2.2 Cardiac action potential phases & refractory periods

The two cardiac cell types

Cardiac cells fall into two electrophysiologic families, and knowing the difference is the key to this whole chapter. Fast-response cells, which include the atrial and ventricular myocytes and the Purkinje fibers, have a stable, very negative resting membrane potential and a steep upstroke. Slow-response cells, the SA and AV nodes, have a less negative, unstable membrane that drifts upward on its own, giving them automaticity.

Phases of the fast-response action potential

The ventricular myocyte action potential is described in five numbered phases:

• Phase 4 (rest): the membrane sits near -90 mV, held there by the sodium-potassium pump and the inward-rectifier potassium current.
• Phase 0 (depolarization): when the cell is driven to threshold (about -70 mV), voltage-gated fast sodium channels open and Na+ floods in, shooting the potential toward +20 to +30 mV. This rapid upstroke is why fast-response tissue conducts quickly.
• Phase 1: a brief downward notch as the sodium channels inactivate and a transient outward potassium current begins repolarization.
• Phase 2 (plateau): the hallmark of cardiac muscle. Inward calcium current through L-type channels roughly balances outward potassium current, holding the membrane depolarized. This sustained plateau triggers calcium-induced calcium release and drives contraction; it also lengthens the action potential far beyond that of skeletal muscle, which prevents tetany.
• Phase 3: calcium channels close while potassium efflux dominates, returning the membrane toward its resting value.

The resting potential itself is created by ionic gradients maintained by the sodium-potassium ATPase, which pumps three Na+ out of the cell for every two K+ it brings in. This keeps potassium high inside and sodium high outside, and the membrane's high resting permeability to potassium holds the interior negative. Anything that disturbs these gradients, such as hyperkalemia or hypokalemia, changes the resting potential and the shape of the action potential, which is exactly why serum electrolyte abnormalities produce recognizable ECG changes like the peaked T waves of high potassium.

Slow-response cells and automaticity

Nodal cells behave differently. Their maximum diastolic potential is only about -60 mV, and instead of a flat phase 4 they show spontaneous diastolic depolarization, a slow upward drift driven mainly by the "funny" current (If, a sodium current) and T-type calcium. When this drift reaches threshold near -40 mV, phase 0 is carried by calcium rather than sodium, producing a slower, more gradual upstroke and therefore slower conduction, which is why the AV node conducts slowly. The steepness of the phase 4 slope sets how fast a pacemaker fires; the SA node has the steepest slope, so it reaches threshold first and fastest. This dependence on calcium is also why calcium-channel blockers and beta-blockers slow the SA and AV nodes so effectively, and why the QT interval on the surface ECG mirrors ventricular action-potential duration: when repolarizing currents are impaired by drugs, ischemia, or inherited channel defects, both the action potential and the QT interval lengthen.

Refractory periods

While the action potential is running, the cell cannot be re-excited normally. This is described in terms of refractory periods:

• Absolute (effective) refractory period: spans phase 0, phase 1, phase 2, and the first part of phase 3. Sodium channels are inactivated, so no stimulus, however strong, can trigger a new propagated action potential. On the ECG this covers the QRS complex, the ST segment, and roughly the first half of the T wave. It protects the ventricle from being re-stimulated too soon and from sustaining a tetanic contraction.
• Relative refractory period: occupies the later part of phase 3 and appears on the downslope of the T wave. Enough sodium channels have recovered that a stronger-than-normal stimulus can elicit an action potential, but conduction is slow and abnormal.
• Supernormal period: a very brief window at the end of phase 3 in which a weaker-than-expected stimulus can excite the cell.

Refractoriness is not only protective within a single beat; it also limits how fast impulses can reach the ventricles. Because the AV node has a long refractory period, it acts as a filter that blocks many impulses during very rapid atrial rhythms such as atrial flutter or atrial fibrillation, protecting the ventricles from dangerously fast rates. In the same way, the long ventricular refractory period makes it harder for a wavefront to circle back and re-excite tissue it has just left, which is the heart's built-in defense against re-entrant tachycardias.

The vulnerable period and R-on-T

The peak of the T wave marks the vulnerable period. At this moment the ventricular cells are repolarizing unevenly, some fully recovered and some still refractory, so the tissue is electrically heterogeneous. A premature impulse landing here, classically a PVC falling on the T wave ("R-on-T"), can fragment into multiple wandering wavefronts and precipitate ventricular tachycardia or ventricular fibrillation. This is precisely why synchronized cardioversion times the shock to the R wave and avoids the T wave. For the rhythm technician, the QT interval is a useful surrogate for total ventricular action-potential duration: a long QT stretches repolarization, widens the vulnerable window, and raises the risk of R-on-T arrhythmias such as torsades de pointes.