Management of tachyarrhythmias in the emergency room

Narrow-QRS tachycardias with regular rhythm

In figure 5 is shown the diagnostic and therapeutic flow chart to be followed in narrow-QRS tachycardias with regular rhythm, by taking into account the response to vagal stimulation and the P wave location.

Figure 5. Diagnostic and therapeutic algorhythm in narrow-QRS tachycardia and regular ventricular rhythm

Atrial tachycardia is a rare arrhythmia. It can be paroxysmal or persistent. The latter form is typical of children. Vagal maneuvers do not interrupt the arrhythmia but may cause a transient AV block.
The P waves (rate between 130-200 bpm) precede the QRS of 80-200 msec and are different from the sinus P (sometimes they may be positive in inferior leads). Atrial tachycardia can be maintained by an intra-atrial reentry circuit or by an automatic focus. The latter mechanism is the most frequent one.

Antiarrhythmic drugs (class IC drugs are of first choice) are often ineffective and DC shock, although able to interrupt the arrhythmia, may not prevent it from restarting immediately after.
The ventricular rate can be reduced by drugs acting on the atrio-ventricular node (tab. III) and an ablation of the ectopic focus may be programmed.

Some patients on chronic treatment with class I antiarrhythmic drugs or amiodarone could have their atrial flutter episodes slowed by the drug mimicking an atrial tachycardia. The treatment is that of atrial flutter.

Table III. Intraveneuos drugs acting on AV node

Atrial flutter may be classified on the basis of either the morphology or the frequency of F waves (tab IV). The Waldo classification is the one clinically useful: the slower type 1 atrial flutter has an excitable gap and it can be interrupted by overdrive atrial pacing; the rarer type 2 has not an excitable gap and it is not manageable by atrial pacing.

When atrial flutter has a 2:1 atrio-ventricular conduction, every other F wave is inside the ventricular complex and may be difficult to identify. Vagal maneuvers, by decreasing the atrio-ventricular conduction, may uncover the typical saw-teeth appearance of the atriogram, thus allowing the diagnosis. Even a careful observation of the patient’s neck could show a double jugular pulse for every heart beat.

Table IV. Atrial flutter classification

Drug therapy of atrial flutter (except for the new pure class III antiarrhythmic agents ibutilide or dofetilide, whose preliminary trials show a 60-70% success rate) is often unsuccessful (less than 40% with class I antiarrhythmic drugs) while a synchronous low energy DC shock interrupt the arrhythmia in nearly 100% of the cases.
Transoesophageal atrial pacing (effective only in type 1 AFl) has an intermediate success rate. In our experience, it converts about 30-40% of the patients, while a shift to atrial fibrillation occurs in 20-30% of cases. Two thirds of them will later convert to sinus rhythm, either spontaneously or by intravenous infusion of an 1C antiarrhythmic drug.

An alternative choice could be to slow the ventricular rate by drugs acting on atrio-ventricular node (tab. III) and to defer the restoration of sinus rhythm.

Figure 6 shows the flow chart we suggest in type 1 atrial flutter.

Figure 6. Treatment of type 1 atrial flutter

In type 2 atrial flutter, an intravenous Class IC antiarrhythmic drug can be successful. Other choices are limited to DC shock or ventricular rate control.

Paroxysmal reentrant tachycardia. The P waves have to be carefully looked for on ECG. If P waves are not detectable, an atrio-ventricular nodal reentry tachycardia is the most likely arrhythmia. In fact, since myocardial activation proceeds almost contemporarily upward - toward the atria - and downwards - towards the ventricles - the P waves are inside the QRS complex or just follow it, slightly modifying its last vector (pseudo-S waves) (fig. 7). If a retrograde P wave follows the QRS by at least 70 msec, a diagnosis of atrio-ventricular reentry tachycardia can be made. In fact, the stimulus descends to the ventricles through the normal pathway and comes back to the atria through an atrio-ventricular accessory pathway (fig. 8 right).

Figure 7. Supraventricular reentrant tachycardias. Location of the retrograde P waves allows differential diagnosis between nodal reentry tachycardia and atrioventricular reentry tachycardia.

Figure 8. Schematic representation of the reentrant circuits responsible of the intranodal reentrant tachycardia and the atrioventricular orthodromic reentrant tachycardia

left: nodal reentrant tachycardia
right: orthodromic atrioventricular reentrant tachycardia

Both the arrhythmias involve the atrio-ventricular node. It follows that any therapy able to block the conduction in this structure will stop them. In table V are listed the drugs acting on atrio-ventricular node conduction.

In patients with known WPW syndrome, it could be safer to administer a drug acting on the atrio-ventricular as well as on the accessory pathway. In fact, in case of transformation of the arrhythmia into atrial fibrillation, the ventricular rate might be dangerously accelerated by a drug acting exclusively on the atrio-ventricular node.

In table V are listed the drugs that may be use intravenously to terminate a reentry tachyarrhythmia and their approximate efficacy.
The most effective drug acting on the atrio-ventricular node is adenosine, the less effective are betablockers. Propafenone and flecainide (1C class drugs) act more on the accessory pathway than on the atrio-ventricular node. Amiodarone action, when acutely administered intravenously, is limited to the atrio-ventricular node without any effect on the accessory pathway.

Table V. Drugs for interruption of supraventricular tachycardias

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