Ventricular tachycardia (VT) is a fast heart rhythm that begins in the lower chambers of the heart, the ventricles. This electrical malfunction causes the heart to beat at an abnormally rapid rate, requiring immediate medical attention. VT usually involves a rate of 100 or more beats per minute. This rapid rhythm severely compromises the heart’s ability to pump blood effectively to the body.
What Defines Ventricular Tachycardia
Ventricular tachycardia is characterized by an abnormal electrical impulse that originates below the atrioventricular (AV) node. This faulty electrical signaling hijacks the heart’s natural pacemaker system, causing the lower chambers to fire independently and quickly. The resulting heart rate is often in the range of 150 to 250 beats per minute. This extremely rapid contraction rate does not allow the ventricles enough time to properly relax and fill with blood between beats, leading to a significant decrease in the amount of blood the heart can eject and resulting in poor circulation.
The Crucial Difference: VT With a Pulse vs. Pulseless VT
Ventricular Tachycardia presents in two distinct forms, and the presence or absence of a palpable pulse is the most important factor determining the patient’s status. When a patient has VT with a pulse, the heart is still generating enough mechanical force to circulate some blood, even though the circulation is highly inefficient. These patients are often conscious but may show signs of instability, such as hypotension, chest pain, or lightheadedness.
The rapid rate in VT with a pulse severely limits the time for the ventricles to fill, but it has not yet caused complete circulatory collapse. This situation is unstable and can quickly degrade, but the presence of a pulse means the heart is still providing some perfusion to the body’s organs. Conversely, pulseless VT is a form of sudden cardiac arrest. In this scenario, the electrical activity of the VT rhythm is present on a monitor, but the ventricular contractions are so rapid or ineffective that no measurable blood pressure or cardiac output is generated.
Pulseless VT means the heart muscle is essentially quivering or beating too quickly to move blood, making it functionally equivalent to ventricular fibrillation. The lack of a pulse signifies a total failure of the circulatory system to deliver oxygen to the brain and other organs. Immediate intervention is required to prevent death because the absence of a pulse confirms that blood flow has stopped entirely.
Immediate Emergency Response Based on Pulse Status
The medical response to ventricular tachycardia is dictated by whether a pulse is present. If the patient has a pulse but is showing signs of instability, treatment involves synchronized cardioversion. This procedure delivers a timed electrical shock to interrupt the abnormal rhythm and restore a normal heartbeat. For patients who are conscious and hemodynamically stable, antiarrhythmic medications like amiodarone or procainamide may be administered intravenously to slow the heart rate and stabilize the electrical system.
If the patient is in pulseless VT, the situation is classified as cardiac arrest, requiring immediate cardiopulmonary resuscitation (CPR). Chest compressions must start immediately to manually pump blood until the heart’s rhythm can be corrected. The definitive treatment is immediate defibrillation, an unsynchronized electrical shock delivered to stop the chaotic electrical activity and allow the heart’s natural pacemaker to restart. Delaying defibrillation makes time a critical factor in this scenario.
Factors That Increase VT Risk
Ventricular tachycardia is most commonly associated with underlying damage or disease in the heart muscle. The most frequent cause is ischemic heart disease, often resulting from a prior heart attack that left behind scar tissue. This scar tissue creates abnormal electrical circuits within the ventricles that can trigger the rapid rhythm. Structural heart diseases, such as cardiomyopathy, which involves a weakened or thickened heart muscle, also increase the risk.
Severe imbalances of electrolytes like potassium and magnesium can destabilize the heart’s electrical system and precipitate VT. Other contributing factors include congenital conditions, like Long QT syndrome, and certain medications that affect the heart’s electrical properties. Addressing these underlying conditions and correcting electrolyte abnormalities are primary goals in preventing future VT episodes.