1), FEV1 / FVC (FEV1 / FVC), peak expiratory volume flow rate (POS vyd, or PEF), MOS25% (MEF25), MOS50% (MEF50), MOC75% (MEF75) and COC25-75% (FEF25-75).

Vital capacity (VC) may remain unchanged or decrease even in the absence of concomitant restrictive disorders. At the same time, it is also important to assess the value of the expiratory reserve volume (ERV), which naturally decreases in obstructive syndrome, especially when early expiratory closure (collapse) of the bronchi occurs.

According to some researchers, a quantitative analysis of the expiratory part of the flow-volume loop also makes it possible to get an idea of the predominant narrowing of large or small bronchi. It is believed that obstruction of the large bronchi is characterized by a decrease in forced expiratory volume velocity, mainly in the initial part of the loop, and therefore such indicators as peak volume velocity (PFR) and maximum volume velocity at the level of 25% of FVC (MOV25%) are sharply reduced or MEF25). At the same time, the volume flow rate of air in the middle and end of expiration (MOC50% and MOC75%) also decreases, but to a lesser extent than POS vyd and MOS25%. On the contrary, with obstruction of small bronchi, a decrease in MOC50% is predominantly detected. MOS75%, while MOSvyd is normal or slightly reduced, and MOS25% is moderately reduced.

However, it should be emphasized that these provisions are currently quite controversial and cannot be recommended for use in general clinical practice. In any case, there are more reasons to believe that the uneven decrease in the volumetric air flow rate during forced expiration reflects the degree of bronchial obstruction rather than its localization. The early stages of bronchial constriction are accompanied by a slowdown in the expiratory air flow at the end and middle of exhalation (decrease in MOS50%, MOS75%, SOS25-75% with little changed values of MOS25%, FEV1 / FVC and POS), whereas with severe bronchial obstruction, a relatively proportional decrease in all speed indicators, including the Tiffno index (FEV1 / FVC), POS and MOS25%.

Of interest is the diagnosis of obstruction of the upper airways (larynx, trachea) using computer spirographs. There are three types of such obstruction:

fixed obstruction;
variable extrathoracic obstruction;
variable intrathoracic obstruction.

An example of a fixed obstruction of the upper airways is deer stenosis due to the presence of a tracheostomy. In these cases, breathing is carried out through a rigid, relatively narrow tube, the lumen of which does not change during inhalation and exhalation. This fixed obstruction limits the flow of air both inspiratory and expiratory. Therefore, the expiratory part of the curve resembles the inspiratory part in shape; volumetric inspiratory and expiratory velocities are significantly reduced and almost equal to each other.

In the clinic, however, more often one has to deal with two variants of variable obstruction of the upper airways, when the lumen of the larynx or trachea changes the time of inhalation or exhalation, which leads to selective limitation of inspiratory or expiratory air flows, respectively.

Variable extrathoracic obstruction is observed with various kinds of stenosis of the larynx (edema vocal cords, tumor, etc.). As is known, during respiratory movements, the lumen of the extrathoracic airways, especially narrowed ones, depends on the ratio of intratracheal and atmospheric pressures. During inspiration, the pressure in the trachea (as well as the intraalveolar and intrapleural pressure) becomes negative, i.e. below atmospheric. This contributes to the narrowing of the lumen of the extrathoracic airways and a significant limitation of the inspiratory air flow and a decrease (flattening) of the inspiratory part of the flow-volume loop. During forced exhalation, intratracheal pressure becomes significantly higher than atmospheric pressure, and therefore the diameter of the airways approaches normal, and the expiratory part of the flow-volume loop changes little. Variable intrathoracic obstruction of the upper airways is also observed in tumors of the trachea and dyskinesia of the membranous part of the trachea. The diameter of the thoracic airways is largely determined by the ratio of intratracheal and intrapleural pressures. With forced exhalation, when intrapleural pressure increases significantly, exceeding the pressure in the trachea, the intrathoracic airways narrow, and their obstruction develops. During inspiration, the pressure in the trachea slightly exceeds the negative intrapleural pressure, and the degree of narrowing of the trachea decreases.

Thus, with variable intrathoracic obstruction of the upper airways, there is a selective limitation of the air flow on exhalation and flattening of the inspiratory part of the loop. Its inspiratory part remains almost unchanged.

With variable extrathoracic obstruction of the upper airways, selective restriction of the volumetric airflow rate is observed mainly on inspiration, with intrathoracic obstruction - on expiration.

It should also be noted that in clinical practice, cases are quite rare when the narrowing of the lumen of the upper airways is accompanied by flattening of only the inspiratory or only the expiratory part of the loop. Usually reveals airflow limitation in both phases of breathing, although during one of them this process is much more pronounced.

Diagnosis of restrictive disorders

Restrictive violations of pulmonary ventilation are accompanied by a limitation of filling the lungs with air due to a decrease in the respiratory surface of the lung, turning off part of the lung from breathing, reducing the elastic properties of the lung and chest, as well as the ability of the lung tissue to stretch (inflammatory or hemodynamic pulmonary edema, massive pneumonia, pneumoconiosis, pneumosclerosis and so-called). At the same time, if restrictive disorders are not combined with the violations of bronchial patency described above, airway resistance usually does not increase.

The main consequence of restrictive (restrictive) ventilation disorders detected by classical spirography is an almost proportional decrease in most lung volumes and capacities: TO, VC, RO ind, RO vy, FEV, FEV1, etc. It is important that, unlike the obstructive syndrome, a decrease in FEV1 is not accompanied by a decrease in the FEV1/FVC ratio. This indicator remains within the normal range or even slightly increases due to a more significant decrease in VC.

In computed spirography, the flow-volume curve is a reduced copy of the normal curve, shifted to the right due to a general decrease in lung volume. Peak volumetric flow rate (PFR) of expiratory flow FEV1 is reduced, although the FEV1/FVC ratio is normal or increased. Due to the limitation of lung expansion and, accordingly, a decrease in its elastic traction, flow rates (for example, COC25-75%, MOC50%, MOC75%) in some cases can also be reduced even in the absence of airway obstruction.

The most important diagnostic criteria for restrictive ventilation disorders, which make it possible to reliably distinguish them from obstructive disorders, are:

an almost proportional decrease in lung volumes and capacities measured by spirography, as well as flow indicators and, accordingly, a normal or slightly changed shape of the curve of the flow-volume loop, shifted to the right;
normal or even increased value of the Tiffno index (FEV1 / FVC);
the decrease in inspiratory reserve volume (RIV) is almost proportional to the expiratory reserve volume (ROV).

It should be emphasized once again that for the diagnosis of even “pure” restrictive ventilation disorders, one cannot focus only on a decrease in VC, since the sweat rate in severe obstructive syndrome can also decrease significantly. More reliable differential diagnostic signs are the absence of changes in the shape of the expiratory part of the flow-volume curve (in particular, normal or increased values of FB1 / FVC), as well as a proportional decrease in RO ind and RO vy.

Determination of the structure of total lung capacity (TLC, or TLC)

As mentioned above, the methods of classical spirography, as well as computer processing of the flow-volume curve, make it possible to get an idea of the changes in only five of the eight lung volumes and capacities (TO, RVD, ROV, VC, EVD, or, respectively - VT, IRV, ERV , VC and 1C), which makes it possible to assess predominantly the degree of obstructive pulmonary ventilation disorders. Restrictive disorders can be reliably diagnosed only if they are not combined with a violation of bronchial patency, i.e. with absence mixed disorders lung ventilation. Nevertheless, in the practice of a doctor, it is precisely such mixed disorders that are most often encountered (for example, in chronic obstructive bronchitis or bronchial asthma complicated by emphysema and pneumosclerosis, etc.). In these cases, the mechanisms of impaired pulmonary ventilation can only be identified by analyzing the structure of the RFE.

To solve this problem, it is necessary to use additional methods for determining functional residual capacity (FRC, or FRC) and calculate indicators of residual lung volume (ROL, or RV) and total lung capacity (TLC, or TLC). Since FRC is the amount of air remaining in the lungs after maximum expiration, it is measured only by indirect methods (gas analysis or using whole body plethysmography).

The principle of gas analysis methods is that the lungs are either injected with an inert gas helium (dilution method), or the nitrogen contained in the alveolar air is washed out, forcing the patient to breathe pure oxygen. In both cases, the FRC is calculated from the final gas concentration (R.F. Schmidt, G. Thews).

Helium dilution method. Helium, as is known, is an inert and harmless gas for the body, which practically does not pass through the alveolar-capillary membrane and does not participate in gas exchange.

The dilution method is based on measuring the helium concentration in the closed container of the spirometer before and after mixing the gas with the lung volume. A covered spirometer with a known volume (V cn) is filled with a gas mixture consisting of oxygen and helium. At the same time, the volume occupied by helium (V cn) and its initial concentration (FHe1) are also known. After a quiet exhalation, the patient begins to breathe from the spirometer, and helium is evenly distributed between the volume of the lungs (FOE, or FRC) and the volume of the spirometer (V cn). After a few minutes, the helium concentration in the general system (“spirometer-lungs”) decreases (FHe 2).

Nitrogen washout method. In this method, the spirometer is filled with oxygen. The patient breathes into the closed circuit of the spirometer for several minutes, while measuring the volume of exhaled air (gas), the initial content of nitrogen in the lungs and its final content in the spirometer. The FRC (FRC) is calculated using an equation similar to that of the helium dilution method.

The accuracy of both of the above methods for determining the FRC (RR) depends on the completeness of the mixing of gases in the lungs, which in healthy people occurs within a few minutes. However, in some diseases accompanied by severe uneven ventilation (for example, with obstructive lung pathology), balancing the concentration of gases takes a long time. In these cases, the measurement of FRC (FRC) by the methods described may be inaccurate. These shortcomings are devoid of the more technically complex method of whole body plethysmography.

Whole body plethysmography. Whole body plethysmography is one of the most informative and complex methods a study used in pulmonology to determine lung volumes, tracheobronchial resistance, elastic properties of the lung tissue and chest, as well as to evaluate some other parameters of pulmonary ventilation.

The integral plethysmograph is a hermetically sealed chamber with a volume of 800 liters, in which the patient is freely placed. The subject breathes through a pneumotachograph tube connected to a hose open to the atmosphere. The hose has a flap that allows you to automatically shut off the air flow at the right time. Special barometric sensors measure the pressure in the chamber (Pcam) and in the oral cavity (Prot). the latter, with the valve of the hose closed, is equal to the alveolar pressure inside. The pneumotachograph allows you to determine the air flow (V).

The principle of operation of an integral plethysmograph is based on Boyle Moriosht's law, according to which, at a constant temperature, the relationship between pressure (P) and gas volume (V) remains constant:

P1xV1 = P2xV2, where P1 is the initial gas pressure, V1 is the initial gas volume, P2 is the pressure after changing the gas volume, V2 is the volume after changing the gas pressure.

The patient inside the plethysmograph chamber inhales and exhales calmly, after which (at the FRC level, or FRC) the hose flap is closed, and the subject makes an attempt to “inhale” and “exhale” (the “breathing” maneuver) With this “breathing” maneuver intra-alveolar pressure changes, and the pressure in the closed chamber of the plethysmograph changes inversely proportional to it. When you try to "inhale" with a closed valve, the volume of the chest increases, which leads, on the one hand, to a decrease in intra-alveolar pressure, and on the other hand, to a corresponding increase in pressure in the plethysmograph chamber (Pcam). On the contrary, when you try to "exhale" the alveolar pressure increases, and the volume of the chest and the pressure in the chamber decrease.

Thus, the whole body plethysmography method makes it possible to calculate intrathoracic gas volume (IGO) with high accuracy, which in healthy individuals quite accurately corresponds to the value of functional residual lung capacity (FRC, or CS); the difference between VGO and FOB usually does not exceed 200 ml. However, it should be remembered that in case of impaired bronchial patency and some other pathological conditions, VGO can significantly exceed the value of the true FOB due to an increase in the number of unventilated and poorly ventilated alveoli. In these cases, it is advisable to combine a study using gas analytical methods of the whole body plethysmography method. By the way, the difference between VOG and FOB is one of the important indicators of uneven ventilation of the lungs.

Interpretation of results

The main criterion for the presence of restrictive disorders of pulmonary ventilation is a significant decrease in the TEL. With a "pure" restriction (without a combination of bronchial obstruction), the structure of the TEL does not change significantly, or a slight decrease in the ratio of TOL/TEL was observed. If restrictive disorders occur against the background of bronchial patency disorders (mixed type of ventilation disorders), along with a clear decrease in the TFR, a significant change in its structure is observed, which is characteristic of broncho-obstructive syndrome: an increase in TRL/TRL (more than 35%) and FFU/TEL (more than 50% ). In both variants of restrictive disorders, VC is significantly reduced.

Thus, the analysis of the structure of the REL makes it possible to differentiate all three variants of ventilation disorders (obstructive, restrictive, and mixed), while the assessment of only spirographic parameters does not make it possible to reliably distinguish the mixed variant from the obstructive variant, accompanied by a decrease in VC).

The main criterion for the obstructive syndrome is a change in the structure of the REL, in particular, an increase in the ROL / TEL (more than 35%) and FFU / TEL (more than 50%). For “pure” restrictive disorders (without a combination with obstruction), the most characteristic is a decrease in the TEL without changing its structure. mixed type ventilation disturbances is characterized by a significant decrease in the TRL and an increase in the ratios of TOL/TEL and FFU/TEL.

Determination of uneven ventilation of the lungs

In a healthy person, there is a certain physiological uneven ventilation of different parts of the lungs, due to differences in the mechanical properties of the airways and lung tissue, as well as the presence of the so-called vertical pleural pressure gradient. If the patient is in an upright position, at the end of exhalation, pleural pressure in the upper lung is more negative than in the lower (basal) sections. The difference can reach 8 cm of water column. Therefore, before the start of the next breath, the alveoli of the tops of the lungs are stretched more than the alveoli of the lower basal regions. In this regard, during inspiration in the alveoli basal departments more air enters.

The alveoli of the lower basal sections of the lungs are normally better ventilated than the areas of the apexes, which is associated with the presence of a vertical intrapleural pressure gradient. However, normally, such uneven ventilation is not accompanied by a noticeable disturbance of gas exchange, since the blood flow in the lungs is also uneven: the basal sections are better perfused than the apical ones.

In some diseases of the respiratory system, the degree of uneven ventilation can increase significantly. Most common causes such pathological uneven ventilation are:

Diseases accompanied by an uneven increase in airway resistance (chronic bronchitis, bronchial asthma).
Diseases with unequal regional extensibility of lung tissue (pulmonary emphysema, pneumosclerosis).
Inflammation of the lung tissue (focal pneumonia).
Diseases and syndromes, combined with local restriction of expansion of the alveoli (restrictive) - exudative pleurisy, hydrothorax, pneumosclerosis, etc.

Often different causes are combined. For example, in chronic obstructive bronchitis complicated by emphysema and pneumosclerosis, regional disorders of bronchial patency and extensibility of the lung tissue develop.

With uneven ventilation, the physiological dead space increases significantly, gas exchange in which does not occur or is weakened. This is one of the reasons for the development of respiratory failure.

To assess the unevenness of pulmonary ventilation, gas analytical and barometric methods are more often used. Thus, a general idea of the uneven ventilation of the lungs can be obtained, for example, by analyzing the curves of helium mixing (dilution) or nitrogen leaching, which are used to measure FRC.

In healthy people, mixing helium with alveolar air or washing out nitrogen from it occurs within three minutes. With violations of bronchial patency, the number (volume) of poorly ventilated alveoli increases dramatically, and therefore the mixing (or washing out) time increases significantly (up to 10-15 minutes), which is an indicator of uneven pulmonary ventilation.

More accurate data can be obtained using a nitrogen leaching test with a single breath of oxygen. The patient exhales as much as possible, and then inhales pure oxygen as deeply as possible. Then he slowly exhales into a closed system of a spirograph equipped with a device for determining the concentration of nitrogen (azotograph). Throughout the exhalation, the volume of the exhaled gas mixture is continuously measured, and the changing concentration of nitrogen in the exhaled gas mixture containing nitrogen of the alveolar air is also determined.

The nitrogen leaching curve consists of 4 phases. At the very beginning of exhalation, air enters the spirograph from the upper airways, which is 100% p. oxygen that filled them during the previous breath. The nitrogen content in this portion of exhaled gas is zero.

The second phase is characterized by a sharp increase in the concentration of nitrogen, which is due to the leaching of this gas from the anatomical dead space.

During the long third phase, the nitrogen concentration of the alveolar air is recorded. In healthy people, this phase of the curve is flat - in the form of a plateau (alveolar plateau). If there is uneven ventilation during this phase, the nitrogen concentration increases due to the gas being washed out from the poorly ventilated alveoli, which are emptied last. Thus, the greater the rise in the nitrogen washout curve at the end of the third phase, the more pronounced is the unevenness of pulmonary ventilation.

The fourth phase of the nitrogen washout curve is associated with the expiratory closure of the small airways of the basal parts of the lungs and the inflow of air mainly from the apical parts of the lungs, the alveolar air in which contains nitrogen of a higher concentration.

Assessment of the ventilation-perfusion ratio

Gas exchange in the lungs depends not only on the level of general ventilation and the degree of its unevenness in various departments organ, but also on the ratio of ventilation and perfusion at the level of the alveoli. Therefore, the value of the ventilation-perfusion ratio (VPO) is one of the most important functional characteristics of the respiratory organs, which ultimately determines the level of gas exchange.

Normal VPO for the lung as a whole is 0.8-1.0. With a decrease in VPO below 1.0, perfusion of poorly ventilated areas of the lungs leads to hypoxemia (decrease in oxygenation of arterial blood). An increase in VPO greater than 1.0 is observed with preserved or excessive ventilation of zones, the perfusion of which is significantly reduced, which can lead to impaired CO2 excretion - hypercapnia.

Causes of HPE violation:

All diseases and syndromes that cause uneven ventilation of the lungs.
The presence of anatomical and physiological shunts.
Thromboembolism small branches pulmonary artery.
Violation of microcirculation and thrombosis in the vessels of the small circle.

Capnography. Several methods have been proposed to detect violations of HPV, of which one of the simplest and most accessible is the capnography method. It is based on the continuous registration of CO2 content in the exhaled mixture of gases using special gas analyzers. These instruments measure the absorption of infrared rays by carbon dioxide as it passes through an exhaled gas cuvette.

When analyzing a capnogram, three indicators are usually calculated:

slope of the alveolar phase of the curve (segment BC),
the value of CO2 concentration at the end of exhalation (at point C),
the ratio of functional dead space (MP) to tidal volume (TO) - MP / DO.

Determination of diffusion of gases

Diffusion of gases through the alveolar-capillary membrane obeys Fick's law, according to which the diffusion rate is directly proportional to:

partial pressure gradient of gases (O2 and CO2) on both sides of the membrane (P1 - P2) and
diffusion capacity of the alveolar-caillary membrane (Dm):

VG \u003d Dm x (P1 - P2), where VG is the gas transfer rate (C) through the alveolar-capillary membrane, Dm is the diffusion capacity of the membrane, P1 - P2 is the partial pressure gradient of gases on both sides of the membrane.

To calculate the diffusion capacity of light POs for oxygen, it is necessary to measure the 62 (VO 2 ) uptake and the average O 2 partial pressure gradient. VO2 values are measured using an open or closed type. To determine the oxygen partial pressure gradient (P 1 - P 2), more complex gas analytical methods are used, since in clinical conditions it is difficult to measure the partial pressure of O 2 in the pulmonary capillaries.

The most commonly used definition of the diffusion capacity of light is ne for O 2, but for carbon monoxide (CO). Since CO binds 200 times more actively with hemoglobin than oxygen, its concentration in the blood of the pulmonary capillaries can be neglected. Then, to determine DlCO, it is sufficient to measure the rate of passage of CO through the alveolar-capillary membrane and the gas pressure in the alveolar air.

The single-breath method is most widely used in the clinic. The subject inhales a gas mixture with a small content of CO and helium, and at the height of a deep breath for 10 seconds holds his breath. After that, the composition of the exhaled gas is determined by measuring the concentration of CO and helium, and the diffusion capacity of the lungs for CO is calculated.

Normally, DlCO, reduced to body area, is 18 ml/min/mm Hg. st./m2. The diffusion capacity of the lungs for oxygen (DlO2) is calculated by multiplying DlCO by a factor of 1.23.

The following diseases most often cause a decrease in the diffusion capacity of the lungs.

Emphysema of the lungs (due to a decrease in the surface area of the alveolar-capillary contact and the volume of capillary blood).
Diseases and syndromes accompanied by diffuse lesions of the lung parenchyma and thickening of the alveolar-capillary membrane (massive pneumonia, inflammatory or hemodynamic pulmonary edema, diffuse pneumosclerosis, alveolitis, pneumoconiosis, cystic fibrosis, etc.).
Diseases accompanied by damage to the capillary bed of the lungs (vasculitis, embolism of small branches of the pulmonary artery, etc.).

For correct interpretation changes in the diffusion capacity of the lungs, it is necessary to take into account the hematocrit index. An increase in hematocrit in polycythemia and secondary erythrocytosis is accompanied by an increase, and its decrease in anemia is accompanied by a decrease in the diffusion capacity of the lungs.

Airway resistance measurement

Measurement of airway resistance is a diagnostically important parameter of pulmonary ventilation. Aspirated air moves through the airways under the action of a pressure gradient between the oral cavity and the alveoli. During inspiration, expansion of the chest leads to a decrease in viutripleural and, accordingly, intra-alveolar pressure, which becomes lower than the pressure in the oral cavity (atmospheric). As a result, the air flow is directed into the lungs. During expiration, the action of the elastic recoil of the lungs and chest is aimed at increasing the intra-alveolar pressure, which becomes higher than the pressure in the oral cavity, resulting in a reverse flow of air. Thus, the pressure gradient (∆P) is the main force that ensures the transport of air through the airways.

The second factor that determines the amount of gas flow through the airways is the aerodynamic drag (Raw), which, in turn, depends on the clearance and length of the airways, as well as on the viscosity of the gas.

The value of the volumetric air flow rate obeys the Poiseuille law: V = ∆P / Raw, where

V is the volumetric velocity of the laminar air flow;
∆P - pressure gradient in the oral cavity and alveoli;
Raw - aerodynamic resistance of the airways.

It follows that in order to calculate the aerodynamic resistance of the airways, it is necessary to simultaneously measure the difference between the pressure in the oral cavity in the alveoli (∆P), as well as the volumetric air flow rate.

There are several methods for determining Raw based on this principle:

whole body plethysmography method;
airflow blocking method.

Determination of blood gases and acid-base status

The main method for diagnosing acute respiratory failure is the study of arterial blood gases, which includes the measurement of PaO2, PaCO2 and pH. You can also measure the saturation of hemoglobin with oxygen (oxygen saturation) and some other parameters, in particular the content of buffer bases (BB), standard bicarbonate (SB) and the amount of excess (deficit) of bases (BE).

The parameters PaO2 and PaCO2 most accurately characterize the ability of the lungs to saturate the blood with oxygen (oxygenation) and remove carbon dioxide (ventilation). The latter function is also determined from the pH and BE values.

To determine the gas composition of the blood in patients with acute respiratory failure in intensive care units, a complex invasive technique for obtaining arterial blood is used by puncturing a large artery. More often, a puncture of the radial artery is performed, since the risk of developing complications is lower. The hand has a good collateral blood flow, which is carried out by the ulnar artery. Therefore, even if the radial artery is damaged during puncture or operation of the arterial catheter, the blood supply to the hand is preserved.

Indications for puncture of the radial artery and placement of an arterial catheter are:

the need for frequent measurement of arterial blood gases;
severe hemodynamic instability against the background of acute respiratory failure and the need for constant monitoring of hemodynamic parameters.

A negative Allen test is a contraindication to catheter insertion. For the test, the ulnar and radial arteries are pinched with fingers so as to turn the arterial blood flow; the hand turns pale after a while. After that, the ulnar artery is released, continuing to compress the radial. Usually the color of the brush is quickly (within 5 seconds) restored. If this does not happen, then the hand remains pale, ulnar artery occlusion is diagnosed, the test result is considered negative, and the radial artery is not punctured.

When positive result test palm and forearm of the patient is fixed. After preparation operating field in the distal parts of the radial guests, the pulse on the radial artery is palpated, anesthesia is performed in this place, and the artery is punctured at an angle of 45°. The catheter is advanced until blood appears in the needle. The needle is removed, leaving the catheter in the artery. To prevent excessive bleeding, the proximal part of the radial artery is pressed with a finger for 5 minutes. The catheter is fixed to the skin with silk sutures and covered with a sterile dressing.

Complications (bleeding, arterial occlusion by a thrombus, and infection) during catheter placement are relatively rare.

It is preferable to draw blood for research into a glass rather than a plastic syringe. It is important that the blood sample does not come into contact with the surrounding air, i.e. collection and transport of blood should be carried out under anaerobic conditions. Otherwise, exposure to the blood sample of ambient air leads to the determination of the level of PaO2.

Determination of blood gases should be carried out no later than 10 minutes after arterial blood sampling. Otherwise, ongoing metabolic processes in the blood sample (initiated mainly by the activity of leukocytes) significantly change the results of the determination of blood gases, reducing the level of PaO2 and pH, and increasing PaCO2. Especially pronounced changes are observed in leukemia and in severe leukocytosis.

Methods for assessing the acid-base state

Measurement of blood pH

The pH value of blood plasma can be determined by two methods:

The indicator method is based on the property of some weak acids or bases, used as indicators, to dissociate at certain pH values, thus changing the color.
The pH-metry method makes it possible to more accurately and quickly determine the concentration of hydrogen ions using special polarographic electrodes, on the surface of which, when immersed in a solution, a potential difference is created that depends on the pH of the medium under study.

One of the electrodes - active, or measuring, is made of a noble metal (platinum or gold). The other (reference) serves as a reference electrode. The platinum electrode is separated from the rest of the system by a glass membrane permeable only to hydrogen ions (H+). Inside the electrode is filled with a buffer solution.

The electrodes are immersed in the test solution (for example, blood) and polarized from a current source. As a result, a current appears in a closed electrical circuit. Since the platinum (active) electrode is additionally separated from the electrolyte solution by a glass membrane permeable only to H + ions, the pressure on both surfaces of this membrane is proportional to blood pH.

Most often, the acid-base state is assessed by the Astrup method on the microAstrup apparatus. Determine the indicators of BB, BE and PaCO2. Two portions of the studied arterial blood are brought into equilibrium with two gas mixtures of known composition, differing in the partial pressure of CO2. pH is measured in each portion of blood. The pH and PaCO2 values in each portion of blood are plotted as two points on a nomogram. Through 2 points marked on the nomogram, a straight line is drawn to the intersection with the standard graphs of BB and BE and the actual values of these indicators are determined. Then measure the pH of the blood under study and find on the resulting straight point corresponding to this measured pH value. The projection of this point onto the y-axis determines the actual pressure of CO2 in the blood (PaCO2).

Direct measurement of CO2 pressure (PaCO2)

In recent years for direct measurement PaCO2 in a small volume is used as a modification of polarographic electrodes designed to measure pH. Both electrodes (active and reference) are immersed in an electrolyte solution, which is separated from the blood by another membrane, permeable only to gases, but not to hydrogen ions. CO2 molecules, diffusing through this membrane from the blood, change the pH of the solution. As mentioned above, the active electrode is additionally separated from the NaHCO3 solution by a glass membrane permeable only to H + ions. After the electrodes are immersed in the test solution (for example, blood), the pressure on both surfaces of this membrane is proportional to the pH of the electrolyte (NaHCO3). In turn, the pH of the NaHCO3 solution depends on the concentration of CO2 in the blood. Thus, the magnitude of the pressure in the circuit is proportional to the PaCO2 of the blood.

The polarographic method is also used to determine PaO2 in arterial blood.

Determination of BE from the results of direct measurement of pH and PaCO2

Direct determination of pH and PaCO2 of the blood makes it possible to significantly simplify the procedure for determining the third indicator of the acid-base state - the excess of bases (BE). The latter indicator can be determined by special nomograms. After direct measurement of pH and PaCO2, the actual values of these indicators are plotted on the corresponding nomogram scales. The points are connected by a straight line and continue it until it intersects with the BE scale.

This method of determining the main indicators of the acid-base state does not require balancing the blood with a gas mixture, as when using the classical Astrup method.

Interpretation of results

Partial pressure of O2 and CO2 in arterial blood

The values of PaO2 and PaCO2 serve as the main objective indicators of respiratory failure. In a healthy adult breathing room air with an oxygen concentration of 21% (FiO 2 \u003d 0.21) and normal atmospheric pressure (760 mm Hg), PaO 2 is 90-95 mm Hg. Art. With a change in barometric pressure, ambient temperature and some other conditions, PaO2 in a healthy person can reach 80 mm Hg. Art.

Lower values of PaO2 (less than 80 mm Hg) can be considered the initial manifestation of hypoxemia, especially against the background of acute or chronic damage to the lungs, chest, respiratory muscles, or the central regulation of respiration. Reducing PaO2 to 70 mm Hg. Art. in most cases, it indicates compensated respiratory failure and, as a rule, is accompanied by clinical signs of a decrease in the functionality of the external respiratory system:

slight tachycardia;
shortness of breath, respiratory discomfort, appearing mainly during physical exertion, although at rest the respiratory rate does not exceed 20-22 per minute;
a noticeable decrease in exercise tolerance;
participation in breathing of the auxiliary respiratory muscles, etc.

At first glance, these criteria for arterial hypoxemia contradict the definition of respiratory failure by E. Campbell: “respiratory failure is characterized by a decrease in PaO2 below 60 mm Hg. st ... ". However, as already noted, this definition refers to decompensated respiratory failure, manifested by a large number of clinical and instrumental signs. Indeed, a decrease in PaO2 below 60 mm Hg. Art., as a rule, indicates severe decompensated respiratory failure, and is accompanied by shortness of breath at rest, an increase in the number of respiratory movements up to 24-30 per minute, cyanosis, tachycardia, significant pressure of the respiratory muscles, etc. Neurological disorders and signs of hypoxia in other organs usually develop when PaO2 is below 40-45 mm Hg. Art.

PaO2 from 80 to 61 mm Hg. Art., especially against the background of acute or chronic damage to the lungs and the respiratory apparatus, should be regarded as the initial manifestation of arterial hypoxemia. In most cases, it indicates the formation of mild compensated respiratory failure. Reducing PaO 2 below 60 mm Hg. Art. indicates moderate or severe precompensated respiratory failure, clinical manifestations which are clearly expressed.

Normally, the pressure of CO2 in arterial blood (PaCO 2) is 35-45 mm Hg. Hypercapia is diagnosed when PaCO2 rises above 45 mm Hg. Art. PaCO2 values are greater than 50 mm Hg. Art. usually correspond to the clinical picture of severe ventilation (or mixed) respiratory failure, and above 60 mm Hg. Art. - serve as an indication for mechanical ventilation, aimed at restoring the minute volume of breathing.

Diagnostics various forms respiratory failure (ventilation, parenchymal, etc.) is based on the results comprehensive examination patients - the clinical picture of the disease, the results of determining the function of external respiration, radiography of the chest, laboratory tests, including the assessment of the gas composition of the blood.

Above, some features of the change in PaO 2 and PaCO 2 in ventilation and parenchymal respiratory failure have already been noted. Recall that for ventilation respiratory failure, in which the process of releasing CO 2 from the body is disturbed in the lungs, hypercapnia is characteristic (PaCO 2 is more than 45-50 mm Hg), often accompanied by compensated or decompensated respiratory acidosis. At the same time, progressive hypoventilation of the alveoli naturally leads to a decrease in the oxygenation of the alveolar air and the pressure of O 2 in arterial blood (PaO 2), resulting in the development of hypoxemia. Thus, a detailed picture of ventilation respiratory failure is accompanied by both hypercapnia and increasing hypoxemia.

The early stages of parenchymal respiratory failure are characterized by a decrease in PaO 2 (hypoxemia), in most cases combined with severe hyperventilation of the alveoli (tachypnea) and developing in connection with this hypocapnia and respiratory alkalosis. If this condition cannot be stopped, signs of a progressive total decrease in ventilation, minute respiratory volume and hypercapnia gradually appear (PaCO 2 is more than 45-50 mm Hg). This indicates the accession of ventilation respiratory failure due to fatigue of the respiratory muscles, a pronounced obstruction of the airways, or a critical drop in the volume of functioning alveoli. Thus, the later stages of parenchymal respiratory failure are characterized by a progressive decrease in PaO 2 (hypoxemia) in combination with hypercapnia.

Depending on the individual characteristics of the development of the disease and the predominance of certain pathophysiological mechanisms of respiratory failure, other combinations of hypoxemia and hypercapnia are possible, which are discussed in subsequent chapters.

Acid-base disorders

In most cases for accurate diagnosis respiratory and non-respiratory acidosis and alkalosis, as well as to assess the degree of compensation for these disorders, it is quite enough to determine blood pH, pCO2, BE and SB.

During the period of decompensation, a decrease in blood pH is observed, and in alkalosis, it is quite simple to determine the values of the acid-base state: with acidego, an increase. It is also easy to determine the respiratory and non-respiratory types of these disorders by laboratory parameters: changes in pCO 2 and BE in each of these two types are multidirectional.

The situation is more complicated with the assessment of the parameters of the acid-base state during the period of compensation for its violations, when the pH of the blood is not changed. Thus, a decrease in pCO 2 and BE can be observed both in non-respiratory (metabolic) acidosis and in respiratory alkalosis. In these cases, an assessment of the overall clinical situation helps to understand whether the corresponding changes in pCO 2 or BE are primary or secondary (compensatory).

Compensated respiratory alkalosis is characterized by a primary increase in PaCO2, which is essentially the cause of this acid-base disorder; in these cases, the corresponding changes in BE are secondary, that is, they reflect the inclusion of various compensatory mechanisms aimed at reducing the concentration of bases. On the contrary, for compensated metabolic acidosis, changes in BE are primary, and shifts in pCO2 reflect compensatory hyperventilation of the lungs (if it is possible).

Thus, comparison of the parameters of acid-base disorders with the clinical picture of the disease in most cases makes it possible to reliably diagnose the nature of these disorders even during the period of their compensation. Establishing the correct diagnosis in these cases can also help evaluate changes in the electrolyte composition of the blood. In respiratory and metabolic acidosis, hypernatremia (or normal concentration of Na +) and hyperkalemia are often observed, and in respiratory alkalosis, hypo- (or normo) natremia and hypokalemia

Pulse oximetry

The supply of oxygen to peripheral organs and tissues depends not only on the absolute values of D2 pressure in arterial blood, but also on the ability of hemoglobin to bind oxygen in the lungs and release it in the tissues. This ability is described by an S-shaped oxyhemoglobin dissociation curve. The biological meaning of this shape of the dissociation curve is that the region of high values of O2 pressure corresponds to the horizontal section of this curve. Therefore, even with fluctuations in oxygen pressure in arterial blood from 95 to 60-70 mm Hg. Art. saturation (saturation) of hemoglobin with oxygen (SaO 2) remains at a sufficiently high level. Yes, healthy young man at PaO 2 \u003d 95 mm Hg. Art. saturation of hemoglobin with oxygen is 97%, and at PaO 2 = 60 mm Hg. Art. - 90%. The steep slope of the middle section of the oxyhemoglobin dissociation curve indicates a very favorable conditions to provide oxygen to the tissues.

Under the influence of certain factors (temperature increase, hypercapnia, acidosis), the dissociation curve shifts to the right, which indicates a decrease in the affinity of hemoglobin for oxygen and the possibility of its easier release in tissues. the same level requires more PaO 2 .

The shift of the oxyhemoglobin dissociation curve to the left indicates an increased affinity of hemoglobin for O 2 and its lower release in tissues. This shift occurs under the action of hypocapnia, alkalosis and lower temperatures. In these cases, a high saturation of hemoglobin with oxygen is maintained even at lower values of PaO 2

Thus, the value of saturation of hemoglobin with oxygen in respiratory failure acquires to characterize the provision of peripheral tissues with oxygen independent meaning. The most common non-invasive method for determining this indicator is pulse oximetry.

Modern pulse oximeters contain a microprocessor connected to a sensor containing a light emitting diode and a light sensitive sensor located opposite the light emitting diode). Usually 2 wavelengths of radiation are used: 660 nm (red light) and 940 nm (infrared). Oxygen saturation is determined by the absorption of red and infrared light, respectively, by reduced hemoglobin (Hb) and oxyhemoglobin (HbJ 2 ). The result is displayed as SaO2 (saturation obtained from pulse oximetry).

Normal oxygen saturation is over 90%. This indicator decreases with hypoxemia and a decrease in PaO 2 less than 60 mm Hg. Art.

When evaluating the results of pulse oximetry, one should bear in mind a rather large error of the method, reaching ± 4-5%. It should also be remembered that the results of an indirect determination of oxygen saturation depend on many other factors. For example, from the presence on the nails of the examined varnish. The varnish absorbs part of the radiation from the anode with a wavelength of 660 nm, thereby underestimating the values of the SaO 2 index.

The readings of the pulse oximeter are affected by a shift in the hemoglobin dissociation curve that occurs under the influence of various factors (temperature, blood pH, PaCO2 level), skin pigmentation, anemia at a hemoglobin level below 50-60 g/l, etc. For example, small pH fluctuations lead to significant changes indicator SaO2, with alkalosis (for example, respiratory, developed against the background of hyperventilation), SaO2 is overestimated, with acidosis - underestimated.

In addition, this technique does not allow taking into account the appearance in the peripheral blood of pathological varieties of hemoglobin - carboxyhemoglobin and methemoglobin, which absorb light of the same wavelength as oxyhemoglobin, which leads to an overestimation of SaO2 values.

Nevertheless, at present, pulse oximetry is widely used in clinical practice, in particular, in intensive care units and intensive care units for simple approximate dynamic monitoring of the state of hemoglobin saturation with oxygen.

Assessment of hemodynamic parameters

For a complete analysis of the clinical situation in acute respiratory failure, it is necessary to dynamically determine a number of hemodynamic parameters:

blood pressure;
heart rate (HR);
central venous pressure (CVP);
pulmonary artery wedge pressure (PWP);
cardiac output;
ECG monitoring (including for the timely detection of arrhythmias).

Many of these parameters (BP, heart rate, SaO2, ECG, etc.) make it possible to determine modern monitoring equipment in intensive care and resuscitation departments. In severely ill patients, it is advisable to catheterize the right heart with the installation of a temporary floating intracardiac catheter to determine CVP and PLA.

Respiratory failure is a pathology that complicates the course of most diseases of internal organs, as well as conditions caused by structural and functional changes in the chest. To maintain gas homeostasis, the respiratory section of the lungs, airways and chest must work in a stressful mode.

External respiration provides oxygen to the body and removal of carbon dioxide. When this function is disturbed, the heart begins to beat hard, the number of red blood cells in the blood increases, and the level of hemoglobin rises. Strengthened work of the heart is the most important element of compensation for insufficiency of external respiration.

In the later stages of respiratory failure, compensatory mechanisms fail, the functional capabilities of the body decrease, and decompensation develops.

Etiology

Pulmonary causes include a disorder in the processes of gas exchange, ventilation and perfusion in the lungs. They develop with lobar, lung abscesses, cystic fibrosis, alveolitis, hemothorax, hydrothorax, water aspiration during drowning, traumatic chest injury, silicosis, anthracosis, congenital malformations of the lungs, chest deformities.

Extrapulmonary causes include:

Alveolar hypoventilation and bronchial obstruction are the main pathological processes of respiratory failure.

At the initial stages of the disease, compensation reactions are activated, which eliminate hypoxia and the patient feels satisfactory. With severe disorders and changes in the gas composition of the blood, these mechanisms do not cope, which leads to the development of characteristic clinical signs, and in the future - severe complications.

Symptoms

Respiratory failure is acute and chronic. The acute form of pathology occurs suddenly, develops rapidly and poses a threat to the life of the patient.

In primary insufficiency, the structures of the respiratory tract and the respiratory organs are directly affected. Its reasons are:

Pain with fractures and other injuries of the sternum and ribs,
Bronchial obstruction with inflammation of the small bronchi, compression of the respiratory tract by a neoplasm,
Hypoventilation and lung dysfunction
Damage to the respiratory centers in the cerebral cortex - TBI, drug or drug poisoning,
Respiratory muscle damage.

Secondary respiratory failure is characterized by damage to organs and systems that are not part of the respiratory complex:

blood loss
Thrombosis of large arteries,
Traumatic shock,
intestinal obstruction,
Accumulation of purulent discharge or exudate in the pleural cavity.

Acute respiratory failure is manifested by rather vivid symptoms. Patients complain of a feeling of lack of air, shortness of breath, difficulty inhaling and exhaling. These symptoms appear before the others. Tachypnea usually develops - rapid breathing, which is almost always accompanied by respiratory discomfort. The respiratory muscles are overstrained, it requires a lot of energy and oxygen to work.

With an increase in respiratory failure, patients become excited, restless, euphoric. They cease to critically assess their condition and the environment. Symptoms of "respiratory discomfort" appear - whistling, remote wheezing, breathing is weakened, tympanitis in the lungs. The skin becomes pale, tachycardia and diffuse cyanosis develop, the wings of the nose swell.

In severe cases, the skin turns grayish and becomes sticky and moist. As the disease develops, arterial hypertension is replaced by hypotension, consciousness is depressed, coma and multiple organ failure develop: anuria, stomach ulcer, intestinal paresis, kidney and liver dysfunction.

The main symptoms of the chronic form of the disease:

Shortness of breath of various origins;
Increased breathing - tachypnea;
Cyanosis of the skin - cyanosis;
Strengthened work of the respiratory muscles;
compensatory tachycardia,
Secondary erythrocytosis;
Edema and arterial hypertension in the later stages.

Palpation is determined by the tension of the muscles of the neck, contraction of the abdominal muscles on exhalation. In severe cases, paradoxical breathing is revealed: on inspiration, the stomach is pulled inward, and on exhalation it moves outward.

In children, pathology develops much faster than in adults due to a number of anatomical and physiological features of the child's body. Babies are more prone to swelling of the mucous membrane, the lumen of their bronchi is rather narrow, the process of secretion is accelerated, the respiratory muscles are weak, the diaphragm is high, breathing is more shallow, and the metabolism is very intense.

These factors contribute to the violation of respiratory patency and pulmonary ventilation.

Children usually develop an upper obstructive type of respiratory failure, which complicates the course, paratonsillar abscess, false croup, acute epiglotitis, pharyngitis, and. The timbre of the voice changes in the child, and "stenotic" breathing appears.

The degree of development of respiratory failure:

First- difficult breathing and restlessness of the child, hoarse, "cock" voice, tachycardia, perioral, intermittent cyanosis, aggravated by anxiety and disappearing when breathing oxygen.
Second- noisy breathing that can be heard from a distance, sweating, constant cyanosis on a pale background, disappearing in an oxygen tent, coughing, hoarseness, retraction of the intercostal spaces, pallor of the nail beds, lethargic, adynamic behavior.
Third- severe shortness of breath, total cyanosis, acrocyanosis, marbling, pallor of the skin, drop in blood pressure, suppressed reaction to pain, noisy, paradoxical breathing, weakness, weakening of heart sounds, acidosis, muscle hypotension.
Fourth the stage is terminal and is manifested by the development of encephalopathy, asystole, asphyxia, bradycardia, seizures, coma.

Development lung failure in newborns, it is due to an incompletely mature surfactant system of the lungs, vascular spasms, aspiration of amniotic fluid with primordial feces, and congenital anomalies in the development of the respiratory system.

Complications

Respiratory failure is a severe pathology requiring urgent therapy. The acute form of the disease is difficult to treat, leads to the development dangerous complications and even death.

Acute respiratory failure is a life-threatening pathology that leads to the death of the patient without timely medical care.

Diagnostics

Diagnosis of respiratory failure begins with the study of the patient's complaints, the collection of an anamnesis of life and illness, and the clarification of comorbidities. Then the specialist proceeds to examine the patient, paying attention to the cyanosis of the skin, rapid breathing, retraction of the intercostal spaces, listens to the lungs with a phonendoscope.

To assess the ventilation capacity of the lungs and the function of external respiration, functional tests are carried out, during which the vital capacity of the lungs, the peak volumetric forced expiratory flow rate, and the minute respiratory volume are measured. To assess the work of the respiratory muscles, measure the inspiratory and expiratory pressure in the oral cavity.

Laboratory diagnostics includes the study of acid-base balance and blood gases.

Additional research methods include radiography and magnetic resonance imaging.

Treatment

Acute respiratory failure develops suddenly and rapidly, therefore you need to know how to provide emergency first aid.

The patient is laid on the right side, the chest is freed from tight clothing. To prevent the tongue from sinking, the head is thrown back, and the lower jaw is pushed forward. Then foreign bodies and sputum are removed from the pharynx using a gauze pad at home or an aspirator in a hospital.

It is necessary to call an ambulance team, since further treatment is possible only in the intensive care unit.

Video: first aid for acute respiratory failure

Treatment chronic pathology It is aimed at restoring pulmonary ventilation and gas exchange in the lungs, delivering oxygen to organs and tissues, pain relief, as well as eliminating the diseases that caused this emergency.

The following therapeutic methods will help restore pulmonary ventilation and airway patency:

After the restoration of respiratory patency, they proceed to symptomatic therapy.

Thanks

The site provides reference information for informational purposes only. Diagnosis and treatment of diseases should be carried out under the supervision of a specialist. All drugs have contraindications. Expert advice is required!

What is respiratory failure?

The pathological condition of the body, in which gas exchange in the lungs is disturbed, is called respiratory failure. As a result of these disorders, the level of oxygen in the blood is significantly reduced and the level of carbon dioxide is increased. Due to insufficient supply of tissues with oxygen, hypoxia or oxygen starvation develops in organs (including the brain and heart).

The normal gas composition of the blood in the initial stages of respiratory failure can be ensured by compensatory reactions. The functions of the respiratory organs and the functions of the heart are closely related. Therefore, when gas exchange in the lungs is disturbed, the heart begins to work hard, which is one of the compensatory mechanisms that develop during hypoxia.

Compensatory reactions also include an increase in the number of red blood cells and an increase in the level of hemoglobin, an increase in the minute volume of blood circulation. With a severe degree of respiratory failure, compensatory reactions are not enough to normalize gas exchange and eliminate hypoxia, the stage of decompensation develops.

Classification of respiratory failure

There are a number of classifications of respiratory failure according to its various features.

According to the mechanism of development

1. hypoxemic or parenchymal pulmonary insufficiency (or type I respiratory failure). It is characterized by a decrease in the level and partial pressure of oxygen in the arterial blood (hypoxemia). Oxygen therapy is difficult to eliminate. Most often occurs in pneumonia, pulmonary edema, respiratory distress syndrome.
2. Hypercapnic , ventilation (or pulmonary insufficiency type II). At the same time, the content and partial pressure of carbon dioxide are increased in the arterial blood (hypercapnia). The oxygen level is low, but this hypoxemia is well treated with oxygen therapy. It develops with weakness and defects of the respiratory muscles and ribs, with violations of the function of the respiratory center.

Due to the occurrence

obstructive respiratory failure: this type of respiratory failure develops when there are obstructions in the airways for the passage of air due to their spasm, narrowing, squeezing or entry foreign body. In this case, the function of the respiratory apparatus is disturbed: the respiratory rate decreases. The natural narrowing of the lumen of the bronchi during exhalation is supplemented by obstruction due to the obstacle, so exhalation is especially difficult. The cause of obstruction can be: bronchospasm, edema (allergic or inflammatory), blockage of the bronchial lumen with sputum, destruction of the bronchial wall or its sclerosis.
Restrictive respiratory failure (restrictive): this type of lung failure occurs when there are restrictions on the expansion and collapse of lung tissue as a result of effusion into the pleural cavity, the presence of air in the pleural cavity, adhesive process, kyphoscoliosis (curvature of the spine). Respiratory failure develops due to limitation of the depth of inspiration.
Combined or mixed pulmonary insufficiency is characterized by the presence of signs of both obstructive and restrictive respiratory failure with a predominance of one of them. It develops with prolonged pulmonary heart diseases.
Hemodynamic respiratory failure develops with circulatory disorders that block ventilation of the lung area (for example, with pulmonary embolism). This type of pulmonary insufficiency can also develop with heart defects, when arterial and deoxygenated blood is mixed.
diffuse type respiratory failure occurs when the pathological thickening of the capillary-alveolar membrane in the lungs, which leads to a violation of gas exchange.

According to the gas composition of the blood

1. Compensated (normal performance blood gases).
2. Decompensated (hypercapnia or hypoxemia of arterial blood).

According to the course of the disease

According to the course of the disease, or according to the rate of development of the symptoms of the disease, acute and chronic respiratory failure are distinguished.

By severity

There are 4 degrees of severity of acute respiratory failure:

I degree of acute respiratory failure: shortness of breath with difficulty inhaling or exhaling, depending on the level of obstruction and increased heart rate, increased blood pressure.
II degree: breathing is carried out with the help of auxiliary muscles; there is a diffuse cyanosis, marbling of the skin. There may be convulsions and blackouts of consciousness.
III degree: severe shortness of breath alternates with periodic stops in breathing and a decrease in the number of breaths; cyanosis of the lips are noted at rest.
IV degree - hypoxic coma: rare, convulsive breathing, generalized cyanosis of the skin, a critical decrease in blood pressure, depression of the respiratory center up to respiratory arrest.

There are 3 degrees of severity of chronic respiratory failure:

I degree of chronic respiratory failure: shortness of breath occurs with significant physical exertion.
II degree of respiratory failure: shortness of breath is noted with little physical exertion; at rest, compensatory mechanisms are activated.
III degree of respiratory failure: shortness of breath and cyanosis of the lips are noted at rest.

Reasons for the development of respiratory failure

Respiratory failure can be caused different reasons when exposed to the respiratory process or the lungs:

obstruction or narrowing of the airways that occurs with bronchiectasis, chronic bronchitis, bronchial asthma, cystic fibrosis, pulmonary emphysema, laryngeal edema, aspiration and foreign body in the bronchi;
lung tissue damage in pulmonary fibrosis, alveolitis (inflammation of the lung alveoli) with the development of fibrous processes, distress syndrome, malignant tumor, radiation therapy, burns, lung abscess, drug effects on the lung;
violation of blood flow in the lungs (with pulmonary embolism), which reduces the flow of oxygen into the blood;
congenital heart defects (non-closure of the oval window) - venous blood, bypassing the lungs, goes directly to the organs;
muscle weakness (with poliomyelitis, polymyositis, myasthenia gravis, muscular dystrophy, spinal cord injury);
weakening of breathing (with an overdose of drugs and alcohol, with respiratory arrest during sleep, with obesity);
anomalies of the rib cage and spine (kyphoscoliosis, chest injury);
anemia, massive blood loss;
defeat of the central nervous system;
increase in blood pressure in the pulmonary circulation.

The pathogenesis of respiratory failure

Lung function can be roughly divided into 3 main processes: ventilation, pulmonary blood flow and gas diffusion. Deviations from the norm in any of them inevitably lead to respiratory failure. But the significance and consequences of violations in these processes are different.

Often, respiratory failure develops when ventilation is reduced, resulting in an excess of carbon dioxide (hypercapnia) and a lack of oxygen (hypoxemia) in the blood. Carbon dioxide has a large diffusion (penetrating) ability, therefore, in violation of pulmonary diffusion, hypercapnia rarely occurs, more often they are accompanied by hypoxemia. But diffusion disturbances are rare.

An isolated violation of ventilation in the lungs is possible, but most often there are combined disorders based on violations of the uniformity of blood flow and ventilation. Thus, respiratory failure is the result of pathological changes in the ventilation/blood flow ratio.

Violation in the direction of increasing this ratio leads to an increase in physiologically dead space in the lungs (areas of lung tissue that do not perform their functions, for example, in severe pneumonia) and the accumulation of carbon dioxide (hypercapnia). A decrease in the ratio causes an increase in bypass or anastomoses of vessels (additional blood flow) in the lungs, resulting in a decrease in blood oxygen (hypoxemia). The resulting hypoxemia may not be accompanied by hypercapnia, but hypercapnia usually leads to hypoxemia.

Thus, the mechanisms of respiratory failure are 2 types of gas exchange disorders - hypercapnia and hypoxemia.

Diagnostics

To diagnose respiratory failure, the following methods are used:

Questioning the patient about past and concomitant chronic diseases. This may help set possible cause development of respiratory failure.
Examination of the patient includes: counting the respiratory rate, participation in breathing of the auxiliary muscles, identifying the cyanotic color of the skin in the area of the nasolabial triangle and nail phalanxes, listening to the chest.
Holding functional tests: spirometry (determination of vital capacity of the lungs and minute breathing volume using a spirometer), peak flowmetry (determination top speed movement of air during forced exhalation after a maximum inspiration using a peak flow meter device).
Analysis of the gas composition of arterial blood.
X-ray of the chest organs - to detect damage to the lungs, bronchi, traumatic injuries of the rib cage and defects of the spine.

Symptoms of respiratory failure

Symptoms of respiratory failure depend not only on the cause of its occurrence, but also on the type and severity. The classic manifestations of respiratory failure are:

signs of hypoxemia (decreased oxygen levels in arterial blood);
signs of hypercapnia (increased levels of carbon dioxide in the blood);
dyspnea;
syndrome of weakness and fatigue of the respiratory muscles.

hypoxemia manifested by cyanosis (cyanosis) of the skin, the severity of which corresponds to the severity of respiratory failure. Cyanosis appears at a reduced partial pressure of oxygen (below 60 mm Hg). At the same time, there is also an increase in heart rate and a moderate decrease in blood pressure. With a further decrease in the partial pressure of oxygen, memory impairment is noted, if it is below 30 mm Hg. Art., then the patient has a loss of consciousness. As a result of hypoxia, dysfunctions of various organs develop.

Hypercapnia manifested by increased heart rate and sleep disturbance (drowsiness during the day and insomnia at night), headache and nausea. The body tries to get rid of excess carbon dioxide with the help of deep and frequent breathing, but even this is ineffective. If the level of partial pressure of carbon dioxide in the blood rises rapidly, then an increase in cerebral circulation and an increase in intracranial pressure can lead to cerebral edema and the development of hypocapnic coma.

When the first signs of respiratory disorders appear in a newborn, they begin to carry out (providing control of the gas composition of the blood) oxygen therapy. For this, an incubator, a mask and a nasal catheter are used. With a severe degree of respiratory disorders and the ineffectiveness of oxygen therapy, an artificial lung ventilation apparatus is connected.

In the complex of therapeutic measures, intravenous administration of the necessary medicines and surfactant preparations (Curosurf, Exosurf) are used.

In order to prevent the syndrome of respiratory disorders in a newborn with the threat of premature birth, pregnant women are prescribed glucocorticosteroid drugs.

Treatment

Treatment of Acute Respiratory Failure (Emergency Care)

The volume of emergency care in case of acute respiratory failure depends on the form and degree of respiratory failure and the cause that caused it. Urgent care aims to eliminate the cause of emergency, restoration of gas exchange in the lungs, anesthesia (for injuries), prevention of infection.

In case of I degree of insufficiency, it is necessary to free the patient from restrictive clothing, to provide access to fresh air.
At the II degree of insufficiency, it is necessary to restore the patency of the respiratory tract. To do this, you can use drainage (lay to bed with a raised leg end, lightly beat on the chest when exhaling), eliminate bronchospasm (intramuscularly or intravenously injected Euphyllin solution). But Eufillin is contraindicated in low blood pressure and a pronounced increase in heart rate.
To liquefy sputum, thinning and expectorants are used in the form of inhalation or medicine. If it was not possible to achieve the effect, then the contents of the upper respiratory tract are removed using an electric suction (the catheter is inserted through the nose or mouth).
If it was still not possible to restore breathing, artificial ventilation of the lungs is used by a non-apparatus method (mouth-to-mouth or mouth-to-nose breathing) or with the help of an artificial respiration apparatus.
When spontaneous breathing is restored, intensive oxygen therapy and the introduction of gas mixtures (hyperventilation) are carried out. For oxygen therapy, a nasal catheter, mask, or oxygen tent is used.
Improving the patency of the airways can also be achieved with the help of aerosol therapy: they carry out warm alkaline inhalations, inhalations with proteolytic enzymes (chymotrypsin and trypsin), bronchodilators (Izadrin, Novodrin, Euspiran, Alupen, Salbutamol). If necessary, antibiotics can also be administered in the form of inhalations.
With symptoms of pulmonary edema, a semi-sitting position of the patient is created with legs down or with the head end of the bed raised. At the same time, the appointment of diuretics is used (Furosemide, Lasix, Uregit). In the case of a combination of pulmonary edema with arterial hypertension, Pentamine or Benzohexonium is administered intravenously.
With severe spasm of the larynx, muscle relaxants (Ditilin) are used.
To eliminate hypoxia, sodium oxybutyrate, Sibazon, Riboflavin are prescribed.
For traumatic lesions of the chest, non-narcotic and narcotic analgesics are used (Analgin, Novocain, Promedol, Omnopon, Sodium hydroxybutyrate, Fentanyl with Droperidol).
To eliminate metabolic acidosis (accumulation of underoxidized metabolic products) use intravenous administration Sodium bicarbonate and Trisamine.
ensuring the patency of the airways;
ensuring a normal supply of oxygen.

In most cases, it is almost impossible to eliminate the cause of chronic respiratory failure. But it is possible to take measures to prevent exacerbations of a chronic disease of the bronchopulmonary system. In severe cases, lung transplantation is used.

To maintain the patency of the airways, drugs are used (dilating the bronchi and thinning sputum) and the so-called respiratory therapy, which includes various methods: postural drainage, sputum suction, breathing exercises.

The choice of method of respiratory therapy depends on the nature of the underlying disease and the patient's condition:

For postural massage, the patient assumes a sitting position with an emphasis on the hands and leaning forward. The assistant gives a pat on the back. This procedure can be carried out at home. You can also use a mechanical vibrator.
With increased sputum formation (with bronchiectasis, lung abscess or cystic fibrosis), you can also use the "cough therapy" method: after 1 calm exhalation, 1-2 forced exhalations should be made, followed by relaxation. Such methods are acceptable for elderly patients or in the postoperative period.
In some cases, it is necessary to resort to suction of sputum from the respiratory tract with the connection of an electric suction (using a plastic tube inserted through the mouth or nose into the respiratory tract). In this way, sputum is also removed with a tracheostomy tube in a patient.
Respiratory gymnastics should be practiced in chronic obstructive diseases. To do this, you can use the device "incentive spirometer" or intensive breathing exercises of the patient himself. The method of breathing with half-closed lips is also used. This method increases the pressure in the airways and prevents them from collapsing.
To ensure normal partial pressure of oxygen, oxygen therapy is used - one of the main methods of treating respiratory failure. There are no contraindications to oxygen therapy. Nasal cannulas and masks are used to administer oxygen.
Of the medicines, Almitrin is used - the only medicine capable of improving the partial pressure of oxygen for a long time.
In some cases, seriously ill patients need to be connected to a ventilator. The device itself supplies air to the lungs, and exhalation is performed passively. This saves the patient's life when he cannot breathe on his own.
Mandatory in the treatment is the impact on the underlying disease. In order to suppress the infection, antibiotics are used in accordance with the sensitivity of the bacterial flora isolated from the sputum.
Corticosteroid drugs for long-term use are used in patients with autoimmune processes, with bronchial asthma.

When prescribing treatment, one should take into account the performance of the cardiovascular system, control the amount of fluid consumed, and, if necessary, use drugs to normalize blood pressure. With the complication of respiratory failure in the form of the development of cor pulmonale, diuretics are used. By prescribing sedatives, a doctor can reduce oxygen requirements.

Acute respiratory failure: what to do if a foreign body enters the child's airways - video

How to properly perform artificial ventilation of the lungs with respiratory failure - video

Before use, you should consult with a specialist.

Respiratory failure- this is a pathological condition of the body, in which the maintenance of the normal gas composition of arterial blood is not ensured, or it is achieved due to such work of the external respiration apparatus, which reduces the functionality of the body. The term "respiratory failure" is synonymous with "lack of external respiration". The term "respiratory failure" is physiologically more justified, since it covers the occurrence of secondary pathological and compensatory changes in the respiratory system in case of damage to the pulmonary link. From the same point of view, it is inappropriate to equate the concepts of "respiratory failure" and "pulmonary failure". Lung failure is caused by a pathological process in them and is characterized not only by the occurrence of respiratory failure, but also by a violation of other functions - immunity, acid-base balance, water-salt metabolism, prostaglandin synthesis, metabolite release, homeostasis regulation, etc.

Respiratory failure can occur during various pathological processes in the body, and in pulmonary pathology it is the main clinical and pathophysiological syndrome.

Pathogenesis respiratory failure in lung disease is most often caused by a violation of the function of the external respiration apparatus. The main pathophysiological mechanisms for the development of respiratory failure are: a) violations of the processes of ventilation of the alveoli, b) changes in the diffusion of molecular oxygen and carbon dioxide through the alveolocapillary membrane, c) impaired perfusion, i.e. blood flow through the pulmonary capillaries.

Violations of ventilation of the alveoli can be caused by disorders in the function of individual links of the external respiration apparatus - centrogenous (respiratory center of the brain), neuromuscular (motor neurons of the spinal cord, peripheral motor and sensory nerves, respiratory muscles), thoraco-diaphragmatic (thorax, diaphragm and pleura) and bronchopulmonary (lungs and airways).

The function of the respiratory center can be impaired due to direct action on the central nervous system of various pathogenic factors or reflexively. Pathogenic factors that cause depression of the respiratory center are drugs and barbiturates, metabolic products that linger in the blood (for example, carbon dioxide or underoxidized organic acids), stroke or any other vascular catastrophe in the brain, neurological diseases or increased intracranial pressure. With violations of the functions of the respiratory center, respiratory failure develops due to a decrease in the depth and frequency of breathing, disorders of its rhythm (various types of periodic breathing - Cheyne-Stokes breathing, Biot).

The function of motor neurons of the spinal cord, which innervates the respiratory muscles, can be impaired during the development of a tumor in the spinal cord, with poliomyelitis. The nature and degree of disturbance of external respiration in this case depend on the site of damage to the spinal cord (for example, if the pathological process affects the cervical part of the spinal cord, the work of the diaphragm is disrupted) and on the number of affected motor neurons.

Violation of ventilation can occur when the nerves innervating the respiratory muscles are damaged (inflammation, beriberi, trauma), with partial or complete paralysis of the muscles (as a result of the use of relaxants, tetanus, botulism, hypokalemia, poisoning with curare-like poisons, etc.), with a violation of the function of the muscles themselves respiratory muscles (myositis, dystrophy).

The function of the thoraco-diaphragmatic link of the external respiration apparatus can be impaired in the following cases: 1) due to pathology of the chest (congenital or acquired deformity of the ribs and spinal column, for example, fracture of the ribs, kyphoscoliosis, Bechterew's disease, ossification of the costal cartilages, etc.) , 2) with a high standing of the diaphragm (paresis of the stomach and intestines, flatulence, ascites, obesity), 3) in the presence of pleural adhesions, 4) compression of the lung with effusion, as well as blood and air with hemo- and pneumothorax. Excursions of the chest can be limited to sharp pains that occur during breathing, for example, with intercostal neuralgia, inflammation of the pleura, etc.

Violations of the function of the bronchopulmonary link of the external respiration apparatus are caused by various pathological processes in the airways and lungs.

Alveolar ventilation disorders, depending on the mechanisms that cause these disorders, are divided into obstructive, restrictive and mixed.

Obstructive insufficiency of ventilation of the alveoli occurs due to narrowing of the airways lat., obstructio - an obstacle) and increase the resistance to air movement. With difficulty in the passage of air in the airways, not only the ventilation of the lungs is disturbed, but also the mechanics of breathing. Due to the difficulty of exhalation, the work of the respiratory muscles sharply increases. Decreased VC, FVC and MVL.

Obstructive disorders of alveolar ventilation are usually caused by bronchial spasm or their local damage (tumor in the bronchi, cicatricial stenosis, inflammatory or congestive swelling of the bronchial mucosa, hypersecretion of bronchial glands, etc.).

Restrictive type of violation of ventilation of the alveoli due to a decrease in the respiratory surface of the lungs or their extensibility (from lat., restrictio - restriction, reduction). The latter limits the ability of the lungs to expand. To compensate for this and achieve the desired change in lung volume, more than usual transpulmonary pressure must be generated during inspiration. This, in turn, increases the work done by the respiratory muscles. Breathing becomes difficult, especially during physical exertion, VC and MVL decrease.

A decrease in lung volume, manifested by a restrictive type of ventilation insufficiency, is observed in acute and chronic massive inflammatory processes and congestion in the lungs, in tuberculosis, pneumonia, chronic heart failure, exudative pleurisy, spontaneous pneumothorax, emphysema, massive obstacles to chest expansion (kyphoscoliosis ), compaction of interstitial tissue (pneumosclerosis), etc. Restrictive insufficiency of external respiration can be caused by the destruction of large areas of lung tissue by a tuberculous process, the removal of a segment, lobe of the lung or the whole lung, atelectasis.

The development of restrictive ventilation disorders is also facilitated by a change in the activity of the lung surfactant as a factor that reduces the surface tension of the fluid lining the inner surface of the alveoli. Insufficient activity of the surfactant leads to the collapse of the alveoli and the development of atelectasis, hindering the diffusion of oxygen.

Mixed type of violation of ventilation of the alveoli characterized by the presence of signs of both obstructive and restrictive ventilation disorders.

Violation of lung ventilation can be caused by uneven air flow into individual zones of the lung. In diseases, their healthy areas are filled faster than the affected ones. Gas is also removed from them faster during exhalation, therefore, with a subsequent inhalation, gas from the dead space of pathologically altered zones of the lungs can enter healthy areas.

A certain role in the pathogenesis of respiratory failure is played by the state of capillary blood flow in the pulmonary artery. Respiratory failure due to a decrease in lung perfusion (the flow of an appropriate amount of blood through the pulmonary capillaries) can lead to left and right ventricular heart failure (myocardial infarction, myocarditis, cardiosclerosis, exudative pericarditis, etc.), some congenital and acquired heart defects ( pulmonary stenosis, stenosis of the right atrioventricular orifice), vascular insufficiency, pulmonary embolism. Since, under these conditions, the minute volume of blood decreases and its movement in the vessels of the systemic circulation slows down, the tissues experience oxygen starvation, and there is a lack of oxygen and an excess of carbon dioxide in the blood.

Respiratory insufficiency is divided according to etiology into primary and secondary; according to the rate of formation of clinical and pathophysiological manifestations - into acute and chronic; by changes in the gas composition of the blood - into latent, partial and global.

Primary respiratory failure due to damage directly to the external respiratory apparatus, and secondary- pathology of other parts of the respiratory system (circulatory organs, blood, tissue respiration).

Acute respiratory failure- this is a special form of gas exchange disorder, in which the supply of oxygen to the blood and the removal of carbon dioxide from the blood are stopped, which often ends in asphyxia (cessation of breathing). In the development of acute respiratory failure, three stages are distinguished - initial, deep hypoxia and hypercapnic coma.

In the initial stage, carbon dioxide, rapidly accumulating in the body, excites the respiratory center, bringing the depth and frequency of breathing to the maximum possible values. In addition, respiration is reflexively stimulated by a decrease in molecular oxygen in the blood.

In the stage of deep hypoxia, the phenomena of hypoxia and hypercapnia increase. The heart rate increases, blood pressure rises. With a further increase in carbon dioxide in the blood, its narcotic effect begins to manifest itself (the stage of hypercapnic coma), blood pH decreases to 6.8 - 6.5. increased hypoxemia and, accordingly, hypoxia of the brain. This, in turn, depresses breathing, lowers blood pressure. The result is respiratory paralysis and cardiac arrest.

Causes of acute respiratory failure may include severe mechanical injury, compression syndrome, foreign body aspiration, upper airway obstruction, sudden bronchospasm (eg, severe choking or asthma in bronchial asthma), extensive atelectasis, inflammation, or pulmonary edema.

Chronic respiratory failure It is characterized by a gradual increase in gas exchange disorders and the tension of compensatory processes, which are manifested by hyperventilation and increased blood flow in the unaffected lung tissue. The timing of the development of chronic respiratory failure (months or years) and its stages depend, respectively, on the rate of aggravation and the degree of violations of alveolar ventilation, gas diffusion and perfusion. As chronic respiratory failure worsens, the work of the respiratory muscles at rest increases more and more, the volumetric blood flow rate and redistributive vascular reactions increase, aimed at increasing the amount of oxygen transported by arterial blood. Increases metabolism and the body's need for oxygen. As a result, there comes a moment when, even at rest, maintaining a normal blood gas composition becomes impossible. Then, with a decrease in the compensatory capabilities of the cardiovascular system and the blood system, tissue hypoxia, hypercapnia and gaseous acidosis develop.

In the development of chronic respiratory failure, three stages or degrees are distinguished: 1 - latent, latent, or compensated, 2 - pronounced, or subcompensated, and 3 - pulmonary-cardiac decompensation, or decompensated.

Depending on changes in the gas composition of the blood, latent, partial and global respiratory failure are distinguished. Latent respiratory failure is not accompanied by disturbance of the blood gas composition at rest, but compensation mechanisms are strained in patients. With partial respiratory failure, arterial hypoxemia or venous hypercapnia is noted. Global respiratory failure is characterized by arterial hypoxemia and venous hypercapnia.

Main clinical manifestations of respiratory insufficiency are shortness of breath and cyanosis, additional - anxiety, euphoria, sometimes drowsiness, lethargy, in severe cases - lack of consciousness, convulsions.

Shortness of breath (dyspnea) - a feeling of lack of air and the associated need to increase breathing. Objectively, shortness of breath is accompanied by a change in its frequency, depth and rhythm, as well as the ratio of the duration of inhalation and exhalation. The presence of a painful feeling of lack of air, which causes the patient not only involuntarily, but also consciously to increase the activity of respiratory movements, is the most significant difference between dyspnea and other types of respiratory dysregulation - polypnea, hyperpnea, etc.

Shortness of breath is caused by excitation of the inhalation center, which extends not only to the periphery to the respiratory muscles, but also to the overlying parts of the central nervous system, so it is often accompanied by a feeling of fear and anxiety, from which patients sometimes suffer more than shortness of breath itself.

Subjective sensations do not always coincide with its objective signs. So, in some cases, patients complain of a feeling of lack of air in the absence of objective signs of shortness of breath, i.e. occurs false sensation shortness of breath. On the other hand, there are cases when, in the presence of constant shortness of breath, the patient gets used to it and ceases to feel it, although there are all external manifestations of shortness of breath (the patient suffocates, often takes a breath when talking) and significant disturbances in the function of external respiration.

Inspiratory dyspnea, which is characterized by difficulty in inhaling, occurs when the lumen of the upper respiratory tract narrows (diphtheritic croup, laryngeal swelling, tracheal compression). At expiratory dyspnea difficulty exhaling, which can be observed during an attack of bronchial asthma. Mixed dyspnea is characterized by difficulty in both the inspiratory and expiratory phases and occurs in lung diseases accompanied by a decrease in the respiratory surface.

The second important clinical sign of respiratory failure is cyanosis - a bluish coloration of the skin and mucous membranes, due to a high content of reduced hemoglobin in the blood. Cyanosis is detected clinically only when the circulating blood contains more than 50 g / l of reduced hemoglobin (the norm is up to 30 g / l). In acute respiratory failure, cyanosis may develop within seconds or minutes; in chronic respiratory failure, cyanosis develops gradually. Cyanosis is more noticeable on the lips, face, fingers, and nails.

It is customary to distinguish between central and peripheral cyanosis. Respiratory failure is characterized by central cyanosis, which is characterized by diffuseness and an ash-gray skin tone. Due to increased blood flow, the skin is warm to the touch (“warm cyanosis”). Peripheral cyanosis is caused by a slowdown in blood flow in the tissues and is observed in diseases of the cardiovascular system. This cyanosis has the character of acrocyanosis - expressed on the hands and feet, on the earlobes, often has a reddish tint, the skin is cold to the touch ("cold cyanosis"). If, after 5 to 10 minutes of inhalation of pure oxygen, cyanosis disappears, this confirms the presence of peripheral cyanosis.

As you know, the respiratory function of the body is one of the main functions of the normal life of the body. The syndrome, in which the balance of blood components is disturbed, and to be more precise, the concentration of carbon dioxide greatly increases and the volume of oxygen decreases, is called "acute respiratory failure", it can also become chronic. How does the patient feel in this case, what symptoms may bother him, what signs and causes of this syndrome - read below. Also from our article you will learn about diagnostic methods and the most modern methods of treating this disease.

What are the characteristics of this disease?

Respiratory failure (RD) is a special condition in which the human body is when the respiratory organs cannot provide the necessary amount of oxygen for it. In this case, the concentration of carbon dioxide in the blood increases significantly and can reach a critical level. This syndrome is a kind of consequence of an inadequate exchange of carbon dioxide and oxygen between circulatory system and light. Note that chronic respiratory failure and acute may differ significantly in their manifestations.

Any respiratory disorders trigger compensatory mechanisms in the body, which for some time are able to restore the necessary balance and bring the composition of the blood closer to normal. If gas exchange in the lungs of a person is disturbed, then the first organ that begins to perform a compensatory function will be the heart. Later, the amount and overall level will increase in the human blood, which can also be considered a reaction of the body to hypoxia and oxygen starvation. The danger lies in the fact that the forces of the body are not infinite and sooner or later its resources are depleted, after which the person is faced with a manifestation of acute respiratory failure. The first symptoms begin to disturb the patient when the partial pressure of oxygen falls below 60 mm Hg, or the carbon dioxide index rises to 45 mm.

How does the disease manifest itself in children?

Respiratory failure in children often has the same causes as in adults, but the symptoms are usually milder. In newborns, this syndrome outwardly manifests itself as a respiratory disorder:

Most often, this pathology occurs in newborns who were born before the due date, or in those newborns who have had a difficult birth.
In premature babies, the cause of insufficiency is the underdevelopment of surfactant, a substance that lines the alveoli.
Also, the symptoms of DN can also appear in those newborns who experienced hypoxia during intrauterine life.
Respiratory dysfunction can also occur in those newborns who swallowed their meconium, swallowed amniotic fluid or blood.
Also, untimely suction of fluid from the respiratory tract often leads to DN in newborns.
Respiratory distress can often be caused by birth defects development of newborns. For example, underdeveloped lungs, polycystic lung disease, diaphragmatic hernia and others.

Most often, in newborn children, this pathology manifests itself in the form of aspiration, hemorrhagic and edematous syndrome, and pulmonary atelectasis is slightly less common. It is worth noting that acute respiratory failure is more common in newborns, and the sooner it is diagnosed, the greater the chance that the child will not develop chronic respiratory failure.

Causes of this syndrome

Often the cause of DN can be diseases and pathologies of other organs of the human body. It can develop due to infectious and inflammatory processes in the body, after severe injuries with damage to vital organs, with malignant tumors of the respiratory organs, as well as with violations of the respiratory muscles and heart. A person may also experience breathing problems due to restriction of chest movement. So, attacks of insufficiency of respiratory function can lead to:

Narrowing of the airways or obstruction, which are characteristic of bronchiectasis, laryngeal edema, and.
The process of aspiration, which is caused by the presence of a foreign object in the bronchi.
Damage to lung tissue due to such pathologies: inflammation of the alveoli of the lung, fibrosis, burns, lung abscess.
Violation of blood flow, often accompanies pulmonary embolism.
Complex heart defects, mainly. For example, if it did not close on time oval window, venous blood flows directly to the tissues and organs, without penetrating into the lungs.
General weakness of the body, decreased muscle tone. This state of the body can occur with the slightest damage to the spinal cord, as well as with muscle dystrophy, and polymyositis.
The weakening of breathing, which does not have a pathological nature, can be caused by excessive fullness of a person or bad habits- alcoholism, drug addiction, smoking.
Anomalies or injuries of the ribs and spine. They can occur with kyphoscoliosis or after a chest injury.
Often the cause of oppressed breathing can be a strong degree.
DN occurs after complex operations and severe injuries with profuse bleeding.
Various lesions of the central nervous system, both congenital and acquired.
Violation of the respiratory function of the body can be caused by a violation of pressure in the pulmonary circulation.
To bring down the usual rhythm of the transmission of impulses to the muscles involved in the breathing process, various infectious diseases, for example, .
Chronic imbalance of thyroid hormones can also serve as the cause of the development of this disease.

What are the symptoms of this disease?

On the primary signs This disease is also affected by the causes of its occurrence, as well as the specific type and severity. But any patient with respiratory failure will experience common symptoms of this syndrome:

hypoxemia;
hypercapnia;
dyspnea;
respiratory muscle weakness.

Each of the presented symptoms is a set of specific characteristics of the patient's condition, we will consider each in more detail.

hypoxemia

The main sign of hypoxemia is a low degree of saturation of arterial blood with oxygen. At the same time, a person’s skin can change color, they acquire a bluish tint. Cyanosis of the skin, or cyanosis, as this condition is called in another way, can be severe or mild, depending on how long and how strongly the signs of the disease in a person appear. Usually, the skin changes color after the partial pressure of oxygen in the blood reaches a critical level - 60 mm Hg. Art.

After overcoming this barrier, the patient may experience an increase in heart rate from time to time. There is also low blood pressure. The patient begins to forget the simplest things, and if the above figure reaches 30 mm Hg. Art., then a person most often loses consciousness, systems and organs can no longer work in the same mode. And the longer hypoxia lasts, the harder it will be for the body to restore its functions. This is especially true for brain activity.

Hypercapnia

In parallel with the lack of oxygen in the blood, the percentage of carbon dioxide begins to rise, this condition is called hypercapnia, it often accompanies chronic respiratory failure. The patient begins to experience problems with sleep, he cannot fall asleep for a long time or does not sleep all night long. At the same time, a person exhausted by insomnia feels overwhelmed all day and wants to sleep. This syndrome is accompanied by increased heart rate, the patient may feel sick, he experiences severe headaches.

Trying to save itself on its own, the human body tries to get rid of an excess of carbon dioxide, breathing becomes very frequent and deeper, but even this measure has no effect. At the same time, the decisive role in the development of the disease in this case is played by how quickly the carbon dioxide content in the blood grows. For the patient, a high growth rate is very dangerous, as this threatens with increased blood circulation in the brain and increased intracranial pressure. Without emergency treatment, these symptoms cause cerebral edema and a coma.

Dyspnea

When this symptom occurs, a person always seems to be short of breath. At the same time, it is very difficult for him to breathe, although he tries to increase his respiratory movements.

Weakness of the respiratory muscles

If the patient takes more than 25 breaths per minute, then his respiratory muscles are weakened, they are not able to perform their usual functions and get tired quickly. At the same time, a person tries with all his might to improve breathing and involves the muscles of the press, upper respiratory tract and even the neck in the process.

It is also worth noting that with a late degree of the disease, heart failure develops and various parts of the body swell.

Methods for diagnosing pulmonary insufficiency

To identify this disease, the doctor uses the following diagnostic methods:

The patient himself can best tell about the state of health and breathing problems, the task of the physician is to ask him in as much detail as possible about the symptoms, and also to study the medical history.
Also, the doctor should, at the first opportunity, find out the presence or absence of concomitant diseases in the patient, which can aggravate the course of DN.
At medical examination the doctor will pay attention to the condition of the chest, listen to the lungs with a phonendoscope and calculate the frequency heart rate and breathing.
The most important diagnostic point is the analysis of the gas composition of the blood, the indicator of saturation with oxygen and carbon dioxide is studied.
The acid-base parameters of the blood are also measured.
A chest x-ray is required.
The spirography method is used to assess the external characteristics of breathing.
In some cases, a consultation with a pulmonologist is necessary.

DN classification

This disease has several classifications depending on the characteristic feature. If we take into account the mechanism of the origin of the syndrome, then we can distinguish the following types:

Parenchymal respiratory failure, it is also called hypoxemic. This type has the following characteristics: the amount of oxygen decreases, the partial pressure of oxygen in the blood drops, this condition is difficult to correct even with oxygen therapy. Most often it is a consequence of pneumonia or distress syndrome.
Ventilatory or hypercapnic. With this type of disease in the blood, first of all, the content of carbon dioxide increases, while its saturation with oxygen decreases, but this can be easily corrected with the help of oxygen therapy. This type of DN is accompanied by weakness of the respiratory muscles, and mechanical defects of the ribs or chest are often observed.

As we noted earlier, most often this pathology can be a consequence of diseases of other organs, on the basis of etiology, the disease can be divided into the following types:

Obstructive DN implies obstructed air movement through the trachea and bronchi, it can be caused by bronchospasm, narrowing of the airways, the presence of a foreign body in the lungs or malignant tumor. With this type of disease, a person hardly takes a full breath, exhaling causes even greater difficulties.
The restrictive type is characterized by a limitation of the functions of the lung tissue in terms of expansion and contraction, a disease of this nature may be the result of pneumothorax, adhesions in the pleural cavity of the lung, and also if the movements of the rib frame are limited. As a rule, in such a situation, it is extremely difficult for the patient to inhale air.
The mixed type combines signs of both restrictive insufficiency and obstructive insufficiency, its symptoms most often manifest themselves with a late degree of pathology.
Hemodynamic DN may occur due to impaired air circulation in the absence of ventilation on separate area lung. Right-to-left shunting of blood, which is carried out through an open oval window in the heart, can lead to this type of disease. At this time, mixing of venous and arterial blood can occur.
Failure diffuse type occurs when the penetration of gases into the lung is impaired due to thickening of the capillary-alveolar membrane.

Depending on how long a person has been experiencing breathing problems and how quickly the signs of the disease develop, there are:

Acute deficiency affects the lungs of a person at a high speed, usually its attacks last no more than a few hours. Such a rapid development of pathology always causes hemodynamic disturbances and is very dangerous for the patient's life. With the manifestation of signs of this type, the patient needs a complex of resuscitation therapy, especially at those moments when other organs cease to perform a compensatory function. Most often it is observed in those who are experiencing an exacerbation of the chronic form of the disease.
Chronic respiratory failure worries a person for a long period of time, up to several years. Sometimes it is the result of an undertreated acute form. Chronic respiratory failure can accompany a person throughout life, weakening and intensifying from time to time.

In this disease, the gas composition of the blood is of great importance, depending on the ratio of its components, compensated and decompensated types are distinguished. In the first case, the composition is normal, in the second, hypoxemia or hypercapnia is observed. And the classification of respiratory failure according to the severity looks like this:

Grade 1 - sometimes the patient feels short of breath with strong physical activity;
Grade 2 - respiratory failure and shortness of breath appear even with light exertion, while compensatory functions of other organs are involved at rest;
Grade 3 - accompanied by severe shortness of breath and cyanosis of the skin at rest, characteristic hypoxemia.

Treatment of respiratory dysfunction

Treatment of acute respiratory failure includes two main tasks:

Restore normal ventilation of the lungs as much as possible and maintain it in this state.
Diagnose and, if possible, treat comorbidities that cause breathing problems.

If the doctor notices a pronounced hypoxia in a patient, then first of all he will prescribe him oxygen therapy, in which doctors carefully monitor the patient's condition and monitor the characteristics of the blood composition. If a person breathes on his own, then a special mask or nasal catheter is used for this procedure. The patient in a coma is intubated, which artificially ventilates the lungs. At the same time, the patient begins to take antibiotics, mucolytics, and bronchodilators. He is prescribed a number of procedures: chest massage, exercise therapy, inhalation using ultrasound. A bronchoscope is used to clear the bronchi.