Pharmacology II - Chapter 14 Antiarrhythmics
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Questions and Answers

Which class of antiarrhythmic drugs is primarily known for blocking sodium channels and prolonging action potential duration?

  • Class 2
  • Class 3
  • Class 1A (correct)
  • Class 1B

Which antiarrhythmic drug is indicated for severe ventricular arrhythmias?

  • Amiodarone
  • Diltiazem
  • Flecainide (correct)
  • Lidocaine

What is the primary action of Class III antiarrhythmic drugs?

  • Reduce sympathetic autonomic effects
  • Shorten action potential duration
  • Block sodium channels
  • Block potassium currents (correct)

Which of the following drugs has minimal to no effect on action potential duration and has a slow binding profile?

<p>Flecainide (D)</p> Signup and view all the answers

Which class of antiarrhythmic drugs is primarily associated with reducing beta adrenergic activity in the heart?

<p>Class II (C)</p> Signup and view all the answers

What is the primary mechanism of action of Quinidine in treating arrhythmias?

<p>Sodium channel blockade (D)</p> Signup and view all the answers

Which statement about Class Ic antiarrhythmic drugs is accurate?

<p>They are effective only after other antiarrhythmics have failed. (A)</p> Signup and view all the answers

What is a major clinical concern associated with Sotalol as a Class III antiarrhythmic?

<p>Precipitation of Torsade de Pointes arrhythmia (D)</p> Signup and view all the answers

How do beta blockers function in the context of treating arrhythmias?

<p>They reduce sodium and calcium currents and suppress abnormal pacemakers. (C)</p> Signup and view all the answers

What distinguishes Class Ib antiarrhythmic drugs from other classes?

<p>They can lead to a high first-pass effect and are used exclusively at sodium channels. (A)</p> Signup and view all the answers

Which of the following is NOT classified as an arrhythmia?

<p>Myocardial infarction (C)</p> Signup and view all the answers

What distinguishes atrial flutter from atrial fibrillation?

<p>Atrial flutter typically involves a single reentrant circuit. (A)</p> Signup and view all the answers

Which of the following factors can cause an arrhythmia?

<p>Change in conduction velocity (D)</p> Signup and view all the answers

In the context of cardiac action potentials, which statement is true?

<p>Different phases of action potentials are determined by specific ion flows. (A)</p> Signup and view all the answers

Which mechanism is NOT associated with arrhythmias?

<p>Normal conduction pathways (C)</p> Signup and view all the answers

Torsade de pointes is typically characterized by which of the following?

<p>Polymorphic ventricular tachycardia with an increased QT interval. (A)</p> Signup and view all the answers

In terms of cardiac cell ion flux, what is true?

<p>Each cardiac myocyte channel is specific to a single ion. (A)</p> Signup and view all the answers

Ohm's Law in relation to cardiac arrhythmias is relevant for understanding what concept?

<p>Current flow relative to voltage and conductance. (B)</p> Signup and view all the answers

What is the primary function of the atrioventricular (AV) node in the cardiac conduction system?

<p>To distribute electrical impulses to the ventricles (D)</p> Signup and view all the answers

Which antiarrhythmic drug is indicated for maintaining normal sinus rhythm in patients with heart failure?

<p>Amiodarone (C)</p> Signup and view all the answers

Which part of the heart's electrical system is referred to as the 'natural pacemaker'?

<p>SA node (C)</p> Signup and view all the answers

What is the primary use of Amiodarone in arrhythmias?

<p>As a broad-spectrum agent used when all other treatments fail. (D)</p> Signup and view all the answers

Which side effect is most commonly associated with Class IV antiarrhythmic drugs?

<p>Constipation. (A)</p> Signup and view all the answers

In the context of antiarrhythmic therapy, what is a critical consideration before initiating treatment?

<p>Confirming the specific type of arrhythmia present. (D)</p> Signup and view all the answers

What significant toxicity is associated with the use of Verapamil, a Class IV drug?

<p>Severe constipation. (B)</p> Signup and view all the answers

Which part of the cardiac conduction system initiates the conduction of an electrical signal?

<p>His bundle (C)</p> Signup and view all the answers

During which phase of the action potential do Class I drugs primarily act?

<p>Phase 0 - Rapid depolarization (C)</p> Signup and view all the answers

Which ion concentration is significantly higher extracellularly compared to intracellularly in cardiac cells?

<p>Na+ (D)</p> Signup and view all the answers

What is the primary consequence of abnormal automaticity in the heart?

<p>Erratic heart rhythms (D)</p> Signup and view all the answers

Which of the following ions is primarily responsible for the plateau phase in cardiac action potentials?

<p>Ca++ (D)</p> Signup and view all the answers

What is the role of the His-Purkinje system in the heart?

<p>To conduct electrical impulses throughout ventricles (D)</p> Signup and view all the answers

What characterizes Class III drugs in relation to cardiac action potentials?

<p>Prolong repolarization phase (A)</p> Signup and view all the answers

What drugs are well tolerated in heart failure (reduced ejection volume) and have the ability to convert or prevent atrial fibrillation?

<p>Dofetilide (A), Amiodarone (B)</p> Signup and view all the answers

What is used to reverse digoxin-induced arrhythmias?

<p>Digoxin immune fab (B)</p> Signup and view all the answers

What may precipitate torsade de pointes arrhythmia?

<p>Sotalol (B)</p> Signup and view all the answers

What is the mechanism of action (MOA) of adenosine?

<p>Activates K+ channels and blocks calcium channels (A)</p> Signup and view all the answers

What is the importance of magnesium?

<p>May act on ATPase enzyme, Na channels, certain K channels, and Ca channels; often used to treat torsades de pointes (A)</p> Signup and view all the answers

What can hypokalemia induce?

<p>Ectopic pacemaker activity (B)</p> Signup and view all the answers

Match each drug glass to its indications

<p>Class 1 A = AF, PVC Class 1B = PVCs Class 2 = AF, atrial flutter, PVCs Class 1C = Severe ventricular arrhythmia</p> Signup and view all the answers

Match each drug class to its indiciations

<h1>Class 3 = AF, Severe ventricular arrythmias Class 4 = AF, atrial flutter</h1> <p>=</p> Signup and view all the answers

Flashcards

Cardiac Conduction System

The electrical system of the heart that controls the heartbeat. It includes the SA node, AV node, and His-Purkinje fibers.

SA Node

The natural pacemaker of the heart, located in the right atrium. It initiates the electrical impulses that cause the heart to beat.

AV Node

Located between the atria and ventricles, it acts as an electrical bridge, passing impulses through to the ventricles.

Atrial Fibrillation

An irregular heartbeat originating in the atria.

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Antiarrhythmic drugs

Drugs used to treat abnormal heart rhythms (arrhythmias).

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His-Purkinje System Location

Located within the ventricles, this system transmits signals for ventricular contraction.

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Cardiac Conduction Phases

Action potentials in cardiac cells have 5 phases: 0 (rapid depolarization), 1 (early repolarization), 2 (plateau), 3 (repolarization), and 4 (resting potential).

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His Bundle

The starting point of the His-Purkinje system.

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Ion Concentrations (Cardiac Cell)

Cardiac cells have specific concentrations of ions (Na+, K+, Ca++, and Cl-) both inside and outside the cell for proper function.

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Purkinje Fibers

The final part of the His-Purkinje system they conduct the signals throughout the ventricles.

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Cardiac Cell Action Potential

A series of changes in the electrical potential across the cardiac cell membrane, driven by ion flow through channels, generating a heartbeat.

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Arrhythmia Mechanisms

Arrhythmias can arise from abnormal automaticity or reentrant conduction of signals.

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Action Potential Phases Importance

The different phases reflect the different types of ion channels opening and closing, leading to the different stages of depolarization and repolarization involved in the heart's electrical activity.

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Class I Antiarrhythmics

Drugs that block sodium channels in the heart, affecting the speed and duration of electrical signals. They are categorized into IA, IB, and IC based on their effects on action potential duration.

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Class II Antiarrhythmics (Beta Blockers)

These drugs reduce the heart's response to adrenaline and noradrenaline by blocking beta receptors. They slow down the heart rate and reduce the force of contraction.

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Class III Antiarrhythmics

Drugs that primarily prolong the action potential duration by blocking potassium channels, thereby delaying the repolarization of heart cells.

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Class IV Antiarrhythmics (Calcium Channel Blockers)

These drugs block calcium channels, slowing down the heart rate and reducing the force of contraction by interfering with muscle contraction in the heart.

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Dominant Action of Antiarrhythmic Drugs

Although most antiarrhythmic drugs have multiple actions, one action is usually more prominent, leading to their classification into specific classes (I-IV).

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Quinidine Class

Quinidine is a Class Ia sodium channel blocker, meaning it prolongs the action potential duration and slows conduction velocity. It's primarily used to treat atrial fibrillation and ventricular tachycardia.

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Quinidine's Major Cardiac Effects

Quinidine can cause significant side effects, particularly QT interval prolongation, which increases the risk of Torsade de Pointes arrhythmia, a potentially life-threatening condition.

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Class Ib Drugs: Lidocaine

Class Ib antiarrhythmics like lidocaine are used to treat acute ventricular arrhythmias caused by ischemia, usually following a heart attack (MI). They primarily act on sodium channels.

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Class Ic Drugs: High Mortality

Class Ic antiarrhythmics are highly effective in treating both atrial and ventricular arrhythmias, but carry a higher risk of mortality compared to placebo. These are only used when other options fail.

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Class II Drugs: Beta-blockers

Beta-blockers, like propranolol, metoprolol, and timolol, are Class II antiarrhythmics that reduce the strength of heartbeats (both atrial and ventricular) and can prevent arrhythmias.

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Arrhythmia

An abnormal heart rhythm caused by a deviation from the normal pattern of electrical impulses in the heart.

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Causes of Arrhythmias

Arrhythmias can be caused by abnormal impulse origin, alterations in the rate or control of impulses, or changes in the speed of impulse conduction.

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Ion Flux

The movement of ions in and out of cardiac cells through membrane channels controls the electrical potential of the heart. These ions are not directly soluble in the cell wall.

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Cardiac Action Potential Phases

The cardiac action potential is divided into phases, each determined by the specific ions flowing during that phase.

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Ohm's Law and Arrhythmias

Arrhythmias can be caused by disturbances in impulse formation, conduction, or both. These disturbances are related to ion conduction and can be explained by Ohm's Law: Current = Voltage (Conductance).

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Torsade de Pointes

A type of polymorphic ventricular tachycardia characterized by a prolonged QT interval, which can be caused by medications or genetics.

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Reentry

Reentry is when the electrical impulse cycles through conductive tissue that has been recently stimulated, often leading to tachycardia and arrhythmias originating in the AV node.

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Drug Induced Arrhythmias

Some medications can cause or worsen arrhythmias by affecting the electrical activity of the heart.

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Amiodarone

A broad-spectrum antiarrhythmic drug that blocks sodium, potassium, and calcium channels, as well as beta receptors. Used as a last resort due to high toxicity.

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Class IV Drugs

Antiarrhythmic drugs that target calcium channels in specific areas of the heart, like the AV node. They are used for arrhythmias that involve the AV node, such as nodal tachycardia.

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Adenosine

A naturally occurring substance that blocks conduction in the AV node, used to treat AV nodal arrhythmias. Administered in high doses intravenously.

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Eliminate the Cause

The first principle in using antiarrhythmic drugs is to identify and address the underlying cause of the arrhythmia, whether it's electrolyte imbalances, medications, or other factors.

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Baseline Condition

Before starting antiarrhythmic drug therapy, a careful assessment of the patient's overall cardiac health is crucial, considering pre-existing conditions like heart failure.

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Study Notes

Pharmacology II - Chapter 14 Antiarrhythmics

  • Case Study 1:

    • 69-year-old female with a one-month history of palpitations, shortness of breath, and fatigue.
    • Hypertension history.
    • ECG shows atrial fibrillation with a ventricular response of 122 bpm.
    • Echocardiogram reveals a 38% left ventricular ejection fraction.
    • Rhythm reverted to normal after seven days of metoprolol treatment.
    • Patient still experiences atrial fibrillation paroxysms.
    • Question: What antiarrhythmic drug is appropriate for maintaining a normal sinus rhythm?
  • Case Study 2:

    • A drug well-tolerated in heart failure (reduced ejection volume) and with the ability to convert or prevent atrial fibrillation is required.
    • Possible drug options: amiodarone or dofetilide.

Normal Cardiac Rhythm

  • Sinoatrial (SA) node initiates electrical impulses at a rate of 60-100 beats per minute.
  • Impulse spreads through the atria and then to the atrioventricular (AV) node.
  • Impulse travels through the His-Purkinje fibers to the ventricles.
  • Ventricles contract.

Cardiac Conduction System

  • SA node (pacemaker) located in the right atrium.
  • Electrical impulses generated by the SA node.
  • AV node located between the atria and ventricles, acting as an electrical bridge.
  • His-Purkinje system composed of His bundle, right bundle branch, left bundle branch, and Purkinje fibers.

Mechanisms of Arrhythmias

  • Abnormal automaticity or reentrant conduction.

  • Examples of arrhythmias include atrial flutter, atrial fibrillation, AV nodal reentry, premature ventricular beats (PVBs), ventricular tachycardia, and ventricular fibrillation.

  • Arrhythmia causes:

    • Abnormal site of impulse origin
    • Change from normal in rate or regulatory control
    • Change in conduction velocity
  • Cardiac cell electrical potential controlled by ion flux through cell pores/gates.

Action Potential Phases (Cardiac Cell)

  • Phase 0: Rapid depolarization.
  • Phase 1: Early-fast repolarization.
  • Phase 2: Plateau.
  • Phase 3: Repolarization.
  • Phase 4: Diastole, resting potential.

ECG/EKG

  • P wave: Atrial depolarization.
  • QRS complex: Ventricular depolarization.
  • T wave: Ventricular repolarization.
  • PR interval: Conduction time from atrium to ventricle.
  • QRS duration: Time required for ventricular activation (intraventricular conduction time).
  • QT interval: Reflects the duration of the ventricular action potential.

Table 1: Antiarrhythmic Drugs

  • Includes different drug classes (1A, 1B, 1C, 2, 3, 4) and their corresponding drugs, like quinidine, lidocaine, flecainide, esmolol, amiodarone, sotalol
  • Provides specific indications for each drug class.

Mechanisms of Antiarrhythmic Drugs

  • Block sodium channels.
  • Block sympathetic autonomic effects.
  • Prolongation of refractory period.
  • Block calcium channels.

Classes of Antiarrhythmic Drugs

  • Class I: Sodium channel blockers (Ia, Ib, Ic).
    • Local anesthetics.
    • Vary in binding affinity to sodium channels.
    • Prolongation or shortening of action potential duration.
  • Class II: Beta-blockers (reduce beta adrenergic activity in the heart).
  • Class III: Potassium channel blockers (prolong action potential duration).
  • Class IV: Calcium channel blockers (block calcium currents).

Additional Antiarrhythmic Drugs

  • Adenosine (endogenous and used in high doses for AV nodal arrhythmias).
  • Magnesium (less specific class designation and mechanism of action)

Principles in Clinical Use of Antiarrhythmic Agents

  • Eliminate underlying causes, such as electrolyte imbalances or drug interactions.
  • Accurately diagnose the arrhythmia.
  • Assess baseline conditions of the patient (e.g., heart failure, other cardiac diseases).
  • Question the necessity for drug therapy.

Specific Drugs (detailed information)

  • Quinidine:

    • Class Ia sodium channel blocker.
    • Prolonged QRS duration.
    • Major cardiac effects: QT interval prolongation, induction of Torsade de Pointes arrhythmia, and syncope.
    • Extraction of quinine from cinchona bark led to quinidine discovery.
  • Procainamide: Hypotension and lupus erythematosus (L. wolf)

  • Lidocaine: Used in acute ventricular arrhythmias caused by ischemia following MI. High first-pass effect.

  • Amiodarone: Used for a broad spectrum of arrhythmias. High toxicity. Deposits in cornea and skin. Causes thyroid dysfunction.

  • Esmolol: Used IV only for acute arrhythmias.

  • Propranolol, metoprolol, timolol: Used as prophylactic drugs in patients following MI.

  • Sotalol: High toxicity. May precipitate torsades de pointes arrhythmia.

  • Flecainide: Used for both atrial and ventricular arrhythmias. High mortality rates.

  • Verapamil: Key toxicity is constipation, nausea, flushing, and dizziness. Can lead to heart failure.

  • Adenosine: Slows or blocks conduction. Blocks AV nodal arrhythmias.

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Explore key concepts in antiarrhythmic pharmacology through case studies. This quiz covers the mechanisms and options for maintaining normal sinus rhythm, especially in patients with atrial fibrillation. Test your knowledge on drug choices and cardiac rhythms.

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