A patient's reentrant circuit has two pathways with fast and nearly equal conduction velocities, and neither pathway has unidirectional block. What will most likely happen to the electrical wavefront?
AThe circuit will sustain itself indefinitely, producing a tachyarrhythmia
BThe wavefront will traverse both pathways and collide in the middle, extinguishing the circuit
CThe faster pathway will develop unidirectional block, enabling reentry
DThe wavefront will conduct only down the slower pathway, creating a bradyarrhythmia
Reentry requires two conditions: unidirectional block in one pathway AND slow conduction in the other. Without these, wavefronts traveling down both pathways simultaneously will meet and collide — each wavefront encounters refractory tissue (the other wavefront's wake) and cannot continue. This collision-and-extinction is normal cardiac conduction. Reentry is only possible when these conditions break down specifically: one pathway blocks forward conduction, and the other is slow enough that the blocked pathway recovers before the circling wavefront arrives.
Question 2 Multiple Choice
A patient with congenital long QT syndrome develops a polymorphic ventricular tachycardia that appears to 'twist' around the baseline on the ECG. Which arrhythmia mechanism is most directly responsible?
ADelayed after-depolarizations from sarcoplasmic reticulum calcium overload
BAbnormal automaticity in partially depolarized ventricular myocytes
CEarly after-depolarizations during prolonged phase 2/3 of the action potential
DReentry around a fixed anatomic scar
This is torsades de pointes, the characteristic arrhythmia of long QT syndrome. EADs occur when repolarization is prolonged — as in long QT — and L-type calcium channels recover and reactivate before the action potential fully repolarizes, creating a secondary upstroke. DADs (option A) occur after repolarization is complete and are associated with calcium overload from digoxin toxicity or catecholamine excess. The common misconception is that long QT causes standard monomorphic VT — it specifically predisposes to torsades via EADs.
Question 3 True / False
Delayed after-depolarizations (DADs) are generated after repolarization is complete, driven by spontaneous calcium release from the sarcoplasmic reticulum activating the sodium-calcium exchanger.
TTrue
FFalse
Answer: True
DADs arise after the action potential has fully repolarized. When sarcoplasmic calcium is overloaded (as in digoxin toxicity or excess catecholamines), the SR releases calcium spontaneously through ryanodine receptors. The NCX expels this calcium while importing sodium, generating a net inward current that can depolarize the cell to threshold — triggering an ectopic beat. This is distinct from EADs, which interrupt the action potential mid-repolarization.
Question 4 True / False
Long QT syndrome increases risk of standard monomorphic ventricular tachycardia.
TTrue
FFalse
Answer: False
Long QT syndrome predisposes specifically to torsades de pointes — a polymorphic VT that twists around the isoelectric baseline — via early after-depolarizations. Standard monomorphic VT is more typically associated with reentry around fixed anatomic scars (e.g., post-MI fibrosis). Understanding the specific arrhythmia mechanism matters clinically because treatment differs: QT-prolonging drugs worsen torsades, while antiarrhythmics targeting the reentry circuit address monomorphic VT.
Question 5 Short Answer
Why does reentry require both unidirectional block AND slow conduction — why isn't either condition alone sufficient to sustain a reentrant circuit?
Think about your answer, then reveal below.
Model answer: Unidirectional block alone is not enough because if conduction in the alternate pathway is fast, the circling wavefront arrives at the blocked pathway before it has recovered its excitability — it encounters refractory tissue and dies. Slow conduction alone is not enough because without unidirectional block, wavefronts traveling both directions will meet and extinguish. Both conditions must coexist: the block forces the wavefront to take the detour through the slow pathway, and the slow conduction gives the blocked pathway time to recover and become excitable again by the time the wavefront returns from behind. This timing window is what sustains the circuit indefinitely.
The reentry circuit is essentially a timing problem: the wavefront must arrive at the recovered pathway just as it becomes excitable again. Unidirectional block creates the directional asymmetry that forces the detour; slow conduction creates the time delay that allows recovery. Remove either and the circuit either self-terminates or never starts. This understanding explains why antiarrhythmic drugs that slow conduction or prolong refractoriness can interrupt reentry from two different directions.