Answers

Short answers

1 Figure 1 shows a supraventricular arrhythmia that could, on the basis of the adenosine test, be either atrial flutter or a focal atrial tachycardia. The adenosine test revealed regular organised atrial activity, which is actually flutter waves occurring at a rate of approximately 250 per min. This activity constitutes atrial flutter with 1:1 conduction. There is also intermittent atrioventricular block with the adenosine, although the rapid ventricular response rate eventually resumes (as seen towards the end of fig 2B).

2 The use of flecainide—alone, without a rate limiting drug such as a β blocker or calcium channel blocker—to treat this patient’s atrial fibrillation could be responsible for his presentation. Flecainide to treat atrial fibrillation raises the risk of atrial flutter and can also increase the ventricular response rate to atrial activity during the arrhythmia. The regular atrial activity shown by the adenosine rules out atrial fibrillation in this patient. The results of the adenosine test also make atrioventricular re-entrant tachycardia or atrioventricular nodal re-entrant tachycardia much less likely, as these arrhythmias incorporate the atrioventricular node as part of the circuit and so tend to terminate when the atrioventricular node is blocked. Atrial flutter and focal atrial tachycardia are thus the main differential diagnoses. The fact that the patient had been taking flecainide for his atrial fibrillation makes it more likely that the arrhythmia is actually atrial flutter.

Long answers
1 Atrial flutter
Atrial flutter is a form of re-entrant atrial tachycardia and is characterised by an organised atrial rhythm discharging at a rate of 250-350 beats/min.¹ The atrial activity appears on electrocardiograms as flutter or "F" waves, which occur at a regular rate and are composed of a P’ wave and a Ta wave (representing atrial repolarisation).² Whereas atrial fibrillation is generated by multiple random and disorganised simultaneous circuits and focal activity within the atrium, atrial flutter is caused by a single large re-entrant circuit. Atrial flutter most commonly originates in the right atrium but can also arise in the left atrium. It can also be scar related; for example, flutter circuit propagation around an electrical barrier caused by an atriotomy.

As is the case with atrial fibrillation, the ventricular response rate in flutter is determined by the conducting ability of the atrioventricular node. The atrioventricular conduction ratio is usually 2:1 or 4:1 in flutter, hence the relatively common presentation of a ventricular response rate of 140-150 beats/min.^{2 3} The sawtooth pattern one commonly associates with atrial flutter is shown in an electrocardiogram from another patient (fig 3), which demonstrates the lack of an isoelectric line in at least one lead in the arrhythmia.² This sawtooth pattern is classically seen in the inferior leads II, III, and aVF, whereas discrete flutter waves are most often visible in lead V1 (see fig 1).

View larger version (53K): [in this window] [in a new window] [PowerPoint Slide for Teaching]   Fig 3 An electrocardiogram showing atrial flutter with 3:1 conduction. The classic sawtooth pattern can be seen in the inferior leads. Discrete F waves can be seen most prominently in lead V1, and are positive in this lead (black arrow) and negative in the inferior leads (green arrows)

 
The initial patient described in this quiz presented with atrial flutter with 1:1 conduction—that is, every atrial discharge was conducted to the ventricles, resulting in a ventricular response rate of 250 beats/min. The QRS complexes are slightly broadened at this rate compared with QRS complexes when the rate is slowed by adenosine, indicating a degree of aberrant conduction during the tachycardia.

Adenosine can be used to transiently block atrioventricular node conduction and consequently slow the ventricular response rate long enough to permit identification of any underlying atrial activity. An electrocardiogram (preferably with 12 leads) should always be recorded during adenosine administration as the trace can aid in the diagnosis of a tachycardia. When adenosine was administered in this patient, F waves could be seen occurring at a rate of approximately 250 per minute (fig 4).

View larger version (46K): [in this window] [in a new window] [PowerPoint Slide for Teaching]   Fig 4 Electrocardiogram showing 1:1 atrial flutter following the administration of adenosine. F waves are shown occurring at a rate of 250 per minute (thin black arrows). An F wave superimposed on a T wave can be seen (thick black arrow). Some normally conducted beats with a narrow QRS complex (red arrow) are also present. The two very broad QRS complexes represent ventricular escape beats

 
Broadly speaking, atrial flutter can be divided into several types on the basis of the direction of propagation of the wave front in the re-entrant circuit. Conduction towards an electrocardiogram lead produces a positive deflection in that lead, whereas conduction away results in a negative deflection. The most common type of atrial flutter is typical or counterclockwise flutter,⁴ where the wave front circulates counterclockwise within the right atrium. This process results in negative F waves in leads II, III, and aVF (inferior leads) and positive F waves in lead V1.³ Figure 3 shows an example of a typical counterclockwise flutter. A circuit that propagates in the opposite direction is called reverse typical or clockwise flutter, which is less common. This type of flutter produces positive F waves in the inferior leads and negative F waves in lead V1.³ Typical flutter circuits propagate around the tricuspid valve, whereas atypical flutter circuits circulate around other anatomical areas.

The conclusions one draws from the surface electrocardiogram may not necessarily represent really what is going on internally; for example, the electrocardiogram may imply reverse typical atrial flutter but an electrophysiological study could show that the abnormalities actually reflect an atypical flutter. Surface electrocardiogram findings are not exclusive and some overlap in representation can occur.² The patient described in this quiz had positive F waves in leads V1 and II. These findings do not fit with the typical flutter patterns described above and comprise what is known as an atypical flutter.

Electrophysiological studies can be carried out to clarify the mechanism of flutter, and cure can be achieved by ablation.⁴ Ablation entails applying energy to a region of endocardium to deliberately cause tissue necrosis, which creates a barrier to electrical conduction and interrupts the path of the re-entrant circuit. Ablation along an area known as the cavotricuspid isthmus (between the inferior vena cava and tricuspid valve annulus) can be performed by cardiac electrophysiologists to interrupt some types of flutter circuit, generally the typical and reverse typical forms. The re-entrant circuit in an atypical flutter can vary in size and location and thus can be more difficult to treat with ablation.²

The patient described in this quiz remained haemodynamically stable and spontaneously cardioverted within 30 minutes of presenting to hospital. If such a patient becomes haemodynamically unstable at any point, immediate external direct current cardioversion should be carried out.

2 Flecainide as a predisposing factor
Atrial flutter has essentially the same aetiologies as atrial fibrillation. The two arrhythmias can coexist; in fact, flutter occurs in 25-35% of patients with atrial fibrillation.⁴ The use of flecainide to treat atrial fibrillation, however, can convert atrial fibrillation to atrial flutter,³ possibly by slowing the atrial conduction velocity and causing "organisation" of the fibrillatory waves into the single re-entrant circuit of flutter.²

The ventricular response of a patient with an atrial arrhythmia depends on the conducting ability of the atrioventricular node. During atrial fibrillation, for example, as many as 400-600 atrial impulses reach the atrioventricular node; however, only a proportion can be conducted through to the ventricles owing to the refractory period of the tissue. The impulses that are not conducted cause "concealed penetration" of the node and thus increase its refractoriness. A healthy atrioventricular node would tend to conduct every second, third, or fourth flutter wave, resulting in a ventricular response rate of anything from 75 to 150 beats/min. Flecainide can precipitate a rapid ventricular response rate by slowing the atrial rate to a level that the atrioventricular node can conduct at a 1:1 ratio, resulting in an extremely rapid tachycardia that can culminate in haemodynamic collapse. Flecainide is also thought to exert an anticholinergic effect on the node, increasing its conducting abilities.⁵

Flecainide is a class 1c antiarrhythmic drug (Vaughn Williams classification) and can be administered orally or parenterally. The half life of flecainide is approximately 16 hours; therefore, the agent is given twice daily. In addition, it has a narrow therapeutic index. Flecainide is generally used in the treatment of paroxysmal atrial fibrillation, atrioventricular nodal re-entry tachycardia, and pre-excitation syndromes, and has a limited use in certain forms of ventricular tachycardia. The drug should not be used in patients with a structural abnormality of the heart.¹ Flecainide has a negative inotropic action and should also be avoided in patients with heart failure, ischaemic heart disease (especially in the context of a recent myocardial infarction⁶), and haemodynamically significant valve disease.³ Just like all other antiarrhythmic drugs, flecainide can be proarrhythmic, especially in patients with a history of sustained ventricular tachycardia and significantly impaired ventricular function.⁵

Flecainide should be prescribed in combination with rate limiting (atrioventricular nodal blocking) drugs such as β blockers (for example, bisoprolol) or nondihydropyridine calcium channel blockers (for example, diltiazem).^{4 7} Flecainide remains a valuable drug in the treatment of paroxysmal atrial fibrillation but increases the risk of 1:1 conduction of atrial flutter by the mechanisms outlined above. Prescribing a rate limiting drug with flecainide would help control ventricular response rate.

Patient outcome
The patient spontaneously cardioverted into sinus rhythm within 30 minutes of presenting to hospital. Flecainide was discontinued and the patient was commenced on bisoprolol. He was referred to the cardiology team and underwent an electrophysiological study and successful ablation of his atypical flutter. The patient declined additional medication other than the bisoprolol for his paroxysmal atrial fibrillation and so was maintained on this therapy and warfarin.

Cite this as: BMJ 2009;339:b2339