MedEducation Flix – Atrial Flutter Self-Assessment

Typical atrial flutter involves a macro-reentrant circuit in the right atrium, circulating counterclockwise around the tricuspid annulus, using the cavotricuspid isthmus (CTI) as a critical slow-conduction pathway. This produces the classic 'sawtooth' flutter waves in the inferior ECG leads, typically at a rate of 240–300 bpm.

Despite more organized atrial contraction, atrial flutter carries a similar risk of thromboembolism as atrial fibrillation. Therefore, stroke prevention strategies, including anticoagulation decisions, are based on CHA₂DS₂-VASc score in both conditions.

Radiofrequency ablation targeting the cavotricuspid isthmus is the first-line curative therapy due to high success rates (>95%) and low complication risk. Rate control and anticoagulation may be used acutely, but ablation is preferred for long-term rhythm management.

Electrical cardioversion is indicated in patients with hemodynamic instability, rapid ventricular response unresponsive to medical therapy, or when pharmacologic conversion is contraindicated or ineffective. Synchronised shocks typically require lower energy (20–50 J).

Beta-blockers and non-dihydropyridine calcium channel blockers (e.g., diltiazem, verapamil) are first-line agents for rate control. Digoxin may be added in heart failure, but often fails to control rate alone due to rapid atrial conduction through the AV node.

Atrial flutter involves a regular, rapid atrial rate that is more efficiently conducted to the ventricles through the AV node. This makes rate control with medications alone less effective, and rhythm control strategies such as ablation or cardioversion more commonly necessary.

Atypical flutter originates outside the cavotricuspid isthmus and may occur post-surgery, post-ablation, or with left atrial scarring. These circuits are often left-sided or incisional and require electroanatomic mapping for effective ablation.

For flutter lasting >48 hours or of uncertain duration, 3 weeks of therapeutic anticoagulation or a transesophageal echo (TEE) to exclude atrial thrombus is recommended prior to cardioversion, followed by at least 4 weeks of anticoagulation post-procedure.

CTI ablation has a long-term success rate exceeding 90%, with low recurrence. However, up to 50% of patients may later develop atrial fibrillation, requiring ongoing rhythm monitoring and stroke risk assessment.

Management remains similar—rate control, anticoagulation, and ablation—but patients with structural heart disease may have atypical circuits or coexisting AF. Comprehensive EP assessment and individualized anticoagulation planning are essential.

1:1 AV conduction results in very rapid ventricular rates (>250 bpm) and may mimic ventricular tachycardia. It often occurs in young patients or those on class 1C agents like flecainide without AV nodal blockade.

Adenosine transiently blocks AV nodal conduction, unmasking underlying flutter waves by slowing or briefly stopping the ventricular response, thus revealing the atrial activity clearly.

Persistent atrial flutter with rapid ventricular rates despite optimal beta-blocker or CCB therapy suggests need for rhythm control—either electrical cardioversion or catheter ablation. Consider thyroid function, electrolyte status, and ischemia as contributors.

Even after successful ablation, anticoagulation is continued based on stroke risk (CHA₂DS₂-VASc), not procedural success. Many patients develop AF later, maintaining long-term thromboembolic risk.

Ablation lines from PVI can create areas of conduction block that predispose to macro-reentrant atrial flutters (especially roof-dependent or perimitral). Mapping is required to localize and treat new circuits.

Because up to 50% of patients develop atrial fibrillation within 12–24 months post-ablation, periodic Holter or event monitoring is advised for early detection and anticoagulation planning.