Unit Converter
Digoxin
(Cardiac Glycoside – Therapeutic Drug Monitoring for Heart Failure & Arrhythmias)
Synonyms
- Digoxin
- Digitalis glycoside
- Lanoxin
- Cardiac glycoside (digoxin type)
- Cardiac inotropic drug
Units of Measurement
- nmol/L
- µg/L
- µg/dL
- µg/100 mL
- µg%
- ng/mL
1 ng/mL = 1 µg/L
1 µg/dL = 10 ng/mL
µg/100 mL = µg% = µg/dL
1 ng/mL = 1.28 nmol/L (MW = 780 g/mol)
Description
Digoxin is a cardiac glycoside extracted from Digitalis lanata.
It increases myocardial contractility and slows AV nodal conduction.
Mechanisms:
- Na⁺/K⁺-ATPase inhibition → ↑ intracellular Ca²⁺ → ↑ contractility
- Vagal stimulation → ↓ heart rate and ↓ AV conduction
Main clinical uses:
- Heart failure with reduced ejection fraction (HFrEF)
- Atrial fibrillation (rate control)
- Atrial flutter
Digoxin requires regular monitoring because of:
- Narrow therapeutic range
- Many drug interactions
- Sensitivity to kidney function
- Electrolyte imbalances affecting toxicity
Physiological Role
Digoxin has no physiological role; it is purely pharmacologic.
Clinical Significance
High Digoxin (Toxicity)
Digoxin toxicity is common, dangerous, and can be fatal.
Cardiac Symptoms
- Bradycardia
- AV block
- Atrial tachycardia with block
- Ventricular arrhythmias
- Bidirectional VT (classic)
Gastrointestinal
- Nausea
- Vomiting
- Anorexia
- Diarrhea
Neurologic
- Confusion
- Weakness
- Visual disturbances (yellow, blurred vision)
Electrolyte Effects
Risk increases with:
- Hypokalemia (most important)
- Hypomagnesemia
- Hypercalcemia
Low Digoxin
Indicates:
- Subtherapeutic dosing
- Drug interactions affecting absorption
- Poor adherence
- Rapid renal clearance
Results in reduced clinical efficacy.
Reference Intervals (Therapeutic Ranges)
(Tietz 8E + AHA/ACC + Mayo + ARUP)
Heart Failure (HFrEF)
- 0.5 – 0.9 ng/mL
(Lower target reduces mortality)
Atrial Fibrillation
- 0.8 – 2.0 ng/mL
Toxicity
- > 2.0 ng/mL
- Toxicity can occur even at “therapeutic” levels, especially in:
- Elderly
- Renal failure
- Hypokalemia
- Elderly
Sampling
- Measure 6–8 hours after last dose (trough).
Diagnostic Uses
1. Therapeutic Drug Monitoring
Used to ensure:
- Effective clinical concentration
- Avoid toxicity
- Adjust dose in renal impairment
- Optimize rate-control therapy in AF
2. Assess Toxicity
Check level if patient has:
- Arrhythmias
- Visual disturbances
- GI symptoms
- Unexplained confusion
- Electrolyte imbalances
3. Special Populations
Digoxin level monitoring essential in:
- Elderly
- CKD patients
- Patients on interacting medications
- Heart failure with reduced ejection fraction
4. Drug Interactions
Digoxin levels increase with:
- Amiodarone
- Verapamil
- Quinidine
- Macrolides
- Azoles
- Spironolactone
- Cyclosporine
Digoxin levels decrease with:
- Rifampicin
- St. John’s wort
Analytical Notes
- Serum sample preferred
- Timing of blood collection critical (6–8 hours post-dose)
- Immunoassays commonly used
- Hemolysis minimal effect
- Assess electrolytes (K⁺, Mg²⁺, Ca²⁺) simultaneously
Clinical Pearls
- Hypokalemia is the strongest risk factor for digoxin toxicity.
- Digoxin immune Fab (Digibind/DigiFab) is used to treat severe toxicity.
- Digoxin does NOT improve survival in HFrEF but improves symptoms & reduces hospitalization.
- Renal function is the biggest determinant of digoxin clearance.
- Toxicity may occur even at “normal” blood levels - always correlate clinically.
Interesting Fact
Digoxin and digitoxin originated from the Digitalis plant used since the 1700s - one of the oldest continuously used drug classes in cardiology.
References
- Tietz Clinical Chemistry & Molecular Diagnostics, 8th Edition - Therapeutic Drug Monitoring.
- AHA/ACC Guidelines - Heart Failure & Arrhythmia Management.
- Mayo Clinic Laboratories - Digoxin.
- ARUP Consult - Digitalis Glycoside Toxicity.
- Pharmacology Texts - Digitalis Drugs.
- MedlinePlus / NIH - Digoxin Testing.