TABAN MD.
Internist & cardiologist
Tabriz medical faculty

 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

 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

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

Automaticity depends on the slope of phase 4

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

Ventricular Tachycardia, wide (>120 ms) the origin of the arrhythmia is within the ventricles
 Re-entrant
 Classic VT
 Monomorphic
 Polymorphic
 Triggered
 Torsade de pointe
 Polymorphic
 long QT on baseline EKG
 Automatic
 Accelerated Idioventricular

Wide Complex Tachycardia
--Sinus tach with aberrancy vs.
--SVT (PSVT, AF, flutter) with aberrancy vs.
--Ventricular tachycardia
 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
 History of heart disease, especially prior myocardial infarction , suggests VT
 Occurrence in a young patient with no known heart disease suggests SVT
 12-lead EKG (if patient stable) should be obtained

 1- QRS:
Wide or Narrow?
Axis?
Shap?
 2- Regularity?



Regular
Regularly irregular
Irregularly irregular
 3- P-waves?
 4- Rate?
HR?
 5- Rate change sudden or gradual?

 Narrow
 Sinus, PSVT, A flutter, A fib
 (All without aberrancy)
 Wide
 SVT with aberrancy
 Ventricular tachycardia

SVT with wide complex
 Abnormal ventricular conduction




RBBB
LBBB
Nonspecific intraventricular conduction defect
Rate-related BBB
 Antidromic Reciprocating
 Goes down through bypass tract

 In RBBB pattern > 140 ms
 In LBBB pattern > 160 ms

1- QRS: Shape?
Typical or atypical LBBB/RBBB
 Look for a true bundle branch block pattern
 Right or left (sinus or SVT with aberrancy)
 absence of RS complex in all leads V1-V6
(negative Concordance)

RBBB
V1 V6
LBBB
V1
V6

 >45 degree
R in aVR

1- QRS
:
Fusion beats / capture beats
 Fusion beats (occasional narrow complex fused with wide one)
 Capture beats

Accelerated Idioventricular
Rhythm
(

Ventricular Escape Rate, but

100 bpm)
Ectopic ventricular activation
Sinus
Fusion beat acceleration
Normal ventricular activation

Ventricular tachycardia in the arrhythmogenic right ventricular dysplasia

 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) or retrograde

More R-Waves Than P-Waves Implies
VT!
II

 P-waves in front of QRS?

SA
Node
AV
Dissociation
ATRIA AND
VENTRICLES
ACT
INDEPENDENTLY
Ventricular
Focus

V1
Ventricular Tachycardia
(VT)
• Rates range from 100-250 beats/min
• Non-sustained or sustained
• P waves often dissociated (as seen here)

 Regular
 VT, Sinus, PSVT, flutter,
 Regularly irregular
 Atrial flutter
 Irregularly irregular
 AF, MAT

 Rate: the faster, the less likely it is sinus
(260 beats/min)

Re-entry vs. automaticity)
 Sinus: gradual
 PSVT: sudden
 Atrial flutter: sudden
 AF: always changing, but sudden onset
 Ventricular tachycardia: Sudden

 Rate gradually changes or always the same?
 Gradual: sinus
 Unchanging: flutter vs. PSVT vs. v tach

Very Fast and Irregular think :
WPW and AF
 Never give AV nodal blocker
 Never give Dig or Calcium channel blocker (IV).
Even adenosine associated with VF
 Electrical or chemical conversion
 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

Regular Wide QRS Tachycardia:
VT or SVT with Aberrant Conduction?

V1

Identify ventricular tachycardia
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.
Step 3: Is there AV dissociation?
 If yes, then rhythm is VT.
> 0.10 sec?
Step 4: Are morphology criteria for VT present
(not typical BBB)?
 If yes, then VT

Ventricular Tachycardia
Concordance
Step 1: Absence of RS in all precordial leads

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

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.

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

 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

 Beta blockers: long term therapy for familial LQTS
Limited role for acute beta blockade in congenital
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

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

 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)

 Patient has serious signs or symptoms? Look for


Chest pain (ischemic? possible ACS?)
Shortness of breath (lungs ‘wet’? possible CHF?)
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

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.






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

 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!!

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.

OR
1.
Left Bundle Branch Block or
RBBB + LAFB (Bifascicular block
1.
AND
3 rd Degree Block
(complete AV dissociation)
2.
2 nd deg Mobitz type 2 block
OR
 Alternating Left and
Right BBB

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

Drug-induced ECG abnormalities

Drug-induced ECG abnormalities

 > 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