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ISBN 9781119066415
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Cover image: Courtesy of Alfons F. Sinnaeve
Before deciding to write this book, we examined many of the multitude of books on electrocardiography to determine whether there was a need for a new book with a different approach focusing on graphics. In our experience the success of our “step by step” books on cardiac pacemakers and implanted cardioverter-defibrillators was largely due to the extensive use of graphics according to feedback we received from many readers. Consequently in this book we used the same approach with the liberal use of graphics. This format distinguishes the book from all the other publications. In this way, the book can be considered as a companion to our previous “step by step” books. The publisher offers a large number of PowerPoint slides obtainable on the Internet. Based on a number of suggestions an accompanying set of test ECG tracings is also provided on the Internet. We are confident that our different approach to the teaching of electrocardiography will facilitate understanding by the student and help the teacher, the latter by using the richly illustrated work.
The authors would also like to thank Garant Publishers, Antwerp, Belgium /Apeldoorn, The Netherlands for authorizing the use of figures from the Dutch ECG book, ECG: Uit of in het Hoofd, 2006 edition, by E. Andries, R. Stroobandt, N. De Cock, F. Sinnaeve and F. Verdonck,
Roland X. Stroobandt
S. Serge Barold
Alfons F. Sinnaeve
This book is accompanied by a companion website, containing all the figures from the book for you to download: www.wiley.com/go/stroobandt/ecg
The ECG provides information on:
History
The Dutch physiologist Willem Einthoven was one of the pioneers of electrocardiography and developer of the first useful string galvonometer. He labelled the various parts of the electrocardiogram using P, Q, R, S and T in a classic article published in 1903. Professor Einthoven received the Nobel prize for medicine in 1924.
The heart is a muscle consisting of four hollow chambers. It is a double pump: the left part works at a higher pressure, while the right part works on a lower pressure.
The right heart pumps blood into the pulmonary circulation (i.e. the lungs). The left heart drives blood through the systemic circulation (i.e. the rest of the body).
The right atrium (RA) receives deoxygenated blood from the body via two large veins, the superior and the inferior vena cava, and from the heart itself by way of the coronary sinus. The blood is transferred to the right ventricle (RV) via the tricuspid valve (TV). The right ventricle then pumps the deoxy- genated blood via the pulmonary valve (PV) to the lungs where it releases excess carbon dioxide and picks up new oxygen.
The left atrium (LA) accepts the newly oxygenated blood from the lungs via the pulmonary veins and delivers it to the left ventricle (LV) through the mitral valve (MV). The oxygenated blood is pumped by the left ventricle through the aortic valve (AoV) into the aorta (Ao), the largest artery in the body.
The blood flowing into the aorta is further distributed throughout the body where it releases oxygen to the cells and collects carbon dioxide from them.
The contractions of the various parts of the heart have to be carefully synchronized. It is the prime function of the electrical conduction system to ensure this synchronization. The atria should contract first to fill the ventricles before the ventricles pump the blood in the circulation.
All in all it takes the electrical impulses less than 200 ms to travel from the sinus node to the myocardial cells in the ventricles.
Cardiac muscle cells are more or less cylindrical. At their ends they may partially divide into two or more branches, connecting with the branches of adjacent cells and forming an anastomosing network of cells called a syncytium. At the interconnections between cells there are specialized membranes (intercalated disks) with a very low electrical resistance.
These “gap-junctions” allow a very rapid conduction from one cell to another.
In the resting state, a high concentration of positively charged sodium ions (Na+) is present outside the cell while a high concentration of positive potassium ions (K+) and a mixture of the large negatively charged ions (PO4---, SO4--, Prot--) are found inside the cell.
There is a continuous leakage of the small ions decreasing the resting membrane potential. Consequently other processes have to restore the phenomenon. The Na+/K+ pump, located in the cell membrane, maintains the negative resting potential inside the cell by bringing K+ into the cell while taking Na+ out of the cell. This process requires energy and therefore it uses adenosine triphosphate (ATP). The pump can be blocked by digitalis. If the Na+/K+ pump is inhibited, Na+ ions are still removed from the inside by the Na+/Ca++exchange process. This process increases the intracellular Ca++ and ameliorates the contractility of the muscle cells.
An external negative electric impulse that converts the outside of a myocardial cell from positive to negative, makes the membrane permeable to Na+. The influx of Na+ ions makes the inside of the cell less negative. When the membrane voltage reaches a certain value(called the threshold), some fast sodium channels in the membrane open momentarily, resulting in a sudden larger influx of Na+.Consequently, a part of the cell depolarizes, i.e. its exterior becomes negative with respect to its interior that becomes positive.Due to the difference in concentration of the Na+ ions, a local ionic current arises between the depolarized part of the cell and its still resting part. These local electric currents give rise to a depolarization front that moves on until the whole cell becomes depolarized.
As soon as the depolarization starts, K+ ions flow out from the cell trying to restore the initial resting potential. In the meantime, some Ca++ ions flow inwards through slow calcium channels. At first, these ion movements and the decreasing Na+ influx nearly balance each other resulting in a slowly varying membrane potential. Next the Ca++ channels are inhibited as are the Na+ channels while the open K+ channels together with the Na+/K+ pump repolarize the cell. Again local currents are generated and a repolarization front propagates until the whole cell is repolarized.
The cells of the sinus node and the AV junction do not have fast sodium channels. Instead they have slow calcium channels and potassium channels that open when the membrane potential is depolarized to about −50 mV.
The major determinant for the diastolic depolarization is the so-called “funny current” If. This particularly unusual current consists of an influx of a mix of sodium and potassium ions that makes the inside of the cells more positive.
When the action potential reaches a threshold potential (about −50/−40mV), a faster depolarization by the Ca++ ions starts the systolic phase. As soon as the action potential becomes positive, some potassium channels open and the resulting outflux of K+ ions repolarizes the cells. The moment the repolarization reaches its most negative potential (−60/−70mV), the funny current starts again and the whole cycle starts all over.
Spontaneous depolarization may be modulated by changing the slope of the spontaneous depolarization (mostly by influencing the If channels). The slope is controlled by the autonomic nervous system.
Increase in sympathetic activity and administration of catecholamines (epinephrine, norepinephrine, dopamine) increases the slope of the phase 4 depolarization. This results in a higher firing rate of the pacemaker cells and a shorter cardiac cycle. Administration of certain drugs decreases the slope of the phase 4 depolarization, reducing the firing rate and lengthening the cardiac cycle.
Spontaneous depolarization is not only present in the sinoatrial node (SAN) but, to a lesser extent, also in the other parts of the conduction system. The intrinsic pacemaker activity of the secondary pacemakers situated in the atrioventricular junction and the His-Purkinje system is normally quiescent by a mechanism termed overdrive suppression. If the sinus node (SAN) becomes depressed, or its action potentials fail to reach secondary pace-makers, a slower rhythm takes over.
Overdrive suppression occurs when cells with a higher intrinsic rate (e.g. the dominant pacemaker) continually depolarize or overdrive potential automatic foci with a lower intrinsic rate thereby suppressing their emergence.
Should the highest pacemaking center fail, a lower automatic focus previously inactive because of overdrive suppression emerges or “escapes” from the next highest level.
The new site becomes the dominant pacemaker at its inherent rate and in turn suppresses all automatic foci below it.
A depolarization front can propagate through the fibers of the heart muscle in the same way as the depolarization front moves through a single cylindrical cell. Local ionic currents between active cells and resting cells depolarize the resting cells and activate them.
Due to the intercalated disks with their gap junctions, a depolarizing electrical impulse spreads out rapidly in all directions. However, the gap junctions with their very low electrical resistance are only present at the short ends of the myocardial cells. Hence, depolarization propagates very fast in the longitudinal direction of the fibers and less fast in the transversal direction.
The voltmeter shows a positive deflection if the voltage vector points towards its positive pole !
A very small current flows through the voltmeter from its positive pole to its negative pole. The internal resistance of the voltmeter has to be extremely high since the small current may not influence the condition of the source, i.e this weak current may not affect the distribution of the ions around the cell.
Due to the high degree of electrical interaction between the branched cells, many cells are depolarizing simultaneously in different regions of the ventricles during the ventricular activation process. The voltage vectors of these many cells may be combined into one resultant vector. When a depolarization front or a repolarization front moves rapidly through a region of the heart it generates a voltage vector and a tiny electrical current flows through the body (which is a good conductor). The ECG recorder acts in the same way as a voltmeter and when the voltage vector points to its positive connector, the ECG registers a positive (+) deflection.
Ventricular activation consists of a series of sequential activation fronts. At each particular time, the vectors of these activation fronts may be combined to form one resultant vector. The resultant vector changes continually as the ventricles are being progressively depolarized. However, at each point in time the multiple activation fronts can be represented by a single resultant vector.
The point of the resultant heart vector traces a closed loop in space. The projection of this path is the vectorcardiogram.
Note:
There is no absolute or fixed zero voltage. All measurements of voltages on ECG are relative to the baseline or isoelectric line.
Upward deflections on an ECG (above the baseline) are called positive. Downward deflections (under the baseline) are called negative.
No calculation needed for a quick estimation of the rate, just count the number of squares between two consecutive R waves !
or with more accuracy
Methods for determining the heart rate during regular rhythm
Example of the 6 s rule during irregular rhythm
Methods for determining the heart rate during irregular rhythm
When the heart rate is irregular (e.g. atrial fibrillation), a longer interval should be measured to provide a more precise rate. “1 second time lines” may be used to measure longer intervals. If no “1 s time lines” are marked on the ECG paper, they can be created by counting 5 large squares (5 x 0.2 s = 1 s).
The lead axis of a lead can theoretically be orientated in any direction or plane relative to the heart. Obviously, this will depend upon electrode placement.
Conventionally, however, there are 12 leads which may be divided into two groups on the basis of their orientation. One group is orientated in the frontal plane of the body, the other in the horizontal plane.
The standard leads are :
Note : Arms and legs are good electrical conductors, hence the position of the electrodes (hand or shoulder, foot or hip) is not critical.
The positive electrodes (+) of the standard limb leads are electrically at about the same distance from a theoretical zero reference in the heart. Hence, the lead axes form an equilateral triangle with the heart and its zero reference in the center. This triangle is called Einthoven's triangle. (Although in reality it is not exactly equilateral, but it is a good approximation.)
If : VLA is the potential at the left arm (LA)
VRA is the potential at the right arm (RA)
VLL is the potential at the left leg (LL)
then the potential difference or voltage in the frontal leads is given by :
Lead I = VLA − VRA
Lead II = VLL − VRA
Lead III = VLL − VLA
It follows that (VLA − VRA) + (VLL − VLA) = (VLL − VRA)
This equation can also be written as :
which is the well-known form of Einthoven's law!
The relationship between the standard limb leads is such that the sum of the electric voltages recorded in leads I and III equals the electric voltage recorded by lead II.
By linking the three limbs RA, LA and LL through large equal resistors a relatively stable reference potential VCT is created. Although it is technically incorrect to label VCT as the zero potential it may be considered as such because the electrocardio-graph only registers variations of voltages and suppresses constant (or DC) voltages.
Since the potential of the central terminal is essentially constant, the potential difference or voltage recorded by the electrocardiograph only reflects the potential variations at the exploring electrode - hence the term “unipolar lead”.
With the Wilson box as a reference potential, additional lead axes were created using one of the three limb electrodes (i.e. RA, LA and LL) as an exploring electrode.
By using only two resistors and omitting the connection between the exploring electrode and the reference point, Dr. Goldberger obtained an amplitude of the deflecton that was 50% larger.
Therefore these leads are called “augmented” hence the letter “a” is applied to the VR, VL and VF leads (aVR, aVL, aVF).
The augmented leads are:
Anatomically the RV lies anteriorly and medially but the LV lies laterally and posteriorly. Leads V1 and V2 are situated over the RV, leads V3 and V4 face the interventricular septum and leads V5 and V6 clearly point towards the free lateral wall of the LV. QRS changes emanating from the LV overshadow those from the RV in the absence of a conduction delay involving the RV. Therefore, V1 and V2 reflect the electrical activity of the interventricular septum (pre-dominantly a left-sided structure), leads V3 and V4 point towards the anterior LV, while leads V5 and V6 reflect the lateral LV.
Locating the 4th intercostal space.
It sounds easy but is not !
WHY DO WE NEED 12 LEADS?
If you want to check the quality of an apple you have to look
for weak spots from many directions !
The same principle applies to the heart !
Lead aVR is directed opposite to that of the other leads and is often ignored (“the forgotten 12th lead”).
Lead aVR does not view any single surface of the heart as do other lead systems. Yet, aVR can be very helpful in diagnosing a number of different entities. Inverted aVR (or minus aVR) can improve the diagnosis of inferior and lateral myocardial infarction.
Lead I is chosen as the reference direction and (0°). The position of the other leads is expressed by the rotation (angle) from this reference. This rotation is positive in clockwise direction and negative in the counter-clockwise direction.
Advantages of the hexaxial diagram:
Note: Lead minus aVL (−aVL) is not used in recording the standard ECG. It is useful in estimating the frontal plane axis and understanding the configuration of the QRS complex. Lead minus aVR (−aVR) is available in relatively few electrocardiographs. It may be used to identify a myocardial infarct (see further on).
A lead axis is selectable. An axis has only a direction and not a magnitude (or amplitude). Therefore axes cannot be vectors and cannot be combined by the parallelogram rule.
The leads themselves are real vector quantities having magnitude and direction. They may be combined in the classical way.
All frontal leads are orthogonal projections of the heart vector upon their specific axes (orthogonal means right angles or 90°). By combining these projections, the heart vector can be reconstructed in a continuously changing format. By doing so at many consecutive times a loop in the frontal plane is formed (i.e. the vectocardiogram).
Since the direction of all lead axes is known, every two leads may be combined by the computer in an ECG machine to find direction and magnitude of the heart vector. Consequently, the resulting heart vector can be decomposed to determine any other lead in the frontal plane. This gives only a good approximation since the human body is not homogeneous and Einthoven's triangle itself is an approximation.
Technicians are commonly trained to place the chest electrodes under the breast of women. The effect of breast tissue on the ECG is smaller than that of misplacement.Therefore it is recommended by some experts to place the electrodes on the breast rather than under the breast to facilitate the precision of electrode placement at the correct horizontal level and at the correct lateral positions. Others believe that there is insufficient evidence to support a switch from traditional sites beneath the left breast to record V4 to V6.
An error in the placement of precordial leads may change the morphology of the ECG and result in inadequate or even wrong diagnosis.
In the example below, the P wave changes from its normal equiphasic appearance to monophasic positive if the electrodes are placed incorrectly too low or monophasic negative if they are placed too high:
The right precordial leads can be placed deliberately too low in order to make a differential diagnosis between left anterior hemiblock (LAH) and an old anteroseptal infarction.
In the example above, there is a QS pattern in V1 and V2.
If the precordial electrodes are placed 2 intercostal places lower the QS morhology changes to rS indicating LAH.
For an old anteroseptal infarction the QS would persist.
Lead switches are a common mistake in ECG recording and can lead to wrong diagnoses. The most common mistake in electrode positioning is reversal of the right and the left arm leads, which occurs in about 3% of ECGs recorded in a hospital setting. Lead I becomes the mirror image of the true lead I so that all deflections (P wave, QRS complex and T wave) are inverted. Lead aVR shows reversed polarity with a positive P wave and QRS complex. Just looking at lead I makes the diagnosis.
Right and left arm lead reversal can be distinguished from the much rarer dextrocardia (where the heart is positioned on the right side) by examination of the precordial R wave progression. This progression is normal with arm lead reversal but is reversed with dextrocardia.
Transposition of the arm and leg electrodes is much less common but quite complex to evaluate, except reversal of the right leg lead with one of the arm leads. In this situation the reversal produces “pseudo-asystole” (a straight line) in either lead II or III because the potential between the two legs is zero. Lead II or III appears “collapsed” (very small voltage), but this sign occurs in only one lead. Consider the switch of the right arm (RA) and the right leg (RL) electrodes. Lead II records the potential difference between the left leg (LL) and RA electrodes (i.e. LL − RA). Now that RA becomes RL as the result of the switch, the electrocardiograph will record lead II with LL − RL which yields an essentially zero potential. The same argument applies to the left arm (LA) and RL switch. Lead III is LL − LA but as LA is now RL, lead III records the difference between LL and RL which is again essentially zero.
The deflection on the ECG will be positive if the projection of the voltage vector points to the positive pole of the lead axis. The deflection on the ECG will be negative if the projection of the voltage vector points to the negative pole of the lead axis.
The magnitude of the deflection on the ECG is determined by the angle between the voltage vector and the lead axis.
The resultant voltage vector of the heart is continuously changing during the heart cycle causing ECG deflections to vary with the passage of time. The tip of the resultant voltage vector describes a closed loop in space.
No deflection is produced when the resultant heart vector is perpendicular to the axis of a lead.
When the heart vector fluctuates at both sides of the perpendicular (partly pointing towards the positive pole and partly towards the negative pole) a biphasic deflection on the ECG is produced.
If the positive and negative deflections are equal in magnitude, an equiphasic deflection is present and the sum of the deflections is zero.
The perpendicular to an axis of a lead serves as a boundary between the predominantly positive and the predominantly negative deflections in any given lead.
No ECG deflection is produced when the resultant heart vector is perpendicular to the axis of a lead: the perpendicular to the lead axis is a “neutral line”, it is the boundary between the positive and the negative deflections for any given lead.
Obviously, there is a positive hemisphere for each lead, i.e. six hemispheres for the frontal plane leads: aVL, I, II, aVF, III, aVR. The same concept also applies to the horizontal plane.
In the normal ECG looking at the precordial leads, the r wave usually progresses from showing an rS complex in V1, with an increasing R and a decreasing S wave when moving towards the left side. There is usually a qR complex in V5 and V6 (the q wave reflecting septal activation) but the absence of q waves in V5 and V6 may be normal. The R wave amplitude is usually taller in V5 (and occasionally in V4) than in V6 because of the attenuating effect of the lungs. The transition zone is the lead with equal R and S wave voltage (i.e. R/S = 1) and occurs normally in V3 or V4. It may be normal to have the transition zone at V2 (called “early transition”), and at V5 (called “delayed transition”). It is normal to have a narrow QS or rSr' pattern in V1.
Normal progression in the precordial plane
R WAVE PROGRESSION
In the normal ECG looking at the precordial leads, the r wave usually progresses from showing an rS complex in V1, with an increasing R and a decreasing S wave when moving towards the left side. There is usually an qR complex in V5 and V6 (the q wave reflecting septal activation) but the absence of q waves in V5 and V6 may be normal. The R wave amplitude is usually taller in V5 (and occasionally in V4) than in V6 because of the attenuating effect of the lungs. The transition zone is the lead with equal R and S wave voltage (R/S = 1) and occurs normally in V3 or V4. It may be normal to have the transition zone at V2 (called “early transition”), and at V5 (called “delayed transition”). It is normal to have a narrow QS or rSr' pattern in V1.
The definition of poor R wave progression in the literature varies considerably. A common definition relies on an R wave being less than 2-4 mm in leads V3 and V4. In addition it requires one or more of the following criteria: R in V4 < R in V3, R in V3 < R in V2, R in V2 < R in V1. If transition occurs at/or before V2 it is called CCW rotation. If it occurs after V4 it is called CW rotation. Poor R wave progression is also defined as a late transition seen in V5 or V6. In other words, poor R wave progression is present when the R wave height does not become progressively taller from leads V1 to V3 or V4, or even remains of low amplitude across the entire precordium. Poor R wave progression is abnormal but is not a diagnosis provided faulty ECG technique is ruled out, remembering that it can also be a normal variant.
The mean QRS axis in the horizontal plane is rarely, if ever, used clinically. Determining the mean QRS axis in the horizontal plane may be useful for determining the origin of ventri-cular premature beats and ventricular tachycardias.
Leads I and aVF divide the thorax into 4 quadrants equal in size. Examine the direction of the QRS complex in leads I and aVF. The combination should place the electrical axis in one of the 4 quadrants of the hexaxial diagram.
1. If leads I and aVF are both upright, the axis is in the left inferior quadrant (yellow area). There is no point in going further to obtain the precise site of the mean axis as it is always normal in this quadrant.
2. If lead I is upright and lead aVF is downward, the axis is in the left superior quadrant (red area) where it may be normal or abnormal because the normal site extends from 90° to −30° moving in a counterclockwise fashion. The site of the axis can be more precisely determined by one step which involves looking at lead II (discussed later). The axis in this quadrant is called left superior axis deviation if it is more superior or more negative than −30°.
3. If lead I is downward and aVF is upright, the axis is in the right inferior quadrant (green area). It is simply called right axis deviation.
4. If both leads I and aVF are downwards, the axis is in the right superior quadrant (blue area). This quadrant has been described by a variety of names: no man's land, marked right axis deviation, marked left axis deviation, indeterminate axis, right shoulder axis and northwest quadrant. It is best called a right superior axis.
Another method related to the quadrant technique involves determining the frontal plane axis by seeking the QRS complex with the greatest amplitude. The axis is parallel to this lead (see step 2).
The lead nearest to (or parallel along) the QRS axis has the largest positive deflection. If two leads have equal positive deflections, the axis is exactly in the middle between these two leads.
The electrical QRS axis is perpendicular to the lead with an isoelectric (equiphasic) QRS complex or the lead with the smallest net amplitude (most equiphasic lead). Since there are two perpendicular directions to each isoelectric lead, choose the direction (positive or negative) that best fits to the adjacent leads.
This method can determine the axis within ± 10°−15°. If there is no isoelectric lead, there are usually two leads that are nearly isoelectric, and these are always 30° apart. Find the perpendiculars for each lead and choose an approximate QRS axis within the 30° range.
Occasionally each of the 6 frontal plane leads is small and/or isoelectric. The axis cannot be determined and is called indeterminate.
I and aVF both positive: left inferior quadrant
tallest R wave in II: QRS axis is along II
most equiphasic in aVL: perpendicular to aVL
I positive; aVF negative: left superior quadrant
tallest S wave in III: QRS axis is along III
most equiphasic in aVR: perpendicular to aVR
aVF is + and lead I is −: QRS is in the right inferior quadrant
tallest R wave in III: QRS axis is close to III
lead III > aVF: axis near III
Note that the sum of R and S waves in lead I is negative which places the axis in the right inferior quadrant
aVF is negative: QRS is oriented superiorly
most equiphasic in lead I: QRS axis is nearly perpendicular to lead I
Note that the largest QRS deflections are in leads II and aVF. Therefore the axis is diame-
trically opposite the line that bisects the angle between the lead II axis and the aVF axis.