Clinical Electrophysiology I Flashcards Preview

Cardiology > Clinical Electrophysiology I > Flashcards

Flashcards in Clinical Electrophysiology I Deck (14):
1

Cellular Basis of Impulse Formation & Propagation

  • Cardiac electrical activity
  • Transmembrane potential
  • Action potential

  • 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

2

Classic APs: 5 Phases

  • 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

3

How Specialized APs Differ from Classic APs

  • 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 (If))

4

Mechanisms of Rhythm Formation: Automaticity

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

  • 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 (If)
    • 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)

5

Mechanisms of Rhythm Formation: Triggered Activity (Triggered Automaticity)

  • Triggered activity
  • After potentials

  • 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

6

Mechanisms of Rhythm Formation: Reentry

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

  • 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

7

How Reentrant Elements Induce Rhythm Abnormality

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

  • 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

8

Cardiac Electrophysiology Studies of Reentrant Circuits

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

  • 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

9

Anatomic Concepts in Cardiac Arrhythmias: SA Node

  • Location
  • Intrinsic pacemaker activity
  • Innervation
  • Impulse

  • Location
    • Heartbeat begins in the anterolateral junciton fo the RA & SVC
  • Intrinsic pacemaker activity: exhibits specialized APs that utilize the pacemaker (If) 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

10

Anatomic Concepts in Cardiac Arrhythmias: AV Node

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

  • 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

11

Anatomic Concepts in Cardiac Arrhythmias: Bundle of His

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

  • 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

12

Consequences of Blocks in the Specialized Conduction System

  • 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

13

Abnormal Anatomic Structures: Scar Tissue

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

  • 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

14

Abnormal Anatomic Structures: Non-Scar Tissue

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

  • 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