Treatment for Potassium 5.2 mmol/L with Bradycardia
For a patient with potassium 5.2 mmol/L and bradycardia, immediately obtain an ECG and assess for signs of BRASH syndrome (Bradycardia, Renal failure, AV nodal blockers, Shock, Hyperkalemia), as this represents a potentially life-threatening synergistic condition requiring urgent intervention beyond standard hyperkalemia or bradycardia protocols. 1, 2
Immediate Assessment and Risk Stratification
Check for BRASH syndrome components: Verify if the patient is on AV-nodal blocking medications (beta-blockers, calcium channel blockers, digoxin), assess for renal dysfunction, evaluate for shock/hypotension, and determine if altered mental status is present 1, 3, 2
Obtain immediate ECG to identify cardiac conduction abnormalities including junctional rhythm (present in 39% of severe cases), peaked T waves (27%), QRS prolongation (30%), or other signs of hyperkalemic cardiotoxicity 4, 5
Assess hemodynamic stability: Check blood pressure, mental status, and signs of end-organ hypoperfusion, as 32% of patients with severe bradycardia and hyperkalemia require hemodynamic support 4
Evaluate renal function immediately: Check BUN, creatinine, and assess for acute kidney injury, as renal failure is a key component of the synergistic cycle in BRASH syndrome 1, 3, 2
Cardiac Stabilization (Priority #1)
If ECG shows any abnormalities or patient is symptomatic:
Administer intravenous calcium immediately (calcium gluconate or calcium chloride) to stabilize cardiac membranes and combat the deleterious effects of hyperkalemia on the heart 6, 1, 5
Do NOT rely solely on atropine for bradycardia in BRASH syndrome, as it often shows poor response when hyperkalemia and AV-nodal blockers are present 1, 3, 2
Consider epinephrine infusion if bradycardia persists despite initial interventions and patient remains hemodynamically unstable 2
Prepare for temporary transcutaneous pacing if severe bradycardia continues, as 14% of patients with severe bradycardia and hyperkalemia require temporary cardiac pacing 4, 2
Hyperkalemia Management (Priority #2)
Acute potassium-lowering therapies:
Administer insulin-dextrose infusion to shift potassium intracellularly 1, 5
Give beta-agonists (albuterol nebulization) for transcellular potassium shift 1, 5
Initiate sodium zirconium cyclosilicate (10 g three times daily for 48 hours, reducing potassium by 1.1 mmol/L) or patiromer (8.4 g twice daily) for potassium binding 7, 1
Avoid sodium polystyrene sulfonate (Kayexalate) due to risk of intestinal necrosis, ischemic colitis, and high mortality rates, especially in patients with renal dysfunction 7, 8, 5
Medication Management
Immediately review and hold AV-nodal blocking agents (beta-blockers, calcium channel blockers, digoxin) until bradycardia and hyperkalemia resolve 1, 3, 2
If patient is on mineralocorticoid receptor antagonists (MRAs), reduce dose by 50% as potassium is >5.0 mmol/L 7, 9
Discontinue NSAIDs and potassium supplements if present 7, 9
Separate administration of potassium binders by at least 3 hours from other oral medications to prevent binding interactions 8
Renal Support
Initiate fluid resuscitation if hypovolemia is present, as this is the most common precipitant of BRASH syndrome 2
Consider urgent hemodialysis if patient has end-stage renal disease, severe renal impairment with ongoing potassium release, or refractory hyperkalemia despite medical management 1, 4, 5
48% of patients with severe bradycardia and severe hyperkalemia require emergent renal replacement therapy 4
Monitoring Strategy
Admit to intensive care unit for continuous cardiac monitoring, as 66% of patients with this presentation require ICU-level care 4
Recheck potassium within 1-2 hours after initial interventions to assess response 7
Monitor for hypotension requiring vasopressor support, as 32% develop shock requiring dopamine or other hemodynamic support 1, 4
Assess for concomitant critical illness including sepsis, hypothermia, or acidemia, which are associated with need for hemodynamic support 4
Critical Pitfalls to Avoid
Do not treat as isolated bradycardia or isolated hyperkalemia - BRASH syndrome requires recognition of the synergistic pathophysiology where hyperkalemia potentiates AV-nodal blocker effects, causing bradycardia and hypotension, which worsens renal perfusion, further increasing potassium 2
Do not follow standard ACLS bradycardia algorithm alone - management extends beyond atropine to include aggressive hyperkalemia treatment, hemodynamic support, and potentially urgent dialysis 1, 2
Do not assume normal ECG excludes significant risk - ECG findings may not correlate with serum potassium levels, and clinical symptoms should guide urgency of treatment 4, 5
Do not overlook missed dialysis as precipitant in dialysis-dependent patients, as this is a common presenting scenario 4
Target Goals
Maintain potassium ≤5.0 mmol/L as recent evidence suggests this is the upper limit of safety for minimizing mortality risk 7, 9, 10
Restore heart rate to >60 beats/min with hemodynamic stability before considering reintroduction of AV-nodal blockers 1, 3
Optimize renal function to break the synergistic cycle of worsening hyperkalemia and bradycardia 2