Pathophysiology

The lungs have a dual vascular supply from both the pulmonary and bronchial circulations. The bronchial arteries originate from the aorta or intercostal arteries and provide nutrition to the pulmonary structures. They give rise to small penetrating arteries which form submucosal plexi supplying the bronchial mucosa. There are anastomoses between the bronchial and pulmonary circulations at the level of medium-sized arteries as well as of microvascular and precapillary vessels. Massive hemoptysis generally involves bleeding from the bronchial arteries or, less frequently, from a pulmonary artery when the pulmonary circulation is pathologically exposed to the high-pressure bronchial circulation through enlarged bronchopulmonary anastomoses ( Sie.rDbach.and Varon 1995).

The response of the bronchial circulation to both acute and chronic disease involves vascular proliferation. Such 'neovascular' development can be seen as early as 4 to 5 days after an acute insult. This ability to proliferate distinguishes the bronchial from the pulmonary circulation. The bronchial circulation, which normally receives less than 1 per cent of the cardic output, can proliferate to the extent that as much as a third of the systemic blood flow passes through it ( Deffebach.efa/ 1987).

Mechanisms by which massive hemorrhage is produced include the following ( SI®Enb§ch.§nd y.a.ro.D 1995).

1. Various vascular alterations, such as aneurysm formation (e.g. 'Rasmussen's aneurysm' in tuberculosis patients), vasculitic reactions (Goodpasture's syndrome, systemic lupus erythematosus, idiopathic hemosiderosis), and pulmonary embolism.

2. Chronic parenchymal inflammation: erosion of bronchial and vascular walls, enlargement and proliferation of bronchial vessels, formation of anastomoses between bronchial and pulmonary circulation, and formation of bronchiectases or lung abscesses.

3. Broncholithiasis: erosion of a calcified lymph node into the tracheobronchial tree with disruption of peribronchial and submucosal bronchial vessels.

4. Vascular invasion by tumor.

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