Dyspnea

DYSPNEA (dyspnoe), a disorder of external respiration, caused by impairment of the function of respiratory organs, auxiliary mechanisms of breathing, or nerve centers regulating respiration. - The pathogenesis of D. appears complex and to this day has not been fully elucidated in all details. Older authors sought explanations for all forms of D., both physiological and pathological, in mechanical changes in the circulation of blood in the lungs. Later, a series of neuro-reflex and then chemical theories were created. Despite the diversity and complexity of the processes whose result is pulmonary and external respiration, it is naturally difficult to seek or give a single explanation for the pathogenesis of D. However, since the basic regulation of respiration is determined by chemical reactions occurring primarily in the tissues of the respiratory center, to some extent the view of most researchers is justified, according to which the basis of D. lies in chemical shifts, while mechanical and nervous moments serve only as supplements for explaining individual forms of D. Mechanical theories attempted to explain respiratory disturbances by changes in circulation in the lesser circle with subsequent disruption of gas exchange in the lungs and accumulation of CO₂ in the blood. The significance of CO₂ as a stimulant of the respiratory center was noted already by Miescher (Mie-scher; 1885). However, Haldane and Priestley (1908) proved that CO₂ does not possess a specific effect and that the stimulant of the respiratory center is the active reaction of the blood. Research by Winterstein and Hasselbalch confirmed that for respiratory function the main factor is the concentration of hydrogen ions in the arterial blood bathing the respiratory center. Somewhat later, research again appeared asserting that CO₂, besides its general influence as an acid, also has a certain specific stimulating effect on the respiratory center. However, these studies did not find acceptance, and the physiological doctrine of Haldane formed the basis of the modern interpretation of the pathogenesis of dyspnea. It was experimentally established that the addition of minimal quantities of acid salts or acids to the blood causes increased pulmonary ventilation. Conversely, an increase in blood alkalinity decreases ventilation. The well-known intensification of breathing during heavy physical work serves as an example of physiological D., which in its pathogenesis is essentially the prototype of prolonged D. in cardiac patients. In physiological dyspnea, ventilation increases to such an extent that it reaches 100-120 liters of air per minute, and in some cases even 150 liters per minute. The intensification of breathing remains for some time after the end of work. It has been proven that physiological work D. depends on the entry of lactic acid into the blood, the content of which, according to Ryffel, can reach 0.07%. When lactic acid enters the blood, there is a decrease in the alkaline reserve, secondary release of carbonic acid, and an increase in blood pH. As a result of these changes, hyperventilation occurs. Thus, physiological D. is an example mainly of chemical D. However, Krogh and Lindhard showed that hyperventilation can occur already at the beginning of work and then is a consequence of increased excitability of the respiratory center. Pathological D. in the vast majority of cases is also the result of chemical shifts and accumulation in the blood or in tissue fluid of volatile or non-volatile acids (lactic, oxalic, butyric, phosphoric, uric, succinic, amino acids, and other still unknown acids). Oxygen starvation is not a direct cause of D., but only contributes to the formation of the mentioned products of incomplete combustion. Slowing of blood flow in the greater circle during decompensation causes oxygen starvation of tissues with its consequences. It has been repeatedly proven that blood contains an increased amount of lactic acid in cardiac insufficiency. Thus, in contrast to the interpretation of cardiac D.

Carbon dioxide dyspnea (D. due to excess CO₂) came to be considered as lactic acid dyspnea, i.e., D. caused by excessive accumulation of lactic acid. Most other cases of severe persistent D. are also explained by the development of acidosis due to the accumulation of non-volatile acids (Lewis), so-called hematogenous D. (Winterstein). The accumulation of the latter in the blood occurs in cardiac patients with increased intermediate metabolism, in particular glycolysis in muscles in connection with physical exertion ('working' D.), as well as at rest with insufficient blood circulation. Slowing of blood flow during decompensation leads to increased 'use' of oxygen by tissues, a drop in its tension in the blood, and difficulty in further release of O₂ by the blood. The respiratory center, maintaining the constancy of blood reaction, responds to increased acidosis with hyperventilation, as a result of which there is increased release of carbon dioxide and its decrease in the blood (see Buffer properties). Thus, in cardiac D., not only is there often no increase in carbon dioxide in the blood, but on the contrary, a decrease is observed (hypocapnia). The development of hypocapnia is the result of that adaptive function inherent in the respiratory center in regulating the active reaction of the blood. However, the occurrence of D. can also be caused by short-term shifts in the active reaction of the blood (decrease in pH), developing locally in the area of the respiratory center. The hyperventilation that arises in such cases depends on the excitation of the respiratory center due to isolated acidosis of the tissue fluid bathing the medulla oblongata (so-called centrogenic D.). 'Hematogenous' and 'centrogenic' D. are also observed in renal patients and in arteriosclerotics and are caused by the same pathogenetic factors. The first occurs in severe kidney damage with impaired function, the second in the early stages of kidney diseases without signs of functional insufficiency (Straub). The first form is accompanied by hypocapnia, which is the result of partial use of the buffer properties of the blood. The second is sometimes accompanied by even alkalosis of the blood (eucapnia or even hypercapnia) due to hyperventilation; it depends on asphyxiation of the respiratory center. Hyperventilation in this form does indeed exist, as evidenced by the decrease in CO₂ content in the alveolar air. In light of the chemical theory, an explanation is obtained for the D. of diabetics, caused by acidosis from the accumulation of ketone bodies in the blood, D. in various autointoxications (cholemia, etc.), in endocrine diseases, e.g., Basedow's disease (Lewis). Apparently many cases of D. in diseases of the respiratory tract also depend on acidosis (Barcroft's pneumonia). However, it is undoubtedly true that the chemical theory does not explain all types of D. completely. It can be said that ultimately every D. is a chemical D. But the paths of occurrence of perversions of the chemical processes of the blood or tissues are different. To understand them, one has to turn to some theories of older authors, namely to the mechanical theories of pulmonary congestion. Traube saw the main cause of D. in the overfilling of pulmonary capillaries and their expansion, leading to their bulging into the alveolar lumen and to a decrease in the volume of pulmonary alveoli. Basch believed that overfilling of capillaries leads to their straightening, and consequently to stretching of the alveoli and the lung as a whole (Lungenschwellung), as well as to rigidity of lung tissue (Lungenstarre), as a result of which the distensibility of the lung decreases and ventilation worsens. Bash's teaching gained general recognition mainly in regard to lung rigidity. The existence of lung rigidity as a result of acute or prolonged congestion has also been confirmed by experiment (Romanoff and others). However, the question of gas exchange in the lungs remains controversial: some believe that in cases of congestion it occurs normally, others point to its changes. While in healthy people and animals the difference in CO₂ tension in arterial blood and alveolar air does not exceed a few millimeters, which is practically insignificant, in cardiac patients much more significant fluctuations are noted. The development of lung rigidity in cardiac patients is confirmed by data on the state of vital capacity (its decrease) and the change in Mittellage. Lung rigidity is a reversible process, disappearing with the restoration of compensation. Accordingly, vital capacity also increases. Some authors believe that as a result of mechanical changes in blood circulation in the lungs, the function of the alveolar epithelium, its permeability, also changes (Peters). The classical theory considered pulmonary congestion as the cause not only of prolonged D., but also of periodic respiratory disorders - cardiac asthma. In the latter case, a 'transient' congestion was assumed. However, the pathogenesis of paroxysmal dyspnea is much more complex. Therefore, clinicians tried to find new explanations for it, particularly in neuro-reflex influences. Hoffmann interpreted cardiac asthma as a 'cardiac neurosis' depending on changes in the cardiac ganglia connected with the respiratory center. Huchard attached particular importance to nervous and toxic factors in the occurrence of 'pseudoasthma aortique' - toxialimentary D.; Vaquez assumed a combination of mechanical and reflex factors. Finally, Koranyi and Eppinger believed that cardiac asthma arises from a reflex from the congested lung. Heymans found confirmation of the reflex theory in experiment. When certain areas of the aorta and sinus caroticus were irritated, he noted, along with changes in blood pressure, reflex irritation of the respiratory center (excitation of the respiratory center with a fall in blood pressure and vice versa). At present, neuro-reflex theories are not widely accepted. Most clinicians adhere to the classical theory of Traube with some additions. Thus, a number of considerations have been put forward to explain the night appearance of attacks. It has been established that during sleep, especially in its first hours, there is a significant drop in blood pressure, which impairs coronary circulation. The second factor is the change in tone of the autonomic nervous system during sleep in the sense of increased influence of the parasympathetic system, which leads to a decrease in systolic tension of the heart. At the same time, in patients with hidden insufficiency of the left heart, there is an increase in venous return at night, placing increased demands on the heart. The increase in venous return is caused by the mobilization of hidden tissue edema that has accumulated during the day and has come into motion under the influence of rest and warmth (Brunn, Koranyi). The fact that asthma is not observed in edematous patients is explained by the greater stability of edema in such cases (Brunn). The clinical fact that a dry diet prevents the appearance of dyspnea (Volhard) serves as proof of the influence of 'clinostatic' flow on the occurrence of asthmatic attacks. Overfilling of the vascular bed with fluid due to the mobilization of edema contributes to the appearance of sudden weakness of the left ventricle, dissociation in the work of the ventricles occurs, i.e., the necessary condition of the classical theory of Traube. Wassermann categorically objects to Traube's theory, considering that pulmonary congestion is a consequence, not a cause, of cardiac asthma. He considers changes in the respiratory center to be the cause. Wasserman opposes the following objections to the classical theory: 1) the appearance of asthma in patients without clinical signs of pulmonary congestion and the absence of dyspnea attacks in mitral patients (this objection has long been put forward by many authors); 2) the impossibility of assuming such a rapid development of pulmonary congestion due to decompensation of the left heart and an equally rapid restitutio-ad-integrum; 3) the absence of clinical symptoms of congestion in the lungs; 4) the presence of sharply expressed subjective disorders characteristic of the participation of the nervous system; 5) the influence on the course of the attack of pressure on the carotid artery. Wassermann believes that cardiac asthma is caused by changes in circulation not in the small, but in the large circle. In his opinion, the functional weakness of the left ventricle is manifested not by gross mechanical changes in the lungs, but by more subtle and early disorders from the respiratory center. The functional insufficiency of the heart is more sharply expressed at night due to anoxia and a decrease in the threshold of irritation of nerve centers. Daytime asthma attacks in the absence of these aggravating factors indicate deeper and more severe changes in the heart. The pathogenesis of another type of periodic respiratory disorder - Cheyne-Stokes breathing - is completely different. This type of breathing can be observed in healthy people if they are placed in conditions of oxygen hunger (Haldane). The main difficulty in explaining the pathogenesis of the Cheyne-Stokes phenomenon is justifying the descending wave of the respiratory curve (see the figure for the article Pneumograph, pneumography). The ascending part of the curve indicates an intensification of breathing, reaching normal physiological magnitude.

The question arises as to why this normal breathing does not remain for a long time, but begins to decline again and reaches the stage of apnea. The old theory of Traubé took as its basis the decreased excitability of the respiratory center. This decrease, with insufficient inflow of arterialized blood to the respiratory center, leads to a respiratory pause—apnea (Traubé). From the moment respiratory movements cease, CO₂ accumulates in the blood. The increased venosity of the blood acts as a strong irritant and causes the reappearance of respiratory movements. As ventilation improves, the venosity of the blood gradually decreases, the irritation of the respiratory center weakens, and breathing ceases again. It is only unclear why, after the elimination of increased blood venosity, normal breathing is not established, but weakness and finally its complete cessation occur again. Rosenbach sought the cause of Cheyne-Stokes breathing in the unusual fatigability of the respiratory center. The frequent occurrence of such dyspnea is observed during sleep (Mosso). At present, the viewpoint of Guldane and Douglas is very widespread, that periodic breathing depends on acapnia (see). 14 7 Apnea depends on the fall in tension of CO₂ in the blood below the threshold of irritation of the respiratory center. During apnea, CO₂ accumulates until its tension reaches a level capable of causing irritation of the respiratory center. As the supply of oxygen increases, there is also a greater release of CO₂, as a result of which acapnia again develops and apnea occurs. Wassermann notes that this theory also does not explain the decrescendo phases, because it remains unclear why the influx of oxygen causes acapnia and not normal ventilation. Furthermore, Wassermann points to the clinical fact that the administration of oxygen to patients leads to the cessation of Cheyne-Stokes breathing, which contradicts the view of Guldane and Douglas. Wassermann believes that the basis of the Cheyne-Stokes symptom complex is chronic oxygen starvation, while the periodicity of breathing depends on the biological peculiarities of the respiratory center, which is characterized by rhythmic activity. During apnea, the oxygen deficit increases, during hyperpnea it decreases, however, this is not the cause but only a consequence of periodic breathing. Nevertheless, even Wassermann's theory cannot be considered fully convincing, and the question of the pathogenesis of Cheyne-Stokes breathing remains unresolved. Types of dyspnea. Physiological dyspnea, occurring after muscular work, represents an adaptation of the respiratory system to the increased needs for tissue blood supply, resp. breathing, and is also, as indicated above, the first and most important means of equalizing those shifts in the active reaction of the blood that occur during work. During prolonged work, and in trained subjects relatively quickly, dyspnea disappears, giving way to the so-called 'second wind,' close to normal. Pathological dyspnea is both a subjective and an objective symptom of numerous diseases. In the clinic, objective dyspnea has dominant significance, however subjective dyspnea is often the first sign revealing one or another disease. In particular, such significance belongs to dyspnea in cardiac patients, in which it is usually an indicator of the state of compensation. Severe subjective dyspnea is most often found in cardiac patients (according to Cabot in 42% of all cases of dyspnea), less frequently in pulmonary tuberculosis (in 28%), chronic bronchitis (11%), emphysema (3.8%), bronchial asthma (4%), pneumonia (9%) and chronic nephritis (8%). Subjective dyspnea is sometimes observed in the absence of objective respiratory disorders in depressive, hysterical patients. It manifests in the form of a subjective sensation of the inability to take a full breath and the need to periodically breathe more deeply. The absence of subjective dyspnea in the presence of visible, objectively confirmable dyspnea indicates 'habituation' to it (in chronic dyspnea in mitral patients) or the severity of the general condition (atonal period, unconscious state). According to some observations, the severity of subjective dyspnea depends to a certain extent on its form; expiratory dyspnea and deep breathing cause more severe subjective disorders; the most severe subjective sensations are given by paroxysmal respiratory disorders, such as cardiac and bronchial asthma. Objective dyspnea is a collective concept under which extremely diverse respiratory disorders are implied. It is characterized by changes in the frequency and depth of breathing, the duration and ratio of its individual phases (inspiration and expiration), and changes in rhythm in the sense of the appearance of more or less long respiratory pauses. Depending on the duration or brevity of dyspnea, as well as the nature of its onset, two large groups can be distinguished: dyspnea of the prolonged type and periodic paroxysmal respiratory disorders. In terms of frequency, there is distinguished rapid breathing—tachypnea, polypnea (in cardiac, nervous, endocrine diseases, poisonings) and slowed breathing—oligopnea, bradypnea (in stenoses of the respiratory tract, comatose states, etc.). In terms of depth, deep breathing—batypnea (in cardiac decompensations, comatose states, narrowing of the respiratory tract) and shallow breathing (in painful sensations in the chest and abdomen, sometimes in cardiac decompensation and hysteria) are distinguished. Usually a combination of rapid and deep breathing is observed, less frequently rapid shallow or slow deep breathing. The ratio between the duration of inspiration and expiration in the pure form of rapid breathing is not disturbed (mixed dyspnea). Dyspnea with slowed breathing is characterized by the predominance of either the inspiratory or expiratory phase, i.e., it represents inspiratory or expiratory dyspnea. Lengthening of inspiration is observed in stenoses of the respiratory tract, some pleuro-pulmonary diseases (croupous pneumonia, lung abscesses, pleurisy, pneumothorax), cardiac diseases (including pericarditis), comatose states. Lengthening of expiration occurs in emphysema, narrowing of the respiratory tract, asthmatic conditions, especially in bronchial asthma, nervous diseases, cardiac decompensation. With deepening of breathing, a predominance of inspiration over expiration is usually observed (Hofbauer), expansion of the chest, and in some cases, for example in stenosis of the respiratory tract, acute pulmonary distension. In some diseases, a peculiar disturbance of breathing is noted, expressed in the appearance of respiratory pauses (apnea). Usually this change is characteristic of periodic respiratory disorders, for example Cheyne-Stokes breathing or 'big breathing,' but it is also found in other conditions, e.g. in dyspnea in Addison's disease, in the agonal period. The duration of the pauses varies, in some cases reaching 30 sec. or more. In some cases, respiratory stops occur with a certain periodicity, in others irregularly. In cardiovascular diseases, several forms of respiratory disorders are observed. In decompensated, predominantly mitral patients, dyspnea of the prolonged type ('valvular dyspnea' of older authors) is often observed, frequently combined with cyanosis. In patients with aortic lesions, as well as with essential hypertension, another form is observed—paroxysmal spontaneous dyspnea. To this group of periodic respiratory disorders in cardiac patients, besides cardiac asthma, belong Cheyne-Stokes breathing and the relatively recently described, close to Cheyne-Stokes breathing 'undulating breathing' (wogende Atmung). Prolonged dyspnea is already found in relatively early stages of subcompensation in the form of 'working dyspnea,' i.e., it occurs with physical exertion (Corvisart). In later stages of decompensation, it becomes permanent and does not leave patients even at rest. In extreme degrees of decompensation, it turns into orthopnea, i.e., dyspnea requiring the forced sitting position of the patient (see below). Changes in breathing in prolonged dyspnea most often come down to an increase in the frequency and depth of breathing, less frequently to rapid shallow breathing. The pneumogram in the stage of decompensation is characterized by a steep descent of the inspiratory and no less steep ascent of the expiratory limb (Hofbauer). Vital capacity of the lungs is reduced sometimes to half, the reserve air is decreased, the residual (residual) is increased, respiratory excursions are decreased compared to normal. The tension of CO₂ in the alveolar air is decreased, that of oxygen is increased. In extreme degrees of decompensation, such a state is observed in which the patient cannot lie down due to difficulty in breathing, but sits in a forced position, leaning with hands on the bed, chair arms, etc. (orthopnea). In this position, patients spend whole days, nights, sometimes weeks, deprived of sleep, unable to lie down. Cyanosis, flaring nostrils, sometimes an open mouth give the face a characteristic expression. The muscles of the shoulder girdle are fixed, which makes possible the participation of accessory muscles in breathing (mm. scaleni, sterno-cleido-mastoidei, serrati anteriores, pectorales majores et minores).

The diaphragm stands low. Additionally, if there is ascites or effusions in the pleural cavities, they shift downward when sitting, as a result of which the lungs expand, their elasticity improves (Lungenspannung), and consequently the respiratory function as well. Finally, in the sitting position, pressure on the v. cava inferior decreases, which together with the action of the abdominal muscles during improved active expiration also promotes the upward propulsion of blood (Hofbauer). During inspiration, however, the diaphragm presses on the liver and squeezes blood out of it (Wenkebach). With the head in a low position, the brain is supplied with blood less well, since most of it goes through the a. carotis externa, and less through the a. carotis interna to the brain (Eppinger, Laszlo and others). In cardiac patients with elevated venous pressure, the impairment of cerebral circulation in the horizontal position is even more pronounced. The vertical position thus improves the blood supply to the respiratory center (Sahli). The second type of O.—paroxysmal dyspnea—in cardiac patients arises suddenly during complete rest, more often at night, in the first hours of sleep. In cases of daytime occurrence (according to Hoffman, relatively frequent), it is still not associated with physical exertion, unlike prolonged dyspnea. The clinical picture varies from mild sensations of breathing difficulty to the most severe attacks of suffocation with difficulty in both inspiration and expiration. In intensity, this dyspnea borders on that observed in pulmonary edema. The duration of suffocation ranges from several minutes to several hours. During an attack, breathing is accelerated to varying degrees, sometimes reaching 40-50 per minute, and is shallow and silent. From the lungs, very few objective symptoms are observed. The attacks proceed 'ohne Sibilus, ohne Stretor, ohne Auswurf' (without whistling, without rales, without sputum) (Traube). Only in some cases do signs of acute left heart failure—acute dilation of the heart, fall in blood pressure, and finally pulmonary edema—accompany but by no means precede the attack of suffocation. The latter is characterized by a peculiar rale-like breathing and the appearance of cough with the expectoration of frothy serous sputum. The pneumogram shows the appearance of a flat curve with lengthening, flattening, and slight height of the inspiratory and expiratory parts of the wave. Respiratory pauses are barely noticeable. To clarify the mechanism of the occurrence of paroxysmal dyspnea, attempts have been repeatedly made to study the pre-paroxysmal stages. Prodromal symptoms are considered to be an increase in blood pressure (Basch, Huchard, Pal), a decrease, and sometimes a sudden sharp drop in vital capacity as an expression of stagnation in the lesser circulation (Gollwitzer-Meier). Sometimes in severe cardiac patients, Cheyne-Stokes breathing (which is most often encountered in kidney diseases, sclerosis of cerebral vessels, etc.) is observed. It is characterized by the appearance of periodic pauses, after which breathing gradually intensifies, respiratory movements deepen and become more frequent. After breathing has reached maximum strength, it also gradually weakens and ends with a new pause. In some cases, during apnea, consciousness fades, bradycardia and pupil constriction are observed. With the resumption of breathing, consciousness is restored, and the other symptoms disappear, and the patient feels that he was 'awakened by dyspnea.' Cheyne-Stokes breathing often appears at night. Sometimes it is provoked by the injection of morphine. A transition to Cheyne-Stokes breathing is 'fluctuating breathing,' often encountered in decompensated cardiac patients (also in other diseases and intoxications). It is observed with consciousness preserved, in the absence of any other disorders, and consists of rhythmic fluctuations in the size of respiratory movements. Respiratory pauses are absent. Fluctuating breathing can directly transition to Cheyne-Stokes breathing and vice versa. Clinically, fluctuating breathing is not determinable; it has been studied only by pneumography. Apparently it occurs much more frequently than has been assumed so far. Some forms of dyspnea, encountered in cardiac patients, are also observed in kidney diseases. Such dyspnea has to be encountered in some patients with acute nephritis, often accompanied by signs of heart failure. In kidney patients, especially in nephrosclerosis, paroxysmal respiratory disorders are sometimes observed, in particular asthmatic attacks. In uremia, two forms of dyspnea are observed: the Cheyne-Stokes breathing described above and the so-called 'great breathing.' Great breathing is characterized by the presence of long respiratory arrests. The inspiratory and expiratory phases quickly follow one another and give on the pneumogram a high and steep rise and fall. In contrast to the great breathing of uremics, the great breathing of diabetics (Kussmaul's) is characterized by an extremely long flat inspiratory phase and a short expiratory phase. Respiratory pauses are prolonged. Clinically, Kussmaul's breathing is distinguished by very noisy inspiration and long arrests; it is observed during diabetic coma. However, respiratory disorders can appear in diabetics before the onset of coma as an early symptom of acidosis. In these cases, breathing is characterized by shallowness, absence of respiratory pauses, and increased frequency. In 'hepatic coma,' e.g., in patients with acute yellow atrophy of the liver, respiratory disorders in the form of expiratory dyspnea (Hofbauer) are observed, less often—fluctuating breathing. In Addison's disease, dyspnea close to Cheyne-Stokes breathing is observed. Bittorf observed in this disease a peculiar form characterized by a gradual decrease in respiratory rate from 24 to 4 per minute. The slowing was accompanied by deep respiratory movements and prolonged—over 10 sec.—respiratory arrests. Dyspnea in obesity is mainly cardiac, and partly related to the high position of the diaphragm.—Sahli found a peculiar dyspnea in anemia. It was characterized by increased and markedly deepened breathing. However, dyspnea in anemias by no means is a constant symptom. In most cases, severe anemias with a significant decrease in Hb and the number of red blood cells are accompanied only by 'work dyspnea,' while at rest breathing remains normal. Changes in breathing are well studied in diseases of the respiratory tract. In stenoses of the respiratory tract, slowing, intensification, and deepening of breathing are observed. In cases where inspiration is predominantly difficult (paralysis of the laryngeal muscles, foreign bodies, polyps, etc.), typical inspiratory dyspnea occurs. Inspiration gives a characteristic wave with initial and final slowing and central acceleration of it. In some cases, dyspnea is relatively inconspicuous and is revealed only when breathing is registered on a curve. Sometimes dyspnea occurs only at night during sleep. In lesions of the small bronchi, mixed dyspnea with increased shallow breathing is observed.—Capillary bronchitis is characterized by marked expiratory dyspnea. Vital capacity of the lungs is reduced by 10-20% in this condition (Wintrich).—In emphysema, mainly lengthening of expiration is observed. Inspiration occurs quickly or normally, expiration is slowed and lengthened; on the pneumogram, a distinct increase in the expiratory phase of the wave is noted due to the action of auxiliary muscles. The frequency and depth of individual respiratory movements are uneven. Residual air is increased, reserve air is decreased, vital capacity is sharply reduced (to 60% according to Wintrich). The diaphragm stands low, the chest has an inspiratory position, ventilation is very difficult. Nevertheless, hyperventilation is usually observed.—In acute lesions of the lungs, dyspnea varies depending on complicating factors (intoxication, condition of the heart). In the absence of special complications, increased breathing and lengthening of both inspiration and expiration are observed.—In exudative pleurisy, the degree of dyspnea depends on the size of the effusion; it is interesting that even with large effusions, dyspnea is observed at rest only during the first 2-3 days.—In pneumothorax, dyspnea fluctuates within very wide limits depending on individual characteristics of the patient. In spontaneous pneumothorax, dyspnea is initially extremely severe. In artificial pneumothorax, breathing is increased and deepened due to the healthy side. The pneumogram reveals slowing and difficulty of expiration. Inspiration is initially unchanged; only with prolonged existence of pneumothorax it becomes more lengthened. Vital capacity is reduced, as are the reserve and additional air. Residual air is reduced by half, Mittellage is increased. In open pneumothorax, residual air is normal, Mittellage is reduced. Pulmonary tuberculosis often proceeds without respiratory disorders. In individual cases, various changes are observed: increased breathing, expiratory and inspiratory dyspnea. In far-advanced cases, lengthening of expiration is usually observed. Vital capacity is reduced to varying degrees. Residual air is relatively high. Nervous respiratory disorders have great diagnostic significance, which can be divided into two groups.

The first group includes severe types of disorders in organic lesions of the central nervous system—Biot's respiration (see). The second group includes functional tachypnea and bradypnea, often observed in hysterical patients, reaching a frequency of 120 respirations per minute. Functional respiratory disorders often superimpose on organic heart lesions (Curschmann). Biot's respiration occurs in meningitis and other organic lesions of the central nervous system. Respiratory movements, unlike Cheyne-Stokes respiration, maintain normal depth, in some cases the inspiration is deepened.—The listed respiratory disorders by no means exhaust all forms of D., but only represent its main types. D. occurs besides the indicated diseases and in a number of others, for example, in diseases of the chest and spine itself, in lesions of muscles, the diaphragm, nerve trunks, in particular the phrenic nerves, diseases of the abdominal cavity, enteroptosis, in cancer intoxication, exogenous intoxications (nicotine), etc. Therapy of D. Since D. is a symptom of disease, its treatment comes down to treating the underlying disease. Symptomatic treatment of D. comes down to prescribing oxygen in some cases (which in particular in Cheyne-Stokes respiration, as indicated above, has a good effect) and morphine. The latter has a beneficial effect in some cases of cardiac asthma. In Cheyne-Stokes respiration, morphine is contraindicated, as it often provokes it (in some cases Cheyne-Stokes respiration developed for the first time after morphine injection). Great importance in the prevention and treatment of asthma is attached to a salt-free diet (Volkhard and others). Prescription of Tincturae Lobeliae, camphor, which stimulate the respiratory center, also helps to eliminate D. In the same sense, bloodletting acts. Worthy of special attention is the method proposed by Wasserman—pressure on the carotid artery, more precisely—on the sympathetic plexus located in the sinus caroticus; with the help of this intervention, it is often possible to stop severe attacks of dyspnea and even incipient pulmonary edema. In some cases of 'congestive' D., pressure on the carotid artery also had a beneficial effect, from which Wasserman concludes that here too the reflex moment plays some pathogenetic role.