R heart TAPSE talk from Cuba.  Also, announcing Resusfest with @criticalcarenow & @emcrit! #FOAMED

And you thought the Summer of R Heart Failure was over……wrong!  Well, actually it is over, but you all can’t seem to get enough.  We’ve got a lot of feedback about how much people enjoyed all the R heart talk, so we’ve got a little more for you.

We were in Havanna, Cuba recently with the DevelopingEM crew and we were lucky enough to catch up with James Daley who’s been doing some pretty sweet research on TAPSE.  As luck would have it, we were also able to corral some other super echo experts, Brian Galovic, Patrick Ockerse, and Jimmy Fair to discuss just how useful TAPSE is and how not to screw it up.
Also, we know you love learning ultrasound in a castle, so why not resuscitation as well!  Our good friends Scott Weingart and Haney Mallemat are putting on Resusfest this year in conjunction with Castlefest and registration is open.  Go to Castlefest2016.com to find our more and register.  Basically it’s 2 days of incredible resuscitation education in a castle on 4/30-5/1.  If you’ve already registered for Castlefest and want to add it on, then just email us.  We’ll sort it out for you.  See you there!


  1. Kudos for at last bringing the right side into the limelight.
    I’m not sure though which group of patients you are having difficulty in distinguishing between and why. I have been looking at the whole PH and RV function over the last 10 years. I have only come across two cases where I needed to distinguish but both weren’t decompensated. One proceeded to CTPA and the other couldn’t lie down for it but as Dr Ryan said , she had RV hypertrophy as well and hence we didn’t feel PE was strong in likelihood.
    For those who are decompensated ie Shock, (in my world – Hyperensive Hypotension) , don’t know about phenylephrine and metaraminol as both have suggestion of affect on Pulm circ. I found NA as the vasopressor to help increase LV afterload thus reducing the septal bowing. Once NA is running, possibly Milrinone as the inodilator with positive affects on Pulm circ. Levosimendan is also being shown to have a good lusotropic effect.
    Shouldn’t we try and identifyt he group that deteriorates early. By the time TAPSE is reduced you are in RV failure territory already. Intend to raise alarms the moment I am able to see greatly increased RVSP. PW at the PV is great but not always achievable at bedside in ED in my experience especially until you have done a lot of echoes.
    In PH with shock reduced TAPSE , AF and pericardial effusion has already been shown to have much higher mortality. We need to get at the group before the onset of reduced TAPSE . Giving inappropriate amount of fluids to this group also risks AF which makes life extra difficult.
    One thing for sure I feel from my experience, indicating this group of patients [ PH with shock or Hypertensive hypotension] without the knowledge of the status of Pulmonary circulation and Rt heart function, leads to near 100% mortality due to the fluid regimen, the early lack of use of vasopressors and inotropes and then Ventilation.
    It’s been great to see this topic come in to ED discussions and as Dr Ryan said, there is no evidence base or consensus. I know for sure though, only EP’s getting more aware of this and doing the research will provide the evidence base.

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  4. Interesting discussion guys. After watching the podcast of TAPSE I asked some of the cardiologists and echo techs about it where I work and they had never heard about it before. I looked in Lang’s ASE’s Comprehensive Echocardiography textbook(second edition) and it had 3 very small paragraphs on TAPSE out of it’s 900 pages. I find it very difficult to integrate this kind of skill into my practice when other specialties are not on the same page. I appreciate the viewpoint that Matt always tries to give “can the common ED doc do this”. Many times it is yes we can do this, however our colleagues in the community setting many times don’t know about it or use it in their practice. I thought that TAPSE along with other metrics used to evaluate the RV in submassive or high risk intermediate PE patients would be helpful in risk stratifying these patients to see if they would benefit from systemic thrombolysis or CDT. The newly updated CHEST guidelines on antithrombotic treatment of VTE has not changed. They do not support thrombolysis in submassive PE. Unfortunately, it does not appear that all of this information we can obtain about the rv changes management. That said, we just had a patient with submissive PE, TAPSE 12mm, positive biomarkers. Was given TPA half dose, doing well. Thanks for all of the great education!!

    1. Hi James,
      Evaluation of the right heart is crucial in critically ill. It is much less forgiving than the left heart. Quite often it is the cause of death but as the clinicians haven’t questioned RV function, they never know.
      I work in a hospital where the incidence of submassive and massive PE presentation is pretty high, yet, I will state that the incidence of Pulmonary hypertension from a non ACUTE PE cause is more common. We have had two cases of submassives not treated with thrombolysis which became massive and arrested and didnt survive.

      But, the real success of evaluating the rt heart and PH is in undiagnosed cases of pulmonary hypertension treated longstanding as COPD and Asthma. When these patients come in critically ill with hypotension, if without evaluating the rt heart you were to continue as you would resuscitate as per normal sepsis resuscitation strategies, there is a higher likelihood of death.

      Even under the care of experts in PH, cases such as these presenting to such tertiary hospitals in shock had a mortality of above 70% when there was seen to be moderate to severe pulmonary hypertension. I’m pretty sure it would be near 90% when the clinician managing this group of patients is unaware of the existence of moderate to severe PH. This is where Rt heart evaluation is crucial.

  5. Ash,

    Thank you for the response. I have been measuring TAPSE on a number of patients without PE and have found results ranging from 20mm up to 35 mm. Is there a normal range for tapse or just a threshold of normal and abnormal?


  6. James, 1.7 is quoted in a lot of texts. I always tend to say anything less than 2 I would be worried and look at everything else.ASH

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