Wide Complex Tachycardia

Wide Complex Tachycardia | Stethoscope overlying a supraventricular tachycardia ECG reading
Credit: Getty Images | Supraventricular Tachycardia

Wide complex tachycardia (WCT) is a general term describing a group of conditions that present with an accelerated heart rhythm, specifically a heart rate of more than 100 beats per minute (bpm) and a QRS duration of more than 120 milliseconds. WCT can be loosely divided into 2 types: ventricular tachycardia (VT) and supraventricular WCT (SWCT).1,2

Ventricular Tachycardia

Ventricular tachycardia is the most common type of wide complex tachycardia. It is defined as a sequence of 3 or more ventricular beats with a frequency greater than 100 bpm. Ventricular tachycardia can be further classified as nonsustained or sustained, depending on the arrhythmia duration.

Nonsustained ventricular tachycardia refers to an arrhythmia with a duration of less than 30 seconds. Sustained ventricular tachycardia describes an arrhythmia lasting more than 30 seconds or one during which the patient experiences hemodynamic instability in less than 30 seconds. Ventricular tachycardia usually manifests as a heart rate ranging from 100 bpm to 200 bpm; in most patients with ventricular tachycardia, the heart rate exceeds 170 bpm.1,3,4

Supraventricular Tachycardia

Supraventricular wide complex tachycardia, a relatively rare form of WCT, is defined as any WCT that does not originate in the ventricles. There are many possible variations of supraventricular wide complex tachycardia, but there are 4 main types5

  • Aberrant conduction;
  • Ventricle pre-excitement via accessory pathway conduction;
  • QRS duration prolongation due to metabolic abnormalities; and 
  • Rapid ventricular pacing.

Historical Background

The evolution in understanding tachycardia and other arrhythmias, including ventricular arrhythmias, is closely related to the history of electrocardiography. The string galvanometer, created in 1901, was the first tool to effectively measure electrical activity from the body’s surface, and its use led to rapid development in the study of tachycardia and related heart conditions.6 

For most of the 20th century, the roving electrode was the primary means of mapping electrical activity in the heart, but it was reliable only for strictly regular forms of arrhythmia. The first intentional activation and stopping of tachycardias occurred in experimental and clinical demonstrations conducted in the 1960s.6

In the late 1970s, systems were developed that enabled measurements to be made simultaneously from multiple electrical positions. As a result of these innovations, arrhythmias could be measured with greater accuracy, and more types could be defined. Clinical data accumulated since that time have informed current approaches to the management of wide complex tachycardia.6


Wide complex tachycardia is a major contributor to sudden cardiac death.4 Approximately 80% of WCT cases are due to ventricular tachycardia,1,7 and this estimate may be even higher given the difficulty in gathering accurate data.7 In the United States, ventricular tachycardia alone accounts for approximately 50% of cardiac deaths and 15% of all-cause deaths. Ventricular tachycardia that progresses to ventricular fibrillation (VF) often results in sudden death.4 

The most common subtype of supraventricular wide complex tachycardia is aberrant conduction. In aberrant conduction, supraventricular electrical impulses are conducted through the ventricle tissues. Aberrant conduction accounts for approximately 15% of WCT cases.8

Etiology & Wide Complex Tachycardia Risk Factors

Distinguishing between the many possible causes of wide complex tachycardia is key to establishing a differential diagnosis of wide complex tachycardia and determining appropriate wide complex tachycardia treatment. Some of the most common causes of WCT include: 

  • Acute myocardial infarction3,4,7
  • Inflammatory disease of the heart3
  • Infectious disease of the heart3
  • Ischemic heart disease3,4
  • Structural heart disease3
  • Electrolyte imbalances, such as hyperkalemia3,7 
  • Side effects of return of spontaneous circulation (ROSC), resuscitation7
  • Pacemaker-mediated tachycardia7
  • Overdose or toxicity of certain illicit drugs, such as cocaine7
  • Effects of digitalis poisoning3,7

Wide complex tachycardias most commonly occur in people older than 35 years, and they generally occur more frequently in men. Other key risk factors contributing to wide complex tachycardias include a history of heart conditions. Regarding ventricular tachycardia in particular, a history of structural heart disease is a strong indicator, especially in a patient with a prior myocardial infarction. Structural heart disease also increases the risk of WCT in children.3,4,9,10

Triggering Agents for Supraventricular Tachycardia

Among people considered to be at increased risk for wide complex tachycardia, the following are believed to be triggering agents for supraventricular wide complex tachycardia: 

  • Caffeine11
  • Alcohol consumption11
  • Stress11
  • Certain medications

A history of using medications specifically known to have proarrhythmic effects also may be a risk factor and can narrow down the possible causes of WCT.9


The prognosis of wide complex tachycardia varies depending on the mechanisms underlying the condition. Urgent wide complex tachycardia treatment is required for any patient with hemodynamic instability. Because many patients with WCT are hemodynamically stable, however, identification of the specific type of WCT in an individual patient is essential to improve prognosis.7,12

Ventricular & Supraventricular Tachycardia Prognosis

As previously noted, sustained ventricular tachycardia in particular contributes significantly to cases of sudden cardiac death.4 Nonsustained ventricular tachycardia has been linked to long-term increases in the risk of death, but this risk typically disappears after associated conditions have been identified and addressed.13 Mortality risk associated with supraventricular wide complex tachycardia varies depending on the type, but it is generally not fatal.12

Sustained ventricular tachycardia can lead to fainting and possibly cardiac arrest. Because at any time ventricular tachycardia can also degenerate into ventricular fibrillation — which can be fatal in a matter of minutes — urgent treatment of sustained ventricular tachycardia is warranted.13,14 

Wide Complex Tachycardia Diagnosis & Presentation

Wide complex tachycardia can cause a wide range of visible symptoms. People who are unstable due to the condition may present with7

  • Hypotension
  • Pulmonary edema
  • Reduced body temperature
  • Altered mental status
  • Unusual pallor

In stable patients, persistent chest pain is common and may occur in conjunction with shortness of breath, nausea, and dizziness.7

Patients with WCT may also be asymptomatic or only present with relatively mild symptoms such as palpitations or slight lightheadedness, especially in cases of hemodynamically stable, nonsustained ventricular tachycardia.9

Medical History

Medical history is a key indicator of wide complex tachycardia, with a history of myocardial infarction, coronary artery disease, and/or congestive heart failure found to be predictive of ventricular tachycardia. Use of antiarrhythmic drugs and pacemakers is also known to cause WCT.7

Diagnostic Wide Complex Tachycardia Workup/Physical Examination

The standard first step to confirm a diagnosis of any type of wide complex tachycardia is use of a 12-lead electrocardiogram (ECG) or another imaging method, such as cardiac magnetic resonance imaging (MRI).4,7

Further testing varies depending on prior results, symptoms, and medical history. Treadmill stress tests are used in cases of symptoms related to exercise or ischemic heart disease. Ambulatory ECG may be used for patients who have experienced fainting and palpitations but had no arrhythmia detected by the first ECG.4,7

Differential Diagnosis of Wide Complex Tachycardia

wide qrs complex tachycardia table

Certain other conditions need to be differentiated from tachycardias and may manifest with similar visible symptoms.

Differential Diagnosis with Bradycardia

Bradycardia, a condition in which the heart rate slows to fewer than 60 bpm, is known to cause15

  • Chest pain,
  • Fainting,
  • Lightheadedness,
  • Dizziness, and
  • Confusion

Because a differential diagnosis of wide complex tachycardia from bradycardia can be accomplished once a patient’s heart rate has been measured, clinical problems usually arise only in the most urgent situations.15

Differential Diagnosis with Noncardiac Conditions

Certain noncardiac conditions may also symptoms similar to those of wide complex tachycardia and can be more difficult to quickly produce a differential diagnosis from cardiac problems. For example, insufficient delivery of oxygen to vital organs due to anemia, hemoglobin malfunction, or respiratory issues may trigger symptoms similar to those associated with cardiac events, including10:

  • Dizziness,
  • Fainting, and
  • Chest pain

Seizures and other brain conditions may cause an increased heart rate and changes to consciousness similar to those seen in patients with primary tachycardias. Some medications and stimulants, such as anticholinergic and antihypertensive agents, can result in similar symptoms, especially in the setting of overdose.10

Wide Complex Tachycardia ICD 10 Codes

These are the relevant ICD 10 codes for wide complex tachycardia.

I47.1Supraventricular tachycardia
I47.2Ventricular tachycardia
I47.9Paroxysmal tachycardia – unspecified
I47.9Paroxysmal tachycardia, unspecified
Wide Complex Tachycardia ICD 10


The key challenge presented by wide complex tachycardia is the need to quickly and accurately identify and treat the specific type of condition in a potential emergency situation. This ability is critical to preserving the patient’s life, especially when there is a history of serious heart conditions.


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9. Lam P, Saba S. Approach to the evaluation and management of wide complex tachycardias. Indian Pacing Electrophysiol J. 2002;2(4):120-126.

10. Marill KA. Tachydysrhythmias. In: Adams JG, Barton ED, Collings JL, DeBlieux PMC, Gisondi MA, Nadel ES, eds. Emergency Medicine. 2nd ed. Saunders; 2013:497-513.e2.

11. Medi C, Kalman JM, Freedman SB. Supraventricular tachycardia. Med J Aust. 2009;190(5):255-260. doi:10.5694/j.1326-5377.2009.tb02388.x 

12. McGill TD, Kashou AH, Deshmukh AJ, LoCoco S, May AM, DeSimone CV. Wide complex tachycardia differentiation: an examination of traditional and contemporary approaches. J Electrocardiol. 2020;60:203-208. doi:10.1016/j.jelectrocard.2020.04.006 

13. Stevenson WG, Zeppenfield K. Ventricular arrhythmias. In: Libby P, Bonow RO, Mann DL, Tomaselli GF, Bhatt DL, Solomon SD, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine.12th ed. Elsevier, Inc; 2022:1288-1311. 

14. Ventricular fibrillation. American Heart Association. Updated November 15, 2022. Accessed November 29, 2022.

15. Kusumoto FM, Schoenfield MH, Barrett C, et al. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(8):16(9):e382-e482. doi:10.1161/CIR.0000000000000628

Author Bio

Martyn Bryson, a medical writer and editor living in Philadelphia, Pennsylvania, has more than a decade of experience covering a wide range of health and wellness topics.