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Pulmonary Embolism

Anna Berry


A thrombus originating in a deep vein (LE > UE) embolizing to the pulmonary arterial circulation.

  • Risk Factors = Virchow’s Triad
    • Stasis: immobilization, hospitalization, spinal cord injury, or long travel
    • Hypercoagulable state: cancer, prothrombotic genetic conditions such as Factor V Leiden, OCPs, antiphospholipid syndrome, nephrotic syndrome, pregnancy, infection, etc.
    • Endothelial Injury: surgery, trauma

Most originate from a DVT in the iliac, femoral, and popliteal veins


  • Dyspnea and tachypnea
  • Respiratory alkalosis on blood gas from hyperventilation
  • Hypoxemia
  • Sinus Tachycardia or atrial arrhythmias
  • Hemoptysis
  • Lower extremity pain, swelling, and redness – occurs in 50% of pts with DVT
  • RV Failure (large PE) – elevated JVP, hypotension, syncope, R parasternal heave, accentuated P2, hepatomegaly


  • If hemodynamically unstable and PE suspected, provide hemodynamic support (ie. O2, pressors, etc.) and perform emergent bedside TTE
  • If no RV strain evident on TTE, low likelihood of hemodynamically significant PE. Consider other causes of shock.

  • Hemodynamically stable

    • EKG
      • Most commonly sinus tachycardia
      • Less commonly and indicative of large PE: RAD, RVH, RBBB, RA enlargement, S1Q3T3 (deep S in lead I, deep Q and inverted T in lead III), TWI in V1-V3
    • CXR: Typically normal. May see linear atelectasis, pleural effusion, PA cutoff sign
    • Labs: ABG, troponin, BNP
    • May consider lower extremity dopplers
    • Imaging vs d-dimer based on pre-test probability:
      • Low pre-test probability (use Wells Criteria) d-dimer
      • For moderate to high pre-test probability CTA Chest PE protocol
        • If high pre-test probability or moderate pre-test probability with >4 hour delay in work-up, start empiric anticoagulation if bleeding risk is acceptable while work-up is ongoing
    • TTE


PE Class: Low risk Submassive Massive

Hemodynamically stable

No evidence of right heart strain or myocardial necrosis on labs or TTE

Hemodynamically stable

Evidence of right heart strain or myocardial necrosis: RV strain on TTE (ex: D-sign), BNP >150, trop >0.05

Hemodynamically unstable (ex: SBP<90)

Evidence of RV strain


Start anticoagulation

LWH or heparin gtt (if renal impairment)

Can also use NOAC. Rivaroxaban & apixaban can be used as initial management. Edoxaban & dabigatran can be used after 5-10 days of parenteral therapy

Provide hemodynamic support, monitor for decompensation

Start anticoagulation with unfractionated heparin gtt

STAT consult cardiology for consideration of catheter directed thrombolysis (EKOS) or embolectomy

Provide hemodynamic support.

Start anticoagulation with unfractionated heparin gtt

Page CCU fellow STAT. Consider systemic tPA (this is a fellow/attending level decision).

Discuss with cardiology catheter directed thrombolysis (EKOS) or embolectomy

tPA Considerations

  • Dose is 100mg tPA over 2hrs
  • Most effective within 24 hours but effective up to 14d
  • Contraindications:
    • Absolute:
      • CNS Pathology: hemorrhagic or ischemic CVA within 3 mo, AVM, CNS neoplasm, recent surgery
      • Trauma: Recent head trauma w/ fx or injury
    • Relative
      • Surgery: surgery w/in 3 wks
      • Heme: active bleeding, bleeding diathesis, plt \< 100, oral AC
      • Age: >75 yo, dementia

Long-term management

  • Anticoagulation

    • NOAC - Remember to give initial loading dose (duration of load varies with each agent)
    • Warfarin (Coumadin): Goal INR 2-3, requires frequent monitoring
      • Need to bridge with heparin or lovenox
      • Pharmacy consult, and will need to be set up with coumadin clinic at the time of dc
  • IVC filter: only if AC is contraindicated, bleeding risk unacceptably high, recurrent PE despite optimal AC (placed by IR or Interventional cards)

## Duration of Anticoagulation:

  • Major reversible/transient risk factors (surgery, trauma): 3-6 months
  • Idiopathic, unprovoked, or with less compelling risk factors: 12 months
  • Major permanent risk factors (cancer, homozygote F5L or prothrombin gene mutation, APLS, protein C/S deficiencies, AT III deficiency): At least 1 year, preferably lifelong.
  • Recurrent DVT/PE: lifelong
    • Consider etiology of recurrent VTE: cancer screenings, family hx of hypercoagulable disorders, features of autoimmune disease