Affirming Arrhythmia Diagnosis Using All Available Electrocardiography Leads.

Abstract

Scenario: The rhythm strip below (leads II and V1) was an alarm for ventricular tachycardia (VT) in a 72-year-old man being treated in the cardiac intensive care unit for an acute exacerbation of heart failure. The patient was intubated and thus unable to report symptoms. His blood pressure was unchanged during the alarm (90/50 mm Hg). The patient has a history of coronary artery disease, heart failure due to ischemic heart disease, and paroxysmal atrial fibrillation. The nurse noted the wide QRS complex in lead II but not V1 and wondered if this was true VT given the wide QRS complex; thus, he printed a rhythm strip with additional electrocardiography (ECG) leads (see next page).The baseline rhythm is sinus tachycardia with left bundle branch block pattern (ie, P waves present, QRS > 120 milliseconds, deep S wave in V1, and discordant T waves). There is a single episode of nonsustained VT (NSVT, ie, >6 consecutive premature beats at rate >120/min and lasting <30 seconds). Throughout, there are low-amplitude QRS segments during baseline rhythm (most likely due to heart failure).Although VT is not entirely distinguishable in leads II and V1, which are typically displayed on the bedside monitor, evaluation of leads I and III confirms that this arrhythmia is NSVT, emphasizing the importance of examining multiple leads during arrhythmia interpretation. Lead V1 is typically very useful for diagnosing wide complex tachycardias versus supraventricular tachycardia with aberrancy; however, lead V1 is not helpful in this example, most likely because the abnormal depolarization of the myocardium is perpendicular to where this lead is on the body surface; thus, visible and distinct QRS waveforms are not seen. Although lead II is somewhat better for assessing the origin of this arrhythmia, leads I and III are very helpful and confirm the presence of NSVT. One strong ECG criterion for VT is a QRS width greater than 0.16 seconds (4 small boxes), which is met in lead I.In patients with underlying structural heart disease, myocardial infarction, and/or heart failure, the chance of a wide complex tachycardia being VT is 90%. Patients with heart failure (this patient’s primary problem) often have VT, and it is a significant cause of mortality in such patients. This patient was taking amiodarone to prevent VT before admission and continued receiving this medication during hospitalization; hence, he was on guideline-based therapy. Given this, his QT interval measured at the upper limit of normal is expected. Although antiarrhythmic drugs are commonly used to prevent and treat VT, this strategy is not always effective for preventing VT in patients with heart failure. Cardiology should be notified. Determine why and for how long this patient has been in sinus tachycardia and treat as indicated. One source of VT is myocardial ischemia, which could be exacerbated in the presence of tachycardia via demand-related ischemia. Given the underlying left bundle branch block, ST-segment interpretation for ischemia is con-founded. Treat this problem if indicated. Measure potassium and magnesium levels to ensure they are not the problem. Vigilant ECG monitoring should be continued because this rhythm could recur and deteriorate into ventricular fibrillation. Consider applying multifunction pads to the patient’s torso if ischemia is suspected and/or electrolyte levels are abnormal. Anticipate an evaluation for an implantable cardioverter defibrillator.