PE is the third leading cause of vascular mortality, after myocardial infarction and stroke. It is an enormously heterogeneous and unpredictable disease, which makes treatment difficult. As such, it should not be surprising that PE therapy remains highly controversial. For example, the new European Society of Cardiology guidelines recommend anticoagulation and watchful waiting for high-risk submassive PE (with salvage thrombolysis as needed). Meanwhile, in the United States, PE response teams (PERT teams) are typically employing more aggressive approaches to these same high-risk submassive PE patients. The use of systemic thrombolysis, interventional radiology strategies, and ECMO remain highly variable across different countries and different centers. Additional research is needed to resolve these controversies.
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The IBCC chapter is located here.
- The podcast & comments are below (the podcast is our longest yet at ~90 minutes of PE insanity! It's taking a little while, but will be out soon.)
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Amazing review. One question I have for you which I can’t seem to find a straight answer for anywhere is, how long do you wait before you check a PTT and fibrinogen after the tPA is done (i.e., 30 minutes, 1 hour? etc…)
Hi Josh, awesome post as usual. What do you think of endotracheal Milrinone? There is this retrospective study, where patients received this after separation from cardiopulmonary bypass and responded wonderfully. (Gebhard et al. J Cardiothorac Vasc Anesth 2019;33(3):651–660. doi:10.1053/j.jvca.2018.09.016) I wonder why there isn’t more literature on the effect of iv. Milrinone in right heart failure? From a pathophysiological this should also work quite well. What are your thoughts on that? Another thing is Levosimendan. This is used quite a lot in Europe (e.g. Austria), I think you guys don’t have it in the States. There is also literature that this improves RV function in patients and reduces sPAP. (Parissis JT et al. Effects of levosimendan on right ventricular function in patients with advanced heart failure. Am J Cardiol. 2006;98(11):1489–1492. doi:10.1016/j.amjcard.2006.06.052) What do you think of that? Vasopressin seems to me like the optimal pressor in right heart failure, as it raises MAP und decreases sPAP unlike e.g. Phenylephrine. (Sugawara et al. Effects of vasopressin during a pulmonary hypertensive crisis induced by acute hypoxia in a rat model of pulmonary hypertension. Br J Anaesth. 2019;122(4):437–447. doi:10.1016/j.bja.2019.01.014) Shouldn’t Milrinone oder Levosimendan (when available) be first line inotropic support in right heart… Read more »