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Approach to Arrhythmias

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) Chest pressure

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Approach to Arrhythmias

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  1. Approach to Arrhythmias Armed Forces Academy of Medical Sciences

  2. 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) • Chest pressure • Dyspnea • Lightheadedness, presyncope, syncope • Triggers • Termination maneuvers: especially vagal

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

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

  5. 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 • Three primary etiologies • AVNRT (most common) • AVRT • Atrial tachycardia (least common in absence of structural heart disease) • Rare: IST, SNRT, junctional tachycardia

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

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

  8. AT AVNRT 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 Paroxysmal Supraventricular Tachycardias: Short RP vs. Long RP no p-wave - AV node reentry AVRT

  9. Differential Diagnosis of NCT

  10. AVNRT • Most common form of Paroxysmal SVT • 50-60% of regular, narrow complex tachycardias • Usual rate: 150-250 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 • Adenosine

  11. AVNRT • Mechanism: Reentry • Required substrate: dual AV nodal physiology • 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 distort terminal QRS pseudo r’ in v1, pseudo S waves in inferior leads

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

  13. 42 yo female with sudden onset palpitations, no PMHx Typical AVNRT

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

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

  16. AVRT • Accounts for 30% of regular, NCTs • More common in males • 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 • Classified based on location along the TV or MV annulus • Degree of preexcitation determined by relative conduction to ventricle over the AVN vs. AP • Minimal preexcitation: latent

  17. Preexcitation Pattern

  18. Types of AVRT Antegrade / Orthodromic Retrograde / Antidromic

  19. 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

  20. 18 year old male with palpitations

  21. 18 year old male with palpitations

  22. AV Reentry - retrograde accessory pathway conduction Sinus rhythm - antegrade accessory pathway conduction delta -wave p p

  23. 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 • AVN blocking agents ineffective in AP-AP tachycardias • 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

  24. AVRT-Antidromic 25 yo with a long history of tachypalpitations

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

  26. AVRT Chronic Management • Management guided by presence of pre-excitation, arrhythmia tolerance • Concealed AP: pharmacologic management same as for AVNRT • Pharmacologic therapy • AVN blocking agents • Verapamil, diltiazem, digoxincontraindicated with manifest pre-excitation • 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) • Risk location dependent: AV block, perforation, embolism • Overall major complication rate should be <3%

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

  28. 62 year old female with occasional palpitations

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

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

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

  32. 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%) AT

  33. Focal Atrial Tachycardia Middle-aged women with palpitations

  34. Multifocal Atrial Tachycardia

  35. Differential Diagnosis ofWide-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

  36. Key ECG Signs • Atrial activity • Width of QRS • QRS Axis • QRS Configuration

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

  38. QRS Width • QRS width • Site of origin- lateral wall vs. near septum • Scar tissue, LVH, HCM • >140ms in RBBB, >160ms LBBB; likely VT • Septal origin may be narrower • VT likely if width narrower than with sinus rhythm Wellens. Heart 2001;86:579-585

  39. QRS Axis • Assists in differentiation, localization and assessing etiology • Inferior Axis- Basal origin • Superior Axis- Apical origin • Wellens et al. (Am J Med 1978)- RBBB with superior axis strongly suggests VT • LBBB with inferior axis argues for RVOT tachycardia Wellens. Heart 2001;86:579-585

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

  41. Capture and Fusion Beats Fusion Capture Wellens. Heart 2001;86:579-585

  42. A-V Dissociation, Fusion, and Capture Beats in VT V1 E F C ECTOPY FUSION CAPTURE Fisch C. Electrocardiography of Arrhythmias. 1990;134.

  43. Concordance • Precodial leads share the same axis • positive or negative Wellens. Heart 2001;86:579-585

  44. Summary ECG Distinctions of VT from SVT with Aberrancy Favors VT Favors SVT with Aberrancy Duration RBBB: QRS > 0.14 sec. < 0.14 sec. LBBB: QRS > 0.16 sec. < 0.16 sec. Axis QRS axis -90° to ±180° Normal

  45. Summary ECG Distinctions of VT from SVT with Aberrancy Favors VT Favors SVT with Aberrancy Morphology Precordial concordance If LBBB: R V1 duration > 30 ms S wave > 70 ms S wave notched or slurred V6: qR or QR R wave monophasic If RBBB: V1: monophasic R wave qR If triphasic, R > R1 R < R1 V6: R < S

  46. 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

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