U01.07.017 Myocardial action potential

Learning Objectives

Master the 5 phases of the ventricular myocardial action potential and their associated ion currents. Distinguish between cardiac and skeletal muscle excitation-contraction coupling. Understand the role of gap junctions in cardiac electrical conduction. Identify which cardiac cells utilize this fast-response action potential.


Phases of the Myocardial Action Potential

This “fast-response” action potential occurs in all cardiac myocytes except for the SA and AV nodes.

  • Phase 0 (Rapid Upstroke): Massive depolarization caused by the opening of fast voltage-gated Na+ channels.
  • Phase 1 (Initial Repolarization): Inactivation of voltage-gated Na+ channels. Transient outward voltage-gated K+ channels begin to open.
  • Phase 2 (Plateau): The “platwo” phase. Ca2+ influx through L-type voltage-gated channels balances K+ efflux. This Ca2+ influx is the trigger for excitation-contraction coupling.
  • Phase 3 (Rapid Repolarization): Massive K+ efflux due to the opening of slow delayed-rectifier K+ channels and closure of Ca2+ channels.
  • Phase 4 (Resting Potential): High K+ permeability is maintained through K+ leak channels.


Unique Characteristics of Cardiac Muscle

Cardiac muscle differs from skeletal muscle in several high-yield ways:

  • Plateau Phase: Unlike skeletal muscle, cardiac muscle has a sustained plateau due to the balance of Ca2+ influx and K+ efflux.
  • Calcium-Induced Calcium Release (CICR): Contraction requires Ca2+ influx from the extracellular fluid (ECF) to trigger the release of much larger amounts of Ca2+ from the sarcoplasmic reticulum.
  • Electrical Syncytium: Myocytes conduct excitation throughout the heart rapidly via gap junctions.

Myocardial vs. Pacemaker Potentials

Feature Myocardial (Fast) Pacemaker (Slow – SA/AV Nodes)
Phase 0 Upstroke Na+ influx Ca2+ influx
Plateau Phase Present (Phase 2) Absent
Resting Potential Stable (Phase 4) Unstable (If “funny” current)

Activity