Pulmonary Embolism for the USMLE Step 3 Exam
Etiology and Risk Factors
- Pulmonary Embolism (PE):
- PE results from a thrombus, usually originating from the deep veins of the legs or pelvis (deep vein thrombosis, DVT), which dislodges and obstructs a pulmonary artery.
- Virchow’s Triad:
- Risk factors for thrombus formation are explained by Virchow's triad:
- Endothelial injury: Vessel wall trauma (e.g., surgery, catheterization).
- Venous stasis: Prolonged immobility (e.g., bed rest, long-distance travel).
- Hypercoagulability: Pregnancy, malignancy, oral contraceptives, or inherited thrombophilias (e.g., factor V Leiden).
- Additional Risk Factors:
- Recent surgery (especially orthopedic procedures), malignancy (e.g., lung, pancreatic cancer), obesity, smoking, and pregnancy.
Pathophysiology
- Thrombus Formation and Migration:
- A thrombus forms in the deep veins, travels through the venous circulation into the right side of the heart, and is pumped into the pulmonary arteries where it obstructs blood flow.
- Hemodynamic Consequences:
- The embolus causes increased pulmonary vascular resistance, leading to right ventricular strain. In large PEs, this can result in right heart failure and cardiogenic shock.
- Ventilation-Perfusion (V/Q) Mismatch:
- The obstruction prevents blood from reaching areas of the lung, causing V/Q mismatch, which leads to hypoxemia.
Clinical Features
- Symptoms:
- Dyspnea: Sudden onset, often the most common presenting symptom.
- Pleuritic chest pain: Sharp pain, worsened by deep breathing.
- Cough: Can be dry or productive, with hemoptysis in some cases.
- Tachycardia and tachypnea: Often seen on physical exam.
- Leg swelling or pain: May indicate the presence of a DVT, the source of the embolism.
- Massive PE:
- Symptoms of syncope, hypotension, or signs of shock indicate a massive PE, usually due to right ventricular failure.
Diagnosis
Clinical Probability
- Wells Score:
- A scoring system used to assess the likelihood of PE, including factors like clinical signs of DVT, recent immobilization, previous DVT/PE, and malignancy.
Diagnostic Testing
- D-dimer:
- A sensitive but nonspecific marker for clot formation. A negative result can rule out PE in low-risk patients.
- CT Pulmonary Angiography (CTPA):
- The gold standard diagnostic test for PE, providing direct visualization of the thrombus in the pulmonary arteries.
- Ventilation-perfusion (V/Q) scan:
- Used when CTPA is contraindicated (e.g., in patients with contrast allergy or renal insufficiency). A V/Q mismatch suggests PE.
- Compression ultrasonography:
- Used to identify DVT in patients with leg symptoms or when PE imaging is unavailable.
Management
Anticoagulation
- Initial Therapy:
- Immediate anticoagulation is critical to prevent further clot formation. Options include:
- Low-molecular-weight heparin (LMWH): Preferred for most stable patients.
- Unfractionated heparin: Used in patients who may require thrombolysis or those with high bleeding risk.
- Direct oral anticoagulants (DOACs): Rivaroxaban and apixaban are commonly used for stable patients, without the need for bridging therapy.
Thrombolysis and Thrombectomy
- Thrombolysis:
- Administered in massive PE with hemodynamic instability. Alteplase (tPA) is the most commonly used agent for clot dissolution.
- Surgical or Catheter-Based Thrombectomy:
- Used for patients who fail thrombolysis or have contraindications to thrombolytic therapy.
Long-Term Anticoagulation
- Duration of Therapy:
- Anticoagulation is continued for 3-6 months in cases of provoked PE (e.g., surgery). For unprovoked PE, longer-term anticoagulation may be required based on the patient’s risk factors.
Complications
- Chronic Thromboembolic Pulmonary Hypertension (CTEPH):
- A long-term complication of unresolved PE, leading to persistent pulmonary hypertension and right ventricular dysfunction.
- Right Heart Failure:
- Acute or chronic right ventricular failure may develop in severe cases of PE due to increased pulmonary pressure.
Key Points
- Pulmonary embolism is caused by thrombi, often from the deep veins of the legs, migrating to the pulmonary arteries and blocking blood flow.
- Risk factors include immobility, recent surgery, malignancy, pregnancy, and inherited hypercoagulable states.
- Clinical presentation includes sudden dyspnea, pleuritic chest pain, tachycardia, and tachypnea, with massive PE presenting with hypotension or shock.
- Diagnosis is confirmed by CT pulmonary angiography (CTPA), and D-dimer is useful for ruling out PE in low-risk patients.
- Management involves prompt anticoagulation, with thrombolysis or thrombectomy for severe cases. Long-term anticoagulation depends on whether the PE was provoked or unprovoked.