Hyperkalemia: Difference between revisions
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(Convert medication dosing to MedicationDose templates for SMW integration (8 medications: calcium gluconate, calcium chloride, insulin, albuterol, sodium bicarbonate, furosemide, kayexalate, lokelma)) |
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''Indicated if there are any ECG changes or evidence of arrhythmias. Consider if K >7 mEq/L'' | ''Indicated if there are any ECG changes or evidence of arrhythmias. Consider if K >7 mEq/L'' | ||
*Either one of the following: | *Either one of the following: | ||
**{{MedicationDose|drug=Calcium gluconate|dose= | **{{MedicationDose|drug=Calcium gluconate|dose=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|route=IV|context=Cardiac membrane stabilization (preferred)|indication=Hyperkalemia|onset=15-30 min|duration=30-60 min|notes=Only 1/3 elemental calcium vs calcium chloride; can cause hypotension}} | ||
**{{MedicationDose|drug=Calcium chloride|dose=1 gram IV over 1-2 min|route=IV|context=Cardiac membrane stabilization (code situations)|indication=Hyperkalemia|onset=15-30 min|duration=30-60 min|notes=Extravasation risk: use a good IV; usually given in code situations}} | |||
*Do serial [[ECG]]s 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 [[Digitalis Toxicity|Digoxin]] although risk of [[Stone heart]] may be unsubstantiated <ref>Erickson CP, Olson KR. Case files of the medical toxicology fellowship of the California poison control system-San Francisco: calcium plus digoxin-more taboo than toxic? J Med Toxicol. 2008 Mar;4(1):33-9</ref> | *Use caution in patients taking [[Digitalis Toxicity|Digoxin]] although risk of [[Stone heart]] may be unsubstantiated <ref>Erickson CP, Olson KR. Case files of the medical toxicology fellowship of the California poison control system-San Francisco: calcium plus digoxin-more taboo than toxic? J Med Toxicol. 2008 Mar;4(1):33-9</ref> | ||
===Shift K+ intracellularly=== | ===Shift K+ intracellularly=== | ||
*{{MedicationDose|drug=Insulin|dose=10 units regular insulin IV with 25-50g of D50 (1-2 ampules)|route=IV|context=Potassium shifting|indication=Hyperkalemia|duration=4-6 hours|notes=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<ref>Sterns R, Grieff M, Bernstein P (2016). Treatment of hyperkalemia: Something old, something new. Kidney International, 89(3), 546-554.</ref> | |||
***Follow glucose levels q30-60 min and supplement dextrose to avoid hypoglycemia (occurs in ~75% of patients)<ref> Apel J, Reutrakul S, Baldwin D. Hypoglycemia in the Treatment of Hyperkalemia With Insulin in Patients With End-Stage Renal Disease. Clin Kidney J. 2014;7(3):248-250</ref> | |||
*{{MedicationDose|drug=Albuterol|dose=15-20 mg nebulized|route=Nebulized|context=Potassium shifting|indication=Hyperkalemia|onset=30 min (peak)|duration=2 hours|notes=Response is dose-dependent}} | |||
***Consider mixing in 10 cc NS syringe to ensure small volume of 10 units insulin fully administered via | *{{MedicationDose|drug=Sodium bicarbonate|dose=3 amps in 1L D5W (isotonic bicarbonate drip)|route=IV drip|context=Potassium shifting (if metabolic acidosis)|indication=Hyperkalemia|notes=Generally not considered unless pH <7.1; pushing ampules of hypertonic bicarb ineffective in RCTs}} | ||
**For '''normovolemic or hypovolemic''' patients with '''metabolic acidosis''' | |||
*** | |||
* | |||
* | |||
**For '''normovolemic or hypovolemic''' patients with '''metabolic acidosis''' | |||
===Remove K+ from body=== | ===Remove K+ from body=== | ||
* | *{{MedicationDose|drug=Furosemide|dose=40-80 mg IV|route=IV|context=Potassium elimination|indication=Hyperkalemia|display=Furosemide (Lasix)|notes=Ensure adequate urine output first}} | ||
**Decreases potassium by dilution, shifting into muscle cells, and promoting renal excretion via alkalosis<ref>[https://emcrit.org/ibcc/hyperkalemia/ IBCC Hyperkalemia Chapter]</ref> | |||
**Decreases | *{{MedicationDose|drug=Sodium polystyrene sulfonate|dose=30 g PO or PR|route=PO/PR|context=Potassium binding|indication=Hyperkalemia|display=Kayexalate (SPS)|notes=Very controversial; high risk of bowel perforation}} | ||
* | **See: [[EBQ: Use of Kayexylate in Hyperkalemia]] | ||
*{{MedicationDose|drug=Sodium zirconium cyclosilicate|dose=10 g PO TID x48 hours, then 10-15 g PO daily maintenance|route=PO|context=Potassium binding (preferred over Kayexalate)|indication=Hyperkalemia|display=Lokelma (SZC)|notes=Similar to Kayexalate but without bowel perforation risk}}<ref>Beccari, Mario V, and Calvin J Meaney. "Clinical utility of patiromer, sodium zirconium cyclosilicate, and sodium polystyrene sulfonate for the treatment of hyperkalemia: an evidence-based review." Core evidence vol. 12 11-24. 23 Mar. 2017, doi:10.2147/CE.S129555</ref> | |||
** | |||
* | |||
*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) | *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) <ref> https://emcrit.org/pulmcrit/fluid-selection-using-ph-guided-resuscitation </ref> | ||
*[[Hydrocortisone]] if suspicious for [[adrenal insufficiency]] | *[[Hydrocortisone]] if suspicious for [[adrenal insufficiency]] | ||
*Definitive treatment is [[hemodialysis]] | *Definitive treatment is [[hemodialysis]] | ||
Revision as of 16:06, 20 March 2026
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
- 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
^Fixed or rate-related
Evaluation
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 [1]
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
- 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 IV — Ensure adequate urine output first
- Decreases potassium by dilution, shifting into muscle cells, and promoting renal excretion via alkalosis[4]
- Kayexalate (SPS) 30 g PO or PR PO/PR — Very controversial; high risk of bowel perforation
- Lokelma (SZC) 10 g PO TID x48 hours, then 10-15 g PO daily maintenance PO — Similar to Kayexalate but without bowel perforation risk[5]
- 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) [6]
- Hydrocortisone if suspicious for adrenal insufficiency
- Definitive treatment is hemodialysis
IV Fluid Choice
- LR is preferred over NS, even in renal failure[7]
- 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
External Links
References
- ↑ Erickson CP, Olson KR. Case files of the medical toxicology fellowship of the California poison control system-San Francisco: calcium plus digoxin-more taboo than toxic? J Med Toxicol. 2008 Mar;4(1):33-9
- ↑ Sterns R, Grieff M, Bernstein P (2016). Treatment of hyperkalemia: Something old, something new. Kidney International, 89(3), 546-554.
- ↑ Apel J, Reutrakul S, Baldwin D. Hypoglycemia in the Treatment of Hyperkalemia With Insulin in Patients With End-Stage Renal Disease. Clin Kidney J. 2014;7(3):248-250
- ↑ IBCC Hyperkalemia Chapter
- ↑ Beccari, Mario V, and Calvin J Meaney. "Clinical utility of patiromer, sodium zirconium cyclosilicate, and sodium polystyrene sulfonate for the treatment of hyperkalemia: an evidence-based review." Core evidence vol. 12 11-24. 23 Mar. 2017, doi:10.2147/CE.S129555
- ↑ https://emcrit.org/pulmcrit/fluid-selection-using-ph-guided-resuscitation
- ↑ O'Malley CM, Frumento RJ, Hardy MA, Benvenisty AI, Brentjens TE, Mercer JS, Bennett-Guerrero E. A randomized, double-blind comparison of lactated Ringer's solution and 0.9% NaCl during renal transplantation. Anesth. Analg. 2005 May;100(5):1518-24.
