What is the emergency management of BRASH syndrome in an older patient on beta‑blockers or non‑dihydropyridine calcium‑channel blockers who develops acute kidney injury, hyperkalaemia, bradycardia and hypotension?

Emergency Management of BRASH Syndrome

In an older patient presenting with BRASH syndrome, immediately discontinue all AV-nodal blocking agents (beta-blockers and non-dihydropyridine calcium channel blockers), aggressively treat hyperkalemia with IV calcium gluconate followed by insulin/glucose and beta-agonists, provide fluid resuscitation for renal hypoperfusion, and use epinephrine infusion (not atropine) for persistent bradycardia with hemodynamic instability. 1

Understanding the Pathophysiology

BRASH syndrome represents a vicious cycle where hyperkalemia and AV-nodal blocking medications synergistically cause profound bradycardia, leading to shock, renal hypoperfusion, worsening kidney injury, further hyperkalemia, and increased drug effects—creating a self-perpetuating spiral toward multiorgan failure. 1, 2 The syndrome is most commonly precipitated by hypovolemia, nephrotoxic insults (NSAIDs, contrast), urinary tract infections, or medications promoting hyperkalemia in older patients with limited renal reserve. 3, 1

Immediate Recognition and Diagnosis

Look for the specific constellation of:

• Bradycardia (often profound, <40 bpm, may present as complete heart block) 4
• Renal dysfunction (elevated creatinine, BUN, decreased urine output) 5, 4
• Current use of beta-blockers (metoprolol, atenolol, carvedilol) or non-dihydropyridine calcium channel blockers (diltiazem, verapamil) 6
• Hypotension/shock (systolic BP <90 mmHg) 5, 4
• Hyperkalemia (typically K+ >5.0-6.0 mEq/L) 4, 1
• Associated symptoms: syncope, altered mental status, oliguria, fatigue 5, 4, 3

Critical pitfall: Do not attribute bradycardia solely to hyperkalemia or drug overdose—BRASH is a distinct entity requiring different management than either condition alone. 1

Step-by-Step Emergency Treatment Algorithm

Step 1: Discontinue Offending Medications Immediately

• Stop all AV-nodal blocking agents (beta-blockers, diltiazem, verapamil) 2, 1
• Discontinue ACE inhibitors, ARBs, and potassium-sparing diuretics 3
• Hold digoxin if prescribed 6

Step 2: Treat Hyperkalemia Aggressively (Do Not Wait for Labs)

Immediate membrane stabilization:

• Calcium gluconate 1-2 grams IV over 2-5 minutes (or calcium chloride 0.5-1 gram if central access available) 4, 1
• This does not lower potassium but protects the myocardium from arrhythmias 1

Shift potassium intracellularly:

• Regular insulin 10 units IV with 50% dextrose (25-50 grams) 4, 1
• Nebulized albuterol 10-20 mg (beta-agonist therapy) 1
• Consider sodium bicarbonate if concurrent metabolic acidosis 1

Remove potassium from body:

• Loop diuretics (furosemide 40-80 mg IV) if adequate renal function and volume status permits 1
• Prepare for emergent hemodialysis if K+ >7.0 mEq/L or refractory to medical management 1

Step 3: Fluid Resuscitation for Renal Hypoperfusion

• Administer IV crystalloid boluses (500-1000 mL normal saline or lactated Ringer's) to restore renal perfusion and reverse prerenal azotemia 3, 2, 1
• Monitor for fluid overload in patients with heart failure 5
• The goal is to break the cycle of renal hypoperfusion worsening hyperkalemia 2

Step 4: Manage Bradycardia and Hypotension

Atropine is typically ineffective in BRASH syndrome because the bradycardia is not vagally mediated but due to direct AV-nodal blockade plus hyperkalemia. 5, 4, 1

For persistent symptomatic bradycardia with hypotension:

• Epinephrine infusion 2-10 mcg/min (first-line chronotropic agent) 1
• Alternative: Isoproterenol infusion (beta-agonist) if epinephrine unavailable 5
• Dopamine 5-20 mcg/kg/min can be used for combined inotropic and chronotropic support 4

Advanced therapies if refractory:

• High-dose insulin infusion (1 unit/kg bolus, then 0.5-1 unit/kg/hour with dextrose) for calcium channel blocker toxicity component 1
• Glucagon 3-5 mg IV bolus, then 3-5 mg/hour infusion for beta-blocker toxicity component 1
• Lipid emulsion therapy (20% intralipid 1.5 mL/kg bolus, then 0.25 mL/kg/min infusion) for severe lipophilic drug toxicity 1

Avoid temporary pacing initially—most patients respond to medical management within 12-24 hours, and pacing may be unnecessary if the underlying cycle is interrupted. 3, 1

Critical Monitoring Parameters

• Continuous cardiac monitoring for rhythm changes 5
• Serial potassium levels every 2-4 hours until normalized 1
• Renal function (creatinine, BUN) every 6-12 hours 4
• Urine output hourly 5
• Blood pressure continuously or every 15 minutes 5
• Mental status for signs of hypoperfusion 3

Special Considerations in Older Patients

Elderly patients are particularly vulnerable to BRASH syndrome due to:

• Reduced renal reserve making them susceptible to acute kidney injury from minor insults 6
• Polypharmacy increasing risk of drug interactions 6, 7
• Delayed drug elimination of beta-blockers and calcium channel blockers 6
• Increased susceptibility to hyperkalemia when combining ACE inhibitors/ARBs with potassium-sparing diuretics 6
• Blunted baroreceptor response worsening hypotension 6

Common Pitfalls to Avoid

1. Attributing bradycardia to isolated hyperkalemia: ECG may show normal QT interval and T waves without classic hyperkalemic changes (peaked T waves, widened QRS), yet profound bradycardia persists due to synergistic drug effects. 4, 1

2. Relying on atropine: Atropine is ineffective because the mechanism is not vagal but direct AV-nodal blockade plus hyperkalemia. 5, 4, 1

3. Rushing to temporary pacemaker placement: Most patients improve with medical management within 24 hours; pacing should be reserved for truly refractory cases. 3, 1

4. Inadequate fluid resuscitation: Hypovolemia is often the precipitant—aggressive fluid therapy breaks the cycle of renal hypoperfusion. 3, 2, 1

5. Continuing AV-nodal blockers: Even low-dose beta-blockers or calcium channel blockers must be discontinued immediately. 2, 1

6. Overlooking concurrent medications: NSAIDs, ACE inhibitors, ARBs, and potassium-sparing diuretics all contribute to the syndrome and must be held. 6, 3

Expected Clinical Course

With appropriate treatment, patients typically show:

• Improvement in heart rate within 12-24 hours as hyperkalemia corrects and drug effects wane 5, 3
• Gradual recovery of renal function over 2-5 days with fluid resuscitation 3
• Resolution of hypotension as bradycardia improves and cardiac output increases 1

Mortality risk is significant (cases report cardiac arrest and death) if the syndrome is not recognized early and the vicious cycle is not interrupted. 4, 1

Disposition and Follow-Up

• ICU admission is mandatory for continuous monitoring and vasopressor/chronotropic support 5, 4
• Medication reconciliation before discharge to prevent recurrence 3
• Nephrology consultation if renal function does not improve or dialysis is needed 1
• Cardiology consultation for evaluation of permanent pacing only if bradycardia persists after syndrome resolution 1