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Cardiac action potentials

One sheet for the three traces you keep mixing up: the fast working myocyte, the slow SA nodal pacemaker, and how they line up against the ECG.

The two shapes, same voltage scale

Everything else follows from this picture: the myocyte sits still at −90 mV until something wakes it. The node never sits still at all — it climbs to its own threshold and fires again.

+20 0 −40 −60 −90 mV Ventricular myocyte SA node flat until stimulated never flat — always drifting up
−90 → +20
myocyte swing
−60 → ≈0
nodal swing
Na⁺
myocyte upstroke
Ca²⁺
nodal upstroke

Fast AP — ventricular myocyte

Also called the non-pacemaker or working myocardial AP. Fast Na⁺ channels, a long plateau, and a refractory period almost as long as the contraction itself.

+20 0 −70 −90 mV TP −70 RMP −90 0 1 2 3 4 Na⁺ in K⁺ out Cl⁻ in L-type Ca²⁺ in balanced by K⁺ out K⁺ out Ca²⁺ closed 3 Na⁺ out 2 K⁺ in ARP ≈ 250 ms RRP ≈ 50 ms
  1. 0

    Rapid depolarisationQRS

    Stimulus drags the membrane to threshold −70 mV → fast Na⁺ channels fly open → Na⁺ rushes in. At about +20 mV they inactivate and close. Steep, brief, all-or-none.

  2. 1

    Early rapid repolarisation

    A small notch back down to ≈ 0 mV. Transient outward K⁺ efflux starts, with a little Cl⁻ entry; Ca²⁺ channels are just beginning to open.

  3. 2

    Plateau — the signature of cardiac muscleST

    Lasts about 200 ms. Inward L-type Ca²⁺ current is balanced by outward K⁺, so voltage holds flat. This Ca²⁺ triggers Ca-induced Ca release from the SR → contraction.

  4. 3

    Rapid repolarisationT wave

    Ca²⁺ channels close while delayed-rectifier K⁺ channels open → K⁺ efflux dominates → membrane falls back to −90 mV.

  5. 4

    Resting membrane potential — restorationdiastole

    IK1 holds the RMP steady at −90. Ionic gradients are reset by the Na⁺/K⁺ ATPase (3 Na⁺ out, 2 K⁺ in) and the Na⁺–Ca²⁺ exchanger (3 Na⁺ in, 1 Ca²⁺ out). No spontaneous drift — it waits.

Why the heart cannot tetanise

  • The absolute refractory period (≈250 ms) covers phases 0, 1, 2 and most of 3 — no stimulus of any strength will fire a second AP.
  • The relative refractory period (≈50 ms) runs from late phase 3 into early 4 — only a stronger-than-normal stimulus works.
  • Because the ARP lasts almost as long as the contraction, the muscle has already relaxed before it can be re-excited. No summation, no tetany — which is exactly what a pump needs.

Atrial and Purkinje myocytes — same plan, different lengths

  • Atrial: shorter (~150 ms), triangular, poorly developed plateau — larger transient outward K⁺ current cuts it short.
  • Purkinje: the longest AP and the steepest phase 0 (fastest conduction, ~4 m/s). It has a slow phase 4 drift, which is why it can act as a latent pacemaker at 15–40/min.

Slow AP — SA node, pacemaker, nodal

Same trace, three names. Its defining feature is phase 4: the membrane refuses to stay put, so it needs no external stimulus at all.

+10 0 −40 −60 mV TP −40 MDP −60 4 0 3 4 funny current Iƒ : Na⁺ in K⁺ efflux falling then T-type Ca²⁺ in L-type Ca²⁺ in K⁺ out, Ca²⁺ closed spontaneous diastolic depolarisation → automaticity
  1. 4

    Slow diastolic depolarisation — the pre-potential

    There is no true resting potential. From the maximum diastolic potential of −60 mV the membrane drifts steadily up to −40 mV: the funny current Iƒ lets Na⁺ leak in through HCN channels, K⁺ efflux fades, and near −50 mV T-type Ca²⁺ channels add the final push. Inside becomes progressively more positive. This slope sets the heart rate.

  2. 0

    Depolarisation — slow, and that is the point

    At threshold −40 mV, L-type Ca²⁺ channels open and carry the upstroke. Because Ca²⁺ channels are slow to open and slow to conduct, the slope is much less steep than a myocyte's — hence slow conduction through the node. Peak reaches roughly 0 to +10 mV. Fast Na⁺ channels play no role: at −60 mV they are permanently inactivated.

  3. 3

    Repolarisation

    Ca²⁺ channels close, K⁺ channels open → K⁺ efflux brings the membrane back down to −60 mV, where phase 4 immediately begins again.

  4. —

    Missing on purpose: phases 1 and 2

    No overshoot notch and no plateau. The whole AP is shorter and rounder — and there is no plateau to correspond to an ST segment, because nodal tissue is far too small to register on the surface ECG at all.

Autonomic control — all of it acts on the phase 4 slope

Sympathetic → faster Noradrenaline → β1 → cAMP rises → more Iƒ and more Ca²⁺ current → steeper phase 4, threshold reached sooner → heart rate rises.
Parasympathetic → slower ACh → M2 → opens K(ACh) channels and lowers cAMP → more negative MDP + flatter phase 4 → longer climb to threshold → heart rate falls.

Side by side

The column you can reconstruct the whole topic from.

Fast — ventricular myocyteSlow — SA / AV node
BaselineTrue RMP, stable at −90 mVNo RMP; max diastolic potential −60 mV
Threshold−70 mV−40 mV
Phase 0 carried byFast Na⁺ channelsL-type Ca²⁺ channels
Upstroke slopeVery steep (~200–500 V/s)Shallow (~1–10 V/s)
Peak≈ +20 mV≈ 0 to +10 mV
Phases present0, 1, 2, 3, 40, 3, 4 only
PlateauYes, ~200 ms, L-type Ca²⁺Absent
AutomaticityNone — needs a stimulusYes, intrinsic ~100/min (≈70 after vagal tone)
Conduction velocityFast (0.3–1 m/s; Purkinje ~4)Slow (0.02–0.1 m/s) → AV delay
RefractorinessVoltage-dependent; ARP ≈250 msTime-dependent; recovery outlasts repolarisation
ECG correlate0→QRS, 2→ST, 3→TToo small to appear on surface ECG
Blocked byClass I antiarrhythmics (Na⁺ channel blockers)Class IV (verapamil, diltiazem), β-blockers, ivabradine on Iƒ

Four things to fix in your notes

Your pages are solid — these are the spots where the labels drifted, and all four are commonly examined.

  • Your slow-AP page has phase 0 driven by T-type Ca²⁺. It is the other way round: T-type belongs to late phase 4 (around −50 mV), and L-type carries phase 0 from −40 mV. The page also says "baseline drift due to slow L Ca" — that drift is Iƒ plus T-type, not L.
  • You wrote the nodal peak as +20 mV. That is the ventricular figure. Nodal overshoot is only about 0 to +10 mV — the Ca²⁺ current is too small to drive it higher.
  • "Hyperpolarisation" is crossed out on your page and it should stay crossed out. Phase 4 in the node is depolarising, not hyperpolarising. What is true is that Iƒ is activated by hyperpolarisation — that is the odd behaviour it is named for.
  • Your phase 1 lists "Ca in" alongside K out and Cl in. Phase 1 is essentially the transient outward K⁺ current (with some Cl⁻); Ca²⁺ entry is what defines phase 2.

Quick recall hooks

  • Na is fast, Ca is slow. Whichever ion carries phase 0 tells you the conduction velocity of that tissue.
  • Only the node has a phase 4 slope, and everything that changes heart rate changes that slope.
  • Plateau = ST = no tetany. One structure explains the ECG segment and the mechanics.
  • 3 out, 2 in for the Na⁺/K⁺ pump; 3 in, 1 out for the Na⁺–Ca²⁺ exchanger.