An dysrhythmia of the heart is an irregular heartbeat rhythm. Ventricular tachycardia is an dysrhythmia in which the lower chambers of the heart, the ventricles, beat unusually fast. The heart rate is measured with an electrocardiogram, or ECG. This is a machine that measures the electrical impulses from the patient’s heart. This is displayed on a monitor or ECG graph paper. The boxes on the graph paper measure time. Five small boxes are equal to one large box. The large box represents two-tenths of a second.
The atrial contraction is represented by the P wave. This is an upward, or positive wave of the line on the graph. The ventricular contraction is displayed by the QRS complex. The QRS complex is composed of three waves, the Q, R, and S waves. The Q wave is the first downward, or negative movement on the graph. The R wave is the positive movement following the Q wave. It rises above the starting point of the Q wave. The S wave is a negative movement following the R wave. The S wave returns the line to the original baseline. The T wave, the repolarization of the ventricle, is a positive wave of the line that ends one beat of the heart. The atrial repolarization is not represented on the graph. It is absorbed by the QRS complex, which is a stronger impulse.
In a normal heart beat, there is one P wave for every QRS complex and T wave. The QRS complex is no larger than three small boxes on the graph paper. Every beat comes at the same interval as the other beats. During ventricular tachycardia, the P wave is not represented. The QRS complex is wide. The T wave is not present on the graph. The intervals between beats can be up to five times shorter than a normal rhythm. A normal heart beats anywhere from sixty to one hundred times per minute. The sinoatrial node or SA node, is an area of specialized tissue in the right atrium at the juncture of the superior vena cavae. The SA node is the primary pacemaker of the heart.
It starts the heartbeat by spontaneously contracting, causing the rest of the heart to contract in a wave. The wave spreads through the atria before reaching the atrioventricular node, or AV node, located just above the right ventricle. The AV node focuses the wave into the ventricles, contracting the ventricles. Should the SA node fail, the AV node can take over as the primary pacemaker at a rate of forty to sixty beats per minute. Should both the SA node and the AV node fail, there is a tertiary pacemaker, the perkinje fibers. Perkinje fibers are located near the bottom of the ventricles and can stimulate contraction at a rate of twenty to forty beats per minute. If the perkinje fibers or the AV node becomes irritated, they can begin contraction of the ventricles at speeds well above normal. Other causes of ventricular tachycardia include heart disease and medications. When the ventricles are contracting at a rate greater than one hundred beats per minute, the heart becomes inefficient.
Blood cannot properly fill the ventricular chambers before it is forced out. This decreases the amount of oxygenated blood circulating through the body. The lack of oxygen in the body causes the heart to attempt to pump more blood, forcing the ventricles to work even harder. Should the ventricular rate rise above one hundred fifty beats per minute, patients usually require cardioversion. Cardioversion is electric shock treatment. It acts like a reset button, stopping all action so that the heart can begin normal beating again. Cardioversion, or defibrillation, should be done up to three times in increasing strength, no less than two hundred joules and no more than three hundred sixty joules. If the patient is still in ventricular tachycardia, defibrillation is used in conjunction with certain medications. The first medication given to a patient in ventricular tachycardia is epinephrine. One milligram is administered rapidly, every three to five minutes.
Epinephrine improves blood flow through the body and holds the heart in a contractile state until it the entire heart can relax. This allows the AV node to regain control of the heart’s beating. After administering epinephrine, the patient is then again defibrillated at three hundred sixty joules, within thirty to sixty seconds. If ventricular tachycardia persists, other medications are given. These include lidocaine, bretylium, and magnesium sulfate.
Lidocaine suppresses the premature or extra beats of the heart. This drug is given rapidly in a dose of one to five milligrams per kilogram. Lidocaine is often effective, but also dangerous. Too much lidocaine can produce a toxicity that can cause slurred speech, muscle twitching and seizures, an altered level of consciousness, and even further heart dysrhythmias. If lidocaine doesn’t work, the next drug to use, after again defibrillating, is bretylium.
Bretylium is administered at a rate of five milligrams per kilogram repeating every five minutes at ten milligrams per kilogram, with a maximum of thirty-five milligrams per kilogram. Side effects of bretylium include vertigo, dizziness, hypotension or low blood pressure, and bradycardia, an abnormally slow heart rate. After administering bretylium, use cardioversion at the same level, three hundred sixty joules. When lidocaine and bretylium both fail to produce positive results, magnesium sulfate can be used.
Magnesium sulfate is an antidysrhythmic, meaning that it establishes a normal heart rhythm. Magnesium sulfate can also cause hypotension, bradycardia, and circulatory collapse among other side effects. It is a last resort drug for ventricular tachycardia. Other medications, however, are indicated for an unusual form of ventricular tachycardia called Torsade de Pointes. Torsade de Pointes is the irregular rhythm of ventricular tachycardia, but it occurs in a pattern of small series of waves that increase to a greater magnitude, and then back in a repeating pattern.For Torsade de Pointes, the drug of choice is magnesium sulfate. It should be administered at a rate of one to two grams in one hundred milliliters of normal saline over one to two minutes.
