Common misconceptions

Common mistake
Wrong: The AV node is supplied by the LAD.
Right: The AV node is supplied by the AV nodal artery, a branch of the RCA in ~90% of people, explaining why inferior MI (RCA occlusion) causes heart block.
The LAD supplies the anterior wall, interventricular septum, and bundle branches — not the AV node itself. The AV nodal artery is a branch of the RCA in about 90% of people, which is why RCA occlusion (inferior MI) is the classic culprit for AV nodal block. If you're seeing complete heart block in the setting of inferior ST elevations, think RCA, not LAD.
Common mistake
Wrong: AV nodal delay exists to allow time for ventricular depolarization to spread.
Right: AV nodal delay allows atrial contraction to complete and fill the ventricles before ventricular systole begins, optimizing stroke volume.
The AV delay isn't buying time for ventricular conduction — the Purkinje system spreads depolarization through the ventricles very rapidly once it gets the signal. The real purpose is mechanical: the 150–200 ms delay allows the atria to fully contract and push blood into the ventricles (atrial kick) before ventricular systole begins. Losing this coordination — as in junctional rhythm or complete heart block — reduces stroke volume because ventricular filling is incomplete.
Common mistake
Gap: Missing that SA node blood supply varies between RCA and LCx, relevant to sinus bradycardia in MI
The SA node is supplied by the SA nodal artery, a branch of the RCA in ~60% and of the LCx in ~40% of individuals.
Most students only memorize that the RCA supplies conduction tissue and leave it there, but the SA node supply is split: RCA in ~60% of people, LCx in ~40%. This matters because a posterior MI (LCx occlusion) can also cause sinus bradycardia or sinus arrest even though it's not an inferior MI in the classic RCA sense. Knowing this variable supply helps you reason through bradyarrhythmias associated with non-RCA territory infarcts.
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What the exam tests

  1. Know the full sequence of the cardiac conduction pathway: SA node → internodal pathways → AV node → Bundle of His → left and right bundle branches → Purkinje fibers → ventricular myocardium.
  2. Understand why the AV node slows conduction: the delay allows atrial contraction to complete ventricular filling (the 'atrial kick') before ventricular systole, which maximizes stroke volume.
  3. Connect nodal blood supply to arrhythmia risk in MI: the AV node is fed by the RCA in ~90% of people, so inferior MI causes AV block; the SA node supply varies (RCA ~60%, LCx ~40%), so sinus bradycardia can occur in inferior or posterior MI.

Can you avoid these mistakes?

A patient with an acute inferior MI develops progressive PR prolongation followed by dropped beats. Which artery occlusion is responsible, and why does this vessel put the AV node at risk?
What is the mechanical consequence of losing AV nodal delay — for example, in a patient with a junctional rhythm at 60 bpm versus normal sinus rhythm at 60 bpm? Why would stroke volume differ?
A patient develops sinus bradycardia after an MI. Imaging shows a posterior wall distribution. Which coronary artery is likely occluded, and how does SA node blood supply explain this finding?
Compare the phase 0 mechanism in an SA nodal cell versus a ventricular myocyte. Which ion carries the current in each, and why does this difference matter for drug targeting (e.g., why do calcium channel blockers slow the SA/AV nodes but not working myocytes at therapeutic doses)?

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