Atrial flutter ( AFL ) is a supraventricular arrhythmia characterized by a fast atrial rate with a fixed or variable ventricular rate.
First described in 1887 by Mac WIlliam as faradic stimulation of the auricles which sets them into rapid flutter The atria depolarize at a regular rate of 250-350 beats / minute ( typically 300 beats ) The AV node cannot conduct at this high rate -this means that the ventricle may contract at 150 BPM ( 2 :1 block ) and the ventricular rate may remain fixed 2 : 1 block is the most common one seen by extension if the atrial rate is 300 3 : 1 conduction results in a VR of 100 BPM 4 :1 in a rate of 75 BPM and 5 :1 in a rate of 60 BPM 1 : 1 conduction is rare but possible if a bypass tract is present This block may vary from moment to moment and can cause an irregular ventricular rhythm – this is called atrial flutter with variable conduction ( this can be difficult to distinguish from atrial fibrillation ) Various types have been described depending on the location of the short-circuit and the direction of the re-entry circuit Typical atrial flutter – also known as macrorentrant atrial tachycardia ( MRT ) -a reentry rhythm that propagate around the tricuspid annulus and is counterclockwise in direction Atypical atrial flutter originates from the left atrium or areas high in the right atrium ( such as surgical scars ) and has a variable appearance on ECG.
Atrial flutter is less common than atrial fibrillation It is the second most common tachyarrhythmia after atrial fibrillation Overall incidence of AFL has been reported at around 88 per 100 000 person-years ( Marshfield epidemiology study ) In the US an estimated 200, 000 new cases are seen annually AFL occurs more frequently with advancing age and is more common in men AFL is uncommon in children or young adults in absence of congenital heart disease.
Underlying structural heart disease ( particularly valvular heart disease ) Congestive cardiac failure / Left ventricular dysfunction Chronic obstructive lung disease ( COPD ) Pulmonary vascular disorders as pulmonary embolism Following open heart surgery ( 1st week ) AFL can happen in up to 10 % to 20 % of patients following cardiac surgery and the incidence peaks at days 2-3 Congenital heart disease Age related degenerative changes Rheumatic heart disease Obesity Pericarditis Use of antiarrhythmia therapy for atrial fibrillation.
diagnosis is made predominantly by surface ECG Narrow complex tachycardia Atrial activity usually between 250-320 beats / minute typical flutter ECG reveals continuous regular atrial activation with a sawtooth appearance most obvious in leads II , III and aVF The Flutter waves – have identical morphology ie all alike in each lead Flutter waves appear prior to QRS complex Flutter waves without an isoelectric base line in between the QRS complexes In typical AFL the flutter waves would be negative in leads II , III and aVF and positive in V1
Atrial fibrillation has f waves -they are irregular and not alike and the QRS rhytm would be irregularly irregular ( ie more chaotic )
can be asymptomatic presentation would depend upon ○ any underlying heart disorder ○ ventricular rate -usually if < 120 may not cause any symptoms other presenting symptoms for e.g if the ventricular rate is faster & causing a decrease in cardiac output ○ chest discomfort ○ palpitations ○ angina ○ lightheadedness ○ fatigue ○ dyspnoea ○ syncope ○ hypotension ○ reduced exercise tolerance presentation may also be with complications as ○ decompensated heart failure ○ tachycardia induced cardiomyopathy ○ embolic stroke Risk of stroke in atrial flutter is less compared to atrial fibrillation as the atrial are usually able to pump all the blood into the ventricles with every beat ie less risk of blood pooling in the atria. Some papers quote an equal risk – this would be a decision made by the specialist team following investigations/ risk assessment
physical often normal Undertake a full CVS examination Obtain vitals Listen to the chest Obtain full past medical history – most cases are associated with predisposing factors ( see causes )
atrial fibrillation multifocal atrial tachycardia paroxysmal supraventricular tachycardia sinus tachycardia junctional tachycardia Wolf-Parkinson-White syndrome.
12 lead surface ECG CXR ( exclude lung disease , heart failure ) Bloods – TSH , FBC , Us&Es , Digoxin level ( if indicated ) Screen for infection ( if suspected ) Coagulation profile ( if considering anticoagulation ) Secondary care options include Echocardiography ( evaluate structural heart disease ) Transthoracic echocardiography Holter monitoring or event recorder Pulmonary function tests Use of risk calculators as CHA2DS2-VaSc score.
Management would be by specialists and would depend upon the clinical circumstances / presentation and may include aspects as rate control rhythm control anticoagulation.
Non-pharmacological measures Vagal maneuvers DC cardioversion Overdrive pacing Radiofrequency ablation Pharmacological antiarrhythmic agents for e.g amiodarone class 1A anti arrhythmic agents calcium channel blockers beta blockers.
AFL often co-exists or precedes atrial fibrillation It has been shown that AF developed in 56 % of patients with AFL Another study has shown that more than 50 % of patients with AFL will go on to develop AF in 3 yrs and more than 80 % will develop AF within 5 yrs Patients treated with ablation for isolated typical ATL – can experience new onset AF This relation ship between AF and ATL is complex – this would be taken into consideration by cardiologists when considering treatment options particularly anticoagulation.
Ablation carries a high success rate Cardioversion is also very successful in restoring sinus rhythm Most patients would be followed up in primary care and it should be noted that patients have a significant risk of developing atrial fibrillation and condition is associted with a high risk of a stroke and other embolic phenomena
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