Ventricular Tachycardia Quiz

Understanding Ventricular Tachycardia

Ventricular Tachycardia (VT) is a critical cardiac arrhythmia that originates in the ventricles. It is characterized by a rapid heart rate, typically over 100 beats per minute, and wide QRS complexes on an electrocardiogram (ECG). Understanding its characteristics, causes, and management is vital for healthcare professionals in emergency and critical care settings.

What are the ECG Characteristics of VT?

Recognizing VT on an ECG is a crucial skill. The classic presentation involves a series of wide, bizarre-looking QRS complexes occurring at a rapid rate. Key features include:

• Rate: Typically 120-250 beats per minute.
• Rhythm: Usually regular, but can be slightly irregular.
• QRS Duration: Greater than 0.12 seconds (i.e., wide).
• AV Dissociation: The atria and ventricles beat independently. This is a specific sign but not always visible.
• Fusion and Capture Beats: Intermittent normal-looking QRS complexes can occur when a supraventricular impulse “captures” the ventricles.

Common Causes and Risk Factors

VT most often occurs in the context of underlying structural heart disease. The damaged myocardial tissue provides a substrate for the re-entrant electrical circuits that sustain the arrhythmia. Common causes include:

• Ischemic heart disease (e.g., prior myocardial infarction)
• Cardiomyopathy (dilated or hypertrophic)
• Valvular heart disease
• Electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia)
• Myocarditis or channelopathies (e.g., Brugada syndrome)
• Drug toxicity (e.g., antiarrhythmics, tricyclic antidepressants)

Monomorphic vs. Polymorphic VT

VT is classified based on the appearance of the QRS complexes. Monomorphic VT features QRS complexes that are uniform in shape and size, suggesting a single, stable ectopic focus. Polymorphic VT, in contrast, shows QRS complexes that vary in shape, axis, and amplitude, indicating multiple or changing ventricular foci. A specific type of polymorphic VT is Torsades de Pointes, which is associated with a long QT interval.

Differentiating VT from SVT with Aberrancy

One of the most challenging diagnostic dilemmas is distinguishing wide-complex tachycardia due to VT from supraventricular tachycardia (SVT) with aberrant conduction. While complex algorithms like the Brugada criteria exist, a simple rule of thumb is to assume any wide-complex tachycardia in an adult with structural heart disease is VT until proven otherwise. This approach is safer, as misdiagnosing VT as SVT can have catastrophic consequences.

Treatment Algorithms for VT

Management depends critically on the patient’s hemodynamic stability.
Unstable VT (with a pulse): Patients with hypotension, altered mental status, or signs of shock require immediate synchronized cardioversion.
Stable VT: Management involves antiarrhythmic medications. Intravenous amiodarone is a common first-line agent. Procainamide and sotalol are other options.
Pulseless VT: This is a cardiac arrest rhythm treated with immediate defibrillation and high-quality CPR, following standard ACLS protocols.

Long-Term Management and Prevention

After an episode of VT is treated, the focus shifts to preventing recurrence. This often involves a combination of beta-blockers, antiarrhythmic drugs, and potentially an implantable cardioverter-defibrillator (ICD). An ICD is a device that can detect and terminate life-threatening ventricular arrhythmias by delivering a shock. Catheter ablation, a procedure to destroy the small area of heart tissue causing the arrhythmia, may also be considered.

This information is intended for exam preparation and knowledge reinforcement. It is not a substitute for clinical guidelines or professional medical advice.