Tachydysrhythmias

TABAN MD.

Internist & cardiologist

Tabriz medical faculty

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) Atrium LA AV node Sinus node LV Ventricle

Mechanism of Reentry

Mechanism of Reentry

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

Cardiac Action Potential

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

WQRST یدراک یکات صیخشت

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

5 Questions in tachyarrhythmia

 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?

1- QRS: Wide or Narrow

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

Aberrancy -

SVT with wide complex

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

Suggest VT

 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)

Morphology criteria for VT

RBBB V1 V6 LBBB V1 V6

1-QRS: Axis

 >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

2- 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) 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)

3- Regularity in tachycardia

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

4- rate

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

5- Sudden vs. Gradual change (

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

: نیرمت دنچ

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

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.

یدراک یکات رورم

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:  Serum K > 4.5

Mg, 2g over 30-60 sec, max 6g   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  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

Accelerated idioventricular rhythm

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

Accelerated idioventricular rhythm

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)

نامرد

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.

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

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!!

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

1.

AND

3 rd Degree Block (complete AV dissociation) 2.

2 nd 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   1 st degree AVB or 2 nd degree AVB, Mobitz I (Wenckebach)

Questions?

Drug-induced ECG abnormalities

Drug-induced ECG abnormalities

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