Digoxin

1. Background information

a. Definition

  • Cardiac glycoside with narrow therapeutic index
  • Used in:
    • Atrial fibrillation (AF) – rate control
    • Heart failure with reduced EF (HFrEF) – symptom relief
  • Does not improve mortality in HF

b. Mechanism of action

Dual mechanism (high-yield):

  • Na⁺/K⁺ ATPase inhibition → ↑ intracellular Ca²⁺ → ↑ contractility
  • ↑ Vagal tone → ↓ AV node conduction → ↓ heart rate

c. Indications

  • AF – rate control (especially sedentary or add-on)
  • HFrEF – symptom improvement and ↓ hospitalisation

2. Assessment


a. Contra-indications

Absolute:

  • Ventricular fibrillation
  • High-degree AV block (without pacemaker)
  • Digoxin toxicity

Avoid:

  • Wolff–Parkinson–White + AF

Caution:

  • Renal impairment (major risk factor for toxicity)
  • Bradycardia
  • Electrolyte imbalance (↓K⁺, ↓Mg²⁺, ↑Ca²⁺)

b. Drug interactions (AKT favourites)

Increase digoxin levels:

  • Amiodarone
  • Verapamil / diltiazem
  • Macrolides

Increase toxicity risk:

  • Loop/thiazide diuretics → hypokalaemia

c. Toxicity (CORE EXAM TOPIC)

Risk factors:

  • Renal impairment (most common cause)
  • Elderly
  • Electrolyte disturbance

Clinical features:

SystemFeatures
GINausea, vomiting, anorexia
CardiacBradycardia, AV block, arrhythmias
NeuroConfusion, weakness
VisualYellow/green vision (xanthopsia)

Key AKT point:

  • Hyperkalaemia = marker of severe toxicity

d. ECG features

Therapeutic (“digoxin effect”):

  • Scooped ST depression (“reverse tick”)
  • PR prolongation
    👉 Normal effect, NOT toxicity

Toxicity:

  • ↑ automaticity + ↓ AV conduction:
    • Bradycardia
    • AV block
    • Atrial tachycardia with block
    • Ventricular ectopics / VT

Classic:

  • Bidirectional VT

e. Monitoring (WITH TIMELINES – VERY HIGH YIELD)

Baseline (before starting)

  • U&Es (especially K⁺)
  • Renal function
  • Ca²⁺, Mg²⁺
  • TFTs

After initiation / dose change

  • Serum digoxin level:
    • Take ≥6–12 hours after last dose
    • Check at ~5–7 days (steady state)

Routine monitoring (stable patients)

  • U&Es + renal function:
    • Annually
  • Increase frequency (every 3–6 months) if:
    • Elderly
    • Renal impairment
    • Interacting drugs
    • Electrolyte risk

Serum digoxin levels (NOT routine)

Check only if:

  • Suspected toxicity
  • Renal deterioration
  • Drug interactions
  • Dose change
  • Poor adherence

Therapeutic range

  • 0.7–2.0 ng/mL

Clinical monitoring

  • Pulse (hold if bradycardic)
  • Symptoms of toxicity
  • ECG if indicated

3. Management (NICE CKS aligned)


a. Side effects AND what to do

Side effectAction
Mild GI upsetReview dose, monitor
BradycardiaWithhold digoxin, check ECG
Confusion/visual symptomsCheck digoxin level + U&Es urgently
Suspected toxicitySTOP digoxin immediately

👉 Important:

  • Toxicity can occur within therapeutic range → treat clinically

b. Use in Primary Care

  • Usually initiated by specialist
  • GP role:
    • Repeat prescribing
    • Monitoring (U&Es, renal ± levels)
  • Used for:
    • AF (add-on rate control)
    • Stable HF
  • Avoid loading doses in primary care

c. Use in Secondary Care

Initiation:

  • Loading (“digitalisation”) if rapid control needed

Indications:

  • Acute AF (especially with HF)
  • Decompensated HF

Management of toxicity

  1. Stop digoxin
  2. Check U&Es, digoxin level
  3. Correct electrolytes (especially K⁺)
  4. Treat arrhythmias
  5. Digoxin-specific antibody (Digoxin immune Fab) if:
    • Life-threatening arrhythmia
    • Severe hyperkalaemia
    • Significant overdose

🔑 AKT ULTRA-HIGH YIELD SUMMARY

  • MOA = ↑ contractility + ↓ AV conduction
  • Indications = AF + HFrEF (symptom only)
  • Check level ≥6–12h post-dose
  • Steady state = ~5–7 days
  • Annual U&Es (3–6 monthly if high risk)
  • ↓K⁺ = biggest toxicity trigger
  • Hyperkalaemia = severe toxicity
  • Yellow vision = classic clue
  • Scooped ST ≠ toxicity
  • Antidote = Digoxin immune Fab

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