WIDE QRS TACHYCARDIA - BEDSIDE DIAGNOSIS Dr.K.Chandrasekaran.MD.DM Interventional cardiologist and Cardiac Electrophysiologist

CLASSIFICATION OF TACHYCARDIAS WITH A BROAD QRS COMPLEX SVT WITH BBB ATRIAL TACHYCARDIA ATRIAL FLUTTER ATRIAL FIBRILLATION AV NODAL RE-ENTRANT TACHYCARDIA CMT WITH AV CONDUCTION OVER AV NODE AND VA CONDUCTION OVER ACC PATHWAY

SVT WITH AV CONDUCTION OVER ACC PATHWAY ATRIAL TACHYCARDIA ATRIAL FLUTTER ATRIAL FIBRILLATION AV NODAL RE-ENTRANT TACHYCARDIA

Antidromic circus movement tachycardia using an accessory pathway in the antegrade direction and AV Node or another acc pathway in the retrograde direction AV Reentry tachycardia using a Mahaim fibre in the antegrade direction and AV Node or another acc pathway in the retrograde direction

VENTRICULAR TACHYCARDIA

VT Regular SVT with BBB SVT with AV conduction Over accessory pathway

AF Irregular PMVT with Normal QT PMVT with long QT BBB Accessory Pathway Irregular PMVT with Normal QT PMVT with long QT

THE ECG DIAGNOSIS IMPORTANCE OF AV DISSOCIATION AVD HALLMARK OF VT . VA CONDUCTION DURING SLOW VT. P WAVES CAN BE DIFFICULT TO RECOGNISE NON ECG SIGNS FUSION CAPTURE BEATS AVD IN AVJT WITH BBB AFTER CARDIAC SURGERY OR DURING DIG INTOXICATION

A 47 year old man with a long history of palpitations and blackouts. Wolf-Parkinson-White syndrome with atrial fibrillation irregularly irregular, wide complex tachycardia impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway producing a broad fusion complex or just the AV node producing a narrow complex (without a delta wave) or just the accessory pathway producing a very broad 'pure' delta wave people who develop this rhythm and have very short R - R intervals are at higher risk of VF 15 15

A 23 year old male with palpitations Wolf-Parkinson-White syndrome with atrial fibrillation irregularly irregular, wide complex tachycardia impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway producing a broad fusion complex or just the AV node producing a narrow complex (without a delta wave) or just the accessory pathway producing a very broad 'pure' delta wave people who develop this rhythm and have very short R - R intervals are at higher risk of VF 16 16

WIDTH OF QRS COMPLEX SITE OF ORIGIN OF VT ORIGIN IN THE LATERALFREE WALL  VERY WIDE QRS ( SEQUENTIAL ACTIVATION OF THE VENTRICLES) ORIGIN IN OR CLOSE TO THE IVS  NARROWER QRS ( SIMULTANEOUS ACTIVATION OF THE VENTRICLES ) SCAR TISSUE , VENTRICULAR HYPERTROPHY AND MUSCULAR DISARRAY QRS WIDTH > 0.14 SECS IN RBBB TACHYCARDIAS AND > 0.16 SECS IN LBBB TACHYCARDIAS  ARGUES FOR A VT.

WIDTH OF QRS COMPLEX SVT WITH QRS WIDTH > 0.14 SECS (RBBB) OR > 0.16 SECS (LBBB) IN THREE CONDITIONS: IN THE PRESENCE OF BBB IN THE ELDERLY WITH FIBROSIS IN THE BB SYSTEM AND VENTRICULAR MYOCARDIUM DURING SVT WITH AV CONDUCTION OVER AN ACCESSORY AV PATHWAY WHEN CLASS 1 C DRUGS ARE PRESENT DURING SVT

QRS AXIS IN THE FRONTAL PLANE SUPERIOR AXIS  VT ORIGIN IN THE APICAL PART OF THE VENTRICLE. RBBB SHAPED QRS + SUPERIOR AXIS  VT INFERIOR AXIS  VT ORIGIN IN THE BASAL VENTRICLE. LBBB SHAPED QRS + INFERIOR AXIS VT

CONFIGURATIONAL CHARACTERISTICS OF THE QRS COMPLEX RBBB SHAPED TACHYCARDIA qR OR R IN VI  VT rSR PATTERN IN VI  SVT R/S RATIO < 1 IN V6  VT R/S RATIO < 1 IN V6 TYPICALLY FOUND WITH LEFT AXIS DEVIATION. WITH INFERIOR AXIS V6 OFTEN SHOWS R/S RATIO > 1 qRS in V6 with R/S in V6 >1 ---- SVT

CONFIGURATIONAL CHARACTERISTICS OF THE QRS COMPLEX LBBB SHAPED VT V1,V2 SHOW INITIAL POSITIVE QRS ( r wave)> 30 mSecs, SLURRING / NOTCHING OF THE DOWN STROKE OF THE S-WAVE, AN INTERVAL BETWEEN THE BEGENNING OF QRS AND THE NADIR OF THE S-WAVE OF 70 msecs . qR PATTERN IN V6  VT IS MORE LIKELY

CONFIGURATIONAL CHARACTERISTICS OF THE QRS COMPLEX SVT WITH LBBB V1 SHOWS NO OR MINIMAL INITIAL POSITIVITY, A VERY RAPID DOWNSTROKE OF THE SWAVE A SHORT INTERVAL BETWEEN THE BEGENNING OF THE QRS AND THE NADIR OF THE SWAVE

INTERVAL ONSET QRS TO NADIR OF SWAVE IN PRECORDIAL LEADS RS INTERVAL > 100 msecs IN 1 OR MORE PRECORDIAL LEADS  VT DIFFERENTIAL DIAGNOSIS SVT WITH AV CONDUCTION OVER AN ACC PATHWAY, SVT DURING ADMINISTRATION OF DRUGS LIKE FLECAINIDE. IN SVT WITH PRE-EXISTENT BBB.

CONCORDANT PATTERN NEGATIVE CONCORDANCY VT ARISING IN THE APICAL AREA POSITIVE CONCORDANCY  VT ARISING IN THE LEFT POSTERIOR WALL OR TACHYCARDIAS USING A LEFT POSTERIOR ACC PATHWAY FOR AV CONDUCTION

TACHYCARDIA QRS MORE NARROW THAN SINUS QRS NARROW QRS DURING TACHYCARDIA THAN DURING SINUS RHYTHM  VT ORIGIN CLOSE TO IVS

PRESENCE OF QR COMPLEXES QR DURING WIDE QRS TACHYCARDIA INDICATES A SCAR IN THE MYOCARDIUM QR COMPLEX DURING VT IN 40% OF VTs AFTER MI

RVOT VT IDIOPATHIC VT ARISING FROM RVOT 3 PATTERNS. QRS AXIS + 70 AND LEAD 1 SHOWS A POSITIVE QRS  ORIGIN OF VT IN THE LATERAL PART OF RVOT INFERIOR QRS AXIS, QRS NEGATIVE IN LEAD 1  VT ORIGIN ON THE SEPTAL SIDE IN THE RVOT INFERIOR QRS AXIS, NEGATIVE QRS IN LEAD 1 & V1,V2 SHOWING INITIAL POSITIVITY OF THE QRS  EPICARDIAL ORIGIN OF VT BETWEEN THE ROOT OF THE AORTA AND THE POSTERIOR PART OF THE RVOT .

IDIOPATHIC LEFT VT LEFT AXIS DEVIATION  ORIGIN OF THE VT IS IN OR CLOSE TO THE POSTERIOR FASCICLE OF THE LBB FURTHER LEFTWARD QRS AXIS (NORTH-WEST AXIS) ORIGIN OF VT MORE ANTERIORLY CLOSE TO THE IVS INFERIOR QRS AXIS VT ORIGIN IN THE ANTERIOR FASCICLE OF THE LBB

ARVD 3 PREDILECTION SITES IN THE RV THE INFLOW THE OUTFLOW THE APEX LEFT AXIS DEVIATION IN A YOUNG PERSON WITH LBBB SHAPED VT  ARVD

BBRT WHEN THE BROAD QRS IS IDENTICAL DURING TACHYCARDIA AND SINUS RHYTHM  BBRT OR SVT WITH PRE-EXISTENT BBB BBRT OCCUR IN PATIENTS WITH ASMI, DCMY, MYOTONIC DYSTROPHY, AFTER AORTIC VALVE SURGERY

VALUE OF ECG DURING SINUS RHYTHM ECG DURING SINUS RHYTHM MAY SHOW PRE-EXISTENT BBB, VENTRICULAR PRE-EXCITATION OR AN OLD MI PRESENCE OF AV CONDUCTION DISTURBANCES DURING SINUS RHYTHM  VERY UNLIKELY THAT A BROAD QRS TACHYCARDIA IN THAT PATIENT HAS A SUPRAVENTRICULAR ORIGIN

Emergency Approach – Wide QRS Tachycardia Do not panic when confronted with WCT Obtain a 12 Lead ECG

If Hemodynamically Unstable Carrdiovert Obtain a history Examine the pre and post cardioversion ECG’S to determine the etiology of the arrhythmia

If Hemodynamically Stable Examine the patient for clinical signs of AVD Systematically evaluate the 12 Lead ECG Obtain a history

If Ventricular Tachycardia Give Procainamide 10mg/kg IV bolus over 5 minutes If Ischemia related – Give Lidocaine If unsuccessful, Cardiovert Examine the ECG during VT and during sinus rhythm to determine the etiology of the arrhythmia

If SVT with aberration Vagal stimulation. If unsuccessful, Adenosine 6 mg rapid IV bolus. If unsuccessful, Give 12 mg rapid IV bolus. May be repeated once. If unavailable , Verapamil 10 mg IV over 3 minutes, reduce to 5 mg if the patient is on beta blocker or hypotensive. If unsuccessful, Procainamide 10 mg/kg IV over 5 minutes. If unsuccessful, Cardiovert

Examine SVT and post- conversion ECG’s to determine the mechanism If in doubt, do not give verapamil, give IV Procainamide If irregular, Do not give AV nodal blocking drugs like BB, CCB, Adenosine or Digitalis Give Procainamide IV or Amiodarone or Propafenone

Polymorphic VT with Normal QT Most frequently caused by Acute ischemia or MI Poorly tolerated Tends to degenerate into VF quickly Rarely it is caused by ARVD, IPMVT (short coupled variant of TDP) or familial catecholaminergic PMVT

Polymorphic VT with long QT Initiation of tachycardia is pause dependent with late coupled PVC (long short initiating sequence) Usually non sustained Syncope ECG abnormalities – Long QTc, abnormally shaped T waves

Treatment Sustained PMVT – unstable rhythm with hemodynamic compromise and frequent degeneration into VF Electrical cardioversion is the first line of therapy to decrease the recurrence and as treatment for NSPMVT BB recommended for PMVT with normal QT Magnesium for PMVT with long QT

CONCLUSION WCT– VT MOST COMMON HISTORY IS IMPORTANT POST MI - WCT IS ALWAYS VT UNLESS PROVED OTHERWISE PMVT WITH NORMAL QT - ACUTE ISCHAEMIA

THANK YOU