Pulmonary Infarction

Pulmonary infarction is ischaemic necrosis of lung parenchyma after a distal pulmonary artery becomes occluded, usually by an embolus. The infarct is not simply a “dead” area created by loss of pulmonary blood flow. The lung normally receives blood from two arterial systems: the low-pressure pulmonary circulation and the higher-pressure bronchial circulation. When a small pulmonary artery is blocked, bronchial arteries can increase perfusion to the affected region. Their higher capillary pressure can force erythrocytes across injured vessels and into the alveoli. The result is haemorrhagic consolidation, which may progress to tissue necrosis. This mechanism explains the characteristic combination of pleuritic pain and haemoptysis. The dual supply makes infarction an uncommon complication rather than the expected result of every pulmonary embolism. It occurs in roughly 10% to 30% of acute pulmonary emboli. A more peripheral embolus is more likely to lodge in a small artery and produce infarction; autopsy data show greater risk when the occluded vessel is less than 3 mm in diameter. The pattern is not the one traditionally taught. Older explanations emphasized heart failure, shock and chronic...