BRASH Syndrome
- Faraz Afzal
- Nov 15
- 4 min read
Case Presentation
An 80-year-old man with hypertension and type 2 diabetes was found confused and somnolent at home. On EMS arrival, his blood pressure was 73/46 mmHg and heart rate fluctuated between 25 and 50 beats per minute. The ECG demonstrated a wide-complex bradycardia (rate 26). Atropine had no effect. He received intravenous adrenaline.
On hospital arrival, the patient appeared pale, cold and hypotensive, with clinical signs of pulmonary edema and acute kidney injury. His creatinine was 260 µmol/L with an eGFR of 19 ml/min/1.73 m². Serum potassium ranged from 6.3 to 6.8 mmol/L, accompanied by metabolic acidosis (pH 7.27, bicarbonate 11). He was taking metoprolol extended-release and had a known prolonged PR interval and right bundle branch block. Bedside echocardiography showed mildly reduced LV systolic function and a small LV cavity, consistent with hypovolemia.
He was treated with intravenous calcium gluconate, insulin with glucose, Lokelma and cautious fluid resuscitation. Isoprenaline infusion was started. Due to persistent instability, a temporary pacemaker was inserted. Over time, both heart rate and blood pressure improved, and p waves gradually reappeared on the ECG.
The overall presentation was consistent with BRASH syndrome, defined by Bradycardia, Renal failure, AV-nodal blockade, Shock and Hyperkalemia.
Discussion
BRASH syndrome represents a synergistic interaction between AV-nodal blockade, impaired renal function and hyperkalemia. Patients develop bradycardia and circulatory failure, which further worsen renal perfusion and potassium retention. This self-reinforcing cycle explains why patients with BRASH often present with profound bradycardia that is disproportionately severe relative to the degree of hyperkalemia alone.
In this patient, advanced age, functional decline, suspected dehydration, diabetes and chronic beta-blocker therapy likely contributed. Even moderate hyperkalemia can precipitate marked bradycardia when AV-nodal blocking agents are present.
Pathophysiology
BRASH syndrome occurs when several mechanisms amplify one another. AV-nodal blocking agents such as beta-blockers and non-dihydropyridine calcium channel blockers reduce heart rate and cardiac output. This leads to reduced renal perfusion and a decline in glomerular filtration rate. As GFR falls, both potassium levels and serum concentrations of AV-nodal drugs (which are largely renally cleared) increase.
Hyperkalemia depolarizes the resting membrane potential of cardiomyocytes and inactivates voltage-gated sodium channels. Conduction through the sinus node, AV node and His-Purkinje system slows. This results in bradycardia, AV block and wide-complex rhythms. When combined with AV-nodal blockade, the effect is significantly magnified.
Bradycardia further reduces cardiac output, worsening renal perfusion, which in turn leads to rising potassium levels and accumulation of AV-nodal blocking drugs. This creates a self-perpetuating cycle, explaining why atropine is often ineffective and why correction of electrolytes and hemodynamics is essential.
ECG Changes in Hyperkalemia and the Findings in This Case
Hyperkalemia can produce several characteristic ECG abnormalities, though they may not appear in a predictable sequence and can be difficult to identify in patients with pre-existing conduction disease.
General ECG changes associated with hyperkalemia
• Tall, peaked T waves• Flattening and eventual disappearance of p waves on surface ECG• PR prolongation• Progressive QRS widening• Conduction disturbances such as second-degree AV block (Mobitz II) or complete heart block
In severe cases, this progression may lead to asystole or ventricular fibrillation. Not all abnormalities must be present simultaneously.
ECG findings in this patient
On arrival, the patient demonstrated a wide-complex bradycardia without visible p waves or other atrial activity such as atrial fibrillation waves, indicating absent or severely suppressed atrial depolarization. QRS duration was similar to his baseline ECG.
The most reliable hyperkalemia sign in this case was the presence of tall, peaked T waves, particularly in leads V2 and V3, although such changes may appear in various precordial leads.
Rhythm interpretation after treatment
Following administration of calcium and potassium-lowering therapy, p waves gradually reappeared. This indicates intact sinus node activity and suggests that the absence of p waves on admission was probably due to hyperkalemia-induced suppression of atrial depolarization.
Once p waves re-emerged, the rhythm was consistent with sinus activity with AV block, likely with 2:1 or 3:1 conduction. This explains both the bradycardia and the stable and unchanged QRS configuration.
Why Atropine Does Not Work in Hyperkalemia
Atropine inhibits parasympathetic influence on the sinus and AV nodes and is effective only in vagally mediated bradycardia. In hyperkalemia and BRASH syndrome, the mechanism is fundamentally different: depolarization of the resting membrane potential and inactivation of sodium channels produce a primary conduction abnormality that is not vagally mediated. Atropine therefore has minimal or no effect.
Calcium gluconate or calcium chloride stabilizes the cardiac membrane and counteracts the electrophysiological effects of hyperkalemia. Insulin with glucose, beta-agonists and dialysis reduce serum potassium. Adrenaline and isoprenaline improve chronotropy and dromotropy. Once potassium and perfusion normalize, the rhythm often returns spontaneously without pacing.
Conclusion
BRASH syndrome should be considered in elderly patients on AV-nodal blocking agents who present with bradycardia, hyperkalemia and circulatory failure. Hyperkalemia may cause significant bradycardia even at moderate potassium levels when AV-nodal block is present. ECG findings can be subtle. Early administration of calcium is critical. Unnecessary pacing should be avoided until hyperkalemia and perfusion are corrected.
Comments