1. ELECTROCARDIOGRAM It is a graphic recording of changes of total electromotive force of heart (a sum vector) during spreading excitation wave in the heart Functions of myocardium that can be evaluated by the electrocardiography : functions of automaticity, conductibility, excitability. But not myocardial contractility!

3. CONDUCTIBILITY It is ability of specialized conducting tissue and ordinary muscles to conduct the activation. Ordinary muscles conduct impulses at a velocity much lower than intraventricular specialized conducting tissue (the His-Purkinje system), but considerably faster than AV node.

4. EXCITABILITY It is ability of specialized conducting tissue cells and ordinary muscle fibers to become excited under the influence exogenous electric impulses. Ordinary muscles conduct impulses at a velocity much lower than intraventricular specialized conducting tissue (the His-Purkinje system), but considerably faster than AV node.

5. BASICS ELECTROCARDIOGRAPHY An extracellular cardiac electrical field is generated by ion fluxes across cell membranes and between adjacent cells. These ion currents are synchronized by cardiac activation and recovery sequences to generate a cardiac electrical field in and around the heart that varies with time during the cardiac cycle. As each site is activated, the polarity of the transmembrane potential is converted from negative to positive. Activation of each fiber creates a dipole oriented in the direction of activation. The net effect of all the dipoles in this wave front is a single dipole equal to the (vector) sum of the effects of all the simultaneously active component dipoles. Thus, an activation front propagating through the heart can be represented by a single dipole that projects positive potentials ahead of it and negative potentials behind it. Isopotential lines of the heart’s electromotive force on the body surface

6. THE CONDUCTION SYSTEM OF THE HEART 1 – sinoatrial node; 2 – anterior internodal tract; 3 – Bachmann's bundle ; 4 – medial internodal tracts; 5 – Kent’s bundle; 6 – trunk of His’ bundle; 7 – left bundle branch; 8 – posterior hemifascicle; 9 – anterior hemifascicle; 10 – Purkinje fibers; 11 – right bundle branch; 12 – Mahaim fibers; 13 – James tract; 14 – atrioventricular node; 15 – posterior internodal tract.

7. THE HIS-PURKINJE CONDUCTION SYSTEM Atrial activation begins with impulse generation in the sinoatrial (SA) node. Once the impulse leaves this pacemaker site, atrial activation spreads in the right atrium and simultaneously impulse spreads along the atrial internodal tracts toward the left atrium and atrioventricular (AV) node. Upon exiting the AV node, the impulse traverses the bundle of His to enter the bundle branches (right and left) and then Purkinje fibers to finally activate working muscle fibers. Sequence of ventricular activation: interventricular septum, lateral walls of the left and right ventricles (from endocardium to epicardium), the basal areas of the ventricles are the last to be activated.

8. WAVE OF DEPOLARISATION Shape of QRS complex in any lead depends on orientation of that lead to vector of depolarisation. An electrode senses positive potentials when an activation front is moving toward it and negative potentials when the activation front is moving away from it.

9. COMPONENTS USED IN THE RECORDING AND PROCESSING OF AN ELECTROCARDIOGRAM A modern electrocardiograph includes the following parts: (1) the sensitive elements, electrodes, which are attached to the body of the patient to pick up the potential differences that arise during excitation of the heart muscle, and lead wires; (2) amplifiers, which amplify the minutest voltage of e.m.f. (1-2 mV) to the level that can be recorded; (3) a galvanometer to measure the voltage; (4) a recording instrument, including a traction mechanism and a time marker; and (5) a power unit (the instrument is supplied either from the AC mains or a battery).

10. OPERATING PRINCIPLES The ECG is recorded on to standard paper travelling at a rate of 50 mm/s. The paper is divided into large squares, each measuring 5 mm wide and equivalent to 0.1 s. Each large square is five small squares in width, and each small square is 1 mm wide and equivalent to 0.02 s. The electrical activity detected by the electrocardiogram machine is measured in millivolts. Machines are calibrated so that a signal with an amplitude of 1 mV moves the recording stylus vertically 1 cm. The amplitude of waveforms is expressed as: 0.1 mV = 1 mm = 1 small square. If an electrocardiogram is recorded at a speed of 25 mm/s, each millimeter of the curve corresponds to 0.04 second.

11. CLINICAL ELECTROCARDIOGRAPHIC LEAD SYSTEMS

12. BIPOLAR LIMB LEADS Left arm Left leg LEAD III Right arm Left leg LEAD II Right arm Left arm LEAD I NEGATIVE INPUT POSITIVE INPUT Lead

13. EINTHOVEN'S LAW I + III = II The heart vector H and its projections on the lead axes of leads I and III. Voltages recorded in lead I will be positive whereas potentials in lead III will be negative

14. AUGMENTED UNIPOLAR LIMB LEADS Dotted lines indicate connections to generate the reference electrode potential Left arm + left arm Left leg aVF Right arm + left leg Left arm aVL Left arm + left leg Right arm aVR NEGATIVE INPUT POSITIVE INPUT Lead

15. HEXAXIAL DIAGRAM Projection of six leads in vertical plane showing each lead's view of the heart. The Bayley hexaxial reference system composed of the lead axes of the six frontal plane leads. The lead axes of the six frontal plane leads have been rearranged so that their centers overlay one another. These axes divide the plane into 12 segments, each subtending 30 degrees. Positive ends of each axis are labeled with the name of the lead.

16. POSITION OF THE SIX CHEST ELECTRODES V1: right sternal edge, 4th intercostal space; V2: left sternal edge, 4th intercostal space; V3: between V2 and V4; V4: mid-clavicular line, 5th space; V5: anterior axillary line, horizontally in line with V4; V6: mid-axillary line, horizontally in line with V4

17. LEAD VECTORS The three bipolar limb leads, the three augmented unipolar limb leads (left), and the six unipolar precordial leads (right).

18. ANATOMICAL RELATIONS OF LEADS IN A STANDARD 12 LEAD ELECTROCARDIOGRAM Lead I: lateral wall of left ventricle Lead II: a sum potential of heart on longitudinal axis Lead III: right ventricle and posterodiaphragmatic (inferior) surface of left ventricle aVR: a sum potential of heart on longitudinal axis (the heart vector is oriented from this electrode, therefore Р wave, maximal wave of QRS complex and Т wave are negative); aVL: high areas of lateral wall of left ventricle aVF: right ventricle and posterodiaphragmatic (inferior) surface of left ventricle V 1 and V 2 : anterior wall of heart V 3 : anterior area of the interventricular septum V 4 : heart apex V 5 : anterolateral wall of left ventricle V 6 : lateral surface of left ventricle.

20. THE NORMAL ELECTROCARDIOGRAM The P wave is generated by activation of the atria, the PR segment represents the duration of atrioventricular (AV) conduction, the QRS complex is produced by activation of both ventricles, the ST-T wave reflects ventricular recovery.

21. THE ECG WAVES The P wave represents the electrical activation (depolarization) of both atria; the Q wave corresponds to excitation of the interventricular septum (beginning of ventricular depolarization); the R wave displays the subsequent spreading of excitation of right and left ventricular myocardium; the S wave represents the completion of ventricular depolarisation (excitation of the basal areas of interventricular septum); the T wave corresponds to the process of rapid late repolarization of the ventricular myocardium. T R S P Q

22. THE ECG INTERVALS The PQ interval represents the time required for impulse to pass from SA node through the atrial internodal tracts, atrioventricular node, His’ bundle, bundle branches, Purkinje fibers to the working muscle fibers ( normal duration of PQ interval is 0.12-0.20 sec ); the RR interval represents the duration of one cardiac cycle; the QT interval shows the duration of electric systole of ventricles; the interval TP displays the duration electric diastole of ventricles. RR TP QT PQ

26. GENESIS OF THE QRS COMPLEX The first phase, directed from left to right across the septum, produces a Q wave in V6 and an R wave in V1. The second phase, due mainly to depolarization of the left ventricle from endocardium to epicardium, results in a tall R wave in V6 and a deep S wave in V1. Finally, depolarization of the basal parts of the ventricles may produce a terminal S wave in V6 and a terminal R wave in V1. The QRS complex represents the electrical forces generated by ventricular depolarisation. The duration of the QRS complex is measured in the lead with the widest complex and should not exceed 0.10 sec.

27. MORPHOLOGY OF THE QRS COMPLEX IN THE PRECORDIAL LEADS In the precordial leads, QRS morphology changes depending on whether the depolarisation forces are moving towards or away from a lead. The forces generated by the free wall of the left ventricle predominate, and therefore in lead V1 a small R wave is followed by a large negative deflection (S wave). The R wave in the precordial leads steadily increases in amplitude from lead V1 to V6, with a corresponding decrease in S wave depth, culminating in a predominantly positive complex in V6. Thus, the QRS complex gradually changes from being predominantly negative in lead V1 to being predominantly positive in lead V6. The lead with an equiphasic QRS complex is located over the transition zone; this lies between leads V3 and V4, but shifts towards the left with age.

28. CHARACTERISTICS OF THE Q WAVE When the wave of septal depolarisation travels away from the recording electrode, the first deflection inscribed is negative. Thus small &quot;septal&quot; Q waves are often present in the lateral leads, usually leads I, aVL, V5, and V6. These non-pathological Q waves are less than 2 mm and less than one 0.03 sec wide, and should be <25% of the amplitude of the corresponding R wave. ‘ Normal’ Q wave in lead III diminishes or disappears on deep inspiration because of an alteration in the position of the heart, whilst the ‘pathological’ Q wave of infarction persists.

29. CHARACTERISTICS OF THE R WAVE The height of the R wave is variable and increases progressively across the precordial leads; it is usually <27 mm in leads V5 and V6. The R wave in lead V6, however, is often smaller than the R wave in V5, since the V6 electrode is further from the left ventricle.

30. CHARACTERISTICS OF THE S WAVE The S wave is deepest in the right precordial leads; it decreases in amplitude across the precordium, and is often absent in leads V5 and V6. The depth of the S wave should not exceed 30 mm in a normal individual, although S waves and R waves >30 mm are occasionally recorded in normal young male adults.

31. CHARACTERISTICS OF THE T WAVE The normal T wave is asymmetrical, the first half having a more gradual slope than the second half. The T wave should generally be at least 1/8 but less than 2/3 of the amplitude of the corresponding R wave; T wave amplitude rarely exceeds 10 mm. T wave orientation usually corresponds with that of the QRS complex, and thus is inverted in lead aVR, and may be inverted in lead III. T wave inversion in lead V1 is also common. It is occasionally accompanied by T wave inversion in lead V2, though isolated T wave inversion in lead V2 is abnormal.

32. CHARACTERISTICS OF THE S T SEGMENT The QRS complex terminates at the J point or ST junction. The ST segment lies between the J point and the beginning of the T wave, and represents the period between the end of ventricular depolarisation and the beginning of repolarisation. The ST segment should be in the same horizontal plane as the TP segment; the J point is the point of inflection between the S wave and ST segment .

33. CHANGE IN ST SEGMENT MORPHOLOGY ACROSS THE PRECORDIAL LEADS In leads V1 to V3 the rapidly ascending S wave merges directly with the T wave, making the J point indistinct and the ST segment difficult to identify. This produces elevation of the ST segment, and this is known as &quot;high take-off.&quot; Non-pathological elevation of the ST segment is also associated with benign early repolarisation, which is particularly common in young men, athletes, and black people.

34. NORMAL AND ABNORMAL ST SEGMENTS AND T WAVES (A) Normal ST segment with J point. (B) Horizontal ST depression in myocardial ischaemia. (C) ST segment sloping upwards in sinus tachycardia. (D) S T sagging in digitalis therapy. (E) Asymmetrical T wave inversion associated with ventricular hypertrophy. (F) Similar pattern sometimes seen without voltage changes in hypertrophy – ‘strain’. (G) ST sagging and prominent U waves of hypokalaemia. (H) Symmetrically inverted T wave of myocardial ischaemia or infarction. (I) ST elevation in acute myocardial infarction. (J) ST elevation in acute pericarditis. (K) Peaked T wave in hyperkalaemia.

35. QT INTERVAL The QT interval is measured from the beginning of the QRS complex to the end of the T wave and represents the total time taken for depolarisation and repolarisation of the ventricles. The QT interval lengthens as the heart rate slows, and thus when measuring the QT interval the rate must be taken into account. As a general guide the QT interval should be 0.35-0.45 sec, and should not be more than half of the interval between adjacent R waves ( R-R interval). The QT interval increases slightly with age and tends to be longer in women than in men. Bazett's correction is used to calculate the QT interval corrected for heart rate ( QTc ): QTc = QT/√ R-R (seconds).

38. THE RHYTHM OF THE HEART As known, electrical activation of the heart can sometimes begin in places other than the SA node. The word ‘rhythm’ is used to refer to the part of the heart which is controlling the activation sequence. The normal heart rhythm, with electrical activation beginning in the SA node, is called ‘sinus rhythm’.

41. CALCULATION OF HEART RATE IN REGULAR RHYTHM (1) Duration of one cardiac cycle (the RR interval) and the number of such cycles in one minute length should be determined. If the ECG is recorded on to paper travelling at a rate of 50 mm/s : or

42. CALCULATION OF HEART RATE IN REGULAR RHYTHM (2) If the ECG is recorded on to paper travelling at a rate of 25 mm/s : or

43. CALCULATION OF HEART RATE IN IRREGULAR RHYTHM (1) The length of five or ten RR intervals is determined, the mean, maximum and minimum RR interval found, and the cardiac rate is finally determined as for regular cardiac rhythm. If the ECG is recorded on to paper travelling at a rate of 50 mm/s :

44. CALCULATION OF HEART RATE IN IRREGULAR RHYTHM (2) The number of RR intervals is determined for certain time, e.g. for 3 seconds. This result is multiplied by 20 in this case because:

45. THE ELECTRICAL AXIS Calculation of the mean electrical axis during the QRS complex from the areas under the QRS complex in leads I and III. Magnitudes of the areas of the two leads are plotted as vectors on the appropriate lead axes, and the mean QRS axis is the sum of these two vectors.

46. THE ELECTRICAL AXIS AND α ANGLE The electrical axis of the heart (ventricles) is a projection of a sum electromotive force vector of ventricular depolarization in the frontal plane. The α angle is the angle formed by a horizontal line, which is parallel to the axis of lead I, and the electrical axis of the heart.

47. POSITIONS OF THE ELECTRICAL AXIS OF THE HEART Normal positions : vertical position: α angle = +70-+90°, normal one: α angle = +40-+69°, horizontal position: α angle = 0-+39°. Pathological positions : left axis deviation: α angle <0°; right axis deviation: α angle > +90°.

48. NORMAL POSITION OF THE ELECTRICAL AXIS  = +40  … + 69  R II  R I  R III R III  S III S aVL  R aVL

49. VERTICAL POSITION OF THE ELECTRICAL AXIS  = + 90  R II = R III  R I R I = S I R aVF max  R I and R II  = +70  … + 90  R II  R III  R I R I  S I S aVL  R aVL

50. HORIZONTAL POSITION OF THE ELECTRICAL AXIS  = 0  … + 30  R I  R II  R III S III  R III R aVF  S aVF  = 0  R I  R II  R III S III  R III R aVF = S aVF

51. LEFT AXIS DEVIATION  = 0  …  30  R I  R II  R III R II  S II S III  R III S avF  R avF  =  30  R I  R II  R III R II = S II S III  R III S avF  R avF    30  R I  R II  R III S II  R II S III  R III S avF  R avF R avR  Q(S) avR

52. RIGHT AXIS DEVIATION   + 90  R III  R II  R I S I  R I   +120  R III  R II  R I S I  R I R aVR  Q (S) aVR

53. CALCULATION OF ELECTRICAL AXIS POSITION Algebraic sum Algebraic sum QRS complex in lead I QRS complex in lead III Table Lead I Lead III

62. CAUSES OF SINUS ARRHYTHMIA It is present in most healthy young persons at rest; it consists of a quickening of the heart rate during inspiration and a slowing during expiration, tends to be intensified by deep breathing, and tends to disappear when the breath is held or when the heart rate is increased by exercise or fever. It has no pathological significance.

64. MECHANISM OF ATRIAL FIBRILLATION Atrial fibrillation is caused by multiple re-entrant circuits or &quot;wavelets&quot; of activation sweeping around the atrial myocardium. These are often triggered by rapid firing foci. The direction of excitation wave varies permanently in atrial fibrillation due to unequal duration of the refractory period of separate muscular fibres. There is a chaotic excitation and their contraction with frequency of 350-600 per a minute. Conduction of atrial impulses to the ventricles is variable and unpredictable.

68. ATRIAL FLUTTER Rapid regular coordinated ectopic atrial rhythm at a rate of 220 to 350 beats/min , accompanied by regular or irregular ventricular contractions of various frequency. As a rule, not all atrial impulses are conducted to the ventricles. Each other, third or fourth impulse, is only conducted to the ventricles since partial (incomplete) atrioventricular block develops simultaneously. Conduction of the AV node sometimes constantly changes: each other impulse is now conducted; then the rhythm changes to conduction of each third impulse, and the ventricles contract arrhythmically. Patients with accelerated heart rate (high conduction of the AV node) complain of palpitation. Examination reveals tachycardia that does not depend on the posture of the patient, exercise or psychic strain, since the SA node does not function as the pacemaker in atrial flutter.

69. MECHANISM AND CAUSES OF ATRIAL FLUTTER Atrial flutter is usually the result of a single re-entrant circuit in the right atrium with secondary activation of the left atrium. The causes of atrial flutter are similar to those of atrial fibrillation, although idiopathic atrial flutter is uncommon. It may convert into atrial fibrillation over time or, after administration of drugs such as digoxin.

71. EXTRASYSTOLE Extrasystole is a premature activation of all heart or its parts (only atriums or only ventricles) that breaks correct sequence of cardiac contractions. Compensatory pause – the pause following an extrasystole, when the pause is long enough to compensate for the prematurity of the extrasystole; the short cycle ending with the extrasystole plus the pause following the extrasystole together equal two of the regular cycles. Coupling interval – the interval, usually expressed in hundredths of a second, between a normal sinus beat and the ensuing premature beat.

72. COMPENSATORY PAUSE Compensatory pause is called fully if the RR interval produced by the two sinus-initiated QRS complexes on either side of the premature complex equals twice the normally conducted RR interval: RRse+RRes=2RRs Noncompensatory pause: RRse+Rres<2RRs Rs Rs Rs Rs Rs Re Rs Re Rs Rs Rs Rs

74. TYPES OF EXTRASYSTOLES (1) a – atrial; b – nodal; c – ventricular; d – polytopic. Extrasystoles are marked by the arrows .

75. TYPES OF EXTRASYSTOLE (2) Interpolated extrasystole – a extrasystole which, instead of being followed by a compensatory pause, is sandwiched between two consecutive sinus cycles. Premature extrasystole – initial wave of extrasystole collides with previous T wave . Group extrasystoles – a normal contraction follows by several extrasystoles at a run. These are 3 and more extrasystoles follows one after another. Ex s s

81. MULTIFOCAL VENTRICULAR EXTRASYSTOLE If excitability of the myocardium is high, several (rather than one) ectopic foci may exist. Extrasystoles generated in various heart chambers and can have different contours and are often called multifocal or polytopic extrasystole . More properly they should be called “multiform,” “polymorphic,” or “pleomorphic” since it is not known whether multiple foci are discharging or whether conduction of the impulse originating from one site is merely changing. Extrasystoles are described as &quot;monomorphic&quot; when their QRS complexes have the same general appearance in the same lead. Polymorphic extrasystoles Monomorphic extrasystoles

82. ALLORHYTHMIA Bigeminy – that cardiac rhythm when each beat of the dominant rhythm (sinus or other) is followed by a premature beat, with the result that the heartbeats occur in pairs. Trigeminy – a cardiac arrhythmia in which the beats are grouped in trios, usually composed of a sinus beat followed by two extrasystoles. Quadrigeminy – a cardiac arrhythmia in which the heartbeats are grouped in fours, each usually composed of one sinus beat followed by three extrasystoles, but a repetitive group of four of any composition is quadrigeminal. Allorhythmia – an irregularity in the cardiac rhythm that repeats itself any number of times . Variants

85. ECG CRITERIA OF SINOATRIAL BLOCK Sinoatrial block is characterised by a transient failure of impulse conduction to the atrial myocardium, resulting in periodic missing of the heart complex in the presence of a regular sinus rhythm (neither P wave nor the QRST complex are recorded); the duration of long pause between two next P (or R ) wave depends on amount of blocked (&quot;missed&quot;) sinus impulses: if one sinus impulse is blocked the length of diastole doubles, if two successive sinus impulses are blocked the length of pause is equal to sum of three usual RR intervals of sinus rhythm.

86. ECG CRITERIA OF INTRAATRIAL BLOCK Intraatrial block is impaired conduction through the atria, manifested by the following: the P wave duration increases more than 0.12 second; it may be notched P wave in all cardiac cycles. notched P wave > 0.12 sec

88. ATRIOVENTRICULAR BLOCK I DEGREE In first degree block there is a delay in conduction of the atrial impulse to the ventricles, usually at the level of the atrioventricular node. This results in prolongation of the PQ interval to more than 0.20 sec (up to 0.36-0.40 sec) , but all impulses are conducted and every QRST complex is preceded by a P wave and the PQ interval remains constant. Speed = 25 mm/sec

89. ATRIOVENTRICULAR BLOCK II DEGREE MOBITZ TYPE I, WENCKEBACH TYPE In second degree block there is intermittent failure of conduction between the atria and ventricles. Some P waves are not followed by a QRS complex. There are two types of second degree block. ECG shows progressive lengthening of the PQ interval until an impulse is not conducted to ventricles and and the P wave is not followed by a QRST complex (“unreciprocated” P wave). After this pause which is equal in duration to one cardiac cycle the first PQ interval becomes short again, and the cycle repeats ( Wenckebach period) .

90. ATRIOVENTRICULAR BLOCK II DEGREE MOBITZ TYPE II There is intermittent failure of conduction of P waves: “ unreciprocated” P waves ( QRST complexes do not follow them) are recorded on ECG without prior measurable lengthening of PQ interval; loss of QRST complexes may be regular ( repetitive ) or chaotic. The more impulses are blocked, the less rate of ventricular contractions is. High degree atrioventricular block, which occurs when a QRS complex is seen only after every three, four, or more P waves, may progress to complete third degree atrioventricular block.

91. ATRIOVENTRICULAR BLOCK III DEGREE In third degree block there is complete failure of conduction between the atria and ventricles, with complete independence of atrial and ventricular contractions. The P waves bear no relation to the QRS complexes and usually proceed at a faster rate. The ECG demonstrates two independent rhythms (the independence of P waves and QRST complexes): atrial rhythm ( P waves are sinus or ectopic with a rate of 60-80 beat/min and more) and ventricular rhythm ( QRST complexes are rhythmical, their rate slows down less than 60-30 beat/min depending on the position of pacemaker in the conduction system) .

92. BUNDLE BRANCH BLOCK Bundle branch blocks result from conduction delay or block in any of several sites in the intraventricular conduction system, including the main bundle branches, in the fascicles, or less commonly, within the fibers of the bundle of His. The intrinsicoid deflection time (J) is the time up to that moment the activation front has reached the subjacent muscle (from the beginning of QRS complex to the peak of its maximum positivity).

93. RIGHT BUNDLE BRANCH BLOCK (RBBB) In this disorder, the right branch of the bundle is blocked, but the septum is activated from left to right, as in the normal heart. The left ventricular q wave is preserved, as is the initial r wave over right chest leads. The left ventricle is then depolarized, producing an S wave in right chest leads and an R wave in left chest leads. Finally, depolarization reaches the right ventricle, and so produces an R in the right chest leads and a deep broad S wave in the left chest leads. An M pattern is thus seen in the right chest leads, such as V1. It is also common to see T wave abnormalities in leads V2 and V3.

96. LEFT BUNDLE BRANCH BLOCK (LBBB) When the left branch of the bundle is blocked, the interventricular septum is activated from the right instead of from the left side and the initial vector (phase 1) is directed to the left. Because of this, the normal initial q wave in the left ventricular leads is lost, being replaced by a small r wave. Right ventricular depolarization, which follows, produces an r in V1 and an s in V6. The left ventricle is finally depolarized resulting in an R in V6 and a broad S in V1. The QRS duration is increased to 0.12 s or more. The abnormal left ventricular depolarization sequence in left bundle branch block causes secondary repolarization changes. Consequently, the ST segment and T wave are abnormal.