Distinguishing Wide Complex Tachycardia

     Correct diagnosis of wide complex tachycardia (WCTs) can be challenging. With EMS providers' ever-expanding scope of practice, it is no longer safe to label any rhythm that is wide and fast as ventricular tachycardia (VT). Though many paramedic curricula do not address advanced cardiac dysrhythmias and treatments, several EMS departments have protocols that require advanced training in 12-lead ECG interpretation and treatment of specific cardiac dysrhythmias.

     With the introduction of new pharmacological interventions that target specific areas of the cardiac conduction system, it has become increasingly important for EMS providers to make an accurate interpretation of an ECG. Though most paramedics have no difficulty distinguishing VT from narrow complex supraventricular tachycardia (SVT), some might fall victim to the "wide + fast = VT" trap when looking at SVT with aberrant conduction. Although VT and SVT with aberrant conduction look similar, they vary greatly in terms of origin, pathophysiology and treatment. Mislabeling dysrhythmias can have severe consequences. Improper identification of VT could place a patient in grave danger by delaying indicated pharmacological and electrical interventions.

     A common aphorism among advanced practitioners is, "When in doubt whether a WCT is VT or SVT, treat patients as if they are experiencing VTs."1 This stems from a statistic showing that approximately 80% of all WCTs are VT.1 Though this aphorism is generally a good rule of thumb, it is also important to acknowledge that one in five WCTs is not VT and therefore requires different treatment regimens. One must possess the proper diagnostic tools and knowledge to decide whether a WCT is VT or SVT with aberrant conduction. EMS providers should be able to differentiate VT and SVT with aberrant conduction with confidence and a high degree of certainty. In order to understand the visual differences between VT and SVT with aberrant conduction, one must first understand the basic pathophysiology behind the two dysrhythmias.

Ventricular tachycardia

There are several types of VT caused by many different mechanisms.

     Polymorphic VTs, like torsade de pointes (TDP), have their own footprints that distinguish them from SVTs and are not pertinent to this particular article. Here we address the most common form of VT (monomorphic VT) and the means by which it may be distinguished from SVT with aberrancy.

     Oftentimes, sustained monomorphic VT is the result of a reentry circuit formed through an area of infarct in the ventricles that contains a small pathway of cells still capable of conducting a signal.2 When a wave of depolarization reaches the area of infarct, most of it is transmitted around the infarcted area; however, a small amount of the depolarization wave is transmitted through the narrow pathway of cells in the area of infarct.1 Most of the time, this detached signal is cancelled out by the much larger depolarization wave that is transmitted around the zone of infarct. This cancellation prevents precipitation of a VT dysrhythmia. In simplistic terms, an outside stimuli (usually a premature beat) causes a circuit to form that loops the signal between the noninfarcted tissue surrounding the area of infarct and the narrow pathway through the area of infarct.1 If this re-entrant circuit causes the signal to cycle at 100 beats per minute or greater, it is labeled VT. (This type of re-entry is similar to that which occurs in SVT, where the signal is looped around dual approaches to the AV node.) Ventricular complexes in VT appear wide, due to the fact that the signal is transmitted outside the normal ventricular conduction system and must rely on more time-consuming direct cell-to-cell transmission.1 Remember that width, or horizontal movement, on an ECG represents elapsed time.

SVT with aberrant conduction