Overview
Mechanism and Clinical Pattern
Pulmonary infarction is ischemic necrosis of lung tissue caused by embolic obstruction of a peripheral pulmonary artery when bronchial collateral flow cannot compensate.
Pulmonary infarction is ischemic necrosis of lung tissue caused by embolic obstruction of a peripheral pulmonary artery when bronchial collateral flow cannot compensate. The lung has dual blood supply, so most pulmonary emboli do not produce true infarction; infarction develops in only a minority of cases, roughly 10–15%. Heart failure, chronic lung disease such as COPD, and other low-flow states reduce the protective bronchial circulation and increase susceptibility. The damaged area is often peripheral and pleural-based. Ischemia and hemorrhage irritate the pleura, producing sharp pain that worsens with inspiration or coughing. Small-volume hemoptysis, dyspnea, hypoxemia, tachycardia, and a low-grade fever may accompany the infarct. A sterile, sometimes hemorrhagic pleural effusion can occur. Fever or an opacity alone does not establish pneumonia. Pulmonary infarction and massive pulmonary embolism are not interchangeable diagnoses. A peripheral infarct may occur while blood pressure remains normal. Conversely, a large central embolus can cause right-ventricular failure and shock without infarcting lung tissue.