This condition, which means difficulty of breathing, is popularly called shortness of breath. In its physiological aspects it means an exaggeration of the respiratory movements. The affected person has the feeling that he does not get sufficient air into his lungs, and there is an actual deficiency of oxygen or excess of carbonic acid in the blood. There arises, therefore, a stimulation of the respiratory centres by the abnormal condition of the blood, and dyspnoea is brought about when the blood passing to the centres concerned is defective in oxygen or contains an excess of carbonic acid. In dyspnoea the muscles of respiration are called into excessive activity. The muscles which raise the chest and the diaphragm act with exceptional vigour so as to increase the inspiratory effect. There is frequently also a call made for muscular effort to increase the force of the expiratory movements. It is in some cases possible in this way to distinguish the dyspnoea as chiefly inspiratory or chiefly expiratory.
From the remarks made above, it will appear that dyspnoea may have its origin either in an insufficiency of air reaching the air-vesicles or in an insufficiency of blood passing through the pulmonary capillaries. In either case the blood is insufficiently oxygenated, and the respiratory centres are stimulated to increased action.
Dyspnoea from insufficient access of air is illustrated most directly by obstruction to the air passages. This may be in the larger air tubes or in the smaller. The obstruction may be a mechanical one as by pressure of tumours, or aneurysms, or from accumulation of exudation in the tubes, or it may be due to spasm of the muscular apparatus. The latter occurs somewhat readily at the glottis, which may be closed by contraction of the laryngeal muscles, but it also occurs in the bronchi, where, as in asthma, there may be a general spasm of the finer tubes. But besides the obstruction of the air-tubes, we may have the air prevented from entering the lung alveoli by the latter getting filled up with solid or fluid exudation. This is of frequent occurrence in pneumonia, in oedema of the lungs, and in tuberculosis of the lungs, and it may lead to severe dyspnoea.
Dyspnoea from insufficiency of the pulmonary circulation has also various modes of origin. Thus the vessels may be seriously obstructed by pressure oh the lung from without, as in cases where the pleural sac is occupied by fluid or gas in large volume, although in these cases there is also obstruction to the entrance of air. Again there may be great occlusion of the pulmonary vessels by disease in the lungs themselves. Thus in tuberculosis of the lungs there is great loss of tissue, including the vessels, and in emphysema there is atrophy of tissue and occlusion of vessels. But there is a most important group of cases in which, from derangements in the circulation itself and without any disease of the lungs, an insufficient amount of blood traverses the lung. This mostly arises from disease of the heart, and the form of dyspnoea is hence called cardiac dyspnoea. It occurs more especially in disease of the mitral valve, which interferes with the return of blood from the lungs. In this case, the pulmonary capillaries are dilated and may bulge into the alveoli, but the circulation is slow, and there is not sufficient oxygen absorbed to satisfy the tissues. Mere weakness of the heart without organic disease often leads to dyspnoea, especially on exertion.
In most cases of dyspnoea the organism in some measure accommodates itself to the altered circumstances, and the dyspnoea is in part at least overcome. This is partly effected by the person limiting the amount of muscular exertion in which he engages, all muscular effort being accompanied by consumption of oxygen and formation of carbonic acid. Persons liable to dyspnoea learn to go quietly and keep themselves as much as possible at rest. There is also in the case of insufficiency of the pulmonary circulation a partial compensation effected by means of the exertions of the right ventricle. By more vigorous contractions and ultimately by hypertrophy of its muscular substance, the right ventricle succeeds in sending more blood through the diminished channels, or in partly overcoming the impediment at the mitral orifice. These various compensations take place more readily when the cause of the dyspnoea is of gradual occurrence. It is matter of common observation that an interference with the circulation which comes on slowly may produce no perceptible dyspnoea, whilst a similar amount of interference suddenly developed has an exceedingly marked effect.
While the urgency of dyspnoea is frequently overcome, yet the blood is permanently abnormal in respect that the oxygen is deficient and the carbonic acid in excess. The patient is mostly conscious that dyspnoea is every moment ready to obtrude itself. Any extra exertion, such as climbing a stair or a hill, involving a slight increase in the consumption of oxygen, at once causes a deficiency in the blood, and by stimulation of the medulla oblongata leads to dyspnoea.
There comes a time in most of the chronic diseases that lead to dyspnoea, when even the imperfect compensation described above is no longer possible. This takes place most readily where the dyspnoea is due to interference with the circulation of the blood. As the interference advances the limits of compensation of the right ventricle are reached. The circulation is impeded not only in the lungs, but by. dilatation of the right ventricle and ultimately by insufficiency of the tricuspid valve interference with the general systemic circulation occurs. There is a general venous hyperemia. With this there is an increase in the entire bulk of the blood, and a further difficulty in keeping up the percentage of oxygen in the increased volume of blood. In such cases the dyspnoea becomes more or less permanent, and there are added to it the phenomena of cyanosis and general oedema, which are indications of failure in the compensatory power of the heart. These phenomena of dyspnoea and failure of the compensatory power of the heart are not limited to cases of cardiac disease proper, but occur in such conditions as emphysema and bronchitis where the pulmonary circulation is obstructed. They are less likely to occur in cases where from general emaciation the volume of the blood and the bulk of the tissues requiring oxygen are diminished.
The dyspnoea may be increased or rendered more permanent by the occurrence of pyrexia. Febrile rise of temperature implying increased oxidation has a similar effect to increased muscular effort in stimulating the respiratory centres. In this connection Cohnheim has called attention to the fact that in pneumonia the occurrence of the crisis with a sudden fall of temperature is usually followed by an almost entire cessation of the dyspnoea, although the air is still shut off from the lung alveoli by the inflammatory exudation as much as it was before.