Antidysrhythmic Drugs - Chapter 52 Study Notes

Antidysrhythmic Drugs - Chapter 52 Study Notes

Objectives

  • Review generation of normal sinus rhythm in heart
  • Review pathophysiology of cardiac muscle electrical activity/contractility
  • Identify classification system for antidysrhythmic drugs
  • Identify prototype drugs and their major uses

A Beating Heart

  • Rate: Defined as the frequency per unit time, generally measured in beats per minute (bpm).
    • Example: Normal heart rate is approximately 70 beats/min.
  • Rhythm: Refers to the regularity or irregularity of the heart beating.

Electrical Activity of the Heart

  • Impulse generation starts at the sinus node (SA node) and passes through the AV node, leading to ventricular impulses.
  • Electrical activity cascades through heart tissue in a coordinated manner due to ion channels in the cell membrane.
    • This electrical activity translates into mechanical activity, facilitating the coordinated contraction of cardiac muscle.

Definition of Key Terms

  • Dysrhythmia: Any deviation from the normal rate or rhythm of the heart.
    • Arrhythmia: Implies “no rhythm.”
    • Asystole: Refers to the absence of a heartbeat.

Types of Dysrhythmias

  • Tachydysrhythmias: Characterized by an increase in heart rate.
    • More common than bradycardias.
    • Management involves drugs and other treatments.
  • Bradydysrhythmias: Characterized by a decrease in heart rate.
    • Management may include electrical pacing and the drug atropine.

Causes of Dysrhythmias

  • Common causes include:
    • Ischemic heart disease
    • Myocardial infarction
    • Cardiomyopathy
    • Myocarditis
    • Electrolyte imbalances (e.g., abnormal potassium levels)

Antidysrhythmics

  • Defined as drugs used for the treatment and prevention of disturbances in cardiac rate and/or rhythm.
    • Most function by suppressing abnormal electrical impulse formation or conduction.

Cardiac Electrical Activity

  • Types of cardiac cells include:
    • SA Node Cells
    • AV Node Cells
    • Purkinje Cells
    • Ventricular Cells
  • Note: Electrical activity varies by cell type.

Action Potentials and Cardiac Muscle Contraction

  • The movement of ions across cardiac cell membranes generates action potentials (AP), which leads to the contraction of myocardial muscle.

Cardiac Physiology

  • Action potentials differ across cardiac cell types, essential for understanding dysrhythmias and contractility.

Dysrhythmia Symptoms

  • Possible symptoms may include:
    • Palpitations
    • Dizziness
    • Fainting (syncope)
    • Dyspnea
    • Some patients may remain asymptomatic.

Types of Dysrhythmias

Supraventricular Tachycardia (SVT)

  • Defined as a heart rate of 120-250 beats/min.
  • Paroxysmal: Events that start suddenly and revert to normal within approximately 24 hours.
  • Persistent: Last longer than seven days, often requiring treatment to revert the heart to normal rhythm.
  • Permanent: Lasts longer than a year despite medications and other treatments.

Atrial Flutter and Atrial Fibrillation

  • Atrial fibrillation is the most common type of dysrhythmia.

Ventricular Dysrhythmias

  • Ventricular Tachycardia (VT): Characterized by problems with ventricular muscle; can be classified as non-sustained (
  • Ventricular Fibrillation: Considered extremely dangerous due to the chaotic electrical activity.

Importance of Dysrhythmias

  • Supraventricular dysrhythmias affect ventricular contraction rates; AV blocks are less critical compared to ventricular dysrhythmias which are deemed more dangerous.

Antidysrhythmic Drugs: Mechanism of Action

  • Antidysrhythmic drugs are categorized based on how they alter heart function, following the Vaughan Williams Classification system.

Major Drug Classes

  1. Class I – Sodium Channel Blockers:

    • Class Ia: Quinidine, procainamide, disopyramide.
      • Mechanism: Block sodium channels, slow atrial and ventricular rates, delay repolarization, increase AP duration (APD).
    • Class Ib: Lidocaine (IV).
      • Mechanism: Block sodium channels, accelerate repolarization, and decrease APD.
      • Uses: Primarily for ventricular dysrhythmias, including premature ventricular contractions (PVC) and ventricular tachycardia.
    • Class Ic: Flecainide, encainide, propafenone.
      • Mechanism: Block sodium channels with minimal effect on APD or repolarization.
      • Uses: Severe ventricular dysrhythmias and atrial fibrillation.

  2. Class II – Beta Blockers:

    • Includes metoprolol, esmolol (IV), propranolol, sotalol (also Class III).
    • Mechanism: Block sympathetic stimulation, reduce electrical activity in the AV node.

  3. Class III – Potassium Channel Blockers:

    • Include amiodarone, dofetilide, sotalol, bretylium.
    • Function: Prolong repolarization and cardiac action potentials, and extend refractory periods.
    • Note: Amiodarone is particularly effective but has serious adverse effects over time, including lung fibrosis and thyroid issues.

  4. Class IV – Calcium Channel Blockers:

    • Includes diltiazem and verapamil.
    • Mechanism: Reduce electrical activity by inhibiting calcium entry, primarily affecting the AV node to reduce conduction velocity.

  5. Other Unclassified Antidysrhythmics:

    • Digoxin: Decreases AV conduction and slows heart rate.
    • Adenosine: Slows AV conduction and is used to convert paroxysmal supraventricular tachycardia to sinus rhythm.
      • Noted for a short half-life (10-20 seconds) and administered as rapid IV push.

Adverse Effects of Antidysrhythmic Drugs

  • All antidysrhythmics have the potential to cause dysrhythmias, either by creating new ones or exacerbating existing conditions.

Nursing Implications

  • Patients should be educated to report worsening dysrhythmias alongside:
    • Shortness of breath
    • Edema
    • Dizziness
    • Syncope
  • Monitoring the effects of medications is critical, especially in patients on beta-blockers or digoxin.
    • Patients should learn how to check their own pulse for 1 full minute and notify a healthcare provider if the pulse is less than 60 beats/minute before further doses of medication.
  • Key therapeutic responses to monitor include:
    • Decreased blood pressure in hypertensive patients.
    • Reduced edema.
    • Regular pulse rate with no significant irregularities.
    • Improved cardiac output.