5: Cardiac Rhythm Monitors & Equipment

Cardiac Conduction System

Overview

  • The cardiac conduction system is a network responsible for initiating and conducting electrical signals throughout the heart.
  • Main components include:
    • Sinoatrial (SA) node
    • Internodal tracts
    • Atrioventricular (AV) node
    • Bundle of His
    • Bundle branches
    • Purkinje fibers
Internodal Tracts
  1. Anterior internodal tract
    • Gives rise to the Bachmann bundle, which depolarizes the left atrium.
  2. Middle internodal tract
    • Also known as the Wenckebach tract.
  3. Posterior internodal tract
    • Referred to as the Thorel tract.
Conduction Velocities
  • The conduction velocities from slowest to fastest are as follows:
    • AV node
    • SA node
    • Myocardial muscle cells
    • His Bundle
    • Bundle branches
    • Purkinje fibers

Anatomy of the Cardiac Conduction System

  • Specialized cells in the cardiac conduction system initiate heartbeats, distribute electrical signals, and coordinate depolarization of cardiac chambers.

  • Main anatomical pathway:

    • SA node → Internodal tracts → AV node → Bundle of His → Bundle branches → Purkinje fibers

Conduction Velocity

  • Defines how quickly an electrochemical impulse propagates.
Velocities in Different Regions:
  • SA and AV nodes: $0.02 - 0.10 \, \text{m/s}$ (slow conduction)
  • Myocardial muscle cells: $0.3 - 1 \, \text{m/s}$ (intermediate conduction)
  • His bundle, bundle branches, Purkinje fibers: $1 - 4 \, \text{m/s}$ (fast conduction)
Factors Influencing Conduction Velocity
  1. Resting membrane potential
  2. Amplitude of the action potential
  3. Rate of change in membrane potential during phase 0
  4. Autonomic nervous system (ANS) tone
  5. Hyperkalemia affecting fast Na extsuperscript{+} channel closure
  6. Ischemia
  7. Acidosis
  8. Antiarrhythmic drugs

Accessory Pathways

  • A band of connective tissue separates the atria from the ventricles, ensuring AV synchrony and making the AV node a critical electrical pathway.
Common Accessory Pathways:
  • Kent bundle
  • James fiber
  • Atrio-hisian fiber
  • Mahaim bundle

EKG Components and Correlation to Events

  1. P wave: Indicates atrial depolarization onset.
  2. PR-interval: Completion of atrial depolarization.
  3. QRS complex: Represents both atrial repolarization and ventricular depolarization.
  4. ST segment: Confirms completion of ventricular depolarization.
  5. T wave: Marks the beginning of ventricular repolarization.
Cardiac Action Potentials and EKG Phases
  • Understand how to correlate phases of the ventricular action potential to components on the EKG waveform (QRS, ST segment, T wave).
    • Phase 0: Depolarization → QRS complex
    • Phase 1: Initial repolarization → QRS complex
    • Phase 2: Plateau → ST segment
    • Phase 3: Final repolarization → T wave
    • Phase 4: Resting phase

Electrical Activity in One Cardiac Cycle

  • Atria:
    • Depolarization begins: P wave
    • Depolarization complete: PR interval
    • Repolarization: T wave
  • Ventricles:
    • Depolarization begins: QRS
    • Depolarization complete: ST segment
    • Repolarization begins: T wave
    • Repolarization complete: After T wave

Abnormal Conditions and EKG Findings

  1. Pericarditis: Causes PR-interval depression.
  2. Q waves: Indicative of myocardial infarction if:
    • Amplitude > 1/3 of the R wave,
    • Duration > 0.04 seconds,
    • Depth > 1 mm.
  3. Peaked T waves: May be caused by:
    • Myocardial ischemia,
    • Hyperkalemia,
    • Left ventricular hypertrophy,
    • Intracranial bleeding.
  4. Hypokalemia: Increases PR interval and QT interval, causes T wave flattening, and produces a U wave.
  5. Hyperkalemia: Produces peaked T waves, P wave flattening, and extends PR and QRS intervals.
  6. Hypercalcemia: Associated with short QT intervals, while hypocalcemia correlates to long QT intervals.
  7. Hypermagnesemia: Linked to heart block and cardiac arrest; hypomagnesemia is related to long QT intervals (risk of torsades de pointes).
Matching Conditions to EKG Abnormalities
  • Hypokalemia → U wave
  • Pericarditis → PR interval depression
  • Wolff-Parkinson-White syndrome → Delta wave

Heart Blocks

Types of Heart Blocks:
  1. First-degree heart block: PR interval > 0.20 seconds.
  2. Second-degree heart block:
    • Mobitz type 1 (Wenckebach): PR interval progressively lengthens until a beat is dropped.
    • Mobitz type 2: Some beats are dropped without lengthening of the PR interval; treatment typically requires pacing.
  3. Third-degree heart block: Complete dissociation between atrial and ventricular rates.
    • Treatment involves pacemaker insertion.

Antiarrhythmic Medications

  1. Class 1 drugs: Inhibit fast sodium channels (e.g., lidocaine, procainamide).
  2. Class 2 drugs: Decrease rate of phase 4 depolarization (e.g., beta-blockers).
  3. Class 3 drugs: Inhibit potassium channels (e.g., amiodarone).
  4. Class 4 drugs: Slow calcium channels, affecting conduction through the AV node (e.g., verapamil).
  5. Adenosine: Slows conduction through the AV node, primarily used for supraventricular tachycardia.
Key Points on Reentry Pathways
  • Reentry pathways: Most common cause of tachyarrhythmias, defined as a cardiac impulse moving backwards and re-exciting areas of myocardium.
  • Conditions increasing reentry risk include left atrial dilation, ischemia, and epinephrine.

Wolff-Parkinson-White Syndrome

  1. Key Features: Characterized by an accessory pathway (Kent's bundle), causing pre-excitation of the ventricles, observable via delta wave on EKG.
  2. Tachydysrhythmias: AV nodal reentry tachycardia (AVNRT) can be orthodromic or antidromic.
  3. Treatment: Vagal maneuvers, procainamide for antidromic, and cardioversion if unstable.

Cardiac Dysrhythmias Overview

  1. Sinus Arrhythmia: Heart rate varies with respiration.
  2. Sinus Bradycardia: HR < 60 BPM, often due to vagal tone; treat with atropine if symptomatic.
  3. Sinus Tachycardia: HR > 100 BPM, increases myocardial oxygen demand; treat underlying causes.
  4. Atrial Fibrillation: Irregular rhythm; loss of atrial kick leads to output reduction; cardioversion for acute onset.
  5. Ventricular Fibrillation: Rapid, disordered electrical activity leads to no cardiac output; requires immediate CPR and defibrillation.

Torsades de Pointes

  • This polymorphic ventricular tachycardia is associated with prolonged QT interval. Common causes involve metabolic disorders and certain medications. Treatment includes magnesium sulfate.
1. **AF and WPW**: Risk of rapid ventricular rates during AF; procainamide preferred; avoid AV node blockers.
2. **Preventative Measures**: Long QT patients may need beta-blockers; acute management involves shortening the QT interval.