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EXTERNAL RESPIRATION AND FUNCTIONS OF THE LUNG RESPIRATORY FUNCTION OF THE LUNGS AND PATHOPHYSIOLOGICAL MECHANISMS OF HYPOXEMIA AND HYPROCHEMISTRY

The main function of the lungs - the exchange of oxygen and carbon dioxide between the external environment and the body - is achieved by a combination of ventilation, pulmonary circulation and diffusion of gases. Acute violations of one, two or all of these mechanisms lead to acute changes in gas exchange.

Pulmonary ventilation. Indicators of pulmonary ventilation include tidal volume (VT), respiratory rate (f), and minute respiratory volume (VE). The effectiveness of pulmonary ventilation is determined by the magnitude of alveolar ventilation (VA), i.e. the difference between VЕ and the minute volume of ventilation of the dead space.

A decrease in alveolar ventilation may be due to a decrease in VE or an increase in dead space (Vp). The determining factor is the value of VT, its relation to the unstable value of the physiological dead space. The latter includes anatomical dead space and the amount of inhaled air, ventilating alveoli, in which the blood flow is absent or significantly reduced. Thus, alveolar ventilation should be considered as the ventilation of blood-perfused alveoli. With adequate alveolar ventilation, a certain concentration of gases in the alveolar space is maintained, ensuring normal gas exchange with the blood of the pulmonary capillaries.

Dead space increases with the use of an anesthetic apparatus or respirator, with the use of long breathing hoses and connectors, impaired gas recirculation. In cases of impaired pulmonary circulation, Vp also increases. A decrease in Vp or an increase in Vp immediately leads to alveolar hypoventilation, and an increase in f does not compensate for this condition.

Alveolar hypoventilation is accompanied by insufficient elimination of CO2 and arterial hypoxemia.

The ratio of ventilation / blood flow. The effectiveness of pulmonary gas exchange largely depends on the distribution of inhaled air through the alveoli in accordance with their blood perfusion. Alveolar ventilation in a person at rest is about 4 l / min, and pulmonary blood flow is 5 l / min. In ideal conditions, per unit time alveoli receive 4 volumes of air and 5 volumes of blood, and thus the ventilation / blood flow ratio is 4/5, or 0.8.

Disruptions in the ventilation / blood flow relationship — the predominance of ventilation over the bloodstream or blood flow over ventilation — lead to impaired gas exchange. The most significant changes in gas exchange occur with absolute predominance of ventilation over the bloodstream (dead space effect) or blood flow over ventilation (venoarterial shunt effect. Under normal conditions, the pulmonary shunt does not exceed 7%. This explains the fact that arterial oxygen saturation is less than 100% and equal to 97.1%.

An example of the effect of dead space is pulmonary embolism. Shunting of blood in the lungs occurs with severe lesions of the lung parenchyma, respiratory distress syndrome, massive pneumonia, atelectasis and obstruction of the respiratory tract of any origin. Both effects lead to arterial hypoxemia and hypercapnia. The effect of the shunt is accompanied by severe arterial hypoxemia, which is often impossible to eliminate even with the use of high oxygen concentrations.

Diffusion of gases. The diffusion capacity of the lungs is the rate at which the gas passes through the alveolar-capillary membrane per unit pressure gradient of this gas. This indicator is different for different gases: for carbon dioxide, it is about 20 times more than for oxygen. Therefore, a decrease in the diffusion capacity of the lungs does not lead to an accumulation of carbon dioxide in the blood; the partial pressure of carbon dioxide in arterial blood (PaCO2) is easily balanced with that in the alveoli. The main sign of impaired pulmonary diffusion capacity is arterial hypoxemia.

Causes of violation of diffusion of gases through the alveolar-capillary membrane:

• reduction of the diffusion surface (the surface of functioning alveoli, in contact with functioning capillaries, is normally 90 m2);

• the diffusion distance (the thickness of the layers through which the gas diffuses) can be increased as a result of changes in the tissues along the diffusion path.

Disorders of diffusion processes, previously considered one of the main causes of hypoxemia ("alveolocapillary blockade"), are currently considered as factors that do not have much clinical significance in ARF. Restrictions on the diffusion of gases are possible with a decrease in the diffusion surface and changes in the layers through which diffusion passes (thickening of the walls of the alveoli and capillaries, their swelling, collapse of the alveoli, filling them with liquid, etc.).

Violations of the regulation of respiration. The rhythm and depth of breathing are regulated by the respiratory center located in the medulla, the gas composition of arterial blood is of the greatest importance in the regulation. Increasing PaCO2 immediately causes an increase in ventilation. PaO2 oscillations also lead to changes in respiration, but with the help of impulses going to the medulla from the carotid and aortic bodies. Chemoreceptors of the medulla oblongata, carotid and aortic bodies are sensitive to changes in the concentration of H + cerebrospinal fluid and blood. These mechanisms of regulation can be impaired with lesions of the central nervous system, the introduction of alkaline solutions, mechanical ventilation in the mode of hyperventilation, increasing the threshold of excitability of the respiratory center.

Violations of oxygen transport to the tissues. 100 ml of arterial blood contains approximately 20 ml of oxygen. If the minute heart volume (MOC) is normally at rest 5 l / min, and oxygen consumption is 250 ml / min, then this means that 50 ml of oxygen is extracted from 1 l of circulating blood. In severe physical exertion, oxygen consumption reaches 2500 ml / min, and the MOC rises to 20 l / min, but in this case too, the oxygen reserve of blood remains unused. Tissues take approximately 125 ml of oxygen from 1 liter of circulating blood. The oxygen content in arterial blood of 200 ml / l is sufficient to meet the tissue needs for oxygen.

However, with apnea, complete airway obstruction, and breathing with an anoxic mixture, the oxygen reserve is depleted very quickly — within a few minutes consciousness is disturbed, and after 4-6 minutes hypoxic cardiac arrest occurs.

Hypoxic hypoxia is characterized by a decrease in all indicators of the arterial blood oxygen level: partial pressure, saturation, and oxygen content.
Its main cause is the reduction or complete cessation of oxygen supply (hypoventilation, apnea). Changes in the chemical properties of hemoglobin (carboxyhemoglobin, methemoglobin) lead to this type of hypoxia.

Primary circulatory hypoxia occurs due to a decrease in cardiac output (CB) or vascular insufficiency, which leads to a decrease in oxygen delivery to the tissues. At the same time, the oxygen parameters of arterial blood are not changed, however, PvO2 is significantly reduced.

Anemic hypoxia, usually observed with massive blood loss, is combined with circulatory failure. The concentration of hemoglobin below 100 g / l leads to disruption of the oxygen transport system of the blood. Hemoglobin levels below 50 g / l, hematocrit (Ht) below 0.20 represent a greater threat to the life of the patient, even if the MOS is not reduced. The main feature of anemic hypoxia is a decrease in the oxygen content in arterial blood with normal PaO2 and SaO2.

The combination of all three forms of hypoxia - hypoxic, circulatory and anemic - is possible if the development of ARF occurs against the background of cardiovascular insufficiency and acute blood loss.

Histotoxic hypoxia occurs less frequently and is characterized by the inability of tissues to utilize oxygen (for example, in cyanide poisoning). All three forms of hypoxia (with the exception of histotoxic) equally cause venous hypoxia, which is a reliable indicator of a decrease in PO2 in the tissues. The partial pressure of oxygen in mixed venous blood is an important indicator of hypoxia. A PvO2 level of 30 mmHg is defined as critical.

The value of the oxyhemoglobin (HbO2) dissociation curve. Oxygen in the blood is present in two forms - physically dissolved and chemically bound to hemoglobin. The relationship between PO2 and SO2 is graphically expressed as an oxyhemoglobin dissociation curve (SLC), which is S-shaped. This form of BWW corresponds to the optimal conditions for blood oxygenation in the lungs and the release of oxygen from the blood in the tissues. With PO2 equal to 100 mm Hg, only 0.3 ml of oxygen is dissolved in 100 ml of water. In the alveoli, PO2 is about 100 mm Hg. 2.9 ml of oxygen is physically dissolved in 1 l of blood. Most of the oxygen is transported in a state associated with hemoglobin. 1 g of hemoglobin, fully saturated with oxygen, binds 1.34 ml of oxygen. If the concentration of hemoglobin in the blood is 150 g / l, then the content of chemically bound oxygen is 150 g / l x1.34 ml / g = 201 ml / l. This value is called the oxygen capacity of the blood (KEK). Since the oxygen content in the mixed venous blood (CvO2) is 150 ml / l, then 1 l of blood passing through the lungs must add 50 ml of oxygen to make it arterial. Accordingly, 1 liter of blood passing through body tissues leaves 50 ml of oxygen in them. Only about 3 ml of oxygen per liter of blood is transferred in a dissolved state.

Displacement of BWW is the most important physiological mechanism that ensures the transport of oxygen in the body. The circulation of blood from the lungs to the tissues and from the tissues to the lungs is due to changes that affect the affinity of oxygen for hemoglobin. At the tissue level, due to a decrease in pH, this affinity decreases (the Bohr effect), thereby improving oxygen delivery. In the blood of pulmonary capillaries, the affinity of hemoglobin for oxygen increases due to a decrease in PCO2 and an increase in pH compared with similar indicators of venous blood, which leads to an increase in arterial oxygen saturation.

Under normal conditions, 50% SO2 is reached at PO2 of about 27 mmHg. This value is designated P50 and characterizes in general the position of BWW. An increase in P50 (for example, to 30–32 mm Hg) corresponds to the shift of BWW to the right and indicates a decrease in the interaction of hemoglobin and oxygen. With a decrease in P50 (to 25–20 mm Hg), there is a shift of BWW to the left, which indicates an increased affinity between hemoglobin and oxygen. Due to the S-shaped form of BWW, with a rather significant decrease in the fractional concentration of oxygen in the inhaled air (CLE) to 0.15 instead of 0.21, oxygen transfer is not significantly disturbed. By reducing PaO2 to 60 mm Hg. SaO2 decreases to about 90% of the level, and cyanosis does not develop. However, a further drop in PaO2 is accompanied by a more rapid drop in SaO2 and the oxygen content in arterial blood. When PaO2 falls to 40 mm Hg. Sa02 is reduced to 70%, which corresponds to PO2 and SO2 in mixed venous blood.

The described mechanisms are not the only ones. Intracellular organic phosphate - 2,3-diphosphoglycerate (2,3-DFG) - enters the hemoglobin molecule, changing its affinity for oxygen. Increasing the level of 2,3-DFG in erythrocytes reduces the affinity of hemoglobin for oxygen, and a decrease in the concentration of 2,3-DFG leads to an increase in the affinity for oxygen. Some syndromes are accompanied by pronounced changes in the level of 2,3-FGD. For example, in chronic hypoxia, the content of 2,3-DFG in erythrocytes increases and, accordingly, the affinity of hemoglobin for oxygen decreases, which gives an advantage in supplying the tissues with the latter. Massive transfusions of canned blood can worsen the release of oxygen in the tissues.

Thus, the factors leading to an increase in the affinity of hemoglobin for oxygen and the shift of BWW to the left include an increase in pH, a decrease in PCO2, a concentration of 2,3-DFG and inorganic phosphate, a decrease in body temperature. Conversely, a decrease in pH, an increase in PCO2, a concentration of 2,3-DFG and inorganic phosphate, an increase in body temperature lead to a decrease in the affinity of hemoglobin for oxygen and a shift in the BWW to the right.

In tab. 1.1 shows the normal functional parameters of the lungs.

Table 1.1.

Normal values ​​of functional lung tests

[Comroe J. et al., 1961] 1

1Data are for a healthy person (body surface 1.7 m2) at rest in the supine position while breathing air. Pulmonary volumes and ventilation rates are given by BTPS, diffuse capacity of the lungs - by STPD.
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