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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 options for gas exchange. As is known, the ratio of alveolar ventilation (V) to the perfusion of alveolar capillaries (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 Figure 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, and the larynx accounts for about half.

Physiological (functional) dead space- all those parts of the respiratory system in which gas exchange does not occur. The physiological dead space includes not only the airways, but also the alveoli, which are ventilated, but not perfused by blood (gas exchange is impossible in such alveoli, although their 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. Delay CO 2 is usually noted when increasing the ratio Vd/Vt up to 0.5.

Dead space increases with overdistension of the alveoli or reduced airflow. The first variant is observed in obstructive pulmonary diseases and mechanical ventilation of the lungs with maintaining positive pressure by the end of exhalation, the second - in heart failure (right or left), acute pulmonary embolism and emphysema.

SHUNT FRACTION

The fraction of cardiac output that is not fully balanced with alveolar gas is called the shunt fraction (Qs/Qt, where Qt is total blood flow and Qs is shunt blood flow). However, the V/Q ratio is less than 1 (see part B of Figure 3-1). There are two types of shunt.

true shunt indicates no gas exchange between blood and alveolar gas (V/Q ratio is 0, i.e. the lung 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 fully balanced with alveolar gas, i.e. does not undergo full oxygenation in the lungs. With increasing venous admixture, this shunt approaches a true shunt.

The influence of the shunt fraction on the partial pressure of O 2 and CO 2 in arterial blood (paO 2 PaCO 2, respectively) 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 is involved in gas exchange. With an increase in the fraction of the shunt, paO 2 progressively decreases, and paCO 2 does not increase until the ratio Qs/Qt 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 proportion of the shunt (Qs/Qt), an increase in the fractional concentration of oxygen in the inhaled air or gas mixture (FiO 2) is accompanied by a smaller increase in paO 2 . When the ratio Qs/Qt reaches 50%, paO 2 no longer responds to changes in FiO 2 ; . In this case, the intrapulmonary shunt behaves like a true (anatomical) shunt. Based on the foregoing, it is possible not to use toxic oxygen concentrations if the value of shunt blood flow exceeds 50%, i.e. FiO 2 can be reduced without significant reduction in p a O 2 . This helps reduce the risk of oxygen toxicity.

Rice. 3-2. Effect of 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 inhaled 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), pulmonary embolism (PTE). With pulmonary edema (mainly non-cardiogenic) and TLA, the violation of gas exchange in the lungs more closely resembles a true shunt and PaO 2 reacts weaker to changes in FiO 2. For example, in PLA, a shunt is the result of switching blood flow from the embolized area (where blood flow through the vessels is difficult and perfusion is impossible) to other parts of the lung with increased perfusion [3].

CALCULATION OF GAS EXCHANGE INDICATORS

The equations that will be discussed below are used to quantify the severity of ventilation-perfusion disorders. These equations are used in the study of lung 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 the exhaled alveolar air and capillary (arterial) blood (more precisely, the blood of the end segments of the pulmonary capillaries). In healthy people in the lungs, capillary blood is completely balanced with alveolar gas and pCO 2 in the exhaled alveolar air is almost equal to pCO 2 in arterial blood. With an increase in physiological dead space (ie Vd/Vt ratio), pCO 2 in exhaled air (P E CO 2) will be lower than pCO 2 in arterial blood. This principle is the basis of the Bohr equation used to calculate the Vd/Vt ratio:

Vd / Vt \u003d (PaCO 2 - reCO 2) / p and CO 2. Normally, the ratio Vd/Vt = 0.3.

To determine pCO 2 exhaled air is collected in a large bag and using an infrared CO 2 -analyzer measure the average pCO 2 in the air. This is quite simple and is usually needed 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 \u003d C c O 2 - C a O 2 / (C c O 2 - C v O 2).

Normally, the ratio Qs / Qt \u003d 0.1.

Since CcO 2 cannot be directly measured, it is recommended to breathe pure oxygen in order to completely saturate the hemoglobin of the blood of the pulmonary capillaries with it (ScO 2 \u003d 100%). However, in this situation, only the true shunt is measured. Breathing 100% oxygen is a very sensitive test for shunts because when PaO 2 is high, a small decrease in arterial oxygen concentration can cause a significant drop in PaO 2 .

ALVEOLAR-ARTERIAL DIFFERENCE IN OXYGEN (GRADIENT А-а рО 2)

The difference between the values ​​of pO 2 in the 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:

R A O 2 \u003d 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 inhaled 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 \u003d FiO 2 (P B - pH 2 O). At normal body temperature, pH 2 O is 47 mm Hg. Respiratory quotient (RQ) is the ratio between CO 2 production and O 2 consumption, and gas exchange occurs between the alveolar cavity and the lumen of the capillaries surrounding it by simple diffusion (RQ = VCO 2 / VO 2). In healthy people, when breathing room air at normal atmospheric pressure, the gradient is A-a P O 2 is calculated taking into account the listed indicators (FiO 2 \u003d 0.21, P B \u003d 760 mm Hg, p a O 2 \u003d 90 mm Hg, p a CO 2 = 40 mmHg, RQ = 0.8) as follows:

P a O 2 \u003d FiO 2 (P B - pH 2 O) - (paCO 2 / RQ) \u003d 0.21 (760 - 47) - (40 / 0.8) \u003d 100 mm Hg.

The normal value of the gradient A-a pO 2 \u003d 10-20 mm Hg.

Normally, the A-a pO 2 gradient changes with age and with the oxygen content in the inhaled 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.Influence of FiO 2 ; on the A-a pO 2 gradient and the a / A pO 2 ratio in healthy people.

An increase in the A-a pO 2 gradient by 5-7 mm Hg is noted. for every 10% increase in FiO 2 . The effect of oxygen at 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 increase the fraction of the shunt.

Artificial ventilation of the lungs. Since normal atmospheric pressure is about 760 mm Hg, positive pressure ventilation will increase p i O 2 . The mean airway pressure should be added to the atmospheric pressure, which increases the accuracy of the calculation. For example, an average airway pressure of 30 cm of water column (aq) can increase the A-a pO 2 gradient to 16 mm Hg, corresponding to a 60% increase.

RATIO а/А рО 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 \u003d 1 - (A-a pO 2) / paO 2

The presence of p A O 2 both in the numerator and denominator of the formula excludes the influence of FiO 2 through p A O 2 on the ratio a/A pO 2 . Normal values ​​for the ratio a/A pO 2 are shown 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 determine the cause of hypoxemia, the presence of a catheter in the pulmonary artery is necessary, 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. The normal value of the gradient indicates the absence of lung pathology (eg, muscle weakness). An increase in the gradient indicates a violation of the ventilation-perfusion relationship or a low partial pressure of oxygen in 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 the mixed venous blood (pulmonary artery), with the addition of oxygen from the alveolar gas. With normal lung function, the indicator p A O 2 mainly determines the value of p a O 2.

Rice. 3-5. Approach to establishing the cause of hypoxemia. Explanation in the text.

When gas exchange is disturbed, the indicator p a O 2 makes a smaller contribution, and venous oxygenation (i.e. the indicator p v O 2) - on the contrary, is larger in 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 exchange (in the figure this is indicated as a shunt), p a O 2 decreases. When the increase rate of p a O 2 is constant but p v O 2 is lowered, 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 an insignificant effect on p a O 2 . With an increase in the shunt fraction, p v O 2 becomes an increasingly significant factor that determines p a O 2 . In the extreme case, a 100% shunt is possible, when p v O 2 may be the only indicator that determines p a O 2 . Therefore, 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 ratio between the amount of metabolic production of CO 2 and the rate of its release by the lungs:

p a CO 2 \u003d K x (VCO 2 / Va),

where p a CO 2 - 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 relation , and then the previous formula becomes:

p a CO 2 \u003d K x,

where ve is the exhaled minute volume (minute ventilation measured on exhalation). It can be seen from the equation that the main reasons for CO 2 delay are the following: 1.) increase in 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 development of hypoxemia. Explanation in the text.

Rice. 3-7. Explanation in the text.

INCREASED CO2 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 that measures its content in the exhaled air (with each exhalation). To determine the rate of CO 2 release, the respiratory rate is recorded.

respiratory rate. 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 rate of absorption (consumption) of oxygen (usual value VO 2 = 250 ml / min). The ratio of VCO 2 /VO 2 is called the respiratory (respiratory) coefficient (RQ), which is widely used in clinical practice. RQ is different in the biological oxidation of carbohydrates, proteins and fats. For carbohydrates, it is the highest (1.0), somewhat less for proteins (0.8) and the smallest for fats (0.7). With a mixed diet, 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 contains 70% of total calories from carbohydrates and 30% from fat. RQ is discussed in more detail in Chapter 39.

etiological factors. Usually, 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. Sepsis is believed to be the most common cause of an increase in VCO 2 . An increase in the work of the respiratory system can lead to CO 2 retention when the patient is disconnected from the ventilator if the elimination of CO 2 through the lungs is impaired. Excessive carbohydrate intake can raise RQ to 1.0 or higher and cause CO 2 retention, so it is important to measure PaCO 2 , which is directly related to VCO 2 and not RQ. Indeed, VCO 2 can also increase with a 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 the breath). On 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 RO 2 gradient. An exception is a significant delay in CO 2 in case of lung disease, when the magnitude of the A-a pO 2 gradient is close to normal. In such a situation, the increase in airway resistance can be so pronounced that the air will be practically unable to reach the alveoli (similar to holding the 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 the 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 respiratory muscle weakness. 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. Injury to the phrenic nerve may occur during cardiopulmonary bypass surgery due to local cooling of the surface of the heart (see Chapter 2).

Weakness of the respiratory muscles can be determined by measuring the maximum inspiratory pressure (P mvd) directly at the patient's bedside. To do this, the patient, after the deepest exhalation (up to the residual volume), must inhale with maximum effort through the closed valve. R MVD depends on age and gender (see Table 30-2) and ranges from 80 to 130 cm of water. in most adults. CO 2 retention is noted when Pmvd drops to 30 cm of water. It should be remembered that R MVD is measured with the participation of all respiratory muscles, excluding the diaphragm. Therefore, dysfunction of the diaphragm alone, including damage to the phrenic nerve, may be missed in the determination of PMVD, because the accessory muscles are able to maintain PMVD 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 (sleep apnea) is characterized by impaired breathing during sleep and is never accompanied by daytime hypoventilation. The condition of patients with THS and sleep apnea improves with a decrease in excess body weight; in addition, progesterone may be effective in THC (see Chapter 26). Dysfunction of the phrenic nerve can 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. Clinic Chest. Med 1983; 4:149-159.
5. Shapiro B. 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 GC. Misapplication of the alveolar gas equation. N Engi J Med 1985; 312:586.
9. Gilbert R, Kreighley 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. ClinSci 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, lung parenchyma, pleura, musculoskeletal skeleton of the chest and diaphragm constitute a single working organ, through which lung ventilation.

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

The intensity of ventilation is determined inspiratory depth And frequency breathing.
The most informative indicator of lung ventilation is minute volume of breathing, defined as the product of tidal volume times the number of breaths per minute.
In an adult male in a calm state, the minute volume of breathing is 6-10 l / min,
during operation - from 30 to 100 l / min.
The frequency of respiratory movements at rest is 12-16 per 1 min.
To assess the potential of athletes and persons of special professions, a sample with arbitrary maximum ventilation of the lungs 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 the human lungs are ventilated differently, depending on the position of the body.. When a person is upright, the lower sections of the lungs are ventilated better than the upper ones. If a person lies on his back, then the difference in ventilation of the apical and lower parts of the lungs disappears, however, while the rear (dorsal) their areas begin to ventilate better than the front (ventral). In the supine position, the lung located below is better ventilated. The uneven ventilation of the upper and lower parts of the lung in the vertical position of a person is due to the fact that transpulmonary pressure(pressure difference in the lungs and pleural cavity) as a force that determines the volume of the lungs and its changes, these sections of the lung are not the same. Since the lungs are weighty, the transpulmonary pressure is less at their base than at their apex. In this regard, the lower parts of the lungs at the end of a quiet exhalation are more squeezed, however, when inhaling, they straighten out better than the tops. This also explains the more intensive ventilation of the lung sections that are below, if a person lies on his back or on his 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. is the so-called (FOE). At the end of inspiration, this volume increases by the value of 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 part of it reaches the alveoli, where it mixes with the alveolar air. The rest, usually a 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 respiratory 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 by blood. In such alveoli, gas exchange is impossible, although their ventilation does occur.

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

The essence of ventilation

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Thus, ventilation provides intake of outside air into the lungs and parts of it into the alveoli and removal instead of it gas mixtures(exhaled air), consisting of alveolar air and that part of the outside air that fills the dead space at the end of inhalation and is removed first at the beginning of exhalation. Since the alveolar air contains less oxygen and more carbon dioxide than the outside air, the essence of lung ventilation is reduced 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 removal of carbon dioxide(entering the alveoli from the blood of the pulmonary capillaries). Between the level of tissue metabolism (the rate of consumption of oxygen by tissues and the formation of carbon dioxide in them) and ventilation of the lungs, there is a relationship close to direct proportionality. Correspondence of pulmonary and, most importantly, alveolar ventilation to the level of metabolism is provided 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 respiratory volume and respiratory rate) with an increase in the rate of oxygen consumption and the formation of carbon dioxide in tissues.

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

Therefore, there is a distinction "pulmonary ventilation" And "alveolar ventilation".

Alveolar ventilation

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Alveolar ventilation cannot be explained only by the convective air currents in the lungs created by active inspiration. 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 - another 200 ml. If all this space, in which there is almost no gas exchange, were "washed" by convective flows 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 means of convective flows, then atmospheric oxygen can reach the alveoli only with an inhalation volume of at least 1500 ml, while the usual tidal volume in humans is 400-500 ml.

Under conditions of calm breathing (respiratory rate 15 a.m., inhalation duration 2 s, average inspiratory volume velocity 250 ml/s), during inhalation (tidal volume 500 ml) outside air fills the entire conductive (volume 175 ml) and transitional (volume 200 ml) zones of the bronchial tree. Only a small part of it (less than 1/3) enters the alveolar passages, the volume of which is several times greater than this part of the respiratory volume. With such an inhalation, the linear velocity of the inhaled air flow in the trachea and main bronchi is approximately 100 cm/s. In connection with the successive division of the bronchi into ever smaller ones in diameter, 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 transitional 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 occur during active inspiration and are due to the difference between the air pressure in the environment and the pressure in the alveoli is very small in the distal parts of the tracheobronchial tree, and air enters the alveoli from the alveolar ducts and alveolar sacs by convection at a low linear speed. However, the total cross-sectional area not only of the alveolar passages (thousands cm 2), but also of the respiratory bronchioles that form the transition zone (hundreds of cm 2), is large enough to ensure the diffusion transfer of oxygen from the distal sections of the bronchial tree to the alveoli, and carbon dioxide - in the opposite direction.

Due to diffusion, the composition of the air in the airways of the respiratory and transitional zones approaches the composition of the alveolar. Hence, diffusion movement of gases increases the volume of the alveolar and reduces the volume of dead space. In addition to a large diffusion area, this process is also provided by a significant partial pressure gradient: 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) higher than in the inhaled air. Within one second, due to diffusion, the concentration of oxygen and carbon dioxide in the alveoli and nearby structures (alveolar sacs and alveolar ducts) almost equalize.

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) and 5.3 kPa (40 mm Hg) in its distal part. Thus, along the bronchial tract there is a layer-by-layer unevenness of the air composition from atmospheric to alveolar (Fig. 8.4).

Fig.8.4. Scheme of alveolar ventilation.
"a" - according to obsolete and
"b" - according to modern ideas. MP - dead space;
AP - alveolar space;
T - trachea;
B - bronchi;
DB - respiratory bronchioles;
AH - alveolar passages;
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 mode of breathing and, first of all, on the rate of inhalation; the greater the inspiratory rate (i.e., as a result, the greater the minute volume of respiration), the more distally along the bronchial tree, convective flows are expressed at a rate that prevails over the diffusion rate. As a result, with an increase in the minute volume of breathing, the dead space increases, and the border 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 discuss how inhaled air enters the alveoli, how gases pass through the alveolar-capillary barrier, and how they are removed from the lungs in the bloodstream. These three processes are provided respectively by ventilation, diffusion and blood flow.

Rice. 2.1. Scheme of the lung. 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 changes)

On fig. 2.1 shows a schematic representation of the lung. The bronchi that form the airways (see Fig. 1.3) are represented here by one tube (anatomical dead space). Through it, air enters the gas exchange departments, limited by the alveolar-capillary membrane and the blood of the pulmonary capillaries. With each breath, about 500 ml of air (tidal volume) enters the lungs. From fig. Figure 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 Figure 1.7).

lung volumes

Before moving on to dynamic ventilation rates, it is useful to briefly review “static” lung volumes. Some of these can be measured with a spirometer (Figure 2.2). During exhalation, the bell of the spirometer rises and the pen of the recorder falls. The amplitude of oscillations recorded during quiet breathing corresponds to respiratory volume. If the subject takes the deepest possible breath, and then exhale as deep as possible, then the volume corresponding to lung capacity(WISH). However, even after maximum expiration, some air remains in them - residual volume(OO). The volume of gas in the lungs after a normal expiration is called functional residual capacity(FOE).

Functional residual capacity and residual volume cannot be measured with a simple spirometer. To do this, we apply the gas dilution method (Fig. 2.3), which consists in the following. The airways of the subject are connected to a spirometer containing a known concentration of helium gas, which is practically insoluble in blood. The subject takes several breaths 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, which are respectively C 1 X V 1 (concentration X volume) and WITH 2 X X (V 1 + V 2). Therefore, V 2 \u003d 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 subjects) and the carbon dioxide released is absorbed.

Functional residual capacity (FRC) can also be measured using a common plethysmograph (Fig. 2.4). It is a large hermetic chamber, resembling 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, the mouthpiece through which the subject breathes is closed with a plug, and he is asked to make several respiratory movements. When you try 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 an 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 you can calculate AV.

Next, you need to apply the Boyle-Mariotte law to the air in the lungs. Here the dependence will look like this: P 3 V 2 \u003d P 4 (V 2 + AV), where P 3 and P 4 are the pressure in the oral cavity, respectively, before and during an attempt to inhale, and V 2 is the FRC, which is calculated by this formula.

Rice. 2.4. Measurement of FRC using general plethysmography. When the subject tries to take a breath with the airways blocked, his lung volume increases slightly, the airway pressure decreases, and the pressure in the chamber increases. From here, using the Boyle-Mariotte law, you can calculate the volume of the lungs (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 gives only the volume of air that communicates with the oral cavity, i.e., participates in ventilation. In young healthy people, these two volumes are almost the same. In persons suffering from lung diseases, the volume involved in ventilation may be significantly less than the total volume, since a large amount of gases is isolated in the lungs due to obstruction (closure) of the airways.

Ventilation

Suppose that 500 ml of air is removed from the lungs with each exhalation (Fig. 2.1) and that 15 breaths are taken per minute. In this case, the total volume exhaled in 1 minute is 500x15 == 7500 ml/min. This so-called general ventilation, or minute volume breathing. The volume of air entering the lungs is slightly larger, 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 value is called alveolar ventilation. It is of the utmost importance, since it corresponds to the amount of “fresh air” that can participate in gas exchange (strictly speaking, alveolar ventilation is measured by the amount of exhaled rather than inhaled air, however, 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 - letting air in when inhaling into the airways and releasing it when exhaling into a special bag. Alveolar ventilation is more difficult to assess. One way to determine it is to measure the volume of the anatomical dead space (see below) and calculate its ventilation (volume X respiratory rate). The resulting value is subtracted from the total lung ventilation.

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

V T n \u003d V D n + V A n,

where n is the respiratory rate; hence,

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

The complexity of this method lies in the fact that the volume of anatomical dead space is difficult to measure, although with a small error it can be taken 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 during expiration (tidal volume, V D) comes from the anatomical dead space (Vo) and alveoli (va). The density of dots 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 (according to J. Piiper with changes)

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

V A \u003d Vco 2 x100 /% CO 2

The value of % CO 2 /100 is often called the fractional concentration of CO 2 and denoted by Fco 2 . Alveolar ventilation can be calculated by dividing the amount of exhaled CO 2 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 Pco 2) is proportional to the concentration of this gas in the alveolar air:

Pco 2 \u003d Fco 2 X K,

where K is a constant. From here

V A = V CO2 /P CO2 x K

Since Pco 2 in alveolar air and arterial blood are practically the same in healthy people, 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 is halved, then (at a constant rate of formation of CO 2 in the body) Р 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 a deep breath, as the bronchi are stretched by the lung parenchyma surrounding them. The volume of dead space also depends on the size of the body and posture. There is an approximate rule according to which, in a seated person, it is approximately equal in milliliters to body weight in pounds (1 pound \u003d \u003d 453.6 g).

Anatomical dead space volume can be measured using the Fowler method. In this case, the subject breathes through the valve system 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 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 go up steeply. With this method, the volume of exhaled air is also recorded.

To determine the volume of dead space build a graph linking the content of N 2 with 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 x-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. Measurement of anatomical dead space volume using the fast N2 analyzer according to 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 abscissa axis with a vertical dotted line drawn in such a way that the areas A and B are equal

Functional dead space

You can also measure dead space Bohr's method. From Fig.2c. Figure 2.5 shows that the exhaled CO2 comes from the alveolar air and not from the dead space air. 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). With quiet breathing, the ratio of dead space to tidal volume is normally 0.2-0.35. In healthy people, Pco2 in alveolar air and arterial blood are almost the same, so we can write the Bohr equation as follows:

asr2"CO-g ^ CO2

It should be emphasized that the Fowler and Bohr methods measure somewhat different indicators. The first method gives the volume of the conducting airways up to the level where the air entering during inhalation quickly mixes with the air already in the lungs. This volume depends on the geometry of the rapidly branching airways with an increase in the total cross section (see Fig. 1.5) and reflects the structure of the respiratory system. For this reason it is called anatomical dead space. According to the Bohr method, the volume of those parts of the lungs in which CO2 is not removed from the blood is determined; since this indicator is related to the work of the body, 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 may significantly exceed the first due to uneven blood flow and ventilation in different parts of the lungs (see Chapter 5).

Regional differences in lung ventilation

So far, we have assumed that the ventilation of all sections of healthy lungs is the same. However, it was found that their lower sections are ventilated better than the upper ones. You can show this by asking the subject to inhale a gas mixture with radioactive xenon (Fig. 2.7). When 133 Xe enters the lungs, the radiation emitted by it penetrates the chest and is captured by radiation counters attached to it. So you can measure the amount of xenon entering different parts of the lungs.

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

On fig. 2.7 shows 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 region of the lower parts of the lungs and gradually decreases towards their tops. It has been shown that if the subject lies on his back, the difference in ventilation of the apical and lower sections of the lungs disappears, however, in this case, their posterior (dorsal) areas begin to be ventilated better than the anterior (ventral). In the supine position, the lower lung is better ventilated. The reasons for such regional differences in ventilation are discussed in Chap. 7.