B.R.A.S.H Syndrome

Bradycardia, Renal Failure, AV Nodal Blockade, Shock, and Hyperkalemia

This infographic provides a comprehensive look at B.R.A.S.H syndrome, a critical condition resulting from the interaction of AV nodal blockade, hyperkalemia, and renal failure, leading to bradycardia and shock.

Differential Diagnosis

• B.R.A.S.H results from the combined effects of AV nodal blockers and renal failure, contributing to hyperkalemia and bradycardia.
• Hyperkalemia can independently cause bradycardia; ECG findings typically show peaked T waves and flattened P waves.
• AV Nodal Blocker Toxicity may also mimic B.R.A.S.H, often triggered by infections, new medications, or electrolyte imbalances.

Etiology

• Contributing factors include medications like beta-blockers, calcium-channel blockers, ACE inhibitors, and diuretics.
• Renal failure leads to reduced excretion of medications and potassium, exacerbating the condition.

Pathophysiology

• Reduced renal function impairs the clearance of AV nodal blockers, causing bradycardia and worsening hyperkalemia.
• This creates a vicious cycle, with shock lowering cardiac output (CO) and renal blood flow, further decreasing GFR and increasing potassium levels.

Presentation

• Patients often present with bradycardia, recent GI illness, dehydration, and multiorgan failure.
• ECG changes include peaked T waves and prolonged PR intervals.

Management Considerations

• Hyperkalemia: Treat with IV calcium, albuterol, insulin, and dextrose to promote intracellular potassium shift.
• Bradycardia and Hypotension: Use epinephrine or isoproterenol; consider temporary pacing if needed.
• Hemodialysis: Indicated in severe cases of hyperkalemia.
• Fluid resuscitation: Use balanced crystalloids if non-anion gap metabolic acidosis is absent.
• For beta-blocker toxicity, consider lipid emulsion therapy; administer digoxin-specific antibody fragments in cases of digoxin toxicity.

Created by Dr. Chelsea Amo-Tweneboah
Reviewed by Dr. Rawan Amir and Dr. Jessie Holtzman

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