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Name the category.
Positive inotropic agents
Name the main drug.
DIGOXIN
General overview.
Drugs: digoxin, ouabain
Mechanism: inhibition of the cardiac and neuronal Na+/K+- ATPase
Onset of effect
Oral: 0.5–2 h
IV: 15–30 min
Half-life: 36–40 hours
Protein binding: 20–40%
Elimination: renal
Describe the mechanism of action of digoxin.
Inhibition of Na+/K+-ATPase → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers → higher intracellular Ca2+ concentration
In cardiomyocytes, this leads to increased contractility (positive inotropic effect), reduced velocity of electric conduction (negative dromotropic effect) via AV node depression, and a reduction of the heart rate (negative chronotropic effect) via SA node depression.
In neurons of the vagal nerve, this leads to increased velocity of electric conduction, which causes reduced heart rate (via increased vagal tone and a reflexive reduction of sympathetic transmission).
Cardiac glycosides inhibit Na+/K+-ATPase, increasing cardiac contractility and decreasing AV conduction and heart rate!
List indications.
Congestive heart failure (symptomatic patients with NYHA ≥ II despite pharmacotherapy)
Atrial fibrillation
Supraventricular tachycardia
List contraindications.
Ventricular fibrillation
Use with caution in pregnant women and in patients with:
Electrolyte and fluid disorders (e.g., volume depletion, hypokalemia, hypomagnesemia, and/or hypercalcemia )
Cardiovascular disorders (e.g., acute coronary syndrome, AV blocks, Wolff-Parkinson-White syndrome, hypertrophic obstructive cardiomyopathy, sick sinus syndrome)
Renal failure (can lead to digoxin overdose and, vice versa, digoxin can also cause/worsen renal failure)
List interactions.
K+-depleting diuretics → hypokalemia → arrhythmias
Verapamil, diltiazem, amiodarone, quinidine → possible overdose (reduce digoxin dose to avoid overdose)
What can happen in the worst case?
Cardiac glycoside poisoning.
List clinical features of glycoside poisoning.
Via cholinergic agonism: nausea, vomiting, diarrhea, abdominal pain, and anorexia
Visual disturbances
Xanthopsia (yellow-tinted vision)
Photophobia
Blurry vision with a yellow tint and halos
Disorientation, weakness
Palpitations (due to arrhythmias or AV block)
List diagnostics used for glycoside poisoining.
ECG: potentially severe cardiac arrhythmias
Premature ventricular beats
T-wave inversion or flattening
Deformed ST segment (“scooped” or “sagging” ST segments)
↓ QT interval
↑ PR interval
Atrial tachycardia with AV block
Laboratory studies
Serum digoxin concentration (ideally, measure 6 hours after ingestion)
Serum electrolyte levels: hyperkalemia (associated with poor prognosis) resulting from inhibition of the Na+/K+-ATPase
Creatinine and blood urea nitrogen to evaluate renal function
Describe the treatment of glycoside poisoning.
Digoxin-specific antibody (œ) fragments (anti-digoxin Fab fragments)
Atropine for symptomatic bradycardia
Slowly normalize serum potassium levels
Magnesium
Class IB antiarrhythmics
Temporary cardiac pacing
Digoxin has a narrow therapeutic index! Serum concentrations of cardiac glycosides must be monitored closely because overdoses can have severe consequences!
“You better visit a hospital directly!”: Yellow blurry vision and halos are the signs of digoxin poisoning.
Last changed2 years ago