tachydysrhythmias taban md. internist & cardiologist tabriz medical faculty

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

Ventricle

AV nodeLA

LVSinus node

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 تاکی تشخیص کاردی

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 VTRBBB

LBBB

V1 V6

V1V6

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

Ectopic ventricular activation

Normal ventricular activation

Fusionbeat

Accelerated Idioventricular Rhythm ( Ventricular Escape Rate, but 100 bpm)

Sinus acceleration

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?

SANode

Ventricular Focus

ATRIA AND VENTRICLESACT INDEPENDENTLY

AV Dissociation

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

تمرین :چند

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

V1

Identify ventricular tachycardia

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.

Step 4: Are morphology criteria for VT present (not typical BBB)? If yes, then VT

> 0.10 sec?

Regular and wide

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

Ventricular TachycardiaVentricular 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 tachRS > 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”

Artifact precedes“VT”

QRS complexes “march through”the pseudo-tachyarrhythmia

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.

کاردی تاکی مرور

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 minActive v tach: Mg, 2g over 30-60 sec, max 6gSerum K > 4.5Overdrive pacing (100-140)

Lowest pacing rate that prevents PVB’s dilantin, lidocaine

Isoproterenol or beta blocker?

Beta blockers: long term therapy for familial LQTSLimited 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 DysrhythmiaFeatures

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)

درمان

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 doubtStable 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 PACsWith Aberrant Conduction

Wide-Complex Tachycardia Followed by Second-Degree AV Block

STEMI: “Warning Arrhythmias”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

1. Left Bundle Branch Block or RBBB + LAFB (Bifascicular block

1. AND

2. 2nd deg Mobitz type 2 block

Alternating Left and Right BBB

OR

3rd Degree Block (complete AV dissociation)

OR

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)

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