Cardiac Action Potential: Phases, Ions, and the Refractory Period

Why the Action Potential Matters for EKG Technicians

Every waveform you record on an EKG tracing — the P wave, QRS complex, and T wave — is the surface reflection of millions of individual cardiac cells firing in sequence. That firing process is called the action potential: a rapid, predictable change in the electrical charge across a cell membrane. Understanding it lets you explain what you are seeing on the strip, recognize dangerous rhythms, and understand why certain interventions (like a defibrillator shock at the wrong moment) can be lethal.

The Basics: Resting Membrane Potential

At rest, the inside of a ventricular myocyte (muscle cell) carries a negative charge relative to the outside — approximately −90 millivolts (mV). This resting state is maintained mainly by potassium ions (K⁺) leaking slowly out of the cell and by the sodium-potassium pump. The cell is described as polarized when it is at rest and ready to fire.

The Five Phases of the Ventricular Action Potential

The ventricular (fast-response) action potential is divided into phases 0 through 4.

Phase 0 — Rapid Depolarization

An electrical stimulus causes fast sodium (Na⁺) channels to open suddenly. Na⁺ rushes into the cell down its concentration and electrical gradient, reversing the membrane potential rapidly from −90 mV to approximately +30 mV. This steep upstroke is Phase 0. On the EKG, the mass of ventricular cells depolarizing together produces the QRS complex.

Phase 1 — Early Rapid Repolarization

Sodium channels close quickly. A brief, transient outward flow of potassium (K⁺) causes a small downward notch in the curve. The membrane voltage drops slightly from its peak.

Phase 2 — Plateau

This is the distinguishing feature of the cardiac action potential and what makes it so different from a nerve or skeletal muscle action potential. Slow calcium (Ca²⁺) channels open, allowing Ca²⁺ to flow into the cell. At the same time, K⁺ continues to leave slowly. These two opposing currents roughly balance, creating a plateau that keeps the cell depolarized for roughly 200–300 milliseconds. This plateau prevents the heart from going into sustained (tetanic) contraction, because the cell cannot accept another stimulus during most of this time. On the EKG the plateau corresponds roughly to the ST segment.

Phase 3 — Rapid Repolarization

Calcium channels close. K⁺ channels open wide, and K⁺ rapidly exits the cell, driving the membrane potential back toward −90 mV. This phase corresponds roughly to the T wave on the EKG.

Phase 4 — Resting Membrane Potential

In ventricular myocytes, Phase 4 is electrically flat. The cell remains at −90 mV until the next stimulus arrives. The sodium-potassium pump and calcium transporters quietly restore ion concentrations to baseline. This is the electrical silence between beats.

Slow-Response Action Potential: SA and AV Nodes

Pacemaker cells in the sinoatrial (SA) node and atrioventricular (AV) node behave differently. Their Phase 4 is not flat — they spontaneously drift upward (depolarize on their own), a property called automaticity. More importantly, their Phase 0 upstroke is driven by slow calcium channels, not fast sodium channels. This makes their upstroke slower and less steep. Because they lack fast Na⁺ channels, these cells are called slow-response cells. The SA node fires fastest and therefore controls the heart rate under normal conditions.

The Refractory Periods

During and after depolarization, cardiac cells pass through two important refractory states.

Absolute Refractory Period (ARP)

From Phase 0 through approximately the middle of Phase 3, the cell cannot respond to any stimulus, no matter how strong. Fast sodium channels are either open or inactivated and cannot reopen yet. This period covers roughly Phases 0, 1, 2, and early Phase 3. On the EKG it corresponds approximately to the QRS complex through the peak of the T wave.

Relative Refractory Period (RRP)

During the latter portion of Phase 3, some (but not all) fast sodium channels have recovered. The cell can respond to a stimulus, but only if that stimulus is stronger than normal. If a premature impulse arrives during this window, the cell is partially recovered and can fire — but its response is disorganized and slower than normal.

Patient Safety: The R-on-T Phenomenon

The relative refractory period is critically important to patient safety. If an ectopic (abnormal) electrical impulse — or an improperly timed pacemaker spike or defibrillator shock — strikes the ventricles during the relative refractory period (falling on or near the peak of the T wave on the EKG), it may trigger a chaotic, life-threatening rhythm called ventricular fibrillation (VF). This is called the R-on-T phenomenon. Ventricular fibrillation is not a perfusing rhythm: the heart quivers instead of pumping, and the patient will lose pulse and consciousness within seconds.

As an EKG technician you are responsible for recognizing and immediately reporting patterns that suggest R-on-T, such as a premature ventricular contraction (PVC) whose R wave falls on the preceding T wave. Recognizing this is within your scope; treatment decisions belong to the supervising clinician or physician — but your prompt reporting can be life-saving.

Summary

| Phase | Name | Primary Ion Movement |

|-------|------|----------------------|

| 0 | Rapid depolarization | Na⁺ into cell |

| 1 | Early repolarization | K⁺ out of cell |

| 2 | Plateau | Ca²⁺ in; K⁺ out |

| 3 | Rapid repolarization | K⁺ out of cell |

| 4 | Resting potential | Pump restores balance |

Mastering these phases gives you a solid foundation for interpreting every waveform on every strip you record.