Dysrhythmias

When in doubt

 Shock a fast rhythm

 Pace a slow rhythm

 But don’t shock sinus tachycardia!!

 (though it will turn out alright)
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/Sx’s & rapid HR due to something else?
 I.e., is it sinus tach due to sepsis, hemorrhage, PE,
tamponade, dehydration, etc.
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
Re-entry
 Requires 2 functional pathways that differ in
their refractory periods.
 Triggered by early beat (e.g., PAC)

Atriu LA
m AV node

Sinu
s L
node V
Ventricle
Cardiac Action Potential

Automaticity
depends on
the slope of
phase 4
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
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
5 Questions
 Wide or Narrow?
 P-waves?
 Regularity?
 Regular
 Regularly irregular
 Irregularly irregular
 Rate?
 Rate change sudden or gradual?
Identify dysrhythmia
5 specific common tachycardias

 Sinus Tachycardia
 Atrial fibrillation
 Atrial flutter
 Paroxysmal supraventricular tachycardia (PSVT)
 Ventricular tachycardia—non-torsade
 Monomorphic, Polymorphic
 Ventricular tachycardia—Torsade
 Polymorphic, long QT on baseline ECG
 Acquired vs. Congenital
 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
Atrial fibrillation (SVT)
 Multiple re-entrant wavelets
 Irregularly irregular
 No consistent p-waves
 Narrow, unless aberrancy
 Atrium 400-700, Ventricle 100-200
 < 100 implies AV nodal disease or drugs
 Ashmann phenomenon
 Short RR after Long RR may result in wide complex
 Atrial fibrillation--Treatment
 Is WPW present?
 Bizarre, Wide complexes, shortest R-R < 250 ms?
 Is duration < or > 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 blocker—but may worsen!

 If > 48 hours, only convert if unstable

 But this will rarely happen and rarely work
Atrial fibrillation—Treatment
If A fib is sole cause of instability, it will be acute

 Cardioversion (chronic usually will not convert)

 Electricity easiest—150-200 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 < 20% or QT > 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.
 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
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 < 48 hours
 Patient must be certain of time of onset
 Enoxaparin if not converting
 Delayed cardioversion
Electrical Cardioversion of emergency
department patients with atrial fibrillation.
Burton JH et al. Ann Emerg Med 2004 Jul; 44:20-30

 4 sites, 388 patients (mean age 61 years;

range 20 to 93 years)
 Duration of atrial fibrillation < 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
Burton JH et al.
Ann Emerg Med 2004 Jul; 44:20-30

 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.
Atrial flutter (SVT)
 Re-entrant loop just above AVN in right atrium
 Atrial rate 240-360 without medications
 2:1 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
Atrial Flutter
lead II
Paroxysmal supraventricular tachycardia
(PSVT)
 Re-entrant, >90% use AV node, < 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
 AVNRT—AV nodal re-entrant tachycardia (60%)
 Orthodromic reciprocating tachycardia (30%)
 P-wave after QRS, (bypass retrograde is slow)
Re-entry
 Requires 2 functional pathways that differ in
their refractory periods.
 Triggered by early beat (e.g., PAC)

Atriu LA
m AV node

Sinu
s L
node V
Ventricle
Aberrancy - SVT with wide complex
 Abnormal ventricular conduction
 RBBB
 LBBB
 Nonspecific intraventricular conduction defect
 Rate-related BBB
 Antidromic Reciprocating
 Goes down through bypass tract
LBBB
RBBB
 Supraventricular Tachycardia
Any can be narrow except antidromic
Or 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
Ventricular Tachycardia, wide (>120 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
Ventricular tachycardia
 > 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 >200 “Ventricular flutter”

Fusion beats
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)
Identify ventricular tachycardia
Brugada P. Circulation
1991, 83:1649
 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 > 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.
> 0.10 sec?
 Step 4: Are morphology criteria for VT present
 (see next slide)? If yes, then VT
Morphology criteria for VT
RBBB

V1 V6

LBBB

V6
V1
Ventricular Tachycardia
Concordance
(different from “concordance” as used for ST-T vs QRS)

Step 1: Absence of RS in all precordial leads

 Ventricular Tachycardia

Step 1: there is no absence of RS in all precordial leads (no

concordance) (V5, V6)
Step 2: RS in V5 > 0.10 ms, therefore v tach
Step 3: No AV dissociation
V tach
RS > 0.10 sec
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
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 > 4.5
 Overdrive pacing (100-140)
 Lowest pacing rate that prevents PVB’s
 dilantin, lidocaine
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
Other tachydysrhythmias
(following 7 slides)

 Junctional tach
 automatic
 Multifocal atrial tachycardia
 automatic
 Atrial tachycardia
 all 3 mechanisms
 Accelerated idioventricular rhythm
 automatic
Junctional Tachycardia
 Uncommon SVT
 Enhanced automaticity
 Gradual acceleration and deceleration
 Beat to beat variability
 Narrow (unless aberration) AV
 Regularly regular node
 Rate 70-130
 No p-waves
 Due to MI/ischemia, cardiomyopathy, or Dig toxicity
Multifocal atrial tachycardia
 Uncommon SVT
 Enhanced automaticity of multiple atrial foci
 ≥ 3 atrial foci (multiform PAC’s)
 Rate 100-180
 Irreg irreg
 Narrow unless aberration
 Multiform p-waves
 Due to underlying resp disease; e.g., COPD
 treat underlying disease
MAT
Accelerated idioventricular
rhythm

 Ventricular (wide)
 Automatic
 Regular
 No p-waves
 60-100 (ventricular escape is 20-40)
 Reperfusion dysrhythmia
Accelerated idioventricular
rhythm
Atrial Tachycardia-uncommon
All 3 types of dysrhythmia
 Narrow, unless aberration, Regular, Rate 150-250
 P’s 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
Atrial Tachycardia
rate 140-170, converted with adenosine
5 Questions
 Wide or Narrow?
 P-waves?
 Regularity?
 Regular
 Regularly irregular
 Irregularly irregular
 Rate?
 Rate change sudden or gradual?
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
P waves
 Ifp 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)
Regularity in tachycardia

 Regular
 Sinus, PSVT, flutter, V tach
 Regularly irregular
 Atrial flutter
 Irregularly irregular
 Atrial fib, MAT
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, > 100 unless AV node disease or drugs
 Ventricular tachycardia > 100
 usually 140-200 (slow is idioventricular rhythm)
 Sudden vs. Gradual change
Re-entry vs. automaticity

 Sinus: gradual
 PSVT: sudden
 Atrial flutter: sudden
 Atrial fib: always changing, but sudden onset
 Ventricular tachycardia: Sudden
Fast, Narrow, and Irregular
 Atrial Fibrillation
 Irregularly irregular
 Atrial Flutter
 Regularly irregular
 Diagnosis may be aided by adenosine
Identify Dysrhythmia
Features
 P-waves, regular, gradual rate change—sinus
 No p-waves, regular, 130-250
 Narrow
 PSVT or flutter—intranodal (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)
Very Fast and Irregular
think 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
What is it?
What is it?
Treatment when in doubt
Stable or unstable-Electricity
 If possible, get 12-lead ECG first
 If electricity does not work
 Automatic rhythm
 Sinus, accelerated junctional, accelerated idioventricular,
automatic atrial, MAT—treatment 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
Sinus Rhythm and PACs
With Aberrant Conduction
Wide-Complex Tachycardia Followed by
Second-Degree AV Block
 STEMI: “Warning Arrhythmias”

Antman and Rutherford. Coronary Care

Medicine. Boston, MA: Martinus Treat resus v fib, and v tach in STEMI, with
Nijhoff Publishing;1986:81. amiodarone or lidocaine bolus and drip.
Class I for Transvenous
Pacing
OR
• Left Bundle Branch Block or
RBBB + LAFB (Bifascicular
block
3rd Degree Block
1. AND (complete AV
dissociation)
• 2nd deg Mobitz type 2 block

OR

 Alternating Left and

Right BBB
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)
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 don’t shock sinus tachycardia!!

Questions?
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 doesn’t work, then it is likely to be PAT
(if not atrial flutter)
 If adenosine does work, you’ll think you treated PSVT
 If you do diagnose PAT, adenosine is worth a try