Approach to Arrhythmias Armed Forces Academy of Medical Sciences

When to Suspect an Arrhythmia Symptoms variable and depend on rate of ventricular response, overall condition of patient, presence of structural heart disease Palpitations (regular vs. irregular, onset/offset) Palpitations (regular vs. irregular, onset/offset) Chest pressure Chest pressure Dyspnea Dyspnea Lightheadedness, presyncope, syncope Lightheadedness, presyncope, syncopeTriggers Termination maneuvers: especially vagal

First Question Stable vs. Unstable Unstable: hypotensive, syncope, imminent death Unstable: hypotensive, syncope, imminent death Unstable: revert to ACLS algorithm Unstable: revert to ACLS algorithm DC Cardioversion Most likely ventricular arrhythmia Most likely ventricular arrhythmiaStable Symptoms but not life threatening Symptoms but not life threatening Differentiate wide complex from narrow complex Differentiate wide complex from narrow complex

Initial Evaluation of Stable Arrhythmias History Physical exam EKG (sinus rhythm, tachycardia) Twelve lead ECG with and without symptoms Twelve lead ECG with and without symptoms Narrow complex: likely a superventricular tachycardia (SVT) Narrow complex: likely a superventricular tachycardia (SVT) Wide complex Wide complex Ventricular arrhythmia SVT with aberrant conduction Echo if structural heart disease suspected

SVTs Any tachycardia requiring the atrium or the AVN for its perpetuation Common arrhythmia with an incidence of 2.5/1000 Twice as common in women Twice as common in women Three primary etiologies AVNRT (most common) AVNRT (most common) AVRT AVRT Atrial tachycardia (least common in absence of structural heart disease) Atrial tachycardia (least common in absence of structural heart disease) Rare: IST, SNRT, junctional tachycardia Rare: IST, SNRT, junctional tachycardia

SVTs Continued Can present at any age, first symptoms occur from 12 to 30 years AVNRT: middle to older age AVNRT: middle to older age AVRT: adolescence AVRT: adolescence Usually occurs in absence of structural heart disease Exceptions: Ebstein’s anomaly, familial preexcitation with hypertrophy, atrial tachycardia Exceptions: Ebstein’s anomaly, familial preexcitation with hypertrophy, atrial tachycardia

Classification of SVTs AV node dependent vs. independent AT: independent AT: independent AVNRT, AVRT: dependent AVNRT, AVRT: dependent Short RP vs. Long RP Short RP (RP<PR): typical AVNRT, AVRT Short RP (RP<PR): typical AVNRT, AVRT Long RP (PR<RP): AT, atypical AVNRT, rare forms of AVRT Long RP (PR<RP): AT, atypical AVNRT, rare forms of AVRT Regular vs. irregular Regular: AVNRT, AVRT, AT, AFL Regular: AVNRT, AVRT, AT, AFL Irregular: AF, AT, AFL Irregular: AF, AT, AFL

no p-wave - AV node reentry AVRT AVNRT Paroxysmal Supraventricular Tachycardias: Short RP vs. Long RP RP < PR - AV node reentry - AV reentry using an accessory pathway RP > PR - Atrial tachycardia - AV reentry using a decremental AP ex. PJRT - AV node reentry - atypical/uncommon form AT

Differential Diagnosis of NCT

AVNRT Most common form of Paroxysmal SVT 50-60% of regular, narrow complex tachycardias 50-60% of regular, narrow complex tachycardias Usual rate: bpm Usual rate: bpm Prototypic patient: young to middle age, healthy female with no Structural Heart Disease Palpitations with sudden onset/offset, may be terminated by maneuvers that lead to AVN block Vagal maneuvers Vagal maneuvers Adenosine Adenosine

AVNRT Mechanism: Reentry Required substrate: dual AV nodal physiology At least 2 separate pathways provide input into the AVN At least 2 separate pathways provide input into the AVN Fast pathway: rapid conduction, slower recovery Slow pathway: slow conduction, rapid recovery Typical form: short RP P waves not seen due to simultaneous A and V activation P waves not seen due to simultaneous A and V activation P waves distort terminal QRS  pseudo r’ in v1, pseudo S waves in inferior leads P waves distort terminal QRS  pseudo r’ in v1, pseudo S waves in inferior leads

Reentry in AVNRT 3 prerequisites 2 anatomically or functionally distinct conduction pathways 2 anatomically or functionally distinct conduction pathways Unidirectional block in 1 pathway Unidirectional block in 1 pathway Slowed conduction down second pathway Slowed conduction down second pathway Sinus Rhythm A: slow B: fast PACReentry

42 yo female with sudden onset palpitations, no PMHx Typical AVNRT

AVNRT Acute Management Hemodynamically unstable Very rare with AVNRT Very rare with AVNRT Use ACLS algorithm Use ACLS algorithm Vagal Maneuvers Adenosine Hemodynamically stable 99% of all AVNRT cases 99% of all AVNRT cases Vagal maneuvers, adenosine, verapamil, diltiazem (Class 1) Vagal maneuvers, adenosine, verapamil, diltiazem (Class 1) BB, digoxin, amiodarone (Class 2b) BB, digoxin, amiodarone (Class 2b) * Digoxin may be ineffective because its pharmacologic effects can be overridden by enhanced sympathetic tone

AVNRT Chronic Management Determined by tolerance and frequency Well tolerated, spontaneous or easy termination Lifestyle modification, vagal maneuvers Lifestyle modification, vagal maneuvers More frequent or bothersome attacks Pharmacotherapy-prophylactic, overall efficacy 30-65% Pharmacotherapy-prophylactic, overall efficacy 30-65% Slow AVN conduction BB, verapamil, diltiazem, digoxin* BB, verapamil, diltiazem, digoxin* Antiarrhythmic agents: Class Ic (no SHD), III Daily therapy Daily therapy Pill-in-the-pocket (infrequent, prolonged, well-tolerated): flecainide, diltiazem + propranolol Pill-in-the-pocket (infrequent, prolonged, well-tolerated): flecainide, diltiazem + propranolol Frequent attacks despite prophylactic therapy Catheter ablation: slow pathway Catheter ablation: slow pathway 90-95% success, 1% risk of permanent AV block

AVRT Accounts for 30% of regular, NCTs More common in males More common in males Presents at younger age than AVNRT Presents at younger age than AVNRT Extranodal accessory pathway connects myocardium of atrium to ventricle May exhibit antegrade (orthodromic) and retrograde conduction (antidromic) Antegrade conduction results in delta wave on surface EKG Incidence is 0.1 to 0.3% in general population Incidence is 0.1 to 0.3% in general population Classified based on location along the TV or MV annulus Classified based on location along the TV or MV annulus Degree of preexcitation determined by relative conduction to ventricle over the AVN vs. AP Degree of preexcitation determined by relative conduction to ventricle over the AVN vs. AP Minimal preexcitation: latent

Preexcitation Pattern

Types of AVRT Antegrade / Orthodromic Retrograde / Antidromic

AVNRT Conduction down accessory pathway is usually rapid, nondecremental During tachycardia if action potential conducted down accessory pathway can have 1:1 conduction Atrial fibrillation or flutter could lead to ventricular tachycardia Atrial fibrillation or flutter could lead to ventricular tachycardia

18 year old male with palpitations

AV Reentry - retrograde accessory pathway conduction Sinus rhythm - antegrade accessory pathway conduction delta -wave pp

AVRT Acute Management Orthodromic (NCT)-same as AVNRT Antidromic (WCT)-goal: slow AP conduction Unless there is strong evidence supporting AVN dependence, adenosine, non-DHP CCB should be avoided Ventricular rate may increase in WCT due to AT or AFL with AP bystander conduction Ventricular rate may increase in WCT due to AT or AFL with AP bystander conduction AVN blocking agents ineffective in AP-AP tachycardias AVN blocking agents ineffective in AP-AP tachycardias Adenosine may produce AF with rapid ventricular rate Adenosine may produce AF with rapid ventricular rate Procainamide, ibutilide IV are agents of choice Pre-excited atrial fibrillation: slow AP conduction, convert AF Procainamide, ibutilide IV, DCCV if unstable

AVRT-Antidromic 25 yo with a long history of tachypalpitations

Unstable: DCCV IV: procainamide, ibutilide Avoid agents that slow AV nodal conduction EPS/RFA Preexcited Atrial Fibrillation

AVRT Chronic Management Management guided by presence of pre-excitation, arrhythmia tolerance Concealed AP: pharmacologic management same as for AVNRT Concealed AP: pharmacologic management same as for AVNRT Pharmacologic therapy AVN blocking agents AVN blocking agents Verapamil, diltiazem, digoxin contraindicated with manifest pre-excitation Slow AP conduction-Class 1c,III antiarrhythmics Slow AP conduction-Class 1c,III antiarrhythmics Catheter ablation: Class 1 for manifest preexcitation with symptoms, poorly tolerated AVRT with concealed AP 95% success, 5% recurrence (higher for right-sided and septal APs) 95% success, 5% recurrence (higher for right-sided and septal APs) Risk location dependent: AV block, perforation, embolism Risk location dependent: AV block, perforation, embolism Overall major complication rate should be <3% Overall major complication rate should be <3%

Focal Atrial Tachycardia Uncommon SVT in structurally normal hearts, common with SHD (atrial scarring) Clinical forms Incessant: tachycardia-induced cardiomyopathy Incessant: tachycardia-induced cardiomyopathy Paroxysmal Paroxysmal Nonsustained (very common on holters) Nonsustained (very common on holters) Mechanisms: triggered activity, enhanced automaticity, reentry (micro) Rapid spread of activation from focal site Rapid spread of activation from focal site Atrial rates 100 to 250bpm (rarely up to 300 bpm) Isoelectric baseline usually present between p waves Isoelectric baseline usually present between p waves Distinguishes focal AT from AFL AV blocks occurs AVN and ventricle are not required AVN and ventricle are not required PR/RP interval depend on AV nodal conduction properties Long RP tachycardia-most common Long RP tachycardia-most common P wave morphology depends on site of origin in atrium P wave often obscured by T wave P wave often obscured by T wave

62 year old female with occasional palpitations

RIV LSV LI V RSV LA A SVC IVC RAA AVL V1 Left atrium Right Atrium Lateral Left Atrium P Waves in Atrial Tachycardia Tang et al JACC 1995 Septal: narrow p wave Cranial: (+) in inferior leads Caudal: (-) in inferior leads

R inf PV L Sup PV L inf PV R sup PV LA A SVC IVC RA App X X Focal Atrial Tachycardia: Sites of Origin RA LA RA: 75-85% -Crista terminalis -TVA -CS os (7%) -RAA LA: 10-15% -MVA -PV ostia -LAA * can be generators for AF Other: 5-10% -PVs (deep) -SVC -IVC -Vein of Marshall -CS muscle

Atrial Tachycardia Acute Treatment Hemodynamically unstable (rare): DCCV Terminates microreentry, triggered activity Terminates microreentry, triggered activity Hemodynamically stable Response/efficacy depends on mechanism Response/efficacy depends on mechanism Adenosine (2a) Termination: triggered activity Termination: triggered activity Persistence with AV block: microreentry Persistence with AV block: microreentry Transient atrial slowing: automaticity Transient atrial slowing: automaticity IV beta-blockers, CCB Termination (2a) Termination (2a) Rate control through AV block (1) Rate control through AV block (1) Second line: Ia, Ic, III AAD (2a) for direct suppression

AT Focal Atrial Tachycardia: Chronic Management Pharmacologic Beta-blockers CCBs Class Ia, Ic, or III antiarrhythmic drugs Catheter Ablation: Efficacy: 80%-85% acute Drug refractory or incessant -tachycardia-induced CMP Problems: Inability to induce tachycardia Multiple tachycardias (10%) Nonsustained tachycardia Recurrence (8-10%)

Focal Atrial Tachycardia Middle-aged women with palpitations

Multifocal Atrial Tachycardia

Differential Diagnosis of Wide-Complex Tachycardia VT SVT with aberrancy (atrial fibrillation/flutter) Antidromic AV reentry via WPW accessory pathway Atrial fibrillation, atrial flutter, atrial tachycardia, or AV nodal reentry in setting of WPW with rapid conduction down accessory pathway Bundle branch reentry

Key ECG Signs Atrial activity Width of QRS QRS Axis QRS Configuration

Identifying Atrial Activity P wave morphology relationship between P and QRS Capture beats Capture beats AV Dissociation a Hallmark, yet VA conduction may be present Physical Exam- JVP, S1, SBP, Response to carotid sinus message

QRS Width QRS width Site of origin- lateral wall vs. near septum Site of origin- lateral wall vs. near septum Scar tissue, LVH, HCM Scar tissue, LVH, HCM >140ms in RBBB, >160ms LBBB; likely VT >140ms in RBBB, >160ms LBBB; likely VT Septal origin may be narrower VT likely if width narrower than with sinus rhythm VT likely if width narrower than with sinus rhythm Wellens. Heart 2001;86:

QRS Axis Assists in differentiation, localization and assessing etiology Inferior Axis- Basal origin Inferior Axis- Basal origin Superior Axis- Apical origin Superior Axis- Apical origin Wellens et al. (Am J Med 1978)- RBBB with superior axis strongly suggests VT Wellens et al. (Am J Med 1978)- RBBB with superior axis strongly suggests VT LBBB with inferior axis argues for RVOT tachycardia LBBB with inferior axis argues for RVOT tachycardia Wellens. Heart 2001;86:

QRS Configuration Capture and Fusion Beats Leads V1 and V6 QRS intervals Concordance QR complexes

Capture and Fusion Beats Capture Fusion Wellens. Heart 2001;86:

A-V Dissociation, Fusion, and Capture Beats in VT Fisch C. Electrocardiography of Arrhythmias. 1990;134. ECTOPYFUSIONCAPTURE V1 EFC

Concordanc e Precodial leads share the same axis positive or negative positive or negative Wellens. Heart 2001;86:

Summary ECG Distinctions of VT from SVT with Aberrancy Favors VTFavors SVT with Aberrancy Favors VTFavors SVT with Aberrancy DurationRBBB:QRS > 0.14 sec sec.< 0.16 sec. AxisQRS axis -90° to ±180°Normal

Summary ECG Distinctions of VT from SVT with Aberrancy Favors VTFavors SVT with Aberrancy MorphologyPrecordial concordance If LBBB:R V 1 duration > 30 ms S wave > 70 ms S wave notched or slurred V 6 :qR or QRR wave monophasic If RBBB:V 1 :monophasic R wave qR If triphasic, R > R 1 R < R 1 V 6 :R < S

Additional Features Left axis deviation >-30 useful Right axis deviation >+90 w/ LBBB pattern R to S nadir >100ms in 1 or more precordial leads QR complexes