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) |
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==Background== | ==Background== | ||
*Serum potassium | *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]] | ||
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===Causes=== | ===Causes=== | ||
* | *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 | ||
**[[Adrenal insufficiency]] (hypoaldosteronism) | **[[Adrenal insufficiency]] (hypoaldosteronism) | ||
**Type 4 renal tubular acidosis | **Type 4 renal tubular acidosis | ||
* | *Transcellular shift (K moves out of cells): | ||
** | **Acidosis (metabolic acidosis shifts K extracellularly) | ||
** | **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) | ||
* | *Pseudohyperkalemia: hemolyzed sample, prolonged tourniquet, thrombocytosis, leukocytosis | ||
** | **Always repeat level if unexpected | ||
==Clinical Features== | ==Clinical Features== | ||
*Often | *Often asymptomatic until severe | ||
* | *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) | ||
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===ECG Changes (Progressive)=== | ===ECG Changes (Progressive)=== | ||
* | *Peaked T waves (earliest change, typically >5.5 mEq/L) | ||
* | *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 | *'''ECG changes do NOT reliably correlate with K level''' — some patients arrest without warning | ||
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==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 | ||
* | *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) | ||
*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) | ||
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==Management== | ==Management== | ||
===Step 1: Cardiac Membrane Stabilization=== | ===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) | **Calcium chloride 10%: 5-10 mL IV (via central line preferred; 3x more elemental calcium) | ||
**Onset: | **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 | ||
===Step 2: Shift Potassium Intracellularly=== | ===Step 2: Shift Potassium Intracellularly=== | ||
* | *Insulin + Glucose (most reliable): | ||
** | **Regular insulin 10 units IV + D50W 25g (50 mL) IV | ||
**Onset: 15-30 min; duration 4-6 hours; lowers K by | **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 | **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 | **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: | ||
** | **50-100 mEq IV over 5-10 minutes | ||
**Minimal effect as monotherapy; useful in setting of severe | **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 | ||
* | *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 | ||
* | *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): | ||
** | **Indicated for: refractory hyperkalemia, severe renal failure, K >7 despite medical therapy | ||
===Cardiac Arrest from Hyperkalemia=== | ===Cardiac Arrest from Hyperkalemia=== | ||
*Standard ACLS + | *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 | ||
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==Disposition== | ==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== | ==See Also== | ||
Revision as of 09:28, 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):
- Acute kidney injury / chronic kidney disease
- Medications: ACE inhibitors, ARBs, K-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin
- Adrenal insufficiency (hypoaldosteronism)
- Type 4 renal tubular acidosis
- 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)
- 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
- Pseudohyperkalemia (hemolyzed specimen)
- Acute kidney injury / chronic kidney disease
- DKA
- Rhabdomyolysis
- Tumor lysis syndrome
- Adrenal insufficiency
- Medication effect
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):
- 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
- Hypokalemia
- Acute kidney injury
- Diabetic ketoacidosis
- Rhabdomyolysis
- Cardiac arrest
- Digoxin toxicity
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
