Questions: Cardiac Pacemaker Activity and the Sinoatrial Node

Question 1

A patient's SA node is completely blocked. Which structure takes over as pacemaker, and at approximately what rate?

• A. Atrial muscle cells, at 80–100 bpm
• B. The AV node, at 40–60 bpm
• C. The Purkinje fibers, at 60–80 bpm
• D. The ventricles cease to contract without SA node input

Answer: (B)

The AV node has an intrinsic automaticity rate of 40–60 bpm and becomes the primary pacemaker when the SA node fails — this is an 'escape rhythm.' Purkinje fibers fire even more slowly (20–40 bpm) and take over only if the AV node also fails. The heart does not stop; the hierarchy of automaticity ensures that the fastest remaining pacemaker always captures the heart.

Question 2

The SA node's funny current (If) is unusual among voltage-gated currents because it:

• A. Activates upon membrane depolarization, like most voltage-gated channels
• B. Carries pure potassium outward, repolarizing the cell toward rest
• C. Activates upon hyperpolarization and carries a mixed inward Na+/K+ current
• D. Only opens when acetylcholine occupies its binding site

Answer: (C)

The 'funny' in funny current refers precisely to its counter-intuitive gating: If channels (encoded by HCN genes) open when the membrane hyperpolarizes below about −60 mV, opposite to most voltage-gated channels. They conduct net inward (depolarizing) Na+ and K+ current, initiating the slow diastolic drift toward threshold that drives spontaneous firing.

Question 3

Sympathetic stimulation increases heart rate partly by steepening the slope of Phase 4 depolarization in SA node cells.

• T. True
• F. False

Answer: True

Norepinephrine activates beta-1 adrenergic receptors, raising cAMP, which phosphorylates HCN (If) channels and L-type Ca2+ channels. This increases inward current during Phase 4, making the membrane potential rise faster — a steeper depolarization slope — so threshold is reached sooner. The three adjustable parameters of pacing rate are Phase 4 slope, maximum diastolic potential, and threshold voltage; sympathetic tone primarily accelerates Phase 4.

Question 4

The SA node action potential upstroke is driven by fast voltage-gated sodium channels, the same mechanism as in ventricular myocytes.

• T. True
• F. False

Answer: False

SA node cells have very few fast Na+ channels. Their action potential upstroke (Phase 0) is driven by L-type Ca2+ channels, which is why SA node action potentials rise slowly with a rounded shape rather than the sharp spike seen in ventricular myocytes. This Ca2+-dependent upstroke is also why SA node cells are sensitive to calcium channel blockers (e.g., verapamil) as rate-controlling agents.

Question 5

Why does the SA node fire spontaneously without any external stimulus, whereas ventricular myocytes or typical neurons do not?

Model answer: SA node cells lack the large inward-rectifier K+ current (IK1) that anchors other excitable cells at a stable negative resting potential. Instead, after each action potential, funny channels (If) open as the membrane hyperpolarizes and pass a slow inward depolarizing current. Without a stable anchor, the membrane drifts continuously toward threshold, generating the pacemaker potential spontaneously — no external stimulus required.

The distinction is ion channel composition, not some special energy source. Neurons and ventricular myocytes have abundant IK1 that clamps the resting potential at a stable negative voltage. SA node cells have minimal IK1 but abundant If. This makes the SA node intrinsically unstable at rest — a feature, not a bug — producing the automaticity that drives every heartbeat.