Pulmonary Embolism
3
Virchow's Triad
Stasis injury hypercoagulability
1
Gold Standard
CT angiography for diagnosis
2
Categories
Massive (unstable) vs submassive (RV strain stable)
Risk Factors and Classification
Virchow's triad (venous stasis, endothelial injury, hypercoagulability) describes the three conditions that predispose to clot formation. Risk factors include immobility, recent surgery, malignancy, oral contraceptives, DVT history, and obesity.
Massive PE with hemodynamic instability = systemic thrombolysis, not just anticoagulation. The distinction between massive and submassive PE drives treatment decisions.
Massive PE
Hemodynamically unstable
SBP <90, shock, cardiac arrest. Needs systemic thrombolytics or embolectomy. Anticoagulation alone is not enough.
Submassive PE
Hemodynamically stable with RV strain
RV dilation on echo, elevated troponin/BNP. Anticoagulation plus close monitoring. Escalate if deterioration occurs.
Diagnosis
CTA is the gold standard. The Wells score stratifies pre-test probability. D-dimer is useful for ruling OUT PE in low-probability patients but is nonspecific (elevated in many conditions). ABGs may show respiratory alkalosis with hypoxemia. ECG findings include sinus tachycardia, S1Q3T3 (classic but uncommon), and right heart strain pattern.
Key Values to Memorize
CTA = gold standard
Massive = SBP <90
Wells score for probability
D-dimer rules OUT only
Alteplase for massive PE
S1Q3T3 on ECG (classic)
PE classification drives treatment, and the CCRN tests that distinction
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Massive PE with hemodynamic instability gets systemic thrombolytics
Massive PE is defined by hemodynamic instability (sustained hypotension SBP <90, pressor requirement, or cardiac arrest). These patients need systemic thrombolysis (alteplase) or surgical/catheter-directed embolectomy. Standard anticoagulation alone is insufficient. The clot burden is too large.
Submassive PE has RV strain but stable hemodynamics
Submassive PE shows right ventricular dysfunction on echo or CT (RV dilation, septal bowing) and/or elevated biomarkers (troponin, BNP) but the patient maintains adequate blood pressure. Treatment is anticoagulation with close monitoring. Thrombolytics may be considered if the patient deteriorates.
CT angiography is the gold standard for diagnosis
CTA provides direct visualization of the clot within the pulmonary arterial system. It also shows RV enlargement, which helps risk-stratify. V/Q scan is an alternative when CTA is contraindicated (contrast allergy, renal insufficiency). D-dimer is a screening tool only, useful for ruling OUT PE in low-probability patients.
Wells score determines pre-test probability
The Wells score for PE assigns points for clinical features (signs of DVT, heart rate >100, immobilization, history of VTE, hemoptysis, cancer, PE as likely or more likely than alternative diagnosis). It stratifies patients into low, moderate, and high probability categories, guiding the diagnostic workup.
Massive = Lytics
Massive PE = hemodynamic instability = systemic thrombolytics. Do not waste time with just anticoagulation. The clot is too big.
Virchow's Prevention
Stasis + endothelial injury + hypercoagulability = clot risk. SCDs, early ambulation, and chemical prophylaxis target all three.
The pulmonary arteries are the highway system that carries blood from the right heart to the lungs for oxygen. It is a high-flow, low-resistance highway. Blood moves through quickly and efficiently.
A PE is a blood clot (usually from the legs) that breaks loose and lodges in the pulmonary highway. A small clot blocks a side road (segmental PE). A massive clot blocks the main interstate (saddle PE). The bigger the blockage, the worse the traffic backup.
When the highway is blocked, traffic (blood) backs up behind the clot. The right ventricle has to pump harder against the obstruction. If the blockage is massive, the RV cannot generate enough pressure to push blood through. It dilates and fails. That is why massive PE causes hemodynamic collapse.
Anticoagulation prevents new clots from forming and lets the body dissolve existing ones slowly. Thrombolytics (alteplase) actively dissolve the clot like a chemical road clearer. For massive blockages, you need the chemical clearer because waiting for natural dissolution means the traffic stops completely.
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