Atrial flutter (AFl) – management principals
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Atrial flutter (AFL) is an uncommon arrhythmia characterized by rapid, regular atrial depolarizations, primarily classified into type I (typical) and type II (atypical) based on flutter rates and formation locations. The diagnosis involves ECG analysis to detect flutter waves and potential pitfalls leading to misdiagnosis, while treatment focuses on restoring normal sinus rhythm through cardioversion, rate control, and ablation strategies. Prognosis varies, with recurrence rates being high and maintaining sinus rhythm often challenging due to structural heart changes and underlying conditions.
Atrial flutter (AFl) – management principals
- 1. ATRIAL FLUTTER (AFl) – AN APPROACH Dr. Pruthviraj Puwar DNB Cardiology Registrar Vijaya Hospital Chennai 1
- 2. Case history 2 • 48 / F • DM – 13 yr, HTN – 16 yr, • k/c/o OS ASD – diagnosed at age of 22, patch closure done in April -99; • Comfortable and not on any treatment since last 11 years • Hypothyroidism – 6 months, on treatment
- 3. - DOE grade II- III since last 6 months - Asso. Nausea, belching, uneasiness - She consulted Dr in Dec’2014 @ apollo - since then on treatment NOW, - h/o Palpitation with uneasiness - since a week 3
- 4. Brief Cl. Examination points: 4 • Moderate built • No other abnormal G/E findings • PR: 118/min, Irregular, normal volume • BP: 96/60 mmHg • SPO2 99% • Chest: S1 normal, S2 split normal, no murmur heard, NVBS b/L
- 5. ECG: 5
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- 8. ECG findings in Atrial flutter: - P waves are absent. - biphasic "sawtooth" flutter waves (F waves) are present - Rate of about >240 to 340 beats/min. - F waves are fairly regular - The F waves usually do not have an isoelectric interval between them - In counterclockwise, typical type I AFL, the F waves have an axis of around 90º and are usually prominently negative in the inferior leads (II, III, aVF). 8
- 9. Typical atrial flutter (type 1) 9
- 10. Reverse typical AFl type I clockwise typical atrial flutter. The flutter waves are positive in the inferior leads (II, III, aVF), and a broad negative F wave in V1 10
- 11. Type II ECG difference: 11 Rate faster than type 1 Do not necessarily appear like saw tooth F waves have positive axis in inferior leads more often F waves have variable morphology Circuit Lacks excitable gap
- 12. Pitfalls of ECG in flutter: 12 • One of the F waves may be obscured by the QRS complex or the ST-T wave in 2:1 conduction- misdiagnosis • In clockwise, typical type I flutter, the F waves may be positive, and if every other F wave is obscured, it may be mistaken for sinus rhythm • The atrial electrical potential may be small and the F waves may be inapparent in the standard leads • Sometimes, the negative F wave merges with the beginning or end of the QRS complex, suggesting a pathologic Q wave in the first case and a conduction delay in the second.
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- 15. Pitfalls of ECG in Afl: 15 • F wave may appear to cause pathologic ST depression • The F wave morphology may appear atypical in those with CHD, atrial fibrosis, or following cardiac surgery or left atrial ablation even though the rhythm is typical type I flutter • pseudo-atrial flutter - Artefacts
- 16. Atrial Flutter: 16 • Relatively uncommon arrhythmia • can be deleterious by impairing the cardiac output and by promoting atrial thrombus formation • Characterized by rapid, regular atrial depolarizations at a characteristic rate of approximately 300 beats/min
- 17. Types: 17 Type I (typical, isthmus-dependent) Type II (atypical, isthmus-independent) Type I was separated from type II on the basis of the flutter rate (240 to 340 beats/min compared to 340 to 440 beats/min in type II), positivity or negativity of flutter waves in lead II and excitable gap
- 18. Type I: - a macroreentrant arrhythmia, - a depolarizing stimulus (such as a single atrial ectopic beat) excites an area of the atrium and then travels sufficiently slowly in a pathway that is sufficiently long that there is an "excitable gap”, can be entrained - located in the low right atrial isthmus. 18
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- 20. Type II (atypical) is isthmus-independent, 20 • Seems to lack an excitable gap, and cannot be entrained. • • Result from an intra-atrial reentrant circuit that is very short (in contrast to the long isthmus in type I atrial flutter) • May be due abnormal anatomy within the right or left atrium (i.e. surgical scars, irregular pulmonary veins, disturbed mitral annulus)
- 21. Entrainment ? 21 • was first described based on observations during rapid (overdrive) pacing of type I atrial flutter. • Entrainment is capture of the reentrant circuit of a tachycardia without interrupting the tachycardia, so that with cessation of pacing, the spontaneous reentrant tachycardia is still present.
- 22. 22 • The principles of entrainment during type I atrial flutter have permitted identification of targets for successful ablation, of mapping sites within or outside the reentrant circuit, and of appropriate pacing rates to successfully interrupt atrial flutter and restore sinus rhythm.
- 23. Epidemiology: 23 • Incidence: 200000 cases/yr in USA • Type II is unusual in normal heart (1.7%) • In general, most often seen in LVDF, RHD (particularly if the mitral valve is involved), unoperated and repaired CHD, and after cardiac surgery even when atriotomy is not part of the procedure
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- 25. Variety of underlying conditions can predispose to Afl. - Thyrotoxicosis, obesity, sick sinus syndrome, pericarditis, pulmonary disease, and pulmonary embolism, autonomic dysfunction - MVP, AMI, Digitalis toxicity - Post Cardiac Surgery: post-op as well as late arrythmias 25
- 26. Morbidity associated with AFl 26 Natural history is variable ranging from asymptomatic condition to hemodynamic collapse to SCD Mortality rate around 16% at 6.5 years follow-up, 10% experiencing sudden cardiac death Increased rates of recurrences Thromboembolic risk is the major concern with prolonged or recurrent episodes
- 27. Mechanism : 27 Atrial activation occurs in a continuous, uninterrupted manner because of a wavefront rotating around an obstacle formed by anatomical structures (venous or valvular orifices), scars, or areas of functional (anisotropic) block Can arises from any of atrial surface, septum, scar, pulmonary vein Atrial fibrosis – may contribute to arrhythmia substrate
- 28. 28 Concomitant sinus node dysfunction or Autonomic denervation of heart associated with surgery affect atrial refractoriness and may further contribute arrhythmogenesis Surgical scars and suture lines alone may be sufficient to support macroentrant arrhythmias
- 29. Evaluation: 29 • history, physical examination • minimum evaluation suggested by the 2006 ACC/AHA/ESC guidelines for AF • ECG, Exercise testing, • Echocardiography • Drugs history • Coronary evaluation • EP study: for mapping pathways and therapeutic ablation • Electrolytes, TFT
- 30. General Treatment Issues: 30 • Reversion to normal sinus rhythm (NSR) • Maintenance of NSR • Control of the ventricular rate in patients • Prevention of systemic embolization, particularly in the patient who also has atrial fibrillation
- 31. Treatment: 31 • In hemodynamically unstable pt:- synchronized internal or external DC cardioversion (Class I AHA and ESC guidelines) • Immediate cardioversion is also indicated in stable patients (since Afl can be converted to NSR with low energy shock) • Therapy of flutter is similar to Atrial fibrillation, includes three considerations: 1. Preventing thromboembolism 2. Control of ventricular rate 3. Conversion of atrial flutter to normal sinus rhythm
- 32. 32 1. Anticoagulation: It is unusual to have thrombus form in the left atrial appendage because of the regularity of atrial contractions in atrial flutter. However, atrial fibrillation can be a rhythm underlying atrial flutter. if atrial flutter persists for more than 48 hours, 4 weeks of adequate anticoagulation or TEE before attempting cardioversion continuation of warfarin for four weeks after cardioversion. Among patients with atrial fibrillation and flutter, the choice between warfarin and aspirin is based upon the estimated stroke risk
- 33. 2. Control of ventricular rate: • Frequently more difficult than atrial fibrillation cases • AV nodal blocking agents – B-blockers, Digoxin, CCBs • Choice depend upon patients clinical status • Guidelines Recommendations: 1. DC cardioversion (class I) (or Transesophageal pacing in stable pt) 2. CCBs / beta blockers (class IIa) – not to use in failure/ hypotension 3. Digoxin or Amiodarone in heart failure or hypotension (IIb) 33
- 34. 3. Conversion to sinus rhythm: 34 • Recurrance is difficult to determine in Afl • Amiodarone or class IA/IC drugs are the choice • RFA is preferred over the long term pharmacological therapy in type I flutter • NAPSE prospective catheter ablation registry of 477 pts, ablation of isthmus for Afl – acute success in 85%, recurrence 15% • Recurrence more common with type II AFl
- 35. Conversion of Atrial flutter to sinus rhythm can be accomplished by any of the following: # anti-arrhythmic drugs # rapid atrial pacing # electrical cardioversion # catheter ablation # anti-tachycardia devices # surgery 35
- 36. Anti- arrhythmic drugs: 36 Generally reserved for stable patients Class IA (Procainamide) Class IC (Fleicanide, Ibutilide, Sotalol) Class III (Amiodarone, Ibutilide, Sotalol) Ibutilide: Class IIa Up to 78% flutter convert to sinus rhythm within 90 minutes Torsades de pointes in 2-4% CI: SSS, LVDF, long QT
- 37. 37 Procainamide: class IIa Should be combined with AV nodal blocking agents because 1:1 AV conduction can occur during infusion Amiodarone: Additional benefit of ventricular rate control Not effective as Ibutilide Least proarrhthmogenic DOC when LVDF present Class IIb recommendation for both rate control and conversion to sinus rhythm
- 38. Right atrial pacing: 38 • Class I recommendation for stable patients, very effective in converting to sinus rhythm • Does not require sedation • Type I AFL: can be converted to NSR • Type II Afl can not be interrupted by pacing • Atrial fibrillation can occur while pacing
- 39. Ablation: 39 increasingly used to interrupt the reentrant circuit supporting atrial flutter in order to permanently restore normal sinus rhythm. becoming more accepted first-line therapy for the long-term maintenance of sinus rhythm in patients with type I atrial flutter usually done electively for preventing the recurrence, rather than for the acute restoration of sinus rhythm
- 40. 40 With recurrent symptomatic Type I atrial flutter, there is a success rate of higher than 95% with ablation. Ablation is commonly performed at the 6:00 position on the tricuspid valve isthmus. Type II atrial flutter is also amenable to ablation and success rate is close to 95%, but recurrence is more common than Type I. In patients with atrial flutter treated with ablation who subsequently develop a fib (56% in one study), ablation of the AV junction may need to be performed with placement of pacemaker.
- 41. Maintenance of sinus rhythm: 41 Maintenance of sinus rhythm in atrial flutter is often problematic with pharmacologic therapy The success rate at 1year only 20 to 30% Recurrence being highest in the patient with an enlarged right atrium & in heart failure. Good prognostic signs for maintaining sinus rhythm are normal atrial size, recent onset, little or no heart failure, and an underlying reversible disorder such as hyperthyroidism, myocardial infarction, or pulmonary embolism
Editor's Notes
- #13: Atypical morphology of F wave may be due to reductions in LA potentials and changes in the atrial activation sequence. Atypical flutters which do not use the cavotricuspid isthmus as part of the circuit may meet the criteria for type I flutter but have different ECG appearances. Patients with prior cardiac surgery may have an incisional scar which can act as a barrier for an atypical flutter, often in the right atrium. Many patients with congenital heart disease, especially with more complex disease or surgical repairs, will present with atypical flutter
- #22: During entrainment, the orthodromic wavefront from the pacing impulse resets the tachycardia to the pacing rate, while the antidromic wavefront either collides with the orthodromic wavefront of the previous beat (usual case) or is blocked by some other mechanism (refractoriness or another cause of block).