Cardinal Features

Classic sawtooth Flutter waves may be seen best in II, III, aVF and V1 (may be made more apparent by turning the ECG upside-down).

Sometimes the sawtooth morphology is absent and diagnosis depends on identifying flutter waves at a rate usually around 300 (variable, depending on factors mentioned previously) or having a high index of suspicion for atrial flutter when faced with an ECG with a ventricular rate of half of this (i.e.150bpm in a 2:1 block).

Adenosine can be used diagnostically where there is doubt, in order to temporarily block the AV node and provide a few seconds of rhythm strip devoid of ventricular complexes. The presence of flutter waves is then obvious. However, use of adenosine can then cause the AV conduction to increase to 1:1 or precipitate AF.

The ventricular rate seen in patients with Flutter is dependent on the degree of AV nodal block: normally the AV node cannot transmit impulses at 300/min, so only alternate impulses reach the ventricles, giving a rate of 150/min. This is called Atrial Flutter with 2:1 block and is the most common ventricular response (see Figure 2).

Morbidity, Mortality and Treatment

• Rate-related complications such as heart failure and ischaemia
• Thrombo-embolic events, caused by a pro-thrombotic atrial state and leading to a risk of embolic events approaching that of atrial fibrillation

Both of these issues need to be considered when intervention for atrial flutter is considered.

Treatment of Atrial Flutter

Treatment of atrial flutter is broadly the same as for atrial fibrillation, though the condition is more sensitive to DC shock and less so to chemical cardioversion.

The urgency and aims of treatment depend on symptoms, which are usually rate-related.

The various therapeutic options include:

(i) DC Cardioversion

The patient with recent-onset flutter and a rapid ventricular rate may be unstable, with haemodynamic compromise, ischaemic pain or overt pulmonary oedema. These patients require emergency synchronised DC cardioversion. Electrical cardioversion may also be used after failure of pharmacological management. 25J may be sufficient though 50-100J is more reliably effective. Sometimes the first shock converts the rhythm to atrial fibrillation, requiring further shocks to achieve sinus rhythm.

(ii) Rate control

For stable patients with high rates, rate control is preferred first line, but may be difficult to achieve. Drugs include amiodarone (may well also result in cardioversion), beta blockers or calcium channel blockers (eg. verapamil or diltiazem).

(iii) Chemical Cardioversion

Chemical cardioversion can be achieved best with class III anti-arrhythmic drugs. Class Ic antiarrhythmic drugs (e.g. propafenone, fleicanide) arent recommended due to risk of slowing atrial rate, resulting in 1:1 AV conduction.

(iv) Electrophysiological ablation therapy

Antiarrhythmic drugs maintain sinus rhythm in only 50-60% of patients. Radiofrequency catheter ablation is successful in more than 90% of cases, interrupting the re-entrant circuit in the right atrium and avoiding the long-term toxicity observed with antiarrhythmic drugs.

(v) Anticoagulation

There are no studies of the effect of anticoagulation on embolic risk in atrial flutter. There is a consensus that since the risk of embolic events seems to be similar to that of atrial fibrillation, anticoagulation should be used similarly, i.e. if the arrhythmia has been present for more than 48 hours then anticoagulate for 4 weeks prior to cardioversion. Long term anticoagulation is rarely required in Flutter as the condition is permanently cured by radio-catheter ablation, or deteriorates into atrial fibrillation.