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Related Concept Videos

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

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

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

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

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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...
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ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias01:25

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

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

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

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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...
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Cardiac Action Potential01:30

Cardiac Action Potential

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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
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Related Experiment Video

Updated: Apr 4, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
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Sex differences in drug-induced changes in ventricular repolarization.

Jose Vicente1, Lars Johannesen2, Jay W Mason3

  • 1Office of Science and Engineering Laboratories, CDRH, US FDA, Silver Spring, MD, USA; Division of Cardiovascular and Renal Products, Office of New Drugs, CDER, US FDA, Silver Spring, MD, USA; BSICoS Group, Aragón Institute for Engineering Research (I3A), IIS Aragón, University of Zaragoza, Zaragoza, Spain.

Journal of Electrocardiology
|September 2, 2015
PubMed
Summary
This summary is machine-generated.

No sex differences were found in drug-induced QT interval prolongation, suggesting other factors contribute to higher torsade de pointes risk in women. This study investigated ECG changes from hERG channel blockers.

Keywords:
DrugsQTc prolongationSex differencesT wave morphologyTorsade de pointeshERG block

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Area of Science:

  • Cardiovascular pharmacology
  • Clinical electrocardiology
  • Pharmacogenetics

Background:

  • QTc interval prolongation predicts drug-induced torsade de pointes, a dangerous arrhythmia.
  • Women are disproportionately affected by torsade de pointes.
  • Investigating sex differences in drug-induced ECG changes is crucial for patient safety.

Purpose of the Study:

  • To assess sex differences in ECG changes induced by four hERG potassium channel blocking drugs.
  • To determine if QTc prolongation varies between men and women.
  • To explore other ECG biomarker differences related to sex.

Main Methods:

  • Double-blind, 5-period crossover study with 22 healthy subjects (11 women).
  • Single oral dose of dofetilide, quinidine, ranolazine, verapamil, and placebo.
  • ECGs and plasma drug concentrations monitored at multiple time points.

Main Results:

  • Dofetilide, quinidine, and ranolazine prolonged the QTc interval.
  • No significant sex differences in QTc prolongation were observed after accounting for drug exposure.
  • Dofetilide showed sex-specific effects on J-Tpeakc, Tpeak-Tend, and T wave amplitude.

Conclusions:

  • No sex differences in QTc prolongation were found for the studied hERG channel blockers.
  • No systematic sex differences in other drug-induced ECG biomarker changes were observed.
  • Higher torsade risk in women is not explained by greater concentration-dependent QTc prolongation.