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BRASH Syndrome: Bad Synergy

"BRASH" is an acronym for the myriad of symptoms shown below... it's really a perfect storm all triggered by an AV nodal blocker. The induces bradycardia, which kicks off a serious cascade of events. The sustained bradycardia leads to poor tissues perfusion (shock), which fulminates into renal failure, which leads to hyperkalemia. The viscous cycle continues with one issue simply exacerbating the next. The syndrome doesn't show up spontaneously though, it is usually brought on by any illness/injury that prompts acute kidney injury. One such example could be hypovolemia.

Bradycardia - this is usually profound and may contribute to dizziness, syncope etc.. Your EKG may or may not have p waves present

Renal Failure - acute kidney injury usually kicks off the syndrome. This could be a consequence of blood loss, UTI's, profound dehydration. When kidneys fail, remember potassium excretion also comes to a halt.

AV node blocker - lots of pharmacologics fit into this category and could include beta blockers (-olol), calcium channel blockers (-dipine) Other drug classes like ACE inhibitors (-pril) and ARB's (-artan) aren't required but may contribute to the syndrome.

Shock - ETCO2 may be reduced, hypotension (from volume depletion) is also a very common finding. Compensatory efforts to vasoconstrict (normalize BP) may not fix the cardiac output conundrum because of the slow HR. (CO=SV X HR)

Hyperkalemia - the hyperkalemia is usually mild at first, don't anticipate the standard t-wave changes on your ECG tracings. Tall, tented T-waves will many times NOT be present.

Who is at risk?? The Venn diagram below courtesy of Life in the fast Lane helps illustrate this nicely.

These patients will usually have vague, non-specific complaints. Treatment is mostly supportive and aimed at treating the problems simultaneously. Don't focus or fixate on just (1) of the symptoms -- please avoid tunnel vision here. The ACLS algorithm will likely not provide you much benefit in these specialized cases. The underlying problem here is toxicological/metabolic in nature. Glucagon isn't the fix either..

Bradycardia - chronotropic/catecholamine agents usually work fine. More advanced therapies like transcutaneous pacing are rarely needed.

Renal Failure - IV hydration goes a long way. Only the most severe cases would need more advanced treatments like renal replacement therapy (dialysis).

AV node blocker - it's really simple, discontinue this therapy.

Shock - IV fluids again help correct the hypovolemic state. Lactated ringers may be better than NSS alone, as it can provide some renal protective functions. On rare occasions pressor support (epi, norepi) could be required.

Hyperkalemia - consider calcium and/or loop diuretics. Keep in mind we need some baseline kidney function for these diuretics to work most effectively. Make sure the fluids are established first before you attempt diuresis of your patient. Albuterol may have some applicability here as well.

Like most things in our industry, early identification and diagnosis leads to the development of appropriate management plans that, in turn, affects patient outcomes for the better. You'll never see what you don't know, until you know it.

June 17, 2024

Author: Joshua Ishmael, MBA, MLS(ASCP)CM, NRP

Pass with PASS, LLC

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