Digoxin Level Interpreter
Digoxin Level Interpreter
Band a serum digoxin concentration from subtherapeutic through to the thresholds for digoxin-specific antibody fragments, and see why toxicity remains a clinical diagnosis.
Serum digoxin level
1 input → ng/mLSerum digoxin 2.6 ng/mL, sampled 8 hours after the last dose
How the level is read
Traditional therapeutic range 0.5–2.0 ng/mL · preferred range in heart failure 0.5–0.9 ng/mL
Antibody fragments: > 15 ng/mL at any time, or > 10 ng/mL at 6 hours post-ingestion
- 6 hours
- digoxin distributes slowly into tissue, so a sample taken earlier reflects the distribution phase and reads falsely high
- 0.5–0.9 ng/mL
- the range now preferred in heart failure; the traditional 0.5–2.0 ng/mL range is wider than current practice supports
- 10 and 15 ng/mL
- the concentration thresholds for digoxin-specific antibody fragments — above 15 at any time, or above 10 measured 6 hours post-ingestion
- potassium
- hyperkalaemia marks severe acute toxicity and predicts mortality better than the digoxin concentration does
Worked example
Serum digoxin 2.6 ng/mL, sampled 8 hours after the last dose
2.60 ng/mL is above the traditional 0.5–2.0 range → toxicity likely
Below both antibody fragment thresholds of 10 ng/mL at 6 hours and 15 ng/mL at any time
The sample is interpretable only because it was taken more than 6 hours after the dose
Check potassium, magnesium, calcium and renal function: toxicity at this concentration is far likelier with hypokalaemia or hypomagnesaemia
Serum digoxin bands
| Digoxin (ng/mL) | Band | Comment |
|---|---|---|
| < 0.5 | Below the therapeutic range | Check adherence and sampling time before increasing the dose |
| 0.5 – 0.9 | Target range in heart failure | The range now preferred; higher adds no benefit |
| 0.9 – 2.0 | Traditional therapeutic range | Does not exclude toxicity, particularly with electrolyte disturbance |
| 2.0 – 10 | Toxicity likely | Nausea, confusion, visual disturbance, bradyarrhythmias, ectopy |
| 10 – 15 | Antibody fragments indicated at 6 hours | Above 10 ng/mL measured 6 hours post-ingestion |
| > 15 | Antibody fragments indicated at any time | Above 15 ng/mL measured at any time |
What raises the level, and what potentiates toxicity
| Factor | Effect |
|---|---|
| Renal impairment | Digoxin is renally cleared, so the concentration rises on an unchanged dose |
| Amiodarone, verapamil, clarithromycin | Raise the digoxin concentration through P-glycoprotein and clearance effects |
| Sampling before 6 hours post-dose | Reads falsely high — the distribution phase is not complete |
| Hypokalaemia | Potentiates toxicity at any concentration, including within the therapeutic range |
| Hypomagnesaemia and hypercalcaemia | Both potentiate toxicity independently of the digoxin concentration |
Why the concentration is only half the assessment
Digoxin has a narrow therapeutic index and a slow distribution phase, and both facts shape how a concentration is read. The sample must be taken at least 6 hours after the dose; earlier than that the drug has not finished moving from plasma into tissue, and the result reads falsely high and prompts unnecessary alarm. The traditional therapeutic range is 0.5 to 2.0 ng/mL, but in heart failure the preferred range is now 0.5 to 0.9 ng/mL, above which no additional benefit has been shown.
Toxicity is a clinical diagnosis. A concentration inside the therapeutic range does not exclude it, and the reason is that several common disturbances potentiate digoxin at any concentration. Hypokalaemia is the important one, because digoxin and potassium compete at the sodium-potassium ATPase, but hypomagnesaemia and hypercalcaemia do the same. An elderly patient with nausea, confusion, visual disturbance and a new bradyarrhythmia can be seriously toxic at 1.5 ng/mL.
Most chronic toxicity is precipitated rather than spontaneous. Digoxin is cleared renally, so any fall in glomerular filtration raises the concentration on an unchanged dose, and interacting drugs do the same — amiodarone, verapamil and clarithromycin are the classic three, acting largely through P-glycoprotein. Diuretics contribute twice over, by lowering potassium and magnesium and by reducing renal clearance, which is why an intercurrent illness in a patient on a stable dose is the usual trigger.
In acute overdose the picture differs. Hyperkalaemia reflects widespread inhibition of the sodium-potassium pump and predicts mortality better than the digoxin concentration does, so it is a marker of severity rather than an incidental result. Digoxin-specific antibody fragments are indicated for a concentration above 15 ng/mL at any time, or above 10 ng/mL measured 6 hours post-ingestion, and once they are given total digoxin assays read high and become uninterpretable. Poisoning management is time-critical and directed by a poisons centre or clinical toxicology service, and this interpreter supports that advice rather than replacing it.
Frequently asked questions
What is the therapeutic range for digoxin?
Traditionally 0.5 to 2.0 ng/mL, but in heart failure the preferred range is now 0.5 to 0.9 ng/mL, because higher concentrations add no benefit. The sample must be taken at least 6 hours after the dose.
Can a patient be toxic with a level in the therapeutic range?
Yes, and this is the commonest trap. Hypokalaemia, hypomagnesaemia and hypercalcaemia all potentiate digoxin at any concentration, so an elderly patient with nausea, confusion, visual disturbance and a new bradyarrhythmia can be seriously toxic at 1.5 ng/mL.
When are digoxin-specific antibody fragments indicated?
For a concentration above 15 ng/mL measured at any time, or above 10 ng/mL measured 6 hours after ingestion. Hyperkalaemia, life-threatening arrhythmia and haemodynamic instability are indications in their own right.
Why does hyperkalaemia matter in digoxin overdose?
It reflects widespread inhibition of the sodium-potassium pump and, in acute overdose, predicts mortality better than the digoxin concentration itself. It is a marker of severity rather than an incidental finding.
Can I repeat the level after giving antibody fragments?
Not usefully. Total digoxin assays read high after antibody fragments are given and become uninterpretable, so the response is judged clinically. Poisoning management is time-critical and directed by a poisons centre or clinical toxicology service, which this interpreter supports rather than replaces.
Related calculators
References
- David MNV, Shetty M. Digoxin. In: StatPearls. Treasure Island (FL): StatPearls Publishing.
- Rathore SS, Curtis JP, Wang Y, Bristow MR, Krumholz HM. Association of serum digoxin concentration and outcomes in patients with heart failure. JAMA. 2003;289(7):871–878.
- Digitalis (cardiac glycoside) poisoning. In: Merck Manual Professional Edition. Merck & Co.