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Related Concept Videos

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

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

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...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias

Arrhythmia is a condition characterized by an irregular heart rhythm, with ECG changes that differ based on its origin and nature. The types of arrhythmias discussed below include atrial, junctional, and ventricular arrhythmias.Atrial ArrhythmiasPremature Atrial Complexes (PACs): PACs are early atrial beats caused by stress, caffeine, alcohol, electrolyte imbalances, hypoxia, hyperthyroidism, or certain medications (e.g., bronchodilators and decongestants). The ECG shows early P waves with an...

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Related Experiment Video

Updated: Jul 7, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
08:28

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus

Published on: April 5, 2011

[Effect of Bunaftine on the ventricular tachycardia due to aconitine in the dog].

A Alella, C Bertin, D Gattullo

    Archivio Per Le Scienze Mediche
    |October 1, 1976
    PubMed
    Summary

    Bunaftine failed to consistently suppress ventricular tachycardia in dogs. High doses of Bunaftine increased the risk of dangerous cardiac fibrillation, suggesting negative effects on myocardial conductivity.

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    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
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    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

    Published on: November 11, 2022

    A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
    07:56

    A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

    Published on: February 17, 2023

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    Last Updated: Jul 7, 2026

    Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
    08:28

    Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus

    Published on: April 5, 2011

    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
    08:11

    Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

    Published on: November 11, 2022

    A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts
    07:56

    A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

    Published on: February 17, 2023

    Area of Science:

    • Pharmacology
    • Cardiology
    • Veterinary Medicine

    Context:

    • Ventricular tachycardia is a life-threatening arrhythmia.
    • Aconitine is a potent cardiotoxin that reliably induces ventricular tachycardia in animal models.
    • Assessing antiarrhythmic drug efficacy and safety is crucial in cardiovascular research.

    Purpose:

    • To evaluate the efficacy of Bunaftine in suppressing aconitine-induced ventricular tachycardia in a canine model.
    • To determine the dose-dependent effects of Bunaftine on cardiac rhythm and myocardial conductivity.

    Summary:

    • Bunaftine was administered at various doses to dogs experiencing aconitine-induced ventricular tachycardia.
    • Successful conversion to sinus rhythm was observed in only 3 out of 15 dogs.
    • Cardiac fibrillation, particularly at higher doses, was a frequent adverse outcome, suggesting impaired myocardial conductivity.

    Impact:

    • The findings indicate limited therapeutic potential for Bunaftine in treating this specific type of ventricular tachycardia.
    • High doses of Bunaftine may pose significant risks due to pro-arrhythmic effects.
    • This study highlights the importance of careful dose-ranging and safety evaluations for novel antiarrhythmic agents.