Which ion drives phase 0 of the ventricular myocyte action potential?

Fast voltage-gated sodium influx drives phase 0 in atrial and ventricular myocytes. Nodal phase 0 is different because it depends on L-type calcium influx.

Why does phase 2 create a plateau?

L-type calcium influx balances potassium efflux, keeping the membrane depolarized long enough for calcium-induced calcium release and contraction.

Which phase is prolonged by potassium channel blockade?

Potassium channel blockade delays phase 3 repolarization, which increases action potential duration, effective refractory period, and QT interval.

Cardiac Myocyte Action Potential

Five-phase board map

The ventricle is a gated hallway

Each phase is a different door opening or closing. Tap each cell below to test yourself, or reveal all at once.

Core sequence

Phase	Dominant current	Board consequence
0	Fast Na+ influx	Conduction velocity and QRS width
1	Na+ inactivation plus transient K+ efflux	Early notch after depolarization
2	L-type Ca2+ influx balanced by K+ efflux	Plateau and contraction
3	Delayed rectifier K+ efflux	Repolarization, refractory period, QT interval
4	K+ conductance maintains resting potential	Readiness for the next beat

walk the curve from left to right

Phase 0 asks, "How fast can this cell conduct?" Phase 2 asks, "Can the muscle contract?" Phase 3 asks, "How long is it refractory?" That is why sodium blockers widen QRS, calcium matters for contraction, and potassium blockers prolong QT.

Animated mechanism

Watch the membrane change jobs

Tap a phase. The marker glides to that point on the voltage curve while only that phase's ion crosses the membrane. One beat, five jobs, and the ECG remembers every one.

Phase 0: fast Na+ floods IN and the voltage shoots from -90 to +20 mV. A steeper upstroke means faster conduction and a narrower QRS.

Working myocyte vs nodal cell

Same organ, different upstroke

The board tests which tissue uses which channel. Tap cells to self-test.

Feature	Working myocyte	Nodal cell
Phase 0 channel	Fast voltage-gated Na+	L-type Ca2+
Phase 0 slope	Steep (fast conduction)	Slow (slow conduction)
Phase 4	Flat resting potential	Slowly depolarizing (funny current)
Drug that slows phase 0	Na+ blockers (class I)	Ca2+ blockers (class IV), beta blockers
ECG if phase 0 slowed	Wide QRS	Long PR, bradycardia
Automaticity	None (waits for impulse)	Spontaneous (pacemaker)

Clinical decision tree

Use the ECG to identify the blocked gate

Answer each challenge before the explanation appears.

Wide QRS after a channel blocker

Which phase of the action potential is most likely impaired?

Wide QRS reflects slowed ventricular depolarization. Phase 0 depends on fast Na+ channels. Class I agents (especially IC) flatten the phase 0 slope, slowing cell-to-cell conduction. Phase 3 delay prolongs QT, not QRS.

Long QT or torsades risk

Which current is most likely delayed?

QT interval spans ventricular depolarization through repolarization. Phase 3 repolarization depends on K+ leaving through delayed rectifier channels. Block that exit and the action potential stays long, ERP increases, and torsades risk rises.

Bradycardia with PR prolongation

Which tissue is being slowed, and by which mechanism?

SA and AV nodal cells use L-type Ca2+ for their phase 0 upstroke, not fast Na+. Blocking that Ca2+ entry slows AV conduction (longer PR) and reduces SA firing rate (bradycardia). The narrow QRS proves ventricular Na+ channels are intact.

Peaked T waves with progressive QRS widening

What is the immediate danger, and what does IV calcium do?

Severe hyperkalemia partially depolarizes resting myocytes, inactivating Na+ channels and slowing conduction. IV calcium raises the threshold potential, restoring the gap between resting and threshold so remaining channels can conduct. It does not lower serum K+.

Board memory hooks

Five rules that cover most stems

Tap each blurred line to reveal. If you can state the rule before tapping, you own it.

1Phase 0 is a sodium door. Flecainide slams it shut. The QRS widens because depolarization crawls through working myocardium.

2Phase 2 is the calcium agreement: inward Ca2+ balances outward K+. Block the calcium and contraction drops. That is the plateau.

3Phase 3 is potassium leaving. Delay the exit and QT grows. Torsades de pointes lives in that delay.

4Digoxin poisons the Na+/K+ ATPase. Hypokalemia opens the binding site wider to the poison. That is why low K+ and digoxin together cause toxicity.

5IV calcium does not lower potassium. It raises the threshold potential so the membrane can survive while you fix the potassium with insulin, bicarbonate, or dialysis.

Anatomy and ECG anchors

Keep the curve tied to the patient

Use the images to connect the cellular event to conduction tissue and the surface tracing.

Board walkthrough

One patient at a time

Right-click or long-press to cross out. Double-click or double-tap to highlight. Then answer and reveal the mechanism beats.

Medically reviewed by Fatima Ali, DO and Kaitlyn Cocuzzo, MD · Last reviewed June 2026

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