Primary Causes & Pathophysiology
Most bleeding comes from bronchial arteries (high-pressure airway feeders). Infection, bronchiectasis (damaged widened airways) and tumours erode lining and fragile new vessels. Cough shear (tearing force) ruptures them. Lung artery bleeding follows infarction (tissue death) or oedema (fluid overload). Blood in air sacs blocks oxygen transfer.
Chronic inflammation breeds fragile bronchial vessels. Repeated infection ulcerates lining and grows weak new vessels. Cough shear ruptures them and floods the airway.
Smoking injury congests lining and raises mucus. Acute infection adds cough and friability (easy tearing). Small surface vessels break and streak the sputum.
Bacterial invasion inflames air sacs and kills tissue. Inflamed capillaries leak and erode into airspaces. Sputum turns rusty or frankly bloody.
Granulomas (immune lumps) and cavities erode bronchial arteries. A Rasmussen aneurysm (inflamed bulge) can burst suddenly. Caseation (cheese-like breakdown) exposes vessels to air.
Tumour invades bronchi and vessels directly. New cancer vessels are fragile and bleed easily. Central necrosis (inner death) plus cough triggers repeat bleeds.
Clot blockage infarcts downstream lung (tissue death). Dead air sacs bleed into airspaces. Pleuritic pain with streaked sputum is typical.
High left atrial pressure backs into lung veins. Engorged capillaries leak red cells into air sacs. Chronic oedema leaves pink frothy sputum with iron pigment.
Autoantibodies injure air-sac capillaries and cause capillaritis (tiny vessel inflammation). Diffuse bleeding fills alveoli (tiny sacs). Kidney filter inflammation often signals systemic disease.