Digoxin Dosing Calculator

Use the Digoxin Dosing Calculator

Free digoxin dosing calculator: loading and maintenance doses from creatinine clearance, lean weight, and target serum level, with drug interaction alerts.

How to Use Digoxin Dosing Calculator

1. Step 1: Choose the indication

   Select Heart failure or AF rate control. Heart failure sets the target to 0.5-0.9 ng/mL and drops the non-renal clearance term from 40 to 20 mL/min per 70 kg; AF rate control targets 0.8-2.0 ng/mL.

2. Step 2: Enter age, sex, weight and height

   Type the patient age and body weight, then the height in cm or inches. The calculator derives Devine ideal body weight and doses on the lower of actual and ideal weight, because digoxin does not distribute into fat.

3. Step 3: Enter serum creatinine

   Add a stable serum creatinine in mg/dL or micromoles per litre. This drives the Cockcroft-Gault creatinine clearance that sets digoxin clearance and volume of distribution.

4. Step 4: Set target level, formulation and interactions

   Pick a target serum digoxin concentration, choose oral tablets (F 0.70), oral solution (F 0.80) or IV (F 1.00), and select any interacting drug such as amiodarone or verapamil to reduce clearance accordingly.

5. Step 5: Add a loading dose if needed

   Tick Include a loading dose and choose 8 to 15 mcg/kg of lean weight to see the total digitalizing dose split 50 percent now, then 25 percent at 6 hours and 25 percent at 12 hours.

6. Step 6: Read the regimen and predicted level

   The suggested maintenance regimen appears with the predicted steady-state concentration on the therapeutic window bar, plus creatinine clearance, volume of distribution, clearance, half-life and the days needed to reach steady state.

Key Features

• Maintenance dose from Koup digoxin clearance (1.303 × CrCl plus a non-renal term)
• Volume of distribution scaled to renal function with the Sheiner equation
• Separate targets for heart failure (0.5–0.9 ng/mL) and atrial fibrillation rate control
• Total digitalizing dose in mcg/kg lean weight with a 50 / 25 / 25 split schedule
• Bioavailability correction for IV, oral tablets, and oral solution
• Clearance reduction for amiodarone, quinidine, verapamil, and other P-glycoprotein inhibitors

Understanding Results

The Equations Behind This Digoxin Dosing Calculator

Four equations run in sequence. Creatinine clearance comes first, because everything downstream depends on it:

The dosing weight is the lower of actual and Devine ideal body weight, since digoxin binds to skeletal muscle and not to fat. The non-renal term is 40 mL/min per 70 kg normally and 20 mL/min per 70 kg in heart failure, where hepatic and splanchnic perfusion falls. Bioavailability is 1.00 intravenously, 0.80 for the oral solution and 0.70 for tablets. The coefficient of 1.303 exceeds one because digoxin is actively secreted by P-glycoprotein in addition to being filtered — which is exactly the pathway amiodarone, quinidine and verapamil block.

Reference Ranges & Interpretation

Target concentration depends on why the drug was started. For heart failure, aim for 0.5–0.9 ng/mL; DIG trial analyses associate 1.2 ng/mL and above with excess mortality. For atrial fibrillation rate control the traditional 0.8–2.0 ng/mL range still applies, though most patients are controlled at rest well below 1.5 ng/mL. Anything above 2.0 ng/mL is toxic territory.

Typical daily doses fall out of the clearance equation predictably: about 0.25 mg daily above 80 mL/min, 0.125–0.1875 mg daily at 50–79 mL/min, 0.125 mg daily at 30–49 mL/min, 0.0625 mg daily at 15–29 mL/min, and 0.0625 mg every other day below 15 mL/min. Half-life tracks the same axis — roughly 30–40 hours with healthy kidneys, past 85 hours at a creatinine clearance of 20 mL/min — which sets how long you must wait before a level means anything. Confirm the input figure with the creatinine clearance calculator if renal function is borderline.

Assumptions & Limitations

These are population estimates for adults with stable renal function. Cockcroft-Gault is unreliable in acute kidney injury, extreme body composition, amputation and advanced cirrhosis, and every error there propagates straight into the dose. The model does not cover children, pregnancy, haemodialysis or continuous renal replacement therapy, thyroid disease, or established digoxin toxicity, where digoxin-specific antibody fragments — not dose arithmetic — are the treatment. Predicted concentrations also assume perfect adherence and no assay interference; spironolactone metabolites and endogenous digoxin-like immunoreactive substances shift immunoassay results in renal failure, pregnancy and liver disease. Finally, no calculator sees potassium, magnesium or calcium, and those decide whether a given concentration is safe. Treat every output as a starting regimen to be confirmed with a measured serum level drawn at least 6 hours after a dose, and defer to the prescribing clinician.

Complete Guide: Digoxin Dosing Calculator

Any digoxin dosing calculator that asks only for body weight is solving the wrong equation. Consider a 72-year-old man, 78 kg, 175 cm, serum creatinine 1.4 mg/dL, admitted with worsening heart failure and already taking 0.25 mg of digoxin daily because that is the dose everyone remembers. His creatinine looks unremarkable. His ventricular rate is controlled. He is also, on the arithmetic below, running about 60% above the concentration his kidneys can sustain.

Digoxin has one of the narrowest therapeutic indices in cardiology: the concentration that helps and the concentration that causes vomiting, confusion, and bidirectional ventricular tachycardia sit within a factor of two or three of each other. About 60 to 80% of a dose leaves through the kidneys unchanged, so renal function — not the number on the scale — sets the daily requirement. This guide walks one patient end to end, then generalises the reasoning to loading doses, drug interactions, and the electrolytes that make a "normal" level dangerous.

A 72-year-old on 0.25 mg daily: walking the numbers

Run the patient above through the calculator step by step. Every figure comes from equations published in clinical pharmacokinetics texts and used by hospital pharmacy services daily.

1. Pick the dosing weight. Devine ideal body weight for a 175 cm male is 50 + 2.3 × 8.9 inches over 60, or 70.5 kg. His actual weight is 78 kg. Digoxin barely enters adipose tissue, so the lower figure — 70.5 kg — is the one that counts.
2. Estimate creatinine clearance. Cockcroft-Gault on that weight: (140 − 72) × 70.5 ÷ (72 × 1.4) = 47.5 mL/min. A "normal-looking" creatinine of 1.4 mg/dL in a 72-year-old is really stage 3 chronic kidney disease.
3. Calculate digoxin clearance. Cl = 1.303 × 47.5 + 20 = 82 mL/min, which is 118 L per day. The 20 mL/min term is the non-renal (hepatic and gut) route, and heart failure halves it from the usual 40.
4. Convert a target level into a daily requirement. Dose = target × clearance ÷ bioavailability. For 0.8 ng/mL on tablets: 0.8 × 118 ÷ 0.7 = 135 mcg per day.
5. Round to a real tablet. 135 mcg sits closest to 0.125 mg daily, which back-calculates to a steady-state level of 0.74 ng/mL — inside the target window.

His current 0.25 mg daily predicts roughly 1.48 ng/mL. Not immediately toxic, but well past the concentration where the DIG trial data stop showing benefit and start showing harm, and only one episode of dehydration or one new dose of amiodarone away from real trouble. The half-life here is about 58 hours, so it took him nearly 12 days to arrive at that level and it will take a similar span to come down. Digoxin never punishes you quickly, which is precisely what makes it easy to get wrong.

The dose follows clearance, not body weight

The clearance equation used above — Cl (mL/min) = 1.303 × CrCl + non-renal term — carries a coefficient greater than one because digoxin is not only filtered at the glomerulus but also actively secreted into the tubule by P-glycoprotein. It leaves the body faster than creatinine does. That single fact explains most digoxin interactions, because every drug that inhibits P-glycoprotein blocks that secretion.

The non-renal term matters more than its size suggests. It is roughly 40 mL/min per 70 kg in a patient with preserved cardiac output and about 20 mL/min per 70 kg in moderate to severe heart failure, where hepatic and splanchnic perfusion falls. At a creatinine clearance of 20 mL/min that difference is the whole ballgame: total clearance is either 46 or 66 mL/min depending on which term applies, a 30% swing in the daily dose from the indication alone. This is why the calculator asks whether you are treating heart failure or atrial fibrillation before it asks anything else.

Because renal function drives everything, an accurate creatinine clearance is not a formality. The digoxin literature was written in Cockcroft-Gault units, so use a creatinine clearance calculator rather than an eGFR value reported in mL/min/1.73m². The two diverge substantially at the extremes of body size, and in a 48 kg woman the body-surface-normalised figure can overstate true clearance by 25% or more — which translates directly into an overdose.

0.5 to 0.9 ng/mL: what the DIG trial changed

For thirty years the therapeutic range printed on lab reports was 0.8 to 2.0 ng/mL. Post-hoc analysis of the Digitalis Investigation Group trial rewrote that for heart failure. Men with serum digoxin concentrations of 0.5 to 0.8 ng/mL had lower mortality than placebo; those at 1.2 ng/mL or above had higher mortality than placebo. The drug did not stop working — the dose-response curve simply turned out to be inverted-U shaped, and the old range put a large share of patients on the wrong side of the peak.

Selecting the heart failure indication in the calculator therefore does two things at once: it shifts the default target down to 0.8 ng/mL and it lowers the non-renal clearance term. Both push the suggested dose downward, which is the correct direction of travel. In practice this is why so many heart failure patients belong on 0.125 mg daily or 0.0625 mg daily rather than the 0.25 mg tablet that dominated prescribing for decades.

Loading dose: when 10 mcg/kg is right and when it overshoots

Digoxin's long half-life means that without a loading dose, a patient in rapid atrial fibrillation would wait ten days for the drug to work. So the textbook total digitalizing dose is 8 to 12 mcg/kg of lean weight for heart failure and 10 to 15 mcg/kg for atrial fibrillation, given as 50% up front and two 25% increments six hours apart. Here is what those ranges actually predict in the 70 kg patient with a creatinine clearance of 50 mL/min, whose volume of distribution works out to 414 L.

Read that table carefully before dismissing it. A transient peak of 2 ng/mL six hours after a load is not automatically toxic — the level decays toward the maintenance steady state over the following days, and the guideline ranges were derived in populations that tolerated it. But the margin at 15 mcg/kg in a patient with a creatinine clearance of 50 mL/min is zero, and the arithmetic makes clear why the upper half of the range belongs to acute atrial fibrillation in someone with intact kidneys, not to a frail inpatient with quietly declining renal function. When heart failure is the indication and the rhythm is sinus, the honest answer is usually to skip the load entirely and let the maintenance dose accumulate.

Kidney failure shrinks the volume of distribution too

Most clinicians reflexively cut the maintenance dose in renal impairment and stop there. The loading dose needs cutting as well, for a separate reason. Digoxin binds to the Na⁺/K⁺-ATPase in skeletal muscle, and uraemia reduces the number of available binding sites, so the drug has less tissue to disappear into. The Sheiner equation captures this: Vd (L per 70 kg) = 226 + 298 × CrCl ÷ (29.1 + CrCl).

Feed it real numbers and the effect is substantial. At a creatinine clearance of 100 mL/min the volume is 457 L, or about 6.5 L/kg. At 20 mL/min it falls to 302 L, and in an anuric patient it bottoms out at 226 L — half the healthy value. Give the same 800 mcg load to both patients and the dialysis patient reaches roughly 3.5 ng/mL where the healthy one reaches 1.75. The calculator applies this automatically, which is why the suggested total digitalizing dose falls as creatinine rises even though the mcg/kg figure you selected has not changed.

The same shrinking volume lengthens the half-life, since half-life is 0.693 × Vd ÷ clearance. Normal renal function gives 30 to 40 hours; a creatinine clearance of 20 mL/min stretches it past 85 hours. That is the difference between reaching steady state in a week and reaching it in nearly three, and it is the single most common reason a level drawn "after a few days" is meaningless. If you want to see how that curve behaves for any elimination rate, a drug half-life calculator plots the accumulation directly.

Amiodarone, quinidine, verapamil: halving the dose is not optional

Because tubular secretion by P-glycoprotein handles a meaningful share of digoxin elimination, inhibitors of that transporter behave like sudden renal failure. The clinical consequence is that a patient stable on 0.25 mg daily for five years can become toxic without any change in kidney function, weight, or digoxin dose at all.

Selecting one of these in the calculator scales the clearance term directly, so the effect propagates through the suggested dose, the predicted level, and the half-life at once. Amiodarone in the worked example above stretches the half-life from 58 hours to 116 — meaning the interaction takes almost three weeks to fully express itself, long after the prescriber has moved on. Check a level at two weeks, not at three days.

Potassium is the variable the level does not show

Digoxin and potassium compete for the same binding site on the Na⁺/K⁺-ATPase pump. Drop serum potassium and more of that site is free for digoxin, so the drug's effect at the tissue increases while the serum concentration stays exactly where it was. A patient with a level of 1.1 ng/mL and a potassium of 3.0 mmol/L can be frankly toxic; the same level at a potassium of 4.2 is unremarkable.

This is not a rare edge case. Loop diuretics are prescribed alongside digoxin in most heart failure patients, and they are the most reliable cause of hypokalaemia in cardiology. Hypomagnesaemia does the same thing through a related mechanism and often travels with low potassium. Hypercalcaemia potentiates the arrhythmogenic effect independently. Aim for a potassium of 4.0 to 5.0 mmol/L in any patient taking digoxin, and treat a low magnesium before you chase a low potassium that will not correct. Hypothyroidism deserves a mention too: it reduces clearance and raises levels, while hyperthyroidism does the reverse and can make an apparently adequate dose look useless.

Five ways a digoxin level gets misread

Drawing the sample too early after a dose. Digoxin needs 6 to 8 hours to move out of plasma and into tissue. A level drawn 2 hours post-dose can read 2 to 3 times higher than the true steady-state value and has caused countless unnecessary dose reductions. Draw at least 6 hours after the dose, ideally just before the next one.

Sampling before steady state. Five half-lives is the rule, which is 7 to 10 days at normal renal function and closer to 3 weeks at a creatinine clearance of 20 mL/min. A level checked on day 4 of a new dose reflects an incomplete accumulation curve and will read low, tempting an increase that later overshoots.

Treating the number instead of the patient. Roughly a tenth of patients with clear clinical toxicity have concentrations under 2.0 ng/mL, usually because of hypokalaemia or hypoxia. Nausea, anorexia, altered colour vision, new bradycardia, or a regularised ventricular response in atrial fibrillation are toxicity until proven otherwise, whatever the assay says.

Forgetting that assays cross-react. Spironolactone and its metabolites, plus endogenous digoxin-like immunoreactive substances found in renal failure, pregnancy, and liver disease, can shift immunoassay results by a clinically relevant margin. After digoxin-specific antibody fragments are given for toxicity, total digoxin assays become uninterpretable for days because they measure antibody-bound drug.

Reusing a dose across formulations. Switching from tablets to the oral solution raises absorbed drug by roughly 14% at the same milligram dose, and switching to intravenous raises it by about 43%. The calculator handles this with the bioavailability term, but a handover note that says only "digoxin 0.25 mg" loses the information. The same discipline applies to any narrow-index drug — see the dosage calculator for weight-based conversions, and the geriatric dose calculator for the age-related clearance adjustments that apply across most renally cleared medicines.

One closing number worth carrying: in the DIG trial, digoxin cut hospitalisation for heart failure without cutting all-cause mortality. It is a symptom and admission drug, not a survival drug. That changes the risk calculus entirely — if the benefit is fewer hospital days, there is no justification for accepting a concentration that carries a mortality signal. When the calculated dose comes back as 0.0625 mg every other day, that is not an error to round up. It is the answer.

References

1. U.S. Food and Drug Administration. Lanoxin (digoxin) prescribing information — pharmacokinetics, bioavailability, loading and maintenance dosing.
2. National Library of Medicine, StatPearls. Digoxin: mechanism, therapeutic monitoring, and toxicity.
3. National Heart, Lung, and Blood Institute. Heart failure: treatment and management.

Frequently Asked Questions