High Risk, Low Prevalence: BRASH Syndrome

BRASH syndrome is a synergistic spiral of bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia. The clue is disproportionate bradycardia with only mild to moderate potassium elevation, often after dehydration, sepsis, or a medication change in an older patient with kidney disease.

Recognizing BRASH Syndrome

• Five-part vicious cycle: BRASH is not just hyperkalemia plus bradycardia; it is a self-amplifying loop of bradycardia, renal failure, AV nodal blocker exposure, shock, and hyperkalemia that requires treating every limb of the syndrome.
• Disproportionate bradycardia clue: Severe bradycardia can appear when potassium is only 5-7 mEq/L, far earlier than the classic hyperkalemia picture, and that mismatch is the bedside clue we emphasize in the episode.
• Atypical EKG pattern: The ECG finding is often mainly bradycardia rather than the full textbook progression of peaked T waves and QRS widening, so a relatively bland tracing should not reassure you.
• High-risk medication stack: AV nodal blockers are central, especially atenolol, nadolol, and labetalol, while ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, trimethoprim, digoxin, tacrolimus, and cyclosporine raise the risk.
• Typical clinical trigger: The syndrome is often unmasked by dehydration, GI illness, sepsis-related hypotension, or a recent dose increase or new nephrotoxic medication in an older patient with baseline renal vulnerability.

Initial Management Priorities

• Treat the whole syndrome: Management has four parallel targets: volume status, bradycardia, hyperkalemia, and the precipitating cause, because fixing only one piece often leaves the cycle running.
• Volume status first pass: Volume management is nuanced because these patients may be oliguric and overloaded; history, exam, and POCUS are key to finding euvolemia, and we walk through that bedside approach in the chapter.
• Calcium as first move: Calcium is the first-line stabilizer for the bradycardic hyperkalemic patient, and repeat dosing is often needed when the initial response is incomplete.
• Epinephrine over atropine: Epinephrine is the preferred pressor for unstable BRASH because it raises heart rate and shifts potassium intracellularly, whereas atropine is usually not helpful in this physiology.
• Dialysis and mimics: If medical therapy fails, dialysis may be required; persistent instability should also prompt reconsideration of beta-blocker, calcium-channel blocker, or digoxin toxicity and adrenal insufficiency.

References: 

1. Farkas JD, et al.. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia. J Emerg Med. 2020 Aug;59(2):216-223. doi: 10.1016/j.jemermed.2020.05.001. Epub 2020 Jun 18. PMID: 32565167.
2. Hegazi MO, et al. Junctional bradycardia with verapamil in renal failure--care required even with mild hyperkalaemia. J Clin Pharm Ther. 2012;37(6):726-728. PMID: 22568727
3. Farkas J. BRASH syndrome: Bradycardia, Renal failure, Av blocker, Shock, and Hyperkalemia. Pulmcrit. Published February 15, 2016. (Link) Accessed August 2018.
4. Sohal S. Syndrome of bradycardia, renal failure, atrioventricular nodal blockers, shock, and hyperkalemia (BRASH syndrome): A new clinical entity?  Chest. 2019;156(4) A74. (Link)
5. Weiss JN, et al. Electrophysiology of Hypokalemia and Hyperkalemia. Circ Arrhythm Electrophysiol. 2017;10(3):e004667. PMID: 28314851