Transcript WQRS-internist

Tachydysrhythmias
TABAN MD.
Internist & cardiologist
Tabriz medical faculty
3 types of tachydysrhythmias
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Re-entrant
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Respond well to electricity
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Atrial fib and flutter
PSVT
Ventricular tachycardia
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Some atrial tachycardias
Automatic
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Monomorphic, Polymorphic (non-torsade)
Sinus, junctional, most atrial tach, MAT, AIVR
Triggered automaticity
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Some atrial tach, Torsades
Re-entry
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Requires 2 functional pathways that differ in
their refractory periods.
Triggered by early beat (e.g., PAC)
Atrium
LA
AV node
Sinus
node
Ventricle
LV
Mechanism of Reentry
Mechanism of Reentry
Enhanced Automaticity--Pacemaker cell
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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
Cardiac Action Potential
Automaticity
depends on the
slope of phase 4
Triggered Automaticity/Dysrhythmias
Afterdepolarizations
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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
Ventricular Tachycardia, wide (>120 ms)
the origin of the arrhythmia is within the ventricles
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Re-entrant
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Classic VT
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Triggered
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Torsade de pointe
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Monomorphic
Polymorphic
Polymorphic
long QT on baseline EKG
Automatic
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Accelerated Idioventricular
‫تشخیص تاکی کاردی ‪WQRST‬‬
Wide Complex Tachycardia
--Sinus tach with aberrancy vs.
--SVT (PSVT, AF, flutter) with aberrancy vs.
--Ventricular tachycardia
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Pretest probability:
 Majority of wide complex tachycardia is
ventricular tachycardia
REMEMBER: VT does not invariably cause
hemodynamic collapse; patients may be conscious
and stable
Clinical Clues to Basis
for Regular Wide QRS Tachycardia
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History of heart disease, especially prior
myocardial infarction, suggests VT
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Occurrence in a young patient with no known
heart disease suggests SVT
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12-lead EKG (if patient stable) should be
obtained
5 Questions in tachyarrhythmia
 1- QRS:
Wide or Narrow?
Axis?
Shap?
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2- Regularity?
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Regular
Regularly irregular
Irregularly irregular
3- P-waves?
4- Rate?
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HR?
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5- Rate change sudden or gradual?
1- QRS: Wide or Narrow
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Narrow
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Sinus, PSVT, A flutter, A fib
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(All without aberrancy)
Wide
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SVT with aberrancy
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Ventricular tachycardia
Aberrancy - SVT with wide complex
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Abnormal ventricular conduction
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RBBB
LBBB
Nonspecific intraventricular conduction defect
Rate-related BBB
Antidromic Reciprocating
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Goes down through bypass tract
Suggest VT
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In RBBB pattern > 140 ms
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In LBBB pattern > 160 ms
1- QRS: Shape?
Typical or atypical LBBB/RBBB
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Look for a true bundle branch block pattern
 Right or left (sinus or SVT with aberrancy)
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absence of RS complex in all leads V1-V6
(negative Concordance)
Morphology criteria for VT
RBBB
V1
V6
LBBB
V1
V6
1-QRS: Axis
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>45 degree
R in aVR
1- QRS : Fusion beats / capture beats
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Fusion beats (occasional narrow complex fused
with wide one)
Capture beats
Accelerated Idioventricular
Rhythm
( Ventricular Escape Rate, but  100
bpm)
Fusion
beat
Ectopic
ventricular activation
Sinus
Normal
acceleration ventricular activation
Ventricular tachycardia in the arrhythmogenic right ventricular dysplasia
2- P waves
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If p waves, and associated with QRS, then
sinus (or, rarely, atrial tachycardia)
PSVT: generally no p wave visible
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A fib and flutter:
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PR short
P wave hidden in QRS, inverted
No p waves, but flutter may fool you
V tach
May rarely see P waves, but with no association
(AV dissociation) or retrograde
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More R-Waves Than P-Waves Implies
VT!
II
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P-waves in front of QRS?
AV
Dissociation
SA
Node
ATRIA AND
VENTRICLES
ACT
INDEPENDENTLY
Ventricular
Focus
Ventricular Tachycardia
(VT)
V1
• Rates range from 100-250 beats/min
• Non-sustained or sustained
• P waves often dissociated (as seen here)
3- Regularity in tachycardia
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Regular
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Regularly irregular
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VT, Sinus, PSVT, flutter,
Atrial flutter
Irregularly irregular
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AF, MAT
4- rate
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Rate: the faster, the less likely it is sinus
(260 beats/min)
5- Sudden vs. Gradual change
(Re-entry vs. automaticity)
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Sinus: gradual
PSVT: sudden
Atrial flutter: sudden
AF: always changing, but sudden onset
Ventricular tachycardia: Sudden
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Rate gradually changes or always the same?
 Gradual: sinus
 Unchanging: flutter vs. PSVT vs. v tach
Very Fast and Irregular think :
WPW and AF
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Never give AV nodal blocker
Never give Dig or Calcium channel blocker (IV).
Even adenosine associated with VF
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Electrical or chemical conversion
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procainamide, amiodarone, ibutilide
WPW with regular rhythm (orthodromic/antidromic), not atrial fib:
•AV nodal blockers are OK
Atrial Fibrillation with Rapid Conduction
Via Accessory Pathway: Degeneration to VF
:‫چند تمرین‬
Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction?
V1
Identify ventricular tachycardia
Regular and wide
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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.
> 0.10 sec?
Step 3: Is there AV dissociation?
 If yes, then rhythm is VT.
Step 4: Are morphology criteria for VT present
(not typical BBB)?
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If yes, then VT
Ventricular Tachycardia
Concordance
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
Step 4: RBBB pattern (tall R in V1). Notching of this monophasic R indicates VT
V tach
RS > 0.10 sec
What is it?
What is it?
Tracing from a young boy with congenital long-QT syndrome. The
QTU interval in the sinus beats is at least 600 milliseconds. Note TU
wave alternans in the first and second complexes. A late premature
complex occurring in the downslope of the TU wave initiates an
episode of ventricular tachycardia
Ventricular tachycardia originating from the right ventricular outflow tract. This
tachycardia is characterized by a left bundle branch block contour in lead V1
and an inferior axis.
Left septal ventricular tachycardia. This tachycardia is characterized by a
right bundle branch block contour. In this instance, the axis was rightward.
The site of the ventricular tachycardia was established to be in the left
posterior septum by electrophysiological mapping and ablation.
Ventricular
Flutter
• VT  250 beats/min, without clear isoelectric line
• Note “sine wave”-like appearance
Ventricular Fibrillation (VF)
• Totally chaotic rapid ventricular rhythm
• Often precipitated by VT
• Fatal unless promptly terminated (DC shock)
Sustained VT  Degeneration to VF
Artifact Mimicking “Ventricular
Tachycardia”
QRS complexes “march through”
the pseudo-tachyarrhythmia
Artifact
precedes
“VT”
Ventricular flutter and ventricular fibrillation. A, The sine wave appearance
of the complexes occurring at a rate of 300 beats/min is characteristic of
ventricular flutter. B, The irregular undulating baseline typifies ventricular
fibrillation.
‫مرور تاکی کاردی‬
polymorphic ventricular tachycardia
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Polymorphic VT
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Long QT on baseline ECG--Torsade de pointes
Normal QT on baseline ECG = not Torsade
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treat ischemia, correct electrolytes, amiodarone
Polymorphic VT and prolonged
QT (Torsade)
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Usually self terminating, may progress to v fib
Treatment: correct electrolytes (K, Mg)
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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
Limited role for acute beta blockade in congenital
LQTS
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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
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Accelerated idioventricular
rhythm
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Ventricular (wide)
Automatic
Regular
No p-waves
60-100 (ventricular escape is 20-40)
Reperfusion dysrhythmia
Accelerated idioventricular
rhythm
Fast, Narrow, and Irregular
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Atrial Fibrillation
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Atrial Flutter
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Irregularly irregular
Regularly irregular
Diagnosis may be aided by adenosine
Identify Dysrhythmia
Features
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P-waves, regular, gradual rate change—sinus
No p-waves, regular, 130-250
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Narrow
 PSVT or flutter—intranodal (AVNRT) or orthodromic bypass
Wide
 Ventricular tachycardia
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PSVT with aberrancy
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[intranodal or bypass tract (orthodromic)]
PSVT due to antidromic reciprocating tachycardia
Atrial Flutter with aberrancy
Regularly irregular
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Most common
Atrial Flutter
Irregularly irregular
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Atrial fibrillation, (V tach can be only slightly irreg irreg)
‫درمان‬
Is patient stable or unstable?
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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
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(poor cerebral perfusion?)
Clinical shock
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(cool and clammy -- peripheral vaso-constriction?)
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Are the signs & symptoms due to the rapid heart rate?
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Or are S/Sx’s & rapid HR due to something else?
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I.e., is it sinus tach due to sepsis, hemorrhage, PE,
tamponade, dehydration, etc.
Treatment when in doubt
Stable or unstable-Electricity
If possible, get 12-lead ECG first
If electricity does not work
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Automatic rhythm
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Sinus, accelerated junctional, accelerated idioventricular,
automatic atrial, MAT—treatment of underlying disorder
Chronic atrial fib
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Be sure it is not physiologic tachycardia
Amiodarone for conversion
Diltiazem or Digoxin to control rate
Refractory ventricular tachycardia
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Amiodarone
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150 mg, may repeat several times
Treat underlying ischemia
Conclusion: When in doubt
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Shock a fast rhythm
Pace a slow rhythm
In anterior STEMI
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Be certain that transcutaneous pacing will capture
if there is high grade block
But don’t shock sinus tachycardia!!
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
Nijhoff Publishing;1986:81.
Treat resus v fib, and v tach in STEMI, with
amiodarone or lidocaine bolus and drip.
Class I for Transvenous
Pacing
OR
1.
Left Bundle Branch Block or
RBBB + LAFB (Bifascicular
block
AND
1.
2.
2nd deg Mobitz type 2 block
OR
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Alternating Left and
Right BBB
3rd Degree Block
(complete AV
dissociation)
Class IIa for transvenous
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Anterior MI
and
New LBBB or new RBBB + ant or post FB
And
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1st degree AVB or
2nd degree AVB, Mobitz I (Wenckebach)
Questions?
Drug-induced ECG abnormalities
Drug-induced ECG abnormalities
Ventricular tachycardia
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> 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