Hemodynamic support in Acute Right Heart Failure due to Pulmonary Embolism

A 68 year old male with a history of a right ankle ORIF three weeks ago is transferred to your ICU for management of a pulmonary embolism. He developed acute dyspnea while at physical therapy and was taken to an ED where he was found to have bilateral pulmonary emboli extending into both segmental and subsegmental pulmonary arteries on CTPE. His workup included elevated troponins and an echocardiogram that showed a dilated RV with hypokinesis of the RV free wall and reduced tricuspid valve annular systolic excursion. He was started on a heparin infusion prior to transport and was hemodynamically stable when you took the transfer call. When he arrived to your facility he was mentating well but his BP was 85/50 with a HR of 115 and an spO2 of 96% on 2L NC. How will you address his hypotension?


This is an unfortunate gentleman in acute right heart failure. Emergency medicine and critical care physicians need to have a thorough understanding of how to support the right ventricle in cases of acute right heart failure for which there are multiple etiologies. Today we will focus on pulmonary embolism. This patient’s RV failure has detorited to the point where he is now in cardiogenic shock. This is not the patient to hang a liter of crystalloid and wait a half hour to repeat the BP.  


The first thing you should be aware of with this patient is to not give fluids unless you have a good reason to believe the patient is volume depleted. PE in itself is not associated with a hypovolemic state. Remember the right ventricle in massive PE has elevated filling pressures and is pumping against a clot burden. The combination of elevated RV afterload with decreased MAP will decrease RV perfusion. If you give the right ventricle additional volume you will worsen afterload, decrease RV perfusion, increase septal bowing into the LV and worsen LVEF, essentially putting the patient into worsening cardiogenic shock. 


Now that we have decided administering fluids in most scenarios of massive PE is the incorrect choice you need to be thinking about a vasopressor. How do you choose the correct agent? A key thing to remember is that the goal is to increase the MAP without increasing the pulmonary vascular resistance. There is pulmonary vasoconstriction in massive PE so you want to avoid worsening PVR. Two good choices here are epinephrine and vasopressin. The mechanisms of these two medications have a favorable profile in hemodynamic support for massive PE. Think of these vasopressors as having a low PVR to SVR ratio (PVR/SVR). The beta-1 and beta-2 agonism of epinephrine will cause increased chronotropy driving up the MAP as well as decreasing pulmonary vascular resistance. Vasopressin acts on the vasopressinergic (V1) receptor and it increases systemic vascular resistance as  well as decreases pulmonary vascular resistance via a NO-dependent mechanism at the V1 receptor. The bottom line is to remember these patients have complex physiology and to use your clinical judgment in these scenarios. There are no large randomized controlled trials comparing different vasopressors in massive PE so you need to have a good grasp on the pathophysiology. Stay on the lookout for additional posts on other therapies for managing the critically ill PE patient. 




Boulain, T., Lanotte, R., Legras, A., Perrotin, D. (1993). Efficacy of Epinephrine Therapy in Shock Complicating Pulmonary Embolism Chest 104(1), 300-302. https://dx.doi.org/10.1378/chest.104.1.300


Price, L., Wort, S., Finney, S., Marino, P., Brett, S. (2010). Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review Critical Care 14(5), R169. https://dx.doi.org/10.1186/cc9264


Cager, Sara. Deep Dive- Hemodynamic Management of Massive Pulmonary Embolism. Retrieved from: https://www.emrap.org/episode/deepdive/deepdive