Dyspnoea: Factors and Causes | Respiration | Humans | Biology

Dyspnoea means difficulty in breathing associated with a sense of distress. It is to be differentiated from hyperpnoea which simply means hyperventilation, as occurs in muscular exercise, and is usually not associated with sense of distress, unless, of course, the exercise very severe.

Factors Responsible for Dyspnoea:

The factors responsible for dyspnoea may be classified into three categories:

i. Alteration in Chemical Composition of Blood:

a. Hypoxia.

b. Hypercapnia or Hypercarbia.

c. Increased H-ion concentration.

ii. Excessive Work of the Respiratory Muscles to Inflate and Deflate the Lungs so as to Provide Adequate Ventilation:

a. Diminished lung compliance, e.g., in congestion, fibrosis, etc.

b. Abnormalities in chest wall and diaphragm.

c. To provide increased demand for O₂ in diseases associated with high metabolic rate.

iii. Psychogenic Dyspnoea:

Due to impulses from higher centres.

Causes of Dyspnoea:

I. Dyspnoea due to Alteration in Chemical Composition of Blood:

i. O₂ lack from causes enlisted under ‘arterial hypoxia.

ii. Hypokinetic anoxia interferes with transport of respiratory gases due to sluggish circulation as occurs in cardiac failure.

iii. Anaemic anoxia, if severe, will lead to O₂ lack in the body.

iv. Factors affecting diffusion of gases across the alveolo-capillary membrane (alveolo-capillary block syndrome) Stimulation of respiration leading to dyspnoea by the factors mentioned above occurs reflexly via the Sino- aortic mechanism. It is believed that the Hering-Breuer reflex also becomes overactive in these conditions, which also augments respiratory rate and supplements the discomfort of dyspnoea.

v. The CO₂ excess and respiratory acidosis occurs in alveolar hypoventilation associated with decrease in ventilation/perfusion ratio. The causes listed above are usually not associated with CO₂ tention because CO₂ diffuses at least 20 times more rapidly than O₂.

vi. Metabolic acidosis will also produce dyspnoea by stimulating respiratory centre both directly as well as reflexly in the same way as CO₂ excess.

II. Excessive Work of the Respiratory Muscles:

i. Obstruction of the larynx or bronchi as in diphtheria or asthma will produce dyspnoea due to excessive work of the respiratory muscles to overcome the resistance.

ii. O₂ lack and CO₂ excess due to hypoventilation will also add to the discomfort of dyspnoea by reflex and direct effect on respiratory centre.

iii. Reduced distensibility of the lungs as occurs in oedema, congestion, fibrosis, and inflammation of the lungs. Due to diminished distensibility of the lungs i.e., diminished compliance, the respiratory muscles are to work hard to maintain adequate ventilation through the rigid alveoli. The Hering-Breuer reflex is said to be overactive in these cases and so accelerate the rate of respiration.

II. Applied Physiology:

i. Dyspnoea on exertion or even at rest in advanced cases is the commonest symptom of heart disease, e.g., Mitral stenosis. It has been proved to be not due to arterial hypoxia or hypercapnia. Engorgement of pulmonary capillaries leading to diminised-distensibility of lungs is the prime cause of cardiac dyspnoea.

When pulmonary oedema supervenes, anoxia will complicate the picture. It has been mentioned elsewhere that distension of pulmonary capillaries causes rapid shallow breathing.

ii. Conditions which cause limitation of movement of the diaphragm or chest wall will lead to distressed breathing resulting from undue effort of the muscles of respiration. In emphysema, for instance, the elasticity of the lungs is lost and the chest is held up in inspiratory position during rest.

The diaphragm is fixed in an elevated position. Inspiration can, therefore, be effected only by unusual effort of the inspiratory muscles. Expiration is also effected by active contraction of the muscles of expiration.

iii. In diseases associated with high metabolic rate, e.g., thyrotoxicosis there is an increased demand for O₂ in the tissues and also an increased demand for elimination of CO₂. This demand is increased during muscular effort. In such patients the respiratory muscles are to work more to meet the increased demand for oxygen and such these patients are liable to be dyspnoea on slight exertion.

In severe diabetic acidosis, Kussmaul breathing, or air hunger may be observed in comatose subject.

III. Psychogenic or Emotional Dyspnoea:

Many persons of neurotic disposition are apprehensive that they may not be able to get sufficient quantity of air if they enter an overcrowded room. These persons develop ‘air hunger’ on entering a crowded room, e.g., cinema hall and sometimes hyperventilates to such an extent that they develop alkalosis and tetany in a crowded place or rather ‘stuffy’ atmosphere.