AHA PE Guidelines

Recently, the AHA published guidelines on the management of pulmonary embolism. I extracted only the stuff relevant to ED w/u and management:

Source: Circulation 2011;123:1788


Anticoagulate with LMWH, IV/Sub-Q UFH, or fondaparinux (IA)

While working up PE, if pretest is moderate or high, and there are no contra-indications, start anticoagulation during the work-up (IC)


Definition of Massive PE-Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Definition of Submassive PE-Acute PE without systemic hypotension (systolic blood pressure >90 mm Hg) but with either RV dysfunction or myocardial necrosis.

  • RV dysfunction means the presence of at least 1 of the following:
    • —RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography

    • —RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT

    • —Elevation of BNP (>90 pg/mL)

    • —Elevation of N-terminal pro-BNP (>500 pg/mL); or

    • —Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

  • Myocardial necrosis is defined as either of the following:
    • —Elevation of troponin I (>0.4 ng/mL) or

    • —Elevation of troponin T (>0.1 ng/mL)


Fibrinolysis is reasonable for pts with massive PE and acceptable risk of bleeding complications (IIa/B)

Fibrinolysis may be considered for pts with submassive PE judged to have clinical evidence of adverse prognosis (hemodynamic instability, worsening resp. insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (IIb/C)

Fibrinolysis is not recommended for patients with submassive PE with only mild dysfunction, i.e. low risk PEs (III/B)

Fibrinolysis is not recommended for undifferentiated cardiac arrest (III/B)

Interventional and Surgical Options

Either catheter embolectomy or surgical embolectomy can be considered depending on institutional and operator preference (IIa/C)

Either of these are reasonable if the pt is still unstable in massive PE after fibrinolysis (IIa/C)

Also reasonable in massive PE, if the pt has a contra-indication to lysis (IIa/C)

May be considered in lieu of fibrinolysis in patients with submassive PE and evidence of adverse prognosis (IIb/C)

Not recommended for pts with PE at low risk (III/C)


Contraindications to Fibrinolysis

Absolute contraindications include

  • any prior intracranial hemorrhage,
  • known structural intracranial cerebrovascular disease (eg, arteriovenous malformation),
  • known malignant intracranial neoplasm,
  • ischemic stroke within 3 months,
  • suspected aortic dissection,
  • active bleeding or bleeding diathesis,
  • recent surgery encroaching on the spinal canal or brain, and
  • recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury.

Relative contraindications include

  • age >75 years;
  • current use of anticoagulation;
  • pregnancy;
  • noncompressible vascular punctures;
  • traumatic or prolonged cardiopulmonary resuscitation (>10 minutes);
  • recent internal bleeding (within 2 to 4 weeks);
  • history of chronic, severe, and poorly controlled hypertension;
  • severe uncontrolled hypertension on presentation (systolic blood pressure >180 mm Hg or diastolic blood pressure >110 mm Hg);
  • dementia;
  • remote (>3 months) ischemic stroke; and
  • major surgery within 3 weeks.

Recent surgery, depending on the territory involved, and minor injuries, including minor head trauma due to syncope, are not necessarily barriers to fibrinolysis.

The clinician is in the best position to judge the relative merits of fibrinolysis on a case-by-case basis.


Further on who should get lytics

It is preferable to confirm the diagnosis of PE with imaging before fibrinolysis is initiated. When direct imaging is unavailable or unsafe because of the patient’s unstable condition, an alternative approach favors aggressive early management, including fibrinolysis, of the patient with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not clearly due to a cause other than PE) when there is a high clinical pretest probability of PE and RV dysfunction on bedside transthoracic echocardiography.We do not endorse the strategy of treating subjects with undifferentiated cardiac arrest with fibrinolysis, because this approach lacks clinical benefit.

PE Fibrinolytic Treatment Algorithm


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  1. Steve says

    Sounds reasonable except for the 2nd statement on anticoagulation…anticoagulate moderate pre-test probability patients while awaiting the workup has a relatively strong IC recommendation? We workup patients with moderate probability all the time, a small fraction of which actually have a PE. Anticoagulating those people exposes them to harm (even if it is only transient from heparin) from a therapy that has never been proven to be of benefit.

    I agree- if you have the pregnant patient who is tachypenic, hypoxic, tachy, hypotensive with Factor V Leiden, who just got off a plane with a swollen leg and is coughing up blood (obviously being slightly dramatic here…) then they should get heparin (and more like an IR suite) post-haste…otherwise I think it’s dangerous to anticoagulate “moderate” pre-test probability patients. Sounds like more fodder for a plaintiff’s lawyer than actual good patient care…

    • says

      Steve–I thought the exact same thing. From what I can see, there is no evidence either. They just link to two other sets of guidelines. Kline studied this and came to the conclusion that it is only worth starting empiric anti-coagulation on high pretest prob patients.

  2. Tallam says

    Recently I had two patients. Both patients received heparin and at the same patient went to interventional radiology for intra arterial thrombolytics.
    First patient did well.
    Second patient 57 years old had massive PE. She had 5 % of the lung perfusing. She went to interventional suite and someone let her get up to go to bath room and she collapsed went into arrest, she was ressusitated, had interventional procedure and she is doing well.
    I understand the protocols of doing different studies before deciding interventional. This takes time and effort to cooridinate the whole world, pulmonologist for consult and cardiology for 2D echo. This may be easy in major intstitution, this is problem in most of the hospitals.
    I have beed discussing with the radiologist and both of us agree, then call the pulmonologist before going further.
    This need to be further studied at the level of ED. I am working with pulmonologists and cardiologist to develop protocol to cut the chase.
    Thank you

  3. don zweig says

    Thanks, i love listening to Jeff’s aggressive approach and lack of waffling. My question regards the pro-bnp. it is often elevated in patients with some decrease in GFR (renally cleared). I wonder how he factors this into his decision to use the proBNP as an indicator of submassive pe that will benefit from tpa?

  4. Jay says

    Tachycardia is most often related with. I’m just curious why bradycardia <40 is related to massive PE, vagally mediated perhaps?

    • says

      I would think more likely acute cor pulmonale affecting the conduction system, but I can’t find a single ref or description. Anyone?????

    • ED_PharmD says

      I think you misread the sentence. The definition of massive PE said hypotension NOT due to a cause other than PE such as profound bradycardia.

  5. Khurshid Ahmed says

    Is it mandatory to give anticoagulation alongwith antiplatelet after catheter directed embolectomy in submassive pulmonary thromboembolism patients ? As we know Anticoagulation prevents further clot formation, but does not lyse existing thromboemboli or decrease thrombus size. Is there any literature supporting this that anticoagulation may not be given and only dual antiplatelet will be ok?


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