The heart operates through a precisely timed electrical sequence. Tachycardia, a rapid heart rhythm, occurs when the heart beats too quickly, disrupting this normal sequence. Understanding the relationship between the electrical signals of the upper chambers (atria) and lower chambers (ventricles) is necessary to determine the source of the fast rhythm. This article explores what happens to the atrial electrical activity, specifically the P waves, during an abnormally fast rhythm originating in the ventricles, known as Ventricular Tachycardia (VT).
The Rhythm of a Healthy Heart
In a healthy heart, the electrical impulse originates in the sinoatrial (SA) node, the heart’s natural pacemaker, located in the right atrium. This impulse spreads across the atria, causing them to contract and is recorded on an electrocardiogram (ECG) as the P wave. The P wave, therefore, represents the electrical activation, or depolarization, of the atria.
The electrical signal then pauses briefly at the atrioventricular (AV) node before continuing down the His-Purkinje system, a network of specialized fibers that allows for rapid, simultaneous activation of the ventricles. The resulting large electrical discharge causes the ventricles to contract and is recorded as the QRS complex. In this normal sinus rhythm, a P wave consistently precedes every QRS complex, demonstrating a unified electrical connection between the upper and lower chambers.
The time between the start of the P wave and the start of the QRS complex, called the PR interval, typically measures between 120 and 220 milliseconds. This interval confirms that the atrial impulse is successfully conducted through the AV node to the ventricles. The QRS complex itself is normally narrow, lasting less than 100 milliseconds, reflecting the speed of the impulse traveling through the His-Purkinje network.
What Happens During Ventricular Tachycardia
Ventricular Tachycardia (VT) is a rapid rhythm, usually exceeding 100 beats per minute, that originates from an abnormal electrical focus within the ventricles. This ectopic focus bypasses the normal conduction sequence that begins in the SA node. The ventricular rate commonly ranges from 120 to 250 beats per minute.
The electrical impulse in VT does not use the fast, specialized His-Purkinje system for its initial spread. Instead, the electrical wave moves slowly through the muscle tissue of the ventricles. This slow movement is reflected on the ECG by a wide and often bizarre-looking QRS complex that typically lasts longer than 120 milliseconds. This wide complex shape is a clear indication that the rhythm is originating from a location below the AV node.
VT is often caused by re-entry circuits, where a damaged area of ventricular tissue creates an electrical loop. Conditions like prior heart attacks or structural heart disease can create the scar tissue necessary for these circuits to form. Because the ventricles fire so rapidly, they do not have enough time to fully relax and fill with blood between beats. This reduces the amount of blood pumped out to the body, which can lead to lightheadedness or collapse.
Why P Waves Go Missing or Become Dissociated
During Ventricular Tachycardia, the atrial activity (P waves) continues independently, usually at a slower rate dictated by the SA node. This state is known as Atrioventricular (A-V) Dissociation. The fast, independent ventricular rhythm overrides normal control, meaning the P waves and QRS complexes are no longer electrically linked.
The P waves, while present, often become invisible or appear to be “marching through” the QRS complexes and T waves on the ECG. This happens because the electrical signal generated by the massive ventricular depolarization (the QRS complex) is significantly larger than the small atrial signal. The larger ventricular signal simply obscures the smaller P wave, making it difficult to find.
In cases where the P waves are visible, they appear completely unrelated to the timing of the QRS complexes. The atria beat at their own pace, while the ventricles are driven by the faster, ectopic focus. The PR interval becomes highly variable and inconsistent, confirming the lack of communication between the upper and lower chambers. Although A-V dissociation is a definitive sign of VT, clear visual evidence of independent P waves is only present in an estimated 30 to 40 percent of cases.
Reading the ECG Strip
When a patient presents with a wide-complex tachycardia, the primary goal of reading the ECG strip is to search for evidence of A-V dissociation. The rhythm is characterized by the rapid sequence of wide, deformed QRS complexes, which confirms the ventricular origin. Finding P waves that are not consistently related to the QRS complexes is the strongest possible clue for diagnosing VT.
The presence of intermittent, normally conducted beats (capture beats) or complexes that blend the wide VT beat and a narrow, normal beat (fusion beats) also confirms A-V dissociation. These fleeting moments occur when a normal atrial impulse manages to pass through the AV node and briefly activate the ventricles. The inability of the atria to contribute their final push of blood, known as the “atrial kick,” due to the dissociation, causes the clinical symptoms of reduced cardiac output.
The lack of a consistent P wave preceding the QRS, along with the wide and rapid ventricular pattern, indicates Ventricular Tachycardia. The visual evidence of dissociation confirms that the rhythm is being driven by a chaotic focus in the ventricles rather than the heart’s normal, coordinated electrical system.