ASTHMA BRONCHIAL in Children Part 1

DEFINITIONS

The National Asthma Education and Prevention Program (NAEPP) defines asthma as a chronic inflammatory disease of the airways in which many cells and cellular elements play a part. In susceptible individuals, inflammation causes recurring episodes of wheezing, breathlessness (shortness of breath), chest tightness (chest felt tight), and coughing. Asthma is a condition in which airways, narrowed due to hyperactivity of certain stimuli, which cause inflammation, constriction is temporary.

Global Initiative for Asthma (GINA) defines asthma as a chronic inflammatory disorder with respiratory tract which many cells play a role, particularly mast cells, eosinophils and T lymphocytes.

National guidelines define asthma as an operational definition of asthma is the wheezing or coughing and to the characteristics and occurrence of an episodic or chronic, likely during the night (nocturnal), seasonality, the originator of factors including physical activity, and is reversible either spontaneously or with treatment , and a history of asthma or other atopic patients or their families, while other cause had been removed .

PATOPHYSIOLOGY

Asthma is a clinical condition characterized by a reversible bronchial constriction period separated by periods where ventilation is relatively close to normal. This situation is on people who suffer from asthma caused by various stimuli easier, it indicates a typical situation hyperactivity of bronchus. Changes in tissue without the complications of asthma and bronchial limited to consist of smooth muscle spasm, pulmonary edema, infiltration of inflammatory cells and mucus hypersecretion are strong. Secret mobilization is inhibited by the narrowing of the lumen of the respiratory system, exfoliation ciliated epithelial cells, which normally helps clear mucus.

In asthma, IgE antibodies attached to mast cells in interstitial lung contained a closely related bronchiolus and small bronchi. If someone inhaled allergens, the antibody immunoglobulin E increases, the allergen reacts with antibodies that have been attached to the mast cells and causes these cells to release various substances, including histamine, slow reacting substance of anaphylaxis (leukotrienes), eosinophilic chemotactic factor and bradykinin. The combined effect of all these factors will make local edema in the walls of small bronkhioulus also secretion of thick mucus in the lumen of bronchiolus and bronchiolus smooth muscle spasm, causing respiratory arrest to be greatly improve.

In the type of allergic asthma, the incidence of asthma induced by immunological mechanisms, which occur induction of IgE complex, slow response, T-opsonitated lymphosit response. While the types of non-allergic asthma, asthma induced by factors that do not trigger immunological character which intermittent or persistent that will cause inflammation and airway obstruction, among other causes of acute bronchoconstriction, swelling / inflammation of bronchial wall, mucus production in chronic, the channel wall remodeling breath.

Airway obstruction causes increased resistance to air flow and a decrease in expiratory flow rates. These changes resulted in decreased ability to remove the air and can lead to hyperinflation. Generated to help maintain airway patency overdistention, thereby improving expiratory flow, but also alter lung mechanics and increased work of breathing. Hyperinflation compensate for airflow obstruction that ultimately only produce alveolar hypoventilation. Changes in uneven air flow resistance, resulting uneven distribution of air, and changes in the circulation of the increase intraalveolar pressure due to hyperinflation all lead to ventilation-perfusion imbalance. Vasoconstriction caused by alveolar hypoxia also contributes to this discrepancy. Vasoconstriction is also regarded as an adaptive response to ventilation / perfusion mismatch.

In the early stages, when the ventilation-perfusion imbalance resulted in hypoxia, hypercarbia prevented by the diffusion of carbon dioxide in the alveolar capillary membrane. Thus, patients with asthma in the early stages of an acute episode have hypoxemia in the absence of carbon dioxide retention. Hyperventilation induced by hypoxia drives also cause a decrease in Pa 2 Increased alveolar ventilation in the early stages of an acute exacerbation prevent hypercarbia. With worsening obstruction and improving ventilation-perfusion mismatch, carbon dioxide retention occurs. In the early phase of acute episodes, respiratory alkalosis results from hyperventilation. Then, the increase in respiratory work, the increase in oxygen consumption, and increased cardiac output resulted in metabolic acidosis. Respiratory acidosis cause respiratory failure.

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