Bronchial Asthma- Pathology And Pathophysiology



In patient who died of acute asthma the most striking feature of lung at

mesopry is their gross over distension and failure to collapse when the pleural

cavities are opened. When the lung is cut, numerous geletinous plugs of

exudates are present in most of bronchical branches down to the terminal

bronchioles. Histological examination shows the hypertrophy of the bronchial

smooth muscle, hyperplasia of mucosal, sub mucosal vessels, mucosal oedema

denudation of the surface epithelium, pronounced thickening of the basement

membrane and eosinophilic infiltration in the bronchial wall. In smaller

proportions of asthmatics that die, the eosinophilic infilteration is replaced by

neutrophils and mucous plugging is conspicuously absent.


The patho physiological hallmark of asthma is a reduction is airway

diameter brought about by contraction of smooth muscles, vascular changes,

congestion, oedema of the bronchial wall and thick tenacious secretions. The

net result is an increase in airway resistance, a decrease in forced expiratory

volumes and flow rates, hyperinflation of the lungs and thorax, increased work

of breathing alternation in respiratory muscle function, changes in elastic

recoil, abnormal distribution in both ventilation and pulmonary blood flow with

mismatched ratios and alternations to the arterial gas concentrations. Thus,

although asthma is considered to be primarily a disease of airways, virtually all

aspects of pulmonary functions are compromised during acute attacks. In

addition in very symptomatic patients the ECG frequently shows right

ventricular hypertrophy and pulmonary hypertension. When a patient is present

for therapy, his or her forced vital capacity tends to be < 50% of normal. The

forced expiratory volume averages 30% of less of predicted, while maximum

and minimum mid-expiratory flow rate are reduced to 20% or less of the

expected value.

In acutely ill patient, RV frequently approaches 400% of the normal,

while functional residual capacity doubles. The patient tends to report that the

attack has ended clinically, when RV has fallen to 200% of its predicted value

and FEV has reached 50% of the predicted level.

Hypoxia is a universal finding during acute exacerbations, but frank

ventilatory failure is relatively uncommon, most asthmatics have hypoapnea

and a respiratory alkalosis. In acutely ill patients the finding of a normal

arterial CO2 tends to be associated with quite severe levels of obstruction.

Cyanosis is a very late sign. Likewise, signs attributes to CO2 retention,

such as sweating, tachycardia, wide pulse pressure or to acidosis, such as

hyperapnea or H+ excess in individual patient, because they are too frequently

seen in anxious patients with more moderate disease.