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<< Tachyarrhythmias In The ED: Best Evidence

Diagnostic Testing

The Electrocardiogram

The ECG plays a central role in the evaluation of patients with tachyarrhythmias. Examination of a single-lead rhythm strip is inadequate. Obtain a high-quality 12-lead ECG with minimal artifact in all patients prior to treatment, unless the patient requires emergent cardioversion or defibrillation. A rhythm strip should be obtained during any intervention, and a 12-lead ECG should be obtained after successful termination of the rhythm. Make liberal use of rhythm strips and calipers, especially when in doubt as to regularity. If you are still unsure whether a rhythm is regular or irregular, obtain an ECG at double paper speed, which will accentuate the irregular nature of the arrhythmia.25

The ECG in sinus tachycardia will demonstrate narrow QRS complexes (unless there is rate-related or underlying conduction delay) at a rate between 100 and150 beats per minute. P waves should be visible, and the P wave axis should be 0º to + 90º. The rate will usually vary with physiologic needs—in other words, faster with agitation, exertion, pain, fever, hypovolemia, or anemia and slower with recumbency, sleep, relief of pain, or fever.

The ECG in SVT will also have narrow QRS complexes (unless there is rate-related or underlying conduction delay) at a rate between 140 and 250 beats per minute that does not vary with physiologic needs. P waves may or may not be discernible on the ECG during the event. Distinct P waves are more likely to be seen inpatients with AV bypass tracts and atrial tachycardia than in patients with AV nodal reentry. (See Figure 8.) In junctional tachycardia, P waves are absent. Don't forget to examine a repeat ECG in patients who are successfully converted from SVT to look for the short PR interval and delta waves diagnostic of Wolff-Parkinson-White syndrome. (See Figure 9.)

The ECG in atrial flutter classically shows narrow QRS complexes at a very steady rate of 150-160 beats per minute with a unique sawtooth pattern in the isoelectric baseline, especially well seen in leads II and V1, which represents regular atrial depolarizations at a rate of 300-320 beats per minute. (See Figure 4.) In some cases, the distinctive sawtooth pattern is not visible because the P waves that form this pattern are hidden within each QRS and T wave. In these patients, vagal maneuvers or agents such as adenosine or calcium-channel blockers will transiently slow the QRS rate (and increase the block), accentuating the classic sawtooth patter.

Atrial fibrillation is recognized by its characteristic irregularly irregular pattern of QRS complexes and absence of discrete P waves. The ventricular rate is typically 140-150 beats per minute but may be slower,even less than 100 beats per minute, in patients who are taking cardioactive drugs or who have impaired conduction at the AV node. The QRS complex is narrow unless there is rate-related or underlying conduction delay.

The ECG diagnosis of multifocal atrial tachycardiarequires the presence of at least three distinct P wave  morphologies in a single lead, presence of an isoelectric baseline between P waves, and an atrial rate in excess of100 beats per minute. (See Figure 2 .) As with all tachyarrhythmias that originate in the atria, the QRS is narrow unless there is rate-related or underlying conduction delay.

Polymorphic ventricular tachycardia features wide QRS complexes (> 0.12 seconds) at a rate over 100 beats per minute and a unique beat-to-beat variation in the QRS amplitude and polarity such that the peaks of the QRS complexes appear to be "twisting" around the isoelectric baseline. This distinctive pattern will be more easily visualized on a rhythm strip or telemetry monitor than on the 12-lead ECG.

The ECG in monomorphic ventricular tachycardia shows wide QRS complexes (in excess of 0.12 seconds) of uniform morphology at a rate over 100 beats per minute. The rate is most commonly between 130 and 170 beats per minute. P waves may or may not be discernible on the 12-lead ECG during monomorphic ventricular tachycardia. Two other findings considered diagnostic of ventricular tachycardia are the presence ofcapture or fusionbeats amidst the uniform wide QRS complexes.(See Figure 10.) These are seen in the presence of AV dissociation when a dissociated P wave completely(capture beat) or partially (fusion beat) depolarizes the ventricles. Capture beats are premature, coming earlier than the next expected QRS complex, and typically have the narrow appearance of a standard sinus beat. Fusion beats are premature and have a QRS duration and morphology that is intermediate between that of a narrow complex and the prevalent wide QRS complex. AV dissociation, ventriculo atrial block, capture beats, and fusion beats are found in only 12%-24% of wide complex tachycardias.8, 26 In wide complex tachycardias without these findings, the ECG diagnosis remains unclear. The wide complex tachycardia could represent monomorphic ventricular tachycardia or SVT with aberrant QRS conduction. The electrocardiographic evaluation of the undifferentiated wide complex tachycardia has been the subject of enormous debate in the literature and deserves special discussion.  

The Wide Complex Tachycardia

Because these four highly reliable ECG findings (AV dissociation, ventriculoatrial block, capture beats, and fusion beats) are seen infrequently in wide complex tachycardias, investigators have endeavored to discover additional ECG criteria that would properly classify a wide complex tachycardia as ventricular tachycardia or aberrant SVT in all cases. Multiple investigators have retrospectively analyzed the ECG in cases of wide complex tachycardia and noted some features that favor ventricular tachycardia and others that favor SVT.8, 26-29 Two investigators have devised formal diagnostic algorithms based on analysis of the ECG and have published sensitivity and specificity information for the proposed diagnostic algorithm.27, 28 Despite these efforts,no one has yet devised a method of ECG analysis that has proven to consistently distinguish ventricular tachycardia from SVT-aberrancy when studied by independent investigators. In 1995, Drew et al studied 133 cases of wide complex tachycardia induced in the electrophysiology laboratory and concluded that 10% of ECGs defy differentiation by any known criteria.29

In 1978, Wellens et al published the first set of electrocardiographic diagnostic criteria for wide complex tachycardia.26 They retrospectively reviewed 140 episodes of wide complex tachycardia in which the final diagnosis had been determined by electrophysiologic study. (See Table 3.)

While this is a landmark paper in the study of wide complex tachycardia, the sensitivity and specificity of these criteria for the diagnosis of ventricular tachycardia and SVT have not been determined. In addition, it has been noted that some wide complex tachycardia ECGs will have contradictory QRS morphology that"favors" ventricular tachycardia in one lead and "favors"SVT in another lead. Akhtar et al evaluated the Wellens criteria and found that 8% of ventricular tachycardia could not be correctly diagnosed and that 14% of aberrant SVT were incorrectly labeled as ventricular tachycardia using these criteria.8

In 1988, Akhtar et al similarly studied 150 consecutive wide complex tachycardia tracings with known electrophysiologic diagnosis and identified eight "highly reliable" ECG criteria for the diagnosis of ventricular tachycardia.8 (See Table 4.) Note that neither Akhtar et alnor subsequent investigators have published sensitivity and specificity data for the eight "highly reliable" ECG criteria when used together for the analysis of wide complex tachycardias.

Brugada et al were the first investigators to devise electrocardiographic diagnostic criteria for wide complex tachycardia that could be applied to all ECG tracings and were the first to publish sensitivity and specificity data. They devised a sequential four-step ECG analysis algorithm. First the clinician looks for absence of an RS complex in all precordial leads. If there is no RS complex in leads V1 through V6, the diagnosis is ventricular tachycardia. If there is at least one RS complex in theprecordial leads, then the clinician proceeds to step two,seeking any precordial RS interval (beginning of R to S wave nadir) greater than 100 milliseconds. If the interval measures 100 milliseconds in anylead, the diagnosis is ventricular tachycardia. If not, step three is to look for AV dissociation. Its presence makes the diagnosis of ventricular tachycardia. If absent, the clinician proceeds to step four, looking to see if both V1 and V6 have morphology characteristic of SVT- aberrancy. If not, the diagnosis's ventricular tachycardia. (See Figure 11.) Brugada et al prospectively analyzed 554 cases of wide complex tachycardia utilizing their algorithm and reported a sensitivity of 98.7% and a specificity of 96.5% for the diagnosis of ventricular tachycardia, potentially an incredible breakthrough in the confusing world of wide complex tachycardia analysis.27 However, in 1996,Herbert et al found that three different emergency physicians utilizing the four-step Brugada algorithm disagreed as to the diagnosis 22% of the time.30 Inaddition, Isenhour et al were unable to independently verify the high sensitivity and specificity published by Brugada, finding sensitivities of 79%-91% and specificities of 43%-70% when the criteria were used by two board-certified emergency physicians and two board-certified cardiologists.31

The most recent diagnostic algorithm for wide complex tachycardia, proposed by Griffith et al in 1994,emphasizes that ventricular tachycardia should be the default diagnosis unless highly reliable ECG criteria for the diagnosis of SVT- aberrancy are present. SVT- aberrancy is diagnosed only if QRS morphology is typical of bundle branch block. (See Table 5.) Any other morphology of the QRS in leads V1 and V6 is diagnosed as ventricular tachycardia by default. Griffith et al found that two observers using these criteria in 102 cases of wide complex tachycardia achieved a sensitivity and specificity for ventricular tachycardia of 90%-91% and67%-85%, respectively.28 If independent P waves diagnostic of AV dissociation were then sought, sensitivity for ventricular tachycardia increased to 96%, with a specificity of 64%. To date no independent investigators have verified the accuracy of the Griffith criteria.

What can we conclude from this look at the evidence on wide complex tachycardia? First, the ECG diagnosis of wide complex tachycardia can be frustrating for even the most expert electrocardiographer. Second, several ECG-based diagnostic criteria have been proposed, and none have been independently verified as being consistently accurate in distinguishing ventricular tachycardia from SVT in all cases. Third, the odds strongly favor ventricular tachycardia rather than aberrant SVT in a patient who presents with wide complex tachycardia, especially if the patient has previously suffered a myocardial infarction. When in doubt, treat a wide complex tachycardia as monomorphic ventricular tachycardia.

Laboratory Studies

Laboratory studies are not needed in all patients,especially those with recurrence of a known and previously evaluated tachyarrhythmia. Most patients with SVT will have no precipitating cause, so very few additional laboratory studies beyond the ECG will be necessary. For other patients with a first presentation of a tachyarrhythmia, laboratory studies may be helpful and should be based on the presenting rhythm.

Measure hemoglobin in patients with unexplained sinus tachycardia to rule out severe anemia. Check thyroid function tests in patients with unexplained tachyarrhythmias, especially in the presence of exophthalmos, goiter, or tremor. A serum digoxin level is indicated in any patient on digoxin who presents with ectopic atrial or junctional tachycardia, especially those with associated second- or third-degree AV block.

In patients with multifocal atrial tachycardia, obtain serum potassium and magnesium levels, since low levels of these electrolytes can precipitate the arrhythmia. Assess arterial oxygenation via pulse oximetry or arterial blood gas analysis and evaluate for digoxin and theophylline toxicity.

In patients with polymorphic ventricular tachycardia, serum potassium, magnesium, and calcium levels may reveal a metabolic precipitant. Obtain a CPK-MB and troponin level to rule out myocardial injury—especially after successful resuscitation from pulseless ventricular tachycardia or ventricular fibrillation.


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Last Modified: 09/22/2017
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