Fundamentals of respiratory physiology

The main (though not the only) function of the lungs is to ensure normal gas exchange. External breathing is the process of gas exchange between atmospheric air and blood in the pulmonary capillaries, as a result of which blood arterialization occurs: the oxygen pressure rises and the pressure of CO2 decreases. The intensity of gas exchange is primarily determined by three pathophysiological mechanisms (pulmonary ventilation, pulmonary circulation, diffusion of gases through the alveolar-capillary membrane), which are provided by the external respiration system.

Pulmonary ventilation

The pulmonary ventilation is determined by the following factors (AP Zilber):

1. mechanical ventilation device, which, first of all, depends on the activity of the respiratory muscles, their nervous regulation and mobility of the walls of the chest;
2. elasticity and elongation of lung tissue and thorax;
3. patency of airways;
4. intrapulmonary air distribution and its correspondence to the blood flow in various parts of the lung.

In case of violations of one or more of the above factors, clinically significant ventilation disorders, manifested by several types of ventilation respiratory failure, may develop.

Of the respiratory muscles, the most important role belongs to the diaphragm. Its active reduction leads to a decrease in intrathoracic and intrapleural pressure, which becomes lower than atmospheric pressure, resulting in an inhalation.

The inhalation is carried out due to the active contraction of the respiratory muscles (diaphragm), and exhalation is mainly due to the elastic thrust of the lung and chest wall, creating an expiratory pressure gradient, under physiological conditions sufficient to remove air through the airways.

If it is necessary to increase the volume of ventilation, the outer intercostal, staircases and sternocleidomastoid muscles (additional inspiratory muscles) decrease, which also leads to an increase in the volume of the chest and a decrease in the intrathoracic pressure, which promotes inhalation. The muscles of the anterior abdominal wall (external and internal oblique, straight and transverse) are considered to be additional expiratory muscles.

Elasticity of lung tissue and thorax

Elasticity of the lungs. The movement of air flow during inspiration (inside the lungs) and expiration (from the lungs) is determined by the pressure gradient between the atmosphere and the alveoli, the so-called transthoracic pressure (P _tp / _t ):

Pm / m = P _alv - P _atm where P _alb, is alveolar, and P _atm is the atmospheric pressure.

At the time of inspiration, R _av and P _{mp / m} become negative, during exhalation - positive. At the end of the inspiration and at the end of the exhalation, when the air does not move along the airways, and the voice gap is open, R _alve equals P _atm.

The level of the R _{av depends,} in turn, on the value of the intrapleural pressure (P _m ) and the so-called elastic pressure of the lung (P _el ):

The pressure of elastic recoil is the pressure created by the elastic parenchyma of the lung and directed into the lung. The higher the elasticity of the lung tissue, the greater the decrease in intrapleural pressure, so that the lung expands during inspiration, and, therefore, the greater the active work of the inspiratory respiratory muscles. High elasticity promotes more rapid collapse of the lung during exhalation.

Another important indicator, the inverse elasticity of lung tissue - the apathetic dilatability of the lung - is a measure of the lung's susceptibility to dilating. The tensile (and elastic pressure value) of the lung is affected by a number of factors:

1. Volume of the lung: with a small volume (for example, at the beginning of inspiration) the lung is more pliable. At large volumes (for example, at the height of the maximum inspiration), the extensibility of the lung sharply decreases and becomes zero.
2. The content of elastic structures (elastin and collagen) in the lung tissue. Emphysema of the lungs, for which, as is well known, a decrease in the elasticity of the lung tissue is associated with an increase in the extensibility of the lung (by decreasing the pressure of the elastic response).
3. Thickening of alveolar walls due to their inflammatory (pneumonia) or hemodynamic (congestion of the blood in the lung) edema, as well as fibrosing of the lung tissue significantly reduce the extensibility (compliance) of the lung.
4. Surface tension forces in the alveoli. They arise at the interface between gas and liquid, which lining the alveoli from within with a thin film, and tend to reduce the area of this surface, creating a positive pressure inside the alveoli. Thus, the surface tension forces together with the elastic structures of the lungs provide effective alveolar relief during exhalation and at the same time prevent the expansion (stretching) of the lung during inspiration.

Surfactant lining the inner surface of the alveoli is a substance that reduces the force of surface tension.

The surfactant activity is higher the more dense it is. Therefore, on inhalation, when the density and, accordingly, the activity of the surfactant decreases, the surface tension forces (i.e., the forces striving to reduce the surface of the alveoli) increase, which contributes to the subsequent collapse of the lung tissue during exhalation. At the end of exhalation, the density and activity of the surfactant increase, and the surface tension forces decrease.

Thus, after the expiration of the exhalation, when the activity of the surfactant is maximal, and the surface tension forces preventing alveolar expansion are minimal, the subsequent expansion of the alveoli on inspiration requires less energy.

The most important physiological functions of the surfactant are:

• Increase in extensibility of the lung due to a decrease in surface tension forces;
• decrease in the probability of collapse (collapse) of the alveoli during exhalation, since at small volumes of the lung (at the end of exhalation) its activity is maximal, and the forces of surface tension are minimal;
• prevention of the redistribution of air from the smaller ones to the larger alveoli (according to Laplace's law).

In diseases accompanied by a deficiency of the surfactant, the rigidity of the lungs increases, the alveoli collapse (atelectasis develops), respiratory failure occurs.

[1]

Plastic recoil of the chest wall

The elastic properties of the chest wall, which also have a great effect on the nature of pulmonary ventilation, are determined by the state of the skeleton, intercostal muscles, soft tissues, parietal pleura.

With minimal volumes of chest and lungs (during maximum exhalation) and at the beginning of inspiration, the elastic response of the chest wall is directed to the outside, which creates a negative pressure and promotes the spreading of the lung. As the volume of the lung increases during inspiration, the elastic response of the chest wall will decrease. When the volume of the lung reaches about 60% of the GEL value, the elastic response of the chest wall decreases to zero, i.е. Up to atmospheric pressure. With further increase in lung volume, the elastic response of the thoracic wall is directed towards the inside, which creates a positive pressure and contributes to the collapse of the lungs during the subsequent exhalation.

Some diseases are accompanied by an increase in the rigidity of the chest wall, which affects the ability of the chest to stretch (during inspiration) and subside (during exhalation). Such diseases include obesity, kypho- scoliosis, emphysema, massive moorings, fibrotorax, and others.

Airway passage and mucociliary clearance

The passage of the airways largely depends on the normal drainage of the tracheobronchial secretion, which is primarily due to the functioning of the mucociliary cleansing mechanism (clearance) and normal cough reflex.

The protective function of the mucociliary apparatus is determined by an adequate and consistent function of the ciliated and secretory epithelium, as a result of which the thin secret film moves along the surface of the bronchial mucosa and the foreign particles are removed. The movement of the bronchial secretion occurs due to rapid tremors of the cilia in the cranial direction with a slower recoil in the opposite direction. The frequency of ciliary oscillations is 1000-1200 per minute, which ensures the movement of bronchial mucus at a rate of 0.3-1.0 cm / min in the bronchi and 2-3 cm / min in the trachea.

It should also be remembered that bronchial mucus consists of 2 layers: the lower liquid layer (sol) and the upper viscoelastic - the gel, which touches the tip of the cilia. The function of the ciliary epithelium largely depends on the ratio of the thickness of the yule and gel: increasing the thickness of the gel or reducing the thickness of the sol leads to a decrease in the effectiveness of mucociliary clearance.

At the level of respiratory bronchioles and alveoli of mucociliary apparatus ist. Here purification is carried out with the help of cough reflex and phagocytic activity of cells.

In inflammatory lesions of the bronchi, especially chronic, the epithelium morphologically and functionally reconstructs, which can lead to mucociliary insufficiency (a decrease in the protective function of the mucociliary apparatus) and congestion in the lumen of the bronchi.

In pathological conditions, the patency of the airways depends not only on the functioning of the mucociliary cleansing mechanism, but also on the presence of bronchospasm, inflammatory edema of the mucous membrane, and the phenomenon of early expiratory closure of small bronchi.

[2], [3], [4], [5], [6], [7], [8], [9], [10]

Regulation of bronchial lumen

The tone of the smooth musculature of the bronchi is determined by several mechanisms associated with the stimulation of numerous specific receptors of the bronchi:

1. Cholinergic (parasympathetic) effects occur as a result of the interaction of the neurotransmitter acetylcholine with specific muscarinic M-cholinergic receptors. As a result of this interaction, bronchospasm develops.
2. Sympathetic innervation of the smooth muscles of the bronchi in a person is expressed to a small extent, in contrast, for example, from the smooth muscles of the vessels and the heart muscle. Sympathetic effects on the bronchi are mainly due to the effect of circulating adrenaline on beta2-adrenergic receptors, which leads to relaxation of smooth muscles.
3. The tone of smooth muscles is also affected by the so-called. "Non-adrenergic, non-cholinergic" nervous system (NANH), the fibers of which pass in the vagus nerve and release several specific neurotransmitters interacting with the corresponding receptors of the smooth muscles of the bronchi. The most important of them are:
   • vasoactive intestinal polypeptide (VIP);
   • substance R.

Stimulation of VIP receptors leads to a pronounced relaxation, and beta receptors to a decrease in smooth muscles of the bronchi. It is believed that the neurons of the NANH system have the greatest influence on the regulation of airway clearance (KK Murray).

In addition, bronchus contains a large number of receptors interacting with various biologically active substances, including inflammatory mediators - histamine, bradykinin, leukotrienes, prostaglandins, platelet activating factor (FAT), serotonin, adenosine, etc.

The tone of the smooth musculature of the bronchi is regulated by several neurohumoral mechanisms:

1. Dilation of the bronchi develops with stimulation:
   • beta2-adrenergic receptors adrenaline;
   • VIP receptors (the NASH system) as a vasoactive intestinal polypeptide.
2. The narrowing of the lumen of the bronchi arises with stimulation:
   • M-cholinergic receptors with acetylcholine;
   • receptors to substance P (NANH system);
   • Alpha-adrenergic receptors (eg, with blockade or decreased sensitivity of beta2-adrenergic receptors).

Intrapulmonary air distribution and its correspondence to blood flow

The uneven ventilation of the lungs, which is normal, is determined, first of all, by the heterogeneity of the mechanical properties of the lung tissue. The most active ventilated basal, to a lesser extent - the upper sections of the lungs. The change in the elastic properties of the alveoli (in particular, with pulmonary emphysema) or the violation of bronchial patency significantly exacerbate the unevenness of ventilation, increase the physiological dead space and reduce the effectiveness of ventilation.

Diffusion of gases

The process of diffusion of gases through the alveolar-capillary membrane depends

1. from the gradient of the partial pressure of gases on both sides of the membrane (in the alveolar air and in the pulmonary capillaries);
2. from the thickness of the alveolar-capillary membrane;
3. from the general surface of the diffusion zone in the lung.

In a healthy person, the partial pressure of oxygen (PO2) in the alveolar air is normally 100 mm Hg. And in venous blood - 40 mm Hg. Art. The partial pressure of CO2 (PCO2) in the venous blood is 46 mm Hg. In the alveolar air - 40 mm Hg. Art. Thus, the oxygen pressure gradient is 60 mm Hg. And, for carbon dioxide, only 6 mm of mercury. Art. However, the rate of diffusion of CO2 through the alveolar-capillary membrane is approximately 20 times greater than O2. Therefore, the exchange of CO2 in the lungs is quite complete, despite the relatively low pressure gradient between the alveoli and capillaries.

The alveolar-capillary membrane consists of a surfactant layer lining the inner surface of the alveolus, alveolar membrane, interstitial space, pulmonary capillary membrane, blood plasma and erythrocyte membrane. Damage to each of these components of the alveolar-capillary membrane can lead to a significant difficulty in the diffusion of gases. As a consequence, with the diseases, the above values of the partial pressures of O2 and CO2 in the alveolar air and capillaries can vary significantly.

[11], [12]

Pulmonary blood flow

In the lungs there are two circulatory systems: bronchial blood flow, referring to a large range of blood circulation, and the actual pulmonary blood flow, or the so-called small circulation. Between them, both under physiological and under pathological conditions, there are anastomoses.

The pulmonary blood flow is functionally located between the right and left halves of the heart. The driving force of pulmonary blood flow is the pressure gradient between the right ventricle and the left atrium (normally about 8 mm Hg). In the pulmonary capillaries along the arteries, oxygen-poor and saturated with carbon dioxide venous blood. As a result of diffusion of gases in the area of the alveoli, oxygen saturation and its purification from carbon dioxide occur, as a result of which the arterial blood flows through the veins from the lungs to the left atrium. In practice, these values can fluctuate in significant limits. This especially applies to the level of PaO2 in the arterial blood, which is usually about 95 mm Hg. Art.

The level of gas exchange in the lungs during normal operation of the respiratory muscles, the good patency of the airways and the little-changed elasticity of the lung tissue is determined by the rate of perfusion of blood through the lungs and the condition of the alveolar-capillary membrane through which the diffusion of gases is effected by the gradient of the partial pressure of oxygen and carbon dioxide.

Ventilation-perfusion ratio

The level of gas exchange in the lungs, in addition to the intensity of pulmonary ventilation and diffusion of gases, is also determined by the value of the ventilation-perfusion ratio (V / Q). Normally, with an oxygen concentration of 21% in inspired air and normal atmospheric pressure, the V / Q ratio is 0.8.

Other things being equal, the decrease in oxygenation of arterial blood can be due to two reasons:

• reduction of pulmonary ventilation with the same level of blood flow, when V / Q <0,8-1,0;
• a decrease in blood flow with preserved ventilation of the alveoli (V / Q> 1.0).