if the arrhythmia has been present for more than 48 hours then anticoagulate for 4 weeks prior to cardioversion. 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. There are no studies of the effect of anticoagulation on embolic risk in atrial flutter. 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. (iv) Electrophysiological ablation therapyĪntiarrhythmic drugs maintain sinus rhythm in only 50-60% of patients. propafenone, fleicanide) arent recommended due to risk of slowing atrial rate, resulting in 1:1 AV conduction. verapamil or diltiazem).Ĭhemical cardioversion can be achieved best with class III anti-arrhythmic drugs. Drugs include amiodarone (may well also result in cardioversion), beta blockers or calcium channel blockers (eg. Sometimes the first shock converts the rhythm to atrial fibrillation, requiring further shocks to achieve sinus rhythm.įor stable patients with high rates, rate control is preferred first line, but may be difficult to achieve. 25J may be sufficient though 50-100J is more reliably effective. Electrical cardioversion may also be used after failure of pharmacological management. These patients require emergency synchronised 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. The urgency and aims of treatment depend on symptoms, which are usually rate-related. 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. Thrombo-embolic events, caused by a pro-thrombotic atrial state and leading to a risk of embolic events approaching that of atrial fibrillationīoth of these issues need to be considered when intervention for atrial flutter is considered.Rate-related complications such as heart failure and ischaemia.This is called Atrial Flutter with 2:1 block and is the most common ventricular response (see Figure 2). 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. However, use of adenosine can then cause the AV conduction to increase to 1:1 or precipitate AF. The presence of flutter waves is then obvious. 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).Īdenosine 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. Fig 1: Type 1, typical atrial flutter, counterclockwise, with 4:1 block
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