Explain the Pathophysiology of Asthma

Asthma is a chronic inflammation of the distal airways characterized by increasing bronchial reactivity to various stimuli and diffuse reversible bronchial obstruction. Clinically, asthma is characterized by paroxysmal expiratory dyspnea, wheezing and coughing with expectoration.

Paroxysmal Expiratory Dyspnea: Sudden and repeated difficulty while exhaling, feeling breathlessness or shortness of breath.

Bronchial obstruction occurs following the activation of three mechanisms:

  • Spasm of the Bronchial Musculature:  sudden constriction of the muscles in the walls of the bronchioles
  • Mucosal Edema: build-up of tissue fluid within the layer of tissue that lines the body’s interior
  • Hypersecretion of Viscous and Adherent Mucus: Excessive secretion of viscous fluids

Inflammation of the distal airways is the result of the interaction between inflammatory cells, inflammatory mediators and the airway cells.

The wheezing occurs due to smooth muscle contraction, mucus hypersecretion and the reduction of the airway caliber.

Dyspnea occurs due to higher muscle effort to overcome airway resistance, hyperinflation due to distal airway obstruction.

Bronchial asthma occurs at all ages, predominantly in the young: almost half of the cases diagnosed are under the age of 10. The male/female ratio is 2/1 in childhood and almost equal around the age of 30. Looking through long-term studies on asthmatic children until the age of 40, it was found that some of them became asymptomatic in adolescence, but the disease may return in adulthood, especially in those with persistent symptoms and severe asthma.

Adults with asthma, especially those with mature onset rarely become asymptomatic. To better understand asthma, we will explain the pathophysiology of asthma.

Trigger factors which determine asthma attacks

  • Physiological and pharmacological mediators of normal muscle contraction: histamine, metacoline, adenosine triphosphate (ATP)
  • Physico-chemical agents: exercise, especially if performed in cold conditions (cold and dry air). Atmospheric pollutants: sulfur dioxide, nitrogen dioxide, inhalation irritants (cigarette smoke, strong odorants, smoke and workplace gases). Respiratory infections such as influenza can determine asthma attacks as well.
  • Allergens: low molecular weight chemical substances, complex organic molecules such as pollen and house dust can determine the apparition of asthma attacks.
  • Emotional stress: which causes bronchospasm through vagal reflex and increased reactivity to other factors by non-inflammatory mechanism.

Theories regarding asthma attacks

I have stated above the factors that trigger asthma attacks, but to better understand them, two theories have been elaborated:

  • The Immunoallergic theory
  • The Beta-adrenergic Blockade theory

The Immunoallergic Theory

The Immunoallergic Theory states that asthma, after allergen penetration has a reaction between the allergen and the antibodies in the tissues. This results in an antibody whose substrate is immunoglobulin e (IgE), which is developed by the bronchi, tonsils, nasal mucosa.

This antibody causes the release of histamine, under the influence of platelet activation factor and acetylcholine. These substances produce bronchoconstriction and mucus secretion. The immunoallergic component of bronchial asthma can be demonstrated by the acetylcholine test which shows the modifications in the inspiratory and expiratory values when lung tests are performed.

The Beta-adrenergic Blockade Theory

The theory of beta-adrenergic blockade results from the fact that the normal physiological tonus of the bronchial musculature is maintained by the sympathetic and parasympathetic nervous system and mediated by cathecolamines and beta-adrenergic substances.

Which fits best?

Neither of these theories explain entirely the various aspects of asthma, and both must be kept in mind because they contain interfering elements.

Taking into the account these ethiopathogenic aspects, bronchial asthma was divided intro: extrinsic asthma (allergic) and inherent asthma (non-allergic and infectious).

So lets Explain the pathophysiology of asthma

The pathophysiological marker of asthma is the reduction of the airway diameter, generated by both contraction of the smooth muscles, vascular congestion, edema of the bronchial wall and hypersecretion.

Having said this, we must understand that although asthma is a disease of the airways, all the pulmonary functions are compromised during an asthma crisis. The increase in airway resistance is parallel to the severity of the clinical picture and is accompanied by the increase to the same extent of resistive ventilation. Maximum expiratory volume per second and average respiratory flow rates are reduced, reflecting slowing airflow through the stenosed pipes.

When the patient presents himself to the emergency room, all his parameters are below 40% of the predicted value. The lungs of a patient in an asthma crisis are hyperinflated, a change translated by the exploration of the pulmonary function of the residual volume, the residual capacity of functionality and the total lung capacity. In acute attacks, the residual volume can be as 400% higher than the normal value.

The increase in the ventilator labor occurs as a result of the increase in airway resistance and is an important factor of the installment of lung failure. Elastic recovery is normal in young asthmatics in crisis, when hyperinflation is not severe but presents reductions, sometimes important, associated with high increases of the residual volume in older patients.

Hypoxia is usually present in seizures, but respiratory insufficiency is only observed at 10-15% percent of the patients. Most asthmatics have hypocapnia with respiratory alkalosis. When in a severe crisis the concentration of carbon dioxide comes back to normal, consideration should be given to the possibility of installation of alveolar hypoventilation associated with a severe level of obstruction.

Patients with asthma suffer from electrocardiographic signs of pulmonary hypertension as well as right ventricular hypertrophy.

Hypocapnia: the reducing of the carbon dioxide values in the blood

 

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