Arrhythmias 101

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Arrhythmias 101

• Fundamentals and what you should know for the
  big, bad BOARDS!

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The Basics

• SA Node and AV node cells are slow conductors
  activated by calcium, thus blocked by calcium
  channel blockers such as verapamil
• Atrium, Bundle of His, and ventricle cells are
  fast conducting and activated by sodium, thus
  blocked by sodium channel blockers (class 1
  anti-arrhythmics) such as quinidine, lidocaine
  and propafenone.

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4 Mechanisms of Arrhythmia

• reentry (most common)
• automaticity
• parasystole
• triggered activity

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Reentry Requires
Electrical Impulse
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery

1. 2 distinct pathways that come together at
   beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
   
3. Slow conduction in the unblocked pathway.

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Reentry Mechanism
Premature Beat Impulse
Cardiac Conduction Tissue
Repolarizing Tissue (long refractory period)
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery
1. An arrhythmia is triggered by a premature
beat 2. The fast conducting pathway is blocked
because of its long refractory period so the beat
can only go down the slow conducting pathway
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Reentry Mechanism
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery
3. The wave of excitation from the premature
beat arrives at the distal end of the fast
conducting pathway, which has now recovered and
therefore travels retrogradely (backwards) up the
fast pathway
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Reentry Mechanism
Cardiac Conduction Tissue
Fast Conduction Path Slow Recovery
Slow Conduction Path Fast Recovery
4. On arriving at the top of the fast pathway it
finds the slow pathway has recovered and
therefore the wave of excitation re-enters the
pathway and continues in a circular movement.
This creates the re-entry circuit
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Reentry Circuits

• AV Nodal Reentry
• SVT

• Ventricular Re-entry
• ventricular tachycardia

• Atrial Reentry
• atrial tachycardia
• atrial fibrillation
• atrial flutter

SA Node

• Atrio-Ventricular Reentry
• WPW
• SVT

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Reentry Requires

• 2 distinct pathways that come together at
  beginning and end to form a loop.
• A unidirectional block in one of those pathways.
  
• Slow conduction in the unblocked pathway.
• Large reentry circuits, like a-flutter, involve
  the atrium.
• Reentry in WPW involves atrium, AV node,
  ventricle and accessory pathways.

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Automaticity

• Heart cells other than those of the SA node
  depolarize faster than SA node cells, and take
  control as the cardiac pacemaker.
• Factors that enhance automaticity include
• ? SANS, ? PANS, ? CO2, ? O2, ? H, ? stretch,
  hypokalemia and hypocalcaemia.
• Examples Ectopic atrial tachycardia or
  multifocal tachycardia in patients with chronic
  lung disease OR ventricular ectopy after MI

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Parasystole

• is a benign type of automaticity problem that
  affects only a small region of atrial or
  ventricular cells.
• 3 of PVCs

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Triggered activity

• is like a domino effect where the arrhythmia is
  due to the preceding beat.
• Delayed after-depolarizations arise during the
  resting phase of the last beat and may be the
  cause of digitalis-induced arrhythmias.
• Early after-depolarizations arise during the
  plateau phase or the repolarization phase of the
  last beat and may be the cause of torsades de
  pointes (ex. Quinidine induced)

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Diagnosis

• What tools to use and when to use it

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Event Monitors

• Holter monitoring Document symptomatic and
  asymptomatic arrhythmias over 24-48 hours. Can
  also evaluate treatment effectiveness in a-fib,
  pacemaker effectiveness and identify silent MIs.
  
• Trans-telephonic event recording patient
  either wears monitor for several days or attaches
  it during symptomatic events and an ECG is
  recorded and transmitted for evaluation via
  telephone. Only 20 are positive, but still
  helpful.

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Exercise testing

• Symptoms only appear or worsen with exercise.
• Also used to evaluate medication effectiveness
  (esp. flecanide propafenone)
• ? You can assess SA node function with exercise
  testing.
• ? Mobitz 1 (Wenkebach) is blockage at the AV
  node, so catecholamines from exercise actually
  help!
• ? Mobitz 2 is blockage at bundle of His, so it
  worsens as catecholamines from exercise increase
  AV node conduction, thus prognosis is worse.
• PVCs occur in 10 without and 60 of patients
  with CAD. PVCs DO NOT predict severity of CAD
  (neither for nor against)!

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Signal Averaged ECG

• Used only in people post MI to evaluate risk for
  v-fib or v-tach.
• Damage around the infarct is variable, so this
  measures late potentials (low-signal, delayed
  action potentials) as they pass through damaged
  areas.
• Positive predictive value is 25-50 but
  negative predictive value is 90-95, thus if
  test is negative, patient is at low risk.

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Electrophysiologic Testing

• Catheters are placed in RA, AV node, Bundle of
  HIS, right ventricle, and coronary sinus (to
  monitor LA and LV).
• Used to evaluate cardiogenic syncope of unknown
  origin, symptomatic SVT, symptomatic WPW, and
  sustained v-tach.
• Ablative therapy is beneficial in AV node
  reentry, WPW, atrial tachycardia, a-flutter, and
  some v-tach. Complication is 1

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Bradyarrhythmias

• The slow pokes (HRlt60)

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Sick Sinus Syndrome

• Conduction problem with no junctional escape
  during sinus pause
• Diagnose with ECG or Holter. If inconclusive,
  need electrophysiologic testing.
• If asymptomatic, leave alone. If symptomatic,
  needs pacemaker.

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First Degree AV Block

• Delay at the AV node results in prolonged PR
  interval
• PR intervalgt0.2 sec.
• Leave it alone

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Second Degree AV Block Type 1 (Wenckebach)

• Increasing delay at AV node until a p wave is
  not conducted.
• Often comes post inferior MI with AV node
  ischemia
• Gradual prolongation of the PR interval before a
  skipped QRS. QRS are normal!
• No pacing as long as no bradycardia.

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Second Degree AV Block Type 2

• Diseased bundle of HIS with BBB.
• Sudden loss of a QRS wave because p wave was not
  transmitted beyond AV node. QRS are abnormal!
• May be precursor to complete heart block and
  needs pacing.

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Third Degree AV Block

• Complete heart block where atria and ventricles
  beat independently AND atria beat faster than
  ventricles.
• Must treat with pacemaker.

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LBBB
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Left Bundle Branch Block

• Left ventricle gets a delayed impulse
• QRS is widened (at least 3 boxes)
• V5 and V6 have RR (rabbit ears)
• Be careful not to miss any hiding q waves!
• Pacemaker if syncope occurs

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Right Bundle Branch Block
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Right Bundle Branch Block

• Right ventricle gets a delayed impulse
• QRS is widened (at least 3 boxes)
• V1 and V2 have rSR
• Pacemaker if syncope occurs.

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Bifascicular Block

• RBBB plus LABB OR RBBB plus LPBB
• QRS is widened (at least 3 boxes)
• V5 and V6 have RR (rabbit ears)
• V1 and V2 have rSR
• Pacemaker if syncope occurs

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Tachyarrhythmias

• The speed demons(HR gt100)

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Tachyarrhythmias

• Supraventricular tachycardia
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia
• Monomorphic
• Polymorphic (Torsades de pointe)
• Ventricular fibrillation

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Supraventricular Tachycardia
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SVT

• Reentrant arrhythmia at AV node that is
  spontaneous in onset
• May have neck fullness, hypotension and/or
  polyuria due to ANP
• Narrow QRS with tachycardia
• First line is vagal maneuvers
• Second line is adenosine or verapamil
• For chronic SVT, class 1A or 1C or amiodarone or
  sotalol work well
• Ablation will cure it too, but we usually do this
  only in young patients

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Multifocal Atrial Tachycardia
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MAT

• Automatic atrial rhythm from various different
  foci
• Seen in hypoxia, COPD, atrial stretch and local
  metabolic imbalance.
• Three or more types of p waves and a rate gt 100
• Digoxin worsens it, so treat with oxygen and slow
  channel blocker like verapamil or diltiazem.

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Wolf Parkinson White
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WPW

• Ventricles receive partial signal normally and
  partially through accessory pathway
• Symptomatic tachycardia, short PR interval
  (lt0.12), a delta wave and prolonged QRS (gt0.12)
• Electrophysiologic testing helps to identify the
  reentry pathway and location of the accessory
  pathway

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WPW

• Because WPW has both normal conduction through
  the AV node and accessory pathway conduction that
  bypasses the AV node, a-fib can happen via the
  accessory pathway
• Inhibition of the AV node will end up in
  worsening the a-fib because none of the signals
  are slowed down by the AV node before hitting the
  ventricle.
• Do not use any meds that will slow AV node
  conduction, ie digoxin, beta-blockers, adenosine
  or calcium channel blockers.
• The best choice is procainamide as it slows the
  accessory pathway. If patient becomes
  hypotensive, cardiovert immediately!

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Atrial Flutter
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Atrial Flutter

• Atrial activity of 240-320 with sawtooth pattern.
  Usually a 21 conduction pattern if it is 31
  or higher, there is AV node damage
• Treatment is to slow AV node conduction with
  amiodarone, propafenone or sotalol
• DC cardiovert if lt48 hours or unstable
• You can also ablate the reentry pathway within
  the atrium between the tricuspid and the IVC.

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Atrial Fibrillation
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A-Fib

• Can be due to HTN, cardiomyopathy, valvular heart
  desease, sick sinus, WPW, thyrotoxicosis or ETOH
• Therapy is either rate control via slowing AV
  node conduction with stroke prophylaxis or rhythm
  control

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Rate control

• Beta-blockers
• Continuation after CABG may prevent a-fib
• Good for hyperthyroid or post-MI patients with
  a-fib
• ? Carvedilol decreases mortality in patients with
  CHF
• ? Esmolol is good for acute management
• ? Digoxin actually increases vagal tone, thus
  indirectly slowing AV node conduction. But it is
  used essentially only in patients with LV
  dysfunction because its inotropic.

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Rate control

• Calcium Channel Blockers
• Nondihydropyridines (verapamil or dilitiazem)
  block AV node conduction but also have negative
  inotropy, so dont use in CHF.
• Dihydropyridines (nifedipine, amlodipine,
  felodipine) have no effect on AV node conduction
• Adenosine is too short acting to be of any use in
  a-fib
• Last choice is AV node ablation and permanent
  pacing

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Rhythm control

• Rhythm control does not decrease thromboembolic
  risk and may be proarrhythmic
• Class 1A (quinidine, procainamide, disopyramide)
  slows conduction through HIS can cause torsades
  de pointes during conversion. They also enhance
  AV node conduction, so they should be used only
  after rate is controlled
• Class 1B (lidocaine, meilitine, tocainide) are
  useless for a-fib
• Class 1C (propafenone, and flecainide) slow
  conduction through HIS are good first choice.
• Amiodarone is good if patient is post-MI or has
  systolic dysfunction.

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Cardioversion for A-Fib

• Cardiovert if symptomatic
• Patients with a-fib for more than 2 days should
  be receive 3 weeks of anticoagulation before
  electrical cardioversion.
• Give coumadin for 4 weeks after cardioversion

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Anticoagulation Rules for A-Fib

• Everybody who has rheumatic heart disease should
  be anticoagulated
• If lt65 yo and with h/o DM, HTN, CHF, CVA,
  prosthetic valves, thyrotoxicosis, LV dysfunction
  or LA enlargement, then give coumadin
• If no risk factors, do nothing.
• 65-75 yo with any of above risk factors, give
  coumadin if no additional risk factors, give
  coumadin or aspirin
• gt75 yo give coumadin but keep INR 2-2.5 due to
  increased risk of bleed

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Ventricular Tachycardia
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Ventricular Tachycardia

• Impulse is initiated from the ventricle itself
• Wide QRS, Rate is 140-250
• If unstable DC cardiovert
• If not, IV Amiodarone and/or DCCV
• Consider procainamide
• Nonsustained ventricular tachycardia needs no
  treatment

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Torsades de Pointes

• Twisting of the points is usually caused by
  medication (quinidine, disopyramide, sotalol,
  TCA), hypokalemia or bradycardia especially after
  MI
• Has prolonged QT interval
• Acute Remove offending medication. Shorten the
  QT interval with magnesium, lidocaine,
  isoproterenol, or temporary overdrive pacing
• Chronic may need pacemaker/ICD, amiodarone,
  beta-blockers

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Ventricular Fibrillation

• Most common in acute MI, also drug overdose,
  anesthesia, hypothermia electric shock can
  precipitate
• Absence of ventricular complexes
• Usually terminal event
• Use Amiodarone if refractory to DCCV.

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Treatment

• Here comes the fun part!

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Classification of Anti-arrhythmics
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Where did you say you worked?
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When in doubtAmiodarone
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Amiodarone.Modes of action.

• Mainly class III action on the outgoing K
  channels.
• Class Ib action on the Na channels.
• Non competitive alpha antagonism (class III)

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Magnesium indications.

• 1. Torsades de point from any reason.
• 2. Arrhythmias in a patient with known
  hypomagnesaemia.
• 3. Consider its use in acute ischaemia to prevent
  early ventricular arrhythmias.
• 4. Digoxin induced arrhythmias.

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Who gets a pacemaker?

• ? Syncope, presyncope or exercise intolerance
  that can be attributed to bradycardia
• Symptomatic 2nd or 3rd degree AV block
• Congenital 3rd degree AV block with wide QRS
• Advanced AV block after cardiac surgery
• Recurrent type 2 2nd degree AV block after MI
• 3rd degree AV block with wide QRS or BBB.

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QUESTIONS
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