Transcript Tachydysrhythmias

Tachydysrhythmias
August 2, 2001
Gavin Greenfield
Bryan Young
1
Outline
• Basic Science
• Mechanisms of Tachydysrhythmias
– impulse formation or impulse conduction
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Anti-dysrhythmics
Classification
Management of Specific Tachydysrhythmias
Diagnosing Etiology of Wide-Complex
Tachycardia
• Practice EKG’s
• Revised ACLS Tachycardia Algorithm
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Basic Science - Anatomy
• 3 basic types of myocardial cells
• contractile, conductive, pacemaker
– 99% of cardiac muscle cells are contractile
• Innervation
– sympathetic via ~T1-T5
• neurotransmitter? receptor?
– parasympathetic via vagus nerve
• neurotransmitter?
– both innervate cells of both the contractile and
conductive systems
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Basic Science - Electrophysiology
• Depolarization
– common to contractile and conductive cells
• Action Potential
• Resting Membrane Potential
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Basic Science - Electrophysiology
Resting Membrane Potential
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Basic Science - Depolarization
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Basic Science - Depolarization
• Differences between contractile cells and
those involved in conduction
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Basic Science – Effect of
Autonomic Nervous System on
Depolarization
• Sympathetic stimulation increases slope of
phase 4 depolarization
• Parasympathetic stimulation decreases
slope of phase 4 depolarization
– parasympathetic stimulation also
hyperpolarizes membrane (potential starts
from lower value)
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Basic Science – Sequence of
Excitation
• SA node is dominant pacemaker – why?
• Blood supply to SA node?
• Pathway of action potential from SA node
to AV node?
• Blood supply to AV node?
• AV node to bundle of His to R and L BB’s
to Purkinje fibers
• Purkinje fibers rapidly distribute impulse to
contractile cells in ventricles
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Basic Science – Refractory Period
• Refractory Period definition
• Cardiac muscle cells have long refractory
period (this prevents tetanic contractions
and therefore allows filling)
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Mechanisms for Tachydysrhythmia
Formation
• Altered automaticity increased
automaticity in normal (enhanced
automaticity) or ectopic (abnormal
automaticity) site
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Mechanisms for Tachydysrhythmia
Formation
• Reentry in normal or accessory pathway
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Mechanisms for Tachydysrhythmia
Formation
• Triggered Dysrhythmias
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Pharmacology of Anti-dysrhythmics
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Pharmacology of Anti-dysrhythmics
• 4 Broad Classes
– based on effect on action potential and impulse
conduction
• Classification system ignores multiple
overlapping properties of drugs
– agents classified according to major effect
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Class I – sodium channel blockers
Class II – beta-adrenergic blockers
Class III – antifibrillatory agents
Class IV – calcium channel blockers
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Pharmacology of Anti-dysrhythmics
• Class I (Sodium Channel Blockers)
– Which part of action potential is therefore
inhibited?
• phase 0 is inhibited resulting in slowed
depolarization and therefore slowed
conduction and membrane stabilization
(therefore prominent anti-ectopic effects)
– varying effects on repolarization
• 3 subclasses 1A, 1B, 1C
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Pharmacology of Anti-dysrhythmics
Class I – sodium channel blockers
• Class 1A
– Procainamide
– Quinidine
– Disopyramide
• Specific Effects
– moderately slow depolarization and conduction
– prolong repolarization and action potential duration
– clinically results in slowed conduction through atria,
AV node, and His-Purkinje system
– also decreases conduction in accessory pathways
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Pharmacology of Anti-dysrhythmics
Class I – sodium channel blockers
• Class 1B
– lidocaine
– phenytoin
– tocainide, mexiletine, moricizine, aprindine
• Specific Effects
– minimally slow depolarization and conduction
– shorten repolarization and action potential
duration (1A and 1C prolong)
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Pharmacology of Anti-dysrhythmics
Class I – sodium channel blockers
• Class 1C
– Propafenone (also some 1A properties)
– Flecainide, Encainide, Lorcainide
• Specific Effects
– profoundly slow depolarization and
conduction
– prolong repolarization and action potential
duration
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Pharmacology of Anti-dysrhythmics
Class II – Beta adrenergic blockers
• Metoprolol, Esmolol, Acebutolol, Nadolol,
Propranolol
• Specific Effects (think of NE and Beta 1
actions on depolarization and contractility)
– slow SA node impulse formation, slow AV
conduction, prolong action potential and can
depress conduction in ischemic tissue
– depress myocardial contractility
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Pharmacology of Anti-dysrhythmics
Class III – antifibrillatory agents
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Amiodarone
Bretylium
Sotalol (shares activity with Class II)
Ibutilide (shares activity with Class II)
• Specific Effects
– prolong action potential duration and
refractory period duration thus exhibiting
antifibrillatory properties
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Pharmacology of Anti-dysrhythmics
Class IV – Calcium (slow) channel
blockers
• Diltiazem, Verapamil
• Specific Effects
– block calcium entry to cells thus causing
depression of anterograde conduction through
AV node and suppression of other calciumdependent dysrhythmias
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Pharmacology of Anti-dysrhythmics
Miscellaneous
• Adenosine
– naturally occurring purine nucleoside
– causes concentration dependent slowing of
AV conduction and slowing of both
anterograde and retrograde paths of a
reentrant circuit
– at antidysrhythmic doses has peripheral
vasodilatory properties
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Pharmacology of Anti-dysrhythmics
Miscellaneous
• Digoxin
– positive inotrope
– variable electrophysiological effects on
myocardial cells – can divide into excitant and
depressant (therapeutic effects are result of
depressant actions)
– Excitant – increase in altered automatic and
triggered ectopic impulses
– Depressant – depresses conduction and
lengthens refractoriness in AV node
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All anti-dysrhythmics are proarrhythmics
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Amiodarone
• Effects
– complex drug with effects on sodium,
potassium, and calcium channels
– alpha adrenergic and beta adrenergic
blocking properties
– prolongs action potential duration and
refractory period
– slows automaticity in pacemaker cells
– slows conduction in AV node
– causes smooth muscle relaxation
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Amiodarone – “ARREST” Trial
• Kudenchuk et al. Amiodarone for resuscitation after outof-hospital cardiac arrest due to ventricular fibrillation,
NEJM 341(12), 871-8, September 16, 1999.
• prospective trial of VF/pulseless Vtach after first 3
shocks, intubation and 1 mg Epi
• Amiodarone vs placebo followed by routine
antiarrhythmic drugs
• statistically significant increase in survival to hospital
admission in amiodarone group
• trial lacked statistical power to detect differences in
survival to hospital discharge, which differed only slightly
between the two groups
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Tachydysrhythmia Classification
• Several ways to classify
tachydysrhythmias:
– mechanism of formation
– anatomic
– EKG appearance
– stable vs. unstable
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Tachydysrhythmia Classification
Decision Point 1
• Stable vs. Unstable: How do we differentiate?
• unstable condition must be related to
tachycardia
• chest pain suggestive of myocardial ischemia
• shortness of breath / pulmonary edema /
congestive heart failure
• shock / decreased LOC / hypotension
• If unstable it doesn’t matter what the rhythm is –
just sedate and cardiovert
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Specific Dysrhythmias
• Narrow QRS (supraventricular tachys)
– Sinus tachycardia
– Ectopic atrial tachycardia
– Multifocal atrial tachycardia
– Atrial fibrillation
– Atrial flutter
– AV nodal reentrant tachycardia
– Atrioventricular reentrant tachycardia
– Junctional tachycardia
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Specific Dysrhtyhmias
• Wide QRS
– ventricular tachycardia
– ventricular fibrillation
– any supraventricular tachycardia with aberrant
conduction
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Narrow-Complex Tachycardias
Sinus Tachycardia
• from acceleration of SA Node discharge rate
• Atrial rate usually between 100 and 160
• sinus tachycardia is a response to: 1.
physiologic stress (exertion, anxiety, etc.) 2.
pharmacologic influence (caffeine, nicotine,
alcohol, sympathomimetics) 3. pathologic (fever,
anemia, hypoxia, hypotension, etc.)
• Treat underlying condition
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Narrow-Complex Tachycardias
Atrial Tachycardia
• from any nonsinus focus above AV Node
• each QRS preceded by P’
• if no old EKG difficult to differentiate from
sinus tachycardia
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Narrow-Complex Tachycardias
Multifocal atrial tachyardia
• subset of atrial
tachycardia aka
wandering pacemaker
• irregular rhythm, often
confused with afib
• at least three foci of
impulse formation,
therefore 3 distinctly
different P waves
• often associated with
pulmonary disease and
hypoxemia
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Treatment of Atrial and Multifocal
Atrial Tachycardia
• causes:
• include electrolyte and acid-base disturbances,
drug toxicity, fever, hypoxemia
• MFAT classically associated with pulmonary
disease and hypoxemia
• Treat underlying disorder
• if pt symptomatic can treat with Beta blocker or
Calcium channel blocker or Amiodarone
• Magnesium second line agent
• Procainamide and digoxin can also be used
– specific antiarrhythmic therapy is rarely indicated
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Narrow Complex Tachycardias
SVT
• regular rapid rhythm that arises from either
reentry or ectopic pacemaker in area
above bifurcation of bundle of His
• reentrant variety often presents as PSVT
• 60% have reentry within AV node
• 20% have reentry involving bypass tract
• remainder have reentry in other sites
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Mechanisms for Tachydysrhythmia
Formation
• Reentry in normal or accessory pathway
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SVT
• 2 types of reentry SVT
• AV Nodal Reentrant Tachycardia (AVNRT)
– dual AV nodal pathways
– initiated with ectopic atrial impulse
encountering AV node during partial refractory
period
• 2nd type of reentry is Atrioventricular
reentry (AVRT)
– What is AVRT dependent upon?
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SVT
Atrioventricular reentrant
tachycardia (AVRT)
• seen in patients with bypass tracts
• What is classic example?
• second connection (other than AV node)
present between atria and ventricles
• like AVNRT, AVRT usually initiated by
ectopic extrasystole
• 2 types of conduction
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SVT
WPW
• 2 types of conduction
• orthodromic conduction (85% of WPW)
– impulse conducted anterogradely down AV
node and retrogradely up bypass tract
– produces narrow QRS
• antidromic conduction (15% of WPW)
– impulse conducted anterogradely down
accessory tract and up AV node
– wide QRS – difficult to differentiate from vtach
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SVT
• etiology of reentrant SVT
– can occur in normal heart, or in association
with rheumatic heart disease, acute
pericarditis, MI, mitral valve prolapse, or one
of the pre-excitation syndromes (WPW)
• with compromised heart can get
– anginal chest pain, dyspnea, pulmonary
edema from decreased diastolic filling
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SVT Treatment
• can treat by impeding conduction through
one limb of reentry circuit
– sustained reentry then impossible and sinus
node can take over
• increase vagal tone – “vagal maneuvers”
– carotid sinus massage (Munro NC, McIntosh S, Lawson J, et
al: Incidence of complications after carotid sinus massage in older patients with
)
– Valsalva – most effective vagal maneuver
– facial immersion in cold water
syncope. J Am Geriatr Soc 1994;42:1248-1251
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SVT Treatment
• Pharmacologic
•
Hood MA, Smith WM: Adenosine versus verapamil in the treatment of supraventricular tachycardia: A
randomized double-crossover trial. Am Heart J 1992;123:1543-1549
•
Taylor DM - Am J Emerg Med - 1999 Mar; 17(2): 214-6
•
Brady WJ Jr. DeBehnke DJ. Wickman LL. Lindbeck G. Treatment of out-of-hospital supraventricular tachycardia:
adenosine vs verapamil. [see comments]. [Journal Article] Academic Emergency Medicine. 3(6):574-85, 1996
Jun.
– Adenosine
• MOA?
• dose?
• side effects?
– Verapamil
• 0.075 to 0.15 mg/kg (3-10 mg) IV over 15-60 sec
• repeat dose in 30 min if necessary
• associated with hypotension
– Diltiazem, Beta blockers, digoxin
– Consider procainamide, amiodarone, sotalol (2000 ACLS)
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Atrial Flutter
• Definition (Rosen)
– regular atrial depolarization rate of 250 to 350 bpm;
classically 300
– distinct EKG manifestations of abnormal atrial
depolarization in a sawtooth appearance
– common association with a 2:1 block (ventricular rate
of 150 or 4:1 block)
– can see irregular rhythm with variable conduction
(sometimes profound bradycardia)
• pathophysiology thought to be reentry and or
abnormal automaticity
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Atrial Flutter
• often associated with
underlying heart
disease
– IHD, CHF, valvular
dysfunction, PE
– metabolic
derangements
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Atrial Flutter - Treatment
• Of course, cardioversion if unstable
– low energy required – start at 25-50 J
• treat underlying cause (if known)
• Pharmacologic (Rate Control)
– ventricular rate control with calcium channel blocker
(Diltiazem or Verapamil) or beta blocker
– if preexisting CHF (EF < 40%) consider diltiazem,
digoxin, amiodarone (ACLS 2000)
– can think of using adenosine to unmask flutter waves
if diagnosis uncertain
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Atrial Flutter - Treatment
• Pharmacologic (Conversion)
– Class 1A (procainamide), Class 1C
(propafenone, flecainide), Class III
(amiodarone, ibutilide) – ACLS 2000
– consider amiodarone if CHF (EF < 40%)
(ACLS 2000)
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Atrial Fibrillation
• Causes (heart, PE, metabolic)
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IHD, acute MI
valvular heart disease (esp. mitral)
hypertensive heart disease
pericarditis
myocardial contusion
cardiomyopathy
cardiac surgery
congestive heart failure
sick sinus syndrome
acute ethanol intoxication (“holiday heart”)
catecholamine excess
hyperthyroidism
accessory pathway (WPW)
pulmonary embolism
idiopathic
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Atrial Fibrillation
• completely irregular rhythm because of irregular
ventricular response
• loss of coordinated atrial activity and potentially
rapid ventricular response can lead to
decreased cardiac output (reduced diastolic
filling)
• paroxysmal or chronic
• fibrillatory waves best seen inferiorly and V1
• multiple atrial microreentry circuits results in
“atrial rate” of 300-600
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Atrial Fibrillation – Rate Control
• rates of 120 and less usually do not
require emergent treatment
• if unstable sedate and cardiovert (start at
50-100J)
• Calcium channel blockers
• Beta blockers
– especially good for hyperthyroid related afib
• Consider Digoxin and Amiodarone in
compromised LV (EF<40%)
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Atrial Fibrillation
Pharmacologic Conversion Studies
•
Roy D. Talajic M. Dorian P. Connolly S. Eisenberg MJ. Green M. Kus T. Lambert J.
Dubuc M. Gagne P. Nattel S. Thibault B. Amiodarone to prevent recurrence of atrial
fibrillation. Canadian Trial of Atrial Fibrillation Investigators. [see comments].
[Clinical Trial. Journal Article. Multicenter Study. Randomized Controlled Trial] New
England Journal of Medicine. 342(13):913-20, 2000 Mar 30.
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amiodarone vs. sotalol and propafenone for prevention of recurrence
pt’s were electrically cardioverted if no spontaneous cardioversion by 3 weeks
35% of pt’s treated with amiodarone had recurrence, 63% treated with sotalol or propafenone
had recurrence
did not specifically look at initial conversion rates – only avoidance of recurrence
Joseph AP. Ward MR. A prospective, randomized controlled trial comparing the
efficacy and safety of sotalol, amiodarone, and digoxin for the reversion of newonset atrial fibrillation. [Clinical Trial. Journal Article. Randomized Controlled Trial]
Annals of Emergency Medicine. 36(1):1-9, 2000 Jul.
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AFib < 24 h duration
sotalol vs amiodarone vs digoxin
time to reversion 13 h with sotalol, 18 h with amiodarone, 26.9 h with digoxin
concluded that sotalol and amiodarone both better than digoxin
in pt’s who were still in atrial fibrillation sotalol provided the best ventricular rate control
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Atrial Fibrillation
Pharmacologic Conversion Studies
•
Vardas PE. Kochiadakis GE. Igoumenidis NE. Tsatsakis AM. Simantirakis
EN. Chlouverakis GI. Amiodarone as a first-choice drug for restoring sinus
rhythm in patients with atrial fibrillation: a randomized, controlled study.
[see comments]. [Clinical Trial. Journal Article. Randomized Controlled Trial]
Chest. 117(6):1538-45, 2000 Jun.
– amiodarone vs. placebo
– no regard to duration of afib
– 80% of amiodarone group and 40% of placebo group converted by 30 days
•
Blanc JJ. Voinov C. Maarek M. Comparison of oral loading dose of
propafenone and amiodarone for converting recent-onset atrial
fibrillation. PARSIFAL Study Group. [see comments]. [Clinical Trial. Journal
Article. Multicenter Study. Randomized Controlled Trial] American Journal of
Cardiology. 84(9):1029-32, 1999 Nov 1.
– oral amiodarone vs. oral propafenone for conversion in Afib < 2 weeks duration
– median time to conversion 2.4 h (propafenone) and 6.9 h (amiodarone)
– after 24 and 48 h same proportion of pt’s recovered sinus rhythm (56 and 47%)
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Atrial Fibrillation
Pharmacologic Conversion Studies
•
. Kochiadakis GE. Igoumenidis NE. Simantirakis EN. Marketou ME.
Parthenakis FI. Mezilis NE. Vardas PE. Intravenous propafenone versus
intravenous amiodarone in the management of atrial fibrillation of recent
onset: a placebo-controlled study. [Clinical Trial. Journal Article.
Randomized Controlled Trial] Pacing & Clinical Electrophysiology. 21(11 Pt
2):2475-9, 1998 Nov.
– propafenone vs. amiodarone vs. placebo in recent onset Afib (<48h duration)
– 78% conversion in propafenone, 83% conversion in amiodarone, 55%
conversion in placebo
– mean time to conversion 2+/- 3 h for propafenone, 7+/- 5 h for amiodarone
– conclusion was both drugs equally effective and safe for conversion but
propafenone faster
•
Mattioli AV. Lucchi GR. Vivoli D. Mattioli G. Propafenone versus
procainamide for conversion of atrial fibrillation to sinus rhythm. [Clinical
Trial. Controlled Clinical Trial. Journal Article. Randomized Controlled Trial]
Clinical Cardiology. 21(10):763-6, 1998 Oct.
– procainamide vs. propafenone
– procainamide (69.5%) more effective than propafenone (48.7%) for conversion to
sinus rhythm
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Atrial Fibrillation 2000 ACLS
Guidelines
• Duration <48 h
• DC cardioversion
• amiodarone, procainamide, propafenone, ibutilide, flecainide
(all class IIa)
• Duration > 48 h
• no DC cardioversion
• use antiarrhythmics with extreme caution
• delayed cardioversion – anticoagulate x 3 weeks, then
cardiovert, and anticoagulate x 4 more weeks OR early
cardioversion – IV heparin, TEE to exclude clot, then
cardiovert and anticoagulate x 4 more weeks (journal club)
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Carlson, Cardiology in Review,
9(2), 2001
• Reviewed numerous trials regarding afib
and summarized their conclusions:
– biphasic waveform shocks more effective than
monophasic waveform shocks for conversion
– amiodarone is more effective than either
propafenone or sotalol for maintaining SR in
pt’s with Afib
– in a trial of several drugs, combination of
atenolol plus digoxin was most effective for
control of ventricular rates
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Atrial Fibrillation
• Ongoing trial called AFFIRM trial
• looking at mortality with allowing afib to
continue while controlling rate and using
anti-thrombotic therapy vs restoring sinus
rhythm with antiarrhythmic drugs
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Falk, NEJM, April 5, 2001
excellent review of atrial fibrillation
• spontaneous conversion to sinus rhythm
within 24 h after onset of new afib is
common (about 2/3rds). Once duration
exceeds 24 h the likelihood of conversion
decreases
• if onset of afib precisely known then
consider rate controlling only for 24 hours
58
Specific Dysrhythmias
• Narrow QRS (supraventricular tachys)
– Sinus tachycardia
– Ectopic atrial tachycardia
– Multifocal atrial tachycardia
– Atrial fibrillation
– Atrial flutter
– AV nodal reentrant tachycardia
– Atrioventricular reentrant tachycardia
– Junctional tachycardia
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Preexcitation and Accessory
Pathway Syndromes
• preexcitation defined as depolarization of
ventricle earlier than would occur by
conduction of impulse through AV node
– implies existence of accessory pathway
(normally AV node only connection)
– WPW most common accessory pathway
syndrome
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Preexcitation and Accessory
Pathway Syndromes
• Any tachycardia at rate of 200 bpm or
greater should raise suspicion for an
accessory pathway syndrome as that is
near limit of AV conduction
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SVT
WPW
• 2 types of conduction
• orthodromic conduction (85% of WPW)
– impulse conducted anterogradely down AV
node and retrogradely up bypass tract
– produces narrow QRS
• antidromic conduction (15% of WPW)
– impulse conducted anterogradely down
accessory tract and up AV node
– wide QRS – difficult to differentiate from vtach
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Ventricular Tachydysrhythmias
• Ventricular Tachycardia
– monomorphic ventricular tachycardia
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morphologically consistent QRS complexes
usually regular rhythm
rate usually 150-200
can occur in presence or absence of IHD
– polymorphic ventricular tachycardia
• QRS complexes that vary in structure or duration
• associated with more severe underlying disease than
monomorphic vtach
• Torsades de pointes is a specific form
– for treatment an important principal to remember is to
correct any underlying causes
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Stable Monomorphic Ventricular
Tachycardia
• Treatment (ACLS 2000)
• Normal Cardiac Function
– procainamide, sotalol
– amiodarone, lidocaine
• EF < 40% or evidence CHF
– amiodarone or lidocaine then synchronized
cardioversion
65
Stable Polymorphic Ventricular
Tachycardia
• ACLS 2000
• Classified based on QT interval
• Normal baseline QT (not torsades)
– treat ischemia
– correct electrolytes
– consider Beta blockers or lidocaine or amiodarone or
procainamide or sotalol
– if EF < 40% or evidence CHF then amiodarone or
lidocaine followed by synchronized cardioversion
66
Stable Polymorphic Ventricular
Tachycardia
• ACLS 2000
• prolonged baseline QT interval (suggests
torsades)
– correct abnormal electrolytes
– consider magnesium, lidocaine, isoproterenol,
phenytoin, overdrive pacing
– 1A and 1C contraindicated because prolong
repolarization
– sustained or unstable torsades - cardiovert
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Torsades de pointes
• Must meet three criteria to be called
torsades
• ventricular rate greater than 200
• QRS displays undulating axis with polarity
of complexes appearing to shift about
baseline
• occurrences are often in short episodes of
less than 90 seconds, although sustained
runs can be seen
69
Torsades de pointes
• often occurs in setting of prolonged QT
interval during sinus rhythm (repolarization
abnormality)
• repolarization abnormality (prolonged QT)
can be congenital or acquired
• acquired QT prolongation often result of
drug therapy, electrolyte disturbances
(hypoK+, hypoMg++)
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Torsades de pointes
• 2 types
• Pause dependent (acquired)
• Adrenergic dependent (acquired or
congenital)
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Torsades de pointes
• Pause dependent (acquired)
– drug induced
– electrolyte abnormalities
– severe bradycardia or AV block
– myocardial ischemia
– hypothyroid
– contrast injection
– CVA (especially intraparenchymal)
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Torsades de pointes
• Adrenergic dependent
– acquired
• subarachnoid hemorrhage
• autonomic surgery (radical neck dissection, carotid
endarterectomy, truncal vagotomy)
– congenital
• Jervell and Lange-Nielsen syndrome (deafness, autosomal
recessive)
• Romano-Ward syndrome (normal hearing, autosomal
dominant)
• sporadic (normal hearing, no family tendency)
• mitral valve prolapse
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Passman, Medical Clinics of North America, 85(2), March 2001
Treatment of PMVT associated with acquired Long QT (Torsades)
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Approach to EKG Dysrhythmia
interpretation
• rate: ventricular rate fast (>100), slow (<60) or normal
• rhythm: regular or irregular or regular with occasional
irregularities
– use calipers for subtle irregularities
– long rhythm strips (2 min) sometimes required
• QRS width: prolonged (>0.12 sec), borderline (0.09-0.12
sec), or normal
• P wave presence and relationship to QRS complexes
– may require mapping of P-waves with calipers to detect those
falling within QRS complex or T wave
– can increase paper speed to better define p – QRS relationship
• examine multiple leads
• compare with previous tracing
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Differential Diagnosis of Wide
Complex Tachycardia
• ventricular tachycardia vs. supraventricular
source (with aberrancy or accessory
pathway)
• Look at history, physical examination and
EKG tracing
• Morady et al. have shown that stable pt’s
are overdiagnosed as SVT with aberrancy,
with sometimes lethal consequences
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Differential Diagnosis of Wide
Complex Tachycardia
• Wellens criteria
– Wellens HJJ, Bar F, Lie KI: The value of the
electrocardiogram in the differential diagnosis
of a tachycardia with a widened QRS
complex, Am J Med 64:27, 1978.
– Wellens HJJ: The wide QRS tachycardia
(editorial), Ann Intern Med 104:879, 1986.
– look at history, physical examination, EKG
77
Ventricular tachycardia
History
Supraventricular
tachycardia plus
aberrancy
Age 50 or older
Age 35 or less
History of myocardial
infarction, congestive heart
failure, CABG, or ASHD
None
Mitral valve prolapse
Mitral valve prolapse
(especially in WolffParkinson-White syndrome)
Previous history of
ventricular tachycardia
Previous history of
supraventricular tachycardia
78
Ventricular tachycardia
Physical examination
Supraventricular
tachycardia plus
aberrancy
Cannon A waves
Absent
Variation in arterial pulse
Absence of variability
Variable first heart sound
Absence of variability
79
EKG
Specific QRS patterns
Ventricular tachycardia
Supraventricular
tachycardia plus
aberrancy
Fusion beats
None
AV dissociation
Preceding P waves with
QRS complexes
QRS >0.14 sec
QRS usually <0.14 sec
Extreme LAD (<-30
degrees)
Axis normal or slightly
abnormal
No response to vagal
maneuvers
Slow or terminate with vagal
maneuvers
V1 : R, qR, or RS
V1: rsR`
V6 : S, rS, or qR
V6: qRs
Identical to previous
ventricular tachycardia
tracing *
Identical to previous
supraventricular tachycardia
tracing *
Concordance of positivity or
negativity
80
Brugada Criteria
• Brugada P, Brugada J, Mont L, et al: A new
approach to the differential diagnosis of a
regular tachycardia with a wide QRS complex,
Circulation 83:1649, 1991.
Rhythm must be regular to apply criteria
– Absence of any RS complexes in the chest leads
– RS duration (measured from beginning of R to
deepest part of S wave) >0.1 sec
– AV dissociation (variation in first heart sound or in
SBP beat to beat, or cannon jugular waves)
• also EKG evidence of AV dissociation
– Specific ventricular tachycardia morphologic criteria
81
The morphology associated with the fourth criterion in the
Brugada system in patients with a right bundle branchappearing complex.
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The morphology associated with the fourth criterion in the
Brugada system in patients with a left bundle branchappearing complex.
83
Brugada Criteria
• Only when none of the four criteria is met
do we diagnose a supraventricular etiology
• as soon as answer yes vtach diagnosed
• original study found sensitivity 98.7% and
specificity 96.5%
84
Bottom Line
• assume any new onset symptomatic widecomplex tachycardia is vtach until proven
otherwise (but can potentially prove otherwise
by history, physical examination and EKG)
• can not use blood pressure and LOC (stable vs.
unstable) to differentiate
• irregularity suggests afib with aberrancy
• When in doubt consider Procainamide because
it is indicated for both (except 1A and 1C
contraindicated in Torsades because prolong
repolarization)
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EKG Rhythm Diagnosis
• Rate
• Rhythm regular or irregular
– irregular is atrial fibrillation, multifocal atrial tachycardia, any
supraventricular rhythm with variable conduction, occasionally
ventricular tachycardia
• P wave presence and relation to QRS
– if normal p’s prior to each QRS and regular rhythm then have
sinus tach, atrial flutter, single focus ectopic atrial tach
• QRS width
• Can’t see p wave?
– look in multiple leads
– can try long rhythm strip
– can increase paper speed to draw out complexes
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