Lab result explainedMetabolic panelLast updated November 8, 2026

Potassium blood test: what high potassium (hyperkalemia) and low potassium mean

Potassium (serum) (K) · Basic or comprehensive metabolic panel (BMP/CMP), electrolyte panel · reported in mEq/L (identical to mmol/L for potassium)

Potassium is the main electrolyte inside your cells, and a potassium blood test measures the small fraction (about 2 percent of the body's total) that circulates in the blood. Normal is 3.5 to 5.0 mEq/L (the same in mmol/L), and the body keeps it there tightly because the gradient between inside and outside cells is what lets nerves fire and muscles, including the heart, contract. Values a little outside the range are common and often harmless; values far outside it can stop the heart.

High potassium (hyperkalemia) is most often a combination of reduced kidney excretion and a medicine that holds potassium back: chronic kidney disease, ACE inhibitors and ARBs, spironolactone, potassium-sparing diuretics, NSAIDs, trimethoprim and potassium supplements or salt substitutes. A surprisingly large share of high readings, however, are false. If red cells break during or after the blood draw (a haemolysed sample, a tight tourniquet, repeated fist clenching), they leak potassium into the tube and the lab reports a level the body never had; this pseudohyperkalemia is the first thing to exclude with a repeat sample.

Low potassium (hypokalemia) is usually caused by losses: loop and thiazide diuretics, vomiting, diarrhoea, laxative misuse, or by potassium shifting into cells with insulin, salbutamol (albuterol) or alkalosis. Low magnesium makes it hard to correct. Both extremes produce muscle weakness and heart rhythm disturbance, which is why a potassium above about 6.0 or below 2.5 mEq/L is treated as an emergency.

K at a glance

  • What it is: the concentration of potassium in blood plasma; most potassium is inside cells, so the blood level is a sensitive but indirect gauge.
  • Normal: 3.5–5.0 mEq/L (mmol/L); many labs use 3.5–5.1 or 5.2. Optimal for the heart is around 4.0–5.0.
  • High (hyperkalemia): above 5.0–5.5. Mild 5.1–5.9; moderate 6.0–6.4; severe 6.5 or more. Above 6.0 with ECG changes or above 6.5 at any time is an emergency.
  • Low (hypokalemia): below 3.5. Mild 3.0–3.4; moderate 2.5–2.9; severe below 2.5, where paralysis and dangerous arrhythmias occur.
  • Common causes: kidney disease, ACE inhibitors/ARBs, spironolactone, haemolysed samples (false high); diuretics, vomiting, diarrhoea, low magnesium (low).
  • Next step: repeat on a carefully drawn sample, check kidney function, glucose, magnesium and medicines; an ECG if the level is above 6.0 or below 3.0 or you have palpitations or weakness.

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What K measures

Potassium is measured with an ion-selective electrode in serum (clotted blood) or plasma, in milliequivalents per litre (mEq/L), which equals millimoles per litre (mmol/L). About 98 percent of body potassium sits inside cells at a concentration of around 140 mEq/L, against roughly 4 in the blood. That 35-fold gradient, maintained by the sodium-potassium pump, sets the electrical resting state of every nerve and muscle cell. Shift a little potassium out of cells and the heart becomes irritable; shift too much in and muscles cannot fire.

Two systems control the blood level. Over minutes to hours, insulin, adrenaline (via beta-2 receptors) and the blood's acid-base state move potassium into or out of cells, which is why a dose of insulin or a salbutamol nebuliser lowers potassium temporarily and why acidosis raises it. Over hours to days, the kidneys excrete what you eat (typically 60 to 100 mEq a day) under the control of aldosterone; healthy kidneys can handle a very large potassium load, so sustained hyperkalemia almost always involves kidney impairment, aldosterone blockade or both.

The measurement is easily corrupted. Red cells contain about 25 times more potassium than plasma, so haemolysis during collection (a small needle, a hard pull on the syringe, a tight or prolonged tourniquet, shaking the tube) raises the reading, as does repeated fist clenching, which can add 1 to 2 mEq/L by itself. Serum runs 0.3 to 0.4 mEq/L higher than plasma because platelets release potassium as blood clots, and in people with very high platelet or white cell counts this can push serum potassium above 6 while plasma potassium is normal. Delayed processing, especially of chilled samples, has the same effect.

Normal range for K

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (mEq/L (identical to mmol/L for potassium))Notes
Adults, normal3.5–5.0 mEq/LMany labs report 3.5–5.1 or 3.5–5.2; a few 3.6–5.3. Use the printed range. Serum runs about 0.3–0.4 higher than plasma.
Mild hyperkalemia5.1–5.9 mEq/LUsually no symptoms. Repeat on a non-haemolysed sample first; then review kidney function and medicines.
Moderate hyperkalemia6.0–6.4 mEq/LNeeds same-day assessment and an ECG. Treatment started if ECG changes, kidney failure or a rising trend.
Severe hyperkalemia6.5 mEq/L or aboveMedical emergency regardless of symptoms: risk of heart block, ventricular arrhythmia and cardiac arrest. Peaked T waves, wide QRS and a 'sine wave' ECG pattern are the warning signs.
Mild hypokalemia3.0–3.4 mEq/LCommon with diuretics. Usually corrected with diet or oral potassium; check magnesium.
Moderate hypokalemia2.5–2.9 mEq/LWeakness, cramps and constipation are likely; ECG changes (flattened T waves, U waves) appear. Oral or IV replacement.
Severe hypokalemiaBelow 2.5 mEq/LEmergency: muscle paralysis, breathing muscle weakness, rhabdomyolysis and life-threatening arrhythmias, particularly in people on digoxin or with heart disease.
Estimated body deficitRoughly 200–400 mEq for each 1 mEq/L below 4.0A fall from 4.0 to 3.0 reflects a total body loss of several hundred mEq, which is why replacement takes days, not one dose.

High potassium (hyperkalemia)

A potassium above 5.0 to 5.5 mEq/L means potassium is either entering the blood faster than the kidneys can clear it or the kidneys cannot clear it normally. The first question is always whether the result is real. Haemolysis is the most common cause of a high potassium in outpatients, and a lab will usually flag the sample as haemolysed; if it does not, or if the result is unexpected, a repeat on a freshly drawn, promptly processed sample (ideally plasma rather than serum, without fist clenching) settles it. A potassium that comes back normal on repeat needs no further action.

Genuine hyperkalemia in someone outside hospital is most often the product of two or more factors acting together: an eGFR below 45 or so, plus an ACE inhibitor, ARB, spironolactone, eplerenone, amiloride, triamterene, an NSAID, trimethoprim or heparin, plus a dietary source such as a potassium-chloride salt substitute or supplement. Hyperkalemia occurs in about 2 to 3 percent of people taking an ACE inhibitor or ARB but in roughly 10 percent when kidney disease or diabetes is also present, and after the RALES trial popularised spironolactone in heart failure, hospital admissions for hyperkalemia rose severalfold. Type 4 renal tubular acidosis (low aldosterone from diabetic kidney disease), Addison's disease, severe acidosis and insulin deficiency are the other recurring explanations.

What makes hyperkalemia dangerous is its effect on the heart. As potassium rises, the ECG shows peaked T waves (often from 5.5 to 6.5), then a prolonged PR interval and widened QRS (6.5 to 8), then a sine-wave pattern and ventricular fibrillation or asystole. The correlation is loose, and some people have a normal ECG at 7.0 while others have changes at 6.0, so any potassium above 6.0 is treated as potentially lethal until an ECG and a repeat level say otherwise. Chronic, slowly developing hyperkalemia is better tolerated than a sudden rise.

Common causes

  1. Haemolysed or poorly collected sample (pseudohyperkalemia)

    Red cells rupturing in the tube, fist clenching, a tight tourniquet, a small needle, delayed processing or very high platelet (above 500,000) or white cell counts release potassium after the blood has left the body. The most common cause of an unexpected high result; repeat before acting.

  2. Chronic kidney disease and acute kidney injury

    The kidneys excrete 90 percent of dietary potassium. Hyperkalemia becomes common once eGFR falls below 30 and is a frequent complication of acute kidney injury, especially with dehydration or obstruction.

  3. ACE inhibitors, ARBs and aliskiren

    Lisinopril, ramipril, losartan, valsartan and similar drugs lower aldosterone, reducing potassium excretion. The rise is usually 0.2 to 0.5 mEq/L but is larger with kidney disease, diabetes or when combined with the drugs below.

  4. Spironolactone, eplerenone, amiloride and triamterene

    Potassium-sparing diuretics block aldosterone or the kidney's sodium channel directly. In the RALES trial, serious hyperkalemia occurred in about 2 percent of patients on spironolactone; in everyday practice, where kidney function and potassium are monitored less closely, the rate has been much higher.

  5. NSAIDs, trimethoprim, heparin, beta-blockers, calcineurin inhibitors

    Ibuprofen and naproxen reduce renin and kidney blood flow; trimethoprim (in co-trimoxazole) blocks the kidney sodium channel like amiloride; heparin suppresses aldosterone; non-selective beta-blockers, tacrolimus and cyclosporine impair cellular uptake or excretion.

  6. Potassium supplements, salt substitutes and high-potassium diet with impaired excretion

    Potassium chloride salt substitutes ('lite' salts) contain 10 to 13 mEq per quarter teaspoon. A healthy person handles this easily; someone on an ACE inhibitor with CKD may not. Potassium pills, some multivitamins and large amounts of juice, dried fruit, potatoes and tomato products add up.

  7. Acidosis and insulin deficiency

    In metabolic acidosis, hydrogen ions move into cells and potassium moves out. In diabetic ketoacidosis and hyperglycaemic states, lack of insulin and high osmolality push potassium out of cells, so blood potassium is high even though the body is depleted; it falls sharply once insulin is given.

  8. Tissue breakdown

    Rhabdomyolysis (crush injury, extreme exercise, statins in rare cases), tumour lysis after chemotherapy, major burns, large haematomas and haemolytic anaemia release intracellular potassium into the blood.

  9. Addison's disease and hypoaldosteronism

    Lack of aldosterone from adrenal failure, or from type 4 renal tubular acidosis in diabetes, means the kidneys cannot excrete potassium. High potassium with low sodium, low blood pressure and fatigue should prompt a morning cortisol.

  10. Digoxin toxicity, succinylcholine and hyperkalemic periodic paralysis

    Digoxin overdose poisons the sodium-potassium pump; the anaesthetic succinylcholine releases potassium from muscle, dangerously so in burns and neuromuscular disease; the rare inherited periodic paralysis causes transient spikes with weakness.

Symptoms that can go with it

  • Usually none until potassium is above about 6.0 to 6.5, which is why it is found on routine testing
  • Muscle weakness or heaviness, typically starting in the legs
  • Tingling or numbness
  • Nausea or vomiting
  • Palpitations, a slow or irregular pulse, light-headedness
  • Shortness of breath
  • Sudden collapse or cardiac arrest at very high levels

Low potassium (hypokalemia)

A potassium below 3.5 mEq/L means potassium has either been lost from the body or has shifted temporarily into cells. Losses are by far the more common explanation. Loop diuretics (furosemide, bumetanide) and thiazides (hydrochlorothiazide, chlorthalidone, indapamide) are the leading cause, lowering potassium by roughly 0.3 to 0.8 mEq/L depending on dose, with about one in ten users dropping below 3.5. Vomiting, diarrhoea, laxative misuse, high-output stomas and sweating are the gut and skin routes. Because the blood holds only 2 percent of body potassium, a fall of 1 mEq/L usually represents a deficit of 200 to 400 mEq, so correction takes several days of replacement rather than a single dose.

Shifts into cells happen with insulin (including the insulin released after a large carbohydrate meal or during refeeding after starvation), with beta-agonists such as salbutamol (albuterol) and adrenaline, with alkalosis (for example after prolonged vomiting), and in the rare condition hypokalemic periodic paralysis. These produce a low reading without any real deficit and resolve as the trigger wears off. Low magnesium deserves special mention: around 40 percent of people with hypokalemia also have hypomagnesemia, and until the magnesium is replaced the kidneys keep wasting potassium and oral or IV replacement seems not to work.

A low potassium with high blood pressure, especially in someone not on a diuretic, raises the question of primary hyperaldosteronism (Conn's syndrome), which is found in 5 to 10 percent of people with hypertension and is more common than once thought; Cushing's syndrome, liquorice (glycyrrhizin) and renal artery stenosis do the same. Hypokalemia matters most in people with heart disease or on digoxin, where even 3.0 to 3.4 increases the risk of arrhythmia; in those groups clinicians often aim for 4.0 or above.

Common causes

  1. Loop and thiazide diuretics

    The most common cause overall. Furosemide, bumetanide, hydrochlorothiazide, chlorthalidone and indapamide increase potassium loss in urine; the effect is dose-related and larger when dietary intake is poor or magnesium is low.

  2. Vomiting, diarrhoea and laxative misuse

    Stool contains 20 to 50 mEq/L of potassium, so prolonged diarrhoea causes large losses. Vomiting loses little potassium directly but the resulting alkalosis and volume depletion make the kidneys waste it. Hidden purging or laxative use is a frequent explanation for unexplained hypokalemia in young adults.

  3. Low magnesium

    Magnesium is needed to close potassium channels in kidney tubule cells. When it is low, potassium leaks into urine and replacement fails until magnesium is corrected. Common with PPIs, alcohol, diuretics and diarrhoea.

  4. Primary hyperaldosteronism (Conn's syndrome)

    An adrenal adenoma or both adrenals over-producing aldosterone drives potassium into urine and raises blood pressure. Suspect it in anyone with hypertension and a potassium below 3.5, especially if not on a diuretic; an aldosterone-to-renin ratio is the screening test.

  5. Insulin, salbutamol (albuterol), adrenaline and refeeding

    Insulin and beta-2 agonists push potassium into cells; a 10 to 20 mg salbutamol nebuliser lowers potassium by 0.5 to 1.0 mEq/L for a few hours. Refeeding a malnourished person triggers insulin release and can cause dangerous drops in potassium, phosphate and magnesium.

  6. Liquorice and glycyrrhizin

    Glycyrrhizin in black liquorice candy, some herbal teas and chewing tobacco blocks the enzyme that protects the kidney from cortisol, mimicking aldosterone excess. Around 100 mg of glycyrrhizin a day (roughly 50 g of liquorice candy) for two weeks is enough to lower potassium and raise blood pressure in susceptible people.

  7. Cushing's syndrome and high-dose steroids

    Excess cortisol, whether from the body or from prescribed corticosteroids, has mineralocorticoid effects at high levels and wastes potassium, particularly with ectopic ACTH production.

  8. Kidney tubular disorders and some drugs

    Renal tubular acidosis types 1 and 2, Bartter and Gitelman syndromes, amphotericin B, high-dose penicillins, cisplatin and aminoglycosides all cause renal potassium wasting.

  9. Poor intake and alcohol use disorder

    Diet alone rarely causes hypokalemia because the kidneys conserve potassium, but very low intake combined with alcohol, vomiting, diarrhoea or diuretics tips the balance. Hypokalemia is found in a substantial minority of people admitted with alcohol withdrawal.

  10. Hypokalemic periodic paralysis and thyrotoxicosis

    A rare inherited channel disorder, and an acquired form in hyperthyroidism (most often in men of East Asian descent), causes episodes of profound weakness with potassium below 2.5 that resolve as potassium shifts back out of cells.

Symptoms that can go with it

  • Often none when potassium is 3.0 to 3.4
  • Muscle weakness, aching, cramps or fatigue
  • Constipation or bloating; in severe cases the bowel stops moving (ileus)
  • Palpitations, skipped beats or an irregular pulse
  • Passing large volumes of urine and excessive thirst (prolonged hypokalemia impairs kidney concentrating ability)
  • Tingling and numbness
  • Profound weakness, paralysis, difficulty breathing or dark urine from muscle breakdown when potassium is below 2.5

Read it alongside

  • Creatinine and eGFR — impaired kidney function is the usual background to genuine hyperkalemia and changes how any potassium level is managed.
  • Sodium — low sodium with high potassium suggests Addison's disease; low sodium with low potassium suggests diuretics or gut losses.
  • Magnesium — low magnesium causes and perpetuates low potassium; check it in every hypokalemia that does not correct easily.
  • CO2 (bicarbonate) and anion gap — acidosis pushes potassium out of cells (high potassium with low bicarbonate); alkalosis from vomiting pushes it in (low potassium with high bicarbonate). Type 4 RTA gives high potassium with a mild normal-gap acidosis.
  • Glucose — diabetic ketoacidosis presents with a high potassium that masks a large body deficit; insulin treatment can then cause a rapid fall.
  • BUN — a high BUN with high potassium points to kidney failure or dehydration; a rising BUN on an ACE inhibitor is a reason to recheck potassium.
  • Platelets and white cells — counts above 500,000 or 100,000 respectively can cause a falsely high serum potassium; ask for a plasma (heparin tube) potassium.
  • Aldosterone-to-renin ratio and morning cortisol — ordered when low potassium accompanies hypertension (hyperaldosteronism) or when high potassium accompanies low sodium and low blood pressure (adrenal insufficiency).

What usually happens next

  1. An unexpected high potassium (5.1 to 6.0) in someone who feels well is repeated on a fresh sample, drawn without a prolonged tourniquet or fist clenching and processed promptly; if the lab noted haemolysis, the result should be disregarded until repeated.
  2. If the high level is confirmed, expect a review of every medicine (ACE inhibitors, ARBs, spironolactone, NSAIDs, trimethoprim, potassium supplements, salt substitutes), kidney function and glucose; often the fix is adjusting a dose or stopping a salt substitute, then rechecking within a week.
  3. A potassium above 6.0, or above 5.5 in someone with kidney disease or on several of these drugs, needs an ECG and same-day assessment; treatment with calcium, insulin and glucose, nebulised salbutamol and potassium binders is given in hospital if the ECG is abnormal or the level is 6.5 or more.
  4. For low potassium, the usual sequence is checking magnesium, reviewing diuretics and laxatives, asking about vomiting or diarrhoea, and starting oral potassium chloride (typically 40 to 100 mEq a day in divided doses for several days) with a recheck in a few days to a week; IV replacement is reserved for levels below 2.5 or for ECG changes.
  5. Low potassium with high blood pressure, or hypokalemia that recurs without an obvious cause, should prompt an aldosterone-to-renin ratio and a check for Cushing's syndrome.
  6. If you take digoxin, have heart failure or a history of arrhythmia, ask what potassium target your clinician wants (often 4.0 to 5.0) and how often it should be checked after any change in diuretics or kidney function.

Diet, lifestyle and natural levers with evidence

What can move K once the cause is known. Nothing here replaces finding the cause.

Potassium-rich foods for people with normal kidney function

Strong evidence

A meta-analysis of 22 randomised trials and 11 cohort studies for the World Health Organization found that raising potassium intake lowered systolic blood pressure by about 3.5 mmHg and diastolic by 2 mmHg in people with hypertension, and that higher intake was associated with a 24 percent lower risk of stroke. Fruits, vegetables, beans, potatoes, dairy and fish provide the 2,600 to 3,400 mg (66 to 87 mEq) a day now recommended for adults, and raise a low-normal potassium by a few tenths of a mEq/L. This is the main reason the DASH diet lowers blood pressure.

Not appropriate for people with an eGFR below 30 to 45, on dialysis, or whose potassium is already above 5.0 on an ACE inhibitor, ARB or spironolactone; they should follow their clinician's dietary potassium limit.

Correct magnesium alongside potassium

Strong evidence

About 40 percent of people with hypokalemia have low magnesium as well, and in those people potassium replacement fails until magnesium is restored, because magnesium deficiency opens kidney channels that leak potassium into urine. Replacing magnesium (dietary sources such as nuts, seeds, legumes and leafy greens, or 300 to 400 mg a day of a well-absorbed supplement) is standard practice in refractory hypokalemia and typically allows potassium to normalise within days.

Magnesium supplements are cleared by the kidneys and can accumulate in kidney disease; magnesium oxide and citrate cause diarrhoea at higher doses, which itself loses potassium.

Avoid liquorice and glycyrrhizin

Strong evidence

In a dose-response study, healthy volunteers eating 50, 100 or 200 g of liquorice a day for 2 to 4 weeks showed a linear rise in systolic blood pressure of about 3 to 14 mmHg and a fall in potassium, with the effect appearing at glycyrrhizin doses around 100 mg a day. Case reports of hypokalemic paralysis and arrhythmia involve people eating liquorice candy daily for weeks. Deglycyrrhizinated (DGL) liquorice products do not have this effect; most European regulators advise keeping glycyrrhizin below 100 mg a day.

Glycyrrhizin also hides in some herbal teas, throat lozenges, chewing tobacco and traditional remedies. People on diuretics, with heart disease or over 40 are most susceptible.

Low-potassium cooking methods and salt-substitute caution in kidney disease

Moderate evidence

For people with CKD who need to limit potassium, boiling cut vegetables and discarding the water (leaching) removes roughly half of the potassium from potatoes and root vegetables, and soaking then double-boiling removes up to about 75 percent in laboratory food studies. The landmark SSaSS trial showed that a 75:25 sodium-chloride to potassium-chloride salt substitute cut stroke by 14 percent and death by 12 percent in the general rural Chinese population, but it deliberately excluded people with serious kidney disease or on potassium-sparing drugs, in whom the same substitute can cause dangerous hyperkalemia.

Anyone with an eGFR below 45 or on an ACE inhibitor, ARB or spironolactone should check with their clinician before using any potassium-chloride salt substitute.

Oral rehydration solution rather than water alone during vomiting or diarrhoea

Moderate evidence

Diarrhoeal stool contains 20 to 50 mEq/L of potassium, and replacing losses with plain water or sugary drinks lowers both sodium and potassium. WHO-formula oral rehydration solution contains 20 mmol/L of potassium along with sodium and glucose and has been shown in decades of trials to correct dehydration and electrolyte losses in children and adults with gastroenteritis, reducing the need for intravenous fluids by around a third. Bananas, potatoes, orange juice and coconut water add potassium once eating resumes.

Sports drinks are not a substitute: most contain under 5 mEq/L of potassium and far too much sugar for diarrhoeal illness. Seek care for vomiting that prevents fluids staying down for more than a day.

When to see a clinician promptly

  • A potassium of 6.5 mEq/L or above, or 6.0 or above with any weakness, palpitations, slow pulse or breathlessness: go to an emergency department. This can cause cardiac arrest with little warning.
  • A potassium below 2.5 mEq/L, or any low potassium with severe weakness, difficulty breathing, palpitations or dark urine.
  • A confirmed potassium above 5.5 if you have kidney disease, diabetes, heart failure or take an ACE inhibitor, ARB, spironolactone or NSAIDs, so doses can be reviewed before the level climbs.
  • Low potassium with high blood pressure not explained by a diuretic: possible primary hyperaldosteronism, which is treatable and often missed.
  • Low potassium that keeps recurring, or that you suspect relates to vomiting, laxative use or an eating disorder.
  • Any abnormal potassium if you take digoxin or have a history of arrhythmia, where even modest changes raise the risk of a dangerous rhythm.

Frequently asked questions

What is a normal potassium level?

Normal serum potassium is 3.5 to 5.0 mEq/L (the same as mmol/L); some labs extend the upper limit to 5.1, 5.2 or 5.3. For people with heart disease, clinicians often prefer 4.0 to 5.0. A value of 5.1 to 5.4 in someone who feels well is most often a sample artefact and is simply repeated.

What level of potassium is dangerous?

A potassium of 6.5 mEq/L or higher is a medical emergency at any time, and 6.0 or higher is treated as one if the ECG is abnormal or you have symptoms, because of the risk of cardiac arrest. At the low end, below 2.5 mEq/L is dangerous, causing muscle paralysis, breathing difficulty and arrhythmias. Values between 5.5 and 6.0 and between 2.5 and 3.0 need prompt attention but are rarely immediately life-threatening in otherwise healthy people.

Is a potassium of 5.3 or 5.5 high?

Slightly. A result of 5.3 is at or just above the upper limit on most labs and 5.5 is mild hyperkalemia. In someone with normal kidneys who is not on an ACE inhibitor, ARB or spironolactone, the most likely explanation is a haemolysed sample or fist clenching during the draw, and a repeat is normal more often than not. In someone with kidney disease or on those medicines it is real more often and the medicines or diet are reviewed.

Can a blood test show falsely high potassium?

Yes, and it is common. If red cells break during collection (haemolysis), if you clench your fist repeatedly, if the tourniquet is on for long, if the sample sits for hours or is refrigerated before processing, or if you have a very high platelet or white cell count, potassium leaks out of cells into the tube. The lab usually flags haemolysis. Asking for a repeat with a relaxed arm, a larger needle and prompt processing, or a plasma rather than serum sample, resolves most of these.

What are the symptoms of low potassium?

Mild hypokalemia (3.0 to 3.4) usually causes nothing you would notice. As it falls further, muscle weakness, aching, cramps, tiredness, constipation and palpitations appear, along with excess urination and thirst if it has been low for a while. Below about 2.5 there can be profound weakness, paralysis, difficulty breathing and dangerous heart rhythms. People on digoxin or with heart disease are at risk of arrhythmia at higher levels than others.

What foods should I avoid if my potassium is high?

Only if your clinician has confirmed genuine hyperkalemia, usually with kidney disease, do you need to limit potassium. The largest sources are potassium-chloride salt substitutes, potassium supplements, orange and tomato juice, bananas, potatoes, dried fruit, beans, nuts, dairy and chocolate. Boiling vegetables and discarding the water removes about half the potassium. Most people with a mildly high reading and normal kidneys do not need to change their diet; the medicine or the sample is usually the issue.

Does spironolactone or lisinopril raise potassium?

Yes. ACE inhibitors (lisinopril, ramipril) and ARBs (losartan, valsartan) typically raise potassium by 0.2 to 0.5 mEq/L, and spironolactone, eplerenone, amiloride and triamterene raise it further by blocking potassium excretion directly. Combining them, or adding an NSAID, trimethoprim or a salt substitute, especially with an eGFR below 45, is the usual recipe for dangerous hyperkalemia. Potassium and creatinine are checked within one to two weeks of starting or increasing these drugs.

How quickly can low potassium be corrected?

Mild hypokalemia usually corrects over a few days with oral potassium chloride (commonly 40 to 100 mEq a day in divided doses) and potassium-rich foods, because each 1 mEq/L below 4.0 represents a deficit of 200 to 400 mEq. If magnesium is also low it must be replaced or the potassium will not hold. Severe hypokalemia or ECG changes are treated with intravenous potassium in hospital, at a controlled rate, with cardiac monitoring.

References

  1. Potassium blood test. MedlinePlus, US National Library of Medicine (2023)View source
  2. High potassium (hyperkalemia). Mayo Clinic (2023)View source
  3. Hyperkalemia. Merck Manual Professional Version (2023)
  4. Hypokalemia. Merck Manual Professional Version (2023)
  5. Viera AJ, Wouk N. Potassium disorders: hypokalemia and hyperkalemia. American Family Physician (2015)
  6. 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 International (2020)
  7. Asirvatham JR, Moses V, Bjornson L. Errors in potassium measurement: a laboratory perspective for the clinician. North American Journal of Medical Sciences (2013)
  8. Aburto NJ, Hanson S, Gutierrez H, Hooper L, Elliott P, Cappuccio FP. Effect of increased potassium intake on cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ (2013)
  9. Neal B, Wu Y, Feng X, et al.. Effect of salt substitution on cardiovascular events and death (SSaSS). New England Journal of Medicine (2021)
  10. Whang R, Whang DD, Ryan MP. Refractory potassium repletion. A consequence of magnesium deficiency. Archives of Internal Medicine (1992)
  11. Sigurjonsdottir HA, Franzson L, Manhem K, Ragnarsson J, Sigurdsson G, Wallerstedt S. Liquorice-induced rise in blood pressure: a linear dose-response relationship. Journal of Human Hypertension (2001)
  12. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. Journal of Renal Nutrition (2006)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.