Rapid Review·Cardiovascular

Select any text to highlight it or add a note.

Cardiovascular Pharmacology

T1Must know

Digoxin Toxicity

Focus on

Key takeaways

digoxin inhibits the sodium-potassium pump, raising intracellular calcium (inotropy), and increases vagal tone (slows the sinus and atrioventricular (AV) nodes).
it is renally excreted, and it competes with potassium for the pump, so hypokalemia potentiates it.
hypokalemia (loop and thiazide diuretics, vomiting); hypomagnesemia.
renal failure (reduced excretion), volume depletion from diuretics, hypothyroidism, advanced age.
amiodarone, verapamil, quinidine, propafenone.
  • Reduce the digoxin dose by 25 to 50 percent when starting amiodarone, with weekly levels.
predisposes by reducing renal clearance of digoxin, independent of its potassium effect.
anorexia, nausea, vomiting, abdominal pain.
fatigue, weakness, confusion, and altered color vision (yellow-green halos).
frequent ventricular ectopy, bradycardia and AV block of every degree.
  • Atrial tachycardia with block: increased automaticity plus AV block is the signature.
  • Bidirectional ventricular tachycardia: nearly pathognomonic.
drawn at least 6 hours after the last dose (earlier levels are falsely high).
  • Toxicity correlates poorly with the level in chronic disease, so treat the patient, not the number.
though hypokalemia causes toxicity, hyperkalemia is seen in toxicity and predicts a poor prognosis (the blocked pump cannot move potassium into cells).
  • Also magnesium, renal function, thyroid function.
toxicity gives inverted or biphasic T waves and a prolonged PR.
  • The therapeutic "digitalis effect" (scooped ST depression, a short QT) does not by itself mean toxicity.
stop digoxin, monitor continuously, correct hypokalemia and hypomagnesemia cautiously.
reverse severe toxicity.
  • Indications: life-threatening arrhythmias, hemodynamic instability, hyperkalemia over 5 to 5.5 in acute toxicity, end-organ dysfunction, or a massive ingestion.
  • After Fab, the measured total level rises (bound, inactive) and potassium falls.
atropine; pacing only if Fab fails.
Fab, lidocaine or phenytoin, magnesium.
Fab first, then insulin-glucose; avoid intravenous calcium (the exam still expects this).
activated charcoal within 1 to 2 hours of an acute ingestion; dialysis does not remove digoxin (large volume of distribution).
dose by renal function and age, reduce the dose when starting amiodarone or verapamil, monitor potassium and creatinine.
fatal ventricular arrhythmias, asystole, cardiogenic shock; hyperkalemic death in acute overdose; misdiagnosis as gastroenteritis or dementia in the elderly.

How it's tested

Go deeper
High-yield images1
Digoxin mechanism at the myocyte membrane. Digoxin inhibits the Na+/K+-ATPase, so intracellular sodium rises; the Na+/Ca2+ exchanger, which depends on the sodium gradient, then stalls, so intracellular calcium rises. More calcium is loaded into the sarcoplasmic reticulum, more binds troponin C, and cardiac contraction increases.

You just read one page of 236

The rest of Step 2 CK, written exactly like this.

Rapid Review is the reading layer of a full Step 1 platform: a schedule fitted to your exam date, flashcards for every page, and a mentor a message away.

  • Every Step 1 system

    Written the same way: what to know, how it’s tested, where to go deeper.

  • A plan built to your exam date

    Tell us when you sit, and the schedule fits the whole library and your question bank to it.

  • Flashcards for every page

    Ready-made spaced-repetition decks linked to each topic, so nothing you read gets forgotten.