- Rapid Reference 🚀
- Diagnosis of hyperkalemia
- Severity & risk stratification
- Causes of hyperkalemia
- Treatment: Moderate hyperkalemia
- Treatment of severe hyperkalemia
- Sodium zirconium cyclosilicate
- Questions & discussion
- Supplemental media
treatment for severe hyperkalemia (>6.5 mM):
volume resuscitation if hypovolemic
- If bicarbonate is low, resuscitate with isotonic bicarbonate (D5W with 150 mEq/L sodium bicarbonate, typically three 50-mEq amps of bicarb in a liter of D5W).
- If bicarbonate is normal/high, use lactated Ringers or plasmalyte.
- ⚠️ Do not give normal saline, because normal saline will increase the potassium.
- Target euvolemia with a bicarbonate of ~24-28 mM.
temporizing measures (more)
- IV calcium (1 gram of calcium chloride, or 3 grams of calcium gluconate).
- 5 units insulin as an intravenous bolus.
- Dextrose: If glucose <250 mg/dL (<14 mM), give ~two ampules of D50W (100 ml total) –or– ~500 ml of D10W infused over four hours.
- Albuterol: 10-20 mg nebulized (e.g., 4-8 standard nebs back-to-back, or a continuous neb).
elimination: diuresis for patients who can produce urine (more)
- Patients with normal renal function or mild renal dysfunction: IV loop diuretic alone may be sufficient (e.g., 60-120 mg IV furosemide).
- Patients with moderate/severe renal dysfunction who might need emergent dialysis: Aggressive attempt to stave off dialysis with multiple diuretics (nephron bomb):
- 💣 Loop diuretic (e.g., 160 mg IV furosemide or 4 mg IV bumetanide).
- 💣 Thiazide (500-1,000 mg IV chlorothiazide, or 5-10 mg metolazone).
- 💣 +/- Acetazolamide (250-1,000 mg IV/PO).
- 💣 +/- Fludrocortisone 0.2 mg PO (esp. patients on ACEi/ARB).
- Replace urine losses with crystalloid to avoid hypovolemia! Use isotonic bicarbonate or balanced crystalloid as described in the section above on volume resuscitation.
elimination: sodium zirconium cyclosilicate (more)
- This is only mildly effective, so it shouldn't be relied upon as the sole treatment.
- In borderline cases, this may help avoid or delay dialysis.
- Dose is 10 mg PO q8hrs.
- Indicated for patients on chronic hemodialysis, or patients who don't respond to the diuretic bomb.
diagnosis of hyperkalemia
- Left untreated, hyperkalemia may manifest in the following ways:
- Neuromuscular weakness (uncommonly seen; may cause muscle fasciculations, paresthesias, depressed reflexes, and ascending weakness).(32852924)
- Ventricular tachycardia/fibrillation, sudden cardiac death.
- In practice, most patients are asymptomatic (even with severe hyperkalemia).
- Hyperkalemia can cause a very wide range of EKG changes.
- The textbook sequence of changes illustrated above often doesn't occur.(29244647) Instead, hyperkalemia can mimic a wide variety of pathologies (including STEMI and all varieties of bundle/conduction blocks).
- Severe hyperkalemia (e.g. K>7 mM) can occur without obvious EKG changes.
- The following patterns are highly suggestive of hyperkalemia. In an unstable patient, it may be reasonable to give IV calcium based on patterns #2-4 below while awaiting a potassium level.
- (1) Peaked T-waves:
- Narrow, pointy, prominent T-waves.
- Often this is the most notable finding on the EKG (may be visible on bedside monitor as well).
- (2) Ventricular tachycardia mimic:
- QRS wave widens and P-waves may disappear. If patient is tachycardic, this will look like ventricular tachycardia.
- Useful clues: Compared to ventricular tachycardia, T-waves can be sharper than would be usual and heart rate is often slower than would be typical.
- (3) Sine-wave pattern:
- Profound widening of QRS complex and peaked T-waves mimics a sine wave.
- (4) Bradycardia:
- Hyperkalemia can manifest with bradycardia (often in the context of other drugs that slow down the AV node).
- There should always be a high suspicion for hyperkalemia in any bradycardic patient, especially if there are other EKG findings to suggest hyperkalemia.
- Hyperkalemia is variably defined as potassium >5.5 mM or >5.0 mM, depending on the source.
- Pseudohyperkalemia refers to artificially elevated potassium due to:
- (a) Hemolysis.
- (b) Severe polycythemias causing potassium release during clotting (e.g., platelets > 1 million or WBC count > 50,000). This can be avoided by point-of-care testing or measuring labs in a heparinized tube.
- (c) Prolonged tourniquet application.
- Point-of-care testing is generally accurate, but it cannot detect hemolysis.(32852924)
- The first response to a lab report of hyperkalemia should be to look at the telemetry tracing and obtain an EKG.
- If the telemetry/EKG shows features of hyperkalemia, this confirms the diagnosis.
- If the lab reports severe hyperkalemia but the EKG is normal, repeat the lab.
severity & risk stratification
The first step of treatment requires determining whether hyperkalemia is life-threatening (severe). No evidence-based definition for “severe” hyperkalemia exists. Clinical judgement is needed, with attention to the following factors:
- Potassium level: above 6.5-7 mM is more worrisome.
- Chronic hyperkalemia is better tolerated (e.g. dialysis patients who frequently have hyperkalemia).
- Acute hyperkalemia is more dangerous.
- EKG changes: bradycardia, QRS widening, or junctional rhythm are particularly worrisome.(28874951)
- Ongoing potassium release (e.g. by tumor lysis syndrome or rhabdomyolysis) increases the likelihood of deterioration.
causes of hyperkalemia
- Normally the kidney will prevent hyperkalemia by increasing urinary potassium excretion. Persistent hyperkalemia implies dysfunction in renal potassium excretion.
- Critically ill patients often develop hyperkalemia due to a combination of several factors (e.g. hypovolemia plus renal dysfunction plus an ACE-inhibitor). Successful treatment may require addressing many of these problems simultaneously.
- Prolonged tourniquet use or fist clenching during blood draw.
- Severe leukocytosis or thrombocytosis.
- Delayed sample processing.
- Potassium supplements.
- ACEi / ARB, aliskiren (renin-inhibitor).
- Nonselective beta-blockers (e.g., labetalol).
- Potassium-sparing diuretics (amiloride, triamterene, spironolactone, eplerenone).
- Antibiotics (trimethoprim, pentamidine, ketoconazole, IV penicillin G-potassium).
- PRBC transfusion.
- Calcineurin inhibitors (cyclosporine, tacrolimus).
- Digoxin toxicity, succinylcholine.
- Normal saline causing hyperchloremic metabolic acidosis.(30820692)
- Diabetic ketoacidosis, hyperglycemic hyperosmolar non-ketotic syndrome (HHNS).
- Cellular lysis:
- Hemolysis, hematoma.
- Tumor lysis syndrome.
- Tissue necrosis of other etiologies (e.g., trauma, infarction).
- Renal failure, primarily if there is:
- GFR <15 ml/min.
- Dysfunction of the renin-angiotensin-aldosterone system (Type IV renal tubular acidosis):
- Review medication list and consider clinical context.
- Consider evaluation for cellular lysis (e.g., measure CK & LDH levels).
- Consider evaluation for adrenal insufficiency (e.g. random cortisol, ACTH stimulation test).
- (For situations where there is no clear cause of hyperkalemia, further investigation may involve measurement of renin and aldosterone levels. These take forever to return and usually aren’t helpful in the acute management phase.)
treatment of moderate hyperkalemia
step 1: treat any definable causes
- Treat all identifiable causes of hyperkalemia.
- Discontinue any nephrotoxins and establish a state of euvolemia with adequate perfusion.
- Consider a renal diet with limited potassium intake.
step 2: gentle kaliuresis (renal excretion of potassium)
- Potassium excretion can generally be promoted using diuretic among patients able to produce urine (otherwise dialysis will be needed).
- Moderate hyperkalemia can generally be treated with a single diuretic (e.g. IV furosemide), followed by volume replacement with Lactated Ringer's to maintain a net even fluid balance.
- If this regimen fails, more aggressive therapies may be utilized with additional medications discussed below.
IV calcium to stabilize the myocardium
- IV calcium is indicated for patients with EKG changes or a potassium >6.5 mM.(32852924)
- Initial dose:
- Peripheral access: 3 grams IV calcium gluconate over 10 minutes.
- Central access: 1 gram IV calcium chloride over 10 minutes or slow IV push.
- Further doses of calcium may be indicated for persistent, dangerous arrhythmias (e.g. ongoing bradycardia with hypoperfusion). Additionally, calcium only lasts for about 30-60 minutes, so the dose may need to be repeated.
- The ideal strategy for re-dosing is unknown. An expert guideline recommended re-dosing once or twice if needed, while admitting the lack of evidence.(28976587)
- Hyperkalemia is generally more dangerous than hypercalcemia, so you're probably better off erring on the side of hypercalcemia. If you have a point-of-care electrolyte monitor available, check calcium levels and avoid pushing the ionized calcium >3 mM.
IV insulin plus dextrose to shift potassium into cells
- Insulin dose: 5 units IV insulin (must be given IV).(27693804)
- Dextrose dose:
- Traditionally, 2 ampules of D50W has often been used (100 ml total, providing 50 grams of dextrose). Only one ampule of D50W may be inadequate to prevent hypoglycemia.(31084947)
- D10W may be used instead (e.g., 500 ml infused over 4 hours). D10W has the advantages of causing less rebound hypoglycemia and less irritation of veins.
- Dextrose administration may be omitted if the baseline glucose level is already >250 mg/dL (14 mM).(27148740) If the baseline glucose is high (e.g. ~180-250 mg/dL or 10-14 mM) then the dose of dextrose might be cut in half, to 25 grams.
- Observe for the occurrence of hypoglycemia
- The potassium shift lasts for several hours, but may need to be redosed periodically if there is a delay to definitive therapy (e.g., diuresis or dialysis).
- Causes a small shift of potassium into cells.
- Requires a lot of albuterol (10-20 mg, equal to about 4-8 nebulized treatments back-to-back). Logistically, the best way to achieve this dose is to provide albuterol as a continuous nebulized therapy.
- IV epinephrine
- Epinephrine should not be used solely for hyperkalemia. However, if the patient does require a vasopressor, then epinephrine may be a sensible choice.
- Epinephrine is phenomenal for hyperkalemia-induced bradycardia, because it simultaneously treats both the hyperkalemia and the bradycardia.
- Hypertonic bicarbonate doesn't work.
- Ampules of hypertonic bicarbonate have been proven to be ineffective in RCTs.(3052050, 1552710, 8852501, 9170015)
- The hypertonic nature of the fluid pulls potassium out of the cells due to osmotic shifts (“solvent drag”).(2402122) This counteracts the effect of increasing the pH, with an overall neutral effect on the potassium.
- Isotonic bicarbonate does work in metabolic acidosis.
- Isotonic bicarbonate is generally obtained by adding three amps of bicarbonate to a liter of D5W (this creates a 150 mM solution of bicarbonate).
- Isotonic bicarbonate decreases the potassium in three ways: (1) dilution, (2) shifting of potassium into muscle cells, (3) renal potassium excretion is promoted by alkalosis.(18936701)
- Isotonic bicarbonate infusions have been demonstrated to work, but only for patients with metabolic acidosis.(1552710, 24132, 1668124) This requires giving 1-2 liters of fluid, so it is not a viable treatment for patients with volume overload.
- Although this is listed in the section on temporizing measures, 1-2 liters of isotonic bicarbonate can cause a durable reduction in potassium levels.
- More discussion of isotonic bicarbonate here and in the section below as well.
Rx severe hyperkalemia: Potassium elimination
dialysis vs. kaliuresis
- Ultimately, most patients will require elimination of excess potassium from the body. This may be achieved either via the kidneys (kaliuresis) or via dialysis.
- Patients with end-stage renal disease on chronic dialysis will require emergent dialysis (there is no point in attempting kaliuresis). For most other patients, kaliuresis should be attempted prior to emergent dialysis.
kaliuresis step #1 = volume resuscitation if hypovolemic
- Many patients present with renal failure and hyperkalemia due to volume depletion. The first step in managing these patients is volume repletion.
- Isotonic bicarbonate is the preferred resuscitative fluid in metabolic acidosis (excluding lactic acidosis or ketoacidosis).
- The isotonic bicarbonate should be dosed with the goal of bringing the patient's serum bicarbonate level back to a high-normal level (e.g. bicarbonate 24-28 mM). The dose can be estimated by calculating the patient's bicarbonate deficit (MDCalc). Divide the bicarbonate deficit by 150 to estimate the number of liters of isotonic bicarbonate needed. The dose is usually 1-2 liters.
- Bicarbonate should be infused rapidly for patients with hypovolemia and severe hyperkalemia (e.g. 500-1,000 ml/hour).
- If the patient remains hypovolemic after receiving enough sodium bicarbonate to normalize the serum bicarbonate level, then residual hypovolemia can be treated with lactated ringers.
- In the absence of metabolic acidosis, lactated ringers is preferred as the resuscitative fluid (whereas normal saline is contraindicated).
kaliuresis step #2 = consider fludrocortisone
- Oral fludrocortisone (0.2 mg daily) may help stimulate the kidneys to secrete potassium.
- (1) Fludrocortisone is primarily useful in patients with mineralocorticoid insufficiency (green boxes above, for example patients on ACEi/ARB or NSAIDs).
- (2) Consider fludrocortisone if the patient starts producing lots of urine, but the potassium level isn't falling.
kaliuresis step #3 = diuretic cocktail
- The backbone of kaliuresis is a combination of potassium-wasting diuretics, which synergize to cause potassium excretion in the urine.
- Diuretic dose should be adjusted based on the severity of the hyperkalemia and the degree of the renal dysfunction (renal dysfunction generally causes diuretic resistance).
- In life-threatening hyperkalemia, it's often better to err on the side of giving excessive diuretic. If the patient experiences a large-volume diuresis, this can be easily corrected by giving back crystalloid. Alternatively, if in inadequate diuretic dose is given, this may lead to arrhythmias or unnecessary dialysis.
- For maximum efficacy, a combination of three diuretics may be used (when given at maximal doses this is termed the nephron bomb).
- 1) Loop diuretic: furosemide 80-160 mg IV or bumetanide 2-4 mg IV.
- 2) Thiazide diuretic: chlorothiazide 500-1000 mg IV, or metolazone 5-10 mg PO.
- 3) Acetazolamide 250-1,000 mg PO/IV.
kaliuresis step #4 = determine response to diuretic
- If the patient doesn't produce urine in response to diuretic, dialysis will generally be required.
- If the patient does produce urine:
- Urine volume should generally be replaced with Lactated Ringers to prevent volume depletion.
- Electrolytes (including magnesium) should be checked frequently and repleted as needed.
sodium zirconium cyclosilicate
no role for kayexalate or patiromer
- Neither kayexalate nor patiromer has been proven to lower potassium acutely.(29731287, 20167700) Neither one currently has a role for emergent therapy of hyperkalemia.
sodium zirconium cyclosilicate
- Sodium zirconium cyclosilicate is an oral potassium binder which is safe and somewhat effective (essentially a next-generation version of Kayexalate).
- Sodium zirconium cyclosilicate causes about ~0.2 mM reduction in potassium within 4 hours and ~0.4 mM reduction within 24 hours. This effect size is small. Whether this is clinically beneficial depends on the context:
- For an anuric patient with severe hyperkalemia, sodium zirconium cyclosilicate will predictably fail. Such patients require emergent dialysis. Don't delay dialysis while hoping that sodium zirconium cyclosilicate will treat the hyperkalemia.
- For patients on the borderline of requiring dialysis, a small reduction in potassium might be beneficial. In some situations, this could stave off dialysis for long enough that kidney function could recover.
- The dose is 10 grams PO q8hrs.
- Further discussion of sodium zirconium cyclosilicate here.
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questions & discussion
To keep this page small and fast, questions & discussion about this post can be found on another page here.
- The following therapies should be avoided: kayexalate, hypertonic bicarbonate (bicarbonate ampules), normal saline.
- Don't provide temporizing measures without definitive therapy (e.g. patient is given insulin/glucose but no other treatment). This will temporarily make the potassium look better, but the hyperkalemia will inevitably recur later on.
- Insulin dosing errors: 5 units must be given intravenously (not subcutaneously).
Guide to emoji hyperlinks
- = Link to online calculator.
- = Link to Medscape monograph about a drug.
- = Link to IBCC section about a drug.
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- = Link to FOAMed site with related information.
- = Link to supplemental media.
- Treatment of severe hyperkalemia (Scott Weingart, EMCrit)
- Management of severe hyperkalemia (PulmCrit)
- BRASH syndrome: Hyperkalemia plus AV blocker (PulmCrit)
- Updates in management of hyperkalemia (Brit Long and Justin Warix, EMDocs).
- Hyperkalemia (Kane Guthrie) & Hyperkalemia Management (Chris Nickson), LITFL
- Hyperkalemia (Anand Swaminathan, CoreEM)
- Management of life-threatening hyperkalemia (First10EM)
- Hyperkalemia management: preventing hypoglycemia from insulin (Bryan Hayes ALiEM)
- EKG in hyperkalemia
- Is kayexalate useless? (Scott Weingart, EMCrit)
- Is kayexalate useful in treatment of hyperkalemia in the ED? (Salim Rezaie, RebelEM)
- Myths in Emergency Medicine: Kayexalate (Anand Swaminathan, EM News)
Video summarizing treatment of hyperkalemia (Christopher Nemeh)
#ECG of an unconscious young man thought to be in "V-Tach"
His rate is ~110 bpm
When the rate is <120, think #Hyperkalemia
K+ was 9.5!
— Sam Ghali, M.D. (@EM_RESUS) January 7, 2018
isotonic bicarbonate (150 mEq/L NaBic) resuscitation for hypovolemic patient with hyperkalemia & uremic acidosis. two liters caused nice improvement in potassium, despite minimal urine output. https://t.co/fX2PsR723I https://t.co/a8DWx7iDUZ pic.twitter.com/iBpIgarCW3
— josh farkas (@PulmCrit) September 18, 2018
Here's an #ECG of a young man presenting in shock
ECG reading is all about pattern recognition. Burn this morphology into your mind and when you see it think ↑K+. If you can recognize this and start treatment without labs one day you will save a life!
— Sam Ghali, M.D. (@EM_RESUS) September 18, 2018
— Manrique Umana McDermott (@umanamd) June 30, 2018
HyperK is known as the Great Masquerader on #ECG bc it can take on the form of many different patterns. Here’s a classic one where it mimics Coved Brugada! The telltale sign is the size and tented shape of all the T waves.
When you see this think ↑K+
— Sam Ghali, M.D. (@EM_RESUS) October 16, 2018
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