Comparison table: Cardiac action potentials

Cardiac action potentials are one of those “if you can table it, you can ace it” topics: Step questions love to swap one ion current or phase and ask you to predict the EKG change, drug effect, or arrhythmia risk. This post gives you a quick-hit comparison table, plus a sticky mnemonic/visual so you can recall which cells have which phases, which channels matter, and what drugs do.

The two big categories you must separate

1) Fast-response AP (non-nodal)

Cells: atrial myocytes, ventricular myocytes, Purkinje fibers
Defining feature: rapid phase 0 upstroke via fast $Na^+$ channels → fast conduction

2) Slow-response AP (nodal)

Cells: SA node, AV node
Defining feature: no true resting potential + slow phase 0 via $Ca^{2+}$ channels → slower conduction, physiologic delay

Visual/Mnemonic Device (shareable)

“W-shaped vs ramp-shaped”

Working myocytes/Purkinje: think W = 0–1–2–3–4 (you see the notch + plateau)
Nodal cells: think ramp = 4 → 0 → 3 (no phases 1 or 2)

One-liner that usually gets you the point

“Myocytes shoot up with $Na^+$ and plateau with $Ca^{2+}$ ; nodes drift up with funny $Na^+$ and fire with $Ca^{2+}$ .”

Comparison Table: Cardiac Action Potentials (High-Yield)

Feature	Atrial/Ventricular Myocytes (Fast)	Purkinje (Fast)	SA/AV Node (Slow)
Primary job	Contractile force	Fast conduction backup pacemaker	Pacemaker + AV delay
Resting membrane potential	Stable ~ −85 to −90 mV	Stable ~ −90 mV	Unstable (no true resting potential)
Phase 0 (upstroke)	Fast $Na^+$ influx (voltage-gated)	Fast $Na^+$ influx (very fast conduction)	$Ca^{2+}$ influx (L-type)
Phase 1 (early repol)	Transient $K^+$ out (Ito)	Present	Absent
Phase 2 (plateau)	$Ca^{2+}$ in (L-type) balanced by $K^+$ out	Prominent/long plateau	Absent
Phase 3 (repol)	$K^+$ out (delayed rectifier)	$K^+$ out	$K^+$ out
Phase 4	Flat resting potential (IK1)	Flat resting potential (IK1)	Spontaneous depolarization via If + $Ca^{2+}$
Automaticity	No (normally)	Yes (latent)	Yes (primary pacemaker SA)
Key “pacemaker” current	N/A	Minor	If (“funny”) = slow inward $Na^+$ (HCN channels)
Most sensitive to ischemia	Ventricular myocardium (arrhythmias)	Purkinje can trigger ectopy	AV node (conduction blocks)
Conduction velocity	Fast (via $Na^+$ )	Fastest in heart	Slow (via $Ca^{2+}$ )
Refractory period purpose	Prevent tetany + allow filling	Prevent reentry + coordinate	Control rate + protect ventricles

Phase-by-Phase: What ions are doing what?

Fast-response cells (0–1–2–3–4)

Phase 0: $Na^+$ in (fast channels) → steep upstroke = fast conduction
Phase 1: brief $K^+$ out
Phase 2: $Ca^{2+}$ in (L-type) balances $K^+$ out → plateau
- High-yield link: plateau = long refractory period
Phase 3: $K^+$ out dominates → repolarization
Phase 4: stable resting potential (mostly $K^+$ conductance)

Nodal cells (4–0–3)

Phase 4 (pacemaker):
- If (funny) current = slow inward $Na^+$ as membrane becomes more negative
- plus T-type $Ca^{2+}$ late in phase 4 helps reach threshold
Phase 0: L-type $Ca^{2+}$ influx (not $Na^+$ ) → slow upstroke
Phase 3: $K^+$ efflux → repolarization

The “USMLE trigger points” (what questions usually test)

1) What sets heart rate?

Slope of phase 4 in SA node
- Steeper slope = faster HR
- Flatter slope = slower HR

2) What sets AV nodal conduction speed?

Phase 0 upstroke in AV node depends on $Ca^{2+}$
- So anything that blocks L-type $Ca^{2+}$ channels slows AV conduction.

3) What sets ventricular conduction speed?

Phase 0 in myocytes depends on fast $Na^+$ channels
- So class I antiarrhythmics widen QRS (slower ventricular depolarization).

Drug hooks you should attach to phases (super testable)

Beta-1 stimulation (sympathetic)

SA/AV node: ↑ cAMP → ↑ If and ↑ $Ca^{2+}$ currents
- Steeper phase 4 → ↑ HR
- ↑ AV conduction (shorter PR)

Beta blockers

SA/AV node: ↓ cAMP → ↓ If and ↓ $Ca^{2+}$ $C a^{2 +}$
- Flatter phase 4 → ↓ HR
- ↓ AV conduction (longer PR)

Non-dihydropyridine CCBs (verapamil, diltiazem)

AV node: block L-type $Ca^{2+}$ $C a^{2 +}$ channels
- Slower phase 0 in nodes → prolong PR, treat AVN-dependent SVTs

Class III antiarrhythmics (K+ channel blockers)

Prolong phase 3 repolarization in fast-response tissue
- ↑ action potential duration and ↑ refractory period
- High-yield adverse effect: torsades de pointes risk via QT prolongation

High-yield mini table: “Which phase is the drug hitting?”

Drug/Class	Cell type most tested	Main phase effect	Classic clue
Class I ( $Na^+$ blockers)	Ventricular/Purkinje	↓ slope of phase 0	Wide QRS
Class III ( $K^+$ blockers)	Ventricular/Purkinje	Prolong phase 3	Long QT ± torsades
Class IV (non-DHP CCBs)	AV node	↓ phase 0 (nodal)	Long PR, AV block risk
Beta blockers	SA/AV node	↓ phase 4 slope	↓ HR, long PR
Adenosine	AV node	↑ $K^+$ out, ↓ $Ca^{2+}$ in	“Stops” AVN-dependent SVT (very short half-life)

Rapid-fire one-liners to memorize

“Plateau = calcium = refractory.” (Phase 2 in myocytes)
“Nodes use calcium for phase 0.” (So CCBs/beta blockers hit AV conduction)
“Funny current is sodium… but it’s weird sodium.” (If in phase 4)
“ $Na^+$ channels determine ventricular conduction; $Ca^{2+}$ channels determine AV nodal conduction.”

Quick self-check (30 seconds)

If you block L-type $Ca^{2+}$ channels, which interval changes most? → PR increases (AV node slows)
If you block fast $Na^+$ channels, what happens to QRS? → QRS widens
If you prolong phase 3, what EKG change do you expect? → QT prolongation (torsades risk)