It’s 3 a.m. on an overnight shift and the resuscitation room nurse runs over, “Hey doc, the patient in R3 is bradycardic and now his blood pressure is dropping”. You rush in, begin thinking through which medications to give and place pads on the patient. Luckily, he begins to stabilize with vasopressors and pacing. You review his labs again; he has worsening renal function and he’s mildly hyperkalemic to 5.7. He has metoprolol on his medication list but denies taking more than prescribed. So what’s actually going on?

Today we will discuss BRASH syndrome, which stands for Bradycardia, Renal failure, AV Blockade, Shock and Hyperkalemia.

Overview of BRASH

BRASH occurs when patients taking AV nodal blocking agents (e.g. Ca channel blockers, Beta blockers), encounter an insult to their renal function which causes a rise in potassium. The decreased renal function can then impair clearance of the AV nodal blocking agents, worsening bradycardia. The worsened bradycardia then perpetuates this vicious cycle by decreasing renal perfusion, which in turn worsens hyperkalemia and bradycardia. See the helpful graphic below:

**Source:** https://litfl.com/brash-syndrome/

A few clinical distinctions…

It is important to see this syndrome as separate from a couple other related disorders. First, this is distinct from AV nodal blockade overdose, as patients are taking their nodal blocking agents as prescribed, below toxic doses.

Secondly, it is distinct from pure hyperkalemia induced bradycardia for multiple reasons. BRASH typically occurs at lower levels of potassium (less than 7mEq/L) and often does not have the other hallmark findings of hyperkalemia on EKG (Peaked T waves, widened QRS etc). Therefore, these patients often will not respond as robustly to calcium. Though marked hyperkalemia is possible in BRASH in more severe cases.

Management

Truthfully, most ED Physicians have likely successfully and thoroughly resuscitated patients with BRASH without identifying the underlying clinical syndrome. The diagnosis is not necessarily critical to knowing steps in management. The treatment of hyperkalemia, bradycardia, shock and renal dysfunction is not unique to BRASH, however, recognizing the underlying cycle may help treat each aspect of the syndrome without fixating solely on just hyperkalemia or bradycardia in isolation, while missing the other components we can successfully address as well.

Bradycardia. For patients symptomatically bradycardic, consider calcium or push dose epinephrine while readying the patient for pacing. You could consider atropine as well though this likely will only help temporarily if at all. Starting a continuous vasopressor likely will help counteract the AV nodal blockade in these patients as well and will be more easily tolerated than temporary pacing. (See below for a video on transvenous pacing for a refresher)

Hyperkalemia. Consider calcium even in patients with moderate hyperkalemia and bradycardia without other EKG changes to assess for improvement. Otherwise review Dr. Frendo’s cheese from last week for the finer points of managing hyperkalemia.

AV Nodal Blockade. The most important step here arguably may be identifying which medications your patients are taking on arrival that could be contributing to this cycle (AV nodal agents, medicines that worsen renal function or cause hyperkalemia). Obviously then avoid those medications, as well as further nephrotoxic agents. Though this syndrome is distinct from beta blocker/Ca channel blocker overdose, severe cases refractory to initial management may benefit from trialing other therapies such as high dose insulin, glucagon or lipid emulsion.

Shock. We all know how to manage shock, though in this situation, if your patient can handle volume, fluid resuscitation should be prioritized to address possible underlying trigger if hypovolemia is suspected to have contributed to the initial renal insult the incited BRASH. Otherwise, often these patients will respond nicely to epinephrine/vasopressors given the opposition it provides to the AV nodal blockade.

Summary

Think of this syndrome next time you see a hypotensive bradycardic patient with an AKI on an AV nodal blocker. It may not drastically change your management but may help you see the pathophysiology more holistically and allow you to identify underlying triggers.

Returning back to our patient in R3, he required transcutaneous pacing and vasopressors in the ED, was admitted to the MICU under the presumptive diagnosis of BRASH. They continued hyperkalemia treatment and was eventually initiated on high dose insulin. He eventually stabilized and was discharged home.

Authored by Kathryn McGregor, MD and Eric Leser, MD.

FOAMed Resources:

EMRAP Transvenous Pacing: https://www.emrap.org/episode/stabbedwitha/transvenous
EMRAP BRASH Overview: https://www.emrap.org/corependium/chapter/recSdHpVvdD2oAbVe/Bradydysrhythmias
EM Crit: https://emcrit.org/ibcc/brash/

References:

Cassidy T, Cadogan M, Cadogan TC and M. Brash syndrome. Life in the Fast Lane • LITFL. April 14, 2021. Accessed June 6, 2025. https://litfl.com/brash-syndrome/.
Farkas JD, Long B, Koyfman A, Menson K. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia. J Emerg Med. 2020;59(2):216-223. doi:10.1016/j.jemermed.2020.05.001

A 74-year-old female with a past medical history of hypertension, diabetes, hyperlipidemia, and tobacco use disorder presents with chest discomfort and indigestion ongoing for the past 2 weeks. She reports radiation to the jaw and left upper extremity. Recently, she has been feeling short of breath and has experienced some exercise intolerance, limiting her mobility to just half a block, which she partially attributes to her osteoarthritis. She has been compliant with her home medications, which include antihypertensives, metformin, and a statin. On presentation at rest, her pain is less than it has been in the last couple weeks but is still present. An ECG is obtained (Figure 1).

Lucas Ferreira, MD and Ari Edelheit, MD

the County Consult