Ventricular Tachycardia (VT) is a fast heart rhythm that originates in the lower pumping chambers of the heart, the ventricles. During VT, the heart rate accelerates, often exceeding 100 beats per minute. This rapid, abnormal electrical activity prevents the ventricles from filling completely, compromising the heart’s ability to pump blood effectively to the body. While VT is often associated with a regular beat, it can be irregular. This distinction between a regular and an irregular VT points to different underlying causes and dictates separate, time-sensitive treatment strategies.
The Typical Regular Rhythm of Monomorphic VT
The most common form of this condition is Monomorphic Ventricular Tachycardia (MVT), characterized by a regular rhythm. The term “monomorphic” means “single shape.” On an Electrocardiogram (EKG), the electrical complexes (QRS complexes) appear identical from one beat to the next. This consistency reflects a single, fixed electrical pathway that the impulse follows repeatedly.
This fixed pathway is typically a “re-entry circuit,” which acts as a short circuit within the heart muscle. This circuit usually forms around scar tissue, most often resulting from a previous heart attack or Ischemic Heart Disease. The damaged muscle tissue conducts electrical signals slowly, allowing the impulse to circle back and re-excite the surrounding tissue in a continuous loop.
The ventricles are forced to contract rapidly and uniformly, often preventing them from relaxing enough to receive adequate blood volume. The regularity of MVT provides a diagnostic clue, suggesting that the underlying cause is likely a fixed structural problem, such as a myocardial scar.
Forms of Irregular Ventricular Tachycardia
Ventricular Tachycardia can become irregular when the electrical activity does not follow a single, predictable circuit. This means the electrical impulses are originating from multiple, shifting sources within the ventricles. The two main types of irregular VT are Polymorphic VT (PVT) and its specific subtype, Torsades de Pointes (TdP).
Polymorphic VT
Polymorphic VT is irregular because the electrical impulses originate from continuously changing sites within the ventricular muscle. On an EKG, the QRS complexes appear to vary in shape, amplitude, and axis from one beat to the next. This shifting electrical activity is often caused by severe structural heart disease or ongoing myocardial ischemia, which is a lack of blood flow to the heart muscle. The most common cause of PVT is an acute heart attack, where the lack of oxygen creates multiple areas of electrical instability.
Torsades de Pointes
Torsades de Pointes (TdP) is a specific and dangerous form of Polymorphic VT, characterized by a unique twisting pattern on the EKG. The French name means “twisting of the points,” describing how the QRS complexes appear to spiral around the baseline. TdP is always associated with a prolonged QT interval, which represents a delay in the heart’s electrical recovery phase, known as repolarization.
This delay in repolarization can be caused by factors outside the heart’s physical structure, such as imbalances in electrolytes like low magnesium or potassium. Certain medications that prolong the QT interval, including some antibiotics and antiarrhythmic drugs, can also trigger TdP. The mechanism involves “early afterdepolarizations,” which are abnormal electrical firings that occur before the cell has fully reset, leading to the erratic, twisting rhythm.
Why Rhythm Characteristics Guide Treatment
The regularity or irregularity of Ventricular Tachycardia is a diagnostic tool that immediately guides medical intervention. A regular (monomorphic) VT suggests a fixed anatomical problem, such as a scar, which requires a targeted approach. Treatment for MVT often involves antiarrhythmic drugs like amiodarone or sotalol, or a procedure called catheter ablation, which uses heat or cold energy to destroy the single, fixed electrical circuit causing the rhythm.
Conversely, an irregular VT, especially Torsades de Pointes, signals widespread, often temporary, electrical instability. The treatment for TdP is different and focuses on immediate correction of the underlying trigger. This typically involves administering intravenous magnesium, correcting potassium levels, and immediately stopping any medication known to prolong the QT interval.
Irregular VT is also generally more unstable and prone to degenerating into Ventricular Fibrillation (V-Fib), a chaotic rhythm where the heart merely quivers instead of pumping blood. Because of this high risk of collapse, both MVT and PVT often require immediate electrical intervention, such as synchronized cardioversion or defibrillation, to reset the heart’s rhythm. The rhythm’s appearance on the EKG is a life-saving clue, allowing clinicians to choose the correct, highly specific therapy within minutes.