Pulmonary diseases of vascular origin — pulmonary embolism, hemorrhage, and infarction

Pulmonary Embolism (PE)

Source

• Blood clots in large pulmonary arteries are almost always embolic in origin
• >95% originate from deep veins (femoral, iliac, popliteal)
• Minority from periprostatic/parametric vein plexus

Risk factors for deep venous thrombosis

• Prolonged bedrest
• Surgery (especially knee/hip orthopedic)
• Severe trauma (burns, fractures)
• Congestive heart failure
• Disseminated cancer
• Primary hypercoagulability (e.g. Factor V Leiden)

Consequences

Two key consequences of embolic pulmonary arterial occlusion:

1. ↑ Pulmonary artery pressure (blockage + vasospasm)
2. Ischemia of downstream lung parenchyma

Occlusion of major vessel:

• ↑ Pulmonary arterial pressure
• ↓ Cardiac output
• Right-sided heart failure
• Hypoxemia (atelectasis perfusion, ↓ CO, possible right-to-left shunt through patent foramen ovale)

Smaller vessel occlusion: less catastrophic; may be clinically silent

Hemorrhagic pulmonary infarct occurs only if bronchial circulation is compromised (e.g. CHF) or bronchial circulation is impaired

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Morphology

Large emboli (saddle embolus at bifurcation):

• Sudden death from hypoxia or acute cor pulmonale; no time for morphological changes

Medium/small emboli:

• Obstruct small/medium pulmonary arteries → lung parenchyma maintained; but ischemic endothelial damage → pulmonary hemorrhage

Infarction (if compromised cardiovascular status):

• Usually affects lower lobes
• Shape: wedge-shaped, apex pointing towards hilus
• Evolution:
  • Early: red-blue hemorrhagic areas
  • After 48 hrs: lysis begins → infarct pales → red-brown (hemosiderin)
  • Final stage: fibrous replacement from margins → whitish scar
• Histology: coagulative necrosis with hemorrhage

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Clinical Features

• 60–80% of pulmonary emboli are clinically silent (small; rapid fibrinolysis)
• Large emboli (60%): sudden death, acute right-sided heart failure (acute cor pulmonale), cardiovascular collapse (shock)
• Recurrent multiple emboli (<3%): pulmonary hypertension, chronic cor pulmonale, pulmonary vascular sclerosis, progressive dyspnea

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Treatment / Prophylaxis

• Anticoagulation for high-risk patients
• Thrombolytic therapy for massive PE
• Elastic stockings
• Pneumatic calf compression
• Isometric leg exercises
• Early ambulation (post-op, post-partum)

💡 High-yield: PE → >95% from DVT; saddle embolus → sudden death/acute cor pulmonale. Infarct = wedge-shaped, lower lobe; red-blue → red-brown → white scar. 60–80% clinically silent. Recurrent emboli → chronic cor pulmonale. Risk factors: Virchow’s triad (stasis, hypercoag, endothelial injury).