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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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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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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 IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

822
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...
822
Disturbances in Heart Rhythm01:28

Disturbances in Heart Rhythm

932
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...
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Flecainide Toxicity in a Patient with a Functioning Pacemaker.

Sneha Chebrolu1, Jonathan Mayl2, Prashant Bhave2

  • 1Department of Internal Medicine, Wake Forest Baptist Health, Winston-Salem, NC, USA.

The Journal of Innovations in Cardiac Rhythm Management
|July 16, 2024
PubMed
Summary
This summary is machine-generated.

Flecainide toxicity, identified by wide QRS complexes, can occur in patients with pacemakers. Adjusting the pacemaker mode (DDD to VVI) resolved tachycardia and improved ECGs in a case study.

Keywords:
Anti-arrhythmicECGflecainide toxicitypacemakeruse dependenceventricular pacing

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Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Flecainide is a Class Ic anti-arrhythmic drug with use-dependent properties, meaning its efficacy increases at higher heart rates.
  • Flecainide toxicity is characterized by wide QRS complexes on an electrocardiogram (ECG).
  • Patients with structural heart disease and acute kidney injury are at increased risk for flecainide toxicity.

Observation:

  • A 75-year-old patient with a pacemaker presented with suspected flecainide toxicity.
  • The initial ECG revealed tachycardia with wide QRS complexes.
  • The patient's pacemaker, in DDD mode, exhibited rapid ventricular pacing and failed to mode switch.

Findings:

  • Modification of the pacemaker to VVI mode led to the resolution of tachycardia.
  • The patient's QRS complexes improved after the pacing mode adjustment.
  • This case highlights the use-dependent nature of flecainide.

Implications:

  • Pacemaker mode manipulation can be a valuable tool in managing flecainide toxicity.
  • Understanding flecainide's use dependence is crucial for patient management.
  • This case underscores the importance of considering pacemaker settings in patients with anti-arrhythmic drug toxicity.