WIDE COMPLEX & Objectives ABERRANCIES  Upon completion of this course, the learner will:

PRESENTED BY:  Describe the electrophysiology of the 3 KATHY J. NOYES, DNP, APRN, FNP, BC, ACNP, BC types of Wide Complex Tachycardias  Describe the criteria for 3 algorithms used to HEALTHCARE EDUCATIONAL RESOURCES & differentiate Ventricular (VT) SEMINARS, LLC and Supraventricular Tachycardia (SVT)with an Aberrancy  Demonstrate the utilization of the diagnostic criteria for differentiating VT and SVT with Aberrancy

1 2

Mechanisms of : Disclosures Classifications

 No Affiliations or Conflicts of Interest  Arrhythmias can be  Rhythms due to classified as either: abnormal impulse  conduction Bonus Slides Included in the Presentation  Rhythms due to including Anti-Arrhythmic Medications abnormal impulse  Ex: A-fib, A-flutter, generation AV nodal reentry, tachycardias with  Ex: Sinus Brady, Sinus associated Tachycardia, accessory Escape Rhythms, pathways, VT, VF Acc. Junctional or Ventricular rhythms

3 4

Types of Wide Complex Wide Complex Tachycardia's Tachycardias

 Intraventricular Blocks: RBBB, LBBB, Hemiblocks, Non-  Definition of WCT : heart rhythms >100 bpm with a specific IVCDs QRS duration of > 0.12 sec

 May be supraventricular (SVT) with an Aberrancy (i.e., with BBB/ Accessory Pathways) or ventricular  Aberrant Ventricular Conduction: Ashman’s (VT, VF) in origin Phenomenon, Re-entry Tachycardias, WPW  Aberrancy: refers to alteration of impulse conduction from a normal pathway characterized  Ventricular Arrhythmias: , by alteration of QRS configuration Ventricular

5 6

1 Causes of WCTs Sudden Cardiac Death

 Known CVD with history of Myocardial Infarctions, CHF, HTN,(LV Hypertrophy) and Valvular Disease

 Thyroid Disease

 Hypoxemia

 Drug Toxicity (including Antiarrhythmic agents)

 Electrolyte Disturbances (Hyperkalemia, Hypermagnesemia)

 Excessive ETOH, Caffeine or Cocaine

 Exercise or Anxiety Induced

 Pacemaker-generated

2017 AHA/ACC/HRS Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. (2018). Circulation. Volume 138, Issue 13, Pages e272-e391 7 8

Assessment of a WCT Must Begin Physical Findings in with the Patient-Not the ECG Wide Complex Tachycardias

 Hemodynamic Stability (ABC Assessment is Critical). Is there End Organ Perfusion (Hypotension, Confusion, ?)  Diaphoretic

 Focused History 

 Patients with CAD are 4x more likely to have VT than SVT  Hypotension

 Previous Arrhythmias ? But this does NOT Exclude Either VT or SVT  Pale, Ashen, or Cyanotic Coloring

 PMH: Thyroid Disease, Renal Disease, Electrolyte Disturbances  Changes in Levels of Consciousness

 Medication Reconciliation/ SH of ETOH or Cocaine Abuse  Jugular Cannon A waves present in VT

 Focused Physical Exam  Varying intensity of S1 in VT

 Irregular Cannon A waves may be visible  Vs. Constant intensity in SVT  Varying Intensity of the S1 heart sound

 Beat to Beat Variability in SBP

9 10

Normal AV Nodal & Ventricular The Conduction System Conduction System

11 12

2 Normal Ventricular Activation Cardiac Electrophysiology

13 14

Refractory Periods Long QT Interval

 Absolute: cell can not be excited  Relative: abnormally strong stimulus can excite the cell  Supernormal: a low intensity stimulus can excite the cell  Refractory periods are directly proportional to cycle length  Long cycles (slow HR)=long refractory period  Short cycles (fast HR)= short refractory period

15 16

AV Nodal and Ventricular Reentry Medications that Prolong QTI Pathways

Examples of QT Prolonging Medications*

Antiarrhythmic Medications Psychotropic Medications Antibiotics Others

Disopyramide Haloperidol Erythromycin Methadone

Procainamide (N- Phenothiazines Pentamidine Probucol acetylprocainamide)

Quinidine Citalopram Azithromycin Droperidol

Dofetilide Tricyclic Chloroquine Ondansetron

Dronedarone antidepressants Ciprofloxacin

Ibutilide Fluconazole Sotalol Levofloxacin Amiodarone† Moxifloxacin Clarithromycin Itraconazole Ketoconazole

17 18

3 AV Reentrant Tachycardia

 Most common paroxysmal SVT (60% of cases)  May be called PSVT or PAT  Usual reentry mode is for the impulse to go ante grade over the slow pathway and retrograde over the fast pathway  Ventricular rate is 160-200  QRS complex may be normal or wide(if BBB is present  P waves usually NOT evident (buried in QRS)  Usually begins and ends abruptly  Immediate termination with Carotid massage, Valsalva, IV Verapamil or Metoprolol

From: Edmonds, J. (1988). ECG STAT.

19 20

Aberrant Ventricular Conduction Abnormalities: AV Reentry Tachycardias Reentry Tachycardias

 Prerequisites: Longer refractory  An anatomic circuit Slowed with 2 pathways joined Conduction period by common tissue  The 2 pathways have different electrophysiological properties (slow vs. fast conduction)  A section within the circuit has a longer refractory period than the other pathway allowing a unidirectional block (allows impulse to remain active while some tissue has time to repolarize)

21 22

AVNRT

23 24

4 Remember the Leads Remember the ECG Axis

25 26

Conditions That Determine Aberrancy

 Length of the cycle (R-R interval) preceding the

 Degree of prematurity of the impulse (coupling interval) i.e. How early is the ectopic beat within a refractory period

 Speed of AV Conduction

 Recovery of excitability within the normal conduction system (full repolarization can occur)

27 28

Intraventricular Blocks: SVT with SVT with Right Bundle Right Branch Block

 Right BBB pattern occurs when RBB is  ECG Characteristics of RBBB: blocked losing the  Wide QRS (> 0.12 sec) simultaneous depolarization of the  ventricles  rSR’ seen in V1, V2 or V3  Depolarization normally  Small q wave in lateral leads (I AVL, V5, V6) occurs from LV to RV  inversion in Anterior leads (V1-V4) but when RBB is blocked a small “r”  QRS with deep S waves in Lateral leads ( I aVL, V5,V6) appears in V1 as impulse travels away from + electrode

29 30

5 SVT with Right Bundle SVT with RBBB pattern Branch Block

 May be seen with or without pathology

 Seen pathologically in Anterior MI, Hypertensive Heart Disease, RVH

 Also associated with conditions of RV strain of Pulmonary etiology ( Pul. HTN, Pul. Embolism, COPD, or Congenital Left to Right shunting)

 Incomplete RBBB is an rSR’ < 0.10 sec

31 32

SVT with SVT with Left Bundle Branch Block

 Blockage of LBB causes the RV to depolarize first then  ECG Characteristics impulse moves cell to cell  S wave is negative in V1 to depolarize LV  R wave is positive in V6  The impulse is moving away  R waves are small with poor R wave progression (R’s do from Anterior precordial NOT get taller) in V1-V4 leads (V1-V4) toward V6  Inverted T waves in Lateral leads are common (I, aVL, V5, V6)  LBBB is frequently  No Q waves are seen associated with pathology i.e., CAD, Anterior MI, Aortic  rSR’ is seen in V5, V6 (First “r” is R to L depolarization of RV, then “s” is depolarization of septum and second “R” is or Disease depolarization across the LV) (Calcification of leaflets) or Idiopathic BB fibrosis

33 34

Aberrant Ventricular Conduction SVT with LBBB pattern Arrhythmias

 Definition of Aberrancy : an alteration of a normal impulse conduction from a normal pathway characterized by an alteration of ventricular morphology (a conduction defect of the QRS)  The Cause of Aberrancies: supraventricular impulses (either single or multiple) are propagated through the ventricles during a partial refractory phase  Ex: Reentry tachycardias, WPW, Ashman’s Phenomenon,

35 36

6 Aberrant AV Node & Ventricular AV Reentrant Tachycardia Reentry Circuitry

Drugs that Affect the Pathways  AV Reentry Tachycardias may be associated with an accessory pathway, either evident or concealed  Example of Evident (Manifested) Pathway is Wolf- Parkinson-White Syndrome  A Concealed accessory pathway allows retrograde conduction but NOT ante grade conduction  In a Concealed pathway, the impulse travels ante grade over the AV node and retrograde over the accessory pathway, therefore no delta wave  Characteristics of Concealed accessory pathway : narrow QRS, V rate is 190-250, regular rhythm, a negative P wave seen behind the QRS seen best in V1  May also be called a circus movement tachycardia (CMT) Aberrancies may occur anywhere along the conduction pathways.

37 38

Aberrant Ventricular Conduction Wolf-Parkinson-White Abnormalities: Wolf-Parkinson-White Syndrome Syndrome

 Definition: a wide complex tachycardia caused by  an accessory pathway conducting an electrical Characteristics during Normal Sinus Rhythm: impulse from the atria directly to the ,  Short PR interval < 0.10 secs bypassing the AV node  Occurs because the dissection of transcardiac  Slurred upstroke delta wave atrial/ventricle threads fail to dissect by the AV ring  during embryonic development ProlongedThis QRS Photo by Unknown Author is licensed under CC BY- SA-NC  May be benign with only intermittent tachycardia  QRS may be a fusion beat occurrences

39 40

Wolf-Parkinson-White Syndrome WPW

 Characteristics During Tachycardia:  Initiated by a PAC or PVC  Heart Rate ranges between 220-250 bpm  Rhythm is regular  Electrical Alternans ( alternating QRS amplitudes) is common  Usually involves a manifested accessory pathway that conducts ante grade or retrograde during a tachyarrhythmia

41 42

7 Aberrant Ventricular Conduction Abnormalities: Ashman’s Ashman’s Phenomenon Phenomenon

 The occurrence of  Diagnostic Criteria  Definition: occurrence of SVT with aberrancy aberrant ventricular following a long cycle (slow HR) then short cycle  When an aberrant conduction seen ventricular conduction (fast HR) due to the HR change during refractory following a long occurs following a long period within the IVC system ventricular cycle (R-R) ventricular cycle  Characteristics: Usually RBBB morphology following preceding the a slow HR w/o compensatory pause “coupling” of a bizarre  When Atrial or Junction beat to the normal beat bigeminy shows  May be seen in Atrial fib/flutter, Repetitive Atrial of the basic rhythm aberrant ventricular Tachycardia, or with Block conduction when the premature beat follows a long ventricular cycle

43 44

Ashman’s Phenomenon Ashman’s Phenomenon

45 46

Ashman’s Phenomenon Ashman’s Phenomenon

From: Chung, E. (1989) Principles of Cardiac Arrhythmias

47 48

8 Aberrancy Vs. Ventricular Ventricular Tachycardia: Tachycardia Definition

 Mechanisms of Aberrancies:  Premature Excitation Cardiac of ≥3 consecutive complexes originating in during Phase 3 of the the ventricles at a rate >100 bpm (cycle length: <600 ms). Types Action Potential (Early Repolarization) of VT: Sustained: VT >30 s or requiring termination due to  Causes Activation of Conduction System (i.e., hemodynamic compromise in <30 s. Early Depolarization ) Nonsustained/unsustained: ≥3 beats, terminating  Timing of depolarization spontaneously. and the state of refractoriness determines Monomorphic: Stable single QRS morphology from beat to what happens next beat.  If a ventricular Polymorphic: Changing or multiform QRS morphology from beat depolarization occurs during late repolarization to beat. (R on T) we get VT not Bidirectional: VT with a beat-to-eat alternation in the QRS frontal aberrancy plane axis, often seen in the setting of digitalis toxicity or catecholaminergic polymorphic VT Monomorphic VT

49 50

Ventricular Tachycardia Torsades de Pointe

Torsades de pointes is polymorphic VT that occurs in the setting of a long QT Monomorphic VT interval and is characterized by a waxing and waning QRS amplitude. The twisting of the points, although characteristic, may not always be seen, especially if the episode is nonsustained or if only a limited number of leads are available. can result from including high-grade AV block that leads to a long-short sequence initiating torsades de pointes.

Polymorphic VT

Bidirectional VT

51 52

Steps to Analyze Wide Complex Tachycardias

 Rapid, grossly irregular electrical activity with marked variability 1) Are there p waves? If not, maybe VT in electrocardiographic waveform, ventricular rate usually >300  2) Any AV dissociation present? If yes=VT bpm (cycle length: <200 ms).  3) What is the Axis? If indeterminate= VT  If Left or Right Axis = SVT  4) Is there concordance present in V1-V6?= VT  5) Look at V1 and V6 morphology

53 54

9 AV Dissociation Dissociation = Disconnected

 AV Dissociation is the independent beating of the atria and ventricles due to depolarization of different sites within the atria and ventricles.

 AV Dissociation is secondary to some other disorder ( It is an effect- not the cause)

 P waves are unrelated to QRS complex

 Results in loss of atrial kick and slower ventricular rates

55 56

AV Dissociation Precordial Concordance

•Precordial concordance, also known as QRS concordance is when all precordial leads (V1-V6) on an electrocardiogram are either positive (positive concordance) or negative (negative concordance).

They must ALL be MONOMORPHIC and ON THE SAME SIDE OF THE BASELINE! If not, THERE IS NO CONCORDANCE! Jerry W. Jones, MD FACEP FAAEM July 8, 2019. Precordial Concordance in VT 57 58

Morphology Differentiation of Wellens’ Criteria for VT Wide Complex Tachycardias V1-2 V6

VT  1) If AV Dissociation is present

Notch  2) If is present Nadir  3) Presence of Capture or Fusion Beats ( a hybrid of atrial and ventricular activation)

>0.06 sec Any Q wave  4) QRS of generally greater than 140 msec (0.14 sec)  5) Precordial QRS Concordance SVT Narrow R  6) rSR1 in V1, mono-or biphasic QRS in V1 or monophasic QS in V6 Quick, sharp down stroke No Q wave

LBBB Aberration

59 60

10 Kindwall’s ECG Criteria for VT in LBBB Brugada Criteria for VT

Criteria:  R wave in V1 or V2 > 30 ms duration Type I: coved ST-segment elevation with J-wave amplitude or ST-  Any Q wave in V6 segment elevation of > mm or 0.2 mV at its peak, followed by a negative T wave with little or no isoelectric separation  Duration of > 60 ms from the onset of the QRS to the nadir of the S wave in V1 or V2 Type II: Saddle-back type ST-segment elevation with J-wave  Notching on the downstroke of the S wave in V1 or amplitude of > 2mm with descending ST elevation of > 1 mm followed V2 by a positive or biphasic T wave

Type III: Right precordial ST-segment elevation with either or both configurations

61 62

Brugada Syndrome

 An inherited arrhythmic disorder whereby pathogenic mutations of multiple genes that regulate the cardiac sodium, potassium and calcium channels resulting in VT

 Responsible for Sudden Cardiac Deaths in patients without

 Most common cause of arrhythmic deaths in individuals < 40 years of age

 More prevalent in Asian and European descents

 First described in 1992 by Josep Brugada, M.D., Ph,D

63 64

Brugada Criteria for VT

Brugada Syndrome R-wave to Peak Time ≥ Configurations 50ms in lead II strongly suggests VT

ECG Pedia. org

65 66

11 Brugada Syndrome: Treatment Recommendations

 In patients with Brugada Syndrome Type I pattern and , sustained VA, or recent history or syncope suspicious for VA, and meaningful survival of > 1year, an ICD is recommended.

 If the patient has recurrent shocks from the ICD, intensify medical antiarrhythmic or VT ablation is recommended.

 Family members of patients with Brugada Syndrome should have genetic testing and counseling.

2017 AHA/ACC/HRS Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. (2018). Circulation. Volume 138, Issue 13, Pages e272-e391

67 68

2017 AHA/ACC/HRS Guidelines For Bi Ventricular Pacer & ICD Management of Ventricular Arrhythmias (VA)

 1) In patients with sporadic symptoms including syncope, suspected to be VA, implanted cardiac monitors may be useful.  2) The use of imaging i.e., CT angiogram or Echo are useful to identify structural heart disease  3) In patients with long QT interval (i.e., QTc > 470 ms) a beta blocker is recommended. If beta blockers are not tolerated or ineffective, left cardiac sympathetic denervation or ICD should be considered.  4) Other specific guidelines are available for patients with ICM, HOCM, Ischemic Heart Disease, NICM, Arrhythmogenic RV , , Sarcoidosis, HFrEF, and LVADs.

69 70

71 72

12 73 74

Aberrancy Vs. VT Summary

ACC Algorithm  QRS < .14 ms  QRS > .14 ms for  “Rabbit Ears” may be  Precordial Concordancy Differentiating present SVT vs. VT  Indeterminate Axis  Check for ectopic beats  Fusion Beats are Common prior to tachycardia (PVC or PAC)  AV Dissociation may be seen  Look at QRS Morphology  Look at QRS Morphology  Responds to Adenosine  Rarely responds to Adenosine

75 76

Pharmacological Management of Ventricular Arrhythmias

77 78

13 Anti Arrhythmic Mechanism of Action

79 80

81 82

Subcutaneous ICD

83 84

14 85 86

References THANK YOU !!!! Thank You !

 2017 AHA/ACC/HRS Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. (2018). Circulation. Volume 138, Issue 13, Pages e272-e391

 Mizusava Y., Arthur, A.M., and Wilde, M.D., (2012). Brugada Syndrome. Circ Arrhythma Electrophysiol. 5. 606-616.

 Verckei, A., Duray, G., Szenasi G. et al. (2007). Application of a new algorithm in the differential diagnosis of Wide QRS Complex tachycardia. Eur Heart J. Mar 28 (5) 589-600.

 Garner, J.B., Miller, J.M. (2013). Wide Complex Tachycardia- VT or Not VT, That Remains the Question. Arrhythmia & Electrophysiology Review. 2 (1). 23-29.

87 88

Ventricular Tachycardia Ventricular Tachycardia

89 90

15 Sustained VT Torsades de Pointes

91 92

Practice Strips: SVT with Aberrancy Aberrant SVT or VT ? or VT?

93 94

Aberrant SVT or VT ? SVT or VT ?

95 96

16 SVT or VT?

This Photo by Unknown Author is licensed under CC BY-SA-NC 97 98

SVT w/Aberrancy or VT

This Photo by Unknown Author is licensed under CC BY-NC This Photo by Unknown Author is licensed under CC BY-SA

99 100

SVT with Right BBB

This Photo by Unknown Author is licensed under CC BY-NC

This Photo by Unknown Author is licensed under CC BY-SA-NC

101 102

17 Sinus Rhythm with LPFB SVT with Left BBB (Hemi block)

103 104

AV Node Reentrant Aberrant SVT or VT or Neither? Tachycardia

105 106

Intraventricular Blocks: Fascicular Blocks SVT w/Aberrancy Vs. VT (Hemi blocks)

 Anatomy: The LBB divides into an Anterior and Posterior Fascicule  Must determine Axis to differentiate  Bi-fasicular Blocks include 2 fascicles: RBB plus either a LPFB or LAFB  May be chronic or acute

107 108

18 Left Anterior Fascicular Block Left Anterior Fascicular Block

 Characteristics:  Left Axis Deviation  qR in Lead I  rS in Leads II, III, aVF

 May be pathological or not. May be transient  Seen in CAD, s/p CABG or Cardiomyopathy  Rarely requires intervention if no pathology found

109 110

Left Anterior Fascicular Block Left Anterior Fascicular Block (Hemi block)

This Photo by Unknown Author is licensed under CC BY-NC-ND

111 112

Left Posterior Fascicular Block Left Posterior Fascicular Block

 Characteristics:  Right Axis Deviation  rS in Lead I  qR in Leads II, III, aVF  Normal QRS width  Pathology is usually present  If LPFB is present with RBBB during Acute MI then CAD is severe and Mortality is high

This Photo by Unknown Author is licensed under CC BY-SA-NC

This Photo by Unknown Author is licensed under CC BY-NC-ND

113 114

19 Left Posterior Fascicular Block Trifasicular Block

 Definition: block pattern involving 3 fascicles

 LBBB + any AV Block

 RBBB + LPFB + any AV Block

 RBBB + LAFB + any AV Block

 When a block occurs in 3 fascicles (RBBB + LAFB + LAFB = Complete ) a pacemaker is required

This Photo by Unknown Author is licensed under CC BY-NC-ND

115 116

117 118

20