In an older adult with chronic kidney disease on an atrioventricular‑nodal blocking medication who presents with profound bradycardia, hypotension/shock, and hyperkalaemia, what is BRASH syndrome and how should it be managed?

BRASH Syndrome: Definition and Management

What is BRASH Syndrome?

BRASH syndrome is a life-threatening synergistic condition where bradycardia, renal failure, AV-nodal blocking medications, shock, and hyperkalemia create a self-perpetuating cycle of cardiovascular collapse that requires immediate recognition and aggressive intervention. 1, 2

The syndrome occurs when:

• Renal dysfunction (acute or chronic) leads to hyperkalemia 3
• Hyperkalemia directly depresses cardiac conduction, causing bradycardia 4
• AV-nodal blocking medications (beta-blockers, calcium channel blockers) synergistically worsen the bradycardia beyond what either factor would cause alone 1, 5
• Bradycardia reduces cardiac output, causing hypotension/shock 2
• Hypotension further worsens renal perfusion, perpetuating the cycle 4

This is not simple drug toxicity—the drug levels are typically therapeutic, but the combination with hyperkalemia and renal dysfunction creates a synergistic effect 5.

Clinical Presentation

Look for this specific constellation in older adults:

• Profound bradycardia (often <40 bpm, may present with complete heart block or junctional rhythm) 1, 3
• Hypotension/shock (systolic BP often <90 mmHg) 2, 3
• Altered mental status (from decreased cerebral perfusion) 2
• Oliguria or anuria (from decreased renal perfusion) 1
• History of chronic AV-nodal blocker use (beta-blockers like atenolol, metoprolol, carvedilol; or calcium channel blockers like diltiazem, verapamil) 6
• Precipitating factors: dehydration, infection (especially UTI), nephrotoxic medications, or any cause of acute kidney injury 2, 4

Immediate Management Algorithm

Step 1: Recognize the Syndrome and Stop the Cycle

• Immediately discontinue all AV-nodal blocking agents (beta-blockers, calcium channel blockers, digoxin) 1, 3
• Do NOT give atropine as first-line therapy—it is typically ineffective because the bradycardia is not purely vagal 1, 3

Step 2: Treat Hyperkalemia Aggressively

• Calcium gluconate 1-2 grams IV immediately to stabilize cardiac membranes 3
• Insulin 10 units IV with 50% dextrose (25-50 grams) to shift potassium intracellularly 1, 3
• Consider sodium bicarbonate if metabolic acidosis present 4
• Avoid potassium-binding resins initially—they work too slowly for acute management 4

Step 3: Increase Cardiac Output and Renal Perfusion

The key therapeutic goal is breaking the cycle by increasing cardiac output, which improves renal perfusion and potassium clearance. 4, 5

• First-line: Isoproterenol infusion (beta-agonist that increases heart rate and cardiac output) 1

  • Start at 2-10 mcg/min IV, titrate to heart rate >50-60 bpm
  • This directly counteracts both the AV-nodal blockade and hyperkalemia effects 1

• Alternative: Epinephrine or dopamine infusion if isoproterenol unavailable 3

  • Epinephrine: 2-10 mcg/min IV
  • Dopamine: 5-20 mcg/kg/min IV 3

• Cautious IV fluid resuscitation if hypovolemia suspected 2, 4

  • Use guided approach—avoid fluid overload in patients with heart failure 2

Step 4: Consider Temporary Pacing

• Transcutaneous pacing if severe bradycardia persists despite medical management 3
• Transvenous pacing may be needed if prolonged support required, but often unnecessary if medical management is prompt 2, 4

Step 5: Renal Replacement Therapy

• Hemodialysis or CRRT if hyperkalemia refractory to medical management or severe renal failure 4
• This is rarely needed if cardiac output is restored quickly 4

Critical Pitfalls to Avoid

Do not mistake BRASH syndrome for pure drug toxicity—the drug levels are usually therapeutic, and standard overdose treatments (like glucagon for beta-blocker toxicity) are less effective 5. The key is recognizing the synergistic interaction with hyperkalemia and renal dysfunction 1, 5.

Do not rely on atropine—multiple case reports show atropine failure in BRASH syndrome because the bradycardia is not vagally mediated 1, 3. Proceed directly to catecholamine infusion 1.

Do not give IV fluids indiscriminately—many of these patients have heart failure and limited cardiac reserve 1, 2. Fluid resuscitation should be guided by clinical assessment of volume status 2.

Do not restart AV-nodal blockers too quickly—wait until renal function improves and potassium normalizes 1, 2. If these medications are essential (e.g., for heart failure), restart at much lower doses with close monitoring 2.

Monitoring and Disposition

• Continuous cardiac monitoring until heart rate stabilizes >50-60 bpm 1
• Serial potassium levels every 2-4 hours until <5.0 mEq/L 3
• Serial renal function to assess recovery 4
• ICU admission is mandatory for all suspected BRASH cases 1, 3

Prevention in High-Risk Patients

Identify patients at risk:

• Older adults with CKD (especially GFR <45 mL/min) on AV-nodal blockers 6
• Patients on multiple medications that affect potassium (ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs) 2
• Patients with heart failure on beta-blockers or calcium channel blockers 6

The ACC/AHA guidelines specifically warn about using beta-blockers and calcium channel blockers in patients with renal dysfunction and recommend dose reduction 6. These precautions exist precisely because of syndromes like BRASH 7, 8.