ELECTROCARDIOGRAPHY (III) THE ANALYSIS OF THE ELECTROCARDIOGRAM

ELECTROCARDIOGRAPHY (III) THE ANALYSIS OF THE ELECTROCARDIOGRAM Scridon Alina, Șerban Răzvan Constantin Recording and analysis of the 12-lead ECG is part of the basic medical assessment performed for every patient, providing an invaluable diagnostic tool. Therefore, every physician is expected to possess a reasonable level of expertise and skill in electrocardiography, regardless of his/her medical specialty. As in the case of physical examination, it is desirable to follow a standardized sequence of steps in order to avoid missing subtle abnormalities in the ECG tracing, some of which may have major clinical relevance. This chapter presents a systematic, eight-step ECG interpretation method, based on the analysis of: 1. Cardiac rhythm 2. Heart rate 3. Electrical axis of the heart 4. Rhythm disorders (arrhythmias) 5. Conduction disorders (heart blocks) 6. Myocardial hypertrophy 7. ECG changes in coronary artery disease 8. Other abnormalities 1. The assessment of the cardiac rhythm The cardiac rhythm is characterized by two main elements: origin and rhythmicity. 1.1. The assessment of the origin of the cardiac rhythm Since the cardiac rhythm is normally initiated by the sinus node, the normal rhythm is designated as sinus rhythm. For the cardiac rhythm to be considered sinus rhythm, all of the following criteria must be fulfilled: - P waves must be present in front of each QRS complex if the electrical impulses originate in the sinus node they first cause the depolarization of the atria (P wave on the ECG) and only then the depolarization of the ventricles (QRS complex on the ECG) - the morphology of the P waves remains constant in each cardiac cycle within the same ECG lead if the electrical impulses originate in the sinus node they cause an atrial depolarization that always follows the exact same sequence, generating identical P waves - the distance between consecutive P waves is constant the sinus node generates electrical impulses rhythmically (at a constant rate); however, small irregularities can occur (See below) - P waves are positive in leads II and avf the vector of atrial depolarization points downwards and leftwards, towards the positive poles of leads II and avf (See the Electrocardiography (II) chapter). If any of these criteria is not fulfilled, the rhythm is not a sinus rhythm arrhythmia is present. 35

1.2. The assessment of the rhythmicity of the cardiac rhythm Given that the sinus node generates electrical impulses rhythmically (at a constant rate), the normal cardiac rhythm is regular (heart cycles have equal length). To determine if the heart cycles are of equal length, one has two options: - to measure precisely the RR intervals if the RR intervals have equal durations (duration of RR interval 1 = duration of RR interval 2 = = duration of RR interval n) the cardiac rhythm is regular - to use a quick approach mark on a piece of paper the position of 3-4 QRS complexes; shift the paper to other parts of the ECG trace and compare the position of the marks with that of the QRS complexes. If the marks correspond to the position of the QRS complexes, the cardiac rhythm is regular. If the RR intervals are not equal (the marks do not correspond to the position of the QRS complexes), the rhythm is irregular arrhythmia is present. When the cardiac rhythm is irregular, this irregularity can be: - intermittent (periodic) there are only occasional irregularities in the RR intervals, but the baseline rhythm is regular (one example of intermittently irregular cardiac rhythm is due to the presence of premature beats, See below) - absolute when the RR intervals are completely irregular, on the entire ECG tracing (one example of absolute irregularity of the cardiac rhythm is atrial fibrillation, See below). However, slight variations of the cardiac rhythm can also occur in perfectly healthy individuals with respiration, causing the so-called physiological respiratory arrhythmia (shortening of the RR intervals during inspiration and lengthening of the RR intervals during expiration). 2. The assessment of the heart rate The normal heart rate, dictated by the discharge rate of the sinus node, is around 70 beats per minute (bpm), but values between 60 bpm and 100 bpm are considered normal, depending on the status of the patient at the moment of heart rate measurement (e.g., higher heart rate after physical training or in anxious patients; lower heart rate during sleep). The physiological variations of the heart rate are defined as: - sinus tachycardia when the rate of the sinus rhythm is greater than 100 bpm; occurs most commonly during physical exercise - sinus bradycardia when the rate of the sinus rhythm is lower than 60 bpm; can be seen at rest in conditioned athletes. Three main methods can be used to determine the heart rate: calculating precisely, using an ECG ruler, or approximating. 1.1. Precise calculation of the heart rate The heart rate can be calculated precisely starting from the equation of velocity: v D t t D v, where: v = speed, D = distance, t = time. 36

From this equation, one can obtain: 1 T V I RR I T, V RR, where: ν = heart rate, V = speed of the ECG paper (usually 25 mm/s), I RR = RR interval measured in mm, T = duration of the cardiac cycle (RR interval) measured in sec. Replacing the constants in the equation, one will obtain: 25 60 1500 I RR I RR, where: I RR = RR interval in mm. Since the heart rate is measured per minute and not per second, the velocity of the ECG paper (25 mm/s) will have to be converted into mm/min, hence the 25 x 60 value in the equation. 1.2. Precise determination of the heart rate using ECG rulers (Figure 1) Figure 1. Electrocardiographic (ECG) ruler. First, the speed of the ECG paper is checked on the ECG trace. Then, the appropriate marker of the ruler (black arrow) is set on a chosen ECG element, usually the peak of the R wave. The value corresponding to the 2 nd, 3 rd, or 4 th R-wave peak, as mentioned on the ECG ruler, is read. This value represents the heart rate measured in bpm. 1.3. Quick approximation of the heart rate For this method, one should find a QRS complex situated on (or close to) a thick line of the ECG paper. If the next QRS complex is situated on the next thick line, the heart rate is 300 bpm (RR interval duration = 5 mm, 1500 / 5 = 300). If this second QRS complex is situated on the second thick line (RR interval duration = 10 mm), the heart rate is 150 bpm; if it is situated on the following thick lines, the heart rate is 100 bpm, 75 bpm, 60 bpm, 50 bpm, and so on (Figure 2). 37

START 300 150 100 75 60 50 Figure 2. Quick approximation of the heart rate. 3. The assessment of the electrical axis of the heart The electrical axis of the heart provides the image of the mean direction of cardiac impulse propagation through the heart. The term electrical axis of the heart usually refers to the electrical axis of the QRS complex assessed in the frontal plane, as measured by the limb leads. Ideally, the electrical axis of the heart is between +30 and +60, but values between 0 and +90 are also accepted as normal (known as intermediate axis). Whenever the electrical axis is outside the 0 to +90 interval, an electrical axis deviation is present (Figure 3). If the electrical axis of the heart is between +90 and 180, we have a right axis deviation; if the electrical axis of the heart is between 0 and -90, we have a left axis deviation; when the electrical axis of the heart is between -90 and 180, we have an extreme axis deviation. Figure 3. The electrical axis of the heart. N = normal range, LAD = left axis deviation, RAD = right axis deviation, ED extreme deviation. The axes of the P and T waves can be defined in the same way as the axis of the QRS complex. The electrical axis of the heart can be determined by: performing a precise measurement, using the quadrant method, or using the method of the equibiphasic waves. 3.1. Precise measurement of the electrical axis of the heart (Figure 4) The precise measurement of the electrical axis of the heart is performed by using the hexaaxial system of Einthoven and the calculated amplitude of the waves (amplitude of the QRS complex). 38

For this method, the following steps are made, in order: - pick any two limb leads (usually leads I and avf) and represent graphically their axes - determine the amplitude of the QRS complex in the two limb leads by calculating the algebraic sum of the amplitudes of the positive and the negative waves of the complex - represent the values (the amplitudes of the QRS complexes) in the hexaaxial system - compute the exact angle (expressed in degrees) of the vector (draw perpendicular lines on the axes of the two leads through the points representing the amplitudes of the QRS complexes the cross point of the two lines will give the orientation and sense of the mean QRS vector). Figure 4. Precise measurement of the mean QRS axis (example). First, the amplitude of the QRS complex is measured in the two leads (I and avf). Then, the measured values are marked in the hexaaxial system. Perpendicular lines are drawn on the axes through these marked points. The cross point of the two perpendiculars will give the orientation and sense of the mean QRS axis (thick arrow). 3.2. Quick determination of the electrical axis of the heart the quadrant method (Figure 5) For this method, the following steps are made, in order: - represent graphically the axes of leads I and avf - check if the QRS complex is predominantly positive or negative in these leads - determine the semicircle in which the axis of the QRS complex lays for each of the two leads - overlap the two semicircles this allows you to find the position of the axis with 90 precision. 39

Figure 5. Quick determination of the mean QRS axis using the quadrant method (example). If in lead avf the QRS complex is predominantly positive (left image), the axis of the QRS complex lays in the lower semicircle (corresponding to the positive pole of lead avf); if in lead I the QRS complex is predominantly positive (middle image), the axis of the QRS complex lays in the right semicircle (corresponding to the positive pole of lead I). When overlapping the first two images (right image), one can see that the mean QRS axis lays between 0 and +90, considered normal. 3.3. Determination of the electrical axis of the heart using the method of the equibiphasic waves (Figure 6) The term equibiphasic refers to the QRS complexes for which the amplitude of the positive waves is equal with the amplitude of the negative waves. For this method, the following steps are made, in order: - find a standard or a unipolar limb lead where the QRS complex is equibiphasic (if there is one). Often this is the lead with the smallest QRS complex. - the axis of the QRS complex is perpendicular to this lead's orientation and therefore parallel with the axis of the lead that is perpendicular on this lead - analyze the QRS complex in the lead that is perpendicular on the lead where the QRS complex is equibiphasic if the QRS in this lead is predominantly positive, then the vector of the QRS complex points towards the positive direction of the axis of this lead; if the QRS in this lead is predominantly negative, then the vector of the QRS complex points towards the negative direction of the axis of this lead. Figure 6. Determining the electrical axis of the heart using the method of the equibiphasic waves (example). If the equibiphasic QRS complex is in lead avl, the axis of the mean vector of the QRS complex is perpendicular to the axis of lead avl, and therefore parallel with the axis of lead II. If the QRS complex is predominantly positive in lead II, the vector of the QRS complex points to the positive direction of the axis of lead II, that is 60. 40

If there is no lead with an equibiphasic complex, there are usually two leads that are nearly equibiphasic, and these are always 30 apart. Find the perpendiculars for each lead and chose an approximate QRS axis within the 30 range. 4. Rhythm disorders (arrhythmias) Cardiac arrhythmias represent a category of cardiac electrical disturbances that includes a wide range of abnormalities. This chapter addresses only the arrhythmias most commonly encountered in clinical practice. 4.1. Premature (ectopic) beats (extrasystoles) Premature beats represent additional heartbeats that are not initiated by electrical impulses generated by the sinus node, but arise from ectopic pacemakers. Depending on the location of the ectopic pacemaker, extrasystoles are classified as: - atrial extrasystoles when the premature beat arises from an ectopic pacemaker located in the atria - junctional extrasystoles when the premature beat arises from the atrioventricular node (the junction between the atria and the ventricles) - ventricular extrasystoles when the premature beat arises from an ectopic pacemaker located in the ventricles. The non-sinus impulse is generated early, initiating a heartbeat before the next anticipated sinus beat, and is usually followed by a compensatory period. Thus, the RR interval between the preceding sinus beat and the premature beat is shorter than normal and the RR interval between the premature beat and the following sinus beat is longer than normal, but the 2 x I RR (the RR interval that includes the premature beat) is usually constant (See Figure 7). Since the direction of impulse propagation and the mass of myocardium depolarized by these ectopic impulses varies significantly depending on the location of the ectopic pacemaker, these premature beats are morphologically different and can be distinguished using a 12-lead ECG. In the case of an atrial premature beat the excitation wave generated by an ectopic pacemaker located in the atria depolarizes the atria prematurely and produces a P wave that looks different from a sinus node-generated P wave because the direction in which the atria depolarize is abnormal (Figure 7). The premature atrial impulse is then conducted in a normal fashion via the atrioventricular node, the His bundle and the bundle branches to depolarize the ventricles, thus the QRS complex associated with the atrial premature beat is normal. Figure 7. Atrial premature beat (APB). Note the early P wave with different morphology from a sinus node-generated P wave, the normal QRS complex following the APB and the compensatory pause. In the case of a ventricular premature beat (Figure 8) the excitation wave generated by an ectopic pacemaker located in the ventricles is not conducted to the rest of the ventricles 41

along the His bundle and bundle branches, but directly through the ventricular myocardium, on a cell-to-cell basis (See lecture notes). Thus, conduction of excitation in the ventricles is slower than normal, producing an abnormally wide QRS complex and a bizarrelooking T wave. Because the premature beat is ventricle-generated, there is no P wave in front of the QRS complex. Figure 8. Ventricular premature beat (VPB). Note the early, broad and deformed QRS complex that is not preceded by a P wave and the bizarre-looking T wave. 4.2. Ectopic tachycardias (tachyarrhythmias) Tachyarrhythmias define tachycardic rhythms (heart rate >100 bpm) arising from ectopic pacemakers. Based on the origin of the rhythm, ectopic tachycardias can be: - atrial tachycardias when the rhythm arises from ectopic pacemaker(s) located in the atria - junctional tachycardias when the rhythm arises from the atrioventricular node (the junction between the atria and the ventricles) - ventricular tachycardias (Figure 9) when the rhythm arises from ectopic pacemaker(s) located in the ventricles. The morphology of the waves during these tachyarrhythmias is the same as in the case of single premature beats arising from the same cardiac region (See above Premature beats ). Based on the duration of the episode, ectopic tachycardias can be: - non-sustained tachycardias when the episode terminates by itself within less than 30 seconds - sustained tachycardias when the episode lasts more than 30 seconds. Based on the morphology of the waves during the tachyarrhythmic episode, ectopic tachycardias can be: - monomorphic tachycardias when all beats arise form a single ectopic pacemaker, causing all ectopic P waves (in case of atrial tachycardias) or all ectopic QRS complexes (in case of ventricular tachycardias) to have the same morphology - polymorphic tachycardias when there are several ectopic pacemakers that generate electrical impulses, causing ectopic P waves (in case of atrial tachycardias) or ectopic QRS complexes (in case of ventricular tachycardias) to have different morphologies. Torsades de pointes ("twisting of the spikes") is a particular form of polymorphic ventricular tachycardia giving a characteristic illusion of twisting of QRS complexes around the isoelectric line. When ectopic tachycardias have sudden onset and end, the term paroxysmal is used to describe the arrhythmia. The heart rate in this type of tachycardia is usually between 150 bpm and 250 bpm, and the duration of the run of premature beats is usually more than 30 seconds (sustained). 42

Figure 9. Monomorphic non-sustained ventricular tachycardia. 4.3. Cardiac fibrillation Fibrillation defines a rapid, irregular, and unsynchronized activation of cardiac cells. Based on the origin of the arrhythmia, fibrillation can be atrial (atrial fibrillation) or ventricular (ventricular fibrillation). Atrial fibrillation is the most common cardiac arrhythmia found in clinical practice. The arrhythmia is due to the genesis of uncoordinated, chaotically electrical impulses generated by numerous ectopic foci, usually located within the left atrium, causing an absolute arrhythmia. During such episodes, the contraction of the atria is fibrillatory (quivering). Because there is no synchronous contraction of the atrial muscle, the ability of the atria to serve as pumps for the ventricles is abolished, affecting the cardiac output. During atrial fibrillation, atrial myocytes depolarize rapidly and randomly at a combined rate that exceeds 400 per minute. P waves are no longer present on the surface ECG, but the quivering of the atria produces fine f waves on the ECG baseline (Figure 10). The atrioventricular node is constantly 'bombed' by electrical impulses coming from the atria, but, because of the long refractory period of the atrioventricular node, only some of these impulses manage to get through. Thus, the ventricular rate is significantly lower, usually between 110 bpm and 180 bpm. Because the impulses that manage to pass through the atrioventricular node are conducted to the ventricles down the His bundle and the bundle branches, the ventricles are activated normally and the QRS complexes are normal in width and have the same morphology as during sinus rhythm. Figure 10. Atrial fibrillation. Note the complete absence of P waves, the presence of small f waves on the ECG baseline, the normal morphology of QRS complexes and the absolute irregularity of the cardiac rhythm. 43

When the same phenomenon occurs at the ventricular level, the arrhythmia is called ventricular fibrillation. This can occur due to the genesis of uncoordinated, chaotically electrical impulses generated by numerous ectopic foci located within the ventricles. In ventricular fibrillation ventricular myocytes depolarize rapidly and randomly at a combined rate of at least 400 per minute. Instead of the normal ECG trace, no baseline (i.e. no isoelectric line) can be seen and there are no clear and reproducible waves (i.e. no P, Q, R, S, T waves). During such episodes, the contraction of the ventricles is fibrillatory (quivering). Because there is no synchronous contraction of the ventricular muscle, the ability of the ventricles to pump the blood into the circulatory system is abolished, resulting in cardiac arrest. If the arrhythmia is not treated immediately (within a few minutes), ventricular fibrillation results in sudden cardiac death. 4.4. Cardiac flutter Literary, the term flutter means to flap or to vibrate. Based on the origin of the arrhythmia, flutter can be atrial (atrial flutter) or ventricular (ventricular flutter). Ventricular flutter is only rarely seen in clinical practice and difficult to distinguish from other ventricular arrhythmias based on a surface ECG. Atrial flutter originates in the atria (usually the right atrium) and is caused by a special circuit in which the wave of depolarization moves in a loop in the atrial wall. The atria are activated at a rate of about 300 per minute. Each atrial depolarization produces a triangular wave on the ECG trace, giving it a saw tooth appearance ( F waves), best seen in the inferior leads (Figure 11). Due to its longer refractory period, the atrioventricular node exerts a protective effect on the heart rate, blocking some of the atrial impulses. Thus, ventricular rate is usually a submultiple of 300 150 bpm in case of 2:1 conduction, 100 bpm in case of 3:1 conduction, 75 bpm in case of 4:1 conduction, etc. Once atrial flutter impulses pass the atrioventricular node, they depolarize the ventricles by passing down the His bundle and bundle branches, thus the accompanying QRS complexes are normal. Figure 11. Atrial flutter. Note the complete absence of P waves, the saw tooth appearance of the ECG baseline, given by the presence of F waves. QRS complexes have normal morphology. Atrioventricular conduction is variable (6-7:1). 5. Conduction disorders (heart blocks) Heart blocks define an abnormal delay or a complete block of electrical impulses at various levels of the electrical conduction system of the heart. Most commonly, conduction disorders occur at the level of the atrioventricular node or in the bundle branches. 5.1. Atrioventricular conduction blocks In atrioventricular blocks there is a pathological delay in the conduction of electrical impulses within the atrioventricular node. The analysis of the PQ (PR) interval and of the P QRS relationship allows us to differentiate between the different types of atrioventricular block. 44

In first-degree atrioventricular block the cardiac rhythm originates in the sinus node and the atrioventricular node conducts each electrical impulse to the ventricles, but slower than normal. Thus (Figure 12): - each P wave of atrial depolarization is followed by a QRS complex of ventricular depolarization - the time from the initial depolarization of the atria to the initial depolarization of the ventricles is abnormally delayed the PQ (PR) interval is longer than normal (above its upper limit of 210 msec). Figure 12. First-degree atrioventricular block. Note the excessive duration of the PR interval (240 msec) and the normal morphology of the QRS complex. In second-degree atrioventricular block the cardiac rhythm originates in the sinus node, but the transmission of the depolarizing impulse from the sinus node through the atrioventricular conduction system is interrupted intermittently. Thus, the P wave of atrial depolarization is not always followed by a QRS complex. Depending on the changes that occur in the PQ (PR) interval, two major types of second degree atrioventricular block are described: Mobitz I and Mobitz II. Mobitz I type second-degree atrioventricular block (with Wenkebach s phenomenon) occurs when the PQ (PR) interval prolongs progressively with each beat (Figure 13) until an electrical impulse is completely blocked by the atrioventricular node (occasionally, some P waves are not followed by QRS complexes). The gradually increasing PQ (PR) intervals are called Wenkebach s intervals and the process of gradual increase in PQ (PR) intervals is called Wenkebach phenomenon. Figure 13. Second-degree atrioventricular block type Mobitz I. Note the progressive prolongation of the PQ interval until a P wave (arrow) is completely blocked (not followed by a QRS complex). When present, QRS complexes have normal morphology. Mobitz II type second-degree atrioventricular block occurs when electrical impulses coming from the sinus node are occasionally blocked by the atrioventricular node (occasionally, some P waves are not followed by QRS complexes), but there is no progressive prolongation of the PQ (PR) interval. The PQ (PR) interval can be normal or prolonged, but remains constant. 45

In third-degree (complete) atrioventricular block (Figure 14), all electrical impulses arising from the sinus node are blocked in the atrioventricular conduction system and none of them is conducted to the ventricles (none of the P waves is followed by a QRS complex). In the absence of an alternative pacemaker, ventricular contraction comes to a standstill and the patient dies. However, an ectopic pacemaker below the block usually takes over ventricular pacing, generating an escape rhythm. The lower pacemaker can be part of the conduction system of the heart or an ectopic focus located in the ventricular wall. Since the sinus node and the ectopic pacemaker stimulate the atria and the ventricles independently, there will be no relationship between the P waves and the QRS complexes (situation called atrioventricular dissociation). If the block is high in the atrioventricular node and the ventricular pacemaker is located lower in the atrioventricular junction, then the QRS complex is normal in width, because ventricular activation occurs via the bundle branches. If the block is located low in the atrioventricular junction, the ventricles are paced by a ventricular pacemaker, and the QRS complexes will be wide. Figure 14. Third-degree (complete) atrioventricular block. Note the lack of any relationship between the P waves (normal arrows) and the QRS complexes (dashed arrows). The atrial rhythm is regular (PP intervals are constant), as well as the ventricular rhythm (RR intervals are constant), but there is no relationship between the two rhythms. 5.2. Bundle branch blocks In bundle branch blocks the conduction defect is in one of the two bundle branches. If the two bundle branches exhibit a block simultaneously, the progress of activation from the atria to the ventricles is completely inhibited; this is regarded as a third-degree atrioventricular block. In case of a bundle branch block the activation of one ventricle (the ventricle serviced by the non-affected bundle branch) is normal, occurring through the normal conduction system of the heart (atrioventricular node His bundle bundle branches), while the other ventricle (the ventricle serviced by the blocked bundle branch) must await initiation from the normally depolarized ventricle. The activation of the ventricle serviced by the blocked bundle branch in this case is done entirely on a cell-to-cell basis and is therefore significantly delayed compared to the activation of the non-affected ventricle. Thus, the normal synchrony of right and left ventricular depolarization is lost. In right bundle branch block (Figure 15) the electrical impulse cannot travel through the right bundle branch to the right ventricle. The depolarization of the left ventricle occurs normally, but the depolarization of the right ventricle is done on a cell-to-cell basis after the depolarization of the left ventricle and the septal muscle mass. This progress is slower than 46

that through the conduction system so that the activation of the right ventricle is so much delayed, that it occurs after the activation of the left ventricle. This produces a number of abnormalities on the ECG tracing: - QRS complexes with abnormally long duration (above the upper limit of 120 msec) - tall, broad, and usually notched ( M -shaped) R waves or rsr -shaped QRS complexes in the right precordial leads (V 1 and V 2 ) - deep and broad S waves in the lateral leads (I, avl, V 5, V 6 ) - right axis deviation due to the abnormal terminal QRS vector that is directed towards the right ventricle (i.e., rightward and anteriorly) - T wave inversion in the right precordial leads (V 1 and V 2 ) due to the abnormal spread of depolarization, which alters the pattern of repolarization. Figure 15. Right bundle branch block. Note the broad QRS complex (160 msec), with a broad, tall, and notched R wave in lead V 1, the inverted T wave in lead V 1, and the deep and broad S wave in lead V 6. In left bundle branch block (Figure 16) the electrical impulse cannot travel through the left bundle branch to the left ventricle. The depolarization of the right ventricle occurs normally, but the depolarization of the left ventricle is done on a cell-to-cell basis after the depolarization of the right ventricle and the septal muscle mass. This progress is slower than that through the conduction system so that the activation of the left ventricle is so much delayed, that it occurs after the activation of the right ventricle. This produces a number of abnormalities on the ECG tracing: - QRS complexes with abnormally long duration (above the upper limit of 120 msec) - disappearance of the normal septal q waves in the lateral leads because the activation of the interventricular septum no longer occurs from left to right - tall, broad, and usually notched ( M -shaped) R waves in the lateral leads (I, avl, V 5, V 6 ) - deep and broad S waves in the right precordial leads (V 1 and V 2 ) - left axis deviation due to the abnormal terminal QRS vector that is directed towards the left ventricle (i.e., leftwards and posteriorly) - T wave inversion in the lateral leads (I, avl, V 5, V 6 ) due to the abnormal spread of depolarization, which alters the pattern of repolarization. Figure 16. Left bundle branch block. Note the broad QRS complex (160 msec), with a broad, tall, and notched R wave in lead V 6, the inverted T wave in lead V 6, and the deep and broad S wave in lead V 1. 47

6. Myocardial hypertrophy The term hypertrophy defines an increase in the volume of an organ or tissue due to an increase in the size of its component cells. In contrast, an increase in the number of cells, but with constant cell size is called hyperplasia. Dilation refers to the enlargement of a cardiac chamber. Hypertrophy can affect either of the two atria or of the two ventricles, separately or in various combinations. Atrial and ventricular hypertrophy can occur as a result of pressure or volume overload. 6.1. Atrial abnormality Since atrial hypertrophy and atrial dilation cause similar changes on the surface ECG, the term atrial abnormality is used to define both conditions. Signs of atrial abnormalities can normally be found in the leads in which the P wave is most prominent: usually lead II, but also leads III, avf, and V 1. Normally, right atrial depolarization precedes the depolarization of the left atrium, the sum of the two generating the normal P wave on the surface ECG. Right atrial abnormality (Figure 17, A) is a consequence of right atrial overload. In such cases, the depolarization of the right atrium lasts longer than normal, its terminal phase overlapping the left atrial depolarization. The amplitude of the right atrial depolarization vector remains unchanged, but its maximal value now falls on top of that of the left atrial depolarization vector. Thus, a number of changes will be present on the surface ECG: - P wave taller than normal (>2.5 mm) and sharp, but with normal duration (shorter than 100 msec). Since this characteristic tall and sharp P wave usually appears in patients with pulmonary disorders, this P wave is called P pulmonale. - tall, biphasic P wave in lead V 1, with the initial positive portion of the biphasic P wave (depicting right atrial depolarization) larger than the terminal negative portion (depicting left atrial depolarization) - right axis deviation of the P wave. Left atrial abnormality (Figure 17, B) is the consequence of left atrial overload. Left atrial depolarization lasts longer than normal, prolonging the total duration of atrial depolarization, but the amplitude of the left atrial depolarization vector remains unchanged. Thus, a number of changes will be present on the surface ECG: - usually notched P wave, with duration longer than normal (>100 msec), but with amplitude within the normal limits (< 2.5 mm). Since this characteristic notched and prolonged P wave usually appears in patients with mitral valve disorders, this P wave is called P mitrale. - deep, biphasic P wave in lead V 1, with its terminal negative deflection (depicting left atrial depolarization) more than 40 msec wide and more than 1 mm deep - left axis deviation of the P wave. Figure 17. (A) Right atrial abnormality. Note the tall (3.5 mm), sharp P wave. (B) Left atrial abnormality. Note the broad (120 msec), notched P wave (P mitrale). 48

6.2. Ventricular hypertrophy Ventricular hypertrophy is characterized by unusually tall R waves and unusually deep S waves in the left or right precordial leads, depending on the affected ventricle (See below). To determine the presence of ventricular hypertrophy, the Sokolov-Lyon index is calculated, as follows: - for the right ventricle: RV 1 + SV 5 = amplitude of the R wave in lead V 1 + amplitude of the S wave in lead V 5 should normally be (in the absence of right ventricular hypertrophy) 10.5 mm - for the left ventricle: RV 5 + SV 1 = amplitude of the R wave in lead V 5 + amplitude of the S wave in lead V 1 should normally be (in the absence of left ventricular hypertrophy) 35 mm. Right ventricular hypertrophy is a consequence of right ventricular overload. The increase in the muscle mass of the right ventricle produces an increase in the ventricular electrical forces directed towards the right ventricle (rightwards and anteriorly). This causes a number of changes on the surface ECG: - predominantly positive QRS complexes with unusually tall and narrow R waves in leads V 1 and V 2 - unusually deep and narrow S waves in leads V 5 and V 6 - Sokolov-Lyon index for the right ventricle >10.5 mm - right axis deviation - signs of right atrial abnormality are often present because the right atrium is forced to pump blood into a thick-wall, non-compliant, hypertrophied right ventricle - T wave inversion in the right precordial leads (V 1 and V 2 ) due to increased oxygen consumption by the hypertrophied ventricle causing myocardial ischemia. Left ventricular hypertrophy (Figure 18) is the consequence of left ventricular overload. The increase in the muscle mass of the left ventricle produces an increase in the ventricular electrical forces directed to the left ventricle (leftwards and posteriorly). This causes a number of changes on the surface ECG: - predominantly negative QRS complexes with unusually deep and narrow S waves in leads V 1 and V 2 - unusually tall and narrow R waves in leads V 5 and V 6 - Sokolov-Lyon index for the left ventricle >35 mm - left axis deviation - signs of left atrial abnormality are often present because the left atrium is forced to pump blood into a thick-wall, non-compliant, hypertrophied left ventricle - characteristic ST segment depression and T wave inversion in the lateral leads (I, avl, V 5, V 6 ) known as ventricular strain due to increased oxygen consumption by the hypertrophied ventricle causing myocardial ischemia (See below). Figure 18. Left ventricular hypertrophy. Note the tall, narrow R wave in lead V 5 and the deep, sharp S wave in lead V 1. The Sokolov-Lyon index for the left ventricle is 36.5 mm. 49

7. Electrocardiographic changes in coronary artery disease Whenever there is a significant stenosis (abnormal narrowing) of one or several of the coronary arteries, the transport of oxygen to the cardiac muscle is impaired, leading to myocardial ischemia. Ischemia causes changes in the resting potential and in the repolarization of muscle cells, leading to various T wave changes on the ECG (Figure 19): - T wave inversion (negative T waves in leads where they should be positive) or pseudonormalization (return of abnormal T waves back to the normal pattern during an episode of myocardial ischemia) - symmetrical T waves - sharp-tall T waves. Figure 19. Myocardial ischemia. Note the negative and symmetrical T waves. More severe abnormalities in coronary circulation can lead to ECG abnormalities described under the electrocardiographic term of lesion. These abnormalities involve ST segment deviations. The ST segment can be: - elevated - usually this is the ECG mark of acute myocardial infarction (See below) or - depressed - by more than 1 mm in leads V 1 -V 2, and/or more than 2 mm in the other leads. The ECG term of lesion is only used for horizontal or descendent ST segment deviations (Figure 20). Figure 20. Three types of ST segment depression: (A) ascendant, (B) horizontal, (C) descendent. Only the last two types correspond to the electrocardiographic term of lesion. The complete occlusion of a coronary artery causes an acute myocardial infarction. If left untreated, myocardial infarction usually leads to the necrosis of myocardial cells affected by the lack of oxygen. The electrocardiographic sign of necrosis is the pathological Q wave. The pathological Q wave is defined as a Q wave with duration of at least 0.04 sec and amplitude of at least 1/4 of the adjacent R wave. Usually, this is the only mark that can be seen on the ECG of a patient that has had a myocardial infarction at a certain point in his/her life. In acute myocardial infarction the ECG depicts five distinct consecutive phases (Figure 21), according to the moment of ECG recording following the occlusion of the coronary artery: - in the first phase (during the first minutes after coronary artery occlusion) T waves become hyperacute (i.e., sharp and tall) 50

- then, the ECG will show ST segment elevation - ST-segment elevation generally occurs with reciprocal ST depression in ECG leads in which the axis is opposite in direction from those with ST elevation - then pathological Q waves appear - within hours to days, an evolving myocardial infarction will typically demonstrate T- wave inversion - finally, after a peak elevation approximately 1 hour after the onset of chest pain, the ST segment reaches a plateau at about 12 hours, and then normalizes completely (goes back to the isoelectric line) within 2 weeks, and the T wave return to normal (becomes positive again). Figure 21. Evolving phases of myocardial infarction. The typical ECG evolution of an acute myocardial infarction can be strongly influenced by revascularization strategies, which can stop the ECG progression in any of the five phases. These signs of myocardial infarction appear only in the leads that view the affected territory of the heart muscle. Since different leads view the heart from different angles, the 12 ECG leads can be used to distinguish the localization of the myocardial infarction: - ECG abnormalities in leads V 1 to V 6 indicate an anterior myocardial infarction (affecting the entire territory serviced by the anterior descending artery) due to an occlusion affecting the proximal segment of the anterior descending artery - ECG abnormalities in leads V 1 to V 4 indicate an anteroseptal myocardial infarction (affecting the anterior wall of the left ventricle and of the interventricular septum) due to an occlusion affecting the middle segment of the anterior descending artery - ECG abnormalities in the lateral leads (I, avl, V 5, V 6 ) indicate a lateral myocardial infarction (affecting the lateral wall of the left ventricle) due to an occlusion affecting a diagonal artery (branch of the anterior descending artery), the circumflex artery, or a marginal artery (branch of the circumflex artery) - ECG abnormalities in the inferior leads (II, III, avf) indicate an inferior myocardial infarction (affecting the inferior wall of the left ventricle) due to an occlusion usually affecting the right coronary artery or occasionally the circumflex artery. Since none of the leads views the posterior wall of the left ventricle, in case of a posterior myocardial infarction only a mirror image appears in leads V 1 -V 2. To confirm the presence of a posterior myocardial infarction the posterior leads (V 7, V 8, and V 9 ) should be used beside the standard 12 ECG leads, by placing the electrodes on the posterior chest wall. 51

8. Other electrocardiographic abnormalities 8.1. Pre-excitation syndromes Pre-excitation syndromes define the situations in which the passage of electrical impulses from the atria to the ventricles does not occur exclusively through the normal atrioventricular conduction system, but also directly from the atrial to the ventricular muscle via an abnormal route (e.g., the bundle of Kent) that bypasses the atrioventricular junction. Thus, part of the ventricular muscle is activated before normal activation reaches it via the normal conduction system. The resulting ECG (Figure 22) depends on the specific location of this accessory pathway, but QRS complexes are usually wider than normal and present an early upstroke called the delta wave, and the PQ (PR) interval is shorter than normal (below the normal limit of 120 msec). Figure 22. Pre-excitation syndrome. Note the short PR interval (80 msec) and the presence of the delta wave (arrow). 8.2. Cardiac pacing Whenever the intrinsic electrical system of the heart is unable to maintain an adequate heart rate, either because the sinus node is to slow or unable to deliver electrical impulses, or there is a block in the heart's electrical conduction system, an artificial pacemaker can be used to restore the normal heart rate. Pacemakers are small electronic devices consisting of a small pulse generator, usually implanted below the subcutaneous fat of the chest wall, above the muscles and bones of the chest, and one or several leads that carry the electrical signals from the pulse generator to the heart, implanted within the heart by transvenous way. These implantable pacemakers monitor the heart's native electrical rhythm. When the pacemaker does not detect a heartbeat within a normal beat-to-beat time period, it will stimulate the heart with a short low-voltage pulse. These sensing and stimulating activities continue on a beat by beat basis. When the cardiac rhythm is stimulated by the artificial pacemaker, this can usually be recognized on the ECG trace, due to the presence of stimulation spikes sharp, vertical signals that represent the electrical activity of the pacemaker. The location of pacemaker spikes in relationship with the ECG elements depicting atrial and ventricular depolarization (P waves and QRS complexes, respectively) depends on the site of stimulation when the pacemaker stimulates electrically the atria there will be a stimulation spike in front of the P wave; when the pacemaker stimulates the ventricles there will be a stimulation spike in front of the QRS complex (Figure 23); when both the atria and the ventricles are stimulated both the P waves and the QRS complexes will be preceded by stimulation spikes. 52

Figure 23. Ventricular stimulation by an artificial pacemaker. Note the stimulation spike preceding the broad, deformed QRS complex. 8.3. Electrolyte disorders In case of hyperkalemia, narrow and tall T waves appear on the ECG trace (Figure 24). Normally, it is unusual for T waves to be taller than 5 mm in the limb leads and taller than 10 mm in the chest leads. As serum potassium concentration continues to rise, PQ intervals become longer, P waves loose amplitude and may disappear, and QRS complexes widen. If the rise in serum potassium continues, the heart arrests in systole. Figure 24. Electrocardiographic changes in hyperkalemia (lead V 4 ). Note the tall (16 mm), sharp T wave and the P wave with low amplitude (1 mm). In case of hypokalemia the T waves flatten and may even become inverted, the ST segment may be depressed, the QT interval widens, and prominent U waves become visible on the ECG trace. Unlike in hyperkalemia, these additional changes are not related to the degree of hypokalemia. If the drop in serum potassium is not corrected, severe ventricular arrhythmias can occur. As a general rule, whenever one has to interpret an ECG trace he/she has to correlate the ECG findings with the patient s clinical presentation. If there is a previous ECG in the patient's file, the current ECG should be compared with it to see if any significant changes have occurred. These changes may have important implications for clinical management decisions. 53

TEST YOUR KNOWLEDGE 1. The pathological Q wave: a. represents the ECG sign of necrosis b. has an amplitude higher than 0.3 mv c. has a duration longer than 0.04 sec d. appears within the QRS complex after the R wave e. may be seen in the natural evolution of myocardial infarction, if left untreated 2. Which of the following ECG abnormalities are usually seen in a patient with left ventricular hypertrophy? a. duration of the QRS complex longer than 120 msec b. amplitude of the P wave higher than 0.3 mv c. RV 1 + SV 5 > 35 mm d. left axial deviation e. pathological Q wave 3. Which of the following ECG abnormalities are usually seen in a patient with left atrial abnormality? a. irregularly spaced QRS complexes b. PQ intervals longer than 210 msec c. notched P waves in leads II, III, and avf d. P wave amplitude higher than 3 mm e. absent P waves 4. Which of the following statements are true regarding second-degree atrioventricular block type Mobitz II? a. the cardiac rhythm originates in the sinus node b. all P waves are followed by a QRS complex c. there is progressive prolongation of the PQ interval d. the PQ interval is shorter than 120 msec e. none of the above 54