As a result of their locations, ventricular activation during sinus rhythm occurs basally and epicardially. Rare APs also exist between the specialised conduction tissues and the ventricle, but are infrequent enough to place them outside the scope of this review. In some ways, a pacemaker can be thought of as an accessory pathway inserting at the site of the ventricular lead s. Obviously, the presence of a pacing device on physical examination is a strong clue to this possible diagnosis.
Modern bipolar pacemakers use so little voltage, confined to such a small area, that pacemaker spikes are frequently difficult to discern or are even invisible on the ECG. Modern ECG systems compensate for this by adding artificial pacing spikes when they detect the frequency characteristics of a pacing output, but this feature is imperfect in its ability to detect these impulses. The primary goal of a correct diagnosis at presentation is the avoidance of harm.
An SVT incorrectly believed to be VT may be treated with amiodarone or electrical cardioversion — not optimal therapy, but not harmful. If the presenting rhythm was instead atrial flutter, cardioversion in an unanticoagulated patient will incur a 1. In this case, agents with negative inotropic effects such as verapamil or diltiazem may be used to control the presumed SVT. The more insidious consequences of misdiagnosed arrhythmia are found in the long term management of such patients.
Incorrectly diagnosing an SVT as VT may result in the patient receiving long-term amiodarone therapy, or even an implantable defibrillator with repeated generator changes ahead. Regardless of which rhythm is misdiagnosed, potentially curative catheter-based therapies may be inappropriately withheld from the patient. It is a common misconception that a haemodynamically stable patient with minimal symptoms during a WCT episode must have SVT.
Often adding to this assumption is a belief that termination by adenosine or verapamil proves SVT. Again, this assumption can lead to misdiagnosis as some VTs are responsive to one or both of these agents.
Fortunately, the vast majority of these VTs are not associated with significant structural heart disease and sudden death with episodes is extraordinarily rare. Immediate cardioversion of the haemodynamically unstable patient with WCT should be the first thought, and only when some measure of stability has been achieved should a provider delay care to look up and apply the various algorithms described below.
In contrast to the SVTs described above, with relatively constrained modes of ventricular activation, VT can originate from literally any location within the ventricular myocardium or its specialised conduction tissues. As a result of this, VT can appear identical to any of the wide complex SVTs above and it is nearly impossible to say with absolute certainty, from an ECG of free-running tachycardia alone, that a wide complex rhythm must be supraventricular.
As such, most algorithms seeking to discriminate the two entities focus on identifying characteristics unique to VTs — that is to say, those with high specificity for VT — and presume all else to be SVT until proven otherwise; the Griffith algorithm is the notable exception to this approach. Algorithms have been unable to reliably distinguish between VT and pre-excited SVT, since initial ventricular activation in the latter is like most VTs extrinsic to the normal conduction system.
Since pre-excited SVTs comprise such a small proportion of WCTs, they will not be considered further in this discussion. One of the first determinations in looking at a WCT should be its bundle branch block morphology. Ordinarily, the term bundle branch block BBB implies failure to conduct over one or more of the specialised fascicles, but in discussion of WCT, the question is designed more to evaluate which chamber activates last.
This is done by looking at the terminal deflection of lead V1. In Table 2 , we list many of the most popular VT criteria. Many of these criteria e. For such criteria, a predictive value is listed.
In all cases, these numbers were stated explicitly in the original reports or derived from them using standard formulas and 2x2 tables. Most of these criteria are visually depicted in Figure 1.
Each of these criteria correctly point to a diagnosis of VT. The work of Sandler and Marriott published in laid the foundation for the use of ECG criteria instead of, or in complement to, physical exam skills for the diagnosis of VT.
The generally accepted morphology criteria from their work as well as that of other investigators are summarised in Figure 1. A QRS, which is predominantly positive or predominantly negative in every precordial lead, overwhelmingly favours VT. By , two advances had allowed a leap forward in the ECG criteria: the development of the His bundle electrogram and simultaneous multi-lead electrocardiography.
Using these new tools, Wellens et al. Of all criteria, this is the most secure. Its weakness is being able to confidently recognise its presence; in many cases, even when AV dissociation is clearly present on intracardiac recordings during VT, it cannot be readily seen on the ECG. To remedy this, the criteria are applied such that presence of any of the four criteria indicates VT, with an overall accuracy of Published in , the Brugada criteria were the first to offer applicability to all WCT without limitation to one BBB configuration or another.
The criteria are applied in stepwise fashion, stopping further analysis if any step suggests VT. Step 4: Morphology criteria see Figure 1 for details.
Recognising that the morphology criteria can be difficult to remember, some advocate using only steps 1 and 2. Over 1,, fellow IT Pros are already on-board, don't be left out!
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