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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

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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 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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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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Mechanism of Cardiac Arrhythmias01:28

Mechanism of Cardiac Arrhythmias

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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.
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Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

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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...
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Optimization of Transesophageal Atrial Pacing to Assess Atrial Fibrillation Susceptibility in Mice
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Omega-3 Fatty Acids as Antiarrhythmic Drugs: Upstream Target Modulators Affecting Acute and Long-Term Pathological

David F Driscoll1,2, Francine K Welty3, Bruce R Bistrian4

  • 1Stable Solutions LLC, Easton MA.

Critical Care Explorations
|September 27, 2023
PubMed
Summary

Postoperative atrial fibrillation (POAF) after coronary artery bypass grafting (CABG) is common. Omega-3 fatty acids show promise in reducing inflammation and mitigating POAF risks.

Keywords:
atrial fibrillationcoronary artery bypass grafting surgeryinflammatory responseomega-3 fatty acidsspecialized pro-resolving mediators

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Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Postoperative atrial fibrillation (POAF) is a frequent complication after coronary artery bypass grafting (CABG) surgery.
  • POAF is linked to increased short-term and long-term morbidity and mortality.
  • Inflammation, both preoperative and postoperative, is a primary driver of POAF pathophysiology.

Purpose of the Study:

  • To review the role of omega-3 fatty acids (Ω-3 fatty acids) in mitigating POAF.
  • To explore the anti-inflammatory and antiarrhythmic properties of Ω-3 fatty acids in the context of CABG surgery.

Main Methods:

  • A literature search was conducted using PubMed.
  • Studies focusing on complications in patients undergoing isolated CABG surgery were selected.
  • Data were qualitatively assessed and summarized.

Main Results:

  • POAF affects approximately 30% of patients following CABG.
  • Inflammation is identified as the leading cause of POAF.
  • Ω-3 fatty acids possess anti-inflammatory properties and may reduce POAF clinical risks.

Conclusions:

  • Currently, no definitive prophylaxis exists for POAF post-CABG.
  • Targeting the inflammatory response may improve treatment outcomes for POAF.
  • Ω-3 fatty acids may reduce acute inflammation by modulating eicosanoids and pro-resolving mediators.