Narrow Complex Tachyarrhythmias PDF

Prof Sudip Ghosh MD, PhD, FESC, FRCS, FRCGP Consultant Physician, LPT Professor of Medicine Supraventricular (Narrow complex) Tachycardias Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle re...

Prof Sudip Ghosh MD, PhD, FESC, FRCS, FRCGP Consultant Physician, LPT Professor of Medicine Supraventricular (Narrow complex) Tachycardias Supraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region. SVT  Sinus Tachycardia and Sinus Node Reentry  Atrial flutter  Atrial Fibrillation  Atrial Tachycardia  AV nodal reentry tachycardia  AV reentry tachycardia - the WPW(Wolff-Parkinson White) Syndrome  EPIDEMIOLOGY  AF is the most common arrhythmia treated in clinical practice.  The most common arrhythmia for which patients are hospitalized;  Approximately 33% of arrhythmia-related hospitalizations are for AF.  MECHANISM Two electrophysiological mechanism of AF:  AUTOMATIC FOCUS{DRIVERS}: These focus discharge impulses at rapid rates which travel at rapid speed throughout atria causing to fibrillate.  MULTIPLE RE-ENTRANT CIRCUITS: These wander throughout the atria  The focal point remains the PULMONARY VEIN esp. in cases of paroxysmal AF. Thus isolation of pulmonary vein causes abolition of paroxysmal AF, than permanent AF. AF Atrial fibrillation  CAUSES  CARDIAC CAUSES: Hypertensive heart disease Ischemic heart disease Mitral valve disease Cardiomyopathies{ hypertropied/dilated} Severe pulmonary hypertension  NON CARDIAC CAUSES: ENDOCRINAL: Thyrotoxicosis,pheochromocytoma IATROGENIC: Ionotrophic drugs,post-operative OTHERS: obesity,excessive alcohol intake,obstructive sleep apnea. CLASSIFICATIONOF AF  PAROXYSMAL < 7 days  PERSISTANT >7 days  LONGLASTING >1 YR  PERMENANT - Cardioversion failed  LONE AF: usually seen in elderly persons{>60 years} who do not have hypertension or heart disease.  DIAGNOSTIC EVALUATION  History  Clinical features  Investigation History and physical examination  Presence and nature of symptoms associated with AF.  Clinical type of AF (first episode, paroxysmal, persistent, or permanent)  Onset of the first symptomatic attack or date of discovery of AF  Frequency, duration, precipitating factors, and modes of termination of AF  Response to any pharmacological agents that have been administered  Presence of any underlying heart disease or other reversible conditions (eg, hyperthyroidism or alcohol consumption)  CLINICAL FEATURES Clinical features of AF varies from being totally asymptomatic to being hemodynamic unstable,thus explaining the two end spectrum of it.  ASYMPTOMATIC AF: 25% of patients with AF are asymptomatic, more commonly elderly patients and patients with persistent AF.  SYMPTOMATIC AF: palpitations fatigue dyspnea effort intolerance lightheadedness Post palpatory-Polyuria{ANP induced} Types  Acute  Chronic > 1 month  Persistent  Paroxysmal  Risk is the same for embolism though smaller with Paroxysmal Investigations-Electrocardiogram  Rhythm (verify AF)  LV hypertrophy  P-wave duration and morphology or fibrillatory waves  Pre-excitation  Bundle-branch block  Prior MI  Other atrial arrhythmias  To measure and follow the R-R, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy Transthoracic echocardiogram  Valvular heart disease  LA and RA size  LV size and function  Peak RV pressure (pulmonary hypertension)  LV hypertrophy  LA thrombus (low sensitivity)  Pericardial disease  Blood tests of thyroid, renal, and hepatic function.  Holter monitoring or event recording.  Transesophageal echocardiography.  Chest radiograph.  All patients with AF (paroxysmal, persistent or permanent), should be stratified using a predictive index for stroke (e.g. CHADS2) and for the risk of bleeding (e.g. HAS-BLED), and that most patients should receive antithrombotic therapy. CHADS2 Score Risk Factor Score CHF 1 Hypertension 1 Age > 75 years 1 Diabetes 1 Stroke/TIA 2 CHADS2 Score and CVA Risk CHADS2 VASc Score Risk Factor Score CHF 1 Hypertension 1 Age > 75 1 Diabetes 1 Stroke/TIA 2 Vascular disease 1 (MI,PVD) Age 65-74 1 Sex Category Female 1 CHADS2 VASc Stroke Rate Predicting Bleeding Risk HAS-BLED Score Hypertension (>160 mmHg systolic 1 Abnormal Renal/Hepatic function 1-2 Stroke 1 Bleeding history or anemia 1 Labile INR (TTR < 60%) 1 Elderly (age > 75 years) 1 Drugs/Alcohol (antiplatelet/NSAIDs) 1-2 High Risk (>4%/year) >4 Moderate Risk (2-4%/year) 2-3 Low Risk (30 CHADS2VASC ≥ 1 or Warfarin – target INR 2.5 mitral stenosis Warfarin – target INR 2.5 Prosthetic valve Warfarin – target INR 3.0 INR Warfarin vs DOAC  When OAC therapy is indicated, DOAC in preference to warfarin. 4 in the UK market – Edoxaban, Rivaroxaban, Dabigatran and Apxiban RR = 0.91, P65 yrs taking diuretics RATE VS RHYTHM Favors Rate Control Favors Rhythm Control Persistent AF Paroxysmal AF Newly Detected AF Less Symptomatic More Symptomatic >65 years of age < 65 years of age Hypertension No Hypertension No History of Congestive Congestive Heart Failure Heart Failure clearly exacerbated by AF Previous Antiarrhythmic No Previous Antiarrhythmic Drug Failure Drug Failure AFFIRM Rhythm Control of AF  Strategy of rhythm control has never been shown to reduce mortality compared to rate control (AFFIRM, RACE, PIAF trials, AF CHF)  Therefore, goals of rhythm control should focus on improving quality of life  Rhythm control does not necessitate elimination of all AF AF – Burden (Ablation)  Patients with AF or AFL who remain symptomatic with rate control therapy.  Improvement in patient symptoms and clinical outcomes, and not necessarily the elimination of all AF.  Maintenance oral antiarrhythmic therapy as first- line therapy for patients with recurrent AF in whom long-term rhythm control is desired  If AF burden >10% -- referral for ablation is justified Atrial Flutter AFL  Atrial flutter is generally used to describe atrial arrhythmias with large reentrant circuits.  Atrial rate is usually 240 to 340 beats/min. TYPES  Typical atrial flutter reentrant rhythm in the right atrium constrained anteriorly by the tricuspid annulus and posteriorly by the crista terminalis and eustachian ridge.  The flutter can circulate in a counterclockwise direction around the tricuspid annulus in the frontal plane (typical flutter, counterclockwise flutter).  Clockwise direction (atypical, clockwise, or reverse flutter). CAUSES OF AFL  COPD  Atrial dilation from septal defects  Pulmonary emboli  Mitral or tricuspid valve stenosis or regurgitation  Chronic ventricular failure  Prior extensive atrial ablation  Aging  Toxic and metabolic - thyrotoxicosis, alcoholism, and pericarditis  Surgical repair for congenital heart disease. counterclockwise CARDIOVERSION  Cardioversion - the initial treatment of choice.  DC -- 50 J. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore sinus rhythm.  Ibutilide - IV. successfully cardiovert- 60% to 90%. prolongs the QT interval, torsades de pointes  Other medications- procainamide Ablation  Highly effective for typical flutter  Stable patients who do not require immediate cardioversion.  Success rate of 90% to 100% Anticoagulation  Indications for anticoagulation in patients with atrial flutter are similar to those with atrial fibrillation AT  Rapid (usually PR AV reentrant (Example slower than more common rate SVT 150-250 beats per min) AT Treatment of AT  Catheter ablation is the primary therapy regardless of the underlying mechanism.  Antiarrhythmic drug choices are similar to that in AF MAT  Multifocal Atrial Tachycardia  Multifocal Atrial Tachycardia (MAT) ECG Characteristics: Discrete P waves with at least 3different morphologies. Absence of one dominant atrial pacemaker Atrial rate > 100 bpm. The PP, PR, and RR intervals all vary. MAT  Signature tachycardia of patients with significant pulmonary disease.  The atrial rhythm is characterized by at least three distinct P- wave morphologies and often at least three different PR intervals.  Atrial and ventricular rates are typically between 100 and 150 beats per minute.  The presence of an isoelectric baseline distinguishes this arrhythmia from AF.  The absence of any intervening sinus rhythm distinguishes MAT from normal sinus rhythm with frequent multifocal APCs. TREATMENT  Correction of the underlying pulmonary problem.  Cardioversion is ineffective.  Calcium channel blockers- limited success.  In selected patients, -blockers may have a role- use is limited by bronchospasm. Sinus tachycardia  Heart rate faster than 100 beats/min that is caused by rapid impulse formation from the sinoatrial node.  It occurs with fever, exercise, emotion, pain, anemia, heart failure, shock, thyrotoxicosis, or in response to many drugs AVNRT  Patients may be asymptomatic except for awareness of rapid heart action, but some experience mild chest pain or shortness of breath. AV NODAL REENTRANT TACHYCARDIA AVNRT  Presence of a narrow complex tachycardia with regular R-R intervals and no visible p waves.  P waves are retrograde and are inverted in leads II,III,avf.  P waves are buried in the QRS complexes –simultaneous activation of atria and ventricles – most common presentation of AVNRT –66%.  If not synchronous –pseudo s wave in inferior leads ,pseudo r’ wave in lead V1---30% cases.  P wave may be farther away from QRS complex distorting the ST segment ---AVNRT ,mostly AVRT. Vagotonic Maneuvers  Carotid sinus massage  Valsalva maneuver (bearing down)  Facial ice pack.  Mueller maneuvers, gagging. Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes  Termination of SVT by Vagotonic Maneuver (Carotid Sinus Massage) Treatment: Many episodes of Supraventricular Tachycardia (SVT) soon stop and no treatment Is needed. If an episode of SVT does last a long time > 1hr or is severe (symptomatic) admit to a hospital to stop it (this is what the books tell you) IV Adenosine is commonly used – 6mg, 3min 12mg and 3 min 12mg Adenosine works by blocking electrical impulses of the heart at the AV node. Verapamil is an alternative if adenosine is not advised. [People with asthma cannot have adenosine] – start with 5mg IV push; wait 10min 10mg IV Electric Shock treatment is rarely needed to stop an episode of SVT. Prevention  Drugs that slow conduction in the antegrade slow pathway, such as digitalis, beta blockers, and calcium channel blockers.  History of exercise-precipitated AVNRT, the use of beta blockers.  Patients who do not respond to drug therapy directed at the antegrade slow pathway, treatment with class IA or IC agents directed at altering conduction of the fast pathway may be considered. Pill in the pocket approach  In whom recurrences are infrequent.  But sustained.well tolerated hemodynamically.  Patients who have had only a single episode of SVT..  100-200mg of flecainide at the onset of SVT is a reasonable approach…until he reaches the hospital.  40-160 mg verapamil –without preexcitation,  Betablockers  Propafenone 150-450 mg.  80% cases interrupted with a combination of CCBand BB in 2 hrs… Catheter ablation  Directed at elimination or modification of slow pathway conduction, is very effective in permanently eliminating AVNRT.  Patients with recurrent AVNRT that produces significant symptoms or heart rates >200 beats/min and patients reluctant to take chronic drug therapy should be considered for ablative therapy.  Cure >95% of patients Catheter Ablation of Cardiac Arrhythmias. CLINICAL FEATURES  Preexcitation occurs in the general population at a frequency of around 1.5 per 1000.  Of these, 50% to 60% of patients become symptomatic.  Symptoms range from palpitations to syncope.  Episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope. AV REENTRANT TACHYCARDIA WPW syndrome  Two types Orthodromic Antidromic  Antidromic is wide complex tachycardia  In NSR detected by delta wave.  Can ppt into AF and VF on use of AV nodal blockers  CONCEALED WPW syndrome – no delta wave.less risk of AF Manifest vs Concealed  Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-White Sinus Syndrome) Hybrid beat “Delta” Wave QRS shape PR <.12 s AP Fusion activation QRS .12 s of the ventricles AVRT  Typical – RP interval < PR interval  RP interval > 80 milli sec  Atypical –RP interval > PR interval  Orthodromic AV Reentrant Tachycardia NSR with V Preex Note SVT: retrograde V Preex P waves gone in the ST segment Orthodromic AVRT Catheter Ablation of Accessory Pathways  Catheter ablation of APs is performed in conjunction with a diagnostic EPS.(TOC)  Success of catheter ablation in curing APs was 93%.  Asymptomatic RR cycle length < 220 ms, a short refractory period is present. These individuals are at highest risk for sudden death, and prophylactic ablation is indicated. Pharmacologic Therapy  Narrow-complex reentry rhythms involving a bypass tract can be managed as discussed for AVNRT.  AF and AFL with antegrade conduction- digoxin, calcium channel blockers, and even -blockers may decrease the refractoriness of the accessory pathway or increase that of the AV node, often leading to faster ventricular rates. Therefore, these agents should be avoided.  The class Ia(procainamide), class Ic(flecainide,propafenone), and class III antiarrhythmic agents will increase the refractoriness of the bypass tract and are the drugs of choice for wide-complex tachycardias involving accessory pathways.  If hemodynamic compromise is present, electrical cardioversion is warranted.  P wave present but not of same morphology as sinus rhythm Pseudo r’ Pseudo S Pwave wave in wave on lead II ST-T changes V1 Positive in Negative in AVNRT AVNRT inferior leads lead I AVRT AVRT Right posteroseptal Left sided accessory Accessory pathway pathway