O2 and CO2 gas exchange through the alveolar-capillary membrane occurs by means of diffusion, which is carried out in two stages. At the first stage, the diffusion transfer of gases occurs through the air-blood barrier, at the second – the binding of gases in the blood of the pulmonary capillaries occurs, the volume of which leaves 80-150 ml with a thickness of the blood layer in the capillaries only 5-8 microns.Blood plasma practically does not prevent the diffusion of gases, in contrast to the erythrocyte membrane.
The structure of the lungs creates favorable conditions for gas exchange: the respiratory zone of each lung contains about 300 million alveoli and about the same number of capillaries, has an area of 40-140 m2 with a thickness of the air-blood barrier of only 0.3-1.2 μm.
Features of the diffusion of gases are quantitatively characterized through the diffusion capacity of the lungs. For O2 the lung diffusion capacity is the volume of gas transferred from the alveoli into the blood in 1 minute with a gradient of alveolar-capillary gas pressure of 1 mm Hg.
The movement of gases occurs as a result of the difference in partial pressures. The partial pressure is that part of the pressure that this gas constitutes of the total mixture of gases. The reduced pressure of the O2V tissue promotes the movement of oxygen to it.
For CO2 pressure gradient in the opposite direction, and CO2 exhaled air escapes into the environment. The study of the physiology of respiration actually comes down to studying these gradients and how they are supported.
The gradient of the partial pressure of oxygen and carbon dioxide is the force with which the molecules of these gases tend to penetrate the alveolar membrane into the blood. The partial tension of a gas in the blood or tissues is the force with which the molecules of the soluble gas tend to enter the gaseous medium.
At sea level, atmospheric pressure averages 760 mm Hg, and the percentage of oxygen is about 21%. In this case, the pO2 in the atmosphere is: 760 x 21/100 = 159 mm Hg. When calculating the partial pressure of gases in the alveolar air, it should be taken into account that there are vapors in this air (47 mm Hg). Therefore, this number is subtracted from the value of atmospheric pressure, and the proportion of the partial pressure of gases accounts for (760 – 47) = 713 mm Hg. When the oxygen content in the alveolar air is 14%, its partial pressure will be 100 mm Hg. Art. With a carbon dioxide content of 5.5%, the partial pressure of CO2 will be approximately 40 mm Hg.
In arterial blood, the partial tension of oxygen reaches almost 100 mm Hg, in venous blood – about 40 mm Hg, and in the tissue fluid, in cells – 10-15 mm Hg. The voltage of carbon dioxide in arterial blood is about 40 mm Hg, in the venous – 46 mm Hg, and in the tissues – up to 60 mm Hg.
Gases in the blood are in two states: physically dissolved and chemically bound. Dissolution occurs in accordance with Henry’s law, according to which the amount of gas dissolved in a liquid is directly proportional to the partial pressure of this gas above the liquid. Each unit of partial pressure in 100 ml of blood dissolves 0.003 ml of O2, or 3 ml / l of blood.
Each gas has its own solubility coefficient. At body temperature, the solubility of CO2 25 times more than O2. Because of the good solubility of carbon dioxide in the blood and tissues of CO2 tolerated 20 times lighter than O2 The desire of a gas to transfer from a liquid to a gas phase is called a gas voltage. Under normal conditions, only 100 ml of O2 is dissolved in 100 ml of blood and 2.6 ml of CO2.Such values cannot provide the body’s requests for O2.
Oxygen gas exchange between alveolar air and blood occurs due to the presence of O2 concentration gradient. between these mediums. Oxygen transport begins in the capillaries of the lungs, where the bulk of O2 entering the blood enters into a chemical bond with hemoglobin. Hemoglobin is able to selectively bind O2 and form oxyhemoglobin (HbO2). One gram of hemoglobin binds 1.36 to 1.34 ml of O2, and 140–150 g of hemoglobin is contained in 1 liter of blood. Per gram of hemoglobin accounts for 1.39 ml of oxygen. Therefore, in each liter of blood, the maximum possible oxygen content in a chemically bound form will be 190–200 ml O2, or 19% by volume — this is the oxygen capacity of the blood. Human blood contains about 700 – 800 g of hemoglobin and can bind 1 liter of oxygen.
Under the oxygen capacity of the blood understand the amount of O2, which is bound by blood to complete saturation of hemoglobin. Changing the concentration of hemoglobin in the blood, for example, with anemia, poisoning with poisons alters its oxygen capacity. At birth, a person’s blood has a higher oxygen-carrying capacity and hemoglobin concentration. The oxygen saturation of the blood expresses the ratio of the amount of bound oxygen to the oxygen capacity of the blood, i.e. under O2 blood saturation implies the percentage of oxyhemoglobin in relation to the hemoglobin present in the blood.Under normal conditions, O2 saturation is 95–97%. When breathing with pure oxygen, the blood saturation of O2 reaches 100%, and when breathing with a gas mixture with low oxygen content, the saturation percentage drops. With 60 – 65% loss of consciousness occurs.
The dependence of oxygen binding by blood on its partial pressure can be represented as a graph, where the pO2 of blood is deposited along the abscissa, and the ordinate shows the saturation of hemoglobin with oxygen. This graph, the oxyhemoglobin dissociation curve, or the saturation curve, shows what proportion of hemoglobin in a given blood is associated with O2 at one or another of its partial pressure, and which one is dissociated, i.e. free from oxygen. The dissociation curve is S-shaped. The plateau of the curve is characteristic of saturated O2 (saturated) arterial blood, and the steep descending part of the curve is venous, or desaturated, blood in the tissues (Fig. 21).
Fig. 21. Dissociation curves of oxyhemoglobin whole blood
at different blood pH [A) and when the temperature changes (B)
The affinity of oxygen for hemoglobin and the ability to release O2 in tissues depends on the metabolic needs of the cells of the body and is regulated by the most important factors of tissue metabolism, causing a shift in the dissociation curve. These factors include: hydrogen ion concentration, temperature, carbon dioxide partial stress, and the compound that accumulates in red blood cells is 2,3-diphosphoglycerate phosphate (DFG). A decrease in blood pH causes a shift in the dissociation curve to the right, and an increase in blood pH causes a shift in the curve to the left. Due to the increased CO2 content in the tissues, the pH is also lower than in the blood plasma. The pH value and CO2 content in body tissues alter the affinity of hemoglobin for O2. Their influence on the oxyhemoglobin dissociation curve is called the Bohr effect (H. Bohr, 1904). With an increase in the concentration of hydrogen ions and the partial stress of CO2 in the medium, the affinity of hemoglobin for oxygen decreases. This “effect” has an important adaptive meaning: CO2 in the tissues enters the capillaries, so the blood at the same pO2 is able to release more oxygen. The metabolite formed during glucose splitting 2,3-FGD also reduces the affinity of hemoglobin for oxygen.
The oxyhemoglobin dissociation curve is also influenced by temperature. An increase in temperature significantly increases the rate of decomposition of oxyhemoglobin and decreases the affinity of hemoglobin for O2. An increase in temperature in the working muscles contributes to the release of O2. O2 binding hemoglobin reduces the affinity of its amino groups to CO2 (the effect of Holden). CO2 diffusion from the blood into the alveoli is provided by the receipt of CO2 dissolved in the blood plasma (5-10%), from bicarbonates (80-90%) and, finally, from erythrocyte carbamine compounds (5-15%), which are able to dissociate.
Carbon dioxide in the blood is in three fractions: physically dissolved, chemically bound in the form of bicarbonates and chemically bound to hemoglobin in the form of carbohemoglobin.
In venous blood carbon dioxide contains only 580 ml. At the same time, the share of physically dissolved gas is 25 ml, the share of carbohemoglobin is about 45 ml, the share of bicarbonates is 510 ml (plasma bicarbonates is 340 ml, erythrocytes is 170 ml). The arterial blood content of carbonic acid is less.
The process of binding CO2 with blood depends on the partial stress of physically dissolved carbon dioxide. Carbon dioxide enters the erythrocyte, where there is an enzyme carbonic anhydrase, which can increase the rate of formation of carbonic acid by a factor of 10,000. After passing through the erythrocyte, carbonic acid is converted to bicarbonate and is transferred to the lungs.
Red blood cells carry 3 times more CO2 than plasma. Plasma proteins are 8 g per 100 cm3 blood, hemoglobin is contained in the blood of 15 g per 100 cm3. Most of the CO2 transported in the body in the bound state in the form of bicarbonates and carbamine compounds, which increases the exchange of CO2.
Except molecular CO2 dissolved in blood plasma CO2 diffuses from the blood into the alveoli of the lungs, which is released from the carbamine compounds of the erythrocytes due to the oxidation of hemoglobin in the capillaries of the lung, as well as from plasma hydrogen carbonate as a result of their rapid dissociation using the enzyme carbonic anhydrase contained in the erythrocytes. This enzyme is absent in the plasma. Plasma bicarbonates to release CO2 must first enter the red blood cells in order to be exposed to carbonic anhydrase. Sodium bicarbonate is found in plasma, and potassium bicarbonate is found in red blood cells. The erythrocyte membrane is well permeable to CO2, so part of the CO2 rapidly diffuses from the plasma into the erythrocytes. The largest amount of plasma bicarbonate is formed with the participation of erythrocyte carbonic anhydrase.
It should be noted that the process of removing CO2 from blood to the alveoli of the lung is less limited than blood oxygenation, since molecular CO2 penetrates more easily through biological membranes than O2.
Various poisons that limit O2 transport, such as CO, nitrite, ferrocyanide, and many others, have little effect on CO2 transport. Carbonic anhydrase blockers also never completely violate the formation of molecular CO2. Finally, the fabrics have a large buffer capacity, but are not protected from O2 deficiency. Removal of CO2 by the lungs can be impaired with a significant decrease in pulmonary ventilation (hypoventilation) as a result of a disease of the lungs, respiratory tract, intoxication, or dysregulation of respiration. CO2 delay leads to respiratory acidosis – a decrease in the concentration of bicarbonates, a shift in blood pH to the acid side. Excessive removal of CO2 during hyperventilation during intense muscle work, when climbing to high altitudes, can cause respiratory alkalosis, a shift in blood pH to the alkaline side.