Atrial flutter

see also: cardiology; cardiac arrhythmias; AF

• clinically, atrial flutter is managed similarly as for Atrial Fibrillation with which it is often in association, although of the two, AF is 7-8x more common as a cause for admission.
• often flutter is not as well tolerated as AF due to the rapid and often difficult to control ventricular rate, especially with minimal exertion.
• The common form of type I atrial flutter has sawtooth flutter (F) waves, best seen in leads II, III, and aVF, with atrial rates of 240-340 bpm and without an isoelectric interval between these F waves.
• It often presents as a HR of 150 due to an atrial rate of 300 with a 2:1 block
• Variable AV conduction can also be seen (commonly present with 2:1 or 3:1 AV conduction). 
• With 1:1 AV conduction, hemodynamic collapse may occur.

• 75% of patients are male
• most patients are older adults with average age 64yrs
• 30% have ischaemic heart disease
• 30% have hypertensive heart disease
• 30% have no underlying cardiac disease
• other associations:
  • cardiomyopathy
  • hypoxia
  • COPD
  • thyrotoxicosis
  • phaeochromocytoma
  • electrolyte imbalance
  • alcohol consumption

• general care is as for Atrial Fibrillation

• if rapidly deteriorating, then synchronised reversion
• if delay in access to synchronised reversion then:
  • metaraminol (Aramine) 0.5mg iv over 1 minute and repeat minutely until either:
    • arrhythmia reversion
    • max dose 5mg metaraminol given
    • systolic BP > 100

• when it is not clear from the ECG, vagal manouvres or IV adenosine may block the AV node to display the underlying rhythm
• is there evidence of, or a history of a pre-excitation syndrome such as WPW - this should be determined because agents that act exclusively at the level of the AV node may enhance accessory pathway conduction and cause rapid ventricular response with 1:1 conduction and ventricular rate of 300/min which may precipitate VF.

• can be difficult and need to watch for adverse effects of Rx such as hypotension & negative inotropic effects (cardiac failure)
• if no pre-excitation syndrome such as WPW, no other C/I (such as poor LV function) then, either:
  • beta blockers - these are the preferred agents
  • calcium channel blockers
• if inadequate rate control with appropriate dosings of the above and if no pre-excitation syndrome such as WPW, no other C/I, then consider either:
  • digoxin
  • amiodarone - but does risk reversion to SR and thus embolic risk.

• if duration < 48hrs after cardiac consultation, DC reversion is effective in 95% & requires less energy than for AF eg. 50J synchronized
• IV amiodarone slows rate and may result in reversion
• other anti-arrhythmics

• avoid precipitants - eg. caffeine, alcohol,
• anti-arrhythmics as for AF - consider sotalol
• referral for radiofrequency ablation or surgery if recurrent & problematic

• risk is ~14% over 4-5yrs, probably more related to unrecognised associated episodes of AF
• see AF.