Hyperkalemia

Background

• Defined as >5.5 mEq/L
• Potassium secretion is proportional to flow rate and sodium delivery through distal nephron
  • Thus, loop & thiazide diuretics cause hypokalmia
• Most common cause is hemolysis from blood draw (pseudohyperkalemia)

Medication Causes

Alter transmembrane potassium movement

• β blockers
• Digoxin
• Potassium-containing drugs
• Potassium supplements
• Salt substitutes
• Hyperosmolar solutions (mannitol, glucose)
• Suxamethonium
• Intravenous cationic amino acids
• Stored red blood cells (haemolysis releases potassium)
• Herbal medicines (such as alfalfa, dandelion, horsetail, milkweed, and nettle)

Reduce aldosterone secretion

• ACE inhibitors; Angiotensin II receptor blockers
• NSAIDs
• Heparin
• Antifungals (ketoconazole, fluconazole, itraconazole)
• Cyclosporine
• Tacrolimus

Block aldosterone binding to mineralocorticoid receptors

• Spironolactone
• Eplerenone
• Drospirenone
• Potassium sparing diuretics (amiloride, triamterene)
• Trimethoprim
• Pentamidine

Clinical Features

Typically non-specific

• Muscle weakness
• Lethargy, fatigue
• Paresthesias
• Nausea and Vomiting
• Difficulty breathing
• Palpitations, chest pain

Differential Diagnosis

Hyperkalemia

• Pseudohyperkalemia: hemolyzed specimen, prolonged tourniquet use prior to blood draw, thrombocytosis or leukocytosis
• Redistribution (shift from intracellular to extracellular space)
  • Acidemia (see DKA)
  • Cellular breakdown: see Rhabdomyolysis/Crush syndrome, electrical/thermal burn, hemolysis, see Tumor lysis syndrome
• Increased total body potassium
  • Inadequate excretion: Acute/chronic renal failure, Addison's disease, type 4 RTA
  • Drug-induced: potassium-sparing diuretic (spironolactone), angiotensin converting enzyme inhibitors (ACE-I), nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Excessive intake: diet, blood transfusion
• Other causes: succinylcholine, digitalis, beta-blockers

Peaked T-waves

• MI (hyperacute T waves)
• Hyperkalemia
• Benign Early Repolarization
• De Winter's T waves (acute LAD occlusion)

Wide-complex tachycardia

Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)

• Regular
  • Monomorphic ventricular tachycardia
  • PSVT with aberrant conduction:
    • PSVT with bundle branch block^
    • PSVT with accessory pathway
    • Atrial flutter with bundle branch block^
  • Sinus tachycardia with bundle branch block^
  • Accelerated idioventricular rhythm (consider if less than or ~120 bpm)
  • Metabolic
    • Hyperkalemia
    • Digoxin toxicity
    • Severe metabolic acidosis
• Irregular
  • Atrial fibrillation/atrial flutter with variable AV conduction AND bundle branch block^
  • Atrial fibrillation/atrial flutter with variable AV conduction AND accessory pathway (e.g. WPW)
  • Atrial fibrillation + hyperkalemia
  • Polymorphic ventricular tachycardia
    • Torsades de pointes
    • Nonsustained ventricular tachycardia

^Fixed or rate-related

Evaluation

Diagrammatic representation of ECG changes with increasing hyperkalemia

ECG in hyperkalemia with peaked T waves and small P waves

ECG with widened QRS complex and tall broad T waves

ECG showing sine wave pattern

Workup

• ECG
• Chem 10 (including potassium, magnesium, and phosphorus)
  • Consider point-of-care lab testing for more rapid result
• Consider ABG/VBG to evaluate pH

ECG

Changes NOT always predictable and sequential

• 6.5 - 7.5 mEq/L: peaked T waves, prolonged PR interval, shortened QT interval
• 7.5 - 8.0 mEq/L: widened QRS interval, flattened P waves
• 10 - 12 mEq/L: sine wave, ventricular fibrillation, heart block

Diagnosis

• Based on lab testing (>5.5 mEq/L), although ECG may provide earlier information
• Consider pseudohyperkalemia (e.g. from hemolysis)

Management

Stabilize cardiac membranes

Indicated if there are any ECG changes or evidence of arrhythmias. Consider if K >7 mEq/L

• Either one of the following:
  • Calcium gluconate 10mL of 10% solution (1 gram) IV over 5-10 min; in severe cases may start with 3 grams (30 mL), repeat doses up to 9-15 grams total IV (onset 15-30 min, duration 30-60 min) — Only 1/3 elemental calcium vs calcium chloride; can cause hypotension
  • Calcium chloride 1 gram IV over 1-2 min IV (onset 15-30 min, duration 30-60 min) — Extravasation risk: use a good IV; usually given in code situations
• Do serial ECGs to track progress: may need to give multiple doses
• (If given for hyperkalemic cardiac arrest, need to continue resuscitation for at least 30 minutes)
• Use caution in patients taking Digoxin although risk of Stone heart may be unsubstantiated

Shift K+ intracellularly

• Insulin 10 units regular insulin IV with 25-50g of D50 (1-2 ampules) IV (duration 4-6 hours) — May withhold dextrose if blood sugar >300 mg/dL; consider 5 units if glucose <150, AKI/CKD, no DM, weight <60kg, or female
  • • Consider mixing in 10 cc NS syringe to ensure small volume of 10 units insulin fully administered via stopcock
    • Follow glucose levels q30-60 min and supplement dextrose to avoid hypoglycemia (occurs in ~75% of patients)
• Albuterol 15-20 mg nebulized Nebulized (onset 30 min (peak), duration 2 hours) — Response is dose-dependent
• Sodium bicarbonate 3 amps in 1L D5W (isotonic bicarbonate drip) IV drip — Generally not considered unless pH <7.1; pushing ampules of hypertonic bicarb ineffective in RCTs
  • For normovolemic or hypovolemic patients with metabolic acidosis

Remove K+ from body

• Furosemide (Lasix) 40-80 mg IV — Ensure adequate urine output first
  • Decreases potassium by dilution, shifting into muscle cells, and promoting renal excretion via alkalosis
• Kayexalate (SPS) 30 g PO or PR PO/PR — Very controversial; high risk of bowel perforation
  • See: EBQ: Use of Kayexylate in Hyperkalemia
• Lokelma (SZC) 10 g PO TID x48 hours, then 10-15 g PO daily maintenance PO — Similar to Kayexalate but without bowel perforation risk
• Intravenous lactated ringers solution for volume expansion if dehydrated, rhabdomyolysis, diabetic ketoacidosis or other acidosis (avoid NS, causes hyperchloremic acidosis which shifts potassium out of cells increasing level)
  • Consider isotonic bicarbonate if significant acidosis (D5W with 3 amps of bicarb per liter)
• Hydrocortisone if suspicious for adrenal insufficiency
• Definitive treatment is hemodialysis

IV Fluid Choice

• LR is preferred over NS, even in renal failure
• The small amount of 4 mEq/L of potassium in lactated ringers does not contribute to worsening hyperkalemia
• Hyperkalemia worsens with metabolic acidosis, and large volume normal saline administration increases risk of hyperchloremic non-anion gap metabolic acidosis

Disposition

• Consideration for ICU for frequent electrolyte checks and close cardiac monitoring

See Also

• Electrolyte abnormalities
• Acute kidney injury
• Hemodialysis/Hemoperfusion
• Crush syndrome

External Links

• ECG Weekly -Hyperkalemia