Tachycardia: Wide-Complex, Cardioversion, Adenosine, VT, SVT
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Differentiating Types Of Wide-Complex Tachycardia To Determine Appropriate Treatment In The Emergency Department

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Table of Contents
Table of Contents
  1. Abstract
  2. Case Presentations
  3. Introduction
  4. Critical Appraisal of the Literature
  5. Etiology And Pathophysiology
  6. Differential Diagnosis
  7. Prehospital Care
  8. Emergency Department Evaluation
    1. History
    2. Physical Examination
  9. Diagnostic Studies
    1. The Diagnostic Utility Of Electrocardiography
      1. Rate
      2. Axis
      3. QRS Duration And Morphology
      4. Concordance
      5. Atrioventricular Dissociation, Capture Beats, And Fusion Beats
      6. Comparison To Prior Electrocardiograms
    2. Diagnostic Algorithms
    3. The Role Of Adenosine
      1. Diagnostic Utility
    4. Laboratory Analysis
      1. Electrolytes
      2. Cardiac Biomarkers
      3. Toxicology Screening
  10. Treatment
  11. Special Circumstances
    1. Irregular Wide-Complex Tachycardia With Wolff-Parkinson-White Syndrome
    2. Ventricular Tachycardia As A Consequence Of Acute Myocardial Infarction
    3. Right Ventricular Outflow Tract Ventricular Tachycardia
    4. Wide-Complex Tachycardia In The Patient With An Implantable Pacemaker
  12. Controversies/Cutting Edge
    1. Predicting Tachydysrhythmias
    2. Electrical Therapy
    3. New Medications
  13. Disposition
    1. Patients Appropriate For Discharge
  14. Summary
  15. Selected Abbreviations
  16. Risk Management Pitfalls In Managing Wide-Complex Tachycardia
  17. Case Conclusions
  18. Clinical Pathway For Initial Management Of Stable, Regular Wide-Complex Tachycardia
  19. Clinical Pathway For Medical Management Of Stable, Irregular Wide-Complex Tachycardia
  20. Tables and Figures
    1. Table 1. Types Of Wide-Complex Tachycardia With Historical Factors And Electrocardiographic
    2. Table 2. Point Estimates Of Pooled Data, Historical Factors And Electrocardiogram Findings In Patients With Ventricular Tachycardia Or Supraventricular Tachycardia
    3. Figure 1. Wide-Complex Tachycardia Due To Hyperkalemia
    4. Figure 2. Wide-Complex Tachycardia With Right Bundle Branch Block Pattern Before And After Adenosine
    5. Figure 3. Types Of Supraventricular Tachycardia
    6. Figure 4. Extreme Right Axis Deviation (Between -180 and -90)
    7. Figure 5. Precordial Concordance
    8. Figure 6. Atrioventricular Dissociation
    9. Figure 7. Capture And Fusion Beats
    10. Figure 8. Supraventricular Tachycardia And Response To Adenosine
    11. Figure 9. Wide-Complex Tachycardia In Special Populations
    12. Figure 10. Pacemaker-Mediated Tachycardia
  21. References


Wide-complex tachycardia is a rare disease entity among patients presenting to the emergency department. However, due to its potential life-threatening nature, emergency clinicians must know how to assess and manage this condition. Wide-complex tachycardia encompasses a range of cardiac dysrhythmias, some of which can be difficult to distinguish and may require specific treatment approaches. This review summarizes the etiology and pathophysiology of wide-complex tachycardia, describes the differential diagnosis, and presents an evidence-based approach to identification of the different types of tachycardias through the use of a thorough history and physical examination, vagal maneuvers, electrocardiography, and adenosine. The treatment options and disposition for patients with various wide-complex tachycardias are also discussed, with attention to special circumstances and select controversial/contemporary topics.

Case Presentations

You're dictating a chart when EMS brings in an ashen-looking middle-aged man clutching his chest and gasping, “I can’t breathe.” You follow him into the room, and, as he’s attached to the monitor, you see a wide-complex tachycardia with a rate of 146 beats/min. His blood pressure is 86/50 mm Hg, and his pulse oximetry is 86%. The tech is already attaching ECG leads, and you note a sternotomy scar on the patient’s chest. You ask for pads to be placed for direct cardioversion; as you’re getting ready to shock, you think, “Should I wait for the ECG? Is this ventricular tachycardia or supraventricular tachycardia? Do I even need to know that before shocking him?”

Later during your shift, you are called into the room by the nurse of a patient you’ve just admitted for syncope. The nurse points at the monitor and yells, "He's in v-tach!" The patient is looking at you quizzically and asks, “What’s going on?” The monitor shows a wide-complex tachycardia. His blood pressure is 135/96 mm Hg, and his pulse oximetry is 94%. You calmly ask for a stat ECG and pads to be placed on the patient. As you watch his ECG print out, you think, “I’m not sure that’s ventricular tachycardia, but it's possibly supraventricular tachycardia with aberrancy. I need to check his potassium levels. Should I use amiodarone first or should I try adenosine?”

In the next room, there is a young female patient you’ve seen every shift for the past 3 days who was checked in with “anxiety.” You think that she is possibly looking for benzodiazepines except, this time, her triage vital signs show a heart rate of 190 beats/min. There is no blood pressure recorded. You go to see her immediately, and she’s hyperventilating and appears anxious. You hook her up to the monitor yourself and note an irregular wide-complex tachycardia. Her blood pressure is 102/69 mm Hg. As you’re calling for a nurse and a tech, you think, “She’s too young for ventricular tachycardia, isn’t she? Maybe she overdosed, or maybe she has a conduction issue. I really need to see this ECG.”


Wide-complex tachycardia (WCT) describes a rhythm in which the heart rate is > 100 beats/min and the QRS complex is > 120 milliseconds. It is essential for emergency clinicians to have a comprehensive understanding of the recognition and management of the different types of WCTs, as many of these rhythms may progress to other sudden, life-threatening dysrhythmias or progressive cardiomyopathy without prompt treatment. Furthermore, if a WCT is misdiagnosed, subsequent delayed or inappropriate therapeutic decisions can portend further hemodynamic compromise.

Unfortunately, despite the numerous algorithms published in the literature, there are no electrocardiographic criteria that can definitively diagnose aspecific WCT, and agreement with regard to rhythm identification is inconsistent.1,2 This issue of Emergency Medicine Practice will provide you with the tools that are required to recognize, diagnose, and treat common etiologies of WCT.

Critical Appraisal Of The Literature

A PubMed literature search was performed using the search terms wide complex tachycardia, broad complex tachycardia, wide complex dysrhythmia, wide QRS complex tachycardia, broad QRS complex tachycardia, ventricular tachycardia, supraventricular tachycardia, and ventricular arrhythmia. These terms were also used in conjunction with the terms emergency department, prehospital, clinical signs, clinical history, vagal maneuvers, hyperkalemia, and tricyclic antidepressant. This search yielded a total of 949 references from 1964 to June 2014, which were reviewed for relevance. A literature search of the Cochrane Database using the same search terms yielded a total of 7 reviews, only 1 of which was relevant for the current topic. The position statements of the American Heart Association (AHA), the American College of Cardiology (ACC), the European Society of Cardiology (ESC), and the European Resuscitation Council (ERC) were also reviewed.

Current consensus guidelines from the cardiology literature, including those put forth by the AHA, ACC, ESC, and ERC, focus on the identification and treatment of ventricular tachycardia rather than wide-complex tachycardia alone.3-5 The 2010 AHA5 and 2010 ERC guidelines4 provide protocols for cardiopulmonary resuscitation, but they do not address the nuances of ventricular dysrhythmia management.

A combined position statement from the ACC, AHA, and ESC on the management of ventricular arrhythmias was issued in 2006, and it provides a considerably more detailed discussion.3 For this guideline, the collaborative performed a comprehensive literature review of specific topics and then issued a consensus statement for each. While broader in scope than the AHA and ERC resuscitation guidelines, it does not include current evidence.

Risk Management Pitfalls In Managing Wide-Complex Tachycardia

1. “There’s no way that’s VT. The patient is completely stable.”
A patient’s hemodynamic status is a poor predictor of VT. The diagnosis should be made based on examination of the 12-lead ECG, and treatment should be tailored appropriately.

2. “Maybe if I just try to shock him at 200 J again, it’ll work.”
Be cautious when repeating treatments, including electrical cardioversion, if the patient is not responding as expected. Hyperkalemia and drug toxicity can mimic VT, as can sinus tachycardia with a BBB, and all such cases will be refractory to DCCV.

3. “She’s got a pacemaker, so I’ll bet that’s just sinus tachycardia on the monitor.”
Patients with pacemakers that trigger ventricular contraction will, by definition, demonstrate a WCT while in sinus tachycardia. However, these patients may also have underlying ischemic or structural heart disease that can put them at risk for slow VT. Always obtain a 12-lead ECG and do not rely solely on the single lead displayed on the monitor.

4. “This kid’s barely 18 years old, so this irregular WCT has to be WPW with AF, right?”
In young adults, be sure to consider the risk of VT before assuming that the dysrhythmia is secondary to SVT. Long-QT syndrome, congenital heart defects, and drugs can increase the risk of ventricular dysrhythmias.

5. “This QRS complex doesn’t look that different from the BBB seen on prior ECGs, so I’m sure it’s just SVT with aberrancy.”
VT in patients with underlying BBB can demonstrate major changes, minor changes, or no change at all in QRS morphology. Look for other ECG criteria associated with VT before assuming that it is SVT with aberrancy.

6. “I know this has to be torsades de pointes! Let’s just give 2 g of magnesium.”
Remember that torsades de pointes secondary to prolonged QT is only one etiology of polymorphic VT, so consider acute cardiac ischemia when a patient presents in this rhythm.

7. “Well, he’s stable, so let’s avoid electrical cardioversion and just use amiodarone.”
Although amiodarone is the first-line agent for treatment of VT in the ERC guidelines, several studies have suggested that amiodarone may be less effective than other drugs, and procainamide is the first-line treatment recommended by the ACC/AHA.

8. “He didn’t respond to adenosine, so it must be VT.”
Although the vast majority of SVTs will demonstrate some response to adenosine, there are some SVTs that will not respond. Furthermore, right ventricular outflow tract tachycardia may terminate with adenosine administration. Keep in mind that adenosine must be pushed rapidly with a flush and that some patients will respond to a 12-mg dose, even when they don’t respond to 6 mg.

9. “This patient’s WCT could be related to hyperkalemia, but she’s pretty stable, so I’ll just start procainamide and wait for her potassium level to come back from the lab.”
WCT secondary to hyperkalemia will not respond to antidysrhythmics, and it carries a high risk of hemodynamic decompensation and cardiac arrest. If hyperkalemia is suspected, administer calcium to stabilize the myocyte membrane. Calcium administration will have minimal adverse effects on other mechanisms of WCT.

10. “This is new-onset SVT, so this patient has got to be admitted.”
Young patients with a primary SVT who do not have symptoms or signs of myocardial ischemia, and who are stable throughout the ED course after conversion to sinus rhythm, can be safely discharged home.

Tables and Figures

Table 1. Types Of Wide-Complex Tachycardia With Historical Factors And Electrocardiographic


Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.

To help the reader judge the strength of each reference, pertinent information about the study will be included in bold type following the reference, where available. In addition, the most informative references cited in this paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference.

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Publication Information

Ian S. deSouza, MD; Alanna C. Peterson, MD, MS; Keith A. Marill, MD

Publication Date

July 1, 2015

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