Anatomical dead space is a part of the respiratory system in which there is no significant gas exchange. The anatomical dead space consists of air passages, namely the nasopharynx, trachea, bronchi and bronchioles up to their transition to the alveoli.

The volume of air filling them is called the volume of dead space (VD). The volume of dead space is variable and in adults is about 150-200 ml (2 ml/kg body weight). Gas exchange does not occur in this space, and these structures play a supporting role in warming, humidifying and purifying the inhaled air.

Functional dead space. Functional (physiological) dead space refers to those areas of the lungs in which gas exchange does not occur. Unlike the anatomical one, the functional dead space also includes alveoli, which are ventilated but not perfused with blood. Collectively, this is called alveolar dead space. In healthy lungs, the number of such alveoli is small, so the volumes of dead anatomical and physiological space differ little. However, in some disorders of pulmonary function, when the lungs are unevenly ventilated and perfused with blood, the volume of functional dead space may be significantly greater than the anatomical one. Thus, the functional dead space represents the sum of the anatomical and alveolar dead space: Tfunk. = Tanat. + Talveoli.

Dead space volume (VD) ratio. to the tidal volume (V^ is the dead space coefficient (VD/V^). Normally, dead space ventilation is 30% of the tidal volume and alveolar ventilation is about 70%. Thus, the dead space coefficient VD/VT = 0.3 When the dead space coefficient increases to 0.70.8, long-term spontaneous breathing is impossible, since respiratory work increases and CO2 accumulates in greater quantities than can be removed.

The recorded increase in the dead space coefficient indicates that in certain areas of the lung perfusion has practically ceased, but this area is still ventilated.

Dead space ventilation is estimated per minute and depends on the value of dead space (VD) and breathing frequency, increasing linearly with it. An increase in dead space ventilation can be compensated by an increase in tidal volume. What is important is the resulting volume of alveolar ventilation (VA), which actually enters the alveoli per minute and is involved in gas exchange. It can be calculated as follows: VA = (VT - VD)F, where VA is the volume of alveolar ventilation; VT - tidal volume; VD - volume of dead space; F - breathing frequency.

Functional dead space can be calculated using the following formula:

VDfunction = VT(1 - RMT CO2/ra CO2), where VT is tidal volume; RMT CO2 - CO2 content in exhaled air; paCO2 - partial pressure of CO2 in arterial blood.

To approximate the CO2 RMT value, the partial pressure of CO2 in the exhaled mixture can be used instead of the CO2 content in the exhaled air.

Tfunk. = VT(1 - pE CO2 /ra CO2,

where pECO2 is the partial pressure of CO2 at the end of expiration.

Example. If a patient weighing 75 kg has a respiratory rate of 12 per minute, a tidal volume of 500 ml, then the MOD is 6 l, of which dead space ventilation is 12,150 ml (2 ml/kg), i.e. 1800 ml. The dead space coefficient is 0.3. If such a patient has a respiratory rate of 20 per minute and a postoperative VT of 300 ml, then the minute respiratory volume will be 6 L, while dead space ventilation will increase to 3 L (20 150 ml). The dead space coefficient will be 0.5. With an increase in respiratory rate and a decrease in DO, dead space ventilation increases due to a decrease in alveolar ventilation. If tidal volume does not change, then an increase in respiratory rate leads to an increase breathing work. After surgery, especially after laparotomy or thoracotomy, the dead space ratio is approximately 0.5 and can increase to 0.55 in the first 24 hours.

VENTILATION-PERFUSION RELATIONSHIPS

Alveolar-capillary units (Fig. 3-1) are used to describe various options gas exchange. As is known, the ratio of alveolar ventilation (V) to alveolar capillary perfusion (Q) is called the ventilation-perfusion ratio (V/Q). For examples of gas exchange related to the V/Q ratio, see Fig. 3-1. The upper part (A) shows the ideal relationship between ventilation and blood flow and ideal attitude V/Q in the alveolar-capillary unit.

DEAD SPACE VENTILATION

The air in airways, does not participate in gas exchange, and their ventilation is called dead space ventilation. The V/Q ratio in this case is greater than 1 (see Fig. 3-1, part B). There are two types of dead space.

Rice. 3-1.

Anatomical dead space- lumen of the airways. Normally, its volume is about 150 ml, with the larynx accounting for about half.

Physiological (functional) dead space- all those parts of the respiratory system in which gas exchange does not occur. Physiological dead space includes not only the airways, but also the alveoli, which are ventilated but not perfused with blood (gas exchange is impossible in such alveoli, although ventilation does occur). The volume of functional dead space (Vd) in healthy people is about 30% of the tidal volume (i.e. Vd/Vt=0.3, where Vt is the tidal volume). An increase in Vd leads to hypoxemia and hypercapnia. CO 2 retention is usually observed when the Vd/Vt ratio increases to 0.5.

Dead space increases when the alveoli are overdistended or air flow decreases. The first option is observed with obstructive pulmonary diseases and artificial ventilation of the lungs while maintaining positive pressure at the end of expiration, the second - in case of heart failure (right or left), acute pulmonary embolism and emphysema.

SHUNT FRACTION

Part cardiac output, which is not completely balanced with alveolar gas, is called the shunt fraction (Qs/Qt, where Qt is the total blood flow, Qs is the blood flow through the shunt). In this case, the V/Q ratio is less than 1 (see part B of Fig. 3-1). There are two types of shunt.

True shunt indicates the absence of gas exchange between blood and alveolar gas (V/Q ratio is 0, i.e. the pulmonary unit is perfused but not ventilated), which is equivalent to the presence of an anatomical vascular shunt.

Venous admixture represented by blood that is not completely equilibrated with alveolar gas, i.e. does not undergo full oxygenation in the lungs. As venous admixture increases, this shunt approaches a true shunt.

The effect of the shunt fraction on the partial pressure of O 2 and CO 2 in arterial blood (respectively paO 2 PaCO 2) is shown in Fig. 3-2. Normally, shunt blood flow is less than 10% of the total (i.e., the Qs/Qt ratio is less than 0.1, or 10%), while about 90% of cardiac output takes part in gas exchange. As the shunt fraction increases, paO 2 progressively decreases, and paCO 2 does not increase until the Qs/Qt ratio reaches 50%. In patients with an intrapulmonary shunt as a result of hyperventilation (due to pathology or due to hypoxemia), paCO 2 is often below normal.

The shunt fraction determines the ability to increase paO 2 when oxygen is inhaled, as shown in Fig. 3-3. With an increase in the shunt fraction (Qs/Qt), an increase in the fractional concentration of oxygen in the inspired air or gas mixture(FiO 2) is accompanied by a smaller increase in paO 2. When the Qs/Qt ratio reaches 50%, paO 2 no longer responds to changes in FiO 2; . In this case, the intrapulmonary shunt behaves like a true (anatomical) one. Based on the above, it is possible not to use toxic concentrations of oxygen if the value of the shunt blood flow exceeds 50%, i.e. FiO 2 can be reduced without significantly reducing p a O 2 . This helps reduce the risk toxic effect oxygen.

Rice. 3-2. The effect of the shunt fraction on pO 2 (From D "Alonzo GE, Dantzger DR. Mechanisms of abnormal gas exchange. Med Clin North Am 1983;67:557-571). Rice. 3-3. The influence of the shunt fraction on the ratio of the fractional concentration of oxygen in the inspired air or gas mixture (From D "Alonzo GE, Dantzger DR. Mechanisms of abnormal gas exchange. Med Clin North Am 1983;67:557-571)

Etiological factors. Most often, an increase in the shunt fraction is caused by pneumonia, pulmonary edema (cardiac and non-cardiac nature), and pulmonary embolism (PTA). With pulmonary edema (mostly non-cardiogenic) and TPA, the disturbance of gas exchange in the lungs is more reminiscent of a true shunt and PaO 2 responds less well to changes in FiO 2. For example, in TPA, the shunt is the result of switching blood flow from the embolized area (where the flow of blood through the vessels is difficult and perfusion is impossible) to other areas of the lung with an increase in perfusion [3].

CALCULATION OF GAS EXCHANGE INDICATORS

The equations that will be discussed below are used for quantification severity of disturbances in ventilation-perfusion relationships. These equations are used to study pulmonary function, in particular in patients with respiratory failure.

PHYSIOLOGICAL DEAD SPACE

The volume of physiological dead space can be measured using the Bohr method. The volume of functional dead space is calculated based on the difference between pCO 2 values in exhaled alveolar air and capillary (arterial) blood (more precisely, the blood of the terminal segments of the pulmonary capillaries). In healthy people in the lungs, capillary blood is completely balanced with alveolar gas and pCO 2 in exhaled alveolar air is almost equal to pCO 2 in arterial blood. As the physiological dead space (i.e., the Vd/Vt ratio) increases, pCO 2 in exhaled air (PE CO 2) will be lower than pCO 2 in arterial blood. The Bohr equation used to calculate the Vd/Vt ratio is based on this principle:

Vd/Vt = (PaCO 2 - reCO 2) / pa CO 2. Normally the ratio Vd/Vt = 0.3.

To determine paCO 2, exhaled air is collected in a large bag and the average pCO 2 in the air is measured using an infrared CO 2 analyzer. This is quite simple and is usually necessary in a respiratory care unit.

SHUNT FRACTION

To determine the shunt fraction (Qs/Qt), the oxygen content in the arterial (CaO 2), mixed venous (CvO 2) and pulmonary capillary blood(CCO2). We have the shunt equation:

Q s /Q t = C c O 2 - C a O 2 / (C c O 2 - C v O 2).

Normally, the ratio Qs/Qt = 0.1.

Since CcO 2 cannot be directly measured, it is recommended to breathe pure oxygen in order to completely saturate the hemoglobin in the blood of the pulmonary capillaries with it (ScO 2 = 100%). However, in this situation, only the true shunt is measured. Breathing 100% oxygen is a very sensitive test for the presence of shunts because when PaO 2 is high, a small decrease in arterial oxygen concentration can cause a significant drop in PaO 2 .

ALVEOLAR-ARTERIAL OXYGEN DIFFERENCE (GRADIENT A-a pO 2)

The difference between the values of pO 2 in alveolar gas and arterial blood is called the alveolar-arterial difference in pO 2, or the A-a pO 2 gradient. Alveolar gas is described using the following simplified equation:

P A O 2 = p i O 2 - (p a CO 2 /RQ).

This equation is based on the fact that alveolar pO 2 (p A O 2) depends, in particular, on the partial pressure of oxygen in the inspired air (p i O 2) and alveolar (arterial) pCO 2 x p i O 2 - a function of FiO 2, barometric pressure (P B) and partial pressure of water vapor (pH 2 O) in humidified air (p i O 2 = FiO 2 (P B - pH 2 O). At normal temperature body pH 2 O is 47 mm Hg. Art. Respiratory coefficient (RQ) is the relationship between the production of CO 2 and the consumption of O 2, and gas exchange occurs between the cavity of the alveoli and the lumen of the capillaries entwining it by simple diffusion (RQ = VCO 2 /VO 2). In healthy people, when breathing room air at normal atmospheric pressure, the A-a PO 2 gradient is calculated taking into account the listed indicators (FiO 2 = 0.21, P B = 760 mm Hg, p a O 2 = 90 mm Hg ., p a CO 2 = 40 mmHg, RQ = 0.8) as follows:

P a O 2 = FiO 2 (P B - pH 2 O) - (paCO 2 /RQ) = 0.21 (760 - 47) - (40/0.8) = 100 mm Hg.

The normal value of the gradient A-a pO 2 = 10-20 mm Hg.

Normally, the A-a pO 2 gradient changes with age and with the oxygen content in the inspired air or gas. Its change with age is presented at the end of the book (see Appendix), and the effect of FiO 2 is shown in Fig. 3-4.

The usual change in the A-a pO 2 gradient in healthy adults at normal atmospheric pressure (inhalation of room air or pure oxygen) is shown below.

Rice. 3-4.Effect of FiO 2 ; on the A-a pO 2 gradient and the a/A pO 2 ratio in healthy people.

There is an increase in the A-a pO 2 gradient by 5-7 mm Hg. for every 10% increase in FiO 2. The influence of oxygen in high concentrations on the A-a pO 2 gradient is explained by the elimination of the action of hypoxic stimuli, which lead to vasoconstriction and changes in the blood supply to poorly ventilated areas of the lungs. As a result, blood returns to poorly ventilated segments, which may result in an increase in shunt fraction.

Artificial ventilation. Since normal atmospheric pressure is about 760 mm Hg, artificial ventilation with positive pressure will increase pi O 2. The average airway pressure should be added to the atmospheric pressure, which increases the accuracy of the calculation. For example, a mean airway pressure of 30 cmH2O can increase the A-a pO2 gradient to 16 mmHg, which corresponds to a 60% increase.

RATIO a/A pO 2

The a/A pO 2 ratio is practically independent of FiO 2, as can be seen in Fig. 3-4. This explains the following equation:

a/A pO 2 = 1 - (A-a pO 2)/raO 2

The presence of p A O 2 in both the numerator and denominator of the formula eliminates the influence of FiO 2 through p A O 2 on the a/A pO 2 ratio. Normal values for the a/A pO 2 ratio are presented below.

RATIO p A O 2 /FiO 2

Calculating the paO 2 /FiO 2 ratio is a simple way to calculate an indicator that correlates quite well with changes in the shunt fraction (Qs/Qt). This correlation looks like this:

PaO2/FiO2

APPROACH TO HYPOXEMIA

The approach to hypoxemia is shown in Fig. 3-5. To establish the cause of hypoxemia, it is necessary to have a catheter in the pulmonary artery, which occurs only in patients in departments intensive care. First, the A-a pO 2 gradient should be calculated to determine the origin of the problem. A normal gradient value indicates the absence of lung pathology (for example, muscle weakness). An increase in the gradient indicates a violation of the ventilation-perfusion relationship or low partial pressure of oxygen in the mixed air. venous blood(p v O 2). The relationship between p v O 2 and p a O 2 is explained in the next section.

MIXED VENOUS BLOOD AND OXYGENATION

Oxygenation of arterial blood occurs due to the oxygen contained in mixed venous blood ( pulmonary artery), with the addition of oxygen from alveolar gas. At normal function In the lungs, the p A O 2 indicator mainly determines the p a O 2 value.

Rice. 3-5. An approach to identifying the cause of hypoxemia. Explanation in the text.

When gas exchange is disturbed, the pa O 2 indicator makes a smaller contribution, and venous oxygenation (i.e., the p v O 2 indicator) - on the contrary, makes a larger contribution to the final value of p a O 2, which is shown in Fig. 3-6 (the horizontal axis on it goes along the capillaries; the transport of oxygen from the alveoli to the capillaries is also shown). With a decrease in oxygen metabolism (in the figure this is indicated as a shunt), p a O 2 decreases. When the degree of increase of p a O 2 is constant but p v O 2 is reduced, the final value of p a O 2 is the same as in the situation described above. This fact indicates that the lungs are not always the cause of hypoxemia.

The effect of p v O 2 on p a O 2 will depend on the shunt fraction. With a normal value of shunt blood flow, p v O 2 has a slight effect on p a O 2 . As the shunt fraction increases, p v O 2 becomes an increasingly significant factor that determines p a O 2 . In extreme cases, a 100% shunt is possible, when p v O 2 can be the only indicator that determines p a O 2. Therefore, the indicator p v O 2 will play important role only in patients with existing pulmonary pathology.

CARBON DIOXIDE RETENTION

The partial pressure (tension) of CO 2 in arterial blood is determined by the relationship between the amount of metabolic production of CO 2 and the rate of its release by the lungs:

p a CO 2 = K x (VCO 2 / Va),

where p a CO 2 is arterial pCO 2 ; VCO 2 - rate of formation of CO 2; V A - minute alveolar ventilation; K is a constant. Alveolar ventilation is established by the well-known relationship, and then the previous formula takes the following form:

p a CO 2 = K x,

where ve is the exhaled minute volume (minute ventilation measured during exhalation). It is clear from the equation that the main reasons for CO 2 retention are the following: 1.) increased CO 2 production; 2) decrease in minute ventilation of the lungs; 3) increase in dead space (Fig. 3-7). Each of these factors is briefly discussed below.

Rice. 3-6. Mechanisms of hypoxemia development. Explanation in the text.

Rice. 3-7. Explanation in the text.

INCREASING CO 2 PRODUCTION

The amount of CO 2 can be measured in intubated patients using a “metabolic cart”, which is used in indirect calorimetry. This device is equipped with an infrared CO 2 analyzer, which measures its content in the exhaled air (with each exhalation). To determine the rate of CO 2 release, the respiratory rate is recorded.

Respiratory coefficient. The amount of CO 2 production is determined by the intensity of metabolic processes and the type of substances (carbohydrates, fats, proteins) that are oxidized in the body. The normal rate of formation of CO 2 (VCO 2) in a healthy adult is 200 ml per 1 min, i.e. about 80% of the oxygen absorption (consumption) rate (usual VO 2 value = 250 ml/min). The VCO 2 /VO 2 ratio is called the respiratory (respiratory) coefficient (RQ), which is widely used in clinical practice. RQ is different for the biological oxidation of carbohydrates, proteins and fats. It is highest for carbohydrates (1.0), slightly lower for proteins (0.8) and lowest for fats (0.7). With mixed food, the RQ value is determined by the metabolism of all three named species nutrients. The normal RQ is 0.8 for the average person on a diet that has 70% of total calories from carbohydrates and 30% from fat. RQ is discussed in more detail in Chapter 39.

Etiological factors. Typically, an increase in VCO 2 is observed with sepsis, polytrauma, burns, increased work of breathing, increased carbohydrate metabolism, metabolic acidosis, and postoperative period. It is believed that sepsis is the most common cause of increased VCO 2 . Increased work of the respiratory system can lead to CO 2 retention while the patient is disconnected from the device artificial respiration, if the elimination of CO 2 through the lungs is impaired. Excessive consumption carbohydrates can increase RQ to 1.0 or higher and cause CO 2 retention, so it is important to determine PaCO 2, which is directly related to VCO 2, not RQ. Indeed, VCO 2 can increase even with normal RQ (if VO 2 is also increased). Considering only one RQ can be misleading, therefore, this indicator cannot be interpreted in isolation from other parameters.

ALVEOLAR HYPOVENTILATION SYNDROME

Hypoventilation is a decrease in minute ventilation of the lungs without a significant change in their function (similar to holding your breath). In Fig. 3-7 show that it is important to measure the A-a PO 2 gradient to identify alveolar hypoventilation syndrome. The A-a PO 2 gradient may be normal (or unchanged) if there is alveolar hypoventilation. In contrast, cardiopulmonary pathology may be accompanied by an increase in the A-a PO 2 gradient. The exception is a significant delay of CO 2 in lung disease, when the value of the A-a pO 2 gradient is close to normal. In such a situation, an increase in resistance respiratory tract may be so severe that air is virtually unable to reach the alveoli (similar to holding your breath). The main causes of alveolar hypoventilation syndrome in patients in intensive care units are given in Table. 3-1. If the A-a pO 2 gradient is normal or unchanged, then the condition of the respiratory muscles can be assessed using maximum inspiratory pressure, as described below.

Weakness of the respiratory muscles. Patients in intensive care units have a number of diseases and pathological conditions may lead to weakness of the respiratory muscles. The most common are sepsis, shock, electrolyte imbalance and the consequences of heart surgery. In sepsis and shock, there is a decrease in blood flow in the diaphragm. Damage to the phrenic nerve may occur during surgical interventions in conditions cardiopulmonary bypass due to local cooling of the surface of the heart (see Chapter 2).

Weakness of the respiratory muscles can be determined by measuring maximum inspiratory pressure (Pmpi) directly at the patient's bedside. To do this, the patient, after exhaling as deeply as possible (up to the residual volume), must inhale with maximum effort through a closed valve. R MVD depends on age and gender (see Table 30-2) and ranges from 80 to 130 cm of water column. in most adults. CO 2 retention is observed when P MVD drops to 30 cm of water column. It should be remembered that P MVD is measured with the participation of all respiratory muscles, excluding the diaphragm. Therefore, dysfunction of the diaphragm alone, including phrenic nerve injury, may be missed when determining PMV because the accessory muscles are able to maintain PMV at the desired level.

Table 3-1

Causes of alveolar hypoventilation in intensive care units

Idiopathic syndromes. The classification of idiopathic hypoventilation syndromes is related to body weight and time of day (or night). Daytime hypoventilation in obese patients is called obese-hypoventilation syndrome (THS), a similar pathology in thin patients is called primary alveolar hypoventilation (PAH). Sleep apnea syndrome (night apnea) is characterized by impaired breathing during sleep and is never accompanied by daytime hypoventilation. The condition of patients with THS and sleep apnea syndrome improves with a decrease in excess body weight; in addition, progesterone may be effective in THS (see Chapter 26). Impaired phrenic nerve function may limit success in the treatment of PAH.

LITERATURE

Forster RE, DuBois AB, Briscoe WA, Fisher A, eds. The lung. 3rd ed. Chicago: Year Book Medical Publishers, 1986.

Tisi GM. Pulmonary physiology in clinical medicine. Baltimore: Williams & Wilkins, 1980.

Dantzger DR. Pulmonary gas exchange. In: Dantzger DR. ed. Cardiopulmonary critical care. Orlando: Grune & Stratton, 1986:25-46.
D"Alonzo GE, Dantzger DR. Mechanisms of abnormal gas exchange. Med Clin North Am 1983; 67:557-571.
Dantzger DR. Ventilation-perfusion inequality in lung disease. Chest 1987; 91:749-754.
Dantzger DR. The influence of cardiovascular function on gas exchange. Clin Chest. Med 1983; 4:149-159.
Shapiro V. Arterial blood gas monitoring. Crit Care Clin 1988; 4:479-492.

VENTILATION-PERFUSION RELATIONSHIPS AND THEIR DISORDERS

Buohuys A. Respiratory dead space. In: Fenn WO, Rahn H. eds. Handbook of physiology: Respiration. Bethesda: American Physiological Society, 1964:699-714.
Dean JM, Wetzel RC, Rogers MC. Arterial blood gas derived variables as estimates of intrapulmonary shunt in critically ill children. Crit Care Med 1985; 13:1029-1033.
Carroll G.C. Misapplication of the alveolar gas equation. N Engi J Med 1985; 312:586.
Gilbert R, Craigley JF. The arterial/alveolar oxygen tension ratio. An index of gas exchange applicable to varying inspired oxygen concentrations. Am Rev Respir Dis 1974; 109:142-145.
Harris EA, Kenyon AM, Nisbet HD, Seelye ER, Whitlock RML. The normal alveolar-arterial oxygen tension gradient in man. Clin Sci 1974; 46:89-104.
Covelli HD, Nessan VJ, Tuttle WK. Oxygen derived variables in acute respiratory failure. Crit Care Med 1983; 31:646-649.

ALVEOLAR HYPOVENTILATION SYNDROME

Glauser FL, Fairman P, Bechard D. The causes and evaluation of chronic hvpercapnia. Chest 1987; 93.755-759,
Praher MR, Irwin RS, Extrapulmonary causes of respiratory failure. J Intensive Care Med 1986; 3:197-217.
Rochester D, Arora NS. Respiratory muscle failure. Med Clin North Am 1983; 67:573-598.

The entire complex process can be divided into three main stages: external respiration; and internal (tissue) respiration.

External breathing- gas exchange between the body and the surrounding atmospheric air. External respiration involves the exchange of gases between atmospheric and alveolar air, as well as pulmonary capillaries and alveolar air.

This breathing occurs as a result of periodic changes in volume chest cavity. An increase in its volume provides inhalation (inspiration), a decrease provides exhalation (expiration). The phases of inhalation and subsequent exhalation are . During inhalation, atmospheric air enters the lungs through the airways, and when exhaling, some of the air leaves them.

Conditions required for external respiration:

tightness chest;
free communication of the lungs with the surrounding external environment;
elasticity of lung tissue.

An adult takes 15-20 breaths per minute. The breathing of physically trained people is rarer (up to 8-12 breaths per minute) and deeper.

The most common methods for studying external respiration

Assessment methods respiratory function lungs:

Pneumography
Spirometry
Spirography
Pneumotachometry
Radiography
X-ray computed tomography
Ultrasound examination
Magnetic resonance imaging
Bronchography
Bronchoscopy
Radionuclide methods
Gas dilution method

Spirometry- a method of measuring the volume of exhaled air using a spirometer device. Spirometers are used different types with a turbimetric sensor, as well as water ones, in which exhaled air is collected under a spirometer bell placed in water. The volume of exhaled air is determined by the rise of the bell. IN lately Sensors sensitive to changes in volumetric air flow velocity connected to a computer system are widely used. In particular, a computer system such as “Spirometer MAS-1”, produced in Belarus, etc., operates on this principle. Such systems make it possible to carry out not only spirometry, but also spirography, as well as pneumotachography).

Spirography - a method of continuously recording the volumes of inhaled and exhaled air. The resulting graphical curve is called spirophamma. Using a spirogram, you can determine the vital capacity of the lungs and tidal volumes, respiratory rate and voluntary maximum ventilation of the lungs.

Pneumotachography - method of continuous recording of the volumetric flow rate of inhaled and exhaled air.

There are many other methods for studying the respiratory system. Among them are plethysmography of the chest, listening to sounds produced when air passes through the respiratory tract and lungs, fluoroscopy and radiography, determination of the oxygen and carbon dioxide content in the exhaled air flow, etc. Some of these methods are discussed below.

Volume indicators of external respiration

The relationship between lung volumes and capacities is presented in Fig. 1.

When studying external respiration, the following indicators and their abbreviations are used.

Total lung capacity (TLC)- the volume of air in the lungs after the deepest possible inspiration (4-9 l).

Rice. 1. Average values of lung volumes and capacities

Vital capacity of the lungs

Vital capacity of the lungs (VC)- the volume of air that a person can exhale with the deepest, slowest exhalation made after a maximum inhalation.

The vital capacity of the human lungs is 3-6 liters. Recently, due to the introduction of pneumotachographic technology, the so-called forced vital capacity(FVC). When determining FVC, the subject must, after inhaling as deeply as possible, make the deepest forced exhalation possible. In this case, exhalation should be made with an effort aimed at achieving the maximum volumetric speed of the exhaled air flow throughout the entire exhalation. Computer analysis of such forced exhalation makes it possible to calculate dozens of indicators of external respiration.

The individual normal value of vital capacity is called proper lung capacity(JEL). It is calculated in liters using formulas and tables based on height, body weight, age and gender. For women aged 18-25, the calculation can be made using the formula

JEL = 3.8*P + 0.029*B - 3.190; for men of the same age

Residual volume

JEL = 5.8*P + 0.085*B - 6.908, where P is height; B—age (years).

The value of the measured VC is considered reduced if this decrease is more than 20% of the VC level.

If the name “capacity” is used for the indicator of external respiration, this means that the composition of such a capacity includes smaller units called volumes. For example, TLC consists of four volumes, vital capacity - of three volumes.

Tidal volume (TO)- this is the volume of air entering and leaving the lungs in one respiratory cycle. This indicator is also called the depth of breathing. At rest in an adult, the DO is 300-800 ml (15-20% of the VC value); one month old baby- 30 ml; one year old - 70 ml; ten years old - 230 ml. If the depth of breathing is greater than normal, then such breathing is called hyperpnea- excessive, deep breathing, if DO is less than normal, then breathing is called oligopnea- insufficient, shallow breathing. At normal depth and frequency of breathing it is called eupnea- normal, sufficient breathing. The normal resting respiratory rate in adults is 8–20 breaths per minute; a month-old baby - about 50; one year old - 35; ten years old - 20 cycles per minute.

Inspiratory reserve volume (IR ind)- the volume of air that a person can inhale with the deepest breath taken after a calm breath. The normal PO value is 50-60% of the VC value (2-3 l).

Expiratory reserve volume (ER ext)- the volume of air that a person can exhale with the deepest exhalation made after a calm exhalation. Normally, the RO value is 20-35% of vital capacity (1-1.5 l).

Residual lung volume (RLV)- air remaining in the respiratory tract and lungs after a maximum deep exhalation. Its value is 1-1.5 l (20-30% of TEL). In old age, the value of TRL increases due to a decrease in the elastic traction of the lungs, bronchial patency, a decrease in the strength of the respiratory muscles and the mobility of the chest. At the age of 60 years, it is already about 45% of the TEL.

Functional residual capacity (FRC)- air remaining in the lungs after a quiet exhalation. This capacity consists of residual lung volume (RVV) and expiratory reserve volume (ERV).

Not all atmospheric air entering the respiratory system during inhalation takes part in gas exchange, but only that which reaches the alveoli, which have a sufficient level of blood flow in the capillaries surrounding them. In this regard, there is something called dead space.

Anatomical dead space (AMP)- this is the volume of air located in the respiratory tract to the level of the respiratory bronchioles (these bronchioles already have alveoli and gas exchange is possible). The size of the AMP is 140-260 ml and depends on the characteristics of the human constitution (when solving problems in which it is necessary to take into account the AMP, but its value is not indicated, the volume of the AMP is taken equal to 150 ml).

Physiological dead space (PDS)- the volume of air entering the respiratory tract and lungs and not participating in gas exchange. The FMP is larger than the anatomical dead space, since it includes it as an integral part. In addition to the air in the respiratory tract, the FMP includes air that enters the pulmonary alveoli, but does not exchange gases with the blood due to the absence or reduction of blood flow in these alveoli (this air is sometimes called alveolar dead space). Normally, the value of functional dead space is 20-35% of the tidal volume. An increase in this value above 35% may indicate the presence of certain diseases.

Table 1. Indicators of pulmonary ventilation

IN medical practice It is important to take into account the dead space factor when designing breathing devices (high-altitude flights, scuba diving, gas masks), and carrying out a number of diagnostic and resuscitation measures. When breathing through tubes, masks, hoses, additional dead space is connected to the human respiratory system and, despite the increase in the depth of breathing, ventilation of the alveoli with atmospheric air may become insufficient.

Minute breathing volume

Minute respiration volume (MRV)— volume of air ventilated through the lungs and respiratory tract in 1 minute. To determine the MOR, it is enough to know the depth, or tidal volume (TV), and respiratory frequency (RR):

MOD = TO * BH.

In mowing, MOD is 4-6 l/min. This indicator is often also called pulmonary ventilation (distinguished from alveolar ventilation).

Alveolar ventilation

Alveolar ventilation (AVL)- the volume of atmospheric air passing through the pulmonary alveoli in 1 minute. To calculate alveolar ventilation, you need to know the value of the AMP. If it is not determined experimentally, then for calculation the volume of AMP is taken equal to 150 ml. To calculate alveolar ventilation, you can use the formula

AVL = (DO - AMP). BH.

For example, if a person’s breathing depth is 650 ml, and the respiratory rate is 12, then AVL is equal to 6000 ml (650-150). 12.

AB = (DO - WMD) * BH = DO alv * BH

AB - alveolar ventilation;
DO alve - tidal volume of alveolar ventilation;
RR - respiratory rate

Maximum ventilation (MVV)- the maximum volume of air that can be ventilated through a person’s lungs in 1 minute. MVL can be determined by voluntary hyperventilation at rest (breathing as deeply as possible and often at a slant is permissible for no more than 15 seconds). Using special equipment, MVL can be determined while a person is performing intensive physical work. Depending on the constitution and age of a person, the MVL norm is within the range of 40-170 l/min. In athletes, MVL can reach 200 l/min.

Flow indicators of external respiration

In addition to lung volumes and capacities, the so-called flow indicators of external respiration. The simplest method for determining one of them, peak expiratory flow rate, is peak flowmetry. Peak flow meters are simple and quite affordable devices for use at home.

Peak expiratory flow rate(POS) - the maximum volumetric flow rate of exhaled air achieved during forced exhalation.

Using a pneumotachometer device, you can determine not only the peak volumetric flow rate of exhalation, but also inhalation.

In conditions medical hospital Pneumotachograph devices with computer processing of the received information are becoming increasingly widespread. Devices of this type make it possible, based on continuous recording of the volumetric velocity of the air flow created during exhalation of the forced vital capacity of the lungs, to calculate dozens of indicators of external respiration. Most often, POS and maximum (instantaneous) volumetric air flow rates at the moment of exhalation are determined as 25, 50, 75% FVC. They are called respectively indicators MOS 25, MOS 50, MOS 75. The definition of FVC 1 is also popular - the volume of forced expiration for a time equal to 1 e. Based on this indicator, the Tiffno index (indicator) is calculated - the ratio of FVC 1 to FVC expressed as a percentage. A curve is also recorded that reflects the change in the volumetric velocity of the air flow during forced exhalation (Fig. 2.4). In this case, the volumetric velocity (l/s) is displayed on the vertical axis, and the percentage of exhaled FVC is displayed on the horizontal axis.

In the graph shown (Fig. 2, upper curve), the vertex indicates the value of PVC, the projection of the moment of exhalation of 25% FVC on the curve characterizes MVC 25, the projection of 50% and 75% FVC corresponds to the values of MVC 50 and MVC 75. Not only flow velocities at individual points, but also the entire course of the curve are of diagnostic significance. Its part, corresponding to 0-25% of the exhaled FVC, reflects the air patency of the large bronchi, trachea, and the area from 50 to 85% of the FVC - the patency of the small bronchi and bronchioles. A deflection in the descending section of the lower curve in the expiratory region of 75-85% FVC indicates a decrease in the patency of the small bronchi and bronchioles.

Rice. 2. Stream breathing indicators. Note curves - volume healthy person(upper), a patient with obstructive obstruction of the small bronchi (lower)

Determination of the listed volume and flow indicators is used in diagnosing the state of the external respiration system. To characterize the function of external respiration in the clinic, four variants of conclusions are used: normal, obstructive disorders, restrictive disorders, mixed disorders(combination of obstructive and restrictive disorders).

For most flow and volume indicators of external respiration, deviations of their value from the proper (calculated) value by more than 20% are considered to be outside the norm.

Obstructive disorders- these are obstructions in the patency of the airways, leading to an increase in their aerodynamic resistance. Such disorders can develop as a result of increased tone of the smooth muscles of the lower respiratory tract, with hypertrophy or swelling of the mucous membranes (for example, with acute respiratory viral infections), accumulation of mucus, purulent discharge, in the presence of a tumor or foreign body, dysregulation of the upper respiratory tract and other cases.

The presence of obstructive changes in the airways is judged by a decrease in POS, FVC 1, MOS 25, MOS 50, MOS 75, MOS 25-75, MOS 75-85, the value of the Tiffno test index and MVL. The Tiffno test rate is normally 70-85%; a decrease to 60% is regarded as a sign moderate impairment, and up to 40% - a pronounced violation of bronchial patency. In addition, with obstructive disorders, indicators such as residual volume, functional residual capacity and total lung capacity increase.

Restrictive violations- this is a decrease in the expansion of the lungs when inhaling, a decrease in respiratory excursions of the lungs. These disorders can develop due to decreased compliance of the lungs, damage to the chest, the presence of adhesions, congestion in pleural cavity fluid, purulent contents, blood, weakness of the respiratory muscles, impaired transmission of excitation at neuromuscular synapses and other reasons.

The presence of restrictive changes in the lungs is determined by a decrease in vital capacity (at least 20% of the proper value) and a decrease in the MVL (nonspecific indicator), as well as a decrease in lung compliance and, in some cases, an increase in the Tiffno test score (more than 85%). At restrictive disorders total lung capacity, functional residual capacity and residual volume decrease.

The conclusion about mixed (obstructive and restrictive) disorders of the external respiration system is made with the simultaneous presence of changes in the above flow and volume indicators.

Lung volumes and capacities

Tidal volume - is the volume of air that a person inhales and exhales in calm state; in an adult it is 500 ml.

Inspiratory reserve volume- this is the maximum volume of air that a person can inhale after a quiet breath; its size is 1.5-1.8 liters.

Expiratory reserve volume - this is the maximum volume of air that a person can exhale after a quiet exhalation; this volume is 1-1.5 liters.

Residual volume - this is the volume of air that remains in the lungs after maximum exhalation; The residual volume is 1 -1.5 liters.

Rice. 3. Changes in tidal volume, pleural and alveolar pressure during lung ventilation

Vital capacity of the lungs(VC) is the maximum volume of air that a person can exhale after the deepest breath. Vital capacity includes inspiratory reserve volume, tidal volume and expiratory reserve volume. The vital capacity of the lungs is determined by a spirometer, and the method for determining it is called spirometry. Vital capacity in men is 4-5.5 l, and in women - 3-4.5 l. It is greater in a standing position than in a sitting or lying position. Physical training leads to an increase in vital capacity (Fig. 4).

Rice. 4. Spirogram of pulmonary volumes and capacities

Functional residual capacity(FRC) is the volume of air in the lungs after a quiet exhalation. FRC is the sum of expiratory reserve volume and residual volume and is equal to 2.5 liters.

Total lung capacity(OEL) - the volume of air in the lungs at the end of a full inspiration. TLC includes residual volume and vital capacity of the lungs.

Dead space is formed by air that is located in the airways and does not participate in gas exchange. When you inhale, the last portions of atmospheric air enter the dead space and, without changing its composition, leave it when you exhale. The dead space volume is about 150 ml, or approximately 1/3 of the tidal volume during quiet breathing. This means that out of 500 ml of inhaled air, only 350 ml enters the alveoli. By the end of a quiet exhalation, the alveoli contain about 2500 ml of air (FRC), so with each quiet breath, only 1/7 of the alveolar air is renewed.

Minute ventilation is total quantity air newly entered into the respiratory tract and lungs and released from them within one minute, which is equal to the tidal volume multiplied by the respiratory frequency. Normal tidal volume is approximately 500 ml and the respiratory rate is 12 times per minute.

Thus, the normal ventilation minute volume averages about 6 liters. When minute ventilation is reduced to 1.5 liters and the respiratory rate is reduced to 2-4 per minute, a person can live only for a very short time, unless he develops severe inhibition of metabolic processes, as happens with deep hypothermia.

The respiratory rate sometimes increases to 40-50 breaths per minute, and the tidal volume can reach a value close to the vital capacity of the lungs (about 4500-5000 ml in young healthy men). However, at high respiratory rates, a person usually cannot maintain a tidal volume greater than 40% of vital capacity (VC) for several minutes or hours.

Alveolar ventilation

The main function of the pulmonary ventilation system is to constantly renew the air in the alveoli, where it comes into close contact with the blood in the pulmonary capillaries. The speed at which newly introduced air reaches the specified contact area is called alveolar ventilation. During normal, quiet ventilation, the tidal volume fills the airways all the way to the terminal bronchioles, and only a small portion of the inspired air travels all the way to contact the alveoli. New portions of air overcome short distance from terminal bronchioles to alveoli by diffusion. Diffusion is caused by the movement of molecules, with molecules of each gas moving at high speed among other molecules. The speed of movement of molecules in the inhaled air is so high, and the distance from the terminal bronchioles to the alveoli is so small that the gases cover this remaining distance in a matter of seconds.

Dead space

Typically, at least 30% of the air a person inhales never reaches the alveoli. This air is called dead space air because it is useless for the gas exchange process. Normal dead space in a young male with a tidal volume of 500 mL is approximately 150 mL (about 1 mL per pound of body weight), or approximately 30 % tidal volume.

The volume of the airways that conduct inspired air to the site of gas exchange is called anatomical dead space. Sometimes, however, some alveoli do not function due to insufficient blood flow to the pulmonary capillaries. From a functional point of view, these alveoli without capillary perfusion are considered pathological dead space.

Taking into account the alveolar (pathological) dead space, the total dead space is called physiological dead space. In a healthy person, the anatomical and physiological dead space is almost identical in volume, since all alveoli are functioning. However, in individuals with poorly perfused alveoli, the total (or physiological) dead space may exceed 60% of the tidal volume.