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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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Allergic Reactions02:06

Allergic Reactions

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Overview
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Allergic Drug Reactions01:27

Allergic Drug Reactions

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Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing...
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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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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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Updated: Jun 17, 2025

Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
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Amiodarone-Induced Anaphylaxis.

Michelle Tang1, Nitya Nunna1, Qing Zhong1

  • 1Department of Biomedical Sciences, Rocky Vista University College of Osteopathic Medicine, Ivins, UT, USA.

Journal of Pharmacy Practice
|August 13, 2024
PubMed
Summary
This summary is machine-generated.

Amiodarone-induced anaphylaxis is rare but serious, often linked to intravenous administration and polysorbate 80. Prompt treatment is crucial for patient recovery from this adverse drug reaction.

Keywords:
IgE-mediated anaphylaxisIgG-mediated anaphylaxisMast cell-specific G protein-coupled receptor-mediated anaphylaxisamiodaroneanaphylaxisiodidepolysorbate 80

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Area of Science:

  • Cardiology
  • Allergy and Immunology
  • Pharmacology

Background:

  • Amiodarone-induced anaphylaxis is a rarely reported but potentially severe adverse drug event.
  • The precise mechanism underlying amiodarone-induced anaphylaxis remains largely unknown.
  • This study investigates reported cases and potential contributing factors.

Purpose of the Study:

  • To review and analyze documented cases of amiodarone-induced anaphylaxis.
  • To identify potential triggers and clinical manifestations of amiodarone-induced anaphylaxis.
  • To assess the role of polysorbate 80 and iodide in amiodarone-induced anaphylaxis.

Main Methods:

  • Conducted a literature search using keywords: "Amiodarone," "Anaphylaxis," "polysorbate 80," and "hypotension."
  • Searched the FDA Adverse Event Reporting System (FAERS) database for amiodarone-associated anaphylaxis cases (1969-2024).

Main Results:

  • Ten literature cases and 89 FAERS reports of amiodarone-induced anaphylaxis were identified.
  • Intravenous amiodarone administration was the most common trigger, often leading to severe hypotension.
  • Clinical presentations included bronchospasm, rash, angioedema, and unconsciousness; prompt treatment led to full recovery in literature cases, while FAERS reported 14 deaths.

Conclusions:

  • Polysorbate 80, amiodarone itself, and iodide may contribute to anaphylaxis.
  • Early recognition and prompt medical intervention are critical for managing amiodarone-induced anaphylaxis.
  • Further research is needed to elucidate the exact mechanisms involved.