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 Einthoven?s 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 heart?s 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 ElectrocardiogramThe 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).
DigitalisDigitalis 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).
QuinidineNormal 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 PhenothiazinesTricyclic 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).
HyperkalemiaIncreasing 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).
HypokalemiaHypokalemia 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).
HypercalcemiaHypercalcemia leads to a shortened QT interval, with the T wave rising from the QRS.
HypocalcemiaHypocalcemia 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).
PericarditisPericarditis 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 EffusionPericardial 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.? AmericanFamily Physician. June, pp. 28-41.
Kaye, D. (1983). Fundamentals of Internal Medicine. St. Louis, Missouri: C. V. MosbyCompany
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.