The ElectrocardiogramWhen activated, the heart is a concentrated locus of time-varying electrical potentials inthe body. When a portion of the myocardium becomes depolarized from an actionpotential, its polarity is temporarily reversed, becoming positive on the inside andnegative on the outside relative to neighboring inactivated tissue. When this reversaloccurs, it temporarily creates two neighboring regions of opposite charge, or polarity,within the myocardium (Fig. 12.6). This difference in polarity between two locations iscalled a dipole. Electrical currents readily flow from one poll of a dipole to the otherthough any media between the poles that can conduct electrical current. The intracellularand extracellular fluids in the body are largely composed of electrolyte solution, which isa good conductor of electricity. For this reason, the heart can be thought of as a potentialgenerator in a volume conductor. Consequently, any dipole formed at any time and in anydirection within the myocardium between depolarized and nondepolarized regions istransmitted through the body as currents between the ends of the dipoles. These currentsradiate outward through the body all the way to the surface of the skin.An electrocardiogram, or ECG, is an amplified, timed recording of the electrical activityof the heart, as it is detected on the surface of the body. The recording gives a plot ofvoltage as a function of time. It results from the composite effect of all the different typesof action potentials generated in the myocardium during activation and the resultingmagnitude and orientation of the dipoles created. Although it is correct to say that theelectrical activity in the heart is responsible for creating the ECG, the physician looks atthis process in reverse; that is, the physician examines the ECG to create a picture of theelectrical activity in the heart.The electrocardiogram is one of the most useful diagnostic tools available in medicine tothe physician, but it is important to understand what information can and cannot begained from the analysis of an ECG. The ECG can be used to detect abnormalities inheart rhythm and conduction, myocardial ischemia and infarction, plasma electrolyteimbalances, and effects of numerous drugs. One can also gain information from the ECGabout the anatomic orientation of the heart, the size of the atria and ventricles, and thepath taken by action potentials through the heart during normal or abnormal activation(e.g., the average direction of activation of the ventricles). The ECG, however, cannotgive direct information about the contractile performance of the heart, which is equallyimportant in the evaluation of myocardial status in a clinical setting.The Moment-to-Moment Orientation and Magnitude of Net Dipoles in the HeartDetermine the Formation of the ElectrocardiogramThe formation of the standard wave forms within the ECG can be explained as arisingfrom the orientation and magnitude of the net, or collective average, dipoles that arecreated throughout the heart during electrical activation of the myocardium. Inexplanation, consider the voltage changes produced in which the body serves as a volumeconductor and the heart generates a collection of changing dipoles (Fig. 12.8). In thisexample, an electrocardiographic recorder is connected between points A and B such thatwhen point A is positive relative to point B, the ECG is deflected upward, and when B ispositive relative to A, a downward deflection results. The black arrows show (in two
dimensions) the direction of the net dipole resulting from the many individual dipolespresent at any one time. The lengths of the arrows are proportional to the magnitude(voltage) of the net dipole, which is related to the mass of myocardium generating the netdipole. The blue arrows show the magnitude of the dipole component that is parallel tothe line between points A and B (the recorder electrodes); this component determines theamplitude and polarity of voltage that will be recorded on the ECG. Atrial excitationresults from a wave of depolarization that originates in the SA node and spreads over theatria, as indicated in panel 1 of Figure 12.8. The net dipole generated by this excitationhas a magnitude proportional to the mass of the atrial muscle involved and a directionindicated by the black arrow. The head of the arrow points toward the positive end of thedipole, where the atrial muscle is not yet depolarized. The negative end of the dipole islocated at the tail of the arrow, where depolarization has already occurred. Point A,therefore, is positive relative to point B, and there will be an upward deflection of theECG. The magnitude of this upward deflection depends on two factors: (1) it isproportional to the amount of tissue generating the dipole (the magnitude of the netdipole), and (2) it depends on the orientation of the dipole relative to a parallel lineconnecting points A and B. This latter relationship is demonstrated in Figure 12.9. Forexample, imagine a wave of depolarization traveling through the atria muscle as a sagittalplane, perpendicular to the ground, proceeding directly along the line connecting point Bto point A. This wave of depolarization then is aimed directly at the positive pole A andwill create a positive deflection as described above. For the sake of example only, weshall assign this deflection an amplitude of +4 mm on the ECG recorder. Should thissame wave of depolarization, however, proceed from point A toward point B, the wavewould be aimed directly at the negative pole, resulting in a 4-mm negative, or downward,deflection of the wave. The amplitude of the deflection will thus vary in this examplebetween -4 mm and +4 mm, depending on the angle of the wave of depolarizationrelative to the line connecting A and B. Should the wave proceed toward A at a 45Â°angle, the deflection would be a positive 2 mm; if it proceeds at 90Â° (perpendicular) tothe line connecting A and B, it would not be pointing at either pole and no deflectionwould be recorded on the ECG. The deflection will also register zero once the atria arecompletely depolarized, because no voltage difference will exist between A and B (i.e.,no dipole exists).
Although the preceding discussion is an oversimplification, it presents the basicprinciples of dipole magnitude and orientation relative to two recording points that createthe pattern of the common ECG. For example, after the P wave, the ECG returns to itsbaseline or isoelectric level. During this time, the wave of depolarization moves throughthe AV node, the AV bundle, the bundle branches, and the Purkinje system. The dipolescreated by depolarization of these structures are too small to produce a deflection on theECG. However, the depolarization of ventricular structures does create deflections on theECG. The net dipole that results from the initial depolarization of the septum is shown inpanel 2 of Figure 12.8. This depolarization is pointed toward point B and away frompoint A because the left side of the septum depolarizes before the right side. Thisorientation creates a small downward deflection produced on the ECG called the Q wave.The normal Q wave is often so small that it is not apparent. Next, the wave ofdepolarization spreads via the Purkinje system across the inside surface of the free wallsof the ventricles. Depolarization of free-wall ventricular muscle proceeds from theinnermost layers of muscle (subendocardium) to the outermost layers (subepicardium).Because the muscle mass of the left ventricle is much greater than that of the rightventricle, the net dipole during this phase has the direction indicated in panel 3. Thedeflection of the ECG is upward because the dipole is directed at point A and is largebecause of the great mass of tissue involved. This upward deflection is the R wave. TheP.233
last portions of the ventricle to depolarize generate a net dipole with the direction shownin panel 4, and thus the deflection on the ECG is downward. This final deflection is the Swave. The ECG tracing returns to baseline when all of the ventricular muscle becomesdepolarized and all dipoles associated with ventricular depolarization disappear. The S-Tsegment, or the period between the end of the S wave and the beginning of the T wave, isgenerally isoelectric. This indicates that no dipoles large enough to influence the ECGexist because all ventricular muscle is depolarized (the action potentials of all ventricularcells are in phase 2).Repolarization, like depolarization, generates a dipole because the voltage of thedepolarized area is different from that of the repolarized areas. The dipole associated withatrial repolarization does not appear as a separate deflection on the ECG because itgenerates a low voltage and because it is masked by the much larger QRS complex,which is present at the same time. Ventricular repolarization is not as orderly asventricular depolarization. The duration of ventricular action potentials is longer insubendocardial myocardium than in subepicardial myocardium. The longer duration ofsubendocardial action potentials means that even though subendocardial cells were thefirst to depolarize, they are the last to repolarize. Because subepicardial cells repolarizefirst, the subepicardium is positive relative to the subendocardium That is, the polarity ofthe net dipole of repolarization is the same as the polarity of the dipole of depolarization.This results in an upward deflection because, as in depolarization, point A is positive withrespect to point B. This deflection is the T wave (see panel 5, Fig. 12.8). The T wave hasa longer duration than the QRS complex because repolarization does not proceed as asynchronized, propagated wave. Instead, the timing of repolarization is a function ofproperties of individual cells, such as numbers of particular K+ channels.