.. sured from the end of the S wave to the beginning o f the T wave. This important segment represents a period of time during which no electrical currents are flowing through the heart. Depolarization finishes with the end of the S wave and ventricular repolarization does not begin until the T wave. The ST segment is therefore isoelectric. This segment is clinically important because currents of injury associated with ischemia and infarction are reflected as elevations or depressions in the level of the ST segment, Murphy, (1991).

QT Interval The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This interval represents the entire time required for ventricular depolarization and repolarization, Murphy, (1991). U Wave The U wave is an infrequent finding on a normal ECG. The U wave appears after the T wave. It is small and of low voltage.

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Its exact significance in the normal ECG is unknown. It has been postulated as representing repolarization of the Purkinje fiber conduction system. Several pathologic states give rise to U waves, the most common of which is hypokalemia, Murphy, (1991). The Conduction System Throughout the heart runs a system of highly specialized tissues capable of conducting impulses more rapidly than surrounding muscle tissue. These special tissues are capable of conducting impulses many times faster than normal cardiac muscle tissue and have an extremely short refractroy period. Furthermore, portions of the conduction system possess inherent automaticity that allows spontaneous depolarization at certain characteristic rates.

Because the SA node is the tissue with the fastest inherent automaticity, it usually functions as the primary pacemaker of the heart. If the SA node is blocked or damaged, the fastest viable site becomes the primary pacemaker of the heart, (Fig. #5), Murphy, (1991). Fig. (#5) The electrical conduction system of the heart, Murphy, (1991).

ELECTRODES AND LEADS Because the heart is surrounded by tissue and body fluids (electrolyte solutions), the electrical action potentials produced in the heart are widely conducted throughout the body. However, ECG tracings are recorded from electrodes positioned at several specific points, Murphy, (1991). An electrode is a sensing device that detects changes in electrical potential at a given point. The electrode is connected to a galvanometer, which measures and records these potential differences. Each electrode thus becomes a different eye through which the hearts electrical activity may be viewed. Whenever the electrical axis of the heart points primarily toward a positive electrode, a positive (upward) deflection is recorded on the ECG.

If the axis is directed away from a positive electrode, the deflection on the ECG is negatively (downwardly) directed. Leads are another term for these electrodes. Three types of leads are currently in use today: (1) Standard bipolar limb leads, (2) Augmented unipolar limb leads, and (3) Unipolar precordial leads, Murphy, (1991). Standard Bipolar Limb Leads (I, II, III) The standard limb leads, designated I, II, and III by convention, represent true bipolar leads, That is, they detect differences in electrical potential between two different points. Lead I connects the two arms, lead III the left arm and the left leg, and lead II (the hypotenuse of the triangle) connects the left leg and right arm.

The result is the well known Einthovens triangle. If each of the sides is now pushed to the center of the triangle, three intersecting lines of reference are produced, which make up the triaxial reference system, (Fig #6), Murphy, (1991). Fig. (#6) Triaxial reference system, Murphy, (1991). Augmented Unipolor Limb Leads (aVR, aVL, aVF) The second set of leads, the augmented unipolar limb leads, are so called because they detect potential differences at a single point. Each lead has one point that serves as a positive electrode and three other points connected to a resistor that serves as the negative electrode. The lines of reference produced between each augmented limb lead and the heart produce a new set of axes.

This new triaxial system is about 30 degrees out of phase with that generated by the standard limb leads, I, II and III. When the two triaxial systems are combined, the hexaxial reference system is produced, (Fig. #7), Murphy, (1991). The hexaxial reference system is the standard limb lead system used today. This system represents a 360 degrees circle used to map the frontal electrical axis of the heart.

Each of the six poles represents 60 degrees of the circle. By convention the poles are assigned designations for axis determination, (Fig. #8), Murphy, (1991). Unipolar Precordial Leads (V1 to V6) The precordial electrodes provide a second dimension for determining the hearts electrical axis and six more views of its anterior and lateral aspects. Like the augmented leads, the precordial leads are unipolar, detecting potential differences at a single point. V4 to V6 are all on the same horizontal plane. V1 and V2 are likewise on a horizontal plane.

V3 is situated midway between V2 and V4. These leads determine whether the electrical axis of the heart points forward (positive) or backward (negative), (Fig. #9), Murphy, (1991). Additionally, the precordial leads provide six more electrical views in a horizontal plane across the anterior and lateral aspects of the heart. The three types of leads (bipolar, augmented unipolar, and precordial provide a total of 12 different electrical views of the heart. This is of great clinical importance in evaluating the many varieties of cardiac pathology manifested on the ECG, Murphy, (1991).

Normal Electrocardiogram The ECG is generally recorded on graph paper at a standard speed of 25 mm/sec. In the standard ECG recording, 0.1 mV produces a 1-mm positive (upward) deflection, (Graph #2), Mosby, (1983). Although the SA node normally is the pacemaker of the heart, it does not contain enough mass the produce a voltage detectable by the surface ECG. The P wave, caused by depolarization of the atria, is the first evidence of electrical activity in the cardiac cycle. After the P wave the ECG returns to baseline as the depolarization wave is slowed in the tissue of the AV node.

When the ventricular muscle depolarizes, the QRS complex is produced. An initial downward or negative deflection is termed a q wave, whereas an initial upward or positive deflection is termed an R wave. A positive deflection following a q wave is also termed an R wave. By convention, r indicated a small upward deflection and R a large upward deflection. The S wave is a negative deflection following an R wave.

If a QRS complex has only a negative deflection without a positive deflection it is known as a QS complex. In a QRS complex with more than one R wave, the additional positive deflection is labeled R. Once the ventricles are completely depolarized, the ECG returns to the baseline (ST segment). The T wave that follows represents ventricular repolarization and may sometimes be followed by a small U wave. Atrial repolarization is generally lost in the PR interval and QRS complex because of the small amount of force produced, Mosby, (1983). DRUG AND ELECTROLYTE EFFECTS Various drugs and alterations in electrolyte levels can affect cellular electrophysiology.

For instance, digoxin (Lanoxin) in a therapeutic dose may cause a downward cove, or recession, of the ST segment that mimics ST segment depression. Digoxin toxicity may produce numerous arrhythmias, including bradycardias, AV blocks, ventricular ectopy, atrial fibrillation, and atrial flutter, Kessler, (1995). At high blood levels, Class 1A antiarrhythmic agents, such as quinidine sulfate (Quindex) and procainmaide, can affect the ECG. The most common effects are a widened QRS complex and a lengthened QT interval. Widening of the QRS complex by 50% or more is a sign of toxicity. Class II antiarrhythmic agents (beta blockers) may widen the PR interval, and Class IV agents (calcium channel blockers) may slow conduction and lengthen the QT interval, Fassler, (1991).

Abnormal serum potassium levels also effect the ECG. Hyperkalemia widens the QRS complex; produces tall peaked or tented T waves; alters repolarization; and eventually slow the heart rate. Acute hyperkalemia may produce ventricular fibrillation. Hypokalemia affects cell membrane competency, may produce premature ventricular complexes, enhances the toxic effects of digoxin, and causes short or flattened T waves and U waves, Fassler, (1991). Digitalis Digitalis is given to cardiac patients for two major reasons; (1) to slow conduction through the AV node, and (2) to increase myocardial contractility in heart failure.

Slowing of AV conduction is useful in atrial fibrillation, where it brings the ventricular response down to a reasonable rate, and in supraventricular tachyarrhythmias that involve conduction through the AV node, such as PSVT, where it may interrupt the arrhythmia, Huang, (1993). The normal effect of digoxin is sagging or scooping ST- segment depression. A prolonged PR interval also can be seen. The effects of toxic levels of digoxin are many and include sinus bradycardia, AV block (first, second, or third degree), atrial fibrillation with slow ventricular response, accelerated junctional tachycardia, PAT, often with AV block, and ventricular ectopy, VT, VF, Huang, (1993). Patients in atrial fibrillation who develop accelerated junctional tachycardia go from an irregular rhythm (AF) to a regular rhythm (junctional tachycardia); because they still have no P waves, they are often said to have regularization of ventricular response. This arrhythmia should immediately raise the suspicion of digoxin toxicity, although other causes that irritate the junctional tissues may lead to the same rhythm, Huang, (1993).

Quinidine Normal quinidine effects include QRS prolongation, ST-segment depression, T- wave inversion, and QT prolongation. Toxic rhythms include ventricular ectopy and polymorphous VT, which in the setting of a prolonged QT interval is torsades de pointes, Huang, (1993). Tricylic Anitdepressants and Phenothiazines Tricyclic antidepressants and phenothiazines have similar effects as quinidine. They prolong the QRS duration and the QT interval and cause ST-segment depression and T-wave inversion. In overdoses of tricyclic antidepressants, the QRS duration is more progranstically important than the absolute level of the drug. The QRS duration acts as a bioassay of the effects of the drug, Huang, (1993). Hyperkalemia Increasing serum concentration so potassium lead the following changes: tall peaked T waves, AV conduction problems and flat P waves that may be difficult to see, prolonged QRS complex duration, ST-segment depression and T-wave inversion, VT and VF, Huang, (1993).

Hypokalemia Hypokalemia leads to ST-segment depression and T-wave flattening. With serum potassium levels less than 3.0, prominent U waves will be seen. These are due to continues ventricular repolarization, but they follow the T wave, Huang, (1993). Hypercalcemia Hypercalcemia leads to a shortened QT interval, with the T wave rising from the QRS. Hypocalcemia Hypocalcemia leads to a prolonged QT interval. However, in contrast to the effects of quinidine, the T-wave duration remains normal and the ST segment is prolonged.

If the hypocalcemia is severe, there may be T-wave inversion as well, Huang, (1993). Pericarditis Pericarditis is an inflammation of the pericardium. The changes seen on ECG are ST-segment elevation and PR-interval depression. The baseline of the tracing should be taken as the segment between one T wave and the next P wave. If the PR segment is below this level, there is PR-interval depression, Huang, (1993). Pericardial Effusion Pericardial effusions may cause low voltage because of the fluid that comes between the heart and the electrodes on the chest.

There also may be electrical alternans, in which the size of the QRS complex varies from beat to beat, Huang, (1993). CONCLUSION Electrocardiography is an essential feature of modern coronary care and of arrhythmia diagnosis; no cardiologic workup is complete without it, Parker, (1996) Previous studies have shown that electrocardiograms (ECGs), are not likely to change the diagnosis of a skilled cardiologist who determines that a patient has heart disease on the basis of history and physical examination. Swenson and colleagues conducted a prospective study to determine whether physicians are more likely to change their diagnosis if they use ECGs in the evaluation of a patient referred for chest pain or heart murmur, Huffman, (1991). Children between one month and fourteen years of age were included in this study if they were referred to a cardiology group for evaluation of either a heart murmur (79 percent) or chest pain (21 percent). The cardiologist made a diagnosis of no heart disease, possible heart disease or definite heart disease based on his or her findings on the history and physical examination.

Definite heart disease was defined as any cardiac lesion that would potentially require follow-up or endocarditis prophylaxis, or that could cause morbidity. ECGs were then performed in all of the patients. Results were reviewed by the cardiologist, who changed the original diagnosis if necessary or ordered an echocardiogram if indicated, Huffman, (1991). Overall, four children (7 percent) who were initially thought to have no heart disease were found to have heart disease. Most (68 percent) of the 25 patients initially diagnosed with possible heart disease had normal ECGs. In nearly one half (48 percent) of the patients, the diagnosis of possible heart disease was changed to no heart disease (28 percent) or definite heart disease (20 percent) based on the ECG results.

Finally, in the group initially diagnosed with definite heart disease, ECGs confirmed these findings in one third of the patients, Huffman, (1991). The authors conclude that the information provided by routine ECGs are valuable in the evaluation of patients with heart murmurs or chest pain, Huffman, (1991). BIBLIOGRAPHY Fassler, M. (1991). Electrocardiogram Interpretation and Emergency Intervention. Springhouse, Pennsylvania: Springhouse Corporation Huang, P. (1993).

Introduction to Electrocardiography. Philadelphia, Pennsylvania: W.B. Saunders Company Huffman, G. (1997). Radiographs and ECGs for assessing pediatric chest pain. American Family Physician.

June, pp. 28-41. Kaye, D. (1983). Fundamentals of Internal Medicine. St.

Louis, Missouri: C. V. Mosby Company Kessler, D. (1995). Ambulatory Electrocardiography.

Archives of Internal Medicine. January 23, 1995, pp 165-170. Murphy, K. (1991). ECG Essentials. Chicago, Illinois: Quintessence Publishing Co.