Hyperkalemia is bread and butter critical care medicine. However, the therapeutic approach has changed substantially within the past 5 years. Myths about kayexalate and normal saline have been exposed, allowing more effective therapies to take their place.
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Some good points made here. A ton of lasix and some IVF are definitely faster and more available options than dialysis. If there is urine output with a response to diuretics, the K will come down. Two other points: – There may be some additional benefit from the sodium load given with isotonic bicarb. Delivery of Na to the distal nephron will promote outward K flow through ROMK channels. I tend to take advantage of this by stretching the definition of “acidosis” to give more bicarb, as it contains more Na than LR. Normal saline would work, but is likely… Read more »
Agree,
1) Increased sodium/bicarb delivery to the tubule will improve K excretion, so theoretically it might be ideal to push the bicarb a wee bit high (e.g. to the 28-32 mEq/L range) to optimize potassium excretion. Was tempted to write this but folks are already accusing me of being obsessed with bicarb.
2) Logistically speaking it takes a *lot* of time to get someone cannulated and running on dialysis. For folks who can make urine, diuresis will work much much faster.
Excellent points Josh.
SQ insulin: I worked for an institution where the practice of SQ insulin was entrenched in a local hyperkalemia protocol. Apprently it was thought to be a “safer” route. Unfortunately it doesn’t work. Drove me nuts until we finally got it changed.
Bicarbonate:. Stopped recommending it years ago. The last ED I served in it garnered no believers, myself included. Nice explanation of why it’s just not helpful at code cart concentrations.
Great stuff!
John Hart, PharmD BCPS
thanks! Many reviews/articles consider all forms of bicarb together (isotonic & hypertonic), when this happens the conclusion reached is that bicarb is junk.
Thanks for your work and the post Josh! Temporizing Measures: – Saying Isotonic Bicarbonate Does Work is probably an inappropriately strong statement, your twitter anectdote is misleading because I doubt (hope) that HCO3 was not the ONLY therapy that pt received, they likely got insulin +/- lasix/albuterol as well, plus other fluids. Even if you want to look at the “data” of those 12 patient studies from the 1970s and 1990s in dialysis patients then your still only talking about those patients, and generally only talking about a small reduciton in K (~0.3meq from direct HCO3 effects) and hours later… Read more »
For the “diuretic bomb,” do you think it’s still a feasible strategy if there are no IV thiazide diuretics available? Where I am, we only have PO thiazides (e.g. HCTZ, indapamide, chlorthalidone, metolazone).
You can use an oral thiazide, some of them have suprisingly rapid oral bioavailability (e.g. indapamide https://www.tandfonline.com/doi/abs/10.1185/03007997709110219?journalCode=icmo20). Maybe it won’t work quite as fast as IV but still worth adding it to the mix.
Much appreciated, thanks Josh.
What is your recommended diuretic dose in this diuretic bomb? What is your waiting time for it to work before you decide for dialysis support? Did you repeat the “diuretic bomb”? Thank you
Nice overview as always. What are your thoughts on terbutaline sc. in the management of hyperK?
Regards, Lukas.
Great question! Terbutaline should work fine, as an alternative to albuterol. The reason that I use albuterol is logistic – it’s much faster for me to get albuterol started on a patient than to order terbutaline. Also terbutaline isn’t a med typically used for hyperkalemia at shops that I’ve worked at. But if you have rapid access to terbutaline that would be a good alternative to albuterol (especially if you’re having logistic difficulties with the continuous neb).
thanks, and sc. should be fine? i also have rapid access to salbutamol neb. but terbutaline sc. seems quite practical to me. the thing is i could’t find data on sc. application of beta-mimetics in this setting.
Hi Josh
Would you comment on the management of the patient in cardiac arrest secondary to hyperkalemia?
What role, if any, would sodium bicarbonate have?
Would you still use the isotonic NaHCO3?
Any pearls with regard to this clinical situation?
Have you ever tried i.v. salbutamol instead of epinephrine? It is avaliable in Poland where I study, our cardiology unit described using it in severe hyperkaliemia.
It would make more sense then epi in my opinion since aplha activity of epi will decrease diuresis.
What is the range of kaliuresis that can be obtained by furosemide and other agents. I understand that this will vary greatly. Also that you can measure it on a spot urine analysis. But just your thoughts. Thanks for all the excellent work. Havent found anything useful in litterature.
Hi, What is the expected kaliuretic effect of the different regimens? What about the effect of furosemide only? I understand this will vary greatly depending on patient factors. And also that it can be measured on a spot urine test. But what are ballpark figures? Thanks. Dominic Larose MD FACEP.