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3 Assessment of gas exchange in the lungs at sick bed

VENTILATION-PERFUSION RELATIONSHIPS

Alveolar-capillary units (Fig. 3-1) are used to describe various types of 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 the ideal V/Q ratio in the alveolar-capillary unit.

DEAD SPACE VENTILATION

The air in the 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 - with heart failure (right or left), acute pulmonary embolism and emphysema.

SHUNT FRACTION

The portion of cardiac output that is not completely equilibrated with alveolar gas is called the shunt fraction (Qs/Qt, where Qt is total blood flow and Qs is 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 of oxygen toxicity.

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 to quantify the 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 arterial (CaO 2), mixed venous (CvO 2) and pulmonary capillary blood (CcO 2) is used. 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 body temperature, pH 2 O is 47 mm Hg. Respiratory coefficient (RQ ) - 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 gradient A- and PO 2 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 typical change in A-a pO 2 gradient in healthy adults at normal atmospheric pressure (inhaling 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 effect 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 increased 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:

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 intensive care units. 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 a low partial pressure of oxygen in the mixed 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. With normal lung function, 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 above situation. 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. Consequently, the p v O 2 indicator will play an 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 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 types of 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 in the 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 artificial respiration apparatus if CO 2 elimination through the lungs is impaired. Excessive carbohydrate consumption 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, the increase in airway resistance may be so pronounced that air will be virtually unable to reach the alveoli (similar to holding one's 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. In patients in intensive care units, a number of diseases and pathological conditions can 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 surgery under 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.

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

VENTILATION-PERFUSION RELATIONSHIPS AND THEIR DISORDERS

6. Buohuys A. Respiratory dead space. In: Fenn WO, Rahn H. eds. Handbook of physiology: Respiration. Bethesda: American Physiological Society, 1964:699-714.
7. 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.
8. Carroll G.C. Misapplication of the alveolar gas equation. N Engi J Med 1985; 312:586.
9. 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.
10. 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.
11. Covelli HD, Nessan VJ, Tuttle WK. Oxygen derived variables in acute respiratory failure. Crit Care Med 1983; 31:646-649.

ALVEOLAR HYPOVENTILATION SYNDROME

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

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The airways, pulmonary parenchyma, pleura, musculoskeletal frame of the chest and the diaphragm constitute a single working organ through which ventilation.

Ventilation is the process of updating the gas composition of alveolar air, ensuring the supply of oxygen and the removal of excess carbon dioxide.

The ventilation intensity is determined depth of inspiration And frequency breathing.
The most informative indicator of pulmonary ventilation is minute volume of respiration, defined as tidal volume multiplied by the number of breaths per minute.
In an adult man at rest, the minute breathing volume is 6-10 l/min,
during operation - from 30 to 100 l/min.
Respiratory rate at rest is 12-16 per minute.
To assess the potential capabilities of athletes and people of special professions, a test with arbitrary maximum ventilation is used, which in these people can reach 180 l/min.

Ventilation of different parts of the lungs

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Different parts of a person’s lungs are ventilated differently, depending on body position. When a person is in an upright position, the lower parts of the lungs are better ventilated than the upper parts. If a person lies on his back, then the difference in ventilation of the apical and lower parts of the lungs disappears, however, the rear (dorsal) their areas begin to be ventilated better than the front ones (ventral). Lying on your side allows the lung underneath to be better ventilated. The uneven ventilation of the upper and lower parts of the lung when a person is in an upright position is due to the fact that transpulmonary pressure(the difference in pressure in the lungs and the pleural cavity) as a force that determines the volume of the lungs and its changes, these areas of the lung are not the same. Because the lungs are heavy, the transpulmonary pressure at their base is lower than at the apex. In this regard, the lower sections of the lungs at the end of a quiet exhalation are more compressed, however, during inhalation they expand better than the apexes. This also explains the more intense ventilation of the lower parts of the lungs if a person lies on his back or side.

Respiratory dead space

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At the end of exhalation, the volume of gases in the lungs is equal to the sum of the residual volume and the expiratory reserve volume, i.e. represents the so-called (FOE). At the end of inspiration, this volume increases by the tidal volume, i.e. the volume of air that enters the lungs during inhalation and is removed from them during exhalation.

The air entering the lungs during inhalation fills the airways, and some of it reaches the alveoli, where it mixes with alveolar air. The remaining, usually smaller, part remains in the respiratory tract, in which the exchange of gases between the air contained in them and the blood does not occur, i.e. in the so-called dead space.

Respiratory dead space - the volume of the respiratory tract in which gas exchange processes between air and blood do not occur.
Distinguish between anatomical and physiological (or functional) dead space.

Anatomical breathing measures your space represents the volume of the airways, starting from the openings of the nose and mouth and ending with the respiratory bronchioles of the lung.

Under functional(physiological) dead space understand all those parts of the respiratory system in which gas exchange does not occur. The functional dead space, in contrast to the anatomical one, includes not only the airways, but also the alveoli, which are ventilated but not perfused with blood. In such alveoli, gas exchange is impossible, although ventilation does occur.

In a middle-aged person, the volume of anatomical dead space is 140-150 ml or approximately 1/3 of the tidal volume during quiet breathing. By the end of a quiet exhalation, the alveoli contain about 2500 ml of air (functional residual capacity), so with each quiet breath, only 1/7 of the alveolar air is renewed.

The essence of ventilation

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Thus, ventilation provides entry of outside air into the lungs and some of it into the alveoli and removal instead gas mixtures(exhaled air), consisting of alveolar air and that part of the external air that fills the dead space at the end of inspiration and is removed first at the beginning of exhalation. Since alveolar air contains less oxygen and more carbon dioxide than external air, the essence of lung ventilation comes down to delivery of oxygen to the alveoli(compensating for the loss of oxygen passing from the alveoli into the blood of the pulmonary capillaries) and removing carbon dioxide from them(entering the alveoli from the blood of the pulmonary capillaries). There is a relationship close to direct proportionality between the level of tissue metabolism (the rate of tissue consumption of oxygen and the formation of carbon dioxide in them) and ventilation of the lungs. The correspondence of pulmonary and, most importantly, alveolar ventilation to the level of metabolism is ensured by the system of regulation of external respiration and manifests itself in the form of an increase in the minute volume of respiration (both due to an increase in tidal volume and respiratory frequency) with an increase in the rate of oxygen consumption and the formation of carbon dioxide in the tissues.

Ventilation of the lungs occurs, thanks to active physiological process(respiratory movements), which causes the mechanical movement of air masses along the tracheobronchial tract in volumetric flows. In contrast to the convective movement of gases from the environment into the bronchial space, further gas transport(transition of oxygen from bronchioles to alveoli and, accordingly, carbon dioxide from alveoli to bronchioles) is carried out mainly by diffusion.

Therefore, the concept is distinguished "pulmonary ventilation" And "alveolar ventilation".

Alveolar ventilation

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Alveolar ventilation cannot be explained only by convective air flows in the lungs created by active inhalation. The total volume of the trachea and the first 16 generations of bronchi and bronchioles is 175 ml, the next three (17-19) generations of bronchioles are another 200 ml. If this entire space, in which there is almost no gas exchange, were “washed” by convective currents of outside air, then the respiratory dead space would have to be almost 400 ml. If the inhaled air enters the alveoli through the alveolar ducts and sacs (the volume of which is 1300 ml) also by convective flows, then atmospheric oxygen can reach the alveoli only with an inhalation volume of at least 1500 ml, whereas the usual tidal volume in humans is 400-500 ml.

Under conditions of quiet breathing (breathing rate 15 a min, inspiratory duration 2 s, average volumetric inspiratory rate 250 ml/s), during inspiration (tidal volume 500 ml), external air fills all conductive (volume 175 ml) and transitional (volume 200 ml) ml) zones of the bronchial tree. Only a small part of it (less than 1/3) enters the alveolar ducts, the volume of which is several times greater than this part of the tidal volume. With such an inhalation, the linear velocity of the flow of inhaled air in the trachea and main bronchi is approximately 100 cm/s. Due to the sequential division of the bronchi into increasingly smaller diameters, with a simultaneous increase in their number and the total lumen of each subsequent generation, the movement of inhaled air through them slows down. At the border of the conducting and transition zones of the tracheobronchial tract, the linear flow velocity is only about 1 cm/s; in the respiratory bronchioles it decreases to 0.2 cm/s, and in the alveolar ducts and sacs - to 0.02 cm/s.

Thus, the speed of convective air flows that arise during active inspiration and are caused by the difference between the air pressure in the environment and the pressure in the alveoli in the distal parts of the tracheobronchial tree is very small, and air enters the alveoli from the alveolar ducts and alveolar sacs by convection with a small linear speed. However, the total cross-sectional area of ​​not only the alveolar ducts (thousands cm2), but also the respiratory bronchioles forming the transition zone (hundreds cm2) is large enough to ensure the diffusion transfer of oxygen from the distal parts of the bronchial tree to the alveoli, and carbon dioxide gas - in the opposite direction.

Thanks to diffusion, the composition of the air in the airways of the respiratory and transition zone approaches the alveolar composition. Hence, the diffusion movement of gases increases the volume of the alveolar and reduces the volume of dead space. In addition to the large diffusion area, this process is also ensured by a significant gradient of partial pressures: in the inhaled air, the partial pressure of oxygen is 6.7 kPa (50 mm Hg) higher than in the alveoli, and the partial pressure of carbon dioxide in the alveoli is 5.3 kPa (40 mm Hg) greater than in the alveoli. Hg) more than in inspired air. Within one second, due to diffusion, the concentrations of oxygen and carbon dioxide in the alveoli and nearby structures (alveolar sacs and alveolar ducts) are almost equalized.

Hence, starting from the 20th generation, alveolar ventilation is provided exclusively by diffusion. Due to the diffusion mechanism of oxygen and carbon dioxide movement, there is no permanent boundary between the dead space and the alveolar space in the lungs. In the airways there is a zone within which the diffusion process occurs, where the partial pressure of oxygen and carbon dioxide varies, respectively, from 20 kPa (150 mm Hg) and 0 kPa in the proximal part of the bronchial tree to 13.3 kPa (100 mm Hg .art.) and 5.3 kPa (40 mmHg) in its distal part. Thus, along the bronchial tract there is a layer-by-layer unevenness of air composition from atmospheric to alveolar (Fig. 8.4).

Fig.8.4. Scheme of alveolar ventilation.
“a” - according to outdated and
“b” - according to modern concepts. MP - dead space;
AP - alveolar space;
T - trachea;
B - bronchi;
DB - respiratory bronchioles;
AH - alveolar ducts;
AM - alveolar sacs;
A - alveoli.
Arrows indicate convective air flows, dots indicate the area of ​​diffusion exchange of gases.

This zone shifts depending on the breathing mode and, first of all, on the inhalation rate; the greater the inhalation rate (i.e., as a result, the greater the minute volume of respiration), the more distally along the bronchial tree convective flows are expressed with a speed prevailing over the diffusion rate. As a result, as the minute volume of respiration increases, the dead space increases, and the boundary between the dead space and the alveolar space shifts in the distal direction.

Hence, the anatomical dead space (if it is determined by the number of generations of the bronchial tree, in which diffusion does not yet matter) changes in the same way as the functional dead space - depending on the volume of breathing.

Ventilation

How does air enter the alveoli?

This and the next two chapters examine how inspired air enters the alveoli, how gases pass through the alveolar-capillary barrier, and how they are removed from the lungs through the bloodstream. These three processes are provided by ventilation, diffusion and blood flow, respectively.

Rice. 2.1. Lung diagram. Typical values ​​of volumes and flow rates of air and blood are given. In practice, these values ​​vary significantly (according to J.B. West: Ventilation/Blood Flow and Gas Exchange. Oxford, Blackwell, 1977, p. 3, with modifications)

In Fig. Figure 2.1 shows a schematic representation of the lung. The bronchi, which form the airways (see Fig. 1.3), are represented here by one tube (anatomical dead space). Through it, air enters the gas exchange sections limited by the alveolar-capillary membrane and the blood of the pulmonary capillaries. With each breath, about 500 ml of air enters the lungs (tidal volume). From Fig. 2.1 shows that the volume of anatomical dead space is small compared to the total volume of the lungs, and the volume of capillary blood is much less than the volume of alveolar air (see also Fig. 1.7).

Lung volumes

Before moving on to dynamic ventilation metrics, it is useful to briefly review “static” lung volumes. Some of them can be measured using a spirometer (Fig. 2.2). During exhalation, the spirometer bell rises and the recorder pen lowers. The amplitude of oscillations recorded during quiet breathing corresponds to tidal volume. If the subject takes a deep breath, and then exhales as deeply as possible, then the volume corresponding to vital capacity of the lungs(VEL). However, even after maximum exhalation, some air remains in them - residual volume(OO). The volume of gas in the lungs after normal exhalation is called functional residual capacity(FOE).

Functional residual capacity and residual volume cannot be measured using a simple spirometer. To do this, we apply the gas dilution method (Fig. 2.3), which consists of the following. The airways of the subject are connected to a spirometer containing a known concentration of helium gas, which is practically insoluble in the blood. The subject takes several inhalations and exhalations, as a result of which the helium concentrations in the spirometer and in the lungs are equalized. Since there is no loss of helium, it is possible to equate its amounts before and after equalization of concentrations, equal respectively to C 1 X V 1 (concentration X volume) and WITH 2 X X (V 1 +V 2). Therefore, V 2 = V 1 (C 1 -C 2)/C 2. In practice, during the equalization of concentrations, oxygen is added to the spirometer (to compensate for the absorption of this gas by the test subject) and the carbon dioxide released is absorbed.

Functional residual capacity (FRC) can also be measured using a general plethysmograph (Fig. 2.4). It is a large sealed chamber, reminiscent of a pay phone booth, with the subject inside.

Rice. 2.2. Lung volumes. Please note that functional residual capacity and residual volume cannot be measured by spirometry.

Rice. 2.3. Measurement of functional residual capacity (FRC) using the helium dilution method

At the end of a normal exhalation, a plug is used to close the mouthpiece through which the subject is breathing, and he is asked to make several breathing movements. When trying to inhale, the gas mixture in his lungs expands, their volume increases, and the pressure in the chamber increases with a decrease in the volume of air in it. According to the Boyle-Mariotte law, the product of pressure and volume at a constant temperature is a constant value. Thus, P1V1 == P2(V1 -deltaV), where P 1 and P 2 are the pressure in the chamber, respectively, before and during the attempt to inhale, V 1 is the volume of the chamber before this attempt, and AV is the change in the volume of the chamber (or lungs ). From here the AV can be calculated.

Next, you need to apply the Boyle-Marriott law to the air in the lungs. Here the relationship will look like this: P 3 V 2 = P 4 (V 2 + AV), where P 3 and P 4 are the pressure in the oral cavity, respectively, before and during the attempt to inhale, and V 2 is the FRC, which is calculated according to this formula.

Rice. 2.4. Measuring FRC using general plethysmography. When the subject tries to take a breath with the airways blocked, the volume of his lungs increases slightly, the pressure in the airways decreases, and the pressure in the chamber increases. From here, using the Boyle-Marriott law, you can calculate the lung volume (for more details, see the text)

The method of general plethysmography measures the total volume of air in the lungs, including areas that do not communicate with the oral cavity due to the fact that their airways are blocked (see, for example, Fig. 7.9). In contrast, the helium dilution method provides only the volume of air communicating with the oral cavity, i.e., participating in ventilation. In young healthy people, these two volumes are almost the same. In persons suffering from pulmonary diseases, the volume involved in ventilation may be significantly less than the total, since a large amount of gases is isolated in the lungs due to obstruction (closure) of the airways.

Ventilation

Let us assume that with each exhalation, 500 ml of air is removed from the lungs (Fig. 2.1) and that 15 respiratory movements are performed per minute. In this case, the total volume exhaled in 1 minute is 500X15 = 7500 ml/min. This is the so-called general ventilation, or minute volume breathing. The volume of air entering the lungs is slightly greater, since the absorption of oxygen slightly exceeds the release of carbon dioxide.

However, not all inhaled air reaches the alveolar space, where gas exchange occurs. If the volume of inhaled air is 500 ml (as in Fig. 2.1), then 150 ml remains in the anatomical dead space and (500-150) X15 = 5250 ml of atmospheric air passes through the respiratory zone of the lungs per minute. This quantity is called alveolar ventilation. It is of utmost importance because it corresponds to the amount of “fresh air” that can participate in gas exchange (strictly speaking, alveolar ventilation is measured by the amount of air exhaled, not inhaled, but the difference in volumes is very small).

General ventilation can be easily measured by asking the subject to breathe through a tube with two valves that allow air to enter into the airways when inhaling and release it into a special bag when exhaling. Alveolar ventilation is more difficult to assess. One way to determine this is to measure the volume of anatomical dead space (see below) and calculate its ventilation (volume X respiratory rate). The resulting value is subtracted from the total ventilation of the lungs.

The calculations look like this (Fig. 2.5). Let us denote V t, V p, V a, respectively, the tidal volume, the volume of the dead space and the volume of the alveolar space. Then V T =V D +V A , 1)

V T n =V D n +V A n,

where n is the breathing frequency; hence,

where V is the volume per unit of time, V E is the total expiratory (estimated by exhaled air) pulmonary ventilation, V D and V A are dead space ventilation and alveolar ventilation, respectively (a general list of notations is given in the Appendix). Thus,

The difficulty with this method is that the volume of anatomical dead space is difficult to measure, although with a small error it can be assumed to be equal to a certain value.

1) It should be emphasized that V A is the amount of air entering the alveoli in one breath, and not the total amount of alveolar air in the lungs.

Rice. 2.5 . The air leaving the lungs when you exhale (tidal volume, V D) comes from the anatomical dead space (Vo) and alveoli (va). The density of the points in the figure corresponds to the concentration of CO 2. F - fractional concentration; I-inspiratory air; E-expiratory air. Cm. for comparison fig. 1.4 (by J. Piiper with modifications)

In healthy people, alveolar ventilation can also be calculated by the CO 2 content in the exhaled air (Fig. 2.5). Since gas exchange does not occur in the anatomical dead space, at the end of inspiration it does not contain CO 2 (the negligible content of CO 2 in atmospheric air can be neglected). This means that CO2 enters the exhaled air exclusively from the alveolar air, from where we have where Vco 2 is the volume of CO 2 exhaled per unit time. Therefore,

V A = Vco 2 x100 / % CO 2

The value of % CO 2 /100 is often called the fractional concentration of CO 2 and is designated Fco 2 . Alveolar ventilation can be calculated by dividing the amount of CO 2 exhaled by the concentration of this gas in the alveolar air, which is determined in the last portions of exhaled air using a high-speed CO 2 analyzer. The partial pressure of CO 2 РСО 2) is proportional to the concentration of this gas in the alveolar air:

Pco 2 = Fco 2 X K,

where K is a constant. From here

V A = V CO2 /P CO2 x K

Since in healthy people Pco 2 in the alveolar air and in arterial blood are almost the same, Pco 2 in arterial blood can be used to determine alveolar ventilation. Its relationship with Pco 2 is extremely important. So, if the level of alveolar ventilation decreases by half, then (at a constant rate of CO 2 formation in the body) P CO2. in alveolar air and arterial blood will double.

Anatomical dead space

Anatomical dead space is the volume of the conducting airways (Fig. 1.3 and 1.4). Normally, it is about 150 ml, increasing with deep inspiration, as the bronchi are stretched by the surrounding lung parenchyma. The amount of dead space also depends on body size and posture. There is an approximate rule according to which for a sitting person it is approximately equal in milliliters to body weight in pounds (1 pound == 453.6 g).

The volume of anatomical dead space can be measured using the Fowler method. In this case, the subject breathes through a system of valves and the nitrogen content is continuously measured using a high-speed analyzer that takes air from a tube starting at the mouth (Fig. 2.6, L). When a person exhales after inhaling 100% Oa, the N2 content gradually increases as the dead space air is replaced by alveolar air. At the end of exhalation, an almost constant nitrogen concentration is recorded, which corresponds to pure alveolar air. This section of the curve is often called the alveolar “plateau,” although even in healthy people it is not completely horizontal, and in patients with lung lesions it can rise steeply. With this method, the volume of exhaled air is also recorded.

To determine the volume of dead space, a graph is constructed that relates the N 2 content to the exhaled volume. Then a vertical line is drawn on this graph so that area A (see Fig. 2.6.5) is equal to area B. The volume of dead space corresponds to the point of intersection of this line with the abscissa axis. In fact, this method gives the volume of the conducting airways up to the “midpoint” of the transition from dead space to alveolar air.

Rice. 2.6. Measuring the volume of anatomical dead space using the fast N2 analyzer using the Fowler method. A. After inhaling from a container with pure oxygen, the subject exhales, and the concentration of N 2 in the exhaled air first increases and then remains almost constant (the curve practically reaches a plateau, corresponding to pure alveolar air). B. Dependence of concentration on exhaled volume. The volume of dead space is determined by the point of intersection of the x-axis with a vertical dotted line drawn in such a way that the areas of A and B are equal

Functional dead space

You can also measure the volume of dead space Bohr's method. From ris2s. 2.5 it is clear that exhaled CO 2 comes from the alveolar air, and not from the air of the dead space. From here

vt x-fe==va x fa.

Because the

v t = v a + v d ,

v a =v t -v d ,

after substitution we get

VT xFE=(VT-VD)-FA,

hence,

Since the partial pressure of a gas is proportional to its content, we write (Bohr’s equation),

where A and E refer to alveolar and mixed exhaled air, respectively (see appendix). During quiet breathing, the ratio of dead space volume to tidal volume is normally 0.2-0.35. In healthy people, the Pco2 in the alveolar air and arterial blood is almost the same, so we can write the Bohr equation as follows:

asp2"SO-g ^COg

It must be emphasized that the Fowler and Bohr methods measure slightly different indicators. The first method gives the volume of the conducting airways up to the level where the air entering during inspiration quickly mixes with that already in the lungs. This volume depends on the geometry of the respiratory tract, which quickly branches with an increase in the total cross-section (see Fig. 1.5) and reflects the structure of the respiratory system. In this regard, it is called anatomical dead space. The Bohr method determines the volume of those parts of the lungs in which CO2 is not removed from the blood; since this indicator is related to the work of the organ, it is called functional(physiological) dead space. In healthy individuals, these volumes are almost the same. However, in patients with lung lesions, the second indicator can significantly exceed the first due to the unevenness of blood flow and ventilation in different parts of the lungs (see Chapter 5).

Regional differences in ventilation

Until now, we have assumed that the ventilation of all parts of healthy lungs is the same. However, it was found that their lower regions were better ventilated than their upper regions. This can be demonstrated by asking the subject to inhale a gas mixture with radioactive xenon (Fig. 2.7). When 133 Xe enters the lungs, the radiation it emits penetrates the chest and is captured by radiation counters attached to it. This way you can measure the volume of xenon entering different parts of the lungs.

Rice. 2.7. Assessing regional differences in ventilation using radioactive xenon. The subject inhales a mixture of this gas, and the intensity of the radiation is measured by meters placed outside the chest. It can be seen that ventilation in the lungs of a person in an upright position is weakened in the direction from the lower sections to the upper

In Fig. Figure 2.7 presents the results obtained using this method on several healthy volunteers. It can be seen that the level of ventilation per unit volume is higher in the lower parts of the lungs and gradually decreases towards their apexes. It has been shown that if the subject lies on his back, the difference in ventilation of the apical and lower parts of the lungs disappears, however, their posterior (dorsal) areas begin to be ventilated better than the anterior (ventral) ones. Lying on your side allows the lung underneath to be better ventilated. The reasons for such regional differences in ventilation are discussed in Chap. 7.