Episode 52: Diastolic Heart Failure with Todd Dorman

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 52: Diastolic Heart Failure with Todd Dorman

In this episode, episode 52, I welcome Dr. Todd Dorman to the show.  Dr. Dorman is a professor of anesthesiology here at Johns Hopkins, is the Vice Chair for Critical Care, and is the immediate past president of the Society of Critical Care Medicine (SCCM).  Dr. Dorman and I discuss diastolic heart failure or heart failure with preserved ejection fraction (HFPEF), how it differs from systolic heart failure or heart failure with reduced ejection fraction (HFREF), how it presents, and how to manage it perioperatively.

CME: https://earnc.me/v55B14

References for peripheral vasopressors:

  1. Medlej K et al. Complications from Administration of Vasopressors Through Peripheral Venous Catheters: An Observational Study. JEM 2018. PMID: 29110979
  2. http://rebelem.com/peripheral-vasopressors-safe-dangerous/

Outline by April Liu

15 thoughts on “Episode 52: Diastolic Heart Failure with Todd Dorman”

  1. Great topic and speaker once again! In the same vein of reminding listeners not to just think about LVEF, I think a topic on the R heart would be well timed.

    A few questions:
    1) Dr Dorman mentioned diastolic failure patients are more at risk of sudden decompensation as opposed to the more progressive symptoms w systolic HF. i guess I could always treat diastolic dysfunction like they are about to decompensate, but as you can imagine, not realistic in private practice. What are some tips for identifying that patient who is closer
    To falling off the curve and decompensating w diastolic failure? Should I be putting most attention to the grade of diastolic dysfunction? Functionality? Symptoms? Do all diastolic dysfunction patients deserve an a line for GA because you never know when they will fall of that compensation curve?

    2) I remember one of my mentors
    At Stanford tell me about the rule of the 70 for diastolic dysfunction pts
    a) HR below 70 (to optimize filling time)
    b) diastolic BP>70 (to optimize coronary perfusion pressure; suggesting keeping afterload normal to high if necessary to do so)
    c) pulse pressure <70 (to minimize LV impedance and stroke work)
    What are your thoughts on this rule of thumb? What would you prioritize?

    3) is there any benefit in your mind under anesthesia of preferentially using CCBs like verapamil or dilt over beta blockers to not only drop HR, but improve lusitropy? Do CCBs have a more positive lusitropic effect than beta blockers?

    Thanks Jed. Always appreciated.

    1. Hi Josh,

      Great questions.

      1. Patients with higher grade diastolic dysfunction are at higher risk so being more vigilant with them makes sense. Anyone acting severe (really volatile with small changes in volume, difficult to control BP), regardless of their grade, should also be managed as if they are severe. I wouldn’t place an a-line in anyone with diastolic dysfunction, but in higher grades and anyone whose symptoms suggest a higher grade it would be a reasonable move.

      2. The rule of 70s makes sense. Dr. Dorman says, and I agree, that if you had to pick one, you should prioritize avoiding tachycardia.

      3. There is no data to support the superiority of CCBs over B-blockers for lusitropy or for the management of diastolic dysfunction. Dr. Dorman prefers CCBs, specifically verapimil, for the most severe diastolic dysfunction.

      All the best,

  2. This was an awesome episode, thank you!

    Request/suggestion for future topic: pulmonary hypertension


  3. The problem is compounded by the fact that systolic and diastolic heart failure commonly coexist when patients present with many ischemic and nonischemic etiologies of heart failure.

  4. Dr. Dorman referred to concentrations of norepinephrine appropriate for peripheral administration for limited time periods (assuming there was an existing infiltration protocol). What is the concentration that is considered appropriate for administration via a peripheral line?

    1. Hi Deborah, we used 8mg diluted in 250cc, which comes out to 32mcg/ml. For central lines the concentration is doubled. Hope that helps.


      1. Thanks, Jed. Your podcast is excellent. I recommend it to all the trainees in our teaching program.

      2. I was going to ask the same question. We use 8mg in 500ml, but never in a peripheral IV unless the patient can’t wait and the central line insertion is underway. Dr. Dorman referenced studies suggesting the safety of vasoactive medications in peripheral IV’s, I’d love to read them if you could add them to the show notes.

        1. Hi Mike,

          I added a study and a nice summary from RebelEM.com. There isn’t a ton of great data to support it but I think an important point is that there isn’t much data against it either. Mostly just case reports. If you are going to do it, the more proximal the vein (AC or higher) the better, the lower the dose, and the more dilute the concentration. We use 8mg in 250cc as our peripheral dose, so yours is already twice as dilute. Definitely interested to hear if others have thoughts on this or know of additional literature.

  5. Great talk! Thank you for emphasizing the importance of maintaining euvolemia despite the fact that the heart can appear dilated with poor function on echo in HFrEF. In either HFrEF or HFpEF, cardiac output and filling pressure drive clinical symptoms. Patients with baseline low EF and a dilated heart in acute distributive shock such as sepsis with low filling pressure still need initial volume resuscitation. The acute pathology dictates patient’s management in the acute setting. With regard to the chronic management of HFpEF, correct me if I am wrong, unlike HFrEF, none of the heart failure regimen has shown a survival benefit other than diuresis for symptom relief as needed. At a recent conference one presenter even advocated for faster heart rate. That sounds reasonable if there is a period of diastasis between the E and A waves, in which case there is room to increase heart rate without compromising diastolic filling and in theory it should lower LV filling pressure and increase CO. There are recent drug studies targeting myocardial relaxation in HFpEF patients with neutral results. There are certainly a lot of new knowledge coming out regarding HFpEF. Even the diastolic echo assessment of the heart might not have as much value in HFpEF patients as we previously thought. (Echocardiographic Evaluation of Diastolic Function Is of Limited Value in the Diagnosis and Management of HFpEF. Gaurang, Abramov FEB 2018) These patients can be difficult to manage. Usually it is a delicate balance between the lungs and the kidneys. I am quite intrigued by your use of verapamil in patients with HFpEF. What is the clinical setting? Are they in acute heart failure exacerbation with hypertension? You mentioned that patients’ extremities become warm after verapamil. I wonder how much of the improved CO is due to peripheral vasodilation from verapamil vs improved relaxation. Thank you very much for a great talk on a difficult subject.

    1. Hi Huayong,

      I’m glad you found the episode useful. Here is Dr. Dorman’s response:

      “Thank you for your response and for you positive comments about the material. I am glad you found it useful.

      We have found that this true in a subset of patients with severe HFpEF who are usually in the first 3 days after surgery ( High risk time frame for high levels of endogenous catecholamines secondary to surgical stress response also sometimes called surgical SIRS). The scenario is typically hypotension and evidence of organ dysfunction like low UOP who respond to a fairly small amount of fluid ( say 250-500) with evidence of pulmonary edema. Diuretics help the oxygenation issue but, in this special subset, usually lead back to hypotension. Lusitropy helps them tolerate the fluid without pulmonary compromise. As their endogenous catecholamines fall over 1-3 days, this usually resolves easily.

      In the rare sub-subset with invasive pulmonary monitoring they usually show improved CO with improved SV at lower PA diastolic and filling pressures despite a fluid challenge. Thus it seems that the major reason for improved perfusion is relaxation facilitated cardiac performance.

      I again, want to stress that the need for luistopic agents acutely is rare in our experience, but may be critical in a small subset.”

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