Antiarrhythmic drugs
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Questions and Answers

Which side effect is commonly associated with Flecainide?

  • Blurred vision (correct)
  • Hepatotoxicity
  • Bronchospasm
  • Pulmonary fibrosis

    • What is the primary mechanism of action of Class II antiarrhythmics?

  • Inhibit ATPase
  • Antagonize β-receptors (correct)
  • Block $K^+$ channels
  • Stimulate Ca$^{2+}$ channels

    • Which drug is known to have mixed class I, II, III, and IV actions?

  • Amiodarone (correct)
  • Digoxin
  • Dronedarone
  • Sotalol

    • Dofetilide is primarily used for what condition?

    <p>Persistent atrial fibrillation</p> Signup and view all the answers

    Which of the following is NOT a known adverse effect of Amiodarone?

    <p>Ectopic ventricular beats</p> Signup and view all the answers

    What aspect of antiarrhythmic drugs can potentially lead to QT interval prolongation?

    <p>Potassium channel blockade</p> Signup and view all the answers

    Which β-blocker is noted as the most commonly used in clinical practice?

    <p>Metoprolol</p> Signup and view all the answers

    What is a significant difference in metabolism between Amiodarone and Dronedarone?

    <p>Amiodarone inhibits other CYPs and P-gp</p> Signup and view all the answers

    What effect do Class IA antiarrhythmics primarily have on ventricular muscle fibers?

    <p>They slow Phase 0 depolarization.</p> Signup and view all the answers

    Which of the following Class IB drugs is known for having a wide therapeutic index?

    <p>Lidocaine</p> Signup and view all the answers

    Which statement about Class IC antiarrhythmics is true?

    <p>They are proarrhythmic and can negatively affect myocardial contractility.</p> Signup and view all the answers

    What characteristic is associated with Class I antiarrhythmics regarding their interaction with $Na^+$ channels?

    <p>They have state-dependent blockade.</p> Signup and view all the answers

    Which adverse effect is commonly associated with the use of Lidocaine?

    <p>Nystagmus</p> Signup and view all the answers

    What is the mechanism of action of Class II antiarrhythmics?

    <p>They block beta-adrenoreceptors.</p> Signup and view all the answers

    Which class of antiarrhythmic drugs is primarily metabolized by CYP2D6?

    <p>Class IB</p> Signup and view all the answers

    Which Class IA medication is most associated with causing peripheral vasoconstriction?

    <p>Disopyramide</p> Signup and view all the answers

    Which mechanism is primarily responsible for the increased risk of arrhythmias due to class I antiarrhythmic drugs?

    <p>Prolongation of the refractory period</p> Signup and view all the answers

    What is a common adverse effect associated with antiarrhythmic medications?

    <p>Bradycardia</p> Signup and view all the answers

    Which class of antiarrhythmic drugs is primarily associated with QT interval prolongation leading to the risk of torsades de pointes?

    <p>Class III</p> Signup and view all the answers

    In what clinical scenario would beta-blockers most commonly be used for arrhythmia management?

    <p>Atrial fibrillation with rapid ventricular response</p> Signup and view all the answers

    What is the primary action of Class I antiarrhythmic drugs on cardiac action potentials?

    <p>Blocking Na+ channels during phase 0</p> Signup and view all the answers

    Which of the following best describes the action of beta-blockers in the context of arrhythmias?

    <p>Decrease heart rate and reduce conduction through the AV node</p> Signup and view all the answers

    Which is a potential consequence of prolonged QT intervals when using antiarrhythmic medications?

    <p>Torsades de pointes</p> Signup and view all the answers

    What distinguishes Dofetilide from other Class III agents?

    <p>It is a pure $K^+$ blocker.</p> Signup and view all the answers

    Which Class IV antiarrhythmic agent is most effective for controlling atrial arrhythmias?

    <p>Verapamil</p> Signup and view all the answers

    What is a common adverse effect associated with the use of Verapamil?

    <p>Pulmonary edema</p> Signup and view all the answers

    Which statement is true regarding Amiodarone?

    <p>It is the least proarrhythmic agent out of Classes I and III.</p> Signup and view all the answers

    What common feature do Verapamil and Diltiazem share in their mechanism of action?

    <p>They bind to open $Ca^{2+}$ channels.</p> Signup and view all the answers

    Which of the following correctly describes Class III antiarrhythmic drugs?

    <p>They primarily block potassium channels.</p> Signup and view all the answers

    Which of the following is NOT a characteristic of Class IV antiarrhythmic drugs?

    <p>They have a strong influence on ventricular muscle contraction.</p> Signup and view all the answers

    Which class of agents is Amiodarone misleadingly similar to, due to its iodine component?

    <p>Thyroid hormones</p> Signup and view all the answers

    In what scenario is Adenosine primarily utilized?

    <p>To control rapid atrial rates</p> Signup and view all the answers

    What is a significant risk factor associated with the use of Class III antiarrhythmic drugs?

    <p>Prolongation of the QT interval leading to torsades de pointes.</p> Signup and view all the answers

    What distinguishes Ibutilide's mechanism from that of other Class III agents?

    <p>It has both class IA and III actions.</p> Signup and view all the answers

    Which class of antiarrhythmic drugs is primarily known for its action on calcium channels?

    <p>Class IV</p> Signup and view all the answers

    Which drug is primarily used to stabilize ventricular arrhythmias but is also associated with potential proarrhythmic effects?

    <p>Amiodarone</p> Signup and view all the answers

    Which of the following statements about Dronedarone is accurate?

    <p>It is less effective in patients with heart failure.</p> Signup and view all the answers

    When considering the risk of QT prolongation, which of the following drugs is primarily associated with this effect?

    <p>Sotalol</p> Signup and view all the answers

    Which of the following accurately describes the action of Class III antiarrhythmic drugs?

    <p>They prolong Phase 3 repolarization.</p> Signup and view all the answers

    What is the primary effect of Class IV antiarrhythmic agents on cardiac action potentials?

    <p>They inhibit action potential in SA and AV nodes.</p> Signup and view all the answers

    What distinguishes Class III antiarrhythmics from Class II agents regarding their mechanism of action?

    <p>Class III agents prolong repolarization.</p> Signup and view all the answers

    Which of the following correctly describes an adverse effect associated with Class III antiarrhythmics?

    <p>QT interval prolongation.</p> Signup and view all the answers

    Which statement is true concerning the effect of Class IV antiarrhythmics on cardiac output?

    <p>They may reduce cardiac output due to negative inotropic effects.</p> Signup and view all the answers

    What characteristic is shared by both Class III and Class IV antiarrhythmics with respect to arrhythmia management?

    <p>Both have a pro-arrhythmic potential.</p> Signup and view all the answers

    Which drug is primarily categorized as a Class III antiarrhythmic?

    <p>Dronedarone.</p> Signup and view all the answers

    What effect do Class IV antiarrhythmics have on action potential conduction in the cardiac tissue?

    <p>Slow conduction in the SA and AV nodes.</p> Signup and view all the answers

    Which Class III antiarrhythmic drug is primarily known to prolong Phase 3 repolarization?

    <p>Dofetilide</p> Signup and view all the answers

    Which Class III agents primarily derive their effects from $K^+$ channel blockade?

    <p>Sotalol</p> Signup and view all the answers

    Disopyramide is known for which adverse cardiovascular effect?

    <p>Peripheral vasoconstriction</p> Signup and view all the answers

    Which of the following best describes the pharmacokinetics of Mexiletine?

    <p>Rapidly absorbed with a narrow therapeutic index</p> Signup and view all the answers

    What is the effect of Quinidine on Phase 0 depolarization?

    <p>It slightly slows Phase 0</p> Signup and view all the answers

    Which characteristic of Class IV agents distinguishes them from Class I and III agents?

    <p>They block $Ca^{2+}$ channels</p> Signup and view all the answers

    Which of the following is TRUE regarding Procainamide's metabolic pathway?

    <p>It becomes a class III drug upon acetylation</p> Signup and view all the answers

    What is a significant characteristic of Dronedarone compared to Amiodarone?

    <p>Is less lipophilic</p> Signup and view all the answers

    Which Class III antiarrhythmic has a duration of action of approximately 10 hours and is first-line for specific atrial conditions?

    <p>Dofetilide</p> Signup and view all the answers

    Which of the following statements is true regarding Ibutilide?

    <p>It possesses mixed class IA and III actions.</p> Signup and view all the answers

    Which of the following is a common adverse effect associated with the use of Sotalol?

    <p>Bradycardia</p> Signup and view all the answers

    What best describes the mechanism of action of Class IV antiarrhythmic agents like Verapamil?

    <p>They inhibit calcium channels to reduce cardiac contractility.</p> Signup and view all the answers

    Which statement accurately describes the pharmacokinetics of Amiodarone?

    <p>It has a termination half-life longer than several weeks.</p> Signup and view all the answers

    Which of the following drugs is primarily associated with the management of atrial fibrillation through AV node conduction properties?

    <p>Digoxin</p> Signup and view all the answers

    What is the primary concern when using Dronedarone for arrhythmia treatment?

    <p>Hepatic failure</p> Signup and view all the answers

    Which of the following correctly identifies a side effect of Verapamil?

    <p>Bradycardia</p> Signup and view all the answers

    Which scenario best describes the use of adenosine in clinical practice?

    <p>Rapid conversion of SVT</p> Signup and view all the answers

    Which of the following is a primary characteristic of Class III antiarrhythmic drugs?

    <p>They prolong the action potential duration.</p> Signup and view all the answers

    What is a significant risk factor associated with the use of Class III antiarrhythmic drugs?

    <p>Proarrhythmic effects leading to torsades de pointes.</p> Signup and view all the answers

    Which property is common among both Class III and Class IV antiarrhythmics?

    <p>They can lead to QT interval prolongation.</p> Signup and view all the answers

    What can result from the administration of Class IV antiarrhythmics?

    <p>Decreased conduction velocity in the AV node.</p> Signup and view all the answers

    Which drug is particularly known for causing bradycardia as a side effect?

    <p>Diltiazem.</p> Signup and view all the answers

    What is considered a dangerous property of Class III antiarrhythmic agents?

    <p>They can induce ventricular tachycardia.</p> Signup and view all the answers

    Which class of antiarrhythmic agents is specifically indicated for controlling supraventricular tachycardias?

    <p>Class IV antiarrhythmics.</p> Signup and view all the answers

    Which of the following classes of antiarrhythmics is known for having effects on both automaticity and conduction?

    <p>Class I.</p> Signup and view all the answers

    What is the primary action of Class III antiarrhythmic drugs on ventricular muscle fibers?

    <p>Prolongs Phase 3 repolarization</p> Signup and view all the answers

    Which of the following statements is true regarding Class III antiarrhythmic drugs?

    <p>They can lead to pro-arrhythmia under certain conditions.</p> Signup and view all the answers

    Which characteristic is associated with Class IV antiarrhythmic agents?

    <p>They inhibit action potentials at the SA and AV nodes.</p> Signup and view all the answers

    Which of the following statements is true regarding Class III antiarrhythmic drugs?

    <p>They have a risk of proarrhythmia.</p> Signup and view all the answers

    What is a key characteristic of Dofetilide among Class III antiarrhythmics?

    <p>It is not metabolized and has a long half-life.</p> Signup and view all the answers

    Which drug is known for its mixed actions as a Class III antiarrhythmic agent?

    <p>Dronedarone</p> Signup and view all the answers

    Which effect is commonly associated with Digoxin use?

    <p>Ectopic ventricular beats at toxicity.</p> Signup and view all the answers

    Study Notes

    Antiarrhythmic Drugs

    • Classification of drugs based on mechanism of action and effects on the cardiac action potential
      • Class I: Sodium channel blockers
        • IA: Quinidine, Procainamide, Disopyramide
          • Slows Phase 0 depolarization and
          • Decreases slope of Phase 4 depolarization
          • Can be used for atrial, AV, and ventricular arrhythmias
        • IB: Lidocaine, Mexiletine
          • Shortens Phase 3 repolarization
          • Used to treat ventricular arrhythmias
        • IC: Flecainide, Propafenone
          • Markedly slows Phase 0 depolarization
          • Used for atrial and refractory ventricular arrhythmias
      • Class II: β-Adrenoreceptor blockers (e.g. Metoprolol, Esmolol)
        • Inhibits Phase 4 depolarization in SA and AV nodes
        • Used for atrial and AV arrhythmias, and prevent ventricular arrhythmias
      • Class III: Potassium channel blockers
        • Amiodarone, Dronedarone, Sotalol, Dofetilide, Ibutilide
          • Prolong Phase 3 repolarization
          • Used for a variety of arrhythmias, including atrial, ventricular, and life-threatening rhythms
      • Class IV: Calcium channel blockers
        • Verapamil, Diltiazem
          • Inhibits action potential in SA and AV nodes
          • More effective for atrial arrhythmias
    • Important points to remember:
      • Some drugs are pro-arrhythmic, meaning they can worsen arrhythmias
        • Prolonging QT intervals leading to torsades de pointes.
      • State dependence: Sodium channel blockers have a stronger effect when the channels are frequently depolarizing.
      • Metabolized by various CYPs, which can interact with other medications.
      • Common adverse effects: Nausea, vomiting, bradycardia, and hypotension.
      • Digoxin and Adenosine are also often used to treat arrhythmias, yet they are not traditionally classified in the main classes above.
      • Adverse effects can include pulmonary fibrosis, corneal deposits, neuropathies, and thyroidosis.

    Cardiac Action Potentials

    • Phase 0 : Na+ influx (rapid upstroke)
    • Phase 1: Partial repolarization (K+ efflux)
    • Phase 2: Plateau (Ca2+ influx, K+ efflux)
    • Phase 3: Repolarization(K+ efflux)
    • Phase 4: Increasing depolarization (increased Na+ permeability)

    EKGs

    • P wave: Atrial depolarization
    • Q wave: Interventricular septum depolarization
    • R wave: Main ventricular mass depolarization
    • S wave: Remaining parts of the ventricle depolarize
    • T wave: Ventricular repolarization

    Types of Arrhythmias

    • Atrial: Atrial flutter, Atrial fibrillation
    • AV Node: AV nodal reentry, Supraventricular tachycardia (SVT)
    • Ventricular: Ventricular tachycardia (VT), Ventricular fibrillation (VF)

    Causes of Arrhythmias

    • Abnormal automacity: Ectopic pacemakers (outside the SA node)
    • Conduction abnormality: Reentry circuits

    EKG Measurements

    • RR interval (Distance between ​​R waves) -Indicates heart rate.
    • PP interval (Distance between P waves)- Indicates atrial rhythm.
    • PR segment - Represents the time it takes for the electrical impulse to travel from the atria to the ventricles.
    • P-Wave Duration - Measures the time atrial depolarization takes.
    • PR interval (0.12-0.22s) - Indicates the time it takes for the electrical impulse to travel from the atria to the ventricles.
    • QRS duration (<0.12s) - Indicates the duration of ventricular depolarization (activation).
    • ST-T segment - Represents the time of ventricular contraction on the EKG.
    • TP interval - Reflects the end of ventricular repolarization.
    • QT duration - Measures the time between the start of ventricular depolarization and the end of ventricular repolarization.
    • Corrected QT duration (men: ≤ 0.45s, women: ≤ 0.47s) - Adjusted for heart rate to help identify potential heart rhythm issues.
    • ST-segment deviation (elevation or depression) - Important for diagnosing heart attacks and other conditions.
    • Remember*: The reference level for measuring ST-segment deviation is not the TP interval. The correct reference level is the PR segment (also known as the baseline or isoelectric level).

    Classification of Drugs

    • Class I, II, III, and IV are Na+Na^+Na+, β-blockers, K+K^+K+, and Ca2+Ca^{2+}Ca2+ channel blockers, respectively
    • Each class acts on a specific phase of the cardiac action potential
    • Class I drugs are further classified into IA, IB, IC based on their rate of dissociation from Na+Na^+Na+ channels
    • Class IA drugs (Quinidine, Procainamide, Disopyramide) block Na+Na^+Na+ channels, shorten Phase 3 repolarization, and decrease Phase 4 depolarization in ventricular muscle fibers
    • Class IB drugs (Lidocaine, Mexiletine) rapidly bind and dissociate from Na+Na^+Na+ channels, shortening Phase 3 repolarization
    • Class IC drugs (Flecainide, Propafenone) slowly dissociate from Na+Na^+Na+ channels, causing negative inotropic effect and proarrhythmia
    • Class II drugs (β-blockers) inhibit Phase 4 depolarization in SA and AV nodes, reducing heart rate and contractility
    • Class III drugs (Amiodarone, Dronedarone, Sotalol, Dofetilide, Ibutilide) prolong Phase 3 repolarization in ventricular muscle fibers, prolonging action potentials
    • Class IV drugs (Verapamil, Diltiazem) inhibit Ca2+Ca^{2+}Ca2+ channels, slowing AV node conduction and decreasing heart rate
    • Digoxin is a cardiac glycoside used for atrial fibrillation and heart failure, inhibiting ATPase and slowing AV node conduction
    • Adenosine is a nucleotide that slows conduction and prolongs the refractory period in the AV node

    Pharmacology of Antiarrhythmic Drugs

    • Quinidine is metabolized by CYP3A4 into active metabolites
    • Procainamide is acetylated into a Class III drug
    • Disopyramide is metabolized by CYP3A4 into inactive metabolites
    • Lidocaine is dealkylated by CYP1A2 and CYP3A4
    • Mexiletine is metabolized by CYP2D6
    • Flecainide and Propafenone are metabolized by CYP2D6
    • Amiodarone has a long half-life of several weeks
    • Amiodarone is metabolized by CYP3A4, inhibits other CYPs and P-gp
    • Dronedarone is a less lipophilic derivative of Amiodarone, with fewer side effects
    • Sotalol is a β-blocker and K+K^+K+ blocker, with both D and L isomers
    • Dofetilide is a pure K+K^+K+ blocker, with a half-life of 10 hours
    • Ibutilide is a K+K^+K+ blocker with mixed Class IA and III action
    • Verapamil and Diltiazem are metabolized by CYP3A4

    Adverse Effects of Antiarrhythmic Drugs

    • Class IA drugs can cause cinchonism, hypotension, anti-M symptoms, and be proarrhythmic
    • Class IB drugs can cause nystagmus, drowsiness, paresthesia, slurred speech, confusion, nausea, vomiting, and dyspepsia
    • Class IC drugs can cause blurred vision, dizziness, nausea, bronchospasm, and proarrhythmia
    • Class III drugs can cause pulmonary fibrosis, corneal deposits, neuropathies, hepatotoxicity, skin discoloration, thyroidosis, hepatic failure, and proarrhythmia (torsades de pointes)
    • Class IV drugs can cause bradycardia, hypotension, and pulmonary edema
    • Digoxin can cause ectopic ventricular beats and V-fib at toxic levels

    Electrocardiogram (ECG) Interpretation

    • The ECG measures electrical activity of the heart, and its components are P, Q, R, S and T waves
    • The P wave reflects atrial depolarization
    • The QRS complex reflects ventricular depolarization
    • The T wave reflects ventricular repolarization
    • The RR interval measures the duration of the heart cycle
    • The QT interval measures the duration of ventricular depolarization and repolarization
    • QT prolongation can lead to torsades de pointes

    Arrhythmias

    • Arrhythmias are classified by their origin into atrial, AV node, and ventricular arrhythmias
    • Arrhythmias can be caused by abnormal automacity or conduction abnormality
    • Abnormal automacity occurs when ectopic foci generate impulses instead of the SA node
    • Conduction abnormality can lead to reentry, the most common cause of arrhythmias
    • Reentry is the cyclical propagation of an impulse within a circuit caused by a unidirectional block

    Phases of the Cardiac Action Potential

    • Phase 0: Rapid upstroke caused by Na+Na^+Na+ influx
    • Phase 1: Partial repolarization caused by K+K^+K+ efflux
    • Phase 2: Plateau caused by Ca2+Ca^{2+}Ca2+ influx and K+K^+K+ efflux
    • Phase 3: Repolarization caused by K+K^+K+ efflux
    • Phase 4: Increasing depolarization caused by increased Na+Na^+Na+ permeability

    Classification of Antiarrhythmic Drugs

    • Antiarrhythmic drugs are used to treat or prevent abnormal heart rhythms (arrhythmias).
    • They are classified into five classes (I-V) based on their mechanism of action.
    • Class I drugs are sodium channel blockers that interfere with the fast sodium current (Phase 0) of the cardiac action potential.
    • Class II drugs are beta-blockers that inhibit the sympathetic nervous system and decrease heart rate and contractility.
    • Class III drugs are potassium channel blockers that prolong the action potential duration.
    • Class IV drugs are calcium channel blockers that slow conduction through the AV node.

    Class I: Sodium Channel Blockers

    • Class IA drugs (quinidine, procainamide, disopyramide) slow the depolarization of ventricular muscle fibers and prolong the action potential duration.
    • Class IB drugs (lidocaine, mexiletine) rapidly bind and dissociate from sodium channels, shortening the action potential duration.
    • Class IC drugs (flecainide, propafenone) bind slowly to sodium channels, markedly slowing depolarization and increasing the refractory period.

    Class II: Beta-Blockers

    • Beta-blockers reduce heart rate and contractility by blocking beta-adrenergic receptors.
    • Metoprolol is a commonly used beta-blocker for arrhythmias.
    • Esmolol is a short-acting beta-blocker that can be used for rapid control of heart rhythm.

    Class III: Potassium Channel Blockers

    • Potassium channel blockers prolong the action potential duration and increase the refractory period.
    • Amiodarone is a mixed class antiarrhythmic that has effects on multiple channels and receptors.
    • Dronedarone is a derivative of amiodarone with fewer adverse effects.
    • Sotalol is a combined beta-blocker and potassium channel blocker.
    • Dofetilide is a pure potassium channel blocker that is effective for atrial fibrillation and heart failure.
    • Ibutilide is a potassium channel blocker with mixed class IA and III actions.

    Class IV: Calcium Channel Blockers

    • Calcium channel blockers reduce heart rate and conduction through the AV node by blocking calcium channels.
    • Verapamil and diltiazem are commonly used calcium channel blockers for arrhythmias.

    Other Drugs

    • Digoxin is a drug that inhibits the sodium-potassium ATPase pump, shortening the refractory period in the myocardium and slowing AV node conduction.
    • Adenosine is a drug that slows conduction, prolongs the refractory period, and decreases automaticity in the AV node.

    Phases of Cardiac Action Potentials

    • Phase 0: Fast upstroke (sodium influx)
    • Phase 1: Partial repolarization (potassium efflux)
    • Phase 2: Plateau (calcium influx, potassium efflux)
    • Phase 3: Repolarization (potassium efflux)
    • Phase 4: Increasing depolarization (increased sodium permeability)

    EKG Components

    • P wave: Atrial depolarization
    • Q wave: Interventricular septum depolarization
    • R wave: Main ventricular mass depolarization
    • S wave: Remaining parts of ventricle depolarize
    • T wave: Ventricular repolarization

    EKG Diagram Measurements

    • RR interval (distance between R waves)
    • PP interval (distance between P waves)
    • PR segment
    • P-Wave Duration
    • PR interval (0.12-0.22s)
    • QRS duration (<0.12s)
    • ST-T segment
    • TP interval
    • QT duration
    • Corrected QT duration (men: ≤ 0.45s, women: ≤ 0.47s)

    Types of Arrhythmias

    • Atrial arrhythmias: Atrial flutter, Atrial fibrillation
    • AV node arrhythmias: AV nodal reentry, Supraventricular tachycardia
    • Ventricular arrhythmias: Ventricular tachycardia, Ventricular fibrillation

    Causes of Arrhythmias

    • Abnormal automaticity: Ectopic foci with enhanced automaticity.
    • Conduction abnormality: Injury or delayed conduction in the myocardium leading to reentry.

    Proarrhythmic Effects

    • Some antiarrhythmic drugs can prolong the QT interval, increasing the risk of torsades de pointes (a dangerous type of arrhythmia).
    • Prolongation of the QT interval can be caused by drugs that block potassium channels or have other proarrhythmic effects.

    Class I Antiarrhythmic Drugs

    • Class I antiarrhythmic drugs are sodium channel blockers that exhibit state dependence, meaning they have a greater affinity for channels that are frequently depolarizing.
    • They interfere with regular heartbeats and can be proarrhythmic in patients with ventricular issues and coronary artery disease (CAD).

    Class IA

    • Class IA drugs include quinidine, procainamide, and disopyramide.
    • These drugs slow Phase 0, decrease the slope of Phase 4, inhibit potassium and calcium channels, and have α- and M-blocking properties.
    • Quinidine is metabolized by CYP3A4 to active metabolites and can cause Cinchonism at high doses. It is also an inhibitor of P-gp and CYP2D6.
    • Procainamide is acetylated into a Class III drug and can cause hypotension.
    • Disopyramide has a greater M-blocking effect than the other two and causes peripheral vasoconstriction and a negative inotropic effect. It is metabolized by CYP3A4 into inactive metabolites.

    Class IB

    • Class IB drugs include lidocaine and mexiletine.
    • These drugs rapidly bind and dissociate from sodium channels and shorten Phase 3.
    • Lidocaine is dealkylated by CYP1A2 and CYP3A4 and has a wide therapeutic index (TI). It can cause adverse effects such as nystagmus, drowsiness, paresthesia, slurred speech, and confusion.
    • Mexiletine is metabolized by CYP2D6 and has a narrow TI. Its adverse effects include nausea, vomiting, and dyspepsia.

    Class IC

    • Class IC drugs include flecainide and propafenone.
    • These drugs slowly dissociate from resting sodium channels and are negative inotropic and proarrhythmic.
    • Flecainide suppresses Phase 0 in Purkinje fibers, increases threshold potential, and blocks potassium channels. It is used for atrial and refractory ventricular arrhythmias.
    • Propafenone, unlike flecainide, does not block potassium channels but has weak β-receptor blocking activity. It is used for atrial arrhythmias and prophylaxis of paroxysmal supraventricular tachycardia (PSVT).
    • Both drugs are metabolized by CYP2D6.
    • Flecainide is well-tolerated but can cause blurred vision, dizziness, and nausea.
    • Propafenone can also cause bronchospasm and is a P-gp inhibitor.

    Class II Antiarrhythmic Drugs

    • Class II drugs are β-blockers.
    • They act on β-receptors to diminish Phase 4, prolong AV conduction, reduce heart rate, and decrease contractility.
    • They are used for atrial and AV arrhythmias and to prevent life-threatening ventricular arrhythmias that follow myocardial infarction (MI).
    • Metoprolol is the most widely used, followed by esmolol which is fast-acting.

    Class III Antiarrhythmic Drugs

    • Class III drugs are potassium channel blockers that prolong action potentials.
    • They are all proarrhythmic.

    Amiodarone

    • Amiodarone has mixed Class I, II, III, and IV actions and α-blocking activity.
    • It contains iodine and is similar to T4.
    • It has a long half-life (T1/2) of several weeks.
    • It is used for all three types of arrhythmias.
    • Its adverse effects include pulmonary fibrosis, corneal deposits, neuropathies, hepatotoxicity, skin discoloration, and thyroidosis. However, it is the least proarrhythmic of the Class I and III drugs.
    • It is metabolized by CYP3A4 but inhibits other CYPs and P-gp.

    Dronedarone

    • Dronedarone is an amiodarone derivative that lacks iodine moieties and is less lipophilic.
    • It has Class I, II, III, and IV actions and fewer side effects than amiodarone but can cause hepatic failure.
    • It is used for atrial arrhythmias but is less effective than amiodarone.

    Sotalol

    • L-sotalol is a β-blocker, while D-sotalol is a potassium channel blocker.
    • It is used for all three types of arrhythmias.

    Dofetilide

    • Dofetilide is a pure potassium channel blocker and is a first-line treatment for persistent atrial fibrillation and heart failure.
    • Its T1/2 is 10 hours, and it is not metabolized.

    Ibutilide

    • Ibutilide is a potassium channel blocker with mixed Class IA and III actions.
    • It is used for atrial flutter.
    • It undergoes extensive metabolism.

    Class IV Antiarrhythmic Drugs

    • Class IV drugs include verapamil and diltiazem.
    • These drugs bind to open, depolarized calcium channels, shortening Phase 2 and decreasing Phase 4 rate.
    • They slow conduction in the SA and AV nodes and are more effective for atrial arrhythmias.
    • They are metabolized by CYP3A4 and their adverse effects include bradycardia, decreased blood pressure, and pulmonary edema.

    Other Antiarrhythmic Drugs

    Digoxin

    • Digoxin inhibits ATPase, which shortens the refractory period in the myocardium and slows AV node conduction.
    • It is used to control the response of ventricles in atrial arrhythmias.
    • At toxic levels, it can result in ectopic ventricular beats and ventricular fibrillation.

    Adenosine

    • Adenosine, at high doses, slows conduction, prolongs the refractory period, and decreases AV node automaticity.

    Cardiac Action Potentials

    • Phase 0: Rapid upstroke due to sodium influx.
    • Phase 1: Partial repolarization due to potassium efflux.
    • Phase 2: Plateau due to calcium influx and potassium efflux.
    • Phase 3: Repolarization due to potassium efflux.
    • Phase 4: Increasing depolarization due to increased sodium permeability.

    Electrocardiogram (EKG) Components

    • P wave: Atrial depolarization.
    • Q wave: Interventricular septum depolarization.
    • R wave: Main ventricular mass depolarization.
    • S wave: Remaining parts depolarize.
    • T wave: Ventricular repolarization.

    EKG Diagram Measurements

    • RR interval: Distance between R waves.
    • PP interval: Distance between P waves.
    • PR segment:
    • P-Wave Duration
    • PR interval: 0.12-0.22 s.
    • QRS duration: < 0.12 s.
    • ST-T segment:
    • TP interval:
    • QT duration:
    • Corrected QT duration: Men ≤ 0.45 s, Women ≤ 0.47 s.

    Important Notes:

    • The reference level for measuring ST-segment deviation is not the TP interval, but rather the PR segment, also known as the baseline level or isoelectric level.

    Arrhythmia Origins

    • Atrial: Atrial flutter, atrial fibrillation.
    • AV node: AV nodal reentry, supraventricular tachycardia (SVT).
    • Ventricular: Ventricular tachycardia (VT), ventricular fibrillation (VF).

    Arrhythmia Causes

    • Abnormal automaticity: When ectopic foci have enhanced automaticity, leading to abnormal impulse generation instead of the SA node. This can be managed by blocking sodium and calcium channels.
    • Conduction abnormality: When a portion of the myocardium is injured or has a prolonged refractory period, causing unidirectional blocks that lead to short circuits and abnormal rhythm. This is called reentry and is the most common cause of arrhythmias.

    Antiarrhythmic Drugs and Proarrhythmia

    • Antiarrhythmic drugs, particularly Class I and III, can be proarrhythmic, prolonging QT intervals and leading to torsades de pointes.

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    Cardiac Action Potentials & EKGs PDF

    Description

    This quiz covers the classification of antiarrhythmic drugs based on their mechanisms of action and effects on cardiac action potentials. Learn about the various classes, including sodium channel blockers, β-adrenoreceptor blockers, and potassium channel blockers, along with their therapeutic uses. Test your knowledge on which drugs are used for specific arrhythmias and their corresponding actions.

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