Hyperkalemia: Difference between revisions
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==Background==
==Background==
*Defined as >6.0 mEq/L  
*Serum potassium >5.0 mEq/L (some define >5.5 mEq/L)
*Consider pseudohyperkalemia (e.g. from hemolysis)
*'''Life-threatening when >6.5 mEq/L''' or with ECG changes
*Potassium secretion is proportional to flow rate and sodium delivery through distal nephron
*Most common electrolyte disorder causing [[cardiac arrest]]
**Thus, loop & thiazide diuretics cause ''hypo''kalmia
*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, glucose)
**Acidosis (metabolic acidosis shifts K extracellularly)
*Suxamethonium
**Insulin deficiency / [[DKA]]
*Intravenous cationic amino acids
**Tissue destruction: [[rhabdomyolysis]], tumor lysis, hemolysis, burns
*Stored 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)
*[[Ciclosporin]]
*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''
*Nausea and Vomiting.
*[[Muscle weakness]]
*[[Parathesias]]
*[[Lethargy]], [[fatigue]]
*[[Difficulty breathing]]
*[[Palpitations]], [[chest pain]]


==Differential Diagnosis==
==Differential Diagnosis==
*Pseudohyperkalemia: hemolyzed specimen, prolonged tourniquet use prior to blood draw, thrombocytosis or leukocytosis
*Pseudohyperkalemia (hemolyzed specimen)
*Redistribution (shift from intracellular to extracellular space)
*[[Acute kidney injury]] / [[chronic kidney disease]]
**Acidemia (see [[Diabetic ketoacidosis|DKA]])
*[[DKA]]
**Cellular breakdown: see [[Rhabdomyolysis]]/[[Crush syndrome]], hemolysis, see [[Tumor lysis syndrome]]  
*[[Rhabdomyolysis]]
*Increased total body potassium
*Tumor lysis syndrome
**Inadequate excretion: Acute/chronic renal failure, Addison's disease, type 4 RTA
*[[Adrenal insufficiency]]
**Drug-induced: potassium-sparing diuretic (spironolactone), angiotensin converting enzyme inhibitors (ACE-I), nonsteroidal anti-inflammatory drugs (NSAIDs)
*Medication effect
**Excessive intake: diet, blood transfusion
*Other causes: succinylcholine, digitalis, beta-blockers
 
{{Peaked T-waves DDX}}


==Evaluation==
==Evaluation==
===[[ECG]]===
*'''Stat ECG''' (most urgent — look for peaked T's, widened QRS)
''Changes NOT always predictable and sequential''
*BMP: potassium level, creatinine (renal function), glucose, bicarbonate
*6.5 - 7.5 mEq/L: peaked T waves, prolonged PR interval, shortened QT interval
*Repeat K level if unexpected (rule out pseudohyperkalemia)
*7.5 - 8.0 mEq/L: widened QRS interval, flattened P waves
*VBG/ABG (acidosis evaluation)
*10 - 12 mEq/L: sine wave, ventricular fibrillation, heart block
*Digoxin level if on digoxin (hyperkalemia potentiates digitalis toxicity)
*Urinalysis (myoglobinuria if rhabdomyolysis)
*Consider: CK, uric acid, phosphorus (tumor lysis), cortisol (adrenal insufficiency)


==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)
**[[Calcium gluconate]]: Give 10ml of a 10% solution over 10 mins
**Calcium chloride 10%: 5-10 mL IV (via central line preferred; 3x more elemental calcium)
***Only 1/3 the calcium compared to calcium chloride
**Onset: 1-3 minutes; duration 30-60 minutes; may repeat in 5-10 min if ECG unchanged
***Can cause hypotension due to osmotic shift
**'''Give immediately if ECG changes present or K >6.5'''
**[[Calcium chloride]] 1 gram IV  
*Caution in [[digoxin toxicity]]: calcium may worsen toxicity → use cautiously or consider digibind first
***Give over 1 - 2 minutes  
***Extravasation is bad: use a good IV
***Usually given in code situations
*Takes effect in 15-30 minutes<ref>http://lifeinthefastlane.com/hyperkalemia/. Accessed 02/22/2016</ref>
**(If given for hyperkalemic cardiac arrest, need to continue resuscitation for at least 30 minutes)
*Duration of action: 30 - 60 minutes <ref> The Effect of Calcium on Severe Hyperkalemia http://hqmeded-ecg.blogspot.com/2015/04/the-effect-of-calcium-on-severe.html</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>
*Do serial [[ECG]]s to track progress: may need to give multiple doses


===Shift K+ intracellularly===
===Step 2: Shift Potassium Intracellularly===
*Intravenous insulin + dextrose
*Insulin + Glucose (most reliable):<ref>Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID 15846652</ref>
**Give 10 units regular insulin intravenously with 25 to 50 grams (1 - 2 50 mL ampules) of 50% dextrose (D50)
**Regular insulin 10 units IV + D50W 25g (50 mL) IV
***May withhold dextrose if blood sugar >300mg/dl (>17 mmol/L)
**Onset: 15-30 min; duration 4-6 hours; lowers K by 0.5-1.2 mEq/L
***Duration of effect: 4 - 6 hours  
**Monitor glucose q30min x 4h (hypoglycemia occurs in up to 20%)
***Consider mixing in 10 cc NS syringe to ensure small volume of 10 units insulin fully administered via IV
**Give D50 before or simultaneously with insulin
***Insulin cleared renally, be careful about inducing hypoglycemia (ESRD patients)
*Albuterol (nebulized):
*Nebulized albuterol 5 - 20mg
**10-20 mg nebulized (4-8x standard asthma dose)
**Response is dose-dependent
**Onset: 15-30 min; lowers K by 0.5-1.5 mEq/L
**Peak effect: 30 minutes
**Additive with insulin; 40% of patients are non-responders
**Duration of effect: 2 hours
*Sodium bicarbonate:
*Intravenous sodium bicarbonate 50ml of 8.4% solution (1 ampoule) given over 5 minutes  
**50-100 mEq IV over 5-10 minutes
**Duration of effect: 1 - 2 hours
**Minimal effect as monotherapy; useful in setting of severe metabolic acidosis
**Generally not required, unless pH <7.1
**'''Do NOT rely on bicarb alone''' to lower potassium


===Remove K+ from body===
===Step 3: Remove Potassium from Body===
*Intravenous furosemide (Lasix) 40 - 80mg
*Loop diuretics (furosemide 40-80 mg IV): if adequate renal function
**Ensure adequate urine output first
*Sodium polystyrene sulfonate (Kayexalate) 15-30g PO:
*[[Sodium polystyrene sulfonate]] (Kayexylate): 30 gm oral or per rectum
**Delayed onset (hours); controversial efficacy; risk of bowel necrosis
**'''Very Controversial, High Risk of Bowel Perforation''', see: [[EBQ: Use of Kayexylate in Hyperkalemia]]
**Not recommended as acute treatment
*Intravenous normal saline solution for volume expansion if dehydrated, rhabdomyolysis, diabetic ketoacidosis or other acidosis
*Patiromer (Veltassa) or sodium zirconium cyclosilicate (Lokelma):
*[[Hydrocortisone]] if suspicious for [[adrenal insufficiency]]
**Newer potassium binders; better tolerated than Kayexalate
*Definitive treatment is hemodialysis
**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==
==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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