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Mechanism of Cardiac Arrhythmias

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 Blockers

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 II Agents as β-Adrenergic Blockers

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...

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

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...

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

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...

Cardiac Action Potential

Cardiac Action Potential

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: May 5, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Short- and long-term effects of amiodarone on the two components of cardiac delayed rectifier K(+) current.

K Kamiya¹, A Nishiyama, K Yasui

¹Department of Circulation, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan. kamiya@riem.nagoya-u.ac.jp

|March 10, 2001

Summary

Amiodarone affects cardiac ion channels differently based on treatment duration. Short-term use inhibits I(Kr), while long-term use reduces I(Ks), impacting tachyarrhythmia treatment.

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Area of Science:

Cardiology
Pharmacology
Molecular Biology

Background:

Amiodarone is crucial for treating life-threatening tachyarrhythmias in patients with structural heart disease.
Its complex effects on cardiac ion channels may vary with short-term versus long-term administration.

Purpose of the Study:

To investigate the differential effects of amiodarone on the two components of the delayed rectifier potassium current (I(K))—I(Ks) and I(Kr)—following short-term and long-term administration.
To compare amiodarone's effects on native rabbit cardiac channels and cloned human channels.

Main Methods:

Whole-cell voltage-clamp technique on rabbit ventricular myocytes to measure I(K), I(Kr), and I(Ks).
Utilized specific blockers (chromanol 293B for I(Ks), E-4031 for I(Kr)).
Assessed effects in Xenopus oocytes expressing cloned HERG (I(Kr)) and KvLQT1/minK (I(Ks)) channels.
Administered oral amiodarone to rabbits for 4 weeks to study long-term effects.

Main Results:

Short-term amiodarone inhibited I(Kr) (IC50=2.8 µmol/L) with minimal effect on I(Ks) in rabbit myocytes.
In oocytes, amiodarone inhibited HERG (I(Kr)) current (IC50=38 µmol/L) but not KvLQT1/minK (I(Ks)) current.
Long-term amiodarone treatment (4 weeks) reduced total I(K) by 55% and altered the I(Kr)/I(Ks) ratio.
No significant changes in mRNA levels of ERG, KVLQT1, or minK were observed after long-term amiodarone treatment.

Conclusions:

Amiodarone exhibits distinct effects on I(Kr) and I(Ks) based on administration duration.
Short-term amiodarone primarily targets and inhibits I(Kr).
Long-term amiodarone administration leads to a reduction in I(Ks).