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

     Most paramedics have little difficulty correctly identifying narrow complex SVTs, but the presence of aberrancy gives rise to some diagnostic complications. Aberrancy, aberrant conduction and aberration are all terms used to describe an abnormal conduction of electrical impulses through the heart.3 Just as previously described in the setting of VT, these waywardly conducted signals of SVT take longer to transmit through the myocardium, and consequently produce a wide QRS complex in an ECG.1 This aberrant conduction may be distinguished from a bundle branch block (BBB), which it resembles, though the distinction is nearly impossible to make in the field. BBBs are physiological blockages of the bundle branches that cause part of the wave of depolarization to travel outside of the normal cardiac conduction system, thus taking more time and widening the QRS. Aberrancy's abnormal mechanism of conduction is caused by a difference in refractory periods between the right and left bundle branches, not a permanent physiological blockage.4 Many SVTs with aberrancy are the result of increased atrial activity (atrial fibrillation, multifocal atrial tachycardia, atrial flutter, etc.), coupled with an increase in automaticity of the AV node. The premature signals caused by the atrial delinquency provide the perfect environment for aberrancy to thrive. Either SVTs with aberrant conduction or SVTs with preexisting BBBs may mimic VTs. We will group SVTs with aberrancy and SVTs with BBBs together and call it SVTs with aberrant conduction.

     At first glance, SVTs with aberrant conduction looks a lot like VTs and are virtually indistinguishable from VT in a single viewing lead.1 When viewed in 12 different ECG leads, however, subtle differences help to differentiate the two rhythms. Following are pieces of a diagnostic puzzle that, when used in conjunction with other assessment tools, will help build a case for either VT or SVT with aberrant conduction. No one piece of this puzzle can stand alone, but combining the diagnostic pieces (electrocardiographical clues) with the assessment factors (clinical clues), one should have a solid foundation on which to build a case for either VT or SVT with aberrant conduction.

     The first few diagnostic puzzle pieces are easy to recognize on a 12-lead ECG and are useful when a quick diagnostic impression needs to be formed. The remaining pieces are more advanced and require a little more time and investigation.

Electrographical clues

Irregularity
One of the most common and obvious characteristics of VT is that it is usually regular in presentation.1 Monomorphic VT originates from one area and is many times a re-entrant process. Regardless if the mechanism is due to re-entry or to a single ectopic foci, the rhythm will be regular. By contrast, the rhythm in SVT is often irregular, as the origin of this tachycardia is often either atrial fibrillation or multi-focal atrial tachycardia, both of which are themselves irregular (see Figure 1). Of course, if the SVT is due to re-entry, then the SVT will be regular, as well. However, most SVTs that are a result of a re-entrant mechanism do not cause aberration and are not commonly associated with a BBB. This leaves VT as the most common regular, wide and fast rhythm.

QRS concordance in precordial leads

Monomorphic VT will be displayed in leads V1--V6 as either all-positive or all-negative complexes (Figure 2). On the other hand, SVT with aberrant conduction will exhibit a mix of upright and inverted complexes throughout the precordial leads (Figure 3).6

Electrical axis

     SVTs with aberrancy will produce either a right or left axis deviation. If the aberrancy is conducted in a RBBB pattern, right axis deviation will be present. If the aberrancy is conducted in a LBBB pattern, left axis deviation will be present. In almost all VT, the axis will be in the extreme right quadrant (Table I).6

QRS width

     As a trend, a QRS complex that is 0.14 seconds or greater favors VT. Aberrant rhythms and BBBs rarely achieve that degree of width.5

Noncorrelated P-waves

     Many times in VT, AV dissociation occurs. The atria and ventricles are both firing impulses and contracting at different rates, which is seen on the ECG tracing as P-waves with no relationship to the presenting wide QRS complexes. In SVT with aberrant conduction, P-waves, if present and identifiable (i.e., not a-fib), will correlate with a following QRS complex (Figure 4--arrows indicate noncorrelated P-waves).5

Capture beats

     Since AV dissociation in VT is temporary and oftentimes intermittent, the atria will occasionally be able to conduct a beat through the AV node that results in a normal QRS complex. These are known as capture beats (Figure 5). SVT does not produce capture beats with a narrow QRS width because, in a sense, all of the beats capture in SVT (but exhibit wide QRS morphology due to the aberrancy).6

Fusion complexes

     Fusion complexes are the result of two waves of depolarization (one from the atria and the other from the ventricles) that meld into one complex unlike those that precede or follow. Much like capture beats, fusion complexes are seen when a physiological AV block, often found in VT, fails to block an atrial impulse and is conducted into the ventricular depolarization wave. The resultant offspring beat has characteristics of both an atrial and ventricular complex (Figure 6). Fusion complexes are usually only found in VT.6

Josephson's sign

     The presence of a notch on the downstroke of the S-wave in the septal leads (called Josephson's sign) builds a case for VT. Josephson's sign is not always easily detected, but as time progresses it will begin to stand out as a common calling card that VT leaves behind (Figure 7).1

Brugada's sign

     Brugada's sign is present when the measurement from the beginning of the QRS complex to its nadir (the center of the QRS complex) is greater than 0.10 seconds. If Brugada's sign is present, VT is heavily favored. This is an indirect correlation between width and VT. As noted previously, SVTs with aberrant conduction are wide, but VTs are usually a bit wider. The naked eye cannot readily distinguish between 0.1 seconds and 0.08 seconds; therefore, it is important to measure the QRS width with a pair of calipers and determine whether Brugada's sign is present (Figure 8).1

QRS morphology

     Approximately 60% of all monomorphic VTs conduct in a RBBB pattern, with 92% of those showing a monophasic R or a diphasic qR wave in V1. In addition, diphasic QS or rS complexes in V6 strongly favor VT.3

     Wide complex rhythms that present in a LBBB pattern or in a diphasic pattern that contains a q wave (qR or QS) in lead V6 strongly favor VT.

     Approximately 80%--85% of aberrant beats are conducted with a RBBB pattern.3 Of those, 70% conduct in a triphasic rsR' pattern in V1. In addition, a triphasic qRs complex in V6 favors aberrancy (Figure 9).3

     Alternating bundle branch block patterns

     In transient aberrancy (not associated with a permanent BBB), it is a common occurrence to have both LBBB and RBBB patterns expressed in the same patient. This bilateral aberrancy occurs when a patient is experiencing ventricular aberrancy of one BBB pattern, and, after conducting a normal beat, experiences ventricular aberrancy of the other BBB pattern.4

Clinical Clues

     It cannot be emphasized enough that both SVT and VT can present with serious signs and symptoms, and that immediate cardioversion of unstable patients, be it SVT or VT, is the gold standard of care. The clinical signs and symptoms manifested in these two dysrhythmias give subtle hints that serve as additional clues. These clinical indicators are not meant to be a defining factor in the diagnosis of a dysrhythmia, nor can they serve as the sole criteria in the choice of pharmacological treatment. But they can be used as clinical indicators to help build a case for either VT or SVT with aberration and should only be used in conjunction with other diagnostic tools.

Heart tones

     In AV dissociation, the S1 heart tone (first heart tone) varies in intensity, due to the fact that it represents closure of the AV valves. The intensity of the S1 heart tone is dependent on the proximity of the valve leaflets to each other at the time of ventricular systole.3 When the leaflets are wide open, they slam shut; when they drift close together, they close with minimal sound. The variable intensity of heart tones is a clinical indicator of AV dissociation, favoring VT. Heart tones heard in SVT could be just S1, just S2, or both S1 and S2. In either case, they will not vary in intensity. If a-fib is the driving force of the SVT with aberrant conduction, the heart tones will be irregular, favoring SVT. It is prudent to listen to heart tones on all patients who have cardiac anomalies, as they can reveal many things about the patient. These heart tones can provide physical verification that the mechanical action is consistent with the electrical display. Remember that a wide fast rhythm is called PEA when there are no heart tones present.

Cannon waves

     Occasionally in AV dissociation, the atria and ventricles contract at the same time, causing a dramatic increase in pressure in the heart. Since the ventricles are the more powerful pump, the blood is forced up the superior vena cava and into the jugular veins. This buildup is known as a cannon wave, and can be seen in a patient's neck as an intermittent pulsation of the external jugular veins. This single pulsation only occurs when the atria and ventricles contract at the same time. It can be frequent, however, if the patient's ventricular rate is in tandem, as in a 2:1 conduction. In this case, the cannon wave will be approximately half that of the actual pulse rate. In SVT, cannon waves do not occur, as the atrial impulse always precedes the ventricular impulse; thus AV dissociation does not occur. Presence of cannon waves therefore favors VT.3

Response to vagal stimuli

     Whereas re-entrant tachycardias that originate above the ventricles often convert with a simple vagal maneuver, ventricular tachydysrhythmias seldom respond to vagal stimuli. The ventricular conduction system is not dependent on vagus enervation, and usually only slows when there is a correlation between atrial and ventricular activity.3

Patient history

     A thorough patient history is always indicated, regardless of the patient's presenting signs and symptoms. A patient's history can be the "grain of rice" that tips the scales when differentiating between SVT or VT, as mainstream trends seem to indicate that certain pathological processes give rise to certain dysrhythmias. CHF, a history of MI or hypoperfusion tend to cause arrhythmogenic foci (VT) in the ventricles. AV valve anomalies tend to give rise to arrhythmogenic foci in the atria (SVT).6

Summary

     It is important to mention that not all rhythms are textbook presentations. Certainty exists only in degrees. While the diagnostic clues offered in this article may help to increase certainty as it pertains to diagnosing a WCT, they are not a replacement for continued investigation and discovery regarding cardiac anatomy, physiology and pathophysiology, nor can they be exacting and precise when taken as isolated events. But taken as a whole these clues can build a convincing case for correctly differentiating and treating a WCT. Diagnosing and treating WCTs can be challenging, but with the proper tools, an accurate diagnosis is well within the reach of prehospital care providers (see Table II for a concise summary of electrographical and clinical clues).

References

1. Garcia TB, Miller GT. Arrhythmia Recognition: The Art of Interpretation. Sudbury, MA: Jones and Bartlett, 2004.
2. Janiera LF. Differentiating wide complex tachycardias. American Family Physician 54:5, Oct 1996.
3. Woods SL, et al. Cardiac Nursing, 3rd Ed. Philadelphia, PA: J.B. Lippincott, 1995.
4. Wagner GS. Marriott's Practical Electrocardiography, 10th Ed. Philadelphia, PA: Lippincott, Williams and Wilkins, 2001.
5. Dubin D. Rapid Interpretation of EKGs, 6th Ed. Tampa, FL: Cover, 2000.
6. Conover MB, Marriott HJL. Advanced Concepts in Arrhythmias, 3rd Ed. St. Louis, MO: Mosby, 1998.

Figures
Figures 1, 4: Jenkins D, Gerred S. ECG Library. www.ecglibrary.com/ecghome.html. Jul 1996.
Figures 2, 3: Yanowitz FG. The Alan E. Lindsay ECG Learning Center in Cyberspace. www.medstat.med.utah.edu/kw/ecg.index/html May 2005.

Thanks to all of the people who helped bring this article to fruition: Tom Duffee, EMT-P; Lt. Carla Blazier, CCEMT-P; Frank Giampetro, EMT-P; Daniel Martin, MD, and his colleagues at The Ohio State University Medical Center; Lt. Tom Lawrence; Chiefs Jay and Steve Scaggs; Carolyn Anderson, EMT-P; Scott Woolf, BS, EMT-P; Dr. Jornel Rivera, D.O.; Jennifer Eggerichs, BS, CCEMT-P; Richard Paulus, MD; Rev. Ruth Paulus, RN, MSN; and Mary Paulus, RN, BSN.

Matthew Paulus, BME, NREMT-P, is a full-time paramedic for Madison County Emergency Medical District in London, OH, where he teaches EMS special topics, ACLS, PALS and GEMS.