Cite this post as:
Scott Weingart, MD FCCM. AHA PE Guidelines. EMCrit Blog. Published on July 10, 2011. Accessed on March 29th 2024. Available at [https://emcrit.org/emcrit/aha-pulmonary-embolism-guidelines-2011/ ].
Financial Disclosures:
Dr. Scott Weingart, Course Director, reports no relevant financial relationships with ineligible companies.
This episode’s speaker(s), (listed above), report no relevant financial relationships with ineligible companies.
CME Review
Original Release: July 10, 2011
Date of Most Recent Review: Jan 1, 2022
Termination Date: Jan 1, 2025
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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… Read more »
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.
‘Anti coagulating people exposes them to harm’, in UK every risk group with a positive DDimer gets LMWHeparin whilst awaiting CTPA. I’ve never heard or seen anyone come to ‘harm’ as the result – the pharmacodynamics and certainly risk profile compaired to the prophylactic dose (which they should prob be getting) is negligible. Indeed in some pts- eg renal, the dose is the same.
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… Read more »
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?
hopefully, Dr. Kline will weigh in as I don’t have access to pro-bnp so I have not read as much as I should about it.
Tachycardia is most often related with. I’m just curious why bradycardia <40 is related to massive PE, vagally mediated perhaps?
I would think more likely acute cor pulmonale affecting the conduction system, but I can’t find a single ref or description. Anyone?????
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.
I think the definition does actually include bradycardia as a manifestation of massive PE
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?