Wide-Complex Tachycardias: What Makes Them Wide
There are multiple factors that determine the width of the QRS interval. These factors include the amount of conduction through the normal electrical conduction system, vagal tone, hormonal influences, electrolyte imbalances, and pharmaceutical agents, to name a few. In addition, we are finding that channelopathies are playing a greater role at the root causes of pathologic diseases or syndromes and can definitely lead to widening of the QRS interval. That said, the most important factor determining the width of the QRS interval is the amount of conduction that occurs either through the normal electrical conduction system of the ventricles, known as the His-Purkinje system (HPS), or through direct cell-to-cell contact. The more distance the wave travels through the HPS, the shorter the QRS interval. The more distance the wave travels by direct cell-to-cell contact, the wider the QRS interval.
As we have seen throughout this text, cardiac activation of the ventricles occurring through the HPS provides a rapid, efficient, and symmetrical contraction sequence that cannot be achieved through direct cell-to-cell activation. Without a synchronized “wringing” of the ventricles, maximum cardiac output would be nearly impossible to achieve. And, there lies the crux of the problem.
WCTs develop because they have no or only a limited amount of conduction through a normally functioning HPS. The ventricular depolarization waves are not transmitted in an orderly fashion, and cardiac contractility is haphazard and unsynchronized, leading to a poor ejection fraction. In addition, the atrial kick is compromised because atrial activity either is absent, contracting abnormally due to retrograde activation, or is not synchronized with valvular opening and closing, leading to little or no ventricular overfilling. Add the decreased filling times due to the rapid rates typically seen in these rhythms and you could have some disastrous outcomes.
It is important to note, however, that WCTs do not always lead to hemodynamic compromise. The ventricular rates and underlying cardiac status may sometimes allow for compensation to occur, even if it occurs only for a short period. For these reasons, we cannot use the presence of hemodynamic instability as a major predictor of whether we are dealing with an SVT or a VTach. The most we can say is that hemodynamic instability favors the diagnosis of VTach.
Additional Information
Dr. W. Proctor Harvey was one of the greatest cardiologists and medical educators of modern times. His life was dedicated to keeping alive the principle that medicine is an art form, especially during his 35 years as the head of cardiology at the prestigious Georgetown University School of Medicine.
To help students remember the specific steps of the clinical approach to cardiac patients and to the physical examination of the heart, he used two easy memory aids. These mnemonics were based on a simple five-finger approach, where each finger represents one step.
The five-finger approach to the general evaluation of a cardiac patient basically includes the history, physical examination, ECG, radiograph, and lab tests.6 Contrary to the more modern approach that glorifies technology, Dr. Harvey emphasized that the sequence of this five-finger technique proceeds in a descending order of clinical usefulness. In other words, the history and physical examination will provide you with most of the information, while lab tests are the least helpful. He was also fond of reminding his students that it takes five fingers to make a fist and that it takes a fist to “crack open” many cardiac problems.
The five-finger approach to the physical examination consists of the evaluation of the general appearance, jugular venous pulsations, palpitation (for thrills and heaves), arterial pulses, and finally cardiac auscultation. His belief was that the clinician should have the diagnosis made before even placing the stethoscope on the patient’s chest.