Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.1K
Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
1.1K
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

832
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...
832
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

704
Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
704
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

654
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...
654
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

424
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
424
Disturbances in Heart Rhythm01:28

Disturbances in Heart Rhythm

722
Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow...
722

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Impact of frailty on outcomes in surgical patients: A systematic review and meta-analysis.

American journal of surgery·2018
Same author

Factors related to the development of acquired von Willebrand syndrome in patients with essential thrombocythemia and polycythemia vera.

European journal of internal medicine·2016
Same author

The fixed flexed and subluxed knee in the haemophilic child: what should be done?

Haemophilia : the official journal of the World Federation of Hemophilia·2016
Same author

The feasibility of using concentrates containing factor IX for continuous infusion.

Haemophilia : the official journal of the World Federation of Hemophilia·2016
Same author

Home therapy with continuous infusion of factor VIII after minor surgery or serious haemorrhage.

Haemophilia : the official journal of the World Federation of Hemophilia·2016
Same author

Multifocal pseudotumour in a single limb.

Haemophilia : the official journal of the World Federation of Hemophilia·2016

Related Experiment Video

Updated: May 13, 2025

A New Single Chamber Implantable Defibrillator with Atrial Sensing: A Practical Demonstration of Sensing and Ease of Implantation
16:40

A New Single Chamber Implantable Defibrillator with Atrial Sensing: A Practical Demonstration of Sensing and Ease of Implantation

Published on: February 28, 2012

26.1K

A New Class of Antiarrhythmic-Defibrillatory Compounds.

M Erez, D Varon

    Journal of Basic and Clinical Physiology and Pharmacology
    |April 15, 2025
    PubMed
    Summary
    This summary is machine-generated.

    Ventricular fibrillation (VF) can self-terminate. Enhancing cardiac norepinephrine levels with certain drugs may promote self-defibrillation, offering a novel therapeutic strategy for sudden cardiac death.

    Keywords:
    antiarrhythmic drugsdefibrillatory compoundsdibenzazepinesnorepinephrinenorepinephrine uptake inhibitorsphenothiazinestricyclic antidepressantsventricular defibrillation

    More Related Videos

    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology
    10:41

    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology

    Published on: September 13, 2022

    2.0K
    Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
    05:12

    Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

    Published on: February 14, 2022

    3.0K

    Related Experiment Videos

    Last Updated: May 13, 2025

    A New Single Chamber Implantable Defibrillator with Atrial Sensing: A Practical Demonstration of Sensing and Ease of Implantation
    16:40

    A New Single Chamber Implantable Defibrillator with Atrial Sensing: A Practical Demonstration of Sensing and Ease of Implantation

    Published on: February 28, 2012

    26.1K
    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology
    10:41

    Laser-Induced Action Potential-Like Measurements of Cardiomyocytes on Microelectrode Arrays for Increased Predictivity of Safety Pharmacology

    Published on: September 13, 2022

    2.0K
    Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
    05:12

    Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

    Published on: February 14, 2022

    3.0K

    Area of Science:

    • Cardiology
    • Pharmacology
    • Sudden Cardiac Death Research

    Background:

    • Ventricular fibrillation (VF) is a primary cause of sudden cardiac death.
    • Current antiarrhythmic drugs targeting arrhythmia initiation are insufficient.
    • Spontaneous termination of VF has been observed in mammals and humans.

    Purpose of the Study:

    • To propose pharmaceutical enhancement of self-ventricular defibrillation as a new therapeutic approach.
    • To investigate the role of cardiac extraneuronal norepinephrine in VF self-termination.
    • To explore the defibrillatory activity of dibenzazepine and phenothiazine compounds.

    Main Methods:

    • Reviewing data on spontaneous VF termination.
    • Analyzing the effect of cardiac norepinephrine levels on self-defibrillation.
    • Studying the defibrillatory activity of dibenzazepine and phenothiazine compounds by examining structure-activity relationships.

    Main Results:

    • High cardiac extraneuronal norepinephrine levels facilitate VF self-defibrillation.
    • Dibenzazepines and phenothiazines elevate norepinephrine by inhibiting reuptake.
    • These drug classes demonstrated defibrillatory activity.

    Conclusions:

    • Pharmaceutical enhancement of self-ventricular defibrillation is a promising therapeutic strategy.
    • Modulating norepinephrine levels offers a novel approach to treating VF.
    • Dibenzazepine and phenothiazine compounds warrant further investigation for their defibrillatory potential.