Published: 5 June 2025

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Hyperkalaemia or BRASH syndrome?

Published: 5 June 2025
Prescriber Update 46(2): 32–33
June 2025

  • Patients with BRASH syndrome may present with a range of symptoms from asymptomatic bradycardia to multiorgan failure. The main differential diagnosis to consider is isolated hyperkalaemia.
  • BRASH syndrome involves the synergistic effects of atrioventricular (AV) node blockers with hyperkalaemia, causing profound bradycardia.
  • Triggers include hypovolaemia due to illness and starting or increasing the dose of medicines such as AV blockers. Medicines that cause acute kidney injury, hyperkalaemia or reduced cardiac output may also contribute to the development of BRASH syndrome.


The New Zealand Pharmacovigilance database recently received a case report of BRASH syndrome in a patient taking propranolol and diltiazem. As this was the first report of BRASH syndrome, we have included this article to explain the symptoms and encourage reporting of any further cases.

What is BRASH syndrome?1

BRASH syndrome is an increasingly recognised clinical entity. The acronym describes the signs of this syndrome: bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock and hyperkalaemia.

In BRASH syndrome, the synergistic effects of AV node blockers with hyperkalaemia result in profound bradycardia that is greater than expected from either factor alone. A reduced cardiac output leads to worsening renal dysfunction that exacerbates the hyperkalaemia, creating a vicious cycle that can progress to multiorgan failure.

Triggers include hypovolaemia due to illness and starting or increasing the dose of medicines such as AV blockers. Older people with underlying cardiac or renal impairment, especially those taking multiple AV blockers, are at greater risk.

Clinical presentation and evaluation

Patients with BRASH syndrome may present with a range of symptoms from asymptomatic bradycardia to multiorgan failure. The main differential diagnosis to consider is isolated hyperkalaemia.

In patients with isolated hyperkalaemia, bradycardia generally results from severe hyperkalaemia. However in BRASH syndrome, bradycardia often occurs with moderate hyperkalaemia. In addition, an electrocardiogram (ECG) may show bradycardia without other features of hyperkalaemia.

Similarly, in patients experiencing BRASH syndrome, the bradycardia is not explained by supratherapeutic levels of AV node blockers. Patients are generally taking their medicines at the correct dose.

Healthcare professionals should consider BRASH syndrome in patients taking AV blocking medicines who present with signs of bradycardia and/or hyperkalaemia, even if they seem relatively well.

Which medicines are associated with BRASH syndrome?

Calcium channel blockers and beta-blockers depress AV node conduction and are most often associated with BRASH syndrome. Renally-cleared beta-blockers may increase the risk, as accumulation can occur as renal function worsens.1

Other medicines that are associated with precipitating factors such as acute kidney injury, hyperkalaemia or reduced cardiac output may also contribute to the development of BRASH syndrome. Examples include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), spironolactone, digoxin and amiodarone.1,2

References

  1. Farkas JD, Long B, Koyfman A, et al. 2020. BRASH syndrome: bradycardia, renal Failure, AV blockade, shock, and hyperkalemia. Journal of Emergency Medicine 59(2): 216-23. DOI: 10.1016/j.jemermed.2020.05.001 (accessed 28 March 2025).
  2. Shah P, Gozun M, Keitoku K, et al. 2022. Clinical characteristics of BRASH syndrome: systematic scoping review. European Journal of Internal Medicine 103: 57-61. DOI: 10.1016/j.ejim.2022.06.002 (accessed 28 March 2025).
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