Further Thoughts: Septic Afib w/ Precision Rate Control


You walk into the ED to find your septic patient has a MAP of 50 and heart rate bouncing between 110 and 140. As you walk closer to the hospital monitor, your suspicion of atrial fibrillation with rapid ventricular (RVR) response is confirmed. At some point in your career you may have asked yourself: "is the rate causing the hypotension, or is the rate compensating for the hypotension?"

I believe most of us would chalk this tachycardia up to compensation, evaluate how much fluid the patient has received, and have a low threshold to pull the trigger on levophed. However, if this patient is coming out of an ICU (or extended resuscitation in the ED), already received an adequate amount of fluid, and currently on pressor therapy - one must assume that the tachycardia may have made a shift from a compensatory mechanism to now a response from circulating exogenous catecholamines. 

We know that preload is manipulated by multiple factors, but heart rate is an independent variable. I think of it like the gigantic buckets at waterparks, they fill up over several minutes and then dump water on all the kids standing underneath. If someone were to manually dump the bucket every few seconds, the amount of water released would be underwhelming to say the least.

A little less than two years ago I did a podcast with Dr. Josh Farkas from Pulmcrit on atrial fibrillation with rapid venticular response (RVR) in the septic patient. As a primer to the podcast, Farkas did an amazing blog which can essentially be summarized with this quote.

The average stroke volume of the heart is 50-100 ml's. If we multiply this by our heart rate we will get our cardiac output. Typically if stroke volume goes down, heart rate will increase to maintain cardiac output. However, just because we decrease rate, does not automatically mean we will increase stroke volume. This can be seen in the two calculations below for a patient whose heart rate is decreased from 120 to 80.

Example A : the heart rate decreased to only 80 and without an increase in stroke volume, the cardiac output dropped by two liters.

Example B: the heart rate decreased to 80 and a generous 25 ml's of stroke volume was added. This is an ideal situation, but not assured.

The ideal agent to reduce heart rate after subjective adequate resuscitation would be one in which the heart rate could be tightly controlled and would have a short half-life if stroke volume did not respond to increased diastolic filling.

A study in 2013 evaluated the use of esmolol for this exact scenario. This was a single center, phase II open label RCT, and outcomes were focused on heart rate control (between 80-94), pressor requirements, and fluid requirements. 

The results were promising and showed excellent precision in regard to rate control, decreased pressor requirements, and decreased fluid requirements within the treatment arm. When 28 day, ICU, and hospital mortality was evaluated as a secondary outcome - there was some signal of a mortality benefit as well. 

Graphics have been re-created and simplified for the blog. It is important to download this article from JAMA and evaluate the evidence for yourself. The link is included in the references.

While larger studies are needed with emphasized patient centered primary outcomes, I anecdotally love how tightly I can dial in heart rate on aortic anuerysm patients who I transport on esmolol. This study was an excellent example of the precision and safety margin that can be obtained with esmolol. The graph below shows the average heart rate for both the treatment and control arms. 

It makes sense to me to use an agent that is titrates as an infusion and has a short half-life. I have seen diltiazem reduce heart rate by barely 10 bpm, and other times reduce by 50 bpm. When diastolic filling is a dependent variable, reducing an independent variable such as heart rate should be carefully calculated. 

In this study they did not begin to treat rate untill 24 hours after hemodynamic resuscitation. This probably is wise and for the acute setting, you will be safer to assume the tachycardia is due to compensation in the presense (or suspicion) of sepsis. 

I do believe there are a subset of patients that have increased their heart rate above compensatory therapy. This is especially true in atrial fibrillation, where cardiac output is already diminished due to loss of atrial kick. In this setting, a shared decision-making model with the referring physician is wise prior to transfer.


Morelli A, Ertmer C, Westphal M, et al. Effect of Heart Rate Control With Esmolol on Hemodynamic and Clinical Outcomes in Patients With Septic ShockA Randomized Clinical TrialJAMA. 2013;310(16):1683–1691. doi:10.1001/jama.2013.278477

Flipping The Podcast: Approach to shocky patient in AF w/ RVR - Dr. Josh Farkas

FOAMfrat Podcast 54 - Approaching The Shocky Patient In Afib w/ RVR.


Podcast 91 - Ketamine "Analgesia to RSI" w/ Michael Perlmutter

Last year at WEMSA2019 we had an amazing session that included speakers like Michael Perlmutter, Leon Eidelman, Michael Lauria, and Chip Lange. Each speaker had 20 minutes and the talks were all recorded.

My goal was to put these out A LOT sooner, but the stupid Catalina Mac update prevented me from opening Adobe Audition files. Utilizing an extensive Google search and Russian hacking skills - I was able to access these talks.

This is a 20ish minute talk by friend of the show, flight medic, and current medical student, Michael Perlmutter (@DitchDoc14). Michael is speaking on the application and use of Ketamine "from analgesia to RSI (yes and DSI)."

If you are looking for an awesome state conference with sharp and influential speakers, check out WEMSA right here in the sunny state of Wisconsin. Link For Conference Here.

Put this podcast on the playlist for your next commute! 

Download Slides Here


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