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Related Concept Videos

Conduction System of the Heart01:19

Conduction System of the Heart

Autorhythmicity is a term that refers to the heart's inherent ability to generate electrical signals and instigate muscle contractions. This self-regulating conduction system within the heart consists of two key components: the pacemaker cells and specialized conducting cells.
The pacemaker cells are located in two primary nodes: the sinoatrial (SA) node and the atrioventricular (AV) node. The SA node pacemaker cells can autonomously depolarize, triggering an action potential that leads to the...
Conduction System of the Heart01:20

Conduction System of the Heart

The cardiac conduction system produces and transmits electrical impulses that prompt myocardial contraction, ensuring efficient heart function. This intricate system ensures that the heart beats in a coordinated and efficient manner, beginning with the atria and then the ventricles. The conduction system optimizes cardiac output by maintaining this precise sequence, which is crucial for adequate blood circulation.
This system relies on the unique properties of nodal and Purkinje cells:...
Cardiac Action Potential01:30

Cardiac Action Potential

Cardiac action potentials are essential for proper heart function, enabling the rhythmic contractions needed for adequate blood circulation. Nodal cells and Purkinje fibers, specialized for electrical conduction, generate these action potentials.
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...

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Related Experiment Video

Updated: May 29, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
09:20

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Rate-dependent AV nodal function: closely bound conduction and refractory properties.

Rafik Tadros1, Jacques Billette

  • 1Département de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Canada.

Journal of Cardiovascular Electrophysiology
|September 30, 2011
PubMed
Summary
This summary is machine-generated.

The study found that AV nodal recovery and refractory curves differ mainly by the His-atrial interval, which is affected by pretest conduction time. Rate-dependent AV nodal function is best assessed using recovery curves adjusted for pretest conduction time changes.

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Isolation of Atrial Myocytes from Adult Mice
08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

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Last Updated: May 29, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
09:20

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Isolation of Atrial Myocytes from Adult Mice
08:34

Isolation of Atrial Myocytes from Adult Mice

Published on: July 25, 2019

Area of Science:

  • Cardiology
  • Electrophysiology
  • Cardiac Physiology

Background:

  • The atrioventricular (AV) node plays a crucial role in regulating cardiac rhythm by slowing and filtering atrial impulses.
  • Disparate rate-dependent changes in AV nodal recovery and refractory curves present a puzzle in understanding AV nodal function.

Purpose of the Study:

  • To investigate the functional origin and significance of the differing rate-dependent changes observed in AV nodal recovery and refractory curves.
  • To clarify the relationship between AV nodal conduction properties and atrial cycle length.

Main Methods:

  • Analysis of 30 steady-state AV nodal responses in rabbit heart preparations using S(1)S(2)S(3) protocols.
  • Assessment of paired combinations of basic and pretest cycle lengths to evaluate recovery and refractory curves.
  • Inclusion of standard premature protocols to compare with steady-state responses.

Main Results:

  • Shortening of basic and pretest cycle lengths increased pretest conduction time, equally shortening the His-atrial interval across all test cycle lengths.
  • This effect predictably shifted the refractory curve downward without altering the recovery curve.
  • Increased pretest conduction time shifted both recovery and refractory curves rightward on the x-axis, potentially biasing comparisons between steady states.

Conclusions:

  • AV nodal recovery and refractory curves primarily differ by the His-atrial interval, which is inversely related to pretest conduction time.
  • Pretest conduction time influences and biases comparisons between AV nodal steady states.
  • Accurate assessment of rate-dependent AV nodal function requires recovery curves that account for or are corrected for variations in pretest conduction time.