Hyperkalemia: Difference between revisions

(Major update: stepwise management (stabilize-shift-remove), insulin dose with glucose monitoring, Lokelma, calcium caution in digoxin, ECG progression, cardiac arrest protocol, references with PMIDs)
(Remove refs with incorrect PMIDs (verified against PubMed))
 
(2 intermediate revisions by the same user not shown)
Line 1: Line 1:
==Background==
==Background==
*Serum potassium '''>5.0 mEq/L''' (some define >5.5 mEq/L)
*Serum potassium >5.0 mEq/L (some define >5.5 mEq/L)
*'''Life-threatening when >6.5 mEq/L''' or with ECG changes
*'''Life-threatening when >6.5 mEq/L''' or with ECG changes
*Most common electrolyte disorder causing [[cardiac arrest]]
*Most common electrolyte disorder causing [[cardiac arrest]]
Line 8: Line 8:


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


==Clinical Features==
==Clinical Features==
*Often '''asymptomatic''' until severe
*Often asymptomatic until severe
*'''Muscle weakness''', fatigue, paresthesias
*Muscle weakness, fatigue, paresthesias
*Ascending paralysis (may mimic [[Guillain-Barre]])
*Ascending paralysis (may mimic [[Guillain-Barre]])
*'''Cardiac dysrhythmias''' (most dangerous manifestation)
*'''Cardiac dysrhythmias''' (most dangerous manifestation)
Line 31: Line 31:


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


Line 50: Line 50:
==Evaluation==
==Evaluation==
*'''Stat ECG''' (most urgent — look for peaked T's, widened QRS)
*'''Stat ECG''' (most urgent — look for peaked T's, widened QRS)
*'''BMP''': potassium level, creatinine (renal function), glucose, bicarbonate
*BMP: potassium level, creatinine (renal function), glucose, bicarbonate
*'''Repeat K level''' if unexpected (rule out pseudohyperkalemia)
*Repeat K level if unexpected (rule out pseudohyperkalemia)
*VBG/ABG (acidosis evaluation)
*VBG/ABG (acidosis evaluation)
*'''Digoxin level''' if on digoxin (hyperkalemia potentiates digitalis toxicity)
*Digoxin level if on digoxin (hyperkalemia potentiates digitalis toxicity)
*Urinalysis (myoglobinuria if rhabdomyolysis)
*Urinalysis (myoglobinuria if rhabdomyolysis)
*Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)
*Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)
Line 59: Line 59:
==Management==
==Management==
===Step 1: Cardiac Membrane Stabilization===
===Step 1: Cardiac Membrane Stabilization===
*'''Calcium''' (does NOT lower K; protects myocardium from arrhythmia):
*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 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)
**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
**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'''
**'''Give immediately if ECG changes present or K >6.5'''
*'''Caution in [[digoxin toxicity]]''': calcium may worsen toxicity → use cautiously or consider digibind first
*Caution in [[digoxin toxicity]]: calcium may worsen toxicity → use cautiously or consider digibind first


===Step 2: Shift Potassium Intracellularly===
===Step 2: Shift Potassium Intracellularly===
*'''Insulin + Glucose''' (most reliable):
*Insulin + Glucose (most reliable):<ref>Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID 15846652</ref>
**'''Regular insulin 10 units IV + D50W 25g (50 mL) IV'''
**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'''
**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%)
**Monitor glucose q30min x 4h (hypoglycemia occurs in up to 20%)
**Give D50 '''before or simultaneously''' with insulin
**Give D50 before or simultaneously with insulin
*'''Albuterol''' (nebulized):
*Albuterol (nebulized):
**'''10-20 mg nebulized''' (4-8x standard asthma dose)
**10-20 mg nebulized (4-8x standard asthma dose)
**Onset: 15-30 min; lowers K by '''0.5-1.5 mEq/L'''
**Onset: 15-30 min; lowers K by 0.5-1.5 mEq/L
**Additive with insulin; 40% of patients are non-responders
**Additive with insulin; 40% of patients are non-responders
*'''Sodium bicarbonate''':
*Sodium bicarbonate:
**'''50-100 mEq IV''' over 5-10 minutes
**50-100 mEq IV over 5-10 minutes
**Minimal effect as monotherapy; useful in setting of severe '''metabolic acidosis'''
**Minimal effect as monotherapy; useful in setting of severe metabolic acidosis
**'''Do NOT rely on bicarb alone''' to lower potassium
**'''Do NOT rely on bicarb alone''' to lower potassium


===Step 3: Remove Potassium from Body===
===Step 3: Remove Potassium from Body===
*'''Loop diuretics''' (furosemide 40-80 mg IV): if adequate renal function
*Loop diuretics (furosemide 40-80 mg IV): if adequate renal function
*'''Sodium polystyrene sulfonate (Kayexalate)''' 15-30g PO:
*Sodium polystyrene sulfonate (Kayexalate) 15-30g PO:
**Delayed onset (hours); controversial efficacy; risk of bowel necrosis
**Delayed onset (hours); controversial efficacy; risk of bowel necrosis
**'''Not recommended as acute treatment'''
**Not recommended as acute treatment
*'''Patiromer''' (Veltassa) or '''sodium zirconium cyclosilicate''' (Lokelma):
*Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma):
**Newer potassium binders; better tolerated than Kayexalate
**Newer potassium binders; better tolerated than Kayexalate
**Lokelma 10g PO may lower K within 1 hour
**Lokelma 10g PO may lower K within 1 hour
*'''Hemodialysis''' (most effective method of K removal):
*Hemodialysis (most effective method of K removal):
**'''Indicated for''': refractory hyperkalemia, severe renal failure, K >7 despite medical therapy
**Indicated for: refractory hyperkalemia, severe renal failure, K >7 despite medical therapy


===Cardiac Arrest from Hyperkalemia===
===Cardiac Arrest from Hyperkalemia===
*Standard ACLS + '''calcium 10-20 mL IV push'''
*Standard ACLS + calcium 10-20 mL IV push
*Insulin + glucose + bicarb + albuterol simultaneously
*Insulin + glucose + bicarb + albuterol simultaneously
*Avoid succinylcholine for intubation
*Avoid succinylcholine for intubation
Line 99: Line 99:


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


==See Also==
==See Also==

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
Retrieved from "https://www.wikem.org/w/index.php?title=Hyperkalemia&oldid=389671"