Last Updated: 12/7/2023

Admission Checklist

-- Gut Check: repeat the K (VBG okay for ballpark) to assess for pseudohyperkalemia if patient asymptomatic without EKG changes

-- ABC’s: STAT EKG (look for peaked T waves, block, arrhythmia) and give calcium gluconate if there are any changes;

-- Triage: hyperkalemic emergency is present one or more of the following:

  • Potassium greater than 6.5 mEq/L
  • Clinical changes including EKG changes, muscle weakness
  • An active process leading to persistently elevated levels - ESRD, GI bleed, rhabdo, TLS

-- Chart Check: CKD/ESRD, dialysis timing, home medications, prior EKGs

-- Can’t Miss: EKG changes, acidosis, renal failure, adrenal insufficiency

-- Admission Orders: continuous telemetry, low K diet; BMP q2-4, LFTs, VBG; consider CK, hemolysis labs, cortisol/renin/aldo

–- Initial Treatment to Consider: In general, Insulin 10 units IV with D50 25mg; furosemide 40+mg IV, Lokelma 10mg TID; treat the underlying cause - acidosis, hypovolemia, DKA, hypoaldo, remove meds, etc;  consider the need for dialysis if severe and initial temporizing efforts are ineffective

HPI Intake

-- Symptoms: weakness, paresthesias, nausea/vomiting, constipation, palpitations

-- Preceding events: missed dialysis, traumas, exercise

-- Medications: ACE/ARB, MRAs, trimethoprim-sulfamethoxazole, NSAIDs, beta-blockers, potassium supplements

-- Comorbidities: CKD/ESRD (make urine?), diabetes, adrenal insufficiency, malignancies

To Note on Exam 

-- Neuro: weakness, decreased reflexes, AMS

-- Cardiac: heart rate, irregular rhythm

-- Skin/Extremities: edema, evidence of dehydration


-- Reduced Elimination - ESRD/CKD/AKI, hypoaldosteronism or hypocortisolism, medications (ACE/ARB, MRAs, Bactrim, NSAIDs), Type IV RTA

-- Shifting into Extracellular Space - Lactic acidosis and DKA, medications (beta-blockers, digoxin, succinylcholine)

-- Extracellular Release - Rhabdomyolysis, TLS, hemolysis, pseudohyperkalemia

-- Excess Intake from Diet

EHR Dotphrase


-- History: CKD, makes urine, missed dialysis, precedingevents, contributing meds,

-- Clinical/Exam: muscle cramps, weakness/paralysis, paresthesias, nausea/vomiting, constipation,heart block, arrhythmia

-- Data: potassium (severity), EKG changes, ABG/VBG, creatinine

-- DDx: AKI/CKD, drugs (BB, ACE/ARB, NSAIDs, spironolactone, TMP-SMX), acidosis, hypoaldo/primary adrenal insufficiency, cell lysis (rhabdo, TLS), transfusion reaction, decreased insulin, type IV RTA



-- Monitor: Trend K q 2-4h and EKG q 2-4h after initial stabilization; Continuous telemetry

-- Consult renal if c/f dialysis need (unable to temporize in emergency)

-- Consider sending CK, hemolysis labs (retic count, LDH, haptoglobin, smear), TLS labs (UA, phos, calcium), or cortisol/renin/aldo in the correct clinical context


-- Membrane Stabilization: If emergency - lasts ~30 minutes

  • Calcium gluconate 1-2g IV over 5-10 minutes, repeat q5 minutes with persistent EKG changes

-- Temporizing: If emergency - lasts ~2 hours

  • Insulin 10 units IV with 50cc (25mg) D50 if BG < 250
  • Albuterol nebulizer (SABA) 10-20 mg can be added, but not used as monotherapy

-- Eliminate: If either an emergency or when hyperkalemia expected to persist

  • Furosemide 40mg IV
  • Sodium zirconium cyclosilicate (Lokelma) 10g TID along with laxative 
  • Dialysis if emergency and unable to lower potassium by other means

-- Consider a bicarb amp if pH is less than 7.2

-- Discontinue any likely causative medications and/or treat any acute underlying cause

-- Low potassium diet

-- If c/f Adrenal Insufficiency - hydrocortisone 15-25mg split 2-3 doses + fludrocort 0.05-0.2 daily

If You Remember Nothing Else

The most common cause of hyperkalemia presenting to the hospital is CKD/ESRD (commonly missed dialysis) and medication use. A hyperkalemic emergency is present if the potassium level is greater than 6.5 mEq/L, there are clinical or EKG changes or an active process that would lead to persistently elevated potassium levels including ESRD, GI bleeding, rhabdomyolysis, or TLS. Get an EKG and give calcium gluconate if there are any changes. You should give insulin 10 units with D50 if you need to momentarily temporize and then give either furosemide and/or Lokelma to eliminate the potassium from the body. Don't wait to see if elimination will work if there is an indication for emergent dialysis such as acute renal failure with evidence of poor urine output.

Clinical Pearls

General Information and Epidemiology

  • Though cutoffs vary, hyperkalemia is generally considered to be an elevated potassium level above 5.5 mEq/L
  • Symptoms are usually not present until the potassium is above 7.0 mEq/L or if the level rapidly rises due to an acute insult
  • There is no consensus definition for what is considered acute vs chronic hyperkalemia
  • Hyperkalemia is present in about 2-3% of the population but can be present in up to half of patients with CKD


  • Hyperkalemia influences resting membrane potential which can lead to increased excitability of cells 
  • Only 2% of total body potassium is extracellular, and this level is tightly regulated
  • The resting membrane potential is -90 mV. This potential becomes lower (LESS negative i.e negative 90 to negative 80) when there is more K outside cells, which means less of a signal is needed to fire an action potential, leading to increased excitability and possibly arrhythmias, especially if the changes to the potential are acute
  • Chronic changes in extracellular potassium leads to compensatory mechanisms to reduce excitability
  • K is exchanged for Na in the distal nephron - if RAAS is on (i.e due to hypovolemia, CHF, cirrhosis), less Na makes it to this portion, and K is not excreted in exchange for the Na, potentially leading to hyperkalemia
  • Acidosis causes hyperkalemia by messing with Na/H antiporter efficacy which leads to decreased intracellular Na, which impacts the efficacy of the Na/K-ATPase, and leads to increased extracellular K, leading to hyperkalemia
  • Insulin stimulates and BB inhibits the Na/K-ATPase pump leading to K+ staying outside the cell
  • Hyperkalemia from acute insults is usually short-lived unless there is a chronic, ongoing process such as hypoaldosteronism, renal disease, or certain medication use

Etiology and Risk Factors

  • The most common cause of hyperkalemia is decreased renal function or missed dialysis sessions in those with ESRD
  • Common outpatient medicines that can cause hyperkalemia include ACE/ARBs, MRAs, NSAIDs, TMP-SMX all of which exert their effects by lowering the release of aldosterone; beta-blockers, digoxin, calcineurin inhibitors, and succinlycholine exert their effect by redistributing potassium
  • Under normal conditions, human kidneys should be able to excrete up to 400 mmol of potassium each day - the risk of hyperkalemia is thus only really possible in those with renal disease
  • Some of the most common sources of dietary K+ are potatoes, cereals (bran products, granola), meat, and dairy (milk, yogurt). Other potassium-rich foods include avocados, bananas, leafy green vegetables (except for kale), root vegetables (beets, carrots), and tomatoes
  • Type IV RTA leads to reduced ability to reabsorb sodium in the distal tubule, thus less K excretion
  • Hypoaldosteronism leads to hyperkalemia due to a lack of mineralocorticoids

Clinical Presentation and Diagnosis

  • Patients with severely elevated or acutely elevated potassium levels are more likely to have symptoms; patients with chronic elevations will often be asymptomatic and may be diagnosed incidentally on lab work
  • VBG/ABG potassium levels may not perfectly correlate with BMP but should be within 0.5 mmol/L
  • In vivo hemolysis is a genuine cause of hyperkalemia, whereas hemolysis in vitro as part of the blood drawing process will lead to pseudohyperkalemia - most labs will report this as “hemolyzed” rather than report an inaccurate level
  • The EKG does not always correlate with the actual K level - it depends in part on the chronicity of the elevation; as such, EKG is not a sensitive test for hyperkalemia but can alert you to the risk of an adverse cardiac event
  • Classic EKG progression - peaked T waves → increased P interval, flattening of P wave → wide QRS and BBB → sine wave → PEA/asystole/VF
  • Note that these changes do not necessarily happen in this order
  • Atria are more susceptible to K which is why we tend to see p-wave flattening earlier than changes in QRS
  • Hypo/Hyperkalemia is one of the H’s in the H’s and T’s for causes of PEA arrest; at very high levels hyperkalemia can lead to asystole - never a bad idea to give calcium gluconate if there is a suspicion
  • The weakness associated with hyperkalemia often starts in the legs and then progresses to the arms (ascending paralysis)
  • If a patient is in DKA, they may be hyperkalemic since insulin is not present to push potassium into cells, but TOTAL body K will be low, so you need to replete when less than 5.2 and hold insulin if less than 3.3


  • Calcium gluconate should reverse EKG changes in 5 minutes, if not, push again
  • Calcium chloride has a higher risk of tissue necrosis at the IV site and should be given centrally
  • Calcium salts have no actual effect on potassium levels, and don’t last more than 30-60 minutes - you must always give other treatments beyond calcium
  • Temporizing and redistributing K can drive the K down ~0.5-1.5 in the short term
  • Patients receiving insulin to temporize should not receive concomitant D50 if the glucose level is >250 - hyperglycemia can lead to worse extracellular potassium levels (like in DKA pathology); if you do administer dextrose, the insulin may outlast it, so watch for the development of hypoglycemia
  • Giving insulin leads to potassium entering cells, commonly in the liver and skeletal muscle; this happens with normal physiology so that some can be released later on when patients are fasting to maintain balance, like with glucose
  • Inhaled SABA (albuterol) should not be used as a monotherapy and is less likely to work in patients taking beta blockers or with CKD
  • In normal conditions, 90% of potassium is eliminated renally, and 10% in stool
  • Elimination via furosemide or Lokelma requires urine or stool output. If the patient cannot do either, the only other way to eliminate potassium is via dialysis
  • Elimination is not required in all patients - especially if the acute insult has been addressed
  • Cation-exchange resins like kayexalate and lokelma work by releasing sodium ions which are in turn exchanged with potassium in the gut
  • Resins commonly lead to constipation and should be given with laxatives
  • Sodium polystyrene sulfonate (also known as Kayexalate) has been shown to have rare but serious adverse effects, specifically gut necrosis
  • Bicarbonate should only be used in patients with severe acidosis 

Trials and Literature

  • Clinical Management of Hyperkalemia (Mayo Clin Proc, 2021)
  • An Integrated View of Potassium Homeostasis (NEJM, 2015)
  • Risk of Hospitalization for Serious Adverse Gastrointestinal Events Associated With Sodium Polystyrene Sulfonate Use in Patients of Advanced Age (JAMA, 2019) - Kayexalate is associated with serious GI adverse events over 30 days (0.2% of people who take vs. 0.1% who don’t) - NNH is 1000; intestinal ischemia is the most common
  • Sodium zirconium cyclosilicate in hyperkalemia(NEJM 2015) - reduces K over placebo

Other Resources