Clinical meaning
Pulmonary infarction occurs when a pulmonary embolism completely obstructs an end-artery, cutting off both pulmonary arterial and bronchial collateral blood supply to a segment of lung tissue. The resulting ischemia causes coagulative necrosis of alveolar tissue, hemorrhagic infarction, and pleural inflammation. Only 10-15% of pulmonary emboli result in true infarction because the lung has dual blood supply (pulmonary and bronchial arteries). Infarction is more likely in patients with compromised bronchial circulation due to heart failure, COPD, or large embolic burden.
Exam relevance
Risk factors: - Pulmonary embolism (prerequisite) - Congestive heart failure (impairs bronchial collateral flow) - COPD or chronic lung disease - Large saddle or lobar emboli - Prolonged immobility - Deep vein thrombosis - Hypercoagulable states
Diagnostics: - CT pulmonary angiography showing filling defect with peripheral wedge-shaped opacity - D-dimer elevation (sensitive but not specific) - Chest X-ray showing Hampton hump (wedge-shaped peripheral opacity) - Pleural fluid analysis (often hemorrhagic exudate) - ECG may show right heart strain pattern (S1Q3T3, right axis deviation) - Troponin and BNP to assess right ventricular strain