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Related Concept Videos

Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

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,...
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...
Disturbances in Heart Rhythm01:29

Disturbances in Heart Rhythm

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 heart...
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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Measurement of Antibody Effects on Cellular Function of Isolated Cardiomyocytes
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Measurement of Antibody Effects on Cellular Function of Isolated Cardiomyocytes

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Delayed ventricular repolarization as an anti-arrhythmic principle.

E M Vaughan Williams

    European Heart Journal
    |November 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    Delaying cardiac repolarization can prevent arrhythmias. Amiodarone prolongs action potential duration (APD), demonstrating an anti-arrhythmic effect by extending the refractory period, unlike Class 1 drugs.

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    Area of Science:

    • Cardiovascular Physiology
    • Pharmacology
    • Electrophysiology

    Background:

    • Cardiac depolarization relies on fast inward currents, with channels inactivating rapidly post-repolarization.
    • Class 1 anti-arrhythmic drugs delay inactivation, extending the refractory period.
    • Theoretical potential exists to prolong refractory period by delaying cardiac repolarization itself.

    Purpose of the Study:

    • To investigate the anti-arrhythmic potential of delaying cardiac repolarization.
    • To evaluate amiodarone's effect on action potential duration (APD) and its anti-arrhythmic properties.

    Main Methods:

    • Review of existing literature on anti-arrhythmic drugs and cardiac repolarization mechanisms.
    • Analysis of amiodarone's effects on APD and its observed anti-arrhythmic actions in preclinical and clinical studies.

    Main Results:

    • Quinidine and disopyramide (Class 1 agents) showed minor repolarization delays and had anticholinergic side effects.
    • Amiodarone prolonged APD and exhibited anti-arrhythmic effects in various species, including humans.
    • Homogeneously prolonged APD is theoretically anti-arrhythmic, despite potential QT prolongation from other causes.

    Conclusions:

    • Amiodarone's ability to prolong APD offers a viable anti-arrhythmic strategy.
    • Agents like amiodarone, bretylium, and sotalol, which prolong APD, are associated with reduced arrhythmia incidence.
    • Further research is needed to fully elucidate the mechanisms by which various agents delay cardiac repolarization.