Clinical Electrophysiology I

Question 1

Cellular Basis of Impulse Formation & Propagation

• Cardiac electrical activity
• Transmembrane potential
• Action potential

Answer 1

• Cardiac electrical activity
  
  • Due to rapid changes in the electrical “charge” of the cell
  • Caused by the rapid movement of + & - charged ions into & out of the cell
• Transmembrane potential
  
  • “Ionic charge” of the cell
  • Difference in potential voltage b/n the inside & outside of the cell
• Action potential
  
  • Recording of the change in transmembrane potential over time
  • Two patterns
    
    • Classic: in myocytes
    • Specialized: SA & AV nodes
  • “All or none” response: signal begins when transmembrane potneital increases to threshold potential
    
    • Changes in potential induce changes in adjacent cells to propagate the signal through the heart

Question 2

Classic APs: 5 Phases

Answer 2

• Phase 0: rapid depolarization
  
  • Transmembrane potential crosses the threshold potential (-80 to -90 mV)
  • Increased permeability to Na+ (& Ca2+)
  • Increased influx of Na+ (& Ca2+) depolarizes the cell
  • Makes the transmembrane potential positive
• Phase 1: rapid short repolarization
  
  • Small efflux of K+
  • Slightly decreases the positive charge of the cell
• Phase 2: plateau
  
  • Balance b/n small inward (K+) & outward (Ca2+) currents
• Phase 3: repolarization
  
  • Efflux of K+ makes transmembrane potential less +
• Phase 4: diastolic portion
  
  • Decreased outward K+ current slowly increases + charge

Question 3

How Specialized APs Differ from Classic APs

Answer 3

• Phase 0: rapid depolarization
  
  • Threshold potential = -40 mV
  • Not as rapid b/c depolarization is due to Ca2+ influx, not Na+
• Phase 1: rapid short repolarization
  
  • Absent
• Phase 2: plateau phase
  
  • Absent
• Phase 3: repolarization
  
  • Less rapid due to inactivation of Ca2+ channels & efflux of K+
• Phase 4: diastolic portion
  
  • Steeper slope due to inward movement of Na+ ions (pacemaker current (I_f))

Question 4

Mechanisms of Rhythm Formation: Automaticity

• Automatic rhythms
• Most common example of automatic rhythm
• Phase 4
• Increasers of sinus rate
• Abnormalities in automaticity

Answer 4

• Automatic rhythms
  
  • Characterized by gradual changes in rate
  • Ex. Tachycardias: automatic warm-up & cool-down behavior
• Most common example of automatic rhythm: sinus rhythm
  
  • SA & AV nodes are the only cardiac sites w/ intrinsic automaticity (pacemaker activity)
• Phase 4
  
  • Enhanced diastolic potential currents (I_f)
  • More positive slope
  • Transmembrane potential increases to threshold potential sooner
  • More APs in a given period of time –> faster rate
• Increasers of sinus rate
  
  • Exercise
  • Stress
  • High catecholamine levels
  • Excess thyroid hormone
• Abnormalities in automaticity
  
  • Enhanced automaticity
    
    • Increased automatic activity in cells w/ intrinsic activity (SA & AV nodes)
    • Ex. inappropriate sinus tachycardia, junctional tachycardia
  • Decreased automaticity
    
    • More common
    • Ex. tachy-brady syndrome, syndrome of chronotropic incompetence
  • Automaticity in cells that don’t have intrinsic activity
    
    • Ex. ectopic atrial tachycardia, accelerated idioventricular rhythms (slow ventricular tachycardia)

Question 5

Mechanisms of Rhythm Formation: Triggered Activity (Triggered Automaticity)

• Triggered activity
• After potentials

Answer 5

• Triggered activity
  
  • Pathological cellular depolarization that occurs spontaneously before another AP is expected
  • After potentials (depolarizations) trigger depolarization of adjacent cells & propagate the cardiac impulse
• After potentials
  
  • Early After Depolarizations (EADs)
    
    • Occur soon after AP initiation (phase 2 or 3)
    • Causes: acidosis, hypoxia, hypokalemia (metabolic abnormalities or ischemia)
  • Delayed After Depolarizations (DADs)
    
    • Occur later after AP initiatoin (phase 4)
    • Causes: digitalis toxicity
    • Responsible for physiological exercise-induced ventricular tachycardia

Question 6

Mechanisms of Rhythm Formation: Reentry

• Reentrant rhythms
• Responsible for…
• Only occur in the precence of 3 elements

Answer 6

• Reentrant rhythms
  
  • Sudden initiation & termination of tachycardia
• Responsible for…
  
  • The majority of supraventricular tachycardia (SVT) other than atrial fibrillation
  • Nearly all ventricular tachycardia associated w/ coronary artery disease
• Only occur in the presence of 3 elements
  
  • Conducting circuit: common upper & lower pathways, 2 separate limbs
  • Different signal conduciton velocities int he two limbs: 1 fast, 1 slow
  • Longer refractory period in the faster limb

Question 7

How Reentrant Elements Induce Rhythm Abnormality

• Normal situation
• Very early premature beat
• If a premature impulse is delivered a little later

Answer 7

• Normal situation
  
  • Impulse –> upper common pathway –> 2 limbs
    
    • Fast limb: moves so quickly that the impulse has time to be conducted up the slow pathway in a retrograde manner
    • Slow limb: moves so slowly that there’s no evidence of limb conduction
  • Normal impulse –> lower common pathway
• Very early premature beat
  
  • Impulse –> upper common pathway –> partway through 2 limbs
  • Limbs are both still within their refractory periods so can’t recover the ability to depolarize again
• If a premature impulse is delivered a little later
  
  • Premature impulse –> upper common pathway –> 2 limbs
    
    • Fast limb has a longer refractory period, so premature impulse is blocked
    • Impulse is conducted in the slower limb
  • Impulse –> lower common pathway –> conducted up fast limb in retrograde manner
  • By the time the impulse –> upper common pathway, the fast limb has recovered from the refractory period
  • Self-perpetuating cycle repeats –> tachycardia

Question 8

Cardiac Electrophysiology Studies of Reentrant Circuits

• Cardiac EP studies
• Reentrant circuit sizes
  
  • Microscopic
  • Intermediate size
  • Macroscopic

Answer 8

• Cardiac EP studies
  
  • Can start reentrant rhythms by adding timed premature impulses
• Reentrant circuit sizes
  
  • Microscopic: in reentrant atrial tachycardia
    
    • Ex. sinus node reentry
  • Intermediate size: dual AV nodal physiology
    
    • Responsible for AV node reentry tachycardia
  • Macroscopic: involves a large circuit of the atrium, AV node, ventricle, & accessory pathway
    
    • Ex. AV reciprocating tachycardia associated w/ Wolff-Parkinson-White (WPW) Syndrome

Question 9

Anatomic Concepts in Cardiac Arrhythmias: SA Node

• Location
• Intrinsic pacemaker activity
• Innervation
• Impulse

Answer 9

• Location
  
  • Heartbeat begins in the anterolateral junciton fo the RA & SVC
• Intrinsic pacemaker activity: exhibits specialized APs that utilize the pacemaker (I_f) current
  
  • Exhibits the highest/fastest activity that sets normal HR
• Innervation: right sided sympathetic & parasympathetic (vagus) nerves
  
  • Parasympathetic tone predominates, so atropine (Ach agent) –> increased HR
• SA node impulse –> atrial tissue –> AV node
  
  • Atrial tissue cells exhibit classic APs & don’t have intrinsic pacemaker activity
  • Some specialized fibers may pass through the atrial tissue & provide preferential conduction to the AV node
    
    • May play a role in some supraventricular tachycardia

Question 10

Anatomic Concepts in Cardiac Arrhythmias: AV Node

• Location
• Intrinsic pacemaker activity
• Innervation
• Delay
• Decremental conduction
• Impulse
• Electrical insulation

Answer 10

• Location
  
  • Apex of triangle of Koch: septal attachment of the tricuspid valve + OS of the coronary sinus + tendon of Todaro
• Intrinsic pacemaker activity
  
  • Slower rate than SA node
  • Pace setting activity is suppressed by higher sinus rates
• Innervation
  
  • Left sided sympathetic & parasympahtetic (vagus) nerves
• Delay
  
  • Delays conduction of the signal from atrium to ventricle
  • Responsible for majority of the delay in the PR interval
  • When AV node is bypassed in teh presence of an accessory pathway (WPW syndrome), PR interval is shorter than normal
• Decremental conduction
  
  • Slows conduction velocity w/ increasing impulse rates
  • Governs ventricular rate: faster atiral rate –> slower signal conduction
  • Helps control rapidity of ventricular rate in presence of rapid atrial rates
• Impulse
  
  • Transmits impulse to Bundle of His
• Electrical insulation
  
  • Cartilaginous structure that supports AV valves b/n atria & ventricles
  • WPW syndrome: muscle fibers bridge this structure & provides a connection other than the AV node / His Bundle pathway

Question 11

Anatomic Concepts in Cardiac Arrhythmias: Bundle of His

• Location
• AV block
  
  • Above the Bundle of His
  • Below the Bundle of His
• Impulse

Answer 11

• Location
  
  • Anatomical & electrical dividng point b/n ventricles & supraventricular structures
  • Unifasicular
  • Bifurcates into left & right bundle branches
• AV block
  
  • Above the Bundle of His (in the AV node)
    
    • Less worrisome, les slikely to be associated w/ fatal bradycardia
    • Allows a higher rate escape rhythm
    • Commonly Mobitz Type I block
    • Congenital complete heart block: has an adequate ventricular response b/c the location is abov ethe Bundle of His
  • Below the Bundle of His
    
    • More worrisome
    • Cells that can initiate ventricular contractoin don’t have intrinsic pacemaker activity to provide an adequate escape rhythm
    • –> slow ventricular rate
• Impulse –> ventricualr myocytes w/ faster velocity than surrounding myocytes
  
  • –> Right bundle
    
    • Terminal named branch on the right side of hte heart
  • –> Left bundle
    
    • –> Anterior fascicle
    • –> Posterior fascicle
• Impulse –> purkinje fibers in ventricular tissue

Question 12

Consequences of Blocks in the Specialized Conduction System

Answer 12

• Rapid conduction through specialized conducting system allows all the ventricular myocytes to depolarize in a short period of time –> narrow QRS
• A block in this system causes the myocytes to rely on the passage of signals from cell to cell –> slower conduction velocity –> wider QRS

Question 13

Abnormal Anatomic Structures: Scar Tissue

• Surgical scars
• Surgical replacement & repair of heart valves
• Scars from a myocardial infarction

Answer 13

• Surgical scars
  
  • Created during correction of congential heart disease
  • Increase risk of atrial & ventricular arrhythmias
  • Concern in surgically corrected Tetralogy of Fallot & congenital repairs that involve incisions or suturing into the atrial or ventricular tissue
• Surgical replacement & repair of heart valves
  
  • Soruce of rhythm abnormalities
  • Frequently takes form of heart block
  • His Bundle: located near the noncoronray cusp of the aortic valve
    
    • Surgery to this valve may cause postoperative conduction problems
  • Mitral valve surgery may lead to conduction problems
    
    • Esp if patient has calcification of the mitral valve annulus
• Scars from a myocardial infarction
  
  • Scarred ventricle w/ multiple reentrant circuits & diverse conduction properties –> ventricular arrhythmias –> death
  • Size of infarciton & extent of LV scarring is proportional to risk of sudden arrhythmic cardiac death
  • Leads to indications for implantation of defibrillators

Question 14

Abnormal Anatomic Structures: Non-Scar Tissue

• Extra electrical connections b/n anatomic structures
• Extra connectoins b/n structures other than the atrium & ventricle

Answer 14

• Extra electrical connections b/n anatomic structures
  
  • Wolff-Parkinson-White (WPW) syndrome: extra connection b/n atrium & ventricle (accessory pathway)
    
    • Band of muscle fibers that bridges the AV node
    • Allows the AV node to be bypassed
    • Allows parts of the ventricular tissue to be depolarized before the signal passes through the AV / His Bundle system
  • WPW syndrome –> supraventricular arrhythmias –> sudden arrhythmic death (w/ atrial fibrillation)
• Extra connectoins b/n structures other than the atrium & ventricle
  
  • Pre-excitation variants (nodofascicular / nodoventricular pathways) –> rhythm abnormalities
  • Less common than WPW syndrome