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Ventricular Arrhythmia Dr Mostafa Hekmat Cardiologist Electrophysiologist VENTRICULAR TACHYCARDIA VT Arises Distal To The Bifurcation Of The HB In The Specialized Conduction System In The Ventricular Muscle Or In Combination Of Both Tissues Dr Mostafa Hekmat 2 Note Any wide QRS complex tachycardia should be treated as ventricular tachycardia until definitive evidence is found to establish another diagnosis Dr Mostafa Hekmat 3 Types of Ventricular Arrhythmia Premature Ventricular Complexes Ventricular Tachycardia Monomorphic Polymorphic Torsade de point Normal QT Ventricular Flutter Ventricular Fibrillation Dr Mostafa Hekmat 4 Ventricular Arrhythmias Definitions Premature Ventricular beats Single beats Ventricular Bigeminy, the appearance of one PVC after each sinus beat Couplets, two consecutive premature beats Triplets, three consecutive premature beats Salvos, runs of 3-10 premature beats Dr Mostafa Hekmat 5 Ventricular Arrhythmias Definitions Accelerated Idioventricular Rhythm (Slow VT), rate 60-100 bpm Ventricular Tachycardia (VT), rate over 100 bpm Ventricular Flutter, regular large oscillations at a rate of 150-300 bpm Ventricular Fibrillation (VF), irregular undulations of varying contour and amplitude Dr Mostafa Hekmat 6 PVC • • • • • Rate? Regularity? P waves? PR interval? QRS duration? 60 bpm Occasionally irreg. None for 7th QRS 0.14 s 0.08 s (7th wide) Interpretation? Sinus Rhythm with 7 1 PVC Dr Mostafa Hekmat VT • • • • • Rate? Regularity? P waves? PR interval? QRS duration? 160 bpm Regular None None Wide (> 0.12 sec) Interpretation? Ventricular Tachycardia 8 Dr Mostafa Hekmat VF • • • • • Rate? Regularity? P waves? PR interval? QRS duration? None Irregularly irreg. None None Wide, if recognizable Interpretation? Ventricular Fibrillation 9 Dr Mostafa Hekmat Premature Ventricular Complexes Premature occurrence of a QRS complex that is abnormal in shape Duration usually exceeding the dominant QRS complex Generally longer than 120 milliseconds The T wave is usually large and opposite in direction to the major deflection of the QRS A fully compensatory pause usually follows a PVC The PVC may not produce any pause and may therefore be interpolated Dr Mostafa Hekmat 10 Dr Mostafa Hekmat 11 Ventricular fusion beat Dr Mostafa Hekmat 12 PVC and ventricular echo Dr Mostafa Hekmat 13 An interpolated PVC Dr Mostafa Hekmat 14 Ventricular Premature Complexes Compensatory Pause Dr Mostafa Hekmat Interpolated VPC 15 Premature Ventricular Complexes Bigeminy Pairs of complexes and indicates a normal and premature complex Trigeminy Premature complex that follows two normal beats Quadrigeminy Premature complex that follows three normal beats is called Dr Mostafa Hekmat 16 Multiform Dr Mostafa Hekmat 18 Salvos Dr Mostafa Hekmat 19 CLINICAL FEATURES The prevalence of premature complexes increases with age Male gender Hypokalemia PVCs are more frequent in the morning in patients after MI This circadian variation is absent in patients with severe left ventricular (LV) dysfunction. Dr Mostafa Hekmat 21 CLINICAL FEATURES Activity that increases the heart rate can decrease The patient’s awareness of the premature systoles Reduce their number. Sleep Usually associated with a decrease in the frequency of ventricular arrhythmias But some patients can experience an increase. Dr Mostafa Hekmat 22 The importance of PVCs Depends on the clinical setting In the absence of underlying heart disease, the presence of PVCs usually has no impact on longevity or limitation of activity Antiarrhythmic drugs are not indicated Patients should be reassured if they are symptomatic Dr Mostafa Hekmat 23 PVC and MI Those occurring close to the preceding T wave More than five or six per minute Bigeminal or multiform complexes Those occurring in salvoes of two or three or more Do not occur in about 50% of patients in whom VF develops And VF does not develop in about 50% of patients who have these PVCs Thus, these PVCs are not particularly helpful prognostically Dr Mostafa Hekmat 24 Idioventricular Rhythm Dr Mostafa Hekmat 25 Accelerated idioventricular rhythm Dr Mostafa Hekmat 26 Dr Mostafa Hekmat 27 ECG Distinction of VT from SVT with Aberrancy Favors VT Favors SVT with Aberrancy Morphology Precordial concordance If LBBB: If RBBB: V1 duration > 30 ms S wave > 70 ms S wave notched or slurred V6: qR or QR V1: V6: Dr Mostafa Hekmat monophasic R wave qR If triphasic, R > R1 R<S R wave monophasic R < R1 28 VENTRICULAR FLUTTER & VENTRICULAR FIBRILLATION Dr Mostafa Hekmat 29 A-V Dissociation, Fusion, and Capture Beats in VT V1 E F C CAPTURE ECTOPY Dr Mostafa Hekmat FUSION 30 Accelerated Idioventricular Rhythm The arrhythmia occurs as a rule in patients who have heart disease, such as those with acute myocardial infarction or with digitalis toxicity. Reperfusion of a previously occluded coronary artery During resuscitation It is transient and intermittent Episodes lasting a few seconds to a minute Does not appear to seriously affect the patient’s clinical course or the prognosis Dr Mostafa Hekmat 31 Therapy when Considered when AV dissociation results in loss of sequential AV contraction An accelerated idioventricular rhythm occurs together with a more rapid VT An accelerated idioventricular rhythm begins with a PVC discharging in the vulnerable period of the preceding T wave The ventricular rate is too rapid and produces symptoms VF develops as a result of the accelerated idioventricular rhythm. Dr Mostafa Hekmat 32 Therapy Increasing the sinus rate with Atropine or atrial pacing suppresses the accelerated idioventricular rhythm Dr Mostafa Hekmat 33 Dr Mostafa Hekmat 34 Clinical Impact of VT/VF PVCs and even runs of nonsustained VT may be frequently seen in people with normal and abnormal hearts Sustained VT and VF usually develop in patients with advanced structural heart disease Dr Mostafa Hekmat 35 Clinical Impact of VT/VF CAD is the most frequent cause of SCD and clinically documented VT and VF 80% There is no reason to neglect the device even if the stable VT has been successfully ablated Dr Mostafa Hekmat 37 VT + RBBB (1) the QRS complex is monophasic or biphasic in V1, with an initial deflection different from that of the sinus-initiated QRS complex (2) the amplitude of the R wave in V1 exceeds the R′ (3) a small R and large S wave or a QS pattern in V6 may be present. Dr Mostafa Hekmat 38 VT + LBBB (1) the axis can be rightward, with negative deflections deeper in V1 than in V6, (2) a broad prolonged (more than 40 milliseconds) R wave in V1 (3) a small Q–large R wave or QS pattern in V6 can exist Dr Mostafa Hekmat 39 VT QRS duration exceeding 140 milliseconds In precordial leads with an RS pattern, the duration of the onset of the R to the nadir of the S exceeding 100 Fusion beat Capture beat AV dissociation has long been considered a hallmark of VT Retrograde VA conduction to the atria from ventricular beats occurs in at least 25% of patients Dr Mostafa Hekmat 40 Supraventricular arrhythmia with aberrancy (1) consistent onset of the tachycardia with a premature P wave (2) very short RP interval (0.1 sec) (3) QRS configuration the same as that occurring from known supraventricular conduction at similar rates (4) P wave and QRS rate and rhythm linked to suggest that ventricular activation depends on atrial discharge (an AV Wenckebach block) (5) slowing or termination of the tachycardia by vagal maneuvers Dr Mostafa Hekmat 41 Dr Mostafa Hekmat 42 A QRS complex in V1 - V6, either all negative or all positive favors a VT The presence of a 2 : 1 VA block VT Positive QRS complex in V1 - V6 can also occur from conduction over a left-sided accessory pathway. Supraventricular beats with aberration Triphasic pattern in V1 An initial vector of the abnormal complex similar to that of the normally conducted beats Wide QRS complex with long-short cycle sequence Dr Mostafa Hekmat 43 Sustained Monomorphic VT Dr Mostafa Hekmat 44 Increased risk in VT Reduced LV function Spontaneous ventricular arrhythmias Late potentials on signal-averaged ECG QT interval dispersion T wave alternans Prolonged QRS duration Heart rate turbulence Inducible sustained VTs Dr Mostafa Hekmat 46 Treatment Dr Mostafa Hekmat 47 Treatment Frequent PVCs, even in the setting of an acute MI, need not be treated unless they directly contribute to hemodynamic compromise Dr Mostafa Hekmat 48 Treatment Beta blockers are often the first line of therapy. If they are ineffective, class IC drugs seem particularly successful in suppressing PVCs Flecainide and Moricizine have been shown to increase mortality in patients treated after MI Should be reserved for patients without coronary artery disease or LV dysfunction Amiodarone Should be reserved for highly symptomatic patients and those with structural heart disease. Dr Mostafa Hekmat 49 Treatment VT that precipitates Hypotension Shock Angina Congestive heart failure Symptoms of cerebral hypoperfusion Should be treated promptly with DC cardioversion Very low energies can terminate VT a synchronized shock of 10 to 50 J. Digitalis-induced VT is best treated pharmacologically. Dr Mostafa Hekmat 50 Thump Version Can terminate VT by mechanically inducing a PVC that presumably interrupts the reentrant pathway necessary to support it. Chest stimulation at the time of the vulnerable period Can accelerate the VT or Possibly provoke VF. Intermittent VT best treated pharmacologically Dr Mostafa Hekmat 51 Treatment In patients in whom procainamide Ineffective Procainamide may be problematic Severe heart failure Renal failure Intravenous Amiodarone is often effective Loading dose of 15 mg/min is given during a 10-minute period Infusion of 1 mg/min for 6 hours Maintenance dose of 0.5 mg/min for the remaining 18 hours and for the next several days Dr Mostafa Hekmat 52 Reversible conditions VT related to ischemia antianginal Hypotension vasopressors Hypokalemia potassium Correction of HF reduce the frequency of ventricular arrhythmias Sinus bradycardia or AV block PVCs and ventricular tachyarrhythmias, which can be corrected by administration Atropine Temporary isoproterenol administration Pacing Dr Mostafa Hekmat 53 Long-Term Therapy Asymptomatic nonsustained ventricular arrhythmias in low-risk populations (preserved LV function) often need not be treated. In patients with symptomatic nonsustained tachycardia, beta blockers are frequently effective in preventing recurrences. In patients refractory to beta blockers, class IC agents, Sotalol, or Amiodarone can be effective Dr Mostafa Hekmat 54 CLASSIFICATION OF IDIOPATHIC MONOMORPHIC VT Dr Mostafa Hekmat 55 RMVT Dr Mostafa Hekmat 56 Both Forms Are Characterized By Adenosine Sensitivity And Are Thought To Be Caused By Cyclic Amp Mediated Triggered Activity Dr Mostafa Hekmat 57 VT Can Be Terminated With Adenosine, Verapamil, The Valsalva Maneuver or CSP Dr Mostafa Hekmat 58 VERAPAMIL-SENSITIVE VT Dr Mostafa Hekmat 59 VERAPAMIL-SENSITIVE VT 90-95% HAS RBBB AND LEFT SUPERIOR-AXIS MORPHOLOGY THE REMAINDER OF PATIENTS HAVE VT WITH RBBB AND RIGHT INFERIORAXIS MORPHOLOGY RS INTERVAL IS USUALLY 60-80 ms (in VTs associated with structural heart disease RS is longer than 100 ms ) Dr Mostafa Hekmat 60 CPVT Inherited VT Children and adolescents Without any overt structural heart disease. Patients typically present with syncope or aborted sudden death Highly reproducible, stress-induced VT Bidirectional Mutations of the ryanodine receptor gene result in an autosomal dominant Mutations in the calsequestrin gene result in an autosomal recessive Dr Mostafa Hekmat 61 CPVT The treatment of choice is beta blockers and an ICD Sympathectomy Avoid Dr Mostafa Hekmat vigorous exercise 62 Dr Mostafa Hekmat 63 Dr Mostafa Hekmat 64 Long QT Syndrome Dr Mostafa Hekmat 66 Congenital LQTS The congenital LQTS is a rare disorder (incidence 1:10,000 to 1:15,000) characterized by Prolongation of the Q–T interval on the surface ECG Recurrent syncope Sudden death Dr Mostafa Hekmat 67 Congenital LQTS Romano-Ward syndrome Autosomal Only dominant inheritance Cardiac Arrhythmias Jervell and Lange-Nielson syndrome Autosomal recessive inheritance Cardiac Arrhythmias Congenital deafness. Andersen-Tawil syndrome Ventricular Arrhythmias Periodic paralysis & Facial/Skeletal dysmorphism 68 The acquired form of long-QT Quinidine Cisapride Procainamide Probucol N-acetylprocainamide Hypokalemia Sotalol Hypomagnesemia Amiodarone liquid protein diet Disopyramide Starvation Phenothiazines Tricyclic antidepressants central nervous system lesions Erythromycin Bradyarrhythmias Pentamidine cardiac ganglionitis mitral valve prolapse Dr Mostafa Hekmat 69 Dr Mostafa Hekmat 71 Dr Mostafa Hekmat 72 K or Na The principal abnormality in LQTS is prolongation of action potential duration caused by a reduction in outward potassium current (LQT1 and LQT2) or, less commonly, a persistent inward sodium current during the plateau phase (LQT3). Dr Mostafa Hekmat 73 Action potential prolongation development of early after depolarizations triggered action potential premature beat can initiate a polymorphic VT known as torsades de pointes, Which underlies the clinical symptoms of palpitations, syncope, or sudden death due to VF. Dr Mostafa Hekmat 74 Dr Mostafa Hekmat 75 Dr Mostafa Hekmat 76 Dr Mostafa Hekmat 77 Triggers of cardiac event 1 The classic description of events in LQTS involves exercise- or emotion-induced clinical events. Symptoms often begin in adolescence, though they may begin earlier in LQT1. Dr Mostafa Hekmat 78 Triggers of cardiac event 2 Adrenergic Stimuli in LQTS with Loss of function of K (iKsLQTS1 , iKr-LQTS2) TDP Adrenergic Stimuli Transmural disturbances Β Blocker are useful in LQTS1 & LQTS2 Dr Mostafa Hekmat 79 Dr Mostafa Hekmat 80 LQTS1 Rhythm disturbances mainly occur during sports especially swimming Dr Mostafa Hekmat 81 LQTS 2 Rhythm disturbances mainly triggered by Auditory stimuli Dr Mostafa Hekmat 82 LQTS 3 Malfunction of iNaL , Symptom mostly occur at rest or during night No adrenergic triggers B Blockers Contraindicated Dr Mostafa Hekmat 83 In 10% of patient SCD is the first & tragic symptom. LQTS1 and LQTS2 are more cardiac events Benign cardiac symptoms such as palpitation and syncope degenerate more easily to SCD in LQTS3 Dr Mostafa Hekmat 84 LQTS The hallmark of this condition is prolongation of the QTc greater than 460 ms, QTc may be normal in up to 1/3 of genotype-positive patients. Dr Mostafa Hekmat 85 LQTS Causes of considerable temporal variation in QTc Repolarization is affected by factors such as Sympathetic Electrolyte outflow balance Pharmacologic Dr Mostafa Hekmat agents 86 LQTS The mean QTc does not differ between the LQT1, LQT2, and LQT3 types But is significantly longer in Jervell and Lange-Neilson syndrome. Other electrocardiographic abnormalities that may be found in LQTS include ST–T wave changes U waves, T wave alternans Increased QT dispersion Sinus bradycardia Dr Mostafa Hekmat 87 MANAGEMENT For patients who have idiopathic longQT syndrome but not Syncope Complex Family QTc ventricular arrhythmias, history of sudden cardiac death longer than 500 milliseconds, No therapy or treatment with a beta blocker is generally recommended. Dr Mostafa Hekmat 89 MANAGEMENT In asymptomatic patients with Complex ventricular arrhythmias, Family history of early sudden cardiac death QTc longer than 500 milliseconds Beta adrenoceptor blockers at maximally tolerated doses are recommended. PPM to prevent the bradycardia or pauses that may predispose to the development of TDP may be indicated Dr Mostafa Hekmat 90 MANAGEMENT In patients with syncope caused by ventricular arrhythmias or aborted sudden death, an ICD is warranted. Concomitant beta blockers Overdrive atrial pacing (via the ICD) to minimize the frequency of ICD discharges Dr Mostafa Hekmat 91 MANAGEMENT Most competitive sports are contraindicated for patients with the congenital long-QT syndrome For patients with the acquired form and TDP, intravenous Mg and atrial or ventricular pacing are initial choices. Dr Mostafa Hekmat 92 Survival is dramatically improved by Aggressive treatment with βBlocker drugs Cardiac pacing Left cervical sympathectomy Implantable cardioverter defibrillator (ICD). Dr Mostafa Hekmat 93 Short QT Syndrome Definition QT of less than 350 milliseconds at rates of less than 100 beats/min Dr Mostafa Hekmat 95 Short-QT interval has recently been identified to carry an increased risk of sudden death due to VF One of the syndromes responsible for “idiopathic VF” Dr Mostafa Hekmat 96 Causes Hyperkalemia Hypercalcemia Hyperthermia Acidosis Digitalis Genetic Dr Mostafa Hekmat abnormalities 97 Treatment ICDs are considered the treatment of choice in symptomatic patients to prevent sudden cardiac death. Quinidine Dr Mostafa Hekmat 98 Dr Mostafa Hekmat 99
