What potassium level is dangerously high?

Potassium above 6.0 mEq/L is considered severe hyperkalemia and requires urgent treatment. Levels above 6.5 mEq/L are a medical emergency — they can cause fatal cardiac arrhythmias including ventricular fibrillation and asystole. However, the rate of rise matters as much as the absolute level — acute hyperkalemia is more dangerous than chronic. ECG changes (peaked T waves, QRS widening, loss of P waves) may appear at 6.0–6.5 mEq/L and should trigger immediate treatment regardless of the exact potassium value.

What are symptoms of low potassium?

Mild hypokalemia (3.0–3.5 mEq/L) is often asymptomatic. As potassium drops below 3.0 mEq/L, symptoms include muscle weakness, fatigue, cramps, and constipation (due to smooth muscle dysfunction). Below 2.5 mEq/L, severe symptoms can develop: rhabdomyolysis, paralysis (ascending, mimicking Guillain-Barré), respiratory failure from diaphragm weakness, cardiac arrhythmias (U waves, ST depression, torsades de pointes), and ileus. Chronic hypokalemia can cause a renal concentrating defect (nephrogenic diabetes insipidus) with polyuria and polydipsia.

What potassium level is too low?

Potassium below 3.5 mEq/L is defined as hypokalemia. Levels of 3.0–3.5 mEq/L are mild and may require oral supplementation. Levels of 2.5–3.0 mEq/L are moderate hypokalemia and require prompt treatment. Below 2.5 mEq/L is severe hypokalemia — a critical lab value that requires urgent IV potassium replacement and cardiac monitoring due to the risk of life-threatening arrhythmias. Most labs flag potassium below 3.0 mEq/L as a critical value requiring immediate clinician notification.

What foods are high in potassium?

Potassium-rich foods include bananas (422 mg per medium banana), potatoes with skin (926 mg per medium potato), sweet potatoes (541 mg), spinach (839 mg per cup cooked), avocados (708 mg per whole), white beans (1,189 mg per cup), salmon (534 mg per 3 oz), oranges/orange juice (496 mg per cup), yogurt (573 mg per cup), and dried apricots (755 mg per half cup). The recommended daily intake is 2,600 mg for women and 3,400 mg for men (NASEM 2019). Patients with CKD or hyperkalemia may need to restrict these foods.

What causes high potassium levels?

The most common causes of hyperkalemia are: (1) Renal failure — reduced excretion (the most important cause); (2) Medications — ACE inhibitors, ARBs, potassium-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin; (3) Acidosis — metabolic acidosis shifts potassium out of cells; (4) Tissue destruction — rhabdomyolysis, tumor lysis syndrome, severe burns, massive hemolysis; (5) Adrenal insufficiency — Addison disease, hypoaldosteronism; (6) Pseudohyperkalemia — hemolyzed specimen, prolonged tourniquet use, fist clenching during draw, very high WBC or platelet count. Always verify an unexpected high potassium with a non-hemolyzed repeat specimen.

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Potassium Levels — Normal Range & Causes

Complete reference on potassium normal ranges, causes of hyperkalemia and hypokalemia, dangerous levels, ECG changes, and clinical management.

⚡ Quick Answer — Normal Potassium Range

3.5–5.0 mEq/L (3.5–5.0 mmol/L)

⚠ Critical LOW: <2.5 mEq/L

⚠ Critical HIGH: >6.5 mEq/L

Potassium is the most important intracellular cation. Even small deviations can cause life-threatening cardiac arrhythmias.

What Is Potassium?

Potassium (K⁺) is the primary intracellular cation — approximately 98% of total body potassium (~3,500 mEq) resides inside cells, with only 2% in the extracellular fluid. This steep intracellular-to-extracellular gradient (approximately 140:4 mEq/L) is maintained by the Na⁺/K⁺-ATPase pump and is critical for establishing the resting membrane potential of excitable cells (cardiac myocytes, skeletal muscle, neurons).

Serum potassium is tightly regulated between 3.5–5.0 mEq/L through three main mechanisms: (1) Renal excretion — the kidneys are the primary regulator, handling ~90% of daily potassium excretion (mainly in the distal nephron under aldosterone control); (2) Transcellular shifts — insulin, catecholamines (β2 receptors), and alkalosis drive potassium into cells; acidosis, hyperosmolality, and cell lysis release it; (3) GI excretion — a minor pathway (~10%), but becomes important in renal failure.

Because potassium directly affects the cardiac action potential, both hypokalemia and hyperkalemia can cause life-threatening arrhythmias — making potassium one of the most clinically important electrolytes. Critical values (<2.5 or >6.5 mEq/L) are universally flagged for immediate clinician notification.

Normal Potassium Range

Category	Conventional (mEq/L)	SI (mmol/L)
Adults (serum)	3.5–5.0	3.5–5.0
Adults (plasma)	3.5–4.5	3.5–4.5
Newborns (0–7 days)	3.7–5.9	3.7–5.9
Infants (7 days–1 year)	4.1–5.3	4.1–5.3
Children (1–16 years)	3.4–4.7	3.4–4.7
Clinical Severity Thresholds (Adults)
Normal	3.5–5.0	3.5–5.0
Mild hypokalemia	3.0–3.4	3.0–3.4
Moderate hypokalemia	2.5–2.9	2.5–2.9
Severe / critical hypokalemia	<2.5	<2.5
Mild hyperkalemia	5.1–5.5	5.1–5.5
Moderate hyperkalemia	5.6–6.4	5.6–6.4
Severe / critical hyperkalemia	>6.5	>6.5

Reference ranges from Tietz Clinical Guide to Laboratory Tests, 4th edition. For potassium, conventional and SI units are equivalent (mEq/L = mmol/L). Serum values are typically 0.1–0.5 mEq/L higher than plasma due to potassium released from platelets during clotting.

What Does a High Potassium Mean? (Hyperkalemia)

Hyperkalemia (K⁺ >5.0 mEq/L) is common in clinical practice, particularly in patients with renal disease. It is a medical emergency when severe (>6.5 mEq/L) because of the risk of fatal cardiac arrhythmias.

Causes of Hyperkalemia

Renal failure — the most important cause. Decreased GFR reduces potassium excretion. Significant hyperkalemia typically occurs when GFR falls below 15–20 mL/min, unless other factors are present.
Medications — ACE inhibitors, ARBs, spironolactone/eplerenone, amiloride, triamterene, NSAIDs, trimethoprim, calcineurin inhibitors (tacrolimus, cyclosporine), heparin, beta-blockers (non-selective).
Metabolic acidosis — hydrogen ions move intracellularly, displacing potassium extracellularly. Each 0.1 decrease in pH raises serum K⁺ by ~0.2–0.4 mEq/L (for mineral acidoses).
Tissue destruction — rhabdomyolysis, tumor lysis syndrome, massive hemolysis, crush injuries, severe burns.
Adrenal insufficiency — Addison disease (primary) or isolated hypoaldosteronism (Type IV RTA). Aldosterone deficiency impairs renal potassium excretion.
Diabetic ketoacidosis (DKA) — insulin deficiency and acidosis shift potassium out of cells, even though total body potassium is actually depleted.
Pseudohyperkalemia — the most common cause of unexpected hyperkalemia! Caused by hemolyzed specimen, prolonged tourniquet time, fist clenching during draw, extreme leukocytosis (>70,000/µL), or extreme thrombocytosis (>500,000/µL). Always repeat an unexpected high potassium.

ECG Changes in Hyperkalemia

ECG changes progress with increasing potassium (though correlation is imperfect):

5.5–6.5 mEq/L: Peaked, narrow T waves (earliest finding). PR prolongation.
6.5–7.5 mEq/L: Flattened/absent P waves. QRS widening. First-degree AV block.
7.0–8.0 mEq/L: Bizarre wide QRS ("sine wave" pattern). Bundle branch blocks.
>8.0 mEq/L: Ventricular fibrillation, asystole, PEA arrest.

⚠ Any ECG changes with hyperkalemia = medical emergency. Give IV calcium gluconate immediately to stabilize the myocardium.

Symptoms of Hyperkalemia

Often asymptomatic until severe. Symptoms include: muscle weakness (may progress to flaccid paralysis), paresthesias, nausea, palpitations, and cardiac arrest. Hyperkalemia is sometimes called the "silent killer" because fatal arrhythmias can occur without warning symptoms.

What Does a Low Potassium Mean? (Hypokalemia)

Hypokalemia (K⁺ <3.5 mEq/L) is extremely common, occurring in up to 20% of hospitalized patients. It is usually due to losses (renal or GI) or transcellular shifts.

Causes of Hypokalemia

Diuretics — the most common cause. Thiazides (hydrochlorothiazide, chlorthalidone) and loop diuretics (furosemide, bumetanide) increase renal potassium wasting.
GI losses — vomiting (alkalosis-mediated renal loss, not directly from gastric fluid), diarrhea (direct colonic loss), nasogastric suction, laxative abuse.
Alkalosis — metabolic or respiratory alkalosis shifts K⁺ into cells. Each 0.1 increase in pH decreases K⁺ by ~0.2–0.4 mEq/L.
Renal tubular acidosis (Type I and II) — renal potassium wasting with metabolic acidosis.
Hypomagnesemia — critically important: magnesium depletion causes refractory potassium loss. Hypokalemia will not correct until magnesium is repleted. Always check magnesium alongside potassium.
Primary hyperaldosteronism (Conn syndrome) — excess aldosterone drives renal potassium excretion. Should be suspected in resistant hypertension with hypokalemia.
Insulin administration — drives K⁺ into cells (therapeutic use in hyperkalemia; iatrogenic cause in DKA treatment).
Beta-2 agonists — albuterol and other β2-agonists shift K⁺ intracellularly.
Amphotericin B — causes renal potassium and magnesium wasting.
Hypokalemic periodic paralysis — rare genetic or thyrotoxic condition causing episodic severe hypokalemia with paralysis.

ECG Changes in Hypokalemia

Mild (3.0–3.5 mEq/L): Flattened T waves, ST depression, prominent U waves.
Moderate (2.5–3.0 mEq/L): Prominent U waves, T-U fusion, prolonged QT/QU interval.
Severe (<2.5 mEq/L): Torsades de pointes, ventricular tachycardia/fibrillation, PEA arrest.

Symptoms of Hypokalemia

Mild hypokalemia (3.0–3.5 mEq/L) is often asymptomatic. As potassium falls below 3.0 mEq/L: muscle weakness (especially proximal/lower extremity), cramps, fatigue, constipation/ileus (smooth muscle dysfunction), polyuria/polydipsia (renal concentrating defect). Severe hypokalemia (<2.5 mEq/L) can cause ascending paralysis, respiratory failure, rhabdomyolysis, and cardiac arrest.

Related Tests & Calculators

Magnesium — always check with potassium. Hypomagnesemia causes refractory hypokalemia.
Anion Gap — Anion Gap Calculator — essential for evaluating the cause of metabolic acidosis that may accompany hyperkalemia.
ABG (Arterial Blood Gas) — ABG Interpreter — acid-base status directly affects transcellular potassium shifts.
Sodium Correction — Sodium Correction Calculator — electrolyte abnormalities often coexist.
Renal function (BUN, creatinine, eGFR) — renal failure is the most important cause of hyperkalemia.
Urine potassium and TTKG — transtubular potassium gradient helps distinguish renal from non-renal potassium losses.
ECG — mandatory in all patients with significant hypo- or hyperkalemia.
Aldosterone / renin — for workup of refractory hypokalemia or hyperkalemia with renal potassium wasting.

About This Test

Clinical Pearls

🔑 Key Points for Clinicians

Pseudohyperkalemia is common. Up to 20% of "hyperkalemia" in clinical practice is spurious. Before treating, always check for hemolysis on the sample and repeat if unexpected. A truly hemolyzed sample should be discarded and redrawn.
The magnesium-potassium connection: If a patient's potassium isn't responding to replacement, check the magnesium. Hypomagnesemia causes renal potassium wasting through the ROMK channel — the K⁺ simply won't stay in the body until Mg²⁺ is corrected.
Potassium deficit estimation: For every 1 mEq/L drop in serum K⁺ below 4.0, total body deficit is roughly 200–400 mEq. A patient with K⁺ of 2.0 may need 400–800 mEq of total replacement. IV replacement should not exceed 10–20 mEq/hour via peripheral line (or 40 mEq/hour via central line with cardiac monitoring).
DKA potassium paradox: Patients in DKA often present with normal or high serum K⁺ despite severe total body potassium depletion (due to acidosis and insulin deficiency pushing K⁺ out of cells). Potassium will plummet when insulin is given. Add K⁺ to fluids when serum K⁺ drops below 5.3 mEq/L; hold insulin if K⁺ <3.3 mEq/L.
Emergency treatment of hyperkalemia: (1) Calcium gluconate IV — stabilizes the myocardium (onset: minutes); (2) Insulin + glucose — shifts K⁺ into cells (onset: 15–30 min); (3) Albuterol nebulized — shifts K⁺ into cells; (4) Sodium bicarbonate — if acidotic; (5) Kayexalate or patiromer — removes K⁺ from body (slow onset); (6) Hemodialysis — definitive removal.
Serum vs. plasma: Serum K⁺ is 0.1–0.5 mEq/L higher than plasma K⁺ because potassium is released from platelets during clotting. Use the same specimen type for serial monitoring.

Specimen Notes

Potassium is measured from serum (red-top or SST tube) or plasma (green-top heparin tube). The specimen must be processed promptly — prolonged contact with cells causes K⁺ leakage. Avoid tourniquet time >1 minute and fist clenching, both of which can raise K⁺ by 1–2 mEq/L. Pneumatic tube transport may cause hemolysis and falsely elevated K⁺ in some systems. Cool temperatures during transport delay cell metabolism and reduce spurious elevation.

References

Burtis CA, Ashwood ER, Bruns DE. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier; 2018:738-745.
Mount DB. Causes and evaluation of hyperkalemia in adults. UpToDate. Accessed January 2025.
Mount DB. Causes of hypokalemia in adults. UpToDate. Accessed January 2025.
Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer. J Am Soc Nephrol. 1998;9(8):1535-1543.
Palmer BF. Regulation of potassium homeostasis. Clin J Am Soc Nephrol. 2015;10(6):1050-1060.
Clase CM, Carrero JJ, Ellison DH, et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference. Kidney Int. 2020;97(1):42-61.
Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med. 2017;18(5):963-971.

References last verified: February 2026