ANA 877 Antiarrhythmics Lecture

Introduction to Antiarrhythmics

• Focus of the lecture: antiarrhythmics.

• Reference materials: Stolting Chapter 21, Nagel Hout Chapter 13 for supplementary information.

• Importance of understanding cardiac conduction and EKG interpretation to grasp antiarrhythmics.

Cardiac Conduction System

• Overview of key components in the cardiac conduction system:

  • SA Node: initiates the impulse.

  • Internodal tracts: pathways for impulse propagation. Three key tracts:

  • Anterior internodal tract (Bachmann bundle)

  • Middle internodal tract (Winkiebach tract)

  • Posterior tract (Thurall tract)

  • AV Node: relays the impulse to the ventricles.

  • Bundle of His: transmits impulses from the AV node to the bundle branches.

  • Bundle branches: carry impulses to the ventricles.

  • Purkinje fibers: distribute impulses throughout the ventricles.

• Arrangement of conduction pathways: SA node → 3 internodal tracts → AV node → Bundle of His → Bundle branches → Purkinje fibers.

Conduction Velocity

• Definition: speed of electrochemical propagation along the neural pathway.

• Influencing factors:

  • Resting membrane potential

  • Amplitude of action potential

  • Rate of change during phase zero

• Influencing elements:

  • Autonomic tone

  • Electrolyte imbalances (hyperkalemia, acidosis)

  • Ischemia

  • Antiarrhythmic drugs.

• Comparative speed of conduction:

  • SA and AV nodes: $0.02 - 0.10$ m/s (relatively slow).

  • Myocardial muscle cells: 0.3-1m/sec (intermediate speed)

  • Bundle branches and Purkinje fibers: 1-4 m/sec (faster conduction.)

EKG and Cardiac Action Potential

• Slide introduction to EKG components and mechanical events.

  • EKG: graphical representation of electrical activities of the heart.

• Ventricular Action Potential:

  • Absolute refractory period: myocytes cannot be depolarized.

  • Relative refractory period: requires larger stimuli for depolarization.

  • KNOW DIAGRAM (HD monitoring APEX)

    

• Wiggers Diagram: illustrates phases of the cardiac cycle, including:

  • Atrial and ventricular pressures.

  • Valves open and close at distinct times.

  • Heart volume changes during different phases: passive filling, active filling, diastasis.

Phases of the Cardiac Action Potential

• 

• Detailed breakdown of action potential phases:

  • Phase 0: Rapid depolarization (sodium influx).

  • Phase 1: Initial repolarization (chloride influx, potassium efflux).

  • Phase 2: Plateau (calcium influx, continued potassium efflux).

  • Phase 3: Final repolarization (potassium efflux).

  • Phase 4: Resting phase (gradual potassium leak).

• Important EKG events correlating with action potential phases are crucial for understanding arrhythmias.

Discussion of EKG Disturbances

• Common EKG disturbances and rhythms:

  • Bradycardia: heart rate < 60 bpm.

  • Tachycardia: heart rate > 100 bpm.

  • Atrial fibrillation, atrial flutter, junctional rhythms, PVCs.

  • Complications: ventricular fibrillation and its implications.

Proarrhythmic Effects

• Potential side effects of medications that can cause arrhythmias (proarrhythmias):

  • Example: Torsades de Pointes (Torsades)

  • Can arise from QTc prolongation.

  • Drugs that cause QT prolongation include class 1A antiarrhythmics, certain antibiotics (e.g., Zofran).

  • Incessant Ventricular Tachycardia (V tach):

  • Caused by slowed conduction, particularly with class 1A and 1C drugs.

  • Reentrant tachycardia circuit requires medication or external shock to interrupt.

Heart Block Review

• Normal PR interval: $0.10 - 0.20$ seconds.

• First-degree heart block: Prolonged PR interval (stable, common in elderly).

• Second-degree heart block types:

  • Mobitz Type I (Wenckebach): progressive PR interval lengthening leading to a dropped beat.

  • Mobitz Type II: intermittent non-conducted beats often requiring intervention.

• Third-degree heart block (complete heart block): independent atrial and ventricular rates (AV dissociation).

Antiarrhythmic Medications Overview

• Classification of antiarrhythmics based on ion channel blockade:

  • Class I: Sodium channel blockers (subdivided into Ia, Ib, Ic).

  • Ia: Lengthens action potential duration (e.g., quinidine, procainamide).

  • Ib: Shortens action potential duration (e.g., lidocaine, mexiletine).

  • Ic: Potent sodium channel inhibitors (e.g., flecainide).

  • Class II: Beta blockers (e.g., propranolol, esmolol): decrease heart rate and myocardial oxygen demand.

  • Class III: Potassium channel blockers (e.g., amiodarone): prolong action potential duration.

  • Class IV: Calcium channel blockers (e.g., diltiazem, verapamil): slow conduction and decrease heart rate.

Specific Antiarrhythmic Drugs

• Lidocaine: Used for ventricular arrhythmias (e.g., PVCs, V tach).

  • Mechanism: Delays phase 4 depolarization.

  • Dosage: $2 ext{ mg/kg}$ bolus, therapeutic levels $1 - 5 ext{ mcg/ml}$.

  • Advantages: Rapid onset, low side effect profile.

• Beta Blockers:

  • Propranolol: non-selective beta blocker, hepatic metabolism, dosage varies.

  • Esmolol: selective beta blocker, rapid onset, short duration of action ($10-15$ mins), careful with concurrent beta blocks.

  • Effects: Reduces heart rate, myocardial oxygen demand.

• Amiodarone: Multifaceted antiarrhythmic, used for various tachyarrhythmias.

  • Dosage: Initial $300 ext{ mg}$ bolus; possible hypotension.

  • Side effects: Bradycardia, QT prolongation, pulmonary toxicity, thyroid dysfunction.

  • Reduces mortality rates post-MI.

• Calcium Channel Blockers (e.g., Verapamil, Diltiazem): Best for rate control in rapid atrial arrhythmias.

  • Dosing of Diltiazem: $20 ext{ mg IV}$; initiate drip thereafter.

  • Side effects: Bradycardia, hypotension, myocardial depression.

• Digitalis (Digoxin): Used to stabilize atrial rhythms, slowing AV conduction.

  • Recognizable toxicity signs: atrial arrhythmias, visual disturbances.

• Adenosine: Treats paroxysmal SVT, rapid infusion required.

  • Dose: Initial $6 ext{ mg}$, followed by $6-12 ext{ mg}$ as needed.

  • Short half-life ($10 ext{ seconds}$), side effects include transient heart block.