Hyperkalemia: Difference between revisions

(Convert medication dosing to MedicationDose templates for SMW integration (8 medications: calcium gluconate, calcium chloride, insulin, albuterol, sodium bicarbonate, furosemide, kayexalate, lokelma))
(Remove refs with incorrect PMIDs (verified against PubMed))
 
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==Background==
==Background==
*Defined as >5.5 mEq/L  
*Serum potassium >5.0 mEq/L (some define >5.5 mEq/L)
*Potassium secretion is proportional to flow rate and sodium delivery through distal nephron
*'''Life-threatening when >6.5 mEq/L''' or with ECG changes
**Thus, loop & thiazide [[diuretics]] cause ''hypo''kalmia
*Most common electrolyte disorder causing [[cardiac arrest]]
*Most common cause is hemolysis from blood draw (pseudohyperkalemia)
*Potassium homeostasis:
**98% intracellular (maintained by Na/K-ATPase)
**Renal excretion is primary mechanism of potassium regulation


===Medication Causes===
===Causes===
====Alter transmembrane potassium movement====
*Decreased excretion (most common mechanism):
*[[β blockers]]
**[[Acute kidney injury]] / [[chronic kidney disease]]
*[[Digoxin]]
**Medications: ACE inhibitors, ARBs, K-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin
*Potassium-containing drugs
**[[Adrenal insufficiency]] (hypoaldosteronism)
*Potassium supplements
**Type 4 renal tubular acidosis
*Salt substitutes
*Transcellular shift (K moves out of cells):
*Hyperosmolar solutions ([[mannitol]], [[dextrose|glucose]])
**Acidosis (metabolic acidosis shifts K extracellularly)
*Suxamethonium
**Insulin deficiency / [[DKA]]
*Intravenous cationic amino acids
**Tissue destruction: [[rhabdomyolysis]], tumor lysis, hemolysis, burns
*Stored [[pRBCs|red blood cells]] (haemolysis releases potassium)
**Succinylcholine, beta-blockers, digitalis toxicity
*Herbal medicines (such as alfalfa, dandelion, horsetail, milkweed, and nettle)
**Hyperkalemic periodic paralysis
*Increased intake: excessive supplementation, salt substitutes (KCl)
*Pseudohyperkalemia: hemolyzed sample, prolonged tourniquet, thrombocytosis, leukocytosis
**Always repeat level if unexpected


====Reduce aldosterone secretion====
==Clinical Features==
*[[ACE inhibitors]]; [[Angiotensin II receptor blockers]]
*Often asymptomatic until severe
*[[NSAIDs]]
*Muscle weakness, fatigue, paresthesias
*[[Heparin]]
*Ascending paralysis (may mimic [[Guillain-Barre]])
*[[Antifungals]] ([[ketoconazole]], [[fluconazole]], [[itraconazole]])
*'''Cardiac dysrhythmias''' (most dangerous manifestation)
*[[Cyclosporine]]
*Nausea, vomiting, diarrhea
*[[Tacrolimus]]


====Block aldosterone binding to mineralocorticoid receptors====
===ECG Changes (Progressive)===
*[[Spironolactone]]
*Peaked T waves (earliest change, typically >5.5 mEq/L)<ref>Montague BT, et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324-330. PMID 18235147</ref>
*[[Eplerenone]]
*Prolonged PR interval
*[[Drospirenone]]
*Widened QRS
*Potassium sparing [[diuretics]] (amiloride, triamterene)
*Loss of P waves
*[[Trimethoprim]]
*Sine wave pattern (pre-arrest)
*[[Pentamidine]]
*Ventricular fibrillation / asystole
 
*'''ECG changes do NOT reliably correlate with K level''' — some patients arrest without warning
==Clinical Features==
''Typically non-specific''
*[[Muscle weakness]]
*[[Lethargy]], [[fatigue]]
*[[Paresthesias]]
*[[Nausea and Vomiting]]
*[[Difficulty breathing]]
*[[Palpitations]], [[chest pain]]


==Differential Diagnosis==
==Differential Diagnosis==
{{Hyperkalemia DDX}}
*Pseudohyperkalemia (hemolyzed specimen)
{{Peaked T-waves DDX}}
*[[Acute kidney injury]] / [[chronic kidney disease]]
{{Tachycardia (wide) DDX}}
*[[DKA]]
*[[Rhabdomyolysis]]
*Tumor lysis syndrome
*[[Adrenal insufficiency]]
*Medication effect


==Evaluation==
==Evaluation==
[[File:PMC4475259 JCHIMP-5-27993-g003.png|thumb|Diagrammatic representation of ECG changes with increasing hyperkalemia]]
*'''Stat ECG''' (most urgent — look for peaked T's, widened QRS)
[[File:HyperK2014.jpg|thumb|ECG in hyperkalemia with peaked T waves and small P waves]]
*BMP: potassium level, creatinine (renal function), glucose, bicarbonate
[[File:PMC4475259 JCHIMP-5-27993-g001.png|thumb|ECG with widened QRS complex and tall broad T waves]]
*Repeat K level if unexpected (rule out pseudohyperkalemia)
[[File:PMC4475259 JCHIMP-5-27993-g005.png|thumb|ECG showing sine wave pattern]]
*VBG/ABG (acidosis evaluation)
===Workup===
*Digoxin level if on digoxin (hyperkalemia potentiates digitalis toxicity)
*[[ECG]]
*Urinalysis (myoglobinuria if rhabdomyolysis)
*Chem 10 (including potassium, magnesium, and phosphorus)
*Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)
**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==
==Management==
===Stabilize cardiac membranes===
===Step 1: Cardiac Membrane Stabilization===
''Indicated if there are any ECG changes or evidence of arrhythmias. Consider if K >7 mEq/L''
*Calcium (does NOT lower K; protects myocardium from arrhythmia):
*Either one of the following:
**Calcium gluconate 10%: 10-20 mL IV over 2-3 minutes (preferred; less tissue necrosis if extravasates)
**{{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}}
**Calcium chloride 10%: 5-10 mL IV (via central line preferred; 3x more elemental calcium)
**{{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}}
**Onset: 1-3 minutes; duration 30-60 minutes; may repeat in 5-10 min if ECG unchanged
*Do serial [[ECG]]s to track progress: may need to give multiple doses
**'''Give immediately if ECG changes present or K >6.5'''
*(If given for hyperkalemic cardiac arrest, need to continue resuscitation for at least 30 minutes)
*Caution in [[digoxin toxicity]]: calcium may worsen toxicity → use cautiously or consider digibind first
*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===
===Step 2: Shift Potassium 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}}
*Insulin + Glucose (most reliable):<ref>Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID 15846652</ref>
***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>
**Regular insulin 10 units IV + D50W 25g (50 mL) IV
***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>
**Onset: 15-30 min; duration 4-6 hours; lowers K by 0.5-1.2 mEq/L
*{{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}}
**Monitor glucose q30min x 4h (hypoglycemia occurs in up to 20%)
*{{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}}
**Give D50 before or simultaneously with insulin
**For '''normovolemic or hypovolemic''' patients with '''metabolic acidosis'''
*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


===Remove K+ from body===
===Step 3: Remove Potassium 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}}
*Loop diuretics (furosemide 40-80 mg IV): if adequate renal function
**Decreases potassium by dilution, shifting into muscle cells, and promoting renal excretion via alkalosis<ref>[https://emcrit.org/ibcc/hyperkalemia/ IBCC Hyperkalemia Chapter]</ref>
*Sodium polystyrene sulfonate (Kayexalate) 15-30g PO:
*{{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}}
**Delayed onset (hours); controversial efficacy; risk of bowel necrosis
**See: [[EBQ: Use of Kayexylate in Hyperkalemia]]
**Not recommended as acute treatment
*{{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>
*Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma):
*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)
**Newer potassium binders; better tolerated than Kayexalate
**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>
**Lokelma 10g PO may lower K within 1 hour
*[[Hydrocortisone]] if suspicious for [[adrenal insufficiency]]
*Hemodialysis (most effective method of K removal):
*Definitive treatment is [[hemodialysis]]
**Indicated for: refractory hyperkalemia, severe renal failure, K >7 despite medical therapy


===IV Fluid Choice===
===Cardiac Arrest from Hyperkalemia===
*LR is preferred over NS, even in renal failure<ref>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.</ref>
*Standard ACLS + calcium 10-20 mL IV push
*The small amount of 4 mEq/L of potassium in lactated ringers does not contribute to worsening hyperkalemia
*Insulin + glucose + bicarb + albuterol simultaneously
*Hyperkalemia worsens with metabolic acidosis, and large volume normal saline administration increases risk of hyperchloremic non-anion gap metabolic acidosis
*Avoid succinylcholine for intubation
*Consider emergent dialysis


==Disposition==
==Disposition==
*Consideration for ICU for frequent electrolyte checks and close cardiac monitoring
*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==
==See Also==
*[[Electrolyte abnormalities]]
*[[Hypokalemia]]
*[[Acute kidney injury]]
*[[Acute kidney injury]]
*[[Hemodialysis/Hemoperfusion]]
*[[Diabetic ketoacidosis]]
*[[Crush syndrome]]
*[[Rhabdomyolysis]]
 
*[[Cardiac arrest]]
==External Links==
*[[Digoxin toxicity]]
*[https://ecgweekly.com/2015/01/case-of-the-week-january-12-2015/ ECG Weekly -Hyperkalemia]


==References==
==References==
<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


[[Category:FEN]]
[[Category:Renal]]
[[Category:Renal]]
[[Category:Critical Care]]

Latest revision as of 10:25, 22 March 2026

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):
  • 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)[1]
  • 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

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):[2]
    • 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

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
  1. ↑ Montague BT, et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324-330. PMID 18235147
  2. ↑ Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID 15846652
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