Cardiac electrophysiology: AV nodal delay: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · Cardiac electrophysiology: AV nodal delay

Sample item

Carotid sinus massage in a patient with supraventricular tachycardia prolongs the PR interval and may terminate the rhythm. What is the cellular mechanism of the slowed AV conduction?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Acetylcholine acting on M2 receptors opens K+ channels and reduces calcium current in nodal cells

The AV node normally delays conduction by about 0.1 s because its cells have small diameter, few gap junctions and calcium-dependent upstrokes; this delay allows ventricular filling. Vagal stimulation releases acetylcholine, which hyperpolarises nodal cells through M2-linked K+ channels and lowers L-type calcium current, slowing conduction further.

Option by option

  • A. Acetylcholine acting on M2 receptors opens K+ channels and reduces calcium current in nodal cells (correct)

    Correct. Both hyperpolarisation and reduced calcium current slow the nodal upstroke and conduction.

  • B. Noradrenaline acting on beta-1 receptors increases the funny current

    Beta-1 stimulation accelerates nodal conduction and shortens the PR interval.

  • C. Blockade of fast sodium channels in the His bundle

    His bundle conduction depends on fast sodium channels and is not the site of vagal delay.

  • D. Increased gap-junction coupling between nodal cells

    More gap-junction coupling would speed conduction, the opposite of the effect observed.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Acetylcholine acting on M2 receptors opens K+ channels and reduces calcium current in nodal cells. The AV node normally delays conduction by about 0.

Why is "Noradrenaline acting on beta-1 receptors increases the funny current" not the answer?

Beta-1 stimulation accelerates nodal conduction and shortens the PR interval.

Why is "Blockade of fast sodium channels in the His bundle" not the answer?

His bundle conduction depends on fast sodium channels and is not the site of vagal delay.

Why is "Increased gap-junction coupling between nodal cells" not the answer?

More gap-junction coupling would speed conduction, the opposite of the effect observed.

What concept does this question test?

It tests Cardiac electrophysiology: AV nodal delay in Physiology. 1 s because its cells have small diameter, few gap junctions and calcium-dependent upstrokes; this delay allows ventricular filling. Vagal stimulation releases acetylcholine, which hyperpolarises nodal cells through M2-linked K+ channels and lowers L-type calcium current, slowing conduction further.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Cardiac electrophysiology: AV nodal delay?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.