A temporary change in the electrical membrane potential of a cell, typically a nerve or muscle cell, that leads to an electrical impulse. In the heart, each cardiac action potential triggers a heartbeat by initiating the contraction of the cardiac muscle cells.
The length of time from the start of a cardiac action potential (depolarization) until repolarization is complete. The APD strongly influences the heart’s refractory period (the period during which cells cannot be re-excited).
Abnormal voltage fluctuations following or during a cardiac action potential. They can trigger extra beats (arrhythmias) if they reach threshold.
Early Afterdepolarization (EAD): Occurs before the action potential has fully ended (during phases 2 or 3). Often linked to excessively prolonged action potentials.
Delayed Afterdepolarization (DAD): Occurs after the cell has fully repolarized (during diastole), typically associated with excessive intracellular calcium.
A common cardiac arrhythmia in which the atria (the heart’s upper chambers) quiver or beat irregularly, leading to an irregular and often rapid heartbeat.
A membrane protein that uses ATP (energy) to move sodium (Na⁺) and potassium (K⁺) ions across the cell membrane (3 sodium ions out, 2 potassium ions in). Helps maintain the resting membrane potential and ionic gradients essential for heart cell function.
A slower than normal heart rate (usually fewer than 60 beats per minute in adults).
In the heart, the influx of calcium through L-type calcium channels triggers a larger release of calcium from the sarcoplasmic reticulum (SR). This rise in intracellular calcium drives cardiac muscle contraction.
I_Ca,L (L-type Calcium Current): The primary inward calcium current responsible for most of the calcium entry during the cardiac action potential plateau.
I_Ca,T (T-type Calcium Current): A transient inward calcium current that activates at more negative voltages than I_Ca,L. It can contribute to pacemaker activity in cells of the sinoatrial (SA) and atrioventricular (AV) nodes.
Ryanodine Receptor (RyR): A channel on the sarcoplasmic reticulum that releases stored calcium into the cytosol, triggering contraction.
Sarcoplasmic/Endoplasmic Reticulum Ca²⁺-ATPase (SERCA): A pump that moves calcium from the cytosol back into the sarcoplasmic reticulum, allowing relaxation.
An abnormal heart rhythm. It can be too fast, too slow, or irregular, and arises from disturbances in how impulses are generated or conducted through the heart.
A heart muscle cell. Cardiomyocytes are specialized for contraction and have unique electrical properties that enable the heartbeat.
A hereditary condition in which the QT interval (on the ECG) is prolonged, usually due to mutations in specific ion channel genes. It can cause dangerous arrhythmias.
Failure of an electrical impulse to propagate normally through the heart. Can be “unidirectional” (the impulse travels in one direction but not the reverse) or “bidirectional” (blocked in both directions). Plays a role in reentry-based arrhythmias.
An explanation of pacemaker function in sinoatrial node cells, stating that both membrane currents (the “membrane clock,” such as the funny current I_f) and rhythmic calcium cycling inside the cell (the “calcium clock”) interact to set and regulate the heart’s natural pacing.
The phase of the cardiac cycle when the heart muscle relaxes and allows the chambers to fill with blood.
Differences in action potential durations (or repolarization timing) across different regions of the heart muscle. Heightened dispersion can create a substrate for reentrant arrhythmias.
The shortest time interval after an action potential during which a new electrical stimulus cannot trigger another action potential in cardiac cells.
A noninvasive recording of the heart’s electrical activity measured from the body surface. Common features include the P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization).
The sequence of events whereby an action potential in a heart cell leads to calcium influx, which then triggers cellular contraction.
A mixed inward current (carried by both sodium and potassium) that activates upon hyperpolarization. Plays a key role in pacemaker activity, particularly in the sinoatrial node.
Specialized cell-cell connections (made of proteins called connexins) that allow direct electrical communication between adjacent heart cells, enabling coordinated propagation of electrical impulses.
A clinical syndrome in which the heart’s ability to pump blood is diminished. HF often involves electrical remodeling, changes in calcium handling, and increased risk of arrhythmias.
A shift of the membrane potential to a more negative value, usually making it harder for a cell to fire an action potential.
I_Na (Fast Sodium Current): Responsible for the rapid upstroke (phase 0) of the cardiac action potential in atrial and ventricular cells.
I_NaLate (Late Sodium Current): A small, persistent sodium current that does not completely inactivate. Can prolong repolarization and contribute to arrhythmias.
I_Ca,L (L-Type Calcium Current): Main inward calcium current during the plateau phase.
I_K1 (Inward Rectifier Potassium Current): Stabilizes the resting membrane potential.
I_Kr (Rapid Delayed Rectifier Potassium Current): An outward current that helps with repolarization (phase 3). Block of I_Kr can markedly prolong the action potential.
I_Ks (Slow Delayed Rectifier Potassium Current): Another outward potassium current helping in repolarization, especially at faster heart rates or during β-adrenergic stimulation.
I_to (Transient Outward Current): A brief outward potassium current that contributes to the notch in phase 1 repolarization.
I_K,ACh (Acetylcholine-Activated Potassium Current): Activated by vagal stimulation (via acetylcholine or adenosine). Prominent in atrial and AV nodal cells.
I_Kur (Ultrarapid Delayed Rectifier Potassium Current): A potassium current mostly found in atria, contributing to their shorter action potentials.
A small but prolonged component of the sodium current that persists beyond the initial fast upstroke. Increased late sodium current can prolong repolarization and predispose cells to arrhythmias.
Commonly known as a heart attack. It occurs when blood flow to part of the heart is blocked, causing cell death and often leading to electrical and structural remodeling that may set the stage for arrhythmias.
A membrane transporter that exchanges 3 sodium ions for 1 calcium ion, moving calcium out of the cell (or in the opposite direction depending on membrane potential and ion gradients). Plays a significant role in shaping the action potential plateau and in generating afterdepolarizations when intracellular calcium is high.
A formula used to calculate the equilibrium potential of an ion (e.g., K⁺) across a membrane based on its concentration gradient and charge.
Automatic (self-initiated) firing of action potentials, typically in sinoatrial node cells, setting the heart rate. Certain disease conditions or ectopic foci can also develop pacemaker-like activity.
Phase 0: Rapid upstroke (usually from fast inward sodium current).
Phase 1: Initial partial repolarization (often by transient outward currents).
Phase 2: Plateau phase, where inward (mostly calcium) and outward (potassium) currents are nearly balanced.
Phase 3: Rapid repolarization, dominated by outward potassium currents.
Phase 4: Resting membrane potential (or spontaneous diastolic depolarization in pacemaker cells).
Specialized conducting fibers in the ventricles that rapidly distribute the electrical impulse to ensure coordinated ventricular contraction. They can also act as subsidiary pacemakers if the primary pacemaker (SA node) fails.
An arrhythmia mechanism in which a wave of electrical excitation keeps re-circulating through a region of tissue (e.g., because of conduction block in one direction, slow conduction, and reactivation in the reverse direction). This can sustain rapid tachyarrhythmias.
The return of the cardiac cell membrane potential from a positive (depolarized) value back toward the negative resting level (phase 3 of the action potential).
How action potential duration (APD) adapts following a preceding beat, often studied by looking at APD as a function of the diastolic interval. A steep APD restitution slope can favor arrhythmias (e.g., EADs or alternans).
A specialized endoplasmic reticulum in muscle cells that stores calcium. Calcium release from the SR initiates contraction, and re-uptake into the SR enables relaxation.
The heart’s primary pacemaker region, located in the right atrium. SAN cells spontaneously depolarize, setting the normal heart rate.
A rapid heart rhythm (often above 100 beats per minute in adults). It can be regular or irregular.
The voltage difference across a cell’s membrane—inside relative to outside. Heart cell transmembrane potential changes drive the cardiac action potential.
Abnormal impulses occurring when afterdepolarizations (EADs or DADs) reach threshold, initiating extra beats that can degenerate into more dangerous arrhythmias.
Laboratory methods for measuring ion currents in isolated cells (or tissue) by controlling or recording the membrane potential. Widely used to identify and quantify specific ion channel behaviors.