Arrhythmias and Antiarrhythmic Drugs Lecture 3
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Questions and Answers

Which of the following conditions is classified as bradycardia?

  • Heart rate greater than 100 bpm
  • Heart rate between 60 and 100 bpm
  • Heart rate fluctuating widely
  • Heart rate less than 60 bpm (correct)
  • What is a primary physiological cause of sinus tachycardia?

  • Electrolyte imbalance
  • Acute stress (correct)
  • Heart block
  • Excessive vagal tone
  • Which drug is commonly used for the treatment of sinus bradycardia?

  • Calcium-channel blocker
  • Amiodarone
  • Digoxin
  • Atropine (correct)
  • What underlying mechanism characterizes ventricular tachycardia?

    <p>Rapid spontaneous firing from ectopic ventricular site</p> Signup and view all the answers

    Which best describes atrial fibrillation?

    <p>Rapid, random depolarizations within the atria</p> Signup and view all the answers

    What is a major contributing factor to the development of premature ventricular complexes (PVC)?

    <p>Spontaneous firing of ectopic foci</p> Signup and view all the answers

    The Vaughn-Williams classification scheme is used to categorize which type of drugs?

    <p>Antiarrhythmic drugs</p> Signup and view all the answers

    What is the primary effect of Class IV antiarrhythmic drugs?

    <p>Block L-type calcium channels at SA and AV nodes</p> Signup and view all the answers

    Which class of sodium channel blockers has the strongest blockade?

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

    What is a therapeutic indication for Class IA antiarrhythmic drugs?

    <p>Ventricular tachyarrhythmias</p> Signup and view all the answers

    Which drug belongs to Class IB antiarrhythmics?

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

    How does Class IA antiarrhythmic drugs primarily affect the action potential duration?

    <p>Increase effective refractory period</p> Signup and view all the answers

    What is the primary action of beta-blockers in treating arrhythmias?

    <p>Decrease heart rate by blocking beta-adrenergic receptors</p> Signup and view all the answers

    What is the effect of Class IB sodium channel blockers on action potential duration?

    <p>Decrease action potential duration</p> Signup and view all the answers

    Which of the following Class IA drugs has strong anticholinergic effects?

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

    Which Class IC drug can induce life-threatening ventricular tachycardia?

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

    What is the primary mechanism of Class I antiarrhythmic drugs?

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

    Which class of antiarrhythmic drugs is most effective in treating tachycardia related to reentry mechanisms?

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

    Which drug is NOT classified within the Vaughan-Williams classification system?

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

    What pharmacologic effect does Class II antiarrhythmic drugs mainly provide?

    <p>Block sympathetic activity</p> Signup and view all the answers

    Which subclass of Class I antiarrhythmic drugs has a strong effect on phase 0 slope?

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

    Which class of antiarrhythmic drugs delays repolarization and prolongs the action potential duration?

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

    What is a common side effect of many Class I and III antiarrhythmic drugs?

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

    What does Class IV antiarrhythmic drugs primarily block?

    <p>Calcium channels</p> Signup and view all the answers

    Which of the following statements is incorrect regarding tissue ablation for treating tachycardia?

    <p>It has no risks associated with the procedure.</p> Signup and view all the answers

    Study Notes

    Arrhythmias and Antiarrhythmic Drugs

    • Lecture 3 covers arrhythmias and antiarrhythmic drugs.
    • Learning objectives include describing various arrhythmias (sinus bradycardia, ventricular bradycardia, sinus tachycardia, atrial tachycardia/fibrillation, premature ventricular complexes, and ventricular tachycardia) and recognizing them on ECGs.
    • Objectives also include understanding how abnormal automaticity and reentry cause arrhythmias.
    • Identifying causes of abnormal conduction, utility/limitations of the Vaughn-Williams classification scheme, and specific drug effects on ion channels and conduction are also included.
    • The lecture details how drugs (adenosine, atropine, and ivabradine) are used in treating arrhythmias.

    Abnormal Heart Rates

    • Abnormal heart rates include bradycardia (rates below 60 bpm) and tachycardia (rates above 100 bpm). These can be normal or pathological.
    • Bradycardia:
      • Physiological causes: Highly trained athletes can exhibit resting heart rates as low as 40 bpm.
      • Pathological causes: SAN ischemia, excessive vagal tone, electrolyte disorders, and drug use (beta-blockers, calcium channel blockers) are common.
    • Tachycardia:
      • Physiological causes: Exercise, acute stress (sympathetic activation).
      • Pathological causes: Chronic stress, hyperthyroidism, fever/infections, structural/ischemic heart disease, and anemia.

    Bradycardia (Rate < 60 bpm)

    • Atrial (sinus) bradycardia:
      • Physiological causes: highly trained athletes.
      • Pathological causes: ischemia of the sinoatrial node (SAN), excessive vagal tone, electrolyte imbalances, and some medications.
    • Ventricular bradycardia:
      • Pathological: SA nodal failure, second-degree AV block (2° AV block), and third-degree AV block (3° AV block), often related to damage or degeneration of the His-Purkinje system.
    • Treatment: addressing underlying causes (if possible), chronotropic drugs (like atropine, beta-agonists), or pacemaker implantation.

    Tachycardia (Rate > 100 bpm)

    • Sinus tachycardia:
      • Physiological causes: Exercise, acute stress
      • Pathological causes: Stress, hyperthyroidism, fever, infections, and structural/ischemic heart disease.
    • Atrial tachycardia -Atrial flutter (250-350 bpm) -Causes: Structural/ischemic heart disease , Electrolyte disorders, thyroid disorders, medications/drugs/alcohol, Genetic diseases. -Atrial fibrillation (rapid, random depolarizations within atria). -Causes: Structural/ischemic heart disease, thyroid disease, excess catecholamines, medications & drugs/alcohol, and genetic diseases.
    • Premature ventricular complex (PVC): -Spontaneous firing of ventricular ectopic foci. -Produces early/premature ventricular contraction. -Wide, atypical QRS complex.
    • Ventricular tachycardia: -Pathological causes: Chronic stress, hyperthyroidism, fever/infection, structural/ischemic heart disease, and anemia. -Mechanism of electrophysiology includes rapid spontaneous firing of ectopic ventricular sites/afterdepolarization, and reentry (local/global).

    Abnormal Conduction

    • Prolonged PR interval, QRS, or QT interval often indicates problems with conduction pathways.
    • Ischemic injuries to coronary arteries or severe hyperkalemia can affect conduction by altering cell depolarization and conduction velocity, often in non-nodal tissues.
    • Abnormal pacemaker sites (like ectopic foci) and excessive vagal activation can also cause disruptions in conduction patterns.

    Antiarrhythmic Drugs

    • Vaughan-Williams classification categorizes antiarrhythmic drugs.
      • Class I (sodium channel blockers: IA, IB, IC, ID).
      • Class II (beta-blockers).
      • Class III (potassium channel blockers).
      • Class IV (calcium channel blockers).
    • Drugs like adenosine, atropine, and ivabradine do not fit into these classes.

    Class I Drugs

    • These drugs block sodium channels in the heart, decreasing conduction velocity.
    •   Different classes (IA, IB, IC, ID) exhibit varying degrees of fast sodium channel blockade, altering action potential duration, effective refractory period, and conduction velocity.

    Class II Drugs (Beta-blockers)

    • Block sympathetic activation
    • Slow ventricular rate by depressing AV nodal conduction
    • Suppress abnormal automaticity and reentry arrhythmias
    • Decrease slope of phase 4 and conduction velocity.

    Class III Drugs

    • Structurally diverse drugs that delay repolarization (phase 3) and raise action potential duration and effective refractory periods (ERP).
    • Very effective in supraventricular and ventricular tachycardia caused by reentry.
    • Increased Q-T interval can lead to potentially dangerous torsades de pointes (TdP).

    Class IV Drugs (Calcium Channel Blockers)

    • Block L-type calcium channels, primarily in SA and AV nodes.
    • Reduce conduction velocity and lengthen action potential duration.
    • Effective in supraventricular tachycardias involving AV nodal reentry.

    Drugs Not Fitting into Vaughan-Williams

    • Adenosine: Rapidly suppresses supraventricular tachycardia caused by AV nodal reentry.
    • Atropine: Used to reverse AV block by blocking excessive vagal influences on nodal tissues, increasing SA node heart rate, and AV nodal conduction velocity.
    • Ivabradine: Blocks sinoatrial funny currents, reducing heart rate without affecting other crucial heart functions.

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    Description

    This quiz covers Lecture 3 on arrhythmias and antiarrhythmic drugs. It addresses different types of arrhythmias, their recognition on ECGs, and the mechanisms behind abnormal heart rates. Additionally, it explores the Vaughn-Williams classification and the application of specific drugs in treatment.

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