Wide QRS Tachycardia (WQRS Tachycardia) is an abnormality in the heart’s electrical system defined by a heart rate that is too fast combined with an unusual pattern of electrical activation in the lower chambers. The rapid rate compromises the heart’s ability to pump blood effectively, potentially leading to symptoms like dizziness, fainting, or more severe consequences. Understanding the source of this abnormal rhythm is paramount, as the treatment for one cause can be harmful if the underlying problem is actually another. A precise diagnostic approach is required to ensure the correct intervention is applied.
What Defines Wide QRS Tachycardia
The designation Wide QRS Tachycardia is an electrocardiogram (ECG) finding composed of two distinct components. Tachycardia refers to a heart rate exceeding 100 beats per minute (bpm). The wide QRS complex indicates that the electrical impulse is traveling through the ventricles in a slow or abnormal manner.
The QRS complex represents the electrical event that causes the ventricles, the heart’s main pumping chambers, to contract. In a normal heart, this impulse travels quickly down a specialized conduction system, resulting in a narrow QRS complex. A QRS complex is considered “wide” when its duration is 0.12 seconds (120 milliseconds) or longer. This widening signifies that the electrical signal is not using the His-Purkinje system but is instead moving slowly from muscle cell to muscle cell.
Primary Origin: Ventricular Tachycardia
The primary cause of WQRS Tachycardia is Ventricular Tachycardia (VT), which originates directly within the ventricles. This rhythm bypasses the heart’s normal electrical control centers in the upper chambers, taking over the heart’s pacing function. VT is responsible for approximately 80% of all WQRS Tachycardia cases, a percentage that climbs to about 90% in people with underlying heart disease.
VT commonly develops in hearts that have been previously damaged, creating electrically unstable areas. The most common underlying cause is scar tissue formed after a prior heart attack (myocardial infarction). This scar tissue disrupts the normal flow of electricity, forcing the impulse to travel around the damaged area and creating a re-entrant electrical circuit. Other conditions that structurally alter the heart muscle, such as cardiomyopathy or severe structural heart disease, also predispose a person to VT.
When the ventricles beat rapidly, they do not have enough time to fill completely with blood between contractions. This reduces the amount of blood pumped out to the body, leading to decreased oxygen supply to organs. Sustained VT can quickly progress to Ventricular Fibrillation (VF), a disorganized electrical chaos where the heart muscle quivers instead of pumping. VF is a direct cause of sudden cardiac arrest and requires immediate intervention.
Secondary Origins: Supraventricular Tachycardia with Conduction Defects
While VT is the most common origin, WQRS Tachycardia can also arise from an impulse beginning in the upper part of the heart, known as Supraventricular Tachycardia (SVT). The rhythm originates above the ventricles, but the electrical signal encounters a defect while traveling through the ventricular wiring. This slow, abnormal travel creates the wide QRS complex, mimicking VT.
One mechanism is called aberrancy, which occurs when the rapid supraventricular impulse encounters a temporary or permanent block in one of the bundle branches. The impulse must travel down the remaining functioning branch and spread through the ventricular muscle, a slower process that widens the QRS complex. This abnormal conduction is often rate-related, meaning the fast heart rate “outruns” the ability of one bundle branch to reset quickly enough.
Another secondary cause involves an accessory pathway, an extra electrical connection between the atria and the ventricles. In conditions like Wolff-Parkinson-White syndrome, the impulse travels down this bypass tract instead of the normal route. Since the bypass tract is not part of the specialized fast conduction system, the impulse enters the ventricles early and spreads slowly. This results in a wide QRS complex pattern known as antidromic atrioventricular re-entrant tachycardia.
Urgency and Implications of Diagnosis
The presence of WQRS Tachycardia is treated as a medical emergency due to the risk of rapid deterioration. Because of the high mortality risk associated with VT, if the exact origin cannot be immediately confirmed, the condition must be treated as VT until proven otherwise. This emphasizes the need for rapid and accurate differentiation.
Distinguishing between VT and SVT with aberrancy is crucial because the treatments are different and sometimes contradictory. Certain antiarrhythmic medications, such as calcium channel blockers, are appropriate for some SVTs but can cause hemodynamic collapse and be fatal if given to a patient with VT. Conversely, drugs like Amiodarone are commonly used as a first-line treatment for VT.
For patients who are hemodynamically unstable—exhibiting low blood pressure, altered mental status, or acute heart failure—immediate electrical cardioversion is necessary. Once stabilized, further risk stratification is performed, especially if VT is confirmed. This assessment determines the likelihood of future sudden cardiac death, which may lead to the recommendation of an Implantable Cardioverter-Defibrillator (ICD) to monitor the heart and deliver shocks if a dangerous rhythm recurs.