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.
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.
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) |
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?
Long QT or torsades risk
Which current is most likely delayed?
Bradycardia with PR prolongation
Which tissue is being slowed, and by which mechanism?
Peaked T waves with progressive QRS widening
What is the immediate danger, and what does IV calcium do?
The pacemaker never rests
Working myocytes wait for a signal. Nodal cells make their own. The whole difference is one drifting line in phase 4, and the autonomic nerves spend all day adjusting how steeply it climbs.
Three phases, no plateau
Nodal cells skip phases 1 and 2. There are no fast Na+ channels and no sustained inward current to hold a plateau, so the curve is only phase 4 (a slow drift up), phase 0 (the upstroke), and phase 3 (repolarization).
Phase 0 is calcium, not sodium
The maximum diastolic potential sits near -60 mV, too positive to reset fast Na+ channels, so they stay inactivated. The upstroke rides slow L-type Ca2+ instead. Slow upstroke → slow conduction → this is the AV nodal delay.
The funny current (If)
Phase 4 drift is driven by If through HCN channels, a slow mixed Na+ and K+ inward current. It is called funny because it turns on when the cell gets more negative (it activates on hyperpolarization), the opposite of the fast Na+ channel. Late in phase 4, T-type Ca2+ adds a final shove toward threshold.
The rate ladder
SA node 60 to 100 → AV junction 40 to 60 → Purkinje and ventricle 20 to 40 bpm. The fastest pacemaker wins, so the SA node drives the heart and overdrive-suppresses the slower ones through the electrogenic Na+/K+ ATPase. When the SA node fails, expect a pause before an escape rhythm appears.
Sympathetic vs parasympathetic
| Lever | Sympathetic (beta-1, Gs) | Parasympathetic (M2, Gi) |
|---|---|---|
| Second messenger | More cAMP, binds HCN and boosts L-type Ca2+ | Less cAMP, plus beta-gamma opens GIRK K+ channels |
| Phase 4 slope | Steeper, threshold reached sooner | Flatter, and starts from a more negative potential |
| Chronotropy (SA rate) | Faster | Slower |
| Dromotropy (AV, PR) | Faster conduction, shorter PR | Slower conduction, longer PR |
| Inotropy | Stronger (more Ca2+ entry and SR load) | Weaker, and mostly atrial only |
| Classic agent | Norepinephrine, isoproterenol | Acetylcholine, adenosine, digoxin |
vagal tone is the resting brake
At rest the heart runs near 70, but the SA node's true intrinsic rate is closer to 100. The gap is vagal tone holding it down. Cut the vagus with atropine, or transplant the heart, and the rate climbs toward 100. That is why atropine treats symptomatic bradycardia. Remember the sides: the right vagus mostly feeds the SA node (rate), the left vagus mostly feeds the AV node (conduction).
The phase 0 trap
The single most tested distractor reads, "pacemaker phase 0 is the fast Na+ current." It is not. It is L-type Ca2+. The fast Na+ channels are permanently inactivated by the unstable, depolarized resting potential. That slow calcium upstroke is exactly why the AV node conducts slowly and why calcium blockers and beta blockers lengthen the PR interval.
Read it on the ECG
The SA node is silent on the surface tracing; the P wave is atrial depolarization downstream. The PR interval (120 to 200 ms) is mostly AV nodal delay, the slow calcium upstroke buying time for the atrial kick before the ventricles fire. Sympathetic tone shortens the R-R and the PR; vagal tone lengthens both, and at the extreme drops beats into AV block.
A spark lights an avalanche
The action potential is only the trigger. Turning that voltage into a squeeze takes calcium, and in the heart a small calcium spark releases a much larger one.
1. Trigger
The action potential runs down the T-tubule and opens sarcolemmal L-type Ca2+ channels (Cav1.2, the dihydropyridine receptor). This inward calcium is the same current that sustains the phase 2 plateau.
2. Amplify (CICR)
That small trigger calcium binds RyR2 on the sarcoplasmic reticulum → RyR2 opens → a much larger calcium store floods the cytosol. A small spark in releases a big wave out.
3. Contract
Cytosolic calcium binds troponin C → tropomyosin slides off the actin binding sites → myosin heads cross-bridge cycle → the sarcomere shortens and the cell contracts.
Switching off: relaxation
Relaxation means clearing cytosolic calcium. SERCA2a pumps it back into the SR (the dominant route), the Na+/Ca2+ exchanger throws it out of the cell (3 Na+ in for 1 Ca2+ out), and PMCA plus the mitochondria handle the rest.
The parking brake on SERCA
Dephosphorylated phospholamban inhibits SERCA. Sympathetic beta-1 → cAMP → PKA phosphorylates phospholamban → the brake comes off → SERCA refills the SR faster → faster relaxation. That speed-up is lusitropy.
Why the heart is graded
Contractile force tracks how much trigger calcium enters through L-type channels, because that sets the size of the release and the cytosolic transient. More calcium in, or a fuller SR, means a stronger beat. That is inotropy.
How digoxin adds force
Digoxin blocks the Na+/K+ ATPase → intracellular Na+ rises → the gradient that powers the Na+/Ca2+ exchanger shrinks → less calcium is extruded → calcium accumulates and the SR loads → stronger contraction. Separately it raises vagal tone to slow the AV node.
the heart cannot fake its calcium
Skeletal muscle couples mechanically: the voltage sensor physically tugs RyR1 open, so it never needs outside calcium. The heart couples chemically, so no extracellular calcium through the L-type channel means no spark, no avalanche, no beat. That is why calcium channel blockers drop cardiac contractility but barely touch a sprinter, and it is the reason the plateau exists in the first place. Cardiac is chemical, skeletal is mechanical. Every time.
Cardiac vs skeletal coupling
| Feature | Cardiac | Skeletal |
|---|---|---|
| Coupling type | Chemical (CICR) | Mechanical (voltage sensor tugs RyR1) |
| Needs extracellular Ca2+? | Yes, mandatory | No |
| Ryanodine receptor | RyR2 (opened by calcium) | RyR1 (opened by voltage pull) |
| L-type channel | Cav1.2 | Cav1.1 |
| Force graded by | Calcium entering per beat | Motor-unit recruitment and tetany |
| Tetany possible? | No (long plateau and refractory period) | Yes |
| Disease hook | CPVT from leaky RyR2 | Malignant hyperthermia from RyR1, treat with dantrolene |
Three reversals boards love
SERCA pumps calcium into the SR; it never throws calcium out of the cell (that job belongs to NCX and PMCA). Phospholamban is backwards from intuition: dephosphorylated phospholamban is the brake on, phosphorylated phospholamban releases it. And calcium binds troponin C, not tropomyosin.
The pause that keeps the heart a pump
The long plateau is not wasted time. It stops the heart from tetanizing, and when repolarization misbehaves it spawns the two triggered rhythms: early and delayed afterdepolarizations.
Why the heart cannot tetanize
The plateau stretches the action potential to roughly 200 to 300 ms, almost as long as the mechanical twitch itself. The effective refractory period covers nearly the whole contraction, so the cell relaxes before it can be re-fired. No summation, no tetanus, just a rhythmic pump. Skeletal muscle has a 2 to 5 ms spike and a short refractory period, so it tetanizes easily.
The three windows
Effective (absolute): phase 0 through most of phase 3. Fast Na+ channels are inactivated and cannot reset until the membrane repolarizes past about -60 to -70 mV. No stimulus, however strong, makes a propagated beat.
Relative: late phase 3. Enough Na+ channels have recovered that a stronger-than-normal stimulus can fire, but the upstroke is weak and slow. This is the vulnerable period (R-on-T) where reentry can start.
Supernormal: the very end of phase 3. Channels are recovered and the membrane already sits near threshold, so a weaker-than-normal stimulus can fire a beat.
Early afterdepolarization (EAD)
Fires DURING repolarization, in phase 2 or 3, before the cell finishes. A prolonged action potential (long QT) gives L-type Ca2+ channels time to reactivate → a depolarizing bump on the way down → reach threshold and you trigger torsades. Favored by bradycardia, low K+, low Mg2+, congenital long QT, and QT-prolonging drugs.
Delayed afterdepolarization (DAD)
Fires AFTER repolarization, in phase 4, once the cell is back to rest. Calcium overload → the SR leaks calcium → the Na+/Ca2+ exchanger runs forward (3 Na+ in per 1 Ca2+ out) → a net inward depolarizing current → a late bump. Driven by digoxin toxicity, catecholamines, fast rates, and CPVT.
rate splits the two cleanly
EADs love a slow heart. Pauses and bradycardia lengthen the action potential and give calcium channels time to wake up, so torsades is pause-dependent (watch for a short-long-short sequence). DADs love a fast heart, because speed and catecholamines load more calcium per minute. So speeding the rate suppresses torsades but provokes digoxin and CPVT beats. E comes before D: Early is during, Delayed is after.
QTc 540 ms, polymorphic VT after a pause
Which afterdepolarization is firing this rhythm?
Digoxin toxicity with bigeminy and bidirectional VT
Speeding the heart rate would most likely do what to these beats?
Read it on the ECG
Map the windows onto the T wave: the QRS through the peak of the T is the effective refractory period; the downslope of the T is the relative refractory (vulnerable) period where R-on-T starts reentry; the very end of the T is the brief supernormal window. EADs show a long QT then torsades. DADs show PVCs, bigeminy, atrial tachycardia with AV block, and bidirectional VT.
Match the drug to the phase it blocks
Every antiarrhythmic earns its class from the phase it touches and the interval it moves on the ECG. Learn the map once and most drug questions answer themselves.
The four-class map
Class I blocks Na+ (phase 0). Class II are beta blockers (phase 4 of nodal cells). Class III blocks K+ (phase 3). Class IV blocks Ca2+ (phase 0 of nodal cells). Sodium, Beta, Potassium, Calcium. Adenosine, digoxin, and magnesium sit outside the four.
The full map
| Class | Drugs | Phase / target | ECG effect | Board pearl |
|---|---|---|---|---|
| IA | Quinidine, procainamide, disopyramide | Na+ (phase 0) plus K+ | Modest wide QRS and long QT | Procainamide gives drug-induced lupus; quinidine gives cinchonism; torsades risk |
| IB | Lidocaine (IV), mexiletine | Na+, fast on and off | Little change, may shorten QT | Best on ischemic, depolarized ventricle and post-MI VT |
| IC | Flecainide, propafenone | Na+, strongest block | Markedly wide QRS, QT barely moves | Contraindicated in structural or ischemic heart disease (CAST raised mortality) |
| II | Metoprolol, esmolol, propranolol | Beta-1, phase 4 of nodal cells | Slower rate, longer PR | Esmolol is ultra-short-acting; rate control and post-MI survival |
| III | Amiodarone, sotalol, dofetilide, ibutilide | K+ (phase 3) | Long QT | Amiodarone is multi-class with LOW torsades despite the longest QT; check PFTs, LFTs, TFTs |
| IV | Verapamil, diltiazem | L-type Ca2+, phase 0 of nodal cells | Slower rate, longer PR | Non-dihydropyridine only; verapamil is negatively inotropic, avoid in HFrEF |
| Adenosine | Adenosine | A1 receptor opens GIRK, cuts AV calcium | Brief AV block or sinus pause | First choice for AVNRT; blocked by caffeine, boosted by dipyridamole; lasts about 10 seconds |
| Digoxin | Digoxin | Vagal AV slowing plus Na+/K+ ATPase block | Scooped ST, short QT, long PR | Rate control in AFib; toxicity gives hyperkalemia, atrial tach with AV block, bidirectional VT |
| Magnesium | Magnesium sulfate | Stabilizes membrane, suppresses EADs | Quiets torsades | First line for torsades even when serum Mg is normal |
two wrong answers that kill
Two distractors carry real mortality. First, flecainide (class IC) in a post-MI or structurally diseased heart: it raised death rates in the CAST trial, so it is contraindicated there. Second, an AV-nodal blocker (adenosine, verapamil, digoxin, or a beta blocker) given in WPW with atrial fibrillation: block the node and conduction races down the accessory pathway into VF. Use procainamide or ibutilide instead. Know your clues.
Rate vs rhythm
Classes II and IV plus digoxin and adenosine act on the AV node, so they are rate control. Classes I and III act on atrial and ventricular muscle, so they are rhythm control. And torsades is treated with magnesium first, never with another QT-prolonging class IA or class III drug.
Read the defect off the curve
Each inherited arrhythmia and each electrolyte shift maps onto one part of the action potential. Lose repolarizing K+ and the QT stretches; overload calcium in diastole and you trigger DADs.
The inherited arrhythmias
| Syndrome | Defect (gene, current) | Trigger and board clue |
|---|---|---|
| LQT1 | KCNQ1 loss, less IKs (slow K+) | Exertion, classically swimming; best beta-blocker response |
| LQT2 | KCNH2 / hERG loss, less IKr (rapid K+) | Emotion and sudden noise (alarm, phone); hERG is the target of nearly all drug-induced long QT |
| LQT3 | SCN5A gain, persistent late Na+ | Events at rest or asleep; mexiletine and pacing help, beta blockers less so |
| Brugada | SCN5A loss of function | Coved ST elevation in V1 to V3, events at rest; unmasked by fever or a Na+ blocker; treat with ICD |
| CPVT | RyR2 (dominant) or CASQ2 (recessive) leak | Exercise or emotion triggers bidirectional VT; resting ECG and QT are NORMAL |
| Romano-Ward vs JLN | Romano-Ward dominant, no deafness; Jervell and Lange-Nielsen recessive, KCNQ1/KCNE1 | JLN comes with congenital deafness because IKs also makes inner-ear endolymph; it is more severe |
The electrolytes
| Electrolyte | Action potential effect | ECG signature |
|---|---|---|
| Hyperkalemia | Raises resting potential, inactivates Na+ channels, slows conduction | Peaked T → flat P and long PR → wide QRS → sine wave → arrest |
| Hypokalemia | Paradoxically lowers IKr, slowing phase 3 and lengthening the AP | Flat T waves, U waves, ST depression, long QT, torsades risk |
| Hypercalcemia | More calcium shortens the plateau | Short QT (short ST segment) |
| Hypocalcemia | Less calcium lengthens the plateau | Long QT (long ST segment), can precipitate torsades |
| Hypomagnesemia | Lowers the threshold for EADs | Long QT with torsades |
calcium protects, it does not lower the potassium
When the T waves peak and the QRS widens, the first move is IV calcium gluconate or chloride, and it does not touch the serum potassium. It raises the threshold potential, rebuilding the gap between the depolarized resting membrane and threshold so the heart survives the next few minutes. The potassium itself still has to be shifted (insulin with glucose, a beta-2 agonist, bicarbonate) and removed (diuretics, binders, dialysis). Stabilize, shift, remove. Every time.
Reversals to lock down
SCN5A loss of function is Brugada; SCN5A gain of function (late Na+) is LQT3, same gene, opposite defect. Peaked T waves are hyperkalemia; flat T waves with U waves are hypokalemia. Calcium runs opposite to the QT: high calcium shortens it, low calcium lengthens it. And CPVT has a normal resting ECG, which separates it from congenital long QT in an exercise-syncope stem.
Read it on the ECG
A long QTc (men over 450 ms, women over 470 ms) that breaks into torsades is the long-QT family; coved (type 1) ST elevation in V1 to V3 is Brugada; a normal resting tracing that turns into bidirectional VT on exertion is CPVT. Hyperkalemia marches from peaked T waves to a wide QRS to a sine wave; hypokalemia gives flat T waves and prominent U waves.
Five rules that cover most stems
Tap each blurred line to reveal. If you can state the rule before tapping, you own it.
Keep the curve tied to the patient
Use the images to connect the cellular event to conduction tissue and the surface tracing.
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.
Sources: Costanzo Physiology; Lilly, Pathophysiology of Heart Disease; Katzung, Basic and Clinical Pharmacology; First Aid 2026.
Educational content for medical education. Use clinical judgment and current institutional guidance for patient care.