Mechanisms of dyspnea development
The symptom is always driven by pathological or excessive stimulation of the respiratory center. This occurs via the afferent pathway through the irritation of receptors in the airways, lung parenchyma, and muscles.
In pulmonary diseases, biomechanical impairment comes to the foreground. Respiratory muscles have to perform greater work either due to tissue stiffness (as in pulmonary fibrosis) or a pathologically increased chest volume (in emphysema or an asthma attack).
Hemodynamic mechanism in cardiac pathology: In heart failure (HF), reduced left ventricular pumping function or mitral stenosis leads to increased pressure in the left atrium and pulmonary capillaries. Three mechanisms are subsequently triggered:
- Reflex: due to high pressure, fluid transudates into the interstitium, irritating juxtacapillary J-receptors. This sharply stimulates the respiratory center (the basis of a cardiac asthma attack).
- Volumetric (restrictive): blood congestion in the lungs decreases their tidal volume and distensibility (compliance).
- Metabolic: in late stages of HF, due to low cardiac output, respiratory muscles suffer from hypoxia and fatigue rapidly.
Clinical types of dyspnea
Depending on which respiratory phase is impaired, three types of dyspnea are distinguished:
- Inspiratory: the patient has difficulty inhaling. The obstruction is localized in the upper respiratory tract (trachea, large bronchi). Causes: vocal cord edema, tumor, foreign body aspiration.
- Expiratory: expiration is difficult. Observed in lesions of small and medium bronchi (bronchial asthma, emphysema).
- Mixed: both phases are impaired. The most common variant, typical for advanced stages of chronic pulmonary and heart failure.
Two mechanisms of expiratory dyspnea: In bronchial asthma, expiration is difficult due to smooth muscle spasm of the small bronchi. In emphysema, the expiratory collapse phenomenon operates. Lung tissue loses elasticity, and the bronchial framework weakens. During inspiration, the parenchyma exerts weak pressure on the bronchi, while during expiration, pressure increases, causing insufficiently rigid bronchi to collapse and blocking the exit of air from the alveoli.
Specific "cardiac" variants
When taking a cardiac patient's history, it is important to clarify the relationship between symptoms and body position and time of day:
- Orthopnea (Orthopnea): severe dyspnea in the horizontal position, forcing the patient to sit up or use multiple pillows for sleep. In the upright position, venous return to the right heart drops, congestion in the pulmonary capillaries decreases, and breathing becomes easier. Interesting fact: orthopnea may paradoxically decrease if the patient develops right ventricular failure (the right ventricle pumps less blood into the lungs).
- Paroxysmal nocturnal dyspnea (cardiac asthma): sudden awakening from suffocation due to interstitial pulmonary edema. Unlike pulmonary dyspnea, where relief often comes after assuming an upright position and coughing up sputum (postural drainage), here it is precisely the reduction of venous return and fresh air that helps.
Types of pathological breathing
These conditions usually indicate central nervous system lesions, severe intoxications, or metabolic shifts rather than primary lung disease:
- Kussmaul breathing ("air hunger"): rare, but very deep, noisy inspirations and forced expirations. Encountered in deep comas (ketoacidotic with acetone breath, lactic acidosis, uremic), methanol poisoning. A prognostically extremely unfavorable sign.
- Cheyne-Stokes breathing: a period of apnea (respiratory arrest up to 1 minute) is replaced by shallow breaths that increase in depth toward the 5th–7th breath and then subside again into apnea. Occurs in comas, marked pulmonary edema, severe hypothermia.
- Grocott breathing: wave-like breathing resembling Cheyne-Stokes, but without periods of apnea. Characteristic of early stages of comatose states.
- Biot breathing: alternation of deep rhythmic breaths with prolonged periods of apnea (20–30 seconds). Indicates severe brainstem damage (shock, severe hypoxia, intoxications, circulatory disorders).
Briefly: answers to topical questions
How to differentiate a cardiac asthma attack from bronchial asthma based on objective symptoms?
For differential diagnosis of the attacks, one can compare the forced posture, the mechanism of respiratory relief, and additional signs.
| Sign | Bronchial asthma | Cardiac asthma (left ventricular failure) |
|---|---|---|
| Forced posture | Sitting, leaning hands on the edge of the bed or chair | Orthopnea: sitting or semi-sitting with a high headrest, often with legs hanging down |
| Mechanism of postural relief | Fixation of the shoulder girdle allows the use of accessory respiratory muscles to facilitate expiration | The upright position reduces venous return to the heart and pulmonary congestion, making breathing easier |
| Character of dyspnea | Expiratory: difficulty exhaling during bronchospasm | Attack of suffocation/paroxysmal nocturnal dyspnea; associated with interstitial pulmonary edema |
| Additional data | Favors asthma: recurrent obstruction, eosinophilia, burdened family allergic history, rapid positive response to bronchodilator inhalation | Rales may resemble asthmatic ones but have a cardiac etiology; in congestive heart failure, a dry unproductive "cardiac cough" is possible |
What scales are used to assess the severity of dyspnea in a patient?
To assess the severity of dyspnea, sources explicitly indicate the mMRC scale (The Modified Medical Research Council Dyspnea Scale).
- mMRC is the modified Medical Research Council questionnaire for assessing dyspnea severity; the patient chooses one of five statements from 0 to 4.
- mMRC grades reflect the relationship of dyspnea with exertion: from dyspnea only during heavy physical exertion to dyspnea when dressing/undressing or inability to leave the house due to severe dyspnea.
Additionally, in chronic pulmonary pathology, the degree of respiratory failure is assessed by the severity of dyspnea, cyanosis, tachycardia, and reduced exercise tolerance: Grade I — dyspnea only on exertion, Grade II — on mild exertion, Grade III — at rest.
How to remember the phase of dyspnea and the level of lesion: I-I (Inspiratory — Foreign body / upper airways), E-E (Expiratory — Emphysema / lower airways).
Class and exam questions
How to differentiate pathological dyspnea from physiological fatigue (due to sports)?
The key criterion of pathology is decreased exercise tolerance. Dyspnea begins to occur during exertion (or daily activities) that the patient previously tolerated easily.
Why does a cough appear in congestive heart failure?
Dry cough is caused by pulmonary hypertension and interstitial edema. When transitioning to alveolar edema, the cough becomes wet with pink frothy sputum.
What is the clinical significance of hemoptysis in mitral stenosis?
It occurs due to marked pulmonary hypertension and is a direct indication for surgical treatment of the valvular defect.
What else to study on this topic
- History-taking algorithm: duration, paroxysmal nature, provoking and relieving factors
- Sleep apnea syndrome and Pickwickian syndrome in obese patients
- Relationship of dyspnea with sputum production and the effect of postural drainage
- Mechanisms of formation of pink frothy sputum in alveolar edema
- Assessment of the degree of orthopnea by the number of pillows used by the patient
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