Case Based Learning for September 2025

A 68-year-old female presented to the ED with chest pain and shortness of breath. Her medical history was significant for hypertension, diabetes, and ESRD on dialysis for one year. She has been compliant with dialysis. Workup in the ED was significant for a junctional bradycardia in the 30s and a systolic blood pressure in the 60s. Lab work was significant for a glucose of 194, a potassium of 5.8, and a creatinine of 8.04 with a calculated GFR of 5.

She was given 1mg atropine, which was ineffective. She was then started on an epinephrine infusion with minimal response. Transcutaneous pacing was initiated, and she was given pain control and sedation as her blood pressure tolerated. A tertiary care center was contacted and after an extended wait she was transferred. At the receiving hospital she was taken to the cath lab. No significant disease was noted, and a temporary venous pacemaker was placed. As her hyperkalemia was corrected and her Carvedilol wore off the pacemaker was discontinued. She was discharged home in good condition two days later.

BRASH syndrome is an acronym for Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalemia. BRASH syndrome is a synergistic process created by a combination of hyperkalemia and medications blocking the atrioventricular (AV) node. The most common precipitants are hypovolemia and medications promoting hyperkalemia or renal injury. Often referred to as a vicious cycle, standard ACLS treatments may prove ineffective, as in this case.

Bradycardia reduces the cardiac output; impairs renal perfusion; precipitates renal dysfunction; and exacerbates hyperkalemia. Left unchecked, the vicious cycle of hyperkalemia, bradycardia, renal dysfunction, and worsening hyperkalemia may progress to multiorgan failure with shock, bradycardia, and renal failure. The most common error in managing BRASH syndrome is fixating on a single component of the syndrome (e.g., hyperkalemia) and focusing solely on management of that problem (e.g., emergent dialysis). Meanwhile, other aspects of the syndrome are overlooked (e.g., the patient might remain under-resuscitated, bradycardic, and malperfused).

The goal of treatment is to treat hyperkalemia, bradycardia, hypovolemia (if present), and renal hypoperfusion. Aggressively manage moderate to severe hyperkalemia; stabilizes the myocardium, which may improve heart rate and cardiac output. A patient with BRASH syndrome may be volume depleted, address with isotonic crystalloid resuscitation. (Note: some patients with BRASH syndrome may develop oliguric renal failure, fluid retention and volume overload. Assess fluid status on an individual basis) Give potassium-wasting diuretics such as frusemide to increase potassium excretion. If the patient is anuric, consider dialysis. If calcium, albuterol, and fluid fail to resolve the bradycardia, epinephrine administration can increase heart rate and cardiac output and renal perfusion and shift potassium intracellularly, improving hyperkalemia. The kidneys need to be perfused to excrete AV blocking drugs and potassium. If the patient is euvolemic but still in shock, then do not hesitate to start an inotrope such as epinephrine for its chronotropic and vasoconstricting properties. Don’t forget that these patients are usually on these drugs to treat their hypertension and will likely have a higher baseline blood pressure than the general population.

https://www.jem-journal.com/action/showPdf?pii=S0736-4679%2820%2930399-1

Written by Joshua Corsa, M.D.

ERx Clinical Partners Medical Director, Three Rivers Hospital, Brewster, WA

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This is for informational purposes only. For medical advice or diagnosis, consult a physician.

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