By Kevin Beck – Updated Mar 24, 2022
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The heartbeat is the most vivid reminder of life’s electrical pulse. From medical jargon to everyday metaphors, the phrase “pulse” connotes vitality. In emergency medicine, the first test of life is a pulse check.
What keeps the heart beating is electricity. The rhythmic contractions that pump blood 70 times per minute—over 100,000 beats each day—stem from a precisely coordinated sequence of ion movements across cardiac cell membranes. This electrical sequence is known as the cardiac action potential and is traditionally broken down into five distinct phases.
An action potential is a rapid, reversible change in a cell’s membrane potential that propagates as a wave along cardiac tissue. Cell membranes maintain an electrochemical gradient via ion pumps: sodium (Na⁺), potassium (K⁺), and calcium (Ca²⁺) are actively transported to create a resting potential of roughly –90 mV in contractile cells. When a stimulus triggers the opening of voltage‑gated channels, the gradient collapses, and ions rush across the membrane, altering the membrane potential.
Phase 0 – Depolarization
Rapid influx of Na⁺ through fast sodium channels drives the membrane potential toward +30 mV. Potassium efflux is temporarily reduced.
Phase 1 – Initial Repolarization
Fast sodium channels close, causing a brief drop in membrane potential as outward K⁺ currents begin.
Phase 2 – Plateau
Inward Ca²⁺ currents balance outward K⁺ currents, stabilizing the membrane potential and maintaining depolarization. This plateau sustains the force of contraction.
Phase 3 – Repolarization
Closure of calcium and sodium channels allows K⁺ to dominate, driving the potential back toward the resting level.
Phase 4 – Resting Potential
The cell rests at –90 mV, maintained by the Na⁺/K⁺ pump. This phase is the longest, occupying the majority of the 300‑ms action potential cycle.
Cardiac muscle, or myocardium, comprises contractile cells that pump blood and a smaller fraction of conducting cells that propagate the action potential. Pacemaker cells generate spontaneous depolarizations, granting the heart its autorhythmicity. Sympathetic, parasympathetic, and hormonal inputs modulate the heart rate, but the underlying ion dynamics remain constant.
During diastole, the myocardium relaxes. In phase 4, a slight depolarization to about –65 mV initiates a positive feedback loop that opens voltage‑gated Na⁺ channels, triggering phase 0 and the next contraction.
Phase 2’s plateau is sustained by a delicate balance: inward Na⁺ and Ca²⁺ currents versus outward K⁺ rectifier currents. This equilibrium not only sustains the action potential but also ensures sufficient Ca²⁺ influx to activate contractile proteins.
Unlike nerve action potentials, cardiac potentials are markedly longer, prolonging the refractory period. This design prevents tetanic contractions and ensures coordinated, life‑sustaining heartbeats, even at high rates.
