Dysrhythmias

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Dysrhythmias

• Stephen W. Smith, MD

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When in doubt

• Shock a fast rhythm
• Pace a slow rhythm
• But dont shock sinus tachycardia!!
• (though it will turn out alright)

3
Is patient stable or unstable?

• Patient has serious signs or symptoms? Look for
• Chest pain (ischemic? possible ACS?)
• Shortness of breath (lungs wet? possible CHF?)
• Hypotension
• Decreased level of consciousness
• (poor cerebral perfusion?)
• Clinical shock
• (cool and clammy -- peripheral vaso-constriction?)
  
• Are the signs symptoms due to the rapid heart
  rate?
• Or are S/Sxs rapid HR due to something else?
• I.e., is it sinus tach due to sepsis, hemorrhage,
  PE, tamponade, dehydration, etc.

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3 types of tachydysrhythmias

• Re-entrant
• Respond well to electricity
• Atrial fib and flutter
• PSVT
• Ventricular tachycardia
• Monomorphic, Polymorphic (non-torsade)
• Some atrial tachycardias
• Automatic
• Sinus, junctional, most atrial tach, MAT, AIVR
• Triggered automaticity
• Some atrial tach, Torsades

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Re-entry

• Requires 2 functional pathways that differ in
  their refractory periods.
• Triggered by early beat (e.g., PAC)

Atrium
LA
AV node
Sinus node
LV
Ventricle
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Cardiac Action Potential
Automaticity depends on the slope of phase 4
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Enhanced Automaticity--Pacemaker cell

• Pacemaker has spontaneous depolarization
• Fires when reaches threshold
• 1) Enhanced Normal automaticity (normal pacer
  cells)
• Steepening of depolarization, usually by
  adrenergic stimulation
• Some Atrial and Junctional tachycardia
• 2) Abnormal automaticity
• Happening in tissues that are not normally
  pacemakers
• Myocardial ischemia or recent cardiac surgery
• Accelerated idioventricular rhythm
• Atrial tachycardia, MAT
• Diagnosis
• Accelerates and decelerates gradually
• Beat to beat variability
• Treatment
• Do not respond well to standard interventions
• May respond to overdrive pacing

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Triggered Automaticity/Dysrhythmias
Afterdepolarizations

• Early or Late afterdepolarizations
• R on T phenomenon
• Long preceding R-R interval
• Conditions that prolong QT
• Occur in salvos
• More likely to occur when sinus rate is slow
• Torsades de Pointes
• Digoxin toxicity

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5 Questions

• Wide or Narrow?
• P-waves?
• Regularity?
• Regular
• Regularly irregular
• Irregularly irregular
• Rate?
• Rate change sudden or gradual?

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Identify dysrhythmia5 specific common
tachycardias

• Sinus Tachycardia
• Atrial fibrillation
• Atrial flutter
• Paroxysmal supraventricular tachycardia (PSVT)
• Ventricular tachycardianon-torsade
• Monomorphic, Polymorphic
• Ventricular tachycardiaTorsade
• Polymorphic, long QT on baseline ECG
• Acquired vs. Congenital

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Sinus Tachycardia (sinus SVT)

• Automatic
• P-waves
• Narrow, unless aberration
• Regular
• Max rate dependent on age 200 0.5 x age
• Gradual variations
• Treat underlying condition

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Atrial fibrillation (SVT)

• Multiple re-entrant wavelets
• Irregularly irregular
• No consistent p-waves
• Narrow, unless aberrancy
• Atrium 400-700, Ventricle 100-200
• lt 100 implies AV nodal disease or drugs
• Ashmann phenomenon
• Short RR after Long RR may result in wide complex

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Atrial fibrillation--Treatment

• Is WPW present?
• Bizarre, Wide complexes, shortest R-R lt 250 ms?
• Is duration lt or gt 48 hours? (Thromboembolic
  risk)
• Is acute atrial fib the etiology of the RVR?
• Chronic atrial fib, now tachycardic?
• Likely sepsis, GI bleed, dehydration, etc.--Treat
• Cardioversion unlikely to succeed in chronic a
  fib
• May improve with AV nodal blockerbut may worsen!
• If gt 48 hours, only convert if unstable
• But this will rarely happen and rarely work

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Atrial fibrillationTreatmentIf A fib is sole
cause of instability, it will be acute

• Cardioversion (chronic usually will not convert)
• Electricity easiest150-200 joules biphasic
• If Cardioversion fails or if rhythm converts to
  NSR but converts back to fib, then
• Amiodarone (150 mg over 10 min) or Ibutilide (1
  mg over 10 min)
• Avoid with EF lt 20 or QT gt 480 ms
• May repeat electrical cardioversion
• Success rate 72 without and 100 with ibutilide
• New Engl J Med June 17, 1999 340(24)1849-54.

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Atrial fibrillation--Treatment

• If Cardioversion contraindicated
• (thromboembolic risk)
• AV nodal blocker (Diltiazem bolus and drip)
• Beware hypotensive effects
• Calcium pretreatment not prophylactic
• J Emerg Med 26(4)395, May 2004
• If poor cardiac function
• Digoxin load
• (0.5 mg IV bolus, then 0.25 mg q 6 hours x 2)
• Works well, but has onset in hours, not minutes

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Atrial Fibrillation

• AV nodal blockers do not convert
• Most paroxysmal atrial fib will convert
  spontaneously within several days
• The longer you wait, the better chance a clot
  will form
• Safe to convert if lt 48 hours
• Patient must be certain of time of onset
• Enoxaparin if not converting
• Delayed cardioversion

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Electrical Cardioversion of emergency department
patients with atrial fibrillation.Burton JH et
al. Ann Emerg Med 2004 Jul 4420-30

• 4 sites, 388 patients (mean age 61 years range
  20 to 93 years)
• Duration of atrial fibrillation lt 48 hours in 99
• Electrical cardioversion successful in 332 (86)
  patients
• Twenty-eight complications in 25 encounters
• 22 attributed to procedural sedation
• 6 attributed to electrical cardioversion
• 4 hypotensive episodes (all responded to
  intravenous fluid management)
• 2 bradycardic events

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Burton JH et al. Ann Emerg Med 2004 Jul
4420-30

• 333 (86) patients were discharged to home from
  the ED
• 301 after electrical cardioversion success
• 32 with electrical cardioversion failure.
• 39 patients (10) returned to the ED within 7
  days
• 25 of these patients (6 of successful electrical
  cardioversion patients) returned because of
  relapse of atrial fibrillation.

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Atrial flutter (SVT)

• Re-entrant loop just above AVN in right atrium
• Atrial rate 240-360 without medications
• 21 block, vent rate 150 most common
• Regular, fixed or regularly irregular
• Narrow if no aberrancy
• Flutter waves, sawtooth pattern--Always visible
  in lead II
• Adenosine can help to diagnose, not treat
• Conversion vs. Ventricular slowing
• 50 Joules, Ibutilide/Amiodarone
• Diltiazem slows at AV node
• Procainamide before Diltiazem is dangerous

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Atrial Flutterlead II
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Paroxysmal supraventricular tachycardia (PSVT)

• Re-entrant, gt90 use AV node, lt 10 PAT
• Adenosine almost always works
• Rate 140-280, constant
• Regular, Narrow unless aberrancy
• Sudden onset and offset (paroxysmal)
• Initiated by PAC
• Atrial stretch (ACS, CHF), catecholamines,
  pericarditis
• AVNRTAV nodal re-entrant tachycardia (60)
• Orthodromic reciprocating tachycardia (30)
• P-wave after QRS, (bypass retrograde is slow)

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Re-entry

• Requires 2 functional pathways that differ in
  their refractory periods.
• Triggered by early beat (e.g., PAC)

Atrium
LA
AV node
Sinus node
LV
Ventricle
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Aberrancy - SVT with wide complex

• Abnormal ventricular conduction
• RBBB
• LBBB
• Nonspecific intraventricular conduction defect
• Rate-related BBB
• Antidromic Reciprocating
• Goes down through bypass tract

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LBBB
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RBBB
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Supraventricular TachycardiaAny can be narrow
except antidromicOr Wide with aberrancy

• Sinus
• Paroxysmal SVT (PSVT)
• Intranodal re-entry (60)
• Orthodromic reciprocating (bypass tract) (30)
• Antidromic reciprocating (bypass tract) (10)
• A fib
• A flutter
• MAT
• Atrial tachycardia
• Junctional tachycardia

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Ventricular Tachycardia, wide (gt120 ms) the
origin of the arrhythmia is within the ventricles

• Re-entrant
• Classic V tach
• Monomorphic
• Polymorphic
• Triggered
• Torsade de pointe
• Polymorphic
• long QT on baseline EKG
• Automatic
• Accelerated Idioventricular

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Ventricular tachycardia

• gt 120 ms QRS
• Rate 140-200
• Slow rates due to anti-arrhythmics, e.g. amio
• V1 positive (RBBB config-origin in LV)
• V1 negative (LBBB config-origin in RV)
• V1 indeterminate, Pos and Neg (RS)
• Rate gt200 Ventricular flutter

Fusion beats
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Wide Complex Tachycardia--Sinus tach with
aberrancy vs.--SVT (PSVT, fib, flutter) with
aberrancy vs. --Ventricular tachycardia

• Pretest probability
• Majority of wide complex tachycardia is
  ventricular tachycardia
• If h/o MI, cardiomyopathy, low EF, V tach more
  likely still
• P-waves in front of QRS?
• Irregularly irregular? A fib V tach is most
  commonly regular
• Regular? (Sinus / flutter / PSVT / v tach)
• Rate gradually changes or always the same?
• Gradual sinus
• Unchanging flutter vs. PSVT vs. v tach
• Rate the faster, the less likely it is sinus
• Look for a true bundle branch block pattern
• Right or left (sinus or SVT with aberrancy)
• Fusion beats (occasional narrow complex fused
  with wide one)

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Identify ventricular tachycardia
Brugada P. Circulation 1991, 831649

• Regular and wide
• Step 1 Is there absence of RS complex in all
  leads V1-V6? (Concordance)
• If yes, then rhythm is VT
• Step 2 Is interval from onset of R wave to nadir
  of the S gt 100 msec (0.10 sec) in any precordial
  leads?
• If yes, then rhythm is VT. If no, step 3.
• Step 3 Is there AV dissociation?
• If yes, then rhythm is VT. If no, step 4.
• Step 4 Are morphology criteria for VT present
• (see next slide)? If yes, then VT

gt 0.10 sec?
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Morphology criteria for VT
RBBB
V1
V6
LBBB
V6
V1
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(No Transcript)
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Ventricular Tachycardia Concordance
(different from concordance as used for ST-T vs
QRS)Step 1 Absence of RS in all precordial
leads
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Ventricular Tachycardia
Step 1 there is no absence of RS in all
precordial leads (no concordance) (V5, V6) Step
2 RS in V5 gt 0.10 ms, therefore v tach Step 3
No AV dissociation Step 4 RBBB pattern (tall R
in V1). Notching of this monophasic R indicates
VT
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V tachRS gt 0.10 sec
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polymorphic ventricular tachycardia

• Polymorphic VT
• Long QT on baseline ECG--Torsade de pointes
• Normal QT on baseline ECG not Torsade
• treat ischemia, correct electrolytes, amiodarone

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Polymorphic VT and prolonged QT (Torsade)

• Usually self terminating, may progress to v fib
• Treatment correct electrolytes (K, Mg)
• At risk of torsade Mg, 2g over 15 min
• Active v tach Mg, 2g over 30-60 sec, max 6g
• Serum K gt 4.5
• Overdrive pacing (100-140)
• Lowest pacing rate that prevents PVBs
• dilantin, lidocaine

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Isoproterenol or beta blocker?

• Beta blockers long term therapy for familial
  LQTS
• Isoproterenol (beta 1 and 2 agonist)
• Can terminate acquired LQTS
• Isoproterenol only if all of the below
• Torsade is definitely the result of acquired LQTS
• Underlying bradycardia
• Pause dependent
• Pacing cannot be started immediately
• Limited role for acute beta blockade in
  congenital LQTS

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Other tachydysrhythmias (following 7 slides)

• Junctional tach
• automatic
• Multifocal atrial tachycardia
• automatic
• Atrial tachycardia
• all 3 mechanisms
• Accelerated idioventricular rhythm
• automatic

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Junctional Tachycardia

• Uncommon SVT
• Enhanced automaticity
• Gradual acceleration and deceleration
• Beat to beat variability
• Narrow (unless aberration)
• Regularly regular
• Rate 70-130
• No p-waves
• Due to MI/ischemia, cardiomyopathy, or Dig
  toxicity

AV node
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Multifocal atrial tachycardia

• Uncommon SVT
• Enhanced automaticity of multiple atrial foci
• 3 atrial foci (multiform PACs)
• Rate 100-180
• Irreg irreg
• Narrow unless aberration
• Multiform p-waves
• Due to underlying resp disease e.g., COPD
• treat underlying disease

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MAT
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Accelerated idioventricular rhythm

• Ventricular (wide)
• Automatic
• Regular
• No p-waves
• 60-100 (ventricular escape is 20-40)
• Reperfusion dysrhythmia

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Accelerated idioventricular rhythm
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Atrial Tachycardia-uncommon All 3 types of
dysrhythmia

• Narrow, unless aberration, Regular, Rate 150-250
• Ps before QRS, different morphology from sinus
• Automatic, due to adrenergic stim of normal
  atrial tissue
• Transient suppression by adenosine
• Re-entrant (paroxysmal, PSVT)
• Intra-atrial re-entry
• Abnormal atrium, esp. after atrial surgery
• Not stopped by adenosine (0/13 pts, 8 with
  flutter)
• Electricity works
• Sinus node re-entry--Adenosine works
• Triggered (paroxysmal)
• Cardiomyopathy, on digoxin, usually some AV block
• Prolonged and difficult to treat

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Atrial Tachycardiarate 140-170, converted with
adenosine
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5 Questions

• Wide or Narrow?
• P-waves?
• Regularity?
• Regular
• Regularly irregular
• Irregularly irregular
• Rate?
• Rate change sudden or gradual?

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Wide or Narrow

• Narrow
• Sinus, PSVT, A flutter, A fib
• (All without aberrancy)
• Wide
• SVT with aberrancy
• LBBB, RBBB, IVCD, rate-related BBB, antidromic
• Ventricular tachycardia

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P waves

• If p waves, and associated with QRS, then sinus
  (or, rarely, atrial tachycardia)
• PSVT generally no p wave visible
• PR short
• P wave hidden in QRS, inverted
• A fib and flutter
• No p waves, but flutter may fool you
• V tach
• May rarely see P waves, but with no association
• (AV dissociation)

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Regularity in tachycardia

• Regular
• Sinus, PSVT, flutter, V tach
• Regularly irregular
• Atrial flutter
• Irregularly irregular
• Atrial fib, MAT

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Rate

• Sinus
• 160 - 200 rarely
• 140-160 fast
• Up to 140 common
• PSVT
• 160-190 very common
• A flutter
• 140-200 (ventricle), 260-340 (atrium) common
• A fib
• Any rate, gt 100 unless AV node disease or drugs
• Ventricular tachycardia gt 100
• usually 140-200 (slow is idioventricular rhythm)

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Sudden vs. Gradual changeRe-entry vs.
automaticity

• Sinus gradual
• PSVT sudden
• Atrial flutter sudden
• Atrial fib always changing, but sudden onset
• Ventricular tachycardia Sudden

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Fast, Narrow, and Irregular

• Atrial Fibrillation
• Irregularly irregular
• Atrial Flutter
• Regularly irregular
• Diagnosis may be aided by adenosine

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Identify DysrhythmiaFeatures

• P-waves, regular, gradual rate changesinus
• No p-waves, regular, 130-250
• Narrow
• PSVT or flutterintranodal (AVNRT) or orthodromic
  bypass
• Wide
• Ventricular tachycardia
• Most common
• PSVT with aberrancy
• intranodal or bypass tract (orthodromic)
• PSVT due to antidromic reciprocating tachycardia
• Atrial Flutter with aberrancy
• Regularly irregular
• Atrial Flutter
• Irregularly irregular
• Atrial fibrillation, (V tach can be only slightly
  irreg irreg)

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Very Fast and Irregularthink WPW and atrial fib

• Any R-R interval close to 250 ms?
• Think Atrial Fib with WPW
• Never give AV nodal blocker
• Never give Dig or Calcium channel blocker.
• Even adenosine associated with v fib
• Electrical or chemical conversion
• procainamide, amiodarone, ibutilide
• But NOT chemical AV nodal blocker

• WPW with regular rhythm (orthodromic/antidromic),
  not atrial fib
• AV nodal blockers are OK

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What is it?
57
What is it?
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Treatment when in doubtStable or
unstable-Electricity

• If possible, get 12-lead ECG first
• If electricity does not work
• Automatic rhythm
• Sinus, accelerated junctional, accelerated
  idioventricular, automatic atrial, MATtreatment
  of underlying disorder
• Chronic atrial fib
• Be sure it is not physiologic tachycardia
• Amiodarone for conversion
• Diltiazem or Digoxin to control rate
• Refractory ventricular tachycardia
• Amiodarone
• 150 mg, may repeat several times
• Treat underlying ischemia

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Sinus Rhythm and PACsWith Aberrant Conduction
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Wide-Complex Tachycardia Followed by
Second-Degree AV Block
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STEMI Warning Arrhythmias
Antman and Rutherford. Coronary Care Medicine.
Boston, MA Martinus Nijhoff Publishing198681.
Treat resus v fib, and v tach in STEMI, with
amiodarone or lidocaine bolus and drip.
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Class I for Transvenous Pacing
OR

• Left Bundle Branch Block or RBBB LAFB
  (Bifascicular block
• AND
• 2nd deg Mobitz type 2 block

3rd Degree Block (complete AV dissociation)
OR

• Alternating Left and Right BBB

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Class IIa for transvenous

• Anterior MI
• and
• New LBBB or new RBBB ant or post FB
• And
• 1st degree AVB or
• 2nd degree AVB, Mobitz I (Wenckebach)

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Conclusion When in doubt

• Shock a fast rhythm
• Pace a slow rhythm
• In anterior STEMI
• Be certain that transcutaneous pacing will
  capture if there is high grade block
• But dont shock sinus tachycardia!!

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Questions?
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Atrial Tachycardia Summary of adenosine

• If PSVT PAT, it will be constant rate and look
  much like AV nodal PSVT
• But should have p-waves
• Adenosine aborts some paroxysmal PAT but not all
• You may not know that the PSVT is PAT
• You might think it is the standard AV nodal
  reentrant PSVT
• If adenosine doesnt work, then it is likely to
  be PAT (if not atrial flutter)
• If adenosine does work, youll think you treated
  PSVT
• If you do diagnose PAT, adenosine is worth a try