From Big Medical Encyclopedia

ASTHMA (dyspnoe) — the complicated, changed breath which is shown as subjective feelings of constraint of breath, a lack of air, and objective changes of the main indicators of the function of external respiration (FER), in particular depth and a respiration rate and their ratios, minute volume and a respiratory rhythm, strengthening of work of respiratory muscles.

Nek-ry clinical physicians (M. M. Gubergrits, 1939; Century of X. Vasilenko, 1974, etc.) distinguish fiziol, and patol. The lake, understanding under fiziol. The lake increase in frequency and depth of breath at healthy faces, adequate to an exercise stress. Pathological O. is observed at a number of diseases, and at healthy faces — only in unusual conditions, in particular at decrease in partial pressure of oxygen (pO 2 ) or increase in partial pressure of carbon dioxide gas (pCO 2 ) in inhaled air, at temperature increase of the environment (thermal O.), and also at the exercise stress exceeding possibilities of an organism. In all these cases excitement of a respiratory center and work of respiratory muscles sharply amplifies. Ya. Shik and A. V. Greenberg (1935) specify that at an extraordinary exercise stress (unlike fiziol, deepening and increase of breath at an adequate exercise stress), breath becomes superficial and frequent, and lung volume decreases; at the certain, individually various level of increase in minute volume of breath (hyperpnea) the burdensome feeling of a lack of air appears.

According to Navratil (M. of Navratil) et al. (1967), the feeling of the complicated or insufficient breath both at healthy, and at sick people is the alarm signal forcing to stop an exercise stress. Adequacy of an exercise stress to opportunities of an organism is defined not only by degree of this loading, but also the state of health, and, above all — level funkts, conditions of the human body which is carrying out it. It gave the grounds to use change of function of external respiration, i.e. objective exponents of O. arising under the influence of standard loading as for determination of level funkts, states, and for assessment of degree of respiratory and heart failure and detection of the hidden respiratory insufficiency, etc.

On the nature of the changes of FVD in diagnostic practice observed at O. allocate various manifestations of O.: a hyperpnea, or a polypnea — increase in minute volume of breath at the expense of depth and frequency; tachypnea (see) — sharp increase of breath (St. 40 in 1 min.); fathers-pnoe — deepening of breath; bradipnoe (see) — an urezheniye of breath; an oligopnea, or small breath — reduction of minute volume of breath at the expense of an urezheniye and reduction of frequency; an apnoea — an apnoea; an orthopnea — very sharp disturbance of breath demanding forced position of the patient for its simplification. Also allocation of nek-ry most typical disturbances of a respiratory rhythm is widespread: wavy breath, Cheyna — Stokes breath (see), biotovsky breath (see), Kussmaulya breath (see).

In relation to separate phases of external respiration distinguish three types of O. — inspiratory (difficulty of a breath), expiratory (difficulty of an exhalation) and mixed. Inspiratory O. is observed at defeats of a diaphragm, pleural exudates, a pneumosclerosis, at the heart failure complicated by ascites and also at a tracheostenosis and large bronchial tubes of any origin when the complicated breath is followed sometimes by noise — stidor breath (see. Stridor ). Expiratory O. is observed by hl. obr. during the narrowing of a gleam of small bronchial tubes (accumulation of a secret in them, swelling of a mucous membrane, a spasm of bronchial tubes etc.). Extreme degree of O. is called by suffocation, and by attacks of suffocation — asthma (see).

Subjective and objective signs of O. are not always combined. At slow increase of disturbances of FVD patients can not feel gradually increasing difficulties of breath. At constantly existing O. the patient as if gets used to it, ceases to feel it and does not complain of it though sometimes considerable disturbances of FVD objectively are defined, and already at survey of the patient O. comes to light (the patient chokes, often takes breath at a conversation). According to B. E. Votchal (1969), it is more often observed at patients who should not hurry, to walk upstairs, etc. On the other hand, in nek-ry cases patients complain of feeling of shortage of air in the absence of any changes of FVD, gas and chemical composition of blood, heart troubles and other reasons and O.'s signs (false sensation of O.) that emphasizes importance of objective signs for O.'s allocation as symptom of certain diseases.

O.'s understanding as the phenomenon which is characterized by both subjective, and objective signs is most widespread; it is inherent, in particular, in many prominent Soviet clinical physicians (to D. D. Pletnev, 1933; To G.F. Lang, 1935; M. M. Gubergritsu, 1939; To A. L. Myasnikov, 1951; B. E. Votchalu, 1973; Century of X. Vasilenko, 1974) and number of foreign scientists. At the same time in medical literature also the extreme points of view on O. — or as on only a subjective sign, or as on only the objective phenomenon are presented.

Existence of various approaches to O.'s definition is explained by the different reasons, among to-rykh considerable value has that circumstance that at the modern level of knowledge not all questions of regulation of breath, origins and assessment of various disturbances of FVD are found rather out. Nevertheless the unity a wedge, approach to O.'s understanding as phenomenon with subjective and objective signs is represented very important for practice because the complaint to O. and O.'s characteristic — important symptoms of certain diseases; besides, O. is the main criterion used for classification of various degrees of heart and respiratory failure.

Pathogeny asthmas it is in many respects not clear therefore all existing theories of its origin are not faultless. Proximate causes of emergence of O.: 1) humoral factors — change of gas composition of blood (increase in content of carbon dioxide gas, decrease in the oxygen content) and change of pH with shift in the acid party; these changes exert direct impact as on the bulbar centers, and peripheral chemoceptors of a vascular bed and chemoceptors of a myelencephalon (central); 2) the impulsation from receptors of the respiratory device (bronchopulmonary and respiratory muscles) coming to a respiratory center; 3) the central, in particular cortical, influences on a respiratory center (e.g., at hysterical O.).

There is a representation that reduction pH and a hypercapnia promote deepening and increase of breath while an anoxemia — only to its increase. However direct compliance between extent of changes of gas composition of blood and FVD can not be. Actually all these ratios it is much more difficult, and the expressed humoral changes can cause also opposite reactions. So, e.g., sharply expressed hypercapnia oppresses respiratory center (see), it is long the keeping hypercapnia causes adaptation of a respiratory center to carbon dioxide gas etc. At assessment of all these influences the condition of a respiratory center is of great importance funkts.

The significant effect on funkts, a condition of a respiratory center is rendered by temperature of the blood washing it: indicators of FVD change both at a hypothermia, and at a hyperthermia. At a hypothermia owing to decrease in excitability of a respiratory center breath urezhatsya and becomes more superficial, at a hyperthermia there is so-called thermal O. — increase and deepening of breath.

Still finally the reasons gipernnoe are not found out at a muscular exercise and influence of metabolic activity of fabrics and bodies on FVD. The solution of this question is complicated by the fact that at adequate increase lung ventilation (see) owing to a moderate exercise stress it is not possible to establish any changes in gas structure and pH of an arterial blood though ventilation sometimes increases by 10 — 15 times and more. At patients with respiratory insufficiency (see) the hyperventilation in certain limits also maintains datum level of these indicators.

At the same time it is known that to increase ventilation by 15 times, it is necessary to inhale air mixture, concentration of carbon dioxide gas in a cut apprx. 10%. The assumption of existence of the receptors muscular chemo reacting to increase in content of carbon dioxide gas is disproved by a run with an overload of muscles a venous blood, in to-ruyu carbon dioxide gas is added. At the same time changes of ventilation do not happen. It indicates the compensatory nature of increase in ventilation during the work directed to maintenance of normal gas composition of blood, but remains not clear that causes this compensatory reaction if there are no changes in the oxygen content and carbon dioxide gas, and also indicators of pH of an arterial blood. Idea of the leading neurogenic regulation of FVD during the work, a cut is upheld by D'Andzhelo and Torelli (E. D’Angelo, G. Torelli, 1971), J. I. Jensen et al. (1972), according to most of researchers, it cannot be accepted as the only thing though it is impossible to deny existence of this component. Lakur, Flandrua (J. Lacour, R. Flandrois, 1977) consider that changes of ventilation at an exercise stress are connected with factors of two types: the first are bystry neurogenic reactions, the second — slower humoral. Peripheral incentives are induced by repeated changes of length of muscles and the movement of joints. M. E. Marshak (1958) attached great value to the iropriotseptivny respiratory reflexes arising during the muscular work. On their base uslovnoreflektorny mechanisms of regulation of breath during the muscular work form. Increase in ventilation at an exercise stress is provided also with influence of incentives, the coming from motor centers. Sensitization of the centers even to the insignificant, not giving in to measurement fluctuations of humoral factors, first of all carbon dioxide gas, is promoted by the level of adrenaline increasing in blood at physical activity. As V. Kolychev (1961) showed, small doses of adrenaline strengthen reflex reaction to eksterotseitivny and proprioceptive irritations, doubling lung ventilation. Wasserman's data are of considerable interest (To. Wasserman, 1977), according to the Crimea increase in ventilation at an exercise stress is caused by increase in content of carbon dioxide gas in the venous blood inflowing in lungs from actively working fabrics. According to its data, in system of a pulmonary artery to pulmonary capillaries there are he-moretseptorny mechanisms, active, sensitive to carbon dioxide gas. This representation finds confirmation in the works which showed that at increase in content of carbon dioxide gas in a venous blood ventilation increases while rs02 the arterial blood does not change. The assumption of existence of the chemoceptors of a pulmonary artery reacting to change of the inflowing venous blood allows to explain the hyperventilation arising at patients with respiratory insufficiency when there are no changes of gas structure of an arterial blood yet. However in a number of experimental works it was not succeeded to prove existence in system of a pulmonary artery chemo of the receptors sensitive to carbon dioxide gas. It is also impossible to exclude influence of fervescence during the work. At an exercise stress points JI to one of the possible reasons of hypo pi for a stub. JI. Chic (1968). He considers that the majority of theories of regulation of breath is based on idea of regulation on a deviation by a feed-back from the receptors, various on localization, perceiving deviations rs02, r02 and pH. On etokhm the principle of a feed-back the theory is based so-called wasps-tsidlyatornaya, according to a cut the crucial role in regulation of breath is played by the fluctuations of gas structure of an arterial blood arising in different phases of a respiratory cycle from the average level, but not the average level. It is obvious that regulation of ventilation on a deviation cannot explain a hyperventilation at physical activity and in nek-ry other cases. According to JI. JI. Chic, in regulation of ventilation essential value belongs to the impulsation coming to a respiratory center, caused not by changes of structure of an arterial blood, and from receptors of the motive and respiratory devices signaling about the arising indignations to-rye can lead to a deviation rs02 and r02. Therefore, in addition to regulation on a deviation, there is also a regulation on indignation. Though regulation only on indignation and is not enough, but elaboration of adequate change of ventilation happens in this case by the self-training directed to the prevention or reduction of possible deviations in gas structure of an arterial blood. This thesis is confirmed also by nek-ry experimental data. According to E. Sh. Ay-rapetyants and A. V. Pogrebkova (1956), there is a device of cortical level which is providing information and integration of the processes developing in respiratory system, catching the minimum fluctuations of structure of a gaseous fluid and preventively using hyper mouthpieces-nichesky reaction. E. Sh. Ayrapet-yants considers that in structure of respiratory system there is a device which is carrying out function of the respiratory analyzer. As for influence of the receptor device on O.'s emergence, it is not clear yet whether those it is receptors, to-rye cause normal process of breath, but with the changed character of an impulsation, or these are other receptors; it is not known also where there are these receptors (in the fabrics surrounding respiratory tracts in alveoluses, a pulmonary parenchyma, in respiratory or other muscles) and what their type; at last, it is not found out whether there are afferent ways from receptors as a part of wandering, sympathetic or somatic nerves.

In a question of the reasons of subjective feelings at O. there is also no unity of opinions. There is a representation that accumulation of products of metabolism at sharp strengthening of work of respiratory muscles excites their sensitive nerve terminations. Wright and Branskomb (G. Wright, V. of Branscomb, 1954) consider that subjective feelings of O. are a consequence of an intensification and prolongation of a discharge of medullary inspiratory neurons at very intensive and long bombings of a respiratory center the corresponding impulses. Campbell and Howell (E. Campbell, J. Howell) connect O.'s feeling with the fact that neuromuscular efforts do not correspond to that level of a hyperpnea, a cut is actually reached. Such disbalance of the system controlling and regulating ventilation is perceived by the highest departments of c. N of page as feeling of difficulty of breath. According to S.Y. Frankstein (1974), L. L. Chic (1975), etc. O.'s feeling always results from superexcitation of a respiratory center, a cut is transferred not only to a spinal cord and respiratory muscles, but also to a brain, in particular to limbic structures where the feeling of a lack of air, fear, alarm forms. Local sensitization or irritations of these structures can give subjective O. without any its objective manifestations.

According to A. G. Dembo (1957), O.'s feeling appears at discrepancy between requirements to increase in volume of ventilation and opportunities of the device of external respiration to their satisfaction. It arises when the need for increase in ventilation for providing normal gas structure of an arterial blood exceeds funkts, possibilities of the device of external respiration, from to-rykh degree of a hyperpnea depends. If they do not allow to increase it, no impacts on a respiratory center of this increase can cause. Essential value in restriction of opportunities of increase in a hyperpnea has a condition of the most ventilating device (ability of a thorax to extend, mobility of a diaphragm, etc.) and the factors influencing mechanics of breath, lying out of system of external respiration (a congestive liver, ascites, abdominal distention, etc.). It is obvious that the lower funkts, possibilities of system of external respiration, the quicker there comes O.'s feeling both at physical activity, and at patol, states.

Clinical value of an asthma

O. can arise at diseases of lungs and bronchial tubes, cardiovascular system, system of blood (anemia), defeats of c. N of page, disbolism, at the diseases leading to immobilization of a thorax and a diaphragm (obesity, damage of respiratory muscles, edges and a backbone, a disease of a pleura). Besides, O. can appear at various emotional influences.

At pulmonary and heart diseases of O. is an early and important symptom of the beginning insufficiency of function of these systems that is shown most often by increase and deepening of breath.

The lake at diseases of lungs and bronchial tubes arises or owing to restrictive processes, i.e. reduction of a respiratory surface of alveoluses, or obstructive processes, i.e. reduction of bronchial passability. The restrictive processes causing O. are observed at acute and hron, massive inflammatory processes in lungs (tuberculosis, pneumonia), spontaneous and medical pheumothorax, passive obstacles to expansion of a thorax (a kyphoscoliosis, a state after a thoracoplasty, etc.), consolidation of intersticial fabric (granulomatoses of lungs, a pneumosclerosis, intersticial fibrosis, a silicosis, etc.) and reduction of ventilation of tissue of lung at the expense of a fibrothorax, an exudate in a pleural cavity, etc. Bronchial obstruction is most often observed at hron, bronchitis (see) and bronchial asthma.

At heart troubles O.'s emergence testifies about heart failure (see), first of all the left ventricular, resulting in stagnation blood in lungs therefore elasticity of pulmonary fabric decreases and its respiratory surface decreases. The lake at heart failure appears at first during the work of various intensity, and then and at rest, sometimes in the form of attacks of suffocation (see. Cardiac asthma ). At heart failure breath is speeded usually up, strengthened and is subjective insufficiently. Character and O.'s degree are considered during the definition of degrees of heart and respiratory failure.

The lake, caused by changes in c. the N of page — so-called central O., first of all depends on dysfunctions of a respiratory center. These disturbances can carry funkts, character also to depend on organic changes (injuries of a skull, various inflammatory diseases, abscesses, tumors, hemorrhages and fibrinferments, etc.). Depending on character and extent of defeat of a respiratory center of manifestation of O. can be various. At decrease in excitability of a respiratory center there is a disturbance of a respiratory rhythm — Cheyn's breath — Stokes, breath the Biota when after several breaths there comes the pause — an apnoea. At abscess of a brain, meningitis, disturbance of cerebral circulation, nek-ry poisonings of O. it is shown variously, quite often in the form of so-called breath of Grokko representing the dissociated breath which is characterized by disorder of coordination between work of a diaphragm and other respiratory muscles. nn (S. of Frugoni) explained to Fr guo it with changes in coordination of work of a respiratory center (the name «Grokko's breath — Frugoni» from here). This of oozes O. is often combined with Cheyn's breath — Stokes. The disturbance of a respiratory rhythm called by wavy breath usually precedes Delkhaniya Cheyn's approach — Stokes and happens after his termination.

At increase in excitability of a cerebral cortex or weakening of brake processes in bark, under the influence of cortical influences there can be emotional O. connected with nervousness, fear, joy and other emotions. Treats such O. and so-called neurogenic O.

Stepen O. at anemia (so-called gemichesky O.) depends on disease severity and on extent of reduction of quantity of erythrocytes — oxygen carriers that creates conditions for emergence of an arterial anoxemia and hypoxias (see).

O. caused by acidosis at a diabetic coma (Kussmaul's breath) belongs to O. caused by disbolism, at uraemia (up to uraemic asthma), at poisoning with various poisons influencing transport function of blood or breaking tissue respiration. In these cases of change of indicators of FVD can be various (increase and urezheny frequencies and increase in depth of breath in various combinations).

See also Breath .

Bibliography: Votchal B. E. Pathophysiology of breath and respiratory insufficiency, M., 1973; Dembo A. G. Insufficiency of function of external respiration, L., 1957; Lang G. F. Questions of cardiology, century 1, L., 1936; Marshak M. E. Regulation of breath at the person, M., 1961; H and in r and t and M.'s l, * To and d-lets To. and D and at S. Patofiziologiya's m of breath, the lane from Czeches., Prague — M., 1967; Naumov L. B. Diagnosis of respiratory insufficiency, Tashkent, 1970; New in physiology and pathology of breath, under the editorship of V. V. Parin, page 104, M., 1961; Frankstein S. I. Respiratory reflexes and mechanisms of an asthma, M., 1974; Sh and to L. L. The schematic diagram of regulation of minute volume of breath, in book: Vopr, fiziol, and patol, breath, under the editorship of A. F. Krasnov, page 135, Kuibyshev, 1968; Sh N of e y M. S. O der some fundamental issues of a problem of respiratory insufficiency, Rubbed. arkh., t. 33, No. 4, page 98, 1961; Anthony A. item Y e n of t h H. Funktionsprufung der Atm ung, Lpz., 1962; Beaver W. L. a. W a s s e r m a n K. Tidal volume and respiratory rate changes at start and end of exercise, J. appl. Physiol., v. 29, p. 872, 1970; With o m r o e J. H. Physiology of respiration, Chicago, 1975; D ’Angel oE. T o r e 1 1 i G. Neural stimuli increasing respiration during different types of exercise, J. appl. Physiol., v. 30, p. 116, 1971; G u z A. Regulation of respiration in man, Ann. Rev. Physiol., v. 37, p. 303, 1975; Jensen J. I., V e j b y - C 1) of i s t e n s e n H. Petersen E. Ventilatory response to work initiated at various times d*uring the respiratory cycle, J. appl. Physiol., v. 33, p. 744, 1972; W a s s e r m a n K. o. Carbon dioxide flow and exercise hyperpnea, Amer. Rev. resp. Dis., v. 115, p. 225, 1977.

A. G. Dembo.