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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 Some atrial tachycardias Automatic Monomorphic, Polymorphic (non-torsade) 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 Ventricle LV 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 Triggered Torsade de pointe Monomorphic Polymorphic Polymorphic long QT on baseline EKG Automatic Accelerated Idioventricular تشخیص تاکی کاردی WQRST 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) Fusion beat Ectopic ventricular activation Sinus Normal acceleration 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 A fib and flutter: PR short P wave hidden in QRS, inverted 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? AV Dissociation SA Node ATRIA AND VENTRICLES ACT INDEPENDENTLY Ventricular Focus Ventricular Tachycardia (VT) V1 • Rates range from 100-250 beats/min • Non-sustained or sustained • P waves often dissociated (as seen here) 3- Regularity in tachycardia Regular Regularly irregular VT, Sinus, PSVT, flutter, 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 :چند تمرین 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. > 0.10 sec? 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 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. مرور تاکی کاردی 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: Mg, 2g over 30-60 sec, max 6g Serum K > 4.5 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 Atrial Flutter Irregularly irregular 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 PSVT with aberrancy [intranodal or bypass tract (orthodromic)] PSVT due to antidromic reciprocating tachycardia Atrial Flutter with aberrancy Regularly irregular Most common 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 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 AND 1. 2. 2nd deg Mobitz type 2 block OR Alternating Left and Right BBB 3rd Degree Block (complete AV dissociation) 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