Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

1.3K
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...
1.3K
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

765
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...
765
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

1.8K
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,...
1.8K
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

930
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...
930
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

1.1K
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...
1.1K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

3.1K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
3.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Chronic Treatment with Renin-Angiotensin System Inhibitors at Hospital Admission is Associated with Improved Reperfusion and Mortality Among STEMI Patients Undergoing Mechanical Reperfusion: Insight from the ISACS-STEMI COVID-19 Registry.

Current vascular pharmacology·2026
Same author

Shared Extracellular Matrix Remodeling and Proteomic Signature in Dupuytren's Disease and Relapsed Clubfoot Tissue.

Cells·2026
Same author

High-density contrast echocardiography for patent foramen ovale assessment: sensitivity and relationship with invasively measured shunt severity and atrial septum morphology.

Echo research and practice·2026
Same author

Persisting Sex Discrepancies in Short-Term Outcomes of Patients with ST-Segment Myocardial Infarction: Results of the ISACS-STEMI COVID-19 Registry.

Journal of clinical medicine·2026
Same author

Adverse side-effects of antifibrotic drugs in idiopathic pulmonary fibrosis-clarification of several points.

Journal of thoracic disease·2026
Same author

Pacemaker recovery after permanent pacemaker implantation post-transcatheter aortic valve implantation: A sub-study of the LANDMARK trial.

International journal of cardiology·2026

Related Experiment Video

Updated: Sep 26, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

4.8K

Amiodarone induced pulmonary toxicity.

Martin Hudec, Petra Vysočanová, Vojtěch Brázdil

    Vnitrni Lekarstvi
    |April 23, 2022
    PubMed
    Summary

    Amiodarone-induced pulmonary toxicity (AIPT) is a rare but severe adverse effect. Early diagnosis and treatment of AIPT, along with adjusting antiarrhythmic therapy, significantly improved patient outcomes.

    Keywords:
    AIPTamiodaroneamiodarone induced pulmonary toxicityamiodarone lung

    More Related Videos

    Percutaneous Contrast Echocardiography-guided Intramyocardial Injection and Cell Delivery in a Large Preclinical Model
    14:24

    Percutaneous Contrast Echocardiography-guided Intramyocardial Injection and Cell Delivery in a Large Preclinical Model

    Published on: January 21, 2018

    11.8K
    A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
    08:09

    A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

    Published on: June 7, 2018

    9.9K

    Related Experiment Videos

    Last Updated: Sep 26, 2025

    A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
    05:14

    A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

    Published on: May 16, 2020

    4.8K
    Percutaneous Contrast Echocardiography-guided Intramyocardial Injection and Cell Delivery in a Large Preclinical Model
    14:24

    Percutaneous Contrast Echocardiography-guided Intramyocardial Injection and Cell Delivery in a Large Preclinical Model

    Published on: January 21, 2018

    11.8K
    A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
    08:09

    A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish

    Published on: June 7, 2018

    9.9K

    Area of Science:

    • Cardiology
    • Pulmonology
    • Clinical Pharmacology

    Background:

    • Amiodarone is a widely used antiarrhythmic medication for supraventricular and ventricular arrhythmias.
    • Adverse effects are common with amiodarone, with amiodarone-induced pulmonary toxicity (AIPT) being a rare but severe complication.
    • AIPT carries a high mortality rate and necessitates prompt recognition and management.

    Purpose of the Study:

    • To present a case of amiodarone-induced pulmonary toxicity (AIPT) in an elderly patient.
    • To highlight the typical clinical presentation, diagnostic procedures, and treatment of AIPT.
    • To discuss alternative therapeutic options for supraventricular arrhythmias.

    Main Methods:

    • Case report of an 80-year-old patient with paroxysmal atrial fibrillation treated with amiodarone.
    • Analysis of repeated hospitalizations for bilateral pneumonia over 3 months.
    • Review of diagnostic procedures and treatment strategies for AIPT.

    Main Results:

    • The patient was diagnosed with amiodarone-induced pulmonary toxicity (AIPT) after recurrent pneumonia.
    • Early diagnosis, appropriate AIPT therapy, and modification of antiarrhythmic treatment led to significant clinical improvement.
    • The case illustrates common clinical features and management approaches for AIPT.

    Conclusions:

    • Amiodarone-induced pulmonary toxicity (AIPT) requires vigilant monitoring due to its potential severity.
    • Prompt diagnosis and multidisciplinary management are crucial for improving patient outcomes in AIPT.
    • Optimizing antiarrhythmic therapy is essential when managing amiodarone-related adverse events.