Hyperkalemia

Background

• Serum potassium >5.0 mEq/L (some define >5.5 mEq/L)
• Life-threatening when >6.5 mEq/L or with ECG changes
• Most common electrolyte disorder causing cardiac arrest
• Potassium homeostasis:
  • 98% intracellular (maintained by Na/K-ATPase)
  • Renal excretion is primary mechanism of potassium regulation

Causes

• Decreased excretion (most common mechanism):
  • Acute kidney injury / chronic kidney disease
  • Medications: ACE inhibitors, ARBs, K-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin
  • Adrenal insufficiency (hypoaldosteronism)
  • Type 4 renal tubular acidosis
• Transcellular shift (K moves out of cells):
  • Acidosis (metabolic acidosis shifts K extracellularly)
  • Insulin deficiency / DKA
  • Tissue destruction: rhabdomyolysis, tumor lysis, hemolysis, burns
  • Succinylcholine, beta-blockers, digitalis toxicity
  • Hyperkalemic periodic paralysis
• Increased intake: excessive supplementation, salt substitutes (KCl)
• Pseudohyperkalemia: hemolyzed sample, prolonged tourniquet, thrombocytosis, leukocytosis
  • Always repeat level if unexpected

Clinical Features

• Often asymptomatic until severe
• Muscle weakness, fatigue, paresthesias
• Ascending paralysis (may mimic Guillain-Barre)
• Cardiac dysrhythmias (most dangerous manifestation)
• Nausea, vomiting, diarrhea

ECG Changes (Progressive)

• Peaked T waves (earliest change, typically >5.5 mEq/L)
• Prolonged PR interval
• Widened QRS
• Loss of P waves
• Sine wave pattern (pre-arrest)
• Ventricular fibrillation / asystole
• ECG changes do NOT reliably correlate with K level — some patients arrest without warning

Differential Diagnosis

• Pseudohyperkalemia (hemolyzed specimen)
• Acute kidney injury / chronic kidney disease
• DKA
• Rhabdomyolysis
• Tumor lysis syndrome
• Adrenal insufficiency
• Medication effect

Evaluation

• Stat ECG (most urgent — look for peaked T's, widened QRS)
• BMP: potassium level, creatinine (renal function), glucose, bicarbonate
• Repeat K level if unexpected (rule out pseudohyperkalemia)
• VBG/ABG (acidosis evaluation)
• Digoxin level if on digoxin (hyperkalemia potentiates digitalis toxicity)
• Urinalysis (myoglobinuria if rhabdomyolysis)
• Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)

Management

Step 1: Cardiac Membrane Stabilization

• Calcium (does NOT lower K; protects myocardium from arrhythmia):
  • Calcium gluconate 10%: 10-20 mL IV over 2-3 minutes (preferred; less tissue necrosis if extravasates)
  • Calcium chloride 10%: 5-10 mL IV (via central line preferred; 3x more elemental calcium)
  • Onset: 1-3 minutes; duration 30-60 minutes; may repeat in 5-10 min if ECG unchanged
  • Give immediately if ECG changes present or K >6.5
• Caution in digoxin toxicity: calcium may worsen toxicity → use cautiously or consider digibind first

Step 2: Shift Potassium Intracellularly

• Insulin + Glucose (most reliable):
  • Regular insulin 10 units IV + D50W 25g (50 mL) IV
  • Onset: 15-30 min; duration 4-6 hours; lowers K by 0.5-1.2 mEq/L
  • Monitor glucose q30min x 4h (hypoglycemia occurs in up to 20%)
  • Give D50 before or simultaneously with insulin
• Albuterol (nebulized):
  • 10-20 mg nebulized (4-8x standard asthma dose)
  • Onset: 15-30 min; lowers K by 0.5-1.5 mEq/L
  • Additive with insulin; 40% of patients are non-responders
• Sodium bicarbonate:
  • 50-100 mEq IV over 5-10 minutes
  • Minimal effect as monotherapy; useful in setting of severe metabolic acidosis
  • Do NOT rely on bicarb alone to lower potassium

Step 3: Remove Potassium from Body

• Loop diuretics (furosemide 40-80 mg IV): if adequate renal function
• Sodium polystyrene sulfonate (Kayexalate) 15-30g PO:
  • Delayed onset (hours); controversial efficacy; risk of bowel necrosis
  • Not recommended as acute treatment
• Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma):
  • Newer potassium binders; better tolerated than Kayexalate
  • Lokelma 10g PO may lower K within 1 hour
• Hemodialysis (most effective method of K removal):
  • Indicated for: refractory hyperkalemia, severe renal failure, K >7 despite medical therapy

Cardiac Arrest from Hyperkalemia

• Standard ACLS + calcium 10-20 mL IV push
• Insulin + glucose + bicarb + albuterol simultaneously
• Avoid succinylcholine for intubation
• Consider emergent dialysis

Disposition

• Admit if K >6.0, ECG changes, renal failure, or ongoing cause
• ICU if severe (>7.0), ECG changes, or refractory to treatment
• Continuous telemetry for all admitted patients
• Consider discharge if mild hyperkalemia (5.0-5.5), known chronic cause, normal ECG, correctable precipitant

See Also

• Hypokalemia
• Acute kidney injury
• Diabetic ketoacidosis
• Rhabdomyolysis
• Cardiac arrest
• Digoxin toxicity

References

• Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system. N Engl J Med. 2004;351(6):585-592. PMID 15295051
• Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251. PMID 18936701
• Montford JR, Linas S. How dangerous is hyperkalemia? J Am Soc Nephrol. 2017;28(11):3155-3165. PMID 28778861
• Long B, et al. An emergency medicine approach to hyperkalemia. Am J Emerg Med. 2018;36(5):918-921. PMID 29548654