## Why "Increased wall stress and risk of aortic rupture due to loss of structural integrity of the medial layer" is right The false lumen (marked **B**) forms when blood enters and dissects longitudinally through the aortic media after an intimal tear. This splits the medial layer, destroying its structural integrity and elastin/collagen framework. The expanding false lumen increases transmural pressure and wall stress, dramatically elevating the risk of aortic rupture—the primary life-threatening consequence of dissection. This is why Stanford Type A dissections (involving the ascending aorta) are surgical emergencies with mortality of 1–2% per hour without intervention. The pathophysiology hinges on the false lumen's mechanical effect on the aortic wall, not secondary organ ischemia. (Robbins 10e Ch 11; Harrison 21e Ch 274) ## Why each distractor is wrong - **Reduced coronary artery perfusion pressure leading to acute myocardial infarction**: While Type A dissection can extend into coronary ostia and cause MI, this is not the primary pathophysiologic consequence of the false lumen itself. The false lumen's main threat is rupture from wall stress, not coronary involvement (which occurs in a minority of cases). - **Compression of the esophagus causing dysphagia and aspiration risk**: The false lumen expands within the aortic media and adventitia, not toward the esophagus. Esophageal compression is not a recognized complication of aortic dissection. - **Obstruction of the left main bronchus causing left-sided atelectasis**: The false lumen dissects within the aortic wall itself, not into the mediastinal structures. Bronchial obstruction is not a direct consequence of the false lumen. **High-Yield:** The false lumen's expansion destroys medial integrity → increased wall stress → rupture risk. This is why Type A dissection is a surgical emergency (1–2% mortality per hour). [cite: Robbins 10e Ch 11; Harrison 21e Ch 274]
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