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Wide Complex Tachycardias & Aberrancies

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WIDE COMPLEX TACHYCARDIAS & 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 Tachycardia (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 Arrhythmias: 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: Ventricular tachycardia, by alteration of QRS configuration Ventricular fibrillation 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, Angina?) Diaphoretic Focused History Palpitations 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 heart sounds 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 ectopic beat 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 Bundle Branch Block 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 Right Axis Deviation 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 T wave 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 Left Bundle Branch Block 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 Mitral Valve 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 ventricle, 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
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