12 lead ecg
TRANSCRIPT
Abstract
Find how the ECG translates the heart's electrical activity into a waveform and what it tells you about your patient's condition.
RESPONDING TO THE CALL bell, you find George Smythe, 67, sitting up in bed and complaining of chest discomfort. Mr. Smythe had a laparoscopic cholecystectomy earlier today. You take his vital signs and perform a chest pain assessment, which includes the onset, location, quality, intensity, duration, and any radiation of the discomfort. You ask about associated signs and symptoms and factors that aggravate or relieve the pain. Following your facility's protocol, you administer supplemental oxygen at 2 to 4 liters/minute via nasal cannula and page the physician on call, who orders stat serum cardiac biomarkers, a 12-lead electrocardiogram (ECG), and sublingual nitroglycerin.
Do you know what to look for to determine if Mr. Smythe's 12-lead ECG is abnormal? Could you recognize signs that he's having a myocardial infarction (MI)? If you can independently interpret a 12-lead ECG, you can anticipate and prepare for the emergency care your patient may need.
In this article, I'll cover the basics of 12-lead ECG interpretation, focusing on a normal ECG. Next month, I'll discuss ECG abnormalities.
What's happening in the heart
The heart's internal conduction circuit initiates each heartbeat and coordinates all parts of the heart to contract at the proper time. A normal heartbeat is initiated in the sinoatrial (SA) node, a specialized group of cells in the right atrium. The SA node depolarizes at a rate of 60 to 100 times/minute, causing the atria to contract and propel blood into the ventricles.
Atrial depolarization produces the first element on the ECG waveform: the P wave. The P wave is the first part of the cardiac cycle and appears as a small, semicircular bump (see Tracing a normal ECG waveform).
The wave of depolarization continues through the atria until it encounters the next important structure, the atrioventricular (AV) node. The AV node receives the atrial impulse and (after a brief pause to let the ventricles fill) transmits it to the ventricles via the bundle of His. A collection of cardiac conduction fibers, the bundle of His splits into the right and left bundle branches.
The bundle branches are high-speed conducting fibers that run down the intraventricular septum and transmit the cardiac impulse to the Purkinje fibers. These fibers form a complex network that mingles with ventricular myocardial cells. The function of the Purkinje fibers is to rapidly stimulate ventricular muscle fibers, resulting in the next major event in the cardiac cycle: ventricular depolarization.
Ventricular depolarization generates the QRS complex, the electrical equivalent of ventricular systole. (Remember that electrical activity precedes mechanical activity, and the ECG shows only electrical activity.) If you palpate a carotid or radial pulse while looking at a cardiac monitor, you should feel a pulse with each QRS complex on the monitor.
The QRS complex normally has a duration of 0.06 to 0.1 second. A duration greater than 0.12 second usually indicates prolonged ventricular conduction caused by a bundle-branch block. The QRS complex is variable in appearance and may have a different shape (or morphology) in different patients or even look different in various ECG leads in the same patient. The QRS
complex may have one, two, or three wave components, depending on the lead and your patient's condition.
The last major wave component of the ECG is the T wave, which is larger than the P wave and rounded or slightly peaked. Immediately following the QRS complex, it represents ventricular repolarization or a metabolic rest period between heartbeats. During repolarization, electrolytes such as potassium, sodium, and calcium cross the cell membrane (back to their original location) to prepare the cardiac cell for the next depolarization.
Besides the three waveforms, the normal ECG cardiac cycle tracing has two important segments, or flat (isoelectric) parts of the tracing between the waveforms: the PR interval and the ST segment.
The PR interval is the period from the beginning of the P wave to the beginning of the QRS complex. It consists of the P wave plus the short isoelectric segment that terminates at the start of the QRS complex. The normal PR interval lasts 0.12 to 0.2 second; this represents the time from SA node depolarization to ventricular depolarization. If the PR interval is less than 0.12 second, then the cardiac impulse didn't follow the normal conduction pathway. If the PR interval is longer than 0.2 second, then a disease process may be affecting the cardiac conduction pathway, keeping it from functioning properly.
The ST segment consists of the isoelectric line between the end of the QRS complex and the beginning of the T wave. The ST segment reveals information about the heart's oxygenation status. For example, myocardial ischemia (a temporary, reversible decrease in oxygenation) often results in an ST segment below the baseline of the ECG tracing. When myocardial cells are injured (reversible physical damage from lack of oxygen), the ST segment often is elevated above the baseline. So ST-segment elevations are a key indicator of MI. I'll discuss this in detail in the next part of this series. For tips on how to use the ECG to calculate heart rates and more, see Paper training.
Figure. No caption available.
Catching the wave
If you examine a 12-lead ECG, you'll notice that some QRS complexes have upward deflections and others have downward deflections. Here's why.
Each ECG lead has a positive (or sensing) electrode and a negative electrode, which acts as an anchor. The positive electrode looks toward its negative electrode and senses whether electrical energy is being directed toward or away from the positive electrode.
When electrical energy is directed toward the positive monitoring electrode, the QRS complex has an upward deflection. When the electrical energy is directed away from the positive monitoring electrode, the QRS complex has a downward deflection. The more directly aligned the direction of the electrical energy with the positive electrode, the more upright the complex. If the electrical energy approaches the positive monitoring electrode at a glancing angle, the complex will still be upright, but less upright than if the energy were directly aligned with the positive electrode.
Energy arriving at a perpendicular angle to the positive electrode results in either a waveform with little deflection (isoelectric) or equal amounts of positive and negative deflection.
As the energy is directed away from the positive electrode, the QRS complex becomes progressively more negative. When energy flow is directed totally away from the positive electrode, the QRS complex is deflected directly downward.
Going with the flow: A look at vectors
All cardiac cells are electrochemical, meaning they generate electrical energy during depolarization. This electrical energy, called a vector, has strength (measured in millivolts) and direction (measured in degrees from an arbitrary zero point called the electrical axis). Each cardiac cell generates its own microvector. The mathematical average of these microvectors is the mean QRS vector or mean vector, which follows the conduction pathway of the heart-downward and to the left. The mean vector flows slightly to the left of the ventricular septum because the left ventricle has more and larger cardiac cells.
Generally, each person has a unique mean vector direction, which remains constant unless his cardiac status changes. For example, left ventricular hypertrophy secondary to heart failure pulls the mean vector even more sharply to the left side.1 A person who has a mean vector in an abnormal direction is said to have an axis deviation. (For details, see Axis deviation: As easy as pie (charts).)
Putting it all together
The mean vector is a representation of the overall electrical properties of the heart. A 12-lead ECG is the electrical record of the mean vector from 12 different monitoring sites (leads) on the surface of the body. As when you look at any object, you need to see all the angles to get a complete picture.
Looking at limb leads
The first six leads of the 12-lead ECG come from four electrodes placed on the patient's arms and legs; the right lower leg electrode is the ground electrode. The limb leads record the mean vector in the up-down and left-right direction along the body's frontal plane. Because they use separate positive and negative electrodes, they're called bipolar or standard leads.
* Lead I has the positive electrode on the left arm and looks toward the negative electrode on the right arm for electrical energy. Because the mean vector travels from upper right to lower left, energy flows toward the positive electrode of lead I, resulting in an upward deflection of the QRS. And because the mean vector doesn't flow directly toward lead I, but approaches it at a somewhat broad angle, the upward deflection of the QRS complex is moderate.
Figure. No caption available.
* In lead II, the positive electrode is on the left foot and the negative electrode is on the right arm. Because the mean vector flows directly at the positive lead II electrode, this lead usually has the most upright QRS complexes and the most prominent P waves of the entire 12-lead ECG. That's why lead II is a favorite monitoring lead in many intensive care and telemetry units.
* Lead III puts the positive electrode on the left foot and the negative one on the left arm. The mean vector flow approaches lead III downward from the right, again producing an upward QRS deflection. Because the angle is narrower than the angle between the mean vector and lead I, the lead III QRS complex is more upright than the lead I QRS complex.The second set of limb leads are called the augmented or unipolar leads and use a single positive monitoring electrode. The negative electrode is an electrically calculated location at the center of the heart.
* Lead aVR is the only limb lead on the right side of the body. Its positive monitoring electrode is located on the right arm and looks downward and to the left. The mean vector also flows downward and to the left, directly away from lead aVR, resulting in a negative deflection for all waveforms. In a normal ECG, lead aVR is the only limb lead with a downwardly deflected QRS.
* Lead aVL positions a positive electrode on the left arm and looks to the right and downward toward to the center of the heart (in contrast to lead I, which looks strictly to the right). The mean vector approaches aVL at a very broad angle, producing the least upright QRS complex among the limb leads.
* Lead aVF has its positive monitoring lead on the left leg and looks straight up to the center of the chest. The mean vector approaches aVF at a fairly direct angle, although not as directly as lead II, so lead aVF has very upright QRS complexes with prominent P waves. Because leads II, III, and aVF all look upward at the oncoming mean vector, their waveforms share many qualities, such as highly positive QRS complexes and prominent P waves. Because these leads look upward at the bottom or inferior ventricular wall of the heart, they're known as the inferior leads.
Six chest leads weigh in
The six chest or precordial leads lie across the anterior chest and measure the mean vector in the horizontal plane.
* Lead V1 is located at the right sternal border, fourth intercostal space, and lies above the right ventricle and septum.
* Lead V2 is at the left side of the sternum, fourth intercostal space.
* Lead V3 is midway between leads V2 and V4.
* Lead V4is at the midclavicular line in the fifth intercostal space.
* Lead V5 is at the anterior axillary line in the fifth intercostal space.
* Lead V6 is at the midaxillary line, fifth intercostal space, and is positioned above the lateral wall of the left ventricle.
The mean vector in the horizontal plane is influenced by the overwhelming power of the left ventricle and can be thought of as flowing toward the left side. Because the mean vector flows away from lead V1, this lead has a downward QRS deflection; the QRS is almost totally upright in leads V5 and V6 because the mean vector flows directly at these leads. The QRS complex becomes progressively more upright across the chest wall from V1 to V6, a change known as R-wave progression (see R-wave ups and downs).3 This is another characteristic of a normal ECG.
Figure. No caption available.
Figure. No caption available.
Putting it all together
Prepared with our new knowledge of 12-lead ECGs, let's examine Mr. Smythe's 12-lead ECG. His heart rate is normal, and you see clear P waves, QRS complexes, and T waves. The PR interval is 0.14 second, which falls within the normal range. The QRS complex should be less than 0.12 second; Mr. Smythe's QRS complexes are 0.08 second wide. The T waves are upright and normal looking. Finally, the ST segment is level with the baseline.
Mr. Smythe's limb leads are all upright with the normal exception of aVR. Lead II is the most upright and aVL is the least upright. The chest leads demonstrate downward lead V1 and upright leads V5 and V6 with normal R-wave progression across the chest wall.
You conclude that Mr. Smythe has a normal 12-lead ECG, indicating no electrical abnormalities in heart function. However, he's not out of the woods yet. Some types of ischemic chest pain aren't apparent on routine ECG, so the physician may consider following up with a stress test.4
Mr. Smythe's normal ECG, negative cardiac enzymes, and benign patient history led the medical team to rule out a cardiac source for his discomfort. He was discharged home the next day with a prescription for pantoprazole and told to follow up with his health care provider if his chest discomfort recurs.
In this article, you've learned to recognize the features of the normal ECG. Next month, I'll examine some abnormalities of the 12-lead ECG and discuss how to assess for MIs and arrhythmias.
Paper training
You can use the markings on ECG paper to calculate events within the cardiac cycle. The ECG paper is a grid of large and small blocks. On the horizontal axis, a large block is equal to 0.2 second and a small block is equal to 0.04 second. The vertical axis represents voltage or electrical energy, with each vertical millimeter (small block) being 0.1 millivolt of electrical energy. However, in practice, deflections are typically described as being in millimeters, not millivolts.
By counting the number of small squares and multiplying by 0.04, you can calculate the duration of any event in the ECG tracing. A QRS complex that's 2.5 small squares wide is 0.1 second. You also can use the ECG paper to calculate heart rates, using one of two methods. In the 6-second method, you start by looking for the markings (usually short vertical lines) at the top of the rhythm strip or ECG paper. These markings divide the ECG paper into 3-second intervals. Count the number of QRS complexes contained in two intervals (6 seconds) and multiply by 10. This method works for both regular and irregular heart rhythms.
In the division method, count the number of small squares between any two heartbeats. Make sure you use the same part in both QRS complexes-usually the peak of the complex works the best. Divide 1,500 by the number of small squares and you'll have the heart rate in beats per minute. This method is accurate only with regular heart rates because irregular heart rhythms have a varying number of small squares between any two QRS complexes.
Axis deviation: As easy as pie (charts)
Combining your assessment skills with an understanding of axis deviation can give you a more detailed picture of your patient's condition. The hexaxial reference system and the quadrant method can help you visualize problems with cardiac conduction.
Hexaxial reference system
The normal QRS complex (or vector) represents the average electrical signal that the heart generates during depolarization. Within the heart, the mean vector generally flows from upper right to lower left. The exact direction of that flow (called the electrical axis) can be used as an assessment tool in the 12-lead ECG because an abnormal axis can give you clues about what's going wrong in the heart's electrical system.
To measure the electrical axis, imagine all six limb leads displayed simultaneously around a central point in a circle, which represents the heart (see the illustration at left). In this hexaxial system, the leads divide the circle into equal 30-degree segments.
Each lead can be assigned a number of degrees, and the mean vector's direction can be given in degrees. If the mean vector is aligned directly with lead I, its axis is 0 degrees. A mean vector directed halfway between leads II and aVF has an axis of 75 degrees. (Although you can calculate your patient's electrical axis, all modern 12-lead ECG machines provide this information automatically.)
The normal electrical axis of the heart falls between -30 and +90 degrees. Although this is a wide range, it's a numeric equivalent of the concept that the electrical conduction of the normal heart is right to left and top to bottom.
A left axis deviation occurs when the electrical axis of the heart is between-30 and -90 degrees. A right axis deviation occurs when the electrical axis is in the +90-to-+180-degree range. A mean vector having an electrical axis within the range of -90 to -180 degrees is called an indeterminate axis or extreme right axis deviation.
Quadrant method
To approximate axis deviation using the quadrant method, divide the circle (which represents the patient's heart) into four quadrants (see the illustration below). You need only two ECG leads to make this assessment. Examine leads I and aVF. If lead I is upright, then the vector is flowing right to left. If lead aVF is upright, the vector is directed top to bottom. If they're both upright, the electrical axis must fall into the lower left or normal quadrant. This quadrant roughly matches the criteria for normal electrical axis, indicating a normal direction of electrical conduction.
Left axis deviation occurs when lead I is upright and lead aVF is down or negative. The electrical axis is located in the upper right quadrant. The mean vector is abnormally directed to the left side of the heart. A left axis deviation can be caused by many different pathologic conditions. Some left bundle-branch blocks will produce a left axis deviation because the cardiac vector flows abnormally from the right side of the heart to the left. Because the mean vector is not conducted by infarcted tissue and flows away from it, an inferior-wall myocardial infarction will produce a left axis deviation (due to a negative QRS in lead aVF). Many patients with pacemakers have a left axis deviation because the pacemaker leads are on the right side of the heart.
Finally, some structural body changes will produce a left axis deviation. In advanced pregnancy, the enlarged uterus may occupy so much space in the abdomen that the elevated diaphragm pushes the heart to a more horizontal or leftward-lying position, producing a left axis deviation. Similarly, short and squat or morbidly obese patients may have a left axis deviation because of the heart's position in the chest.
You can recognize a right axis deviation when lead I is negative and lead aVF is upright. The mean vector is abnormally directed to the right side of the heart. Causes of right axis deviation include chronic obstructive pulmonary disease and right ventricular hypertrophy. In both instances, enlargement of the right cardiac chambers pulls the mean vector to the right side. A right bundle-branch block causes the mean vector to flow from left to right, resulting in right axis deviation. Children and tall, thin adults may have a normal right axis deviation if the heart hangs down in a more vertical position.
Figure. No caption available.
If both leads I and aVF are negative, then the axis deviation is termed indeterminate axis or extreme right axis deviation. The mean vector is directed upward and to the right. If you find an indeterminate axis deviation on your patient's ECG, check the leads; incorrect ECG lead placement is a common cause of this finding. Other causes are some types of pacemakers, abnormal cardiac rhythms such as ventricular tachycardia, congenital heart disease, or dextrocardia (heart positioned on the right side of the chest).
Guy Goldich is assistant nurse-manager of the cardiac intensive care unit at Abington (Pa.) Memorial Hospital and an adjunct faculty member at the hospital's Dixon School of Nursing.
The author has disclosed that he has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.
12-Lead ECG System
15.1 LIMB LEADSPRECONDITIONS:SOURCE: Two-dimensional dipole (in the frontal plane) in a fixed locationCONDUCTOR: Infinite, homogeneous volume conductor or homogeneous sphere with the dipole in its center (the trivial solution)
Augustus Désiré Waller measured the human electrocardiogram in 1887 using Lippmann's capillary electrometer (Waller, 1887). He selected five electrode locations: the four extremities and the mouth (Waller, 1889). In this way, it became possible to achieve a sufficiently low contact impedance and thus to maximize the ECG signal. Furthermore, the electrode location is unmistakably defined and the attachment of electrodes facilitated at the limb positions. The five measurement points produce altogether 10 different leads (see Fig. 15.1A). From these 10 possibilities he selected five - designated cardinal leads. Two of these are identical to the Einthoven leads I and III described below.
Willem Einthoven also used the capillary electrometer in his first ECG recordings. His essential contribution to ECG-recording technology was the development and application of the string galvanometer. Its sensitivity greatly exceeded the previously used capillary electrometer. The string galvanometer itself was invented by Clément Ader (Ader, 1897). In 1908 Willem Einthoven published a description of the first clinically important ECG measuring system (Einthoven, 1908). The above-mentioned practical considerations rather than bioelectric ones determined the Einthoven lead system, which is an application of the 10 leads of Waller. The Einthoven lead system is illustrated in Figure 15.1B.
Fig. 15.1. (A) The 10 ECG leads of Waller. (B) Einthoven limb leads and Einthoven triangle. The Einthoven triangle is an approximate description of the lead vectors associated with the limb leads. Lead I is shown as I in the above figure, etc.
The Einthoven limb leads (standard leads) are defined in the following way:
Lead I: VI = ΦL - ΦR
Lead II: VII = ΦF - ΦR (15.1)Lead III: VIII = ΦF - ΦL
where VI = the voltage of Lead IVII = the voltage of Lead IIVIII = the voltage of Lead IIIΦL = potential at the left armΦR = potential at the right armΦF = potential at the left foot
(The left arm, right arm, and left leg (foot) are also represented with symbols LA, RA, and LL, respectively.) According to Kirchhoff's law these lead voltages have the following relationship:
VI + VIII = VII (15.2)
hence only two of these three leads are independent. The lead vectors associated with Einthoven's lead system are conventionally found based on the
assumption that the heart is located in an infinite, homogeneous volume conductor (or at the center of a homogeneous sphere representing the torso). One can show that if the position of the right arm, left arm, and left leg are at the vertices of an equilateral triangle, having the heart located at its center, then the lead vectors also form an equilateral triangle.
A simple model results from assuming that the cardiac sources are represented by a dipole located at the center of a sphere representing the torso, hence at the center of the equilateral triangle. With these assumptions, the voltages measured by the three limb leads are proportional to the projections of the electric heart vector on the sides of the lead vector triangle, as described in Figure 15.1B. These ideas are a recapitulation of those discussed in Section 11.4.3, where it was shown that the sides of this triangle are, in fact, formed by the corresponding lead vectors.
The voltages of the limb leads are obtained from Equation 11.19, which is duplicated below (Einthoven, Fahr, and de Waart, 1913, 1950). (Please note that the equations are written using the coordinate system of the Appendix.)
(11.19)
If one substitutes Equation 11.19 into Equation, 15.2, one can again demonstrate that Kirchhoff's law - that is, Equation 15.2 - is satisfied, since we obtain
(15.3)
15.2 ECG SIGNAL
15.2.1 The Signal Produced by the Activation Front
Before we discuss the generation of the ECG signal in detail, we consider a simple example explaining what kind of signal a propagating activation front produces in a volume conductor.
Figure 15.2 presents a volume conductor and a pair of electrodes on its opposite surfaces. The figure is divided into four cases, where both the depolarization and repolarization fronts propagate toward both positive and negative electrodes. In various cases the detected signals have the following polarities:
Case A: When the depolarization front propagates toward a positive electrode, it produces a positive signal (see the detailed description below).
Case B: When the propagation of activation is away from the positive electrode, the signal has the corresponding negative polarity.
Case C: It is easy to understand that when the repolarization front propagates toward a positive electrode, the signal is negative (see the detailed description below). Although it is known that repolarization does not actually propagate, a boundary between repolarized and still active regions can be defined as a function of time. It is "propagation" in this sense that is described here.
Case D: When the direction of propagation of a repolarization front is away from the positive electrode, a positive signal is produced.
The positive polarity of the signal in case A can be confirmed in the following way. First we note that the transmembrane voltage ahead of the wave is negative since this region is still at rest. (This condition is described in Figure 15.2 by the appearance of the minus signs.) Behind the wavefront, the transmembrane voltage is in the plateau stage; hence it is positive (indicated by the positive signs in Figure 15.2). If Equation 8.25 is applied to evaluate the double layer sources associated with this arrangement, as discussed in Section 8.2.4, and if the transmembrane voltage under resting or plateau conditions is recognized as being uniform, then a double layer source arises only at the wavefront.
What is important here is that the orientation of the double layer, given by the negative spatial derivative of Vm, is entirely to the left (which corresponds to the direction of propagation). Because the dipoles are directed toward the positive electrode, the signal is positive. (The actual time-varying signal depends on the evolving geometry of the source double layer and its relationship to the volume conductor and the leads. In this example we describe only the gross behavior.).
Fig. 15.2. The signal produced by the propagating activation front between a pair of extracellular electrodes.
The negative polarity of the signal in case C can be confirmed in the following way. In this case the direction of repolarization allows us to designate in which regions Vm is negative (where repolarization is complete and the membrane is again at rest) and positive (where repolarization has not yet begun, and the membrane is still in the plateau stage). These are designated in Figure 15.2 by the corresponding minus (-) and plus (+) markings. In this highly idealized example, we show repolarization as occurring instantly at the - to + interface (repolarization wavefront). But the source associated with this spatial distribution of Vm is still found from Equation 8.25. Application of that equation shows that the double layer, given by the negative spatial derivative, is zero everywhere except at the repolarization wavefront, where it is oriented to the right (in this case opposite to the direction of repolarization velocity). Since the source dipoles are directed away from the positive electrode, a negative signal will be measured.
For the case that activation does not propagate directly toward an electrode, the signal is proportional to the component of the velocity in the direction of the electrode, as shown in Figure 15.2E. This conclusion follows from the association of a double layer with the activation front and application of Equation 11.4 (where we assume the direction of the lead vector to be approximated by a line connecting the leads). Note that we are ignoring the possible influence of a changing extent of the wave of activation with a change in direction. Special attention should be given to cases A and D, marked with an asterisk (*), since these reflect the fundamental relationships.
15.2.2 Formation of the ECG Signal
The cells that constitute the ventricular myocardium are coupled together by gap junctions which, for the normal healthy heart, have a very low resistance. As a consequence, activity in one cell is readily propagated to neighboring cells. It is said that the heart behaves as a syncytium; a propagating wave once initiated continues to propagate uniformly into the region that is still at rest. We have quantitatively examined the electrophysiological behavior of a uniform fiber. Now we can apply these results to the heart if we consider it to be composed of uniform fibers. These equivalent fibers are a valid representation because they are consistent with the syncytial nature of the heart. In fact, because the syncytium reflects connectivity in all directions, we may choose the fiber orientation at our convenience (so long as the quantitative values of conductivity assigned to the fibers correspond to those that are actually measured).
Much of what we know about the activation sequence in the heart comes from canine studies. The earliest comprehensive study in this area was performed by Scher and Young (1957). More recently, such studies were performed on the human heart, and a seminal paper describing the results was published by Durrer et al. (1970). These studies show that activation wavefronts proceed relatively uniformly, from endocardium to epicardium and from apex to base.
One way of describing cardiac activation is to plot the sequence of instantaneous depolarization wavefronts. Since these surfaces connect all points in the same temporal phase, the wavefront surfaces are also referred to as isochrones (i.e., they are isochronous). An evaluation of dipole sources can be achieved by applying generalized Equation 8.25 to each equivalent fiber. This process involves taking the spatial gradient of Vm. If we assume that on one side cells are entirely at rest, while on the other cells are entirely in the plateau phase, then the source is zero everywhere except at the wavefront. Consequently, the wavefront or isochrone not only describes the activation surface but also shows the location of the double layer sources.
From the above it should be possible to examine the actual generation of the ECG by taking into account a realistic progression of activation double layers. Such a description is contained in Figure 15.3. After the electric activation of the heart has begun at the sinus node, it spreads along the atrial walls. The resultant vector of the atrial electric activity is illustrated with a thick arrow. The projections of this resultant vector on each of the three Einthoven limb leads is positive, and therefore, the measured signals are also positive.
After the depolarization has propagated over the atrial walls, it reaches the AV node. The propagation through the AV junction is very slow and involves negligible amount of tissue; it results in a delay in the progress of activation. (This is a desirable pause which allows completion of ventricular filling.)
Once activation has reached the ventricles, propagation proceeds along the Purkinje fibers to the inner walls of the ventricles. The ventricular depolarization starts first from the left side of the interventricular
septum, and therefore, the resultant dipole from this septal activation points to the right. Figure 15.3 shows that this causes a negative signal in leads I and II.
In the next phase, depolarization waves occur on both sides of the septum, and their electric forces cancel. However, early apical activation is also occurring, so the resultant vector points to the apex.
Fig. 15.3. The generation of the ECG signal in the Einthoven limb leads. (After Netter, 1971.)
After a while the depolarization front has propagated through the wall of the right ventricle; when it first arrives at the epicardial surface of the right-ventricular free wall, the event is called breakthrough. Because the left ventricular wall is thicker, activation of the left ventricular free wall continues even after depolarization of a large part of the right ventricle. Because there are no compensating electric forces on the right, the resultant vector reaches its maximum in this phase, and it points leftward. The depolarization front continues propagation along the left ventricular wall toward the back. Because its surface area now continuously decreases, the magnitude of the resultant vector also decreases until the whole ventricular muscle is depolarized. The last to depolarize are basal regions of both left and right ventricles. Because there is no longer a propagating activation front, there is no signal either.
Ventricular repolarization begins from the outer side of the ventricles and the repolarization front "propagates" inward. This seems paradoxical, but even though the epicardium is the last to depolarize, its action potential durations are relatively short, and it is the first to recover. Although recovery of one cell does not propagate to neighboring cells, one notices that recovery generally does move from the epicardium toward the endocardium. The inward spread of the repolarization front generates a signal with the same sign as the outward depolarization front, as pointed out in Figure 15.2 (recall that both direction of repolarization and orientation of dipole sources are opposite). Because of the diffuse form of the repolarization, the amplitude of the signal is much smaller than that of the depolarization wave and it lasts longer.
The normal electrocardiogram is illustrated in Figure 15.4. The figure also includes definitions for various segments and intervals in the ECG. The deflections in this signal are denoted in alphabetic order starting with the letter P, which represents atrial depolarization. The ventricular depolarization causes the QRS complex, and repolarization is responsible for the T-wave. Atrial repolarization occurs during the QRS complex and produces such a low signal amplitude that it cannot be seen apart from the normal ECG.
Fig. 15.4. The normal electrocardiogram.
15.3 WILSON CENTRAL TERMINALFrank Norman Wilson (1890-1952) investigated how electrocardiographic unipolar potentials could be defined. Ideally, those are measured with respect to a remote reference (infinity). But how is one to achieve this in the volume conductor of the size of the human body with electrodes already placed at the extremities? In several articles on the subject, Wilson and colleagues (Wilson, Macleod, and Barker, 1931; Wilson et al., 1934) suggested the use of the central terminal as this reference. This was formed by connecting a 5 kΩ resistor from each terminal of the limb leads to a common point called the central terminal, as shown in Figure 15.5. Wilson suggested that unipolar potentials should be measured with respect to this terminal which approximates the potential at infinity.
Actually, the Wilson central terminal is not independent of but, rather, is the average of the limb potentials. This is easily demonstrated by noting that in an ideal voltmeter there is no lead current. Consequently, the total current into the central terminal from the limb leads must add to zero to satisfy the conservation of current (see Figure 15.5). Accordingly, we require that
(15.4)
from which it follows that
(15.5)
Since the central terminal potential is the average of the extremity potentials it can be argued that it is then somewhat independent of any one in particular and therefore a satisfactory reference. In clinical practice good reproducibility of the measurement system is vital. Results appear to be quite consistent in clinical applications.
Wilson advocated 5 kΩ resistances; these are still widely used, though at present the high-input impedance of the ECG amplifiers would allow much higher resistances. A higher resistance increases the CMRR and diminishes the size of the artifact introduced by the electrode/skin resistance.
It is easy to show that in the image space the Wilson central terminal is found at the center of the Einthoven triangle, as shown in Figure 15.6..
Fig. 15.5. The Wilson central terminal (CT) is formed by connecting a 5 kΩ resistance to each limb electrode and interconnecting the free wires; the CT is the common point. The Wilson central terminal represents the average of the limb potentials. Because no current flows through a high-impedance voltmeter, Kirchhoff's law requires that IR + IL + IF = 0.
Fig. 15.6. (A) The circuit of the Wilson central terminal (CT). (B) The location of the Wilson central terminal in the image space (CT'). It is located in the center
of the Einthoven triangle.
15.4 GOLDBERGER AUGMENTED LEADSThree additional limb leads, VR, VL, and VF are obtained by measuring the potential between each limb electrode and the Wilson central terminal. (Note that V in Roman denotes a lead and V in italics a lead voltage.) For instance, the measurement from the left leg (foot) gives
(15.6)
In 1942 E. Goldberger observed that these signals can be augmented by omitting that resistance from the Wilson central terminal, which is connected to the measurement electrode (Goldberger, 1942a,b). In this way, the aforementioned three leads may be replaced with a new set of leads that are called augmented leads because of the augmentation of the signal (see Figure 15.7). As an example, the equation for the augmented lead aVF is:
(15.7)
A comparison of Equation 15.7 with Equation 15.6 shows the augmented signal to be 50% larger than the signal with the Wilson central terminal chosen as reference. It is important to note that the three augmented leads, aVR, aVL, and aVF, are fully redundant with respect to the limb leads I, II, and III. (This holds also for the three unipolar limb leads VR, VL, and VF.)
Fig. 15.7. (A) The circuit of the Goldberger augmented leads. (B) The location of the Goldberger augmented lead vectors in the image space.
15.5 PRECORDIAL LEADSPRECONDITIONS:SOURCE: Dipole in a fixed locationCONDUCTOR: Infinite, homogeneous volume conductor or homogeneous sphere with the dipole in its center (the trivial solution)
For measuring the potentials close to the heart, Wilson introduced the precordial leads (chest leads) in 1944 (Wilson et al., 1944). These leads, V1-V6 are located over the left chest as described in Figure 15.8. The points V1 and V2 are located at the fourth intercostal space on the right and left side of the sternum; V4 is located in the fifth intercostal space at the midclavicular line; V3 is located between the points V2 and V4; V5 is at the same horizontal level as V4 but on the anterior axillary line; V6 is at the same horizontal level as V4 but at the midline. The location of the precordial leads is illustrated in Figure 15.8.
Fig. 15.8. Precordial leads.
15.6 MODIFICATIONS OF THE 12-LEAD SYSTEMThe 12-lead system as described here is the one with the greatest clinical use. There are also some other modifications of the 12-lead system for particular applications.
In exercise ECG, the signal is distorted because of muscular activity, respiration, and electrode artifacts due to perspiration and electrode movements. The distortion due to muscular activation can be minimized by placing the electrodes on the shoulders and on the hip instead of the arms and the leg, as suggested by R. E. Mason and I. Likar (1966). The Mason-Likar modification is the most important modification of the 12-lead system used in exercise ECG.
The accurate location for the right arm electrode in the Mason-Likar modification is a point in the infraclavicular fossa medial to the border of the deltoid muscle and 2 cm below the lower border of the clavicle. The left arm electrode is located similarly on the left side. The left leg electrode is placed at the left iliac crest. The right leg electrode is placed in the region of the right iliac fossa. The precordial leads are located in the Mason-Likar modification in the standard places of the 12-lead system.
In ambulatory monitoring of the ECG, as in the Holter recording, the electrodes are also placed on the surface of the thorax instead of the extremities.
15.7 THE INFORMATION CONTENT OF THE 12-LEAD SYSTEMThe most commonly used clinical ECG-system, the 12-lead ECG system, consists of the following 12 leads, which are:
I, II, IIIaVR, aVL, aVF
V1, V2, V3, V4, V5, V6
Of these 12 leads, the first six are derived from the same three measurement points. Therefore, any two of these six leads include exactly the same information as the other four.
Over 90% of the heart's electric activity can be explained with a dipole source model (Geselowitz, 1964). To evaluate this dipole, it is sufficient to measure its three independent components. In principle, two of the limb leads (I, II, III) could reflect the frontal plane components, whereas one precordial lead could be chosen for the anterior-posterior component. The combination should be sufficient to describe completely the electric heart vector. (The lead V2 would be a very good precordial lead choice since it is directed closest to the x axis. It is roughly orthogonal to the standard limb plane, which is close to the frontal plane.) To the extent that the cardiac source can be described as a dipole, the 12-lead ECG system could be thought to have three independent leads and nine redundant leads.
However, in fact, the precordial leads detect also nondipolar components, which have diagnostic significance because they are located close to the frontal part of the heart. Therefore, the 12-lead ECG system has eight truly independent and four redundant leads. The lead vectors for each lead based on an idealized (spherical) volume conductor are shown in Figure 15.9. These figures are assumed to apply in clinical electrocardiography.
The main reason for recording all 12 leads is that it enhances pattern recognition. This combination of leads gives the clinician an opportunity to compare the projections of the resultant vectors in two orthogonal planes and at different angles. This is further facilitated when the polarity of the lead aVR can be changed; the lead -aVR is included in many ECG recorders.
In summary, for the approximation of cardiac electric activity by a single fixed-location dipole, nine leads are redundant in the 12-lead system, as noted above. If we take into account the distributed character of cardiac sources and the effect of the thoracic surface and internal inhomogeneities, we can consider only the four (of six) limb leads as truly redundant..
Fig. 15.9. The projections of the lead vectors of the 12-lead ECG system in three orthogonal planes when one assumes the volume conductor to be spherical homogeneous and the cardiac source centrally located.