Management of tachyarrhythmias in the emergency room

Wide-QRS tachycardias

In figure 4 are listed the most common forms of wide-QRS tachycardias (QRS > 120 msec). The QRS sequence can be regular or irregular. About 50% of them are of supraventricular origin, with aberrant atrio-ventricular conduction (fig. 11). In these cases the wide QRS may be due to any of the following:

1. preexisting bundle branch block;

2. functional bundle branch block (tachycardia-dependent phase 3 block);

3. ventricular pre-excitation;

4. aberrancy due to sodium channel-blocking antiarrhythmic drugs.

In the patient presenting with a wide-QRS tachycardia associated with haemodynamic impairment, a DC shock must be performed without delay, deferring a precise diagnosis, which will be based on a subsequent retrospective analysis of the ECG. If the haemodynamic situation is not worrisome, a correct diagnosis will be the first step toward an optimal treatment.

Figure 11. Schematic representation of two paroxysmal supraventricular reentry tachycardias with wide QRS.

A: nodal reentry tachycardia witn right BBB;
B: antidromic AV reentrant tachycardia

Wide-QRS tachycardia with irregular rhythm

Except for the easily-recognizable cases of torsade de pointes - the differential diagnosis is limited to atrial fibrillation as well as atrial flutter (with variable AV conduction), both coexistent with either bundle branch block or ventricular preexcitation (Wolf-Parkinson-White syndrome).

Wide-QRS tachycardia with regular rhythm

The diagnosis may be more difficult. The age of the patient and the haemodynamic status are not helpful: a ventricular tachycardia is observed at every age and it may be surprisingly well tolerated even by patients with ventricular dysfunction. On the contrary, a history of previous myocardial infarction or organic cardiac disease orientates toward a ventricular genesis of the arrhythmia. The availability of previous ECGs (preexisting conduction disturbances?) and the knowledge of the current therapy can be helpful. Even in this setting, vagal maneuvers are to be attempted: any electrocardiographic modification may help clarify the origin of the arrhythmia, testifying its supraventricular nature.

When vagal stimulation fails to bring about any change, a careful analysis of the ECG may reveal essential diagnostic features. The first think to look for are the P waves. When these are dissociated from QRS and/or fusion or capture beats are present, the diagnosis of ventricular tachycardia is certain. Even a careful clinical examination can disclose the mechanical equivalents of the electrical atrio-ventricular dissociation such as a variable intensity of the first heart sound or a jugular venous pulse dissociated from the arterial pulse. However, about 50% of ventricular tachycardias have 1:1 ventriculo-atrial retroconduction, or are coexistent with atrial fibrillation. In these cases the diagnosis has to rely upon the QRS morphology.

In figure 12 are listed the ECG features that have to be considered in the differential diagnosis.

In the precordial leads, a concordant negative QRS pattern or a Q-peak S interval > 100 msec are nearly diagnostic for ventricular tachycardia. More subtle morphological criteria are listed in table X.

Figure 12. Approach to the patient with wide-QRS tachycardia.

Table X. Differiential criteria considering the QRS morphology in leads V1 and V6 in case of right bundle brach block (RBBB) or left bundle brach block (LBBB) aspect.

Legend PP+ = positive predictive value; V=ventricular origin; SV=supraventricular origin

The Brugada diagnostic algorithm for wide-QRS tachycardias is
reported in figure 13.

Fig 13 Brugada diagnostic algorhythm for wide-QRS tachycardias.

It must be kept in mind that these criteria are not helpful in case of supraventricular tachycardias with aberrant ventricular conduction due to class IA or IC drugs. This arrhythmias (e.g. "slow" atrial flutter with 1:1 atrio-ventricular conduction) are not distinguishable from ventricular tachycardias. Only the patient history and vagal maneuvers can be of help.

It must be underscored that, whenever a diagnostic doubt exists, the arrhythmia has to be considered and treated as ventricular tachycardia. Drugs as Verapamil or Diltiazem must be avoided because, by depressing contractility and lowering blood pressure, they might worsen the clinical status. A bolus of adenosine, a ultra-short acting agent, profoundly depressing atrio-ventricular node conduction, has been proposed for the differential diagnosis in these cases.

In figures 15 and 16 is reported the treatment for wide-QRS tachycardias. In every kind of ventricular tachycardia, electrolyte disorders must be searched for and promptly corrected.

Figure 14. Treatment of Wide-QRS tachycardias with regular rhythm

Figure 15. Treatment of wide-QRS tachycardias with irregular rhythm

In ventricular tachycardia, a lidocaine bolus may be tried, keeping in mind that it has an high success rate in the setting of myocardial infarction or acute myocardial ischemia, whereas it is rarely effective in ventricular tachycardias arising from an arrhythmogenic chronic substrate (previous myocardial infarction, myocardiopathy, etc.). A synchronous DC shock is the treatment of choice in case of lidocaine failure.

Magnesium solfate is the treatment of choice in torsade de pointes.
This arrhythmia is typically due to an excessive lengthening of repolarization and is facilitated by bradycardia. Ventricular pacing (100-110 bpm) - by shortening repolarization - is very effective in preventing recurrences of the arrhythmia.

In patients where a definite diagnosis of supraventricular tachycardia with aberrant conduction has been made, the treatment is the same as for narrow-QRS tachycardias, avoiding drugs adversely affecting intraventricular conduction (namely IC class agents). Conversely, these drugs are of first choice in antidromic atrio-ventricular reentry tachycardias or in pre-excited atrial fibrillation.

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