Episode 24: The Evils of Sodium Bicarbonate

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 24: The Evils of Sodium Bicarbonate

In this episode I first suggest you take a look at the recently published (ahead of print) VANCS study on the use of vasopressin as a sole agent in the treatment of vasoplegic shock.  Then I review the reasons never to use sodium bicarbonate in lactic acidosis.

CME: https://earnc.me/3CX3ha

The Vancs study: https://www.ncbi.nlm.nih.gov/pubmed/27841822

The two articles I recommend on bicarb:

Forsythe: https://www.ncbi.nlm.nih.gov/pubmed/10631227

Sabatini: https://www.ncbi.nlm.nih.gov/pubmed/18322160

Outline by Brian Park: Outline

11 thoughts on “Episode 24: The Evils of Sodium Bicarbonate”

  1. The use of vasopressin is increasing where I work (mixed med/surg, CT surgical ICU). We currently use it in vasoplegic shock that is refractory to catecholemines (also used as second line pressors in sepsis). Just wondering if others care to comment on the titration of vaso: some medical intensivists say it is an either on or off drug at 0.04 u/min (in sepsis); however as a first line pressor for vasoplegia it would seem that it would need to be titrated to effect. What time intervals are you waiting between dose changes and how much are you titrating by? Is there any worry about the increased coronary vasoconstriction in post-CT surg patients?

    1. Hi Alex,

      Excellent questions and I hope we’ll hear from others who are using vasopressin in these settings. In the Hajjar study they didn’t find any increased cardiac events in the vasopressin group. In fact, they found a trend toward fewer MIs with vasopressin which would seem to be reassuring. In our cardiac SICU we do titrate vaso, though at the moment we only go up to 0.04. In the Hajjar study they went up to 0.06. We usually titrate by 0.01 and we make changes just as we would with norepinephrine or epinephrine, every 10-15 minutes usually, depending on hemodynamics and assuming a reasonably brisk carrier rate (at least 100ml/hr). Thanks for listening and thanks for all you do out there every day.


    2. I know this is an old Podcast so you likely know the answer to your question by know. But my facility uses Vasopressin Post Cardiac Surgery when Vasoplegic Syndrome is suspected. We do go up to 0.06 and typically titrate as Jed said, by 0.01. If the patient is very hypotensive I break these rules and will jump straight to 0.04 and go from there based off the response I see. Has seemed to work very well other than on one patient I’ve had recently which was still slightly hypotensive on 0.06 of Vaso and 3mcg/min of Epi.

      Question for you Jed, since the VANCS study, are facilities going to low dose Levophed as a second line medication in the presence of Vasoplegic Shock following Cardiac Surgery if Vaso alone isn’t sufficient?
      We always have Epi going when the patient comes out which I always leave running to help with Myocardial Stunning and once I rewarm the patient will wean if Cardiac Output is adequate. I’ve always leaned away from cranking up the Epi to a “pressor dose” and going to Vaso if BP support is needed but just curious on Levophed vs Epi as a second line “pressor”. It always seems like Epi induces more Ectopy than I’d like to see.

      Thank you and I hope this isn’t confusing.

      1. Hi CJ, thanks for sharing your practice. As for your question, I don’t know the answer but would love to hear from others. I agree that patients often come out on low dose epi but if CO is fine and vasoplegia is the problem then Vaso and/or levo makes sense. What do others think?

        1. I spoke with a CT Surgeon at my facility and he confirmed that Levophed is acceptable for a second line agent if Vasopressin alone isn’t sufficient. He was also seemed very impressed that I knew what the VANCS study was (thanks ACCRAC lol).

  2. This was a great podcast! Thank you for posting. I like how you addressed each point. This Podcast gave me a lot of food for thought and some great discussion points with colleagues!

    1. Hi Genie,

      I’m not sure I understand your question. If you give bolus after bolus of the traditional amp of 50meq of sodium bicarbonate you will increase your serum sodium. If you have an intact blood brain barrier that won’t allow the Na to leak out into the brain tissue you should get some amount of decrease in ICP just as you would with hypertonic saline. Is that what you were asking?


  3. How do you explain an increase in BP seen with a 50cc bolus of bicarb, in light of the “no absorption rule” (revised Starling equation). Agree that bicarb is evil, just wanted to comment on your statement about fluid being drawn into the intravascular space. Thanks!

    1. Hi Molly,

      Interesting question. I’m not familiar with the “no absorption rule” but I assume the idea is that hypertonic solutions don’t pull fluid into the intravascular space. I’d certainly be interested to see data to support this. The whole idea behind using, for example, hypertonic saline in patients with increased ICP is that it will reduce brain swelling by pulling in fluid. Part of this may be that in very sick patients the glycocalyx is likely not intact and so membranes are more permeable.


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