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Cardiology > Clinical Electrophysiology II > Flashcards

Clinical Electrophysiology II Flashcards

1
Q

Sinus Rhythm

  • General
  • P waves
  • Innervation of the sinus node
  • Changes in sinus rate
A
  • General
    • Most common cardiac rhythm
    • Begins in sinus node w/ intrinsic pacemaker activity at the junction of the RA & SVC in the crista terminalis
  • P waves are upright (+) in lead II
    • pattern of atrial activation begins in high, right lateral locaiton & spreads inferioly towards the left
  • Innervation of the sinus node
    • Right sided sympathetic & parasympathetic trunks
    • Parasympathetic (vagal) tone: predominates w/ normal sinus rate
  • Sinus rhythm is automatic, so changes in rate occur gradually over time
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2
Q

Sinus Bradycardia

  • Due to…
  • More seriously due to…
  • Vagus nerve influence
A
  • Due to…
    • Medication side effects: beta blockers, digoxin
    • Metabolic problems: electrolyte abnormalities, hypothyroidism
  • More seriously due to…
    • Ischemia: myocardial infarction
      • Associated w/ bradycardia due to SA or AV nodal dysfunction
    • Late sequella of cardiac surgery, cancer chemotherapy, or radiation therapy
  • Vagus nerve influence
    • Hyper vagal state: vagal input depresses sinus node output & slows HR
    • Vaso-vagal faint: become queasy at sight of blood
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3
Q

Sinus Tachycardia

  • General
  • Appropriate sinus tachycardia
  • Inappropriate sinus tachycardia
A
  • General
    • Most comon cause of rapid HR
  • Appropriate sinus tachycardia
    • In response to a stimulus like stress, fever, pain, blood loss, dehydration, thyroid disease, or drug use
  • Inappropriate sinus tachycardia
    • Diagnosis of exclusion: absence of a definable cause
    • Resting HR is persistently elevated
      • Even minor activity causes further increases
    • Difficult to treat
    • Most commonly seen in young women
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4
Q

Sick Sinus Syndrome

  • General
  • Tachy-brady syndrome
  • Chronotropic incompetence
  • Junctional rhythm
A
  • General
    • Most common indication for implantation of a pacemaker
  • Tachy-brady syndrome
    • Peroids of tachycardia (most commonly atrial fibrillation) followed by symptomatic bradycardia
    • Occasionally: sinus pauses >3sec
  • Chronotropic incompetence
    • Increase HR in response to exercise
  • Junctional rhythm
    • SA activity is suppressed or AV junctional activity is enhanced
    • Narrow complex rhythm w/ rates 40-60 bpm that’s driven by intrinsic automatic activity of the AV node
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5
Q

Normal Impulse Propagation

  • Cardiac signal initiation
  • Atrial myocytes
  • Insulation
  • Delayed PR interval
  • Decremental conduction
  • Specialized conducting system
A
  • Cardiac signal initiation
    • Initiatied in SA node in atrium
    • Depolarizes atrial tissue (p wave) while traveling to AV node
  • Atrial myocytes
    • Show anisotropic conduction properties
    • Arranged to allow preferential conduction to the AV node
      • Multiple inputs play a role in AV node reentry tachycardia
  • Insulation
    • Fibrous cardiac skeleton supports two AV valves
      • Electrically isolates atria from ventricle
    • AV node / His Bundle: only normal conduction where the signal can passf rom atrium to ventricle
  • Delayed PR interval
    • Due to time required for signal to traverse the AV node
  • Decremental conduction
    • AV node governs ventricular response
    • Sinus rate increases –> impulses impact AV node more rapidly –> impulses conducted through AV node at a slower velocity
  • Specialized conducting system
    • His Bundle –> right & left bundle branches –> left anterior & posterior fascicles –> purkinje fibers
    • Conduct the cardiac impulse at a faster velocity than the ventricular myocytes
    • Bundle branch blocks: longer conduction time (wider QRS)
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6
Q

AV Nodal Blocks

  • First degree
  • Second degree
  • Third degree
A
  • First degree
    • Delay in AV node –> slowed impulse propagation
    • All signals from the atrium are transmitted to the ventricle
      • Just takes longer than usual
    • Prolonged PR interval
  • Second degree
    • Failure of some impulses to reach the ventricle
    • Mobitz Type I (Wenkebach)
      • Above the His Bundle in the AV node
      • Progressive prolongation of the PR interval (& shortening of the RR interval) in consecutive beats before the non-conducted impulse
    • Mobitz Type II
      • Below the His Bundle
      • Constant PR (& RR) intervals in consecutive beats before the non-conducted impulse
  • Third degree
    • Many impulses aren’t conducted to the ventricle
      • May include multiple consecutive impulses not propagated to the ventricle
    • Complete heart block
      • Extreme example when none of the impulses are propagated
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7
Q

Bundle Branch Blocks

  • Right bundle branch block (RBBB)
  • Left bundle branch block (LBBB)
  • Functional bundle branch block (aberancy)
    • Ashman’s (“long-short”) phenomena
    • Rate dependent BBB
A
  • Right bundle branch block (RBBB)
    • Common, typically benign
    • Wide rSR’ in QRS complexes in right precordial leads
    • Seen in coronary artery disease, rheumatic heart disease, hypertensive heart disease, & congenital abnormalities (incomplete RBBB w/ ASD)
    • Transient RBBB: caused by catheter-induced trauma (swan-ganz catheter placement)
  • Left bundle branch block (LBBB)
    • More worrisome
    • Seen in coronary artery disease & hypertension
    • Frequently asymptomatic, worrisome if symptomatic
      • Suggests acute MI since complete LBBB suggests interruption in blood supply by left anterior descending & right coronary arteries
  • Functional bundle branch block (aberancy)
    • One of the bundle branches becomes “refractory” to conduction
    • Ashman’s (“long-short”) phenomena
      • Long coupled beat –> premature beat –> wider QRS –> FBBB (aberrant conduction)
    • Rate dependent BBB
      • Appears as HR increases
      • Disappears as HR decreases
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8
Q

Atrial Fibrillation

  • General
  • Recurrent
    • Paroxysmal
    • Persistent
    • Permanent
  • Etiologies
  • Pathophysiology
A
  • General
    • Most common supraventricular tachycardia
    • Presence increases mortality
  • Recurrent: 2 or more episodes
    • Paroxysmal: AF terminates by itself
    • Persistent: requires pharmacologic or electrical therapy for termination
    • Permanent: AF for a long period of time (>1 year)
  • Etiologies
    • Hypertension, CAD, COPD, ETOH (Holiday Heart), thyroid disease
  • Pathophysiology
    • Due to multiple circulating wavelets that activate the atrium in a random pattern
    • Frequently: irritation of regions of atrial muscle lead to the rhythm (ex. open-heart surgery)
    • Sometimes: rhythm is initiated from a single irritable focus (often within a pulmonary vein)
      *
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9
Q

Atrial Fibrillation Risk Groups

  • High risk
    • Clinical risk factors
    • Anticoagulation
  • Moderate risk
    • Clinical risk factors
    • Anticoagulation
  • Low risk (lone atrial fibrillation)
    • Clinical risk factors
    • Anticoagulation
A
  • High risk
    • Clinical risk factors
      • Rheumatic valvular disease
    • Anticoagulation
      • Strongly recommended
  • Moderate risk
    • Clinical risk factors
      • CHF within last 3 months
      • History of hypertension
      • History of arterial thromboemboli
      • Global LV dysfunction
      • LA size > 4.7 cm
      • Left sided valvular abnormalities
    • Anticoagulation
      • Benefits
  • Low risk (lone atrial fibrillation)
    • Clinical risk factors
      • Absence of all other risk factors
      • < 60 years old
    • Anticoagulation
      • Doens’t reduce already low risk
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10
Q

Atrial Flutter

  • General
  • Classic atrial flutter
  • Key to classic atrial flutter
  • Antithrombotic therapy
A
  • General
    • Macroscopic reentrant rhythm
    • Related to atrial fibrillation
    • May involve either atrium
  • Classic atrial flutter
    • Negative flutter waves in inferior leads
    • Corresponds to a counter-clockwise circuit w/ movement…
      • Upwards along the atrial septum
      • Laterally along the superior (anterior) aspect of the tricuspid valve
      • Medially along the inferior (posterior) aspect of the tricuspid valve
    • Circuit passes b/n the isthmus (coronary sinus OS, IVC, & tricuspid annulus)
  • Key to classic atrial flutter
    • Amenable to both pace termination & curative ablation therapy in the isthmus region
  • Antithrombotic therapy
    • Same recommendations as for atrial fibrillation
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11
Q

Atrioventricular Nodal Reentry Tachycardia (AVNRT)

  • General
  • Due to…
  • Results in…
A
  • General
    • Most common paroxysmal supraventricular tachycardia
  • Due to reentrant circuit
    • Formed by 2 inputs into the AV node (slow & fast pathways) & an upper & lower common pathway
    • Small, located close to the AV node
  • Results in simultaneous activation of atria & ventricles
    • Short RP interval
    • most common cause of a short RP tachycardia in adults
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12
Q

Ectopic Atrial Tachycardias

  • Location
  • RP tachycardias
  • Sinus tachycardia
A
  • Location
    • Originates int he atrium at a location other than the sinus node
    • Exceptoin: sinus node reentrant tachycardia
  • RP tachycardias
    • Long RP tachycardias
    • Interval from QRS to P is greater htan half the RR interval
  • Sinus tachycardia
    • Long RP tachycardia
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13
Q

Wolff-Parkinson-White (WPW) Syndrome

  • Accessory AV connection
  • Accessory pathways
    • Manifest
    • Concealed
  • Normal conduction
  • Right-sided pathway
  • Left-sided pathway
A
  • Accessory AV connection
    • Muscle bands traverse the fibrous skeleton supporting hte tricuspid & mitral valves
  • Accessory pathways: allow the electrical signal to bypass the AV node & pre-excite the ventricular muscle sooner than expected
    • Manifest: delta wave is seeon in ECG
    • Concealed: surface ECG looks normal
  • Normal conduction
    • Inherent delay in AV node –> normal PR interval
  • Right-sided pathway
    • Atrial signal can quickly reach the accessory pathway & start to activate the ventricle while the signal is still being delayed in the normal AV node
    • Pathways on the right side of the heart show max pre-excitation (delta waves)
  • Left-sided pathway
    • Atrial activation mus ttravel to the left-sided pathway before activating the ventricle
    • Signal will also have time to pass through the AV node & provide normal activation of the ventricle
    • Less common to see a delta wave
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14
Q

Wolff-Parkinson-White (WPW) Syndrome: SVT

  • 2 types of SVT
    • Similarities
    • Differences
  • Orhodromic tachycardia
A
  • 2 types of SVT
    • Similarities
      • Involve atrium, AV node, ventricle, & accessory pathway
    • Differences
      • Whether antegrade conduction (from atrium to ventricle) is through the AV ndoe or the accessory pathway
  • Orthodromic tachycardia
    • Most common type of AV reentry tachycardia
    • Narrow QRS complex tachycardia
      • B/c ventricular activation occurs over the normal conducting system
    • Antegrade conduction (atrium –> ventricle): AV node
    • Retrograde conduction (ventricle –> atrium): accessory pathway
  • Antidromic tachycardia
    • Less common
    • Wide QRS complex tachycardia
      • B/c of accessory pathway delta wave
    • Antegrade conduction (atrium –> ventricle): accessory pathway
    • Retrograde conduction (ventricle –> atrium): AV node
      • Could also be a second accessory pathway
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15
Q

Wolff-Parkinson-White (WPW) Syndrome: Atrial Fibrillation

  • AF can coexist w/ WPW
  • AV nodal blocking agents
  • Increased risk for SCD
A
  • AF can coexist w/ WPW
    • If manifest WPW is present, it’s possible to conduct rapidly down the accessory pathway during AF –> ventricular fibrillation –> sudden cardiac death
  • AV nodal blocking agents
    • Ex. Digoxin
    • Can lead to sudden cardiac death
    • Contraindicated in patients w/ a wide QRS during AF
  • Increased risk for SCD
    • COnsecutive preexcited (wide) QRS complexes during AF that are < 250 ms apart
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16
Q

Wolff-Parkinson-White (WPW) Syndrome: Assessment & Treatment

  • Asymptomatic
    • No symptoms
    • High risk occupations
  • Symptomatic
    • First step
    • If syncope or sudden cardiac death
  • Treatment
    • Class IA, IC, & III drugs
    • AV nodal blocking agents
    • Radio frequency energy
A
  • Asymptomatic WPW diagnosed on incidental screening
    • No symptoms: no further evaluation or treatment
    • High risk occupations (ex. pilots): require further evaluation
      • Advocate exercise treadmill testing or AF induction to assess risk of SCD
  • Symptomatic
    • First step: correlate symptoms w/ SVT
      • Esp if patient only complains of palpitations
    • If syncope or sudden cardiac death: diagnostic electrophysiology study (EPS)
      • Characterizes number, location, & characteristics of accessory pathway
  • Treatment
    • Class IA, IC, & III drugs
      • Change properties of the accessory pathway
      • Prevent recurrences of SVT
    • AV nodal blocking agents
      • Ex. Digoxin, beta & calcium channel blockers
      • When used alone, little effect on accessory pathway properties
      • May not be effective & may be dangerous
    • Radio frequency energy
      • Ablates the accessory pathway
      • Curative, successful, & low mortality

Cardiology (40 decks)

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