From Big Medical Encyclopedia

BREATH — set of the processes providing receipt in an organism of oxygen, its use in biol, oxidation of organic matters and removal from an organism of carbon dioxide gas. As a result biol, oxidations in cells the energy going for ensuring life activity of an organism is released (see. Metabolism and energy ). At the elementary animals exchange of gases with the environment is carried out directly through a body surface. At metazoans in process of increase in the sizes of a body bodies of external respiration (the gill easy) were formed; they developed in close connection with the blood circulatory system. At vertebrate animals and the person D. includes external D., transport of gases blood (see. Gas exchange ) and fabric D. (see. biological oxidation ).

D.'s essence as oxidizing process was opened in 1777 for A. Lavoisier. Bases of the theory of gas exchange in lungs and transport of gases blood are put by I. M. Sechenov.

A. Krog in 20 — proved the 30th that gas exchange in lungs is carried out by diffusion, and developed model of gas exchange between capillaries and fabrics. Properties of an alveolar air and pattern of maintenance of constancy of its structure are studied by J. Haldane with sotr. In the 30th J. Barkroft developed the theory of transport hemoglobin of oxygen and carbon dioxide gas. Rorer (F. Rohrer, from 1915 to 1935) laid the foundation of the theory of ventilation of the lungs as biomechanical act, edges gained broad development in Fenn's works (W. The lake of Fenn, from 1946 to 1973), etc. Neergard (To. Neergard, from 1927 to 1929) and Pattl (R. E. Pattle, 1955) showed the nature of an elastic energy of lungs. The big contribution to studying of processes of regulation of D. was made Breyer (J. Breuer, 1868) and E. Goering, the opened reflex influences of lung volume on frequency and D.'s depth, Vinterstein (H. Winterstein, from 1911 to 1958) who formulated bases of the theory of humoral regulation of D., K. Geymans who found out with the sotr. a role of arterial chemoceptors in regulation of breath, AA. Adrian (1933) who studied properties of stretch receptors of lungs.

Understand the processes providing exchange of gases between the environment and blood as external D. At the majority of the animals living in water, external D. is carried out by a body surface and gills. At insects the body is penetrated by dense network of tubules — the tracheas bringing air to fabrics. At vertebrate animals (amphibians) upon transition to land dwelling the lungs which developed as a pair outgrowth of the tail of branchiate area of intestines were created. Reptiles already have a trachea and bronchial tubes. At birds gas exchange happens in lungs and in a trapped air between internals, muscles, and also in bones; a trapped air is continuation of large bronchial tubes. At mammals and the person gas exchange happens generally in alveoluses of lungs and only apprx. 2% of the oxygen coming to blood gets through skin. Pneumatic ways in lungs form similarity of a dense tree (see. Bronchial tubes , Lungs ). At the person on an extent from a trachea to the smallest bronchial tubes pneumatic ways branch on average 17 times, each branching gives on average apprx. three affiliated branches. Alveoluses are located on walls of respiratory bronchioles and the alveolar courses. The quantity of alveoluses in one lung of the person averages 375 million. Diameter of alveoluses changes at D., increasing at breaths, and makes 150 — 300 microns. The area of contact of capillaries of a small circle of blood circulation with alveoluses apprx. 90 sq.m. Blood from an alveolar air is separated by the so-called pulmonary membrane consisting of endothelial cells, two main membranes, a flat alveolar epithelium and a surface-active lipoid and proteinaceous vystilka (see. Surfactant ). Thickness of a pulmonary membrane is 0,4 — 1,5 microns. Expired air represents mix of alveolar and free air of pneumatic ways (see tab. 1).

Table 1. Structure of the inhaled, exhaled and alveolar air, in % (according to A. G. Ginetsinsky)

Gas exchange between an alveolar air and blood happens by diffusion of molecules of gases on a gradient of partial pressures (or tension of dissolved gases). With the barometric pressure equal to 760 mm of mercury., pressure of gases is equal in an alveolar air to 713 mm of mercury. (a difference — 47 mm of mercury. — makes pressure of water vapors). Respectively pressure of oxygen makes about 106, carbon dioxide gas — 39, nitrogen — 568 mm of mercury. Nitrogen is dissolved in liquids of an organism (with an atmospheric pressure apprx. 1,5 l), but does not participate in a metabolism. Tension of oxygen in the mixed blood apprx. 40 mm of mercury. Swing pressure of oxygen between an alveolar air and blood at the beginning of pulmonary capillaries makes apprx. 60 mm of mercury. By the end of a capillary tension of oxygen in blood is practically leveled with partial pressure in an alveolar air. Permeability of a pulmonary membrane for gas is expressed the size of diffusion capacity of lungs, edges are represented by amount of the gas getting through a pulmonary membrane in 1 min. on 1 mm of mercury. gradient of pressure. This size is directly proportional to a surface, through to-ruyu there is a gas exchange, to a diffusion coefficient, solubility of gas in a membrane and is inversely proportional to thickness of a membrane. Normal diffusion capacity of lungs for oxygen — apprx. 25 ml / (min. • mm of mercury.). Tension of oxygen in an arterial blood on 5 — 15 mm of mercury. below, than in an alveolar air. It is explained by an adulteration of a venous blood from bronchial and coronary vessels, irregularity of the relations between ventilation of alveoluses (VA) and perfusion by blood of their capillaries (Q). Normal the relation of VA:Q is close to 0,8 — 1,0. Ventilation of various sites of lungs and rate of volume flow of a blood flow through capillaries of alveoluses are not identical. From alveoluses with insufficient ventilation flows blood with the low tension of oxygen.

Tension of carbon dioxide gas in a venous blood apprx. 46 mm of mercury. The gradient of pressure apprx. a pulmonary membrane is small (6 — 7 mm of mercury.), but it is sufficient for alignment of pressure by the end of a capillary. It is explained high (more than by 20 times bigger, than at oxygen) by solubility of carbon dioxide gas in a pulmonary membrane. But irregularity of the relation between ventilation of alveoluses and perfusion by blood of their capillaries (VA:Q) and an adulteration of a venous blood increase tension of carbon dioxide gas in an arterial blood on 1 — 3 mm of mercury. in comparison with an alveolar air.

Ventilation of the lungs is provided with periodic change of breaths (inspiration) and exhalations (expiration). Frequency of respiratory movements at rest on average 14 — 18 in min. The exhalation is usually 10 — 20% longer than a breath. Ventilation of the lungs is carried out due to energy of reductions of system respiratory muscles (see). Muscles of a breath (a muscle of a diaphragm, outside intercostal, interchondral parts of internal intercostal muscles) increase the volume of a chest cavity. Muscles of an exhalation (a muscle of an abdominal wall, interosseous parts of internal intercostal muscles) reduce the volume of a chest cavity. Lungs are surrounded hermetically with the closed pleural cavity, in a cut 1 — 5 ml of the serous liquid distributed on a pulmonary surface by a layer 5 — 10 microns thick contains.

Fig. 1. The curve of changes of intrapleural pressure at a quiet dykhanii:v the end of a quiet exhalation reaches intrapleural pressure — 5 cm w.g., and at the end of a quiet breath — 8 cm w.g.
Fig. 2. The scheme of a ratio of intra pulmonary and intrapleural pressure at quet breathing: and — a way of definition intra pulmonary and intrapleural pressure during a breath and an exhalation (1 — the manometer determining intra pulmonary pressure by the probe entered into a gullet; 2 — the manometer determining intrapleural pressure); — the curves characterizing reduction during a breath and increase during an exhalation intra pulmonary (1) and intrapleural (2) pressure, the horizontal line — the level of atmospheric pressure.

Lung volume is defined by force of PL, edges P A — Ppl is equal to a difference between pressure in alveoluses of RA and intrapleural (intrathoracic) pressure of Ppl PL =). The size PL is called transpulmonic pressure. In normal conditions lungs are always stretched, the elastic energy of lungs aims to reduce their volume. At disturbance of tightness of a pleural cavity it includes air — develops pheumothorax (see), and lungs are fallen down. The elastic energy of lungs normal provides negative pressure in a pleural cavity (in relation to pressure in alveoluses). Ppl therefore to in number equally elastic energy of easy EL. At the end of a quiet exhalation of Ppl fluctuates from — 2 to — 5 cm w.g. At a breath owing to increase in volume of a chest cavity of Ppl becomes more negative: at quiet breaths from — 4 to — 8 cm w.g. (fig. 1), at strong breaths to — 20 cm w.g. Owing to increase in transpulmonic pressure lung volume increases. Quiet exhalations occur without participation of reductions of muscles of an exhalation, at the expense of the elastic forces which are saved up during a breath. Such exhalations call passive. At ventilation of the lungs with intensity more than 40 l/min exhalations become active due to reductions of muscles of an exhalation.

Changes of intrapleural pressure at the person can be registered by means of the esophageal probe since pressure in a cavity of a gullet rather precisely reproduces changes of intrapleural pressure. For this purpose on depth apprx. 45 cm enter into a gullet thin (1,5 — 2,0 mm) the probe with a rubber bulb on the end, connect other end of the probe to the manometer (fig. 2, a).

Fig. 3. Scheme of model of Donders: 1 — a glass bell; 2 — a rubber membrane; 3 — «pleural cavity»; 4 — «lungs»; 5 — the manometer for measurement of intrapleural pressure; 6 — a tube in «pleural cavity»; 7 — branch with a clip for various manipulations; 8 — a «tracheal» tube. Solid lines — a condition of quiet «exhalation», a dotted line — a condition of «breath».

Pressure in alveoluses (PA) at open pneumatic ways and lack of an air flow to equally atmospheric pressure (PB). But when on pneumatic ways air moves, on their length owing to power consumption on friction there is a pressure drop. RA changes the stronger, than the speed of an air flow and airway resistance to an air flow is more. During a breath pressure in alveoluses decreases, during an exhalation increases in relation to the atmospheric pressure (fig. 2,6). At quet breathing the size PA deviates PB on 1 — 2 cm w.g. At the closed pneumatic ways the attempt to make a breath leads to pressure decrease in lungs to — 70 mm of mercury. (Müller's experience). In these conditions the attempt to make an exhalation causes pressure boost in a chest cavity to 100 mm of mercury., and inflow of blood to heart (Valsalva's experience) is at a loss. The sizes of pressure received in Müller and Valsalva's experiences use for assessment of force of muscles of a breath and an exhalation. The mechanics of ventilation of the lungs is illustrated by Donders's (fig. 3) model. The glass bell corresponds to motionless parts of walls of a chest cavity, a rubber membrane — mobile. Under a bell place the isolated «lungs», connect «trachea» by means of a tube to the atmosphere. The second tube connects to the atmosphere or to the manometer «pleural cavity». Having created in «pleural cavity» a nek-swarm depression and having pressurized it, observe increase in volume of «lungs». Delaying a rubber membrane, increase the volume of «a chest cavity» and observe «breath». Release of a membrane conducts to «a passive exhalation», cave-in of a membrane in a bell — to «an active exhalation». If at the stretched «lungs» to connect to the manometer «a tracheal tube», and «pleural cavity» with the atmosphere, the manometer will show positive pressure in «lungs» — manifestation of an elastic energy of lungs.

Air volume in lungs at the end of a quiet exhalation is called functional residual capacity and makes the sum of reserve volume of the exhalation (about 1500 ml) brought out of lungs at a deep exhalation and the residual volume remaining in lungs after a deep exhalation (about 1500 ml). During one breath respiratory volume (comes to lungs at quet breathing of 400 — 500 ml), and at the deepest breath — still the reserve volume of a breath (about 1500 ml). The air volume leaving lungs at the deepest exhalation after the deepest breath makes so-called. vital capacity of lungs (see). The Vital Capacity of Lungs (VCL) represents the total size of respiratory volume, reserve volume of a breath and reserve volume of an exhalation and averages 3500 ml. Total capacity of lungs is defined by size ZhEL and residual volume. Lung volume, except for residual volume, is determined by method of spirometry (see. Spirography ); functional residual capacity — on the volume of the nitrogen which is washing away from lungs at breath by pure oxygen. The minute volume of ventilation of the lungs (MOV) — the volume of the inhaled or expired air in 1 min. (see. Lung ventilation ). When respiratory coefficient (see) less than 1, the volume of expired air is a little less than inhaled. MOV equals to the work of respiratory volume on a respiration rate. In rest of MOV it is equal to 6 — 9 l. Maximal ventilation of lungs most often fluctuates within 80 — 90 l/min, and at the trained persons can reach 170 l/min. For definition of MOV use gas meters and a method pnevmotakhografiya (see).

Not all inhaled air volume reaches alveoluses. The gleam of pneumatic ways in which gas exchange does not happen is called the anatomic dead or harmful space (see). Gas exchange does not happen also in alveoluses or sites of the alveoluses deprived of contact with capillaries or at the termination of a blood-groove in them. This part of respiratory volume which is not participating in gas exchange is called physiological dead space. Its volume is changeable — increases at breaths, especially deep. The air volume replaced for a unit of time in alveoluses makes the size of alveolar ventilation. It is equal to MOV minus the volume of ventilation of dead space (see. Harmful space ). Gas exchange in lungs happens continuously — during breaths and exhalations. For one D. is replaced apprx. 1/10 parts of an alveolar air. Therefore at quet breathing the structure of an alveolar air depends on a phase D a little. At D.'s deepening fluctuations of structure of an alveolar air increase.

The structure of an alveolar air on rather fixed level is supported by mechanisms of regulation of external. Insufficient ventilation of the lungs (hypoventilation) leads to increase in tension of carbonic acid (hypercapnia) and reduction of tension of oxygen, dissolved in an arterial blood (an anoxemia and asphyxia). (See below) increase in ventilation of the lungs is a consequence of these changes.

Excess ventilation of the lungs leads to undervoltage of carbonic acid in blood (hypocapny) and to increase in tension of oxygen (hyperoxia). As a result the respiratory movements weaken or temporarily stop (apnoea). D.'s weakening and its stop occur also at the progressing hypoxia. This state is extremely life-threatening.

Size MOV is defined by tension of carbonic acid in an arterial blood and cerebrospinal liquid. Tension of carbonic acid is perceived peripheral and central chemoceptors (see). Peripheral receptors are located in the field of branching of the general carotid artery on outside and internal (a carotid ball) and under an aortic arch (aortal balls). At reduction of tension of oxygen, increase in tension of carbonic acid and decrease in pH in an arterial blood, and also at irritation of the sympathetic fibers innervating balls the afferent impulsation amplifies. Impulsation weakens at a hyperoxia and irritation of efferent fibers of a sinus nerve.

Carotid chemoceptors provide bystry reactions respiratory center (see) on changes of tension of O 2 and CO 2 in blood. The central chemoceptors are located on the ventral surface of a medulla. D.'s strengthening at a hypercapnia results from irritation of both peripheral, and central chemoceptors.

Excitement of chemoceptors defines «request» for MOV which can be carried out at different ratios of depth and D. No's frequency to each size MOV there corresponds the frequency range of D. which provides ventilation of the lungs during the minimum work of respiratory muscles. At D. with other frequencies more energy is spent for unit of volume of ventilation. For D. of animals and the person energetically optimum frequencies are inherent. Information of a brain on mechanical characteristics of the peripheral device D. and their changes is necessary for the choice of the optimum mode of ventilation. In lungs there are 3 groups of mechanioreceptors.

1. Stretch receptors of lungs react to increase in lung volume at a breath; in one receptors categories arise at a breath and stop at an exhalation, and in others — categories are available also at an exhalation, but at a breath the frequency of impulses increases. Slow adaptation is inherent to receptors. Frequency of categories of stretch receptors of lungs decreases at increase in content of carbon dioxide gas in inhaled air. These receptors are located in unstriated muscles of walls of pneumatic ways (apprx. a half — in a trachea and extra pulmonary bronchial tubes, the others — in intra pulmonary bronchial tubes). Impulsation goes to c. N of page on thick afferent fibers of vagus nerves with a speed of 14 — 59 m/s.

2. Irritantnye (or epithelial) receptors react on rather bystry reduction and increase in lung volume, to slight mechanical attachments on a mucous membrane of pneumatic ways (e.g., dust particles), on vapors of pyretics. These receptors are excited also at pheumothorax, reductions of unstriated muscles of bronchial tubes, some patol, conditions of lungs (bronchial asthma, stagnation of blood in a small circle of blood circulation, a fluid lungs etc.). Receptors quickly adapt to irritants. They are located in an epithelium or under an epithelium of pneumatic ways. Speed of carrying out impulses afferent fibers of 4 — 26 m/s.

3. J-receptors (yukstakapillyarny receptors) of lungs are irritated at an inflammation and a fluid lungs, at introduction to a blood stream of a small circle of a fenildiguanid. Are near pulmonary capillaries. Send impulses to a brain on the fine fibers which are carrying out them with a speed of 0,5 — 3,0 m/s.

There are no chemoceptors which main irritants would be a carbon dioxide gas and oxygen in easy mammals.

Impulses from mechanioreceptors of lungs define reflex dependence of frequency and D.'s depth on the lung volume (Breyer and Goering's reflexes). At stretching of lungs stretch receptors which send the impulses activating neurons of a respiratory center which brake inspiratory neurons on a vagus nerve are excited. When excitement of inhibitory neurons reaches a certain level, the breath stops and replaced by an exhalation. The pulmonary collapse is resulted by the reflex incentive (weakening of irritation of stretch receptors, irritation of irritantny receptors) accelerating change of an exhalation by a breath. Breyer and Goering's reflexes provide increase in frequency of and MOV at a hyperpnea. At animals after section of a vagus nerve of D. does not stop, but becomes more rare and deeper. At the person quiet D.'s frequency does not depend on impulses from lungs, they participate in regulation only of the strengthened D. Znacheniye irritantny and J-receptors in usual D.'s regulation it is found out not completely; impulses of both groups of receptors increase activity of a respiratory center, they participate in genesis of an asthma at pneumonia, a fluid lungs, bronchial asthma. The irritation of stretch receptors of lungs causes a reflex bronchiectasia, and irritation of irritantny receptors — narrowing.

Participate in regulation of reductions of respiratory muscles being in them proprioceptors (see). Various respiratory muscles are unequally supplied with proprioceptors. The diaphragm, e.g., contains few stretch receptors, and their irritation poorly influences. Reductions of a diaphragm substantially depend on excitement of mechanioreceptors of lungs which in essence are its proprioceptors. Reductions of the diaphragm which is attached to the lower edges by irritation of stretch receptors of intercostal muscles can strengthen excitement of phrenic motor-neurons. Intercostal muscles are supplied with a large number of muscle spindles (apprx. 100 in each intercostal space). These muscles, in addition to participation in ventilation of the lungs, actively participate in maintenance of a pose. Impulses of the sensitive terminations of muscle spindles by means of a reflex on stretching strengthen both respiratory, and postural tonic contractions of intercostal muscles. Usual (extrafusal) muscle fibers are innervated by axons of oc-motor-neurons. On muscle fibers of spindles axons of the fusimotor gamma motor-neurons regulating sensitivity of spindles to stretching terminate. The descending impulses from a respiratory center excite both alpha, and gamma motor-neurons, and gamma motor-neurons of muscles of a breath and exhalation are activated in a phase with excitement of the corresponding alpha motor-neurons. At reduction of extrafusal muscle fibers stretching of spindles weakens. But the impulsation in afferent fibers amplifies owing to excitement gamma motoneyrsnov, the intrafusal fibers causing reduction. This impulsation strengthens excitement of alpha motor-neurons.; At increase in resistance of D. (e.g., narrowing of pneumatic ways) at the same muscular effort shortening of extrafusal fibers decreases, amplifies irritation of the sensitive terminations of spindles and, reflex, reduction of muscles. Thus, stretch receptors of intercostal muscles regulate their reductions depending on resistance of. Impulses of the sensitive terminations of spindles facilitate excitement of alpha motor-neurons not only this, but also the next intercostal spaces. Coordination of activity of separate intercostal muscles is provided to these. Force of reductions of respiratory muscles is defined also by properties of muscle fibers: after switching off of reflexes tension developed by a muscle at reduction the is more, than more length of muscle fibers. D.'s frequency increases at fervescence (5 — 6 acts of D. in 1 min. on 1 °). Frequency and D.'s depth change under the influence of protective and orientative reflexes, at contagious excitation etc. Important adaptive value has uslovnoreflektorny change of D., napr, at athletes before start. In the course of the training their compliance of rhythms of the movement and D. is established, MOV increases, oxygen consumption decreases. As a result the general stability of an organism increases.

Regulation of D. providing speech function is especially difficult. The person is capable to change randomly D. — from a delay to the maximum MOV. But any management D. has limits. So, any delay of D. through a nek-swarm time becomes impossible (the main reason — the accruing hypercapnia). Determination of the maximum duration of any delay of D. is carried out by means of a Stange's test — Gencha. Normal at the level of a quiet exhalation the delay makes 30 — 40 sec., on a breath — 55 — 60 sec.; at cardiac and pulmonary pathology D.'s delay is shortened, in the course of the trainings to physical. to work it is extended.

Transport of gases blood — see. Gas exchange .

Biophysical mechanisms of breath

the Respiratory system of an organism in a broad sense has no accurate space restriction and occupies practically all organism since in each cell D. V processes narrower understanding are made understand specialized bodies of D. as respiratory system (lungs, gills, etc.), and also capillaries of fabrics in which processes actually of gas exchange proceed. The mechanisms providing ventilation of the lungs and gas exchange in capillaries have various nature and are carried out under the influence of various forces.

Ventilation of the lungs is carried out thanks to change of volume of a chest cavity in the sagittal, vertical and frontal directions; it leads to pressure drop in a pleural crack, lungs extend, pressure in them falls, becomes lower atmospheric and air comes into force of swing pressure into lungs in pneumatic ways (see. Lung ventilation ).

At an exhalation the volume of a thorax decreases, pressure in a pleural crack increases, the stretched pulmonary fabric compresses, intra pulmonary pressure becomes higher atmospheric and air begins to leave lungs. Lung volume changes passively — due to the changes of volume of a chest cavity leading to change of pressure in a pleural crack and intra pulmonary pressure.

At change of the size of lungs the large role is played by an elastic energy of lungs — force, about a cut lungs aim to be reduced and edges counteracts atmospheric pressure. Atmospheric pressure stretches lungs, densely presses a pleura to a chest wall, and from a pleural cavity there is a narrow pleural crack (see. Pleura ). Sil, aiming to reduce lung volume, is and there is an elastic energy of lungs, edges increases at a breath and decreases at an exhalation. About 2/3 elastic energies of lungs depend on surface intention of walls of alveoluses. As the proof preservation of elastic properties of lungs after destruction of elastic tissue of lungs enzyme elastin can serve.

During a breath force of respiratory muscles is spent for overcoming elastic resistance, for movement of not elastic fabrics (edges, a diaphragm, a breast, contents of an abdominal cavity) and for overcoming resistance of air at its passing on a trachea and bronchial tubes.

At a quiet breath force of reduction of muscles is generally spent for overcoming resistance of an elastic energy of lungs. At forced ventilation force, overcoming not elastic resistance, and force spent for overcoming resistance to an air flow on a tracheobronchial tree sharply increases.

Work of pectoral muscles is aimed at providing adequate aeration of lungs and maintenance of constancy of structure of an alveolar air, than the gradient of partial pressure for oxygen and carbon dioxide gas is reached. As permeability of biomembranes for molecules of carbon dioxide gas is more than 20 times higher than their permeability for molecules of oxygen, existence of such differences of partial pressures provides constancy of intake of oxygen and removal of carbon dioxide gas from capillaries of lungs at the expense of mechanisms of diffusion for a short time of stay of the inflowing blood in capillaries of lungs and in capillaries of bodies and fabrics (see. Gas exchange, diffusion of blood gases ).

Features of breath at children

the Most important feature of a structure of bodies of D. at children is the small size of all departments of respiratory tract that promotes generalization patol, processes in system D. and complicates their topical and functional diagnosis. So, children have nasal courses already, language is rather big and complicates D. through a mouth. A maximum of development of lymphatic fabric at the age of 4 — 10 years; at the same age diseases of a nasopharynx and the related pneumopathies and pathology of other bodies and systems are frequent. A throat relatively already, than at adults, and more long. Diameter it at the newborn 3,5, in 1 year — 6, in 4 years — 8 mm (at adult 10 — 12 mm). The small gleam along with friability and the raised vascularization of this area complicates an intubation and is the main reason for bystry hypostasis of subcopular space (false croup). The less child, the already respiratory tracts: diameter of lobar bronchi of the newborn — 1,5, in 1 year — 3, in 4 years — 3,5 mm (adults have 5 — 6 mm). Elastic tissue of lungs is developed insufficiently that promotes bystry development of emphysema. Obstruction of respiratory tracts, emphysema and atelectases arise that easier, than the child is younger. Tendency to obstruction, an atelektazirovaniye, and also the raised vascularization of mucous membranes promote generalization of inflammatory processes. The framework of a thorax is soft. The horizontal otkhozhdeniye of edges inherent to children of younger age D. Chem less age of the child reduces reserve opportunities, that muscles are weaker. D. Meteorizm, an aerophagia prevails phrenic, a hepatolienal syndrome are capable to reduce alveolar ventilation significantly.

Owing to immaturity of a respiratory center at newborn and premature children the respiratory arrhythmia is expressed. The age of the child is less, the impact on D. of drugs and various toxicants is stronger.

Functionally children of the first days of life are adapted to acidosis and a hypoxia. Indicators of acid-base equilibrium at them in comparison with advanced age are shifted towards acidosis (tab. 2). Availability of fetalis hemoglobin in blood at newborns promotes the best binding of oxygen in the conditions of low pH.

Table 2. Age dynamics of some normal indicators of function of lungs and indicators of gas exchange in a condition of quiet wakefulness (on M. To I. Anokhin)

Smaller stability of functional standards of D., but deviation from individual fiziol is characteristic of children of younger age. norms children transfer not worse or even slightly better, than adults. So, cases of successful treatment of children after very heavy hypoventilation are frequent (PACO 2 it is higher than 60 mm of mercury.) and hypoxias (Russian joint stock company 2 it is lower than 50 mm of mercury.).

Diseases of bodies of D. (Qatar nasopharynxes, bronchitis, pneumonia, etc.) at children often begin sharply, emphysema quickly develops. It is necessary to consider that disturbances of activity of other bodies (paresis of intestines, a diarrhea, vomiting, spasms, etc.) can mask symptomatology of pathology of bodies of. At recovery many patol, changes, as a rule, are completely liquidated.

Features of breath at advanced age

Fig. 4. The chart characterizing maximal ventilation of lungs (in liters — on ordinate axis) at men during various age periods (advanced in years — on abscissa axis); with increase in age the size of maximal ventilation of lungs considerably decreases.

During the aging of an organism owing to age changes of the musculoskeletal device of a thorax, pneumatic ways, a pulmonary parenchyma, vessels of a small circle of blood circulation conditions of lung ventilation change. It becomes less effective to what increase in a ventilation equivalent and decrease in an oxygen utilization quotient testifies. If in 20 — 29 years the ventilation equivalent averages 2,7 l at men, then in 70 — 79 years it is equal to 4 l, and the oxygen utilization quotient respectively decreases by 1,5 times. Owing to reduction of elasticity of lungs negative intrathoracic pressure decreases. Naturally maximal ventilation of easy (fig. 4) — the indicator which is fullestly reflecting functional capacities and mechanical ventilating characteristics of respiratory system decreases. As a result of increase anatomic and fiziol. dead space the share of alveolar ventilation in the minute volume of decreases. Decrease in efficiency of ventilation is connected with disturbance of equitability of inhaled air because of loss by pulmonary fabric of elasticity, existence of atelectatic sites, and also disturbances of bronchial passability. It clearly is shown in decrease in the forced vital capacity of lungs for 1 sec. — Tiffno's test (see. Votchala — Tiffno test ), inspiratory rate and exhalation (indicators of pneumotachometry).

Disturbance of respiratory function during the aging of an organism causes emergence of various compensatory and adaptive reactions. At the same time adaptive mechanisms of external D. are imperfect.

Test with physical testifies to it. loading. So, at elderly and old people the minute volume of breath increases preferential at the expense of frequency, but not the depth of D., the maximum of respiratory reactions is displaced by the end of loading, the accurate ratio between intensity of work and change of respiratory function is broken, the period of recovery of shifts is extended, the oxygen debt increases. It is often possible to observe respiratory arrhythmias as in the conditions of rest, and during sleep; respiratory reflexes are developed difficult.

Breath under pressure

D. under pressure is the method of ensuring life activity of the person in the conditions of the changed barometric pressure which is applied in aircraft and astronautics during the diving, lacunar works and some other conditions of activity of the person. It is applied also to creation of a possibility of adequate gas exchange and external D. at artificial ventilation of the lungs, in laboratory or a wedge, conditions (see. Hyperbaric oxygenation , Hyperoxia ). There are kinds of this method: Under raised and D. under excessive pressure.

Breath under the m increased pressure when pressure of gas (air, oxygen or gas mixtures) is equal in lungs to pressure of gas or water upon a body surface and when it more than standard barometric atmosphere pressure, is applied during the divings in soft diving space suits, with aqualungs, and also in recompression cameras and cameras of hyperbaric oxygenation.

The increase in gas density created by supertension of a gaseous fluid can significantly influence D.'s mechanics, in particular the aerodynamic resistance of respiratory tracts. The size of resistance depends on length and the cross-sectional area of respiratory tracts, density and gas viscosity, and also on the mode of a flow: laminar or turbulent. This dependence is expressed by Rorer's equation:

PA = k1 + k2V2

where PA — the alveolar pressure necessary for overcoming resistance of respiratory tracts, V — volumetric flow rate, k1 and k2 — constants of viscosity and gas density respectively. The first member of equation reflects linear relation of a flow rate from pressure, characteristic of streamline flow, the second — the square dependence characteristic of a turbulent flow.

The flow of air passing on respiratory tracts has the mixed laminar and turbulent character. At increase in a flow rate or gas density there is a dominance of the turbulent mode. As gas density increases approximately in proportion to a root of the second degree from the size of a gain of barometric pressure, becomes clear why D. in hyperbaric conditions is followed by essential increase in resistance of respiratory tracts and works of respiratory muscles.

As at build-up of pressure of a gaseous fluid D.'s difficulty becomes one of the major factors limiting efficiency of the person, at deep-water immersions apply oxygen-helium mixes which density is 7 times less than density of air and nitrogen-oxygen gas mixtures and at which respiratory resistance considerably decreases.

Other important factor limiting resistance of a human body to D. under supertension of a gaseous fluid is its structure as such components of air, harmless with a standard barometric atmosphere pressure, as oxygen and nitrogen, gain toxic or narcotic properties at increase in their partial pressures. E.g., at D. compressed air at a depth of 37 m the partial pressure of oxygen makes 1 at and long stay at this depth can be followed by development of giperoksichesky intoxication (see. Hyperoxia ). Long D. by pure oxygen further at small depths, about 10 — 12 m is for the same reason even more dangerous. The first signs of narcotic effect of nitrogen at D. are observed by air at different people at a depth from 40 to 60 m.

Prevention of oxygen poisoning and nitric anesthesia is based on maintenance of safe partial pressures of these gases by change of their percentage in the mixes applied to D. under different supertension and also on observance of safe terms of stay in hyperbaric conditions.

Breath by oxygen under excessive pressure. It is applied as a method of protection of pilots from acute hypoxemic hypoxias (see) at disturbance of tightness of cabins of airplanes during flights in a stratosphere.

At this method of oxygen providing an organism the intra pulmonary pressure of gas exceeds pressure of the gaseous fluid surrounding a body and is excessive in relation to atmospheric pressure at this height. Its fundamental difference from D. ped supertension consists in it.

The hypoxias used in aircraft for the purpose of prevention oxygen apparatuses during flight in the depressurized cabin provide datum level of partial pressure of oxygen in an alveolar air by means of gradual, in process of rise on height, enrichment of inhaled air with oxygen (see. the Oxygen and respiratory equipment, in aircraft ). However at the heights more than 10 000 m owing to very big reduction of barometric pressure the level of partial pressure of oxygen begins to decrease even at D. pure oxygen and already at the height of 12 000 m falls to 60 mm of mercury. — i.e. reaches an upper limit of a safe hypoxia, equivalent D. air at height apprx. 4000 m.

Maintenance of the minimum tolerance level of partial pressure of oxygen at further rise on height is carried out

by D. pure oxygen under excessive intra pulmonary pressure. Fiziol. effects of this impact on an organism are very diverse and depend on the size of excessive pressure, speed of its increase, fluctuations on phases D. and degree of the counter-pressure rendered on a body by the high-rise compensating equipment (see. High-rise equipment ).

Fig. 5. Curve (pnevmotakhogramma), characterizing influence of excessive intra pulmonary pressure on structure of a respiratory cycle: and — a pnevmotakhogramma at usual breath; — a pnevmotakhogramma at breath under the excessive pressure of 300 mm w.g.

Excessive pressure in lungs stretches extrathoracic airways and a thorax, displaces down a diaphragm therefore the dead space of respiratory tracts and lung volume increases. Sharply the structure of a respiratory cycle changes: the breath is facilitated, its duration decreases, and the exhalation is extended, becomes complicated, auxiliary muscles are involved in its implementation. At small sizes of excessive pressure on a pnevmotakhogramma the alternating short breaths and the long, proceeding at a small speed exhalations are visible rhythmic. At increase in this pressure up to 300 — 400 mm w.g. Is broken (fig. 5): the abrupt breath is replaced by excessively long exhalation with the chaotic sharp fluctuations of a flow rate testimonial of the increasing resistance to an exhalation and irregularity of efforts of respiratory muscles for its overcoming. If at usual D. work of respiratory muscles is performed only during a breath and is directed to overcoming an elastic energy of lungs, a thorax and resistance of respiratory tracts, and the exhalation is process passive, then at increase in excessive pressure in lungs there comes such moment when excessive pressure counterbalances an elastic energy of fabric structures of lungs and a thorax and, therefore, need for active muscular effort for their stretching disappears. Therefore at achievement of a certain size of excessive pressure, usually apprx. 300 mm w.g., the breath from active process becomes completely passive from the point of view of the termination of energy expenditure on its production. However rhythmic activity of a respiratory center does not change therefore neuroreflex activity of a breath remains. Moreover, in the course of a breath, especially at the end of it, the increased bioelectric activity of respiratory muscles testimonial of their efforts directed to prevention of hyperdystension of lungs by excessive pressure is observed.

On the other hand, the potential energy which is saved up in elastic structures of lungs and a thorax during their stretching at a breath becomes insufficient for overcoming excessive pressure and implementation of an exhalation. Therefore expiratory respiratory muscles which efforts increase in process of increase in excessive pressure begin to take part in the act of an exhalation, i.e. the exhalation becomes active.

The described functional reorganization of a respiratory cycle happens under the influence of interoceptive and the proprioceptive inflow proceeding from receptor zones of lungs and the musculoskeletal device of a thorax.

Change mechanics D. under the influence of excessive pressure is followed by moderate increase of lung ventilation that leads to an alveolar hypocapny, in genesis the cut plays a part also disturbance of the regional ventilating and perfused relations in lungs and reduction of venous return with a delay of carbonic acid on the periphery.

Excessive pressure in lungs owing to difficulty of venous return to the right auricle creates conditions for stagnation of blood on the periphery, reduction of volume of the circulating blood and increase in the general venous pressure, a cut very closely correlates with the size of excessive pressure and makes from 80 to 100% of its size. Nek-roye lag of venous pressure from excessive is explained by power consumption on overcoming elastic forces of fabrics.

As a result of a compression of heart the increased intra pulmonary pressure and increases of peripheric vascular resistance increases as well the ABP. However it raises less, than venous therefore the gradient of arteriovenous pressure decreases that is one of the reasons of decrease in rate of volume flow of the blood-groove taking place at D. under excessive pressure both in small and in a big circle of blood circulation.

Changes of bioelectric activity of heart are characterized by sinus tachycardia, increase in a tooth of P and reduction of a tooth of T. At the expressed tension of compensatory mechanisms of heart decrease in an interval S — T below the isoline, the accompanying reduction of rate of volume flow of a coronary blood-groove is observed.

Heart rate at D. under excessive pressure usually moderately increases, however the expressed tachycardia, especially with the subsequent tendency to bradycardia, is a terrible harbinger of the coming cardiovascular collapse.

The described D.'s changes and blood circulations leading to considerable functional disturbances and decrease in working capacity, as a rule, arise at D. under excessive pressure in lungs exceeding 30 mm of mercury. Therefore for prevention of these adverse effects pulmonary pressure needs to create the external counter-pressure equal in size inside.

Such counter-pressure on a body is rendered by special vysotnokompensiruyushchy vests, suits or high-rise space suits which designs are based on the mechanical, pneumomechanical or pneumatic principles of compensation of excessive intra pulmonary pressure. Modern sets of the oxygen equipment provide reliable protection of pilots and astronauts against a hypoxemic hypoxia and other adverse factors of high-rise flights.

Pathology of external respiration

the Main type of inadequacy of external D. is so-called. respiratory insufficiency (see). In narrow sense understand the states which are characterized by shifts in gas structure of an arterial blood as respiratory insufficiency: undervoltage in it of oxygen and increase in tension of carbon dioxide. In broader understanding carry to respiratory insufficiency also those cases when there are no explicit disturbances of gas exchange and gas composition of blood, but it is reached at the price of increase in total amount of operation of the respiratory device not inherent to a healthy organism. At the XV All-Union congress of therapists (1962) the recommendation to understand such condition of an organism as respiratory insufficiency was accepted, at Krom normal intensity of external D. is insufficient for ensuring normal partial tension of O 2 and CO 2 in an arterial blood.

Efficiency of function of system of external D. is defined by three closely connected processes: ventilation of alveolar space, a pulmonary capillary blood-groove (perfusion) and diffusion of gases adequate to ventilation through an alveolocapillary (aerogematichesky) membrane. Respectively distinguish three main categories of the disturbances of external D. having various patofiziol, a basis: alveolar hypo - and a hyperventilation, disturbance of the ventilating and perfused relations and disturbance of diffusion. Often various combinations of the specified disturbances meet.

Disturbances of alveolar ventilation. Alveolar hypoventilation arises when ventilating exchange of gases in alveoluses is insufficient, decrease the partial pressure of oxygen in an alveolar air and tension of oxygen in the blood flowing from alveoluses therefore can decrease saturation of hemoglobin oxygen and contents it in an arterial blood. Along with it removal from an organism of carbon dioxide gas is usually broken. Thus, primary shifts of gas structure characterizing alveolar hypoventilation are an arterial anoxemia (see. Hypoxia ) and arterial hypercapnia (see).

The disturbances of passability of respiratory tracts caused by a foreign body, a tumor, inflammatory process (abscess, diphtheria, hypostasis of a throat), a spasm of small bronchial tubes and bronchioles (bronchial asthma, poisoning with organophosphorous connections) and other factors can be the reasons of alveolar hypoventilation. Can lead sharp reduction of a respiratory surface of lungs as a result of extensive resections of pulmonary fabric, destruction to alveolar hypoventilation its any patol, process (tuberculosis, a tumor, some forms of emphysema), filling of alveoluses with liquid (pneumonia, hypostasis, pulmonary bleeding), and also an atelectasis because of obturation of a bronchial tube. Reduction of ventilation can also occur at pheumothorax, a hemothorax and big pleural exudates, and also at diffusion reduction of distensibility of pulmonary fabric.

At the same time various changes of character vnesh-py D. Tak can take place, narrowing of respiratory tracts in typical cases is followed by lengthening of both phases of a respiratory cycle, urezheniy D. at simultaneous increase in amplitude of respiratory excursions (respiratory volume), inclusion in the respiratory act of auxiliary muscles; at a spasm of small bronchial tubes preferential lengthening and difficulty of an exhalation (so-called stenotic D.) is characteristic. The speeded-up superficial respiratory movements, on the contrary, are characteristic of extensive pneumonia. At pheumothorax, a hydrothorax, obturatsionny atelectases asymmetry of respiratory excursions etc. is quite often observed. Mechanisms of changes of nature of respiratory movements are in some cases difficult and various. These changes in most cases in itself are not a proximate cause of disturbances of alveolar gas exchange. However at the same time work of respiratory muscles increases, external D.'s efficiency decreases, there can be a feeling asthmas (see).

Along with it quite often alveolar hypoventilation results from primary disturbances of frequency and (or) amplitude of respiratory excursions. Such gipopnoichesky forms D. can externally be shown in the form of complete cessation of respiratory movements (apnoea), their sharp urezheniye (bradipnoe) up to so-called agonal, or terminal, D. (gasping), by long inspiratory delays (apneyzis), periodic forms D. — breath the Biota, Cheyna — Stokes (see. Biotovsky breath , Cheyna — Stokes breath ), so-called chaotic D., and also D. of small amplitude with its various frequency. Quite often combinations of some of the forms stated above take place.

Primary disturbances of respiratory movements can be caused by different injuries of a thorax or defects in its osteoarticular device most often representing an effect of the diseases postponed at children's age (rickets, a tubercular spondylitis, etc.). Inborn defects of a structure of a body can also play a part. Disturbance of respiratory excursions in the form of shallow hurried breathing is observed in connection with excessive ossification of costal cartilages and small mobility of the svyazochnosustavny device of a thorax. In certain cases respiratory excursions can be complicated by external influences of mechanical character (a prelum heavy objects, the earth, sand at various accidents, clothes or objects of production equipment, etc.).

Severe forms of alveolar hypoventilation can result from disturbance of the respiratory excursions connected with inflammatory, atrophic or dystrophic processes in respiratory muscles and also at frustration of its innervation. These frustration can be caused by disturbance of carrying out excitement in peripheral neuromuscular synapses, on trunks of intercostal and phrenic nerves, bulbospinalny conduction paths, and also patol, changes of motor-neurons of cervical and verkhnegrudny departments of a spinal cord. As a proximate cause of such frustration mechanical factors (injuries, tumors), dystrophic processes (myelosyringosis), infectious and toxic influences (diphtheria, poliomyelitis, botulism, tetanus), poisonings with neurotropic poisons can serve. Function of respiratory muscles can sharply be broken at the system disturbances of mediator exchange leading to permanent decrease in lability of neuromuscular synapses (e.g., at a myasthenia).

Frustration of an innervation of respiratory muscles along with weakening of respiratory excursions can lead to disturbance of synchronism of reductions of synergistic muscles up to full disintegration of a respiratory cycle. Depending on localization, character and extent of defeat unilateral disturbances of depth of D., a diskoordination of upper and nizhnegrudny departments of respiratory muscles, the «paradoxicality» of separate components of the respiratory act interfering its normal implementation (e.g. are possible, at a phrenoplegia), etc. In some cases at the expressed phenomena of widespread paralysis of respiratory muscles independent D. becomes in general impossible and patients should be translated on temporary (e.g., at so-called residual curarization after the surgeries performed using muscle relaxants at a disease of poliomyelitis) or constant (a myelosyringosis, high injuries of a spinal cord) an artificial respiration (see. Artificial respiration, artificial ventilation of the lungs ).

Sharply expressed hypoventilation up to asphyxia (see) can arise not only at paralysis, but also at long spastic conditions of respiratory muscles, usually observable at the general spasms of skeletal muscles (poisoning with convulsive poisons, tetanus). In similar cases artificial ventilation of the lungs in combination with muscle relaxants is also quite often applied.

Alveolar hypoventilation of a myogenetic origin can be observed also at almost healthy people with insufficiently developed respiratory muscles at big physical. to loading. The actual volume of ventilation at the most intensive activity of respiratory muscles at them does not correspond to the needs of an organism for oxygen.

Disturbances of normal function can be the cause of alveolar hypoventilation respiratory center (see). These disturbances are caused by various deviations in afferent system of regulation of breath (i.e. have the reflex nature) or patol, changes of the most respiratory center.

The reflex forms of hypofunctional conditions of a respiratory center can be had in the basis insufficiency of an exciting afferentation from various receptors perceiving gas composition of blood and other parameters of internal environment of an organism. Essential value can have also weakening of the activating descending influences from the highest departments of c. N of page and general decrease in a tone of a reticular formation of a brainstem. So, the hypocapny caused by artificial or any hyperventilation is followed by temporary lack of rhythmic activity of a respiratory center after the termination of a hyperventilation; passing hypoventilating states can arise at luxury call an alkalosis, at substantial increase of the ABP, etc. Easing of activity of a respiratory center during a deep sleep is also connected with reduction of inflow of an exciting afferentation and decrease in a tone of a reticular formation. The similar mechanism, apparently, is the cornerstone of D.'s suppression by nek-ry hypnotic drugs and drugs.

Gipoafferentation along with more or less long hypoventilation can lead to difficult shifts in system of regulation of D. and internal environment of an organism. The fact that the control system of external D. represents system of many and coherent regulation is the cornerstone of these phenomena, in a cut there is no self-control of each of the main respiratory indicators separately. These indicators are closely connected among themselves at the level of the central regulation, and the shift of one of them involves the interfaced shifts of other indicators. So, decrease in ion concentration of H + at not gas alkalosis is followed by reduction of an exciting afferentation from the corresponding receptors and easing of inspiratory activity of a respiratory center. Arising thereof hypoventilation leads to decrease in PAO 2 and to corresponding strengthening of an afferentation from «oxygen» receptors of carotid balls. As a result the volume of ventilation can be normalized, however it will occur in the conditions of the new established ratio of gas indicators.

Inhalation of the increased concentration of oxygen can also lead to the hypoventilation resulting from the termination of tonic excitement of sinocarotid «oxygen» chemoceptors. Especially clear hypoventilation at inhalation of oxygen can be observed at patients with hron, the respiratory insufficiency which is followed by an anoxemia, a hypercapnia and acidosis. The gas composition of blood which was established at such patients under the influence of inhalation of oxygen is broken because of reduction of alveolar ventilation, and there is an aggravation of a hypercapnia and acidosis. Through a nek-swarm time the volume of ventilation can be recovered, but against the background of growth of a hypercapnia and acidosis. Cases of an aggravation of symptoms of patients, known in clinic, after inhalation of pure oxygen quite often have such mechanism in a basis.

Hypoventilating states in certain cases have in a basis surplus of an exciting afferentation, napr, frequent and shallow breathing at some neurotic states (a hysterical attack) when the share of dead space in the total amount of ventilation sharply increases, and the share of alveolar ventilation considerably decreases. Such D. results from the inadequate intensive descending exciting afferentation coming to a respiratory center from the highest departments of a brain. There are data in favor of the fact that at the heart of sharp increase and reduction of depth of D. at some diffusion and focal defeats of pulmonary fabric (e.g., at pneumonia) strengthening of the tonic exciting afferentation coming to a respiratory center on S-fibers of pulmonary branches of vagus nerves also lies.

Reflex hypoventilation can result from strengthening of the brake afferentation coming to a respiratory center from receptors of upper respiratory tracts at their sharp irritation the impurity (vapors of ammonia, smoke, etc.) which are contained in air and also at pain at D. (e.g., at fractures of edges, pleurisy, intercostal neuralgia etc.). Such reflex inhibition of D. having character of protective reflexes by the nature can lead to sharp restriction of respiratory excursions or to a full apnoea, creating threat of acute asphyxia.

Hypoventilation can take place and when in D.'s regulation the factors which are not connected with gas exchange and gas composition of blood when performance of this or that activity begin to play a significant role (e.g., singing, playing a wind instrument etc.) interferes with implementation of the normal respiratory act. Such frustration of D. especially clearly are shown at insufficiently made or broken reflex coordination of.

Hypoventilating states can arise iod influence coming to a respiratory center from overlying departments of a brain or from the periphery of the chaotic disorder afferentation that takes place, e.g., at various affects, hard mental work etc. In such cases disturbance of depth and D.'s rhythm, its temporary delays, etc. are quite often observed. More expressed disturbances of ventilation of the reflex nature arise at various heavy patol, the processes (e.g., massive mechanical injuries, burns, visceral damages, some intoxications) which are followed by strong pain stimulation of the various receptors in one way or another connected with a respiratory center. The powerful disorder flow of an afferentation arising at the same time can lead to considerable disorganization of the respiratory act.

Hypoventilation of neurogenic character can be connected with disturbances of the most respiratory center (hemorrhages, hypostases, tumors of a brain), inflammatory processes, local disturbances of blood supply and dystrophic processes in a trunk part of a brain, toxic influences on a respiratory center, the general cooling of an organism, a hypoxia, etc.

Specific forms D. at it is central the caused gipopnoichesky states are very various. Are most characteristic the expressed urezheniye of respiratory excursions (see. Bradipnoe ) at various combinations to change of their depth; sharp reduction of depth of D. without change of frequency or in combination with increase of respiratory excursions (see. Tachypnea ); periodic forms D. (Cheyna — Stokes and Kussmaul); chaotic or alternating D.; so-called apneystichesky D. with long inspiratory delays and terminal (agonal, or gasping-breath) in the form of very deep, but rare short convulsive respiratory movements. Quite often various combinations of the specified forms D meet. Mechanisms of most of them are still insufficiently studied and receive various explanations.

The alveolar hyperventilation arises when the minute volume of ventilation exceeds the needs of an organism for gas exchange. It can be caused by inadequate strengthening of activity of a respiratory center as a result of organic lesions of a brain (an inflammation, a tumor), neurotic states, excessive exciting reflex influences on a respiratory center from various receptors (temperature, baroreceptors, chemoceptors of carotid balls, etc.) and direct influence on brain structures of some chemical agents (respiratory analeptics of the central action, microbic toxins, etc.). It is also accepted to carry to hyper-ventilating states cases of strengthening of D. caused by decrease in partial pressure of oxygen in inhaled air. The short-term hyperventilation arises at any forcing

of D. Giperventilyation leads to increase in partial pressure of oxygen in an alveolar air, to increase in tension of oxygen in plasma of an arterial blood and to decrease in tension of carbon dioxide in it (see. Hypocapny ).

Disturbances of the ventilating and perfused relations. Among external D.'s frustration regional disturbances of functions of lungs in the form of the neravnomernosty ventilation and a pulmonary blood-groove which are going beyond fiziol figure prominently. norms. At disturbance of adequacy of ventilation and a blood-groove separate alveoluses, their groups or considerable sites of pulmonary fabric become partially useless for gas exchange. The pulmonary space ventilated, but deprived of a blood-groove is included fiziol. dead space. The groups of alveoluses washed by blood, but deprived of ventilation also do not participate in gas exchange, and the blood flowing from them is a part of the so-called venous impurity increasing a share of not arterialized blood in the blood flowing from easy.

Uneven alveolar ventilation can be caused by unequal distensibility and elasticity of different sites of pulmonary fabric or unequal extent of disturbance of bronchial passability in different sites of a bronchial tree, and also lacks of coordination of a breath and an exhalation. The last can be a consequence unilateral patol. the changes of a thorax limiting the respiratory movements of one lung (e.g., at a unilateral fibrothorax, an extensive thoracoplasty), a unilateral phrenoplegia, etc. Due to the small mobility of a mediastinum in the corresponding pleural cavity more expressed negative pressure is created that leads to bigger alveolar ventilation, than on the party of defeat; the second lung limited in expansion is ventilated insufficiently. At an exhalation, on the contrary, pressure in alveoluses of the straightened lung intact better will be higher, than in a lung on the struck party. Swing pressure in both lungs at a breath and an exhalation along with uneven distribution of inhaled air can cause on certain phases of a respiratory cycle movement of air from one lung in another in the direction of smaller pressure — so-called pendular ventilation.

Uneven changes of distensibility and elasticity of pulmonary fabric can be caused as the limited pulmonary processes leading to fibrous regeneration, scarring or local stretching of certain sites of pulmonary fabric and diffusion forms of pathology (emphysema, a pneumoconiosis, etc.). The redistribution of pressure and volumes connected with various conditions of stretching and fall of alveoluses in the course of a respiratory cycle leads to a combination hypo - and the hyper ventilated sites of pulmonary fabric, to pendulum movement of air from one alveoluses in others, to increase fiziol, dead space and venous impurity as a result of so-called functional shunting of a venous blood.

The similar phenomena arise at uneven disturbance of bronchial passability in different sites of a bronchial tree. Switching off of some sites of lungs from D. owing to narrowing of bronchial tubes can take place and in fiziol, conditions. However in such cases exact compliance between ventilation and a blood-groove is established. Poorly ventilated sites at the same time poorly are perfused, and saturation of an arterial blood oxygen does not worsen. At some patol, states (a local spasm of bronchioles, existence of a viscous secret, abscess, a tumor) there is a narrowing more or less large, branches of a bronchial tree without corresponding change of perfusion. The partial hypoventilation of normally perfusing alveoluses arising because of an unequal stenozirovaniye of the bringing respiratory tracts can be also followed by pendulum movement of air in lungs, increase fiziol, dead space and leads to decrease in saturation of an arterial blood oxygen.

Uneven perfusion of alveoluses can be caused by reduction of a blood-groove on separate branches of a pulmonary artery, a local reduction of capillaries or a local spasm of pulmonary vessels. Embolism in system of a pulmonary artery, squeezing of its branches, Obliterating processes, influence of the increased concentration of a histamine, serotonin, some microbic toxins, etc. can be the reasons of the specified phenomena.

In all these cases ventilation not perfusing (or poorly perfusing) alveoluses depreciates, fiziol, the dead space increases though the total respiratory amount can remain normal.

Excess anatomic intra pulmonary shunting, as a result to-rogo venous can be the cornerstone of disturbance of the normal ventilating and perfused relations (on gas structure) blood passes on an anastomosis from bronchial veins and system of a pulmonary artery into system of pulmonary veins, passing alveoluses. Distinguish pulmonary precapillary arterio-arterial shunts (bronchial arteries — a pulmonary artery), post-capillary veno-venous (bronchial veins — pulmonary veins), arteriovenous (precapillary system of a pulmonary artery — post-capillary system of pulmonary veins), etc. Carrying out an important role in regulation of pulmonary blood circulation in fiziol, conditions, an intra pulmonary anastomosis in patol, states can pass excess amount of blood. Such phenomenon is observed at some forms of emphysema of lungs, bronchiectasias, extensive pleural processes, heart diseases, etc.

Distinguish also endocardiac shunting (dumping of blood from the right departments of heart in left) connected with anatomic defects of a structure of heart. On the effects for delivery in an organism of oxygen of such disturbance are similar to true insufficiency of external D., though treat not to respiratory, and circulator frustration.

In disturbance of the normal ventilating and perfused relations essential significance is attached to disturbance of the thin coordination mechanisms connected with alveolo - vascular and bronkhiolovaskulyarny reflexes, to influence of surface intention of alveoluses on a pulmonary capillary blood stream, regulation of production of surfactant and other factors.

Disturbance of diffusion. Disturbance of diffusion of gases through an alveolocapillary membrane is referred generally to oxygen since diffusion capacity of carbon dioxide is more than 20 times higher, than oxygen. It can be caused by reduction of a diffusion (respiratory) surface in connection with reduction of quantity of the functioning pulmonary units (the capillaries contacting to alveoluses), change of quality of an aerogematichesky membrane or thickness of separate layers through which diffuse gases (an alveolar membrane, intersticial liquid, a membrane of a capillary, a plasma layer, a membrane of an erythrocyte). The change of quality of an aerogematichesky membrane interfering diffusion (so-called alveolocapillary blockade) is observed in a typiform at such damages of lungs as Beck's sarcoidosis, asbestosis, a berylliosis, etc.

Decrease in diffusion capacity of lungs can be caused by lengthening of a diffusion way of oxygen in connection with increase in a nappe on an inner surface of alveoluses, puffiness of an alveolar membrane, increase in volume of intersticial liquid between an alveolar epithelium and a wall of a capillary, increase in a plasma fraction of blood. It takes place at alveolites, intersticial hypostasis, toxic damages of lungs, and also at some forms of anemia.

Processes of ventilation, perfusion and diffusion are so closely interfaced among themselves that in a wedge, practice the mixed forms of disturbances of external D. including frustration of each of these processes very often meet.

Methods of a research

Transport of oxygen and carbonic acid blood depends on the factors regulating tension of these gases in air cells and in capillaries: from cardiac performance and lungs, the speed of a blood-groove, redox potential of fabrics, permeability of cellular membranes. In this regard exhaustive assessment of a condition of respiratory function of blood can be received only at complex researches of the gas-transporting properties of hemoglobin, oxygen capacity of blood, curves of binding of blood gases, an arteriovenous difference on oxygen and carbonic acid, the external respiration and a hemodynamics allowing to create mathematically; models of gas exchange between lungs, blood and fabrics.

Apply a complex of the functional methods allowing to differentiate rather precisely character patol, process to a research of disturbances of external D. These are the methods allowing to measure pulmonary volumes, to obtain qualitative and quantitative data on ventilation of the lungs at rest and at various loadings, about work of respiratory muscles, gas structure of an arterial blood etc. Such methods as a stratidensitografiya, scintillation are developed elektrokimografiya (see), a share bronkhospirografiya (see. Spirography ), pulmofonografiya (see), localizations, especially important for definition, patol, process. Tracer techniques with use of soluble radioactive gases in blood (oxygen, an oxide and carbon dioxide, nitrogen, xenon, krypton), and also radioactive aerosols, drugs for intravenous administration (e.g., iodine-131-albumine), etc. were widely adopted.

For determination of amount of oxygen and carbonic acid in blood samples manometrical devices of Van-Slayka are used (see. Van-Slayka methods ), Barkrofta (see. Mikrorespirometra ), Skolander's syringe — Raftona, gas chromatographs (see. Chromatography ).

For measurement of partial pressure and concentration of oxygen in small volumes of blood, and also directly in an intact organism use oxygen electrodes (membrane electrodes of Clark, ultramicroelectrodes, all-glass electrodes of Glaykhman — Lyubersa, electrodes catheters). Apply to these purposes also gas analyzers of which device the polyarografichesky principle of measurement of oxygen (is the cornerstone see. Polyarografiya ), and also gas analyzers with use ion-selective electrodes (see). Distinctiveness of membrane electrodes and ultramicroelectrodes is speed of response and the fact that their indications do not depend on a blood-groove. Saturation rate of blood decides by oxygen on the help oksigemografiya (see).

At a research gas exchange (see) in the course of breath measure rate of volume flow of oxygen consumption and rate of volume flow of release of carbon dioxide gas by means of volume devices (the closed type) and gas-analytical (open type).

The principle of operation of volume devices is based on measurement of deficit of gas in the tight system «the patient — the device» at breath of inspected. The majority of these devices measures only one, key parameter of gas exchange — the speed of oxygen consumption. There are 2 groups of volume devices: devices of the oxygen mode (at breath inspected by pure oxygen) and devices of the kislorodnovozdushny mode (breath by oxygen air mixture). The device of the oxygen mode represents the tight respiratory system consisting of a lung-tester, an adsorber for the absorption of carbon dioxide gas, the gas-distributing device connected by gas pipelines and the chart recorder. The respiratory system before a research is filled with oxygen. Results are fixed by the recorder on coordinate paper a feather, a cut is mechanically connected with a mobile element of a lung-tester.

The domestic industry releases the figurative device of the META 1-25 oxygen mode. The device consists of a dry lung-tester (fur) with a capacity of 10 l and the valve gas-distributing device. Change of volumes in time registers on a chart tape, the speed of the movement cover 50 and 600 mm/min.] a measuring range of volume from 1 to 8 l.

The group of devices of the oxygen-air mode is divided into two subgroups: 1) devices with parallel connection of additional capacity of constant volume to the respiratory system of the oxygen mode described above; 2) devices with oxygen stabilization when the automatic delivery in respiratory system of oxygen in the quantity equal consumed by the examinee is made.

Fig. 6. The diagrammatic representation of the domestic camera for measurement of oxygen consumption at newborns and children till 1 year.

With an additional capacity it is possible to carry cameras for definition of gas exchange at children to devices. The domestic industry releases the camera for measurement of oxygen consumption at newborns and children till 1 year (fig. 6). The 90 l Comer, in to-ruyu the child, a lung-tester water, with a capacity of 3 l is located. Oxygen consumption is registered on a chart tape at a speed of its movement of 10 mm/min.

Devices with oxygen stabilization are subdivided into devices of the general research (parameters of gas exchange are measured in both lungs together) and separate (parameters of gas exchange are measured for each lung separately). Devices of the general research contain: a) respiratory system, edges are included by a lung-tester, an adsorber and the gas-distributing device; b) system of oxygen stabilization, in to-ruyu the lung-tester enters: century) chart recorder. The respiratory system is filled with air, and system of oxygen stabilization — oxygen; intake of oxygen in respiratory system happens automatically.

The majority of devices with oxygen stabilization contains two identical tight systems consisting of a lung-tester, an adsorber, the gas-distributing device connected by gas pipelines and the chart recorder. Such devices allow to make a research of both lungs together at breath of the examinee kislorodnovozdushny mix and each lung separately at breath by oxygen.

In the USSR release devices with oxygen stabilization for the general research — the spirocolumns SG-2M (for adults and children) and the spirocolumns SG-1M which allows to make also separate research at breath by oxygen. The lung-tester of respiratory system of the SG-2M device — water, is supplied with two replaceable bells: with a capacity of 6 l — for adult and with a capacity of 3 l — for children. Capacity of a lung-tester of system of oxygen stabilization — 10 l. Record — on a chart tape.

In the spirocolumn SG-1M lung-testers of both systems water, with a capacity of 6 l. Record — on a chart tape. Devices for a separate research of each lung at D. oxygen air mixture contain two identical respiratory systems and two identical systems of oxygen stabilization.

A component of devices for researches of gas exchange of open type are gas analyzers on oxygen and carbon dioxide gas and the spirocount of open type (cm, Spirography ).

The device of the open PGI-2 type released by the domestic industry registers on a chart tape curve changes of the oxygen content and carbon dioxide gas in expired air and to spiro-gram. The spirocount contains two dry lung-testers with a capacity of 10 l in PGI-2. Gas distribution — valve. Gas analyzers: konduktometricheskiya — on carbon dioxide gas and thermomagnetic — on oxygen (see. Gas analyzers ). Measurement ranges: 0 — 8% for CO 2 and 13 — 21% for O 2 .

Parameters of gas exchange can decide on the help of a gas analyzer of GVV-2 [like J. S. Haldane] and the gas meter or the device for measurement of volume of gas — the gasometer. The examinee during certain time exhales through a valve box in a bag for gas collection (a bag of Douglas) then by means of a gas analyzer measure concentration of O 2 and CO 2 in the exhaled air, and the volume of the air exhaled in a bag is measured by the gas meter or the gasometer.

The method of a research of gas exchange based on measurement of concentration of O is widespread 2 and CO 2 in the test which is automatically selected from a gas flow to Krom the air exhaled by the examinee is added. The expense of a flow, from to-rogo is selected test, supported to constants by means of the blower. The analysis is made continuously by means of gas analyzers.

At children 6 — 7 years are more senior the research of function D. is conducted by means of the methods and devices accepted at adults; the spirography and tests with physical. loading are impossible, it is not always possible to measure also depth of breath by means of the mask connected to a lung-tester. In a wedge, conditions function D. is estimated according to auskultativny data, on D.'s frequency, visual symptoms of short wind (retraction of compliant places of a thorax, inflating of wings of a nose etc.). From tool methods the major is the research of concentration of oxygen and carbon dioxide gas and acid-base equilibrium of blood. For assessment mechanics D. use a combination of impedance pneumography (see) and the general pletizmografiya (see). By results of measurements energy costs of a human body are calculated. At the same time special tables, nomograms and spirometabolic rulers are widely used.

Bibliography: Breslav I. S. Any management of breath at the person, L., 1975, bibliogr.; Votchal B. E. Pathophysiology of breath and respiratory insufficiency, M., 1973; Dembo A. G. Nedostatochnost of function of external respiration, L., 1957, bibliogr.; Zilber A. P. Regional functions of lungs, Petrozavodsk, 1971, bibliogr.; Ivanov D. I. and Hromushkin A. I. Life support systems of the person at high-rise and space flights, M., 1968, bibliogr.; And with and to about in P. K. and d river. Theory and practice of an air medicine, M., 1975; Komro Dzh. And d river. Lungs, clinical physiology and functional trials, the lane with English, M., 1961, bibliogr.; Myles S. Underwater medicine, the lane with English, page 59, M., 1971; Marshak M. E. Regulation of breath at the person, M., 1961; H and in-ratil M., Kadlec K. and Daum S. A pathophysiology of breath, the lane from Czeches., M., 1967, bibliogr.; Fundamentals of gerontology, under the editorship of D.F. Chebotaryov, etc., page 211, M., 1969; Sergiyevsky M. V. of ides of river. Respiratory center, M., 1975; Tikhonov M. A. Mechanics of breath, in book: Results of science and tekhn., Fiziol, person and animals, t. 9, under the editorship of G. A. Stepan-sky, page 72, M., 1972; Physiology of breath, under the editorship of L. L. Shik, etc., L., 1973; Frankstein S. I. Respiratory reflexes and mechanisms of an asthma, M., 1974, bibliogr.; Frankstein S. I. and Sergeyev 3. H. Self-control of breath is normal also of pathology, M., 1966, bibliogr.; H and r N y y And. M. Pathophysiology of hypoxemic states, M., 1961, bibliogr.; Altman P. L.a. Dittmer D.S. Respiration and circulation, Bethesda, 1971; Bouhuys A. Breathing, N. Y. — L., 1974; With o m r o e J. H. Physiology of respiration, Chicago, 1966; D i j o u r s P. Respiration, N.Y. — Oxford, 1966; Handbook of physiology, sect. 3, v. 1 — 2, ed. by W. O. Fenn a. H. Rahn, Washington, 1964; The respiratory muscles, Mechanics and neural control, ed. by E. J. M. Campbell a. E. Agostoni, L., 1970; Respiratory physiology, ed. by J. G. Widdi-combe, L., 1974.

V. D. Glebovsky; M. I. Anokhin (ped.), O. V. Korkushko (rep.), N. I. Losev (patol.), N. S. Mironova, L. I. Nemerovsky (devices), M. A. Tikhonov (tousle.), V. P. Shmelyov (biophysical.).