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Dysrhythmias IV: Characteristics of Bradyarrhythmias01:18

Dysrhythmias IV: Characteristics of Bradyarrhythmias

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Bradyarrhythmias are cardiac rhythm disorders characterized by a slower-than-normal heart rate, typically defined as fewer than 60 beats per minute. Some of which are discussed here:Sinus BradycardiaSinus bradycardia presents a heart rate lower than 60 beats per minute, with a regular rhythm originating from the SA node. The ECG typically shows normal P waves preceding each QRS complex, a normal PR interval (0.12 to 0.20 seconds), and a normal QRS duration (0.06 to 0.10 seconds).First-Degree AV...
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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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Depolarizing Blockers: Mechanism of Action01:28

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Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
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Disturbances in Heart Rhythm01:29

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

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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 IV Agents as Calcium Channel Blockers01:20

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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.
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Pembrolizumab-Induced Mobitz Type 2 Second-Degree Atrioventricular Block.

Alisha Khan1, Sana Riaz1, Robert Carhart2

  • 1Department of Medicine, SUNY Upstate Medical University, USA.

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Pembrolizumab, a cancer immunotherapy, can rarely cause heart problems. A patient developed severe heart block after pembrolizumab treatment, highlighting the need for careful monitoring of immune-related adverse events.

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Area of Science:

  • Oncology
  • Cardiology
  • Immunology

Background:

  • Pembrolizumab is an immune checkpoint inhibitor targeting PD-1, widely used in oncology.
  • Immune-related adverse events (IRAEs) are known complications, with cardiotoxicity being infrequent but serious.
  • Reported cardiotoxicities include myocarditis, arrhythmias, and heart failure.

Observation:

  • A case report details a 67-year-old female with stage IV non-small-cell lung cancer.
  • The patient received pembrolizumab and developed Mobitz type 2 second-degree atrioventricular block.
  • Progression to symptomatic complete heart block occurred within hours, necessitating a temporary pacemaker.

Findings:

  • Pembrolizumab treatment was associated with the rapid onset of high-grade atrioventricular block.
  • The case illustrates a rare but severe cardiotoxicity of PD-1 inhibitors.
  • Proposed mechanisms for IRAEs and their management are discussed.

Implications:

  • Physicians should exercise heightened caution and awareness regarding potential cardiotoxicity in patients receiving immunotherapy.
  • A multidisciplinary approach is recommended for managing IRAEs and considering the resumption of immune checkpoint inhibitor therapy.
  • Early recognition and intervention are crucial for managing severe cardiac events associated with pembrolizumab.