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Related Concept Videos

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

892
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...
892
Disturbances in Heart Rhythm01:28

Disturbances in Heart Rhythm

884
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...
884
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.2K
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,...
1.2K
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

763
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...
763
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

705
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...
705
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

505
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...
505

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Related Experiment Video

Updated: May 30, 2025

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

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Therapeutic Flecainide Toxicity Causing VT Storm.

Kiriti Vattikonda1, Christopher J Peterson1, Brian Anyanwu1

  • 1Department of Internal Medicine, Virginia Tech Carilion School of Medicine, Roanoke, Virginia, USA.

JACC. Case Reports
|January 31, 2025
PubMed
Summary

Ventricular tachycardia (VT) storm can be fatal. This case highlights flecainide toxicity, even at therapeutic levels, as a potential cause of VT storm in patients taking this medication.

Keywords:
COVID-19electric stormflecainideventricular tachycardia

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Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
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Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
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Area of Science:

  • Cardiology
  • Clinical Toxicology

Background:

  • Ventricular tachycardia (VT) storm is a life-threatening cardiac arrhythmia.
  • Multiple factors can contribute to the development of VT storm.
  • Flecainide is an antiarrhythmic medication used to treat certain heart rhythm disorders.

Observation:

  • A case study of a 71-year-old woman experiencing VT storm is presented.
  • The patient developed VT storm while on flecainide therapy.
  • The flecainide levels in this patient were within the therapeutic range.

Findings:

  • Flecainide toxicity can precipitate VT storm, even when drug levels are considered therapeutic.
  • This suggests a need for careful monitoring of patients on flecainide, irrespective of standard therapeutic ranges.

Implications:

  • Clinicians should consider flecainide toxicity in the differential diagnosis for any patient presenting with VT storm.
  • This case underscores the importance of recognizing atypical drug toxicity presentations.
  • Further investigation into the mechanisms of flecainide-induced cardiotoxicity at therapeutic levels may be warranted.