Ventricular Tachycardia
Christopher P. Kovach, MD, MSc
Mala M. Sanchez, MD
You admit a 68-year-old woman with atrial fibrillation, hypertension, and hyperlipidemia who presented with 15- to 30-second episodes of lightheadedness and palpitations. She reports weight gain and leg swelling after a recent holiday celebration with family, after which she has not been able to sleep without propping herself with pillows. Shortly after admission, you are paged that she is experiencing active palpitations. At the bedside, you find the patient awake and without acute distress. She is tachycardic with heart rate in the 170s and a normal blood pressure.
Her telemetry rhythm strip demonstrates the following wide-complex tachycardia (WCT):
You compare this tracing to the patient’s baseline ECG (shown below) and weigh whether the patient’s current WCT is more consistent with sustained monomorphic ventricular tachycardia (hereafter stable VT) or supraventricular tachycardia (SVT) with aberrancy.
How can VT and SVT with aberrancy be distinguished by ECG?
Algorithmic ECG interpretation approaches can be used to differentiate VT from SVT with aberrancy. In particular, the presence of atrioventricular (AV) dissociation or precordial QRS concordance or northwest QRS axis (>270°) by ECG is nearly 100% predictive of VT.
In a narrative review,1 authors discussed selected studies published over a period of 50 years that focused on deriving and/or validating the ability of ECG findings to predict VT. Stratifying their findings by QRS morphology, the authors reported positive predictive value (PPV) for a range of ECG findings (Table 23.1). Of these, they found that the presence of AV dissociation, QRS concordance in the precordial leads, and extreme “northwest” QRS axis (i.e., >270°) were the most suggestive of VT in both left and right bundle branch QRS morphologies. Three ECG findings that suggest AV dissociation are (1) QRS complexes occurring more rapidly than, and independently of, P waves, (2) the presence of intermittent normal, nonwide QRS complexes interrupting the WCT (known as “capture beats”), and (3) the presence of hybrid atrial/ventricular complexes interrupting the WCT (known as “fusion beats”).
TABLE 23.1 PPV of Specific ECG Criteria for the Identification of VT | ||||||||||||||||||||||||
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Multiple algorithms for interpreting ECG findings and differentiating between VT and SVT with aberrancy have been established. A retrospective analysis2 of 260 WCTs evaluated the performance characteristics of the Brugada, Bayesian, Griffith, lead aVR, and lead II R-wave peak time algorithms in a sample of 204 patients. ECGs from unselected, consecutive patients were analyzed using algorithms by a blinded cardiologist and cardiac electrophysiologist. Ultimate diagnoses were confirmed by the study team via either electrophysiology (EP) study, intracardiac ECG from an implanted device, or subsequent ECGs. The algorithms were found to have similarly moderate diagnostic accuracy for VT (i.e., arrived at the correct diagnosis approximately 69%-77% of the time). The Brugada algorithm was found to have superior accuracy compared to R-wave peak time (P = .04).
Upon recheck, her heart rate continues to be elevated in the 160s-170s with normal blood pressure. Based on these vital signs and her ECG and rhythm strip findings, which show AV dissociation and fusion beats, you conclude that she is currently in stable VT and consider pharmacologic options for terminating the rhythm.
Which antiarrhythmic drugs can be used to terminate stable VT?
Several medications have efficacy for terminating stable VT, including amiodarone, lidocaine, and procainamide. In particular, evidence supports the effectiveness of procainamide.
This question was addressed in a 2013 systematic review3 that screened 574 studies and ultimately identified 5 high-quality studies (3 prospective, 2 retrospective) comparing the effect of IV antiarrhythmics on stable VT. Studies measuring the suppressive effect of IV drugs on electrophysiologic inducibility of VT were excluded. The authors determined that procainamide was superior to lidocaine (RR 2.2, 95% CI 1.2-4.0; P-value not reported; number needed to treat [NNT] 2.5) but that amiodarone and procainamide were equivalent (RR 4.3, 95% CI 0.8-23.6; NNT 3.0). A major study caveat was limited available evidence.