Bidirectional VT in Digoxin Toxicity MCQ — NEET PG Practice Question | NEETPGAI
Bidirectional VT in Digoxin Toxicity
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stethoscope Medicine
A 72-year-old man with chronic atrial fibrillation on digoxin presents with palpitations, nausea, and visual disturbances (yellow-green halos). ECG shows a wide-complex tachycardia with beat-to-beat alternation of the QRS axis between approximately +120° and −60°. The rhythm marked **B** in the diagram is identified. His serum potassium is 3.2 mEq/L and serum creatinine is 2.1 mg/dL. Which of the following is the PRIMARY mechanism underlying the arrhythmia marked **B**?
A. Reentrant circuit within the ventricular myocardium due to structural scar
B. Delayed afterdepolarizations triggered by sarcoplasmic reticulum calcium overload due to Na+/K+-ATPase inhibition
C. Early afterdepolarizations from prolonged QT interval and abnormal repolarization
D. Abnormal automaticity from ectopic ventricular pacemaker cells in the Purkinje system
Explanation
Why "Delayed afterdepolarizations triggered by sarcoplasmic reticulum calcium overload due to Na+/K+-ATPase inhibition" is right
Bidirectional VT (marked B) in digoxin toxicity arises from delayed afterdepolarizations (DADs) caused by intracellular calcium overload. Digoxin inhibits the sarcolemmal Na+/K+-ATPase, raising intracellular sodium and impairing Na+/Ca²⁺ exchanger-driven calcium extrusion, leading to sarcoplasmic reticulum calcium loading. When calcium is released during diastole, it triggers DADs that originate alternately from the left posterior and left anterior fascicles, producing the characteristic beat-to-beat alternation of QRS morphology. This mechanism is pathognomonic for digoxin toxicity (and CPVT). The patient's hypokalemia (3.2 mEq/L) and renal impairment (creatinine 2.1) are classic risk factors that worsen digoxin toxicity by competing at the Na+/K+-ATPase and reducing digoxin clearance, respectively (Harrison 21e Ch 257; Goldfrank 11e).
Why each distractor is wrong
Early afterdepolarizations from prolonged QT interval and abnormal repolarization: Early afterdepolarizations (EADs) occur during repolarization and are the mechanism of torsades de pointes (marked A), not bidirectional VT. Digoxin toxicity shortens the QT interval (digitalis effect), not prolongs it. EADs are seen with QT-prolonging drugs and electrolyte abnormalities like hypokalemia alone, but not with digoxin.
Reentrant circuit within the ventricular myocardium due to structural scar: While reentry can cause monomorphic VT (marked C), bidirectional VT is a triggered arrhythmia (DAD-mediated), not a reentrant mechanism. Reentry requires anatomical or functional block and a unidirectional conduction delay, which does not explain the alternating axis pattern of BVT.
Abnormal automaticity from ectopic ventricular pacemaker cells in the Purkinje system: Although digoxin toxicity can cause increased automaticity (e.g., junctional tachycardia, frequent PVCs), simple automaticity does not explain the beat-to-beat alternation of QRS axis that defines bidirectional VT. The alternating morphology requires triggered activity (DADs) from competing foci on either side of the bundle of His.
High-YieldNEET PG
Bidirectional VT = beat-to-beat QRS alternation = DADs from calcium overload = digoxin toxicity (or CPVT). Correct hypokalemia and stop digoxin; use DigiFab for life-threatening toxicity.
Harrison 21e Ch 257; Goldfrank Toxicologic Emergencies 11e
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