Electrocardiography (ECG)

In this chapter, we address the basic notions of electrophysiology required for the understanding of electrocardiography. Depolarization and repolarization of the cardiac fibers are described extensively. The action potential represents the transmembranar potential changes measured with 2 electrodes during cardiac fiber activation. The 4 phases of the action potential, related to sodium, calcium and potassium transmembranair flow are described. The electrocardiogram (ECG) is obtained by measuring electrical potential between various points of the body using a biomedical instrumentation amplifier. A lead records the electrical signals of the heart from a particular combination of recording electrodes which are placed at specific points on the patient's body. Cardiac activation is a depolarisation, with constant changes in direction and amplitude, recorded by the ECG. Four electrodes with conventional colours are placed on the patient's arms and legs to approximate the signals obtained with buckets of salt water. These 4 electrodes define 6 derivations: 3 bipolar, lead I records a dipole between the left and the right arm, lead II records a dipole between the right arm and the left leg and lead III records the dipole between the left arm and the left leg. There are 3 other unipolar derivations, called augmented (aVR, aVL, aVF), recording the same phenomenon but referenced to a zero reference called Wilson central terminal. To obtain standadized traces 6 unipolar electrodes are placed on the chest at a specific place. Because of their specific position each electrode explores a specific portion of the ventricles: V1 and V2 explore the right ventricle and the high septum, V3 the mid septum, V4 the low septal portion and the left ventricular apex. V5 and V6 explore the medium and lateral part of the left ventricle. Cardiac activation is the sum of all the phenomena of depolarisation and repolarisation of the atrium and the ventricles. The cardiac electrical activity arises from the sinus node, the physiological pacemaker, located at the junction of the superior vena cava and the right atrium; its activity is not visible on the ECG. The main electrical vector is directed from the sinus node towards the A-V node. The atrial activation turns into a P wave on the ECG. From the atrium to the ventricles the depolarisation uses specific conduction pathways. The A-V conduction is the PR or PQ interval. The ventricular activation follows the progression of the depolarisation along the His bundle and activates the ventricles sequentially. It is the QRS complex. The T wave represents ventricular repolarisation. Electrical axis of the P wave and QRS complex has to be calculated and is considered as normal between 0° and 90° for the P wave and between -30° to +90° for the QRS complex. In sinus rhythm, depolarisation is transmitted to the atrium and afterwards to the ventricle. On the surface ECG the consequences are a positive P wave in all derivations except aVR, a constant PR interval and a regular RR interval equal to the PP interval. At rest, the heart rate is around 60 bpm with a slight variation due to respiratory activity. A heart rate < 60 bpm is called bradycardia and a heart rate > 100 bpm is called tachycardia. With high heart rate the P waves are sometimes non visible because they are concealed in the preceding T wave.

A systematic analysis of the surface ECG is crucial in the diagnostic process (Fig. 1). A good description allows comprehension of the trace and definition of the problem [1-4]. Paper speed and dimensions of grids on ECG paper have to be checked. The rhythm should be precisely defined. If it is not sinus rhythm the following criteria are useful to aid rhythm determination. The heart rate is usually calculated during determination of the rhythm. A small square represents 40 ms. When heart rate is below 60 bpm it is a bradycardia and when it is over 100 bpm it is a tachycardia. The duration, the axis and the morphology of the P wave have to be carefully checked. The P-R interval is the time required for completion of atrial depolarisation; conduction through the A-V node, His bundle and bundle branches; and arrival at the ventricular myocardial cells. Its value is between 120 and 200 ms. The duration, the axis, the morphology and the presence of Q waves should be evaluated. Abnormal Q waves have a duration > 40 ms and an amplitude of at least 25% of the QRS complex. Position of the ST segment should be checked to detect elevation or depression. Non specific changes should be placed in the clinical context. The T wave can be positive, negative or flat. It must also be analyzed within the clinical context. Conduction abnormalities will also modify the T wave and we should not forget that when depolarisation is abnormal, repolarisation is also abnormal. It is measured from the beginning of the QRS complex to the end of the T wave. QT interval duration varies with heart rate and shortens with tachycardia. Its correct value can be calculated with the Bazett formula.

In this chapter, we address the basic notions of conduction abnormalities. Impairment can occur in any part of the conduction system. Prolongation of the PR interval over 200 ms is the characteristic feature of first degree A-V block. Second degree A-V block includes Wenckebach, Mobitz II A-V block and 2:1 A-V block. The characteristic ECG feature of Wenckebach block, also called Mobitz I, is progressive lengthening of the PR interval until finally a beat is dropped. This is a more severe form of second degree block. The characteristic ECG picture is that of a series of one or more non-conducted P waves, 2:1, 3:1, 4:1 block. Two to one A-V block (2:1 block) can be of the types Mobitz I or II. It can be nodal or infra-hisian. A P wave is conducted, the following one is blocked and so on. Third degree A-V block, also known as complete A-V block, is a complete disruption of A-V conduction. The atria and the ventricles are paced independently. Block of conduction in the left bundle branch, prior to its bifurcation, results primarily in delayed depolarisation of the left ventricle. In LBBB, the septum depolarizes from right to left, since in this case depolarisation is initiated by the right bundle branch. In rigth bundle branch block (RBBB) conduction along the right branch of the His bundle no longer exists. The ventricles are activated only by the left branch.

Sinus activity is not visible on the surface ECG. Thus first degree sino-atrial block is only theoretical without electrophysiological sequelae. Only second and third degree sino-atrial blocks are visible on the surface ECG and these do have some clinical importance. Second degree block of the type Wenckebach occurs with a progressive shortening of the PP interval and a slight increase of the heart rate followed by a pause with a duration greater than the PP interval preceding it but less than the next PP interval. Third degree block or complete block cannot be distinguished at all from true atrial standstill: absence of atrial activity, His bundle escape rhythm with narrow QRS complexes and sometimes retrograde P' waves with a polarity opposite to sinus P wave polarity. The pacemaker rhythm can easily be recognized on the ECG. It shows pacemaker spikes: vertical artifact signals that represent the electrical activity of the pacemaker. Usually these spikes are more visible in unipolar than in bipolar pacing. The morphology of the QRS complex helps to locate the site of ventricular pacing, typically right bundle branch block morphology for left ventricular pacing and left bundle branch block morphology for right ventricular pacing.

In this chapter, we address the basic notions of cardiac arrhythmias. Premature ventricular and atrial contractions, also known as “extrasystoles”, are “extra” heartbeats. Atrial premature beats, describes premature beats arising from the atrium. Ectopic P' wave morphology differs from sinus beats and varies depending on the origin of the premature beat. The mechanism of the tachycardia is macro-reentry or automaticity \and the rate varies between 140 and 220 bpm. There are two types of atrial flutter, the common type I and the rarer type II. Most individuals with atrial flutter will manifest only one of these. Rarely someone may manifest both types. Flutter originates either from the right or left atrium depending on its cause. Typical atrial flutter (90% of cases) is caused by a macro re-entry in the right atrium, with a regular rate of about 300 beats per minute. Atrial fibrillation is a consequence of multiple atrial micro reentry circuits. The arrhythmia is described as irregularly irregular because of the complete disorganization of the atrial electrical activity. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place (“f” waves), at a rate of 350 to 500/minute and irregularity of the R-R interval due to irregular conduction of impulses to the ventricles.

AV nodal reentrant tachycardia (AVNRT) is also called junctional tachycardia. AVNRT is usually a reentrant tachycardia using a reentry circuit located within the AV node area. In the typical form of AVNRT (> 90% of the cases), the reentry circuit uses the slow pathway antegradely and the fast pathway retrogradely. Antegrade ventricular activation occurs simultaneously with the retrograde atrial activation. The P' wave is hidden in the QRS complex, sometimes visible as a small r' wave in V1 at the end of the QRS complex. Rarely it can be seen as a small q wave in the inferior leads. Comparison of the trace in tachycardia and in sinus rhythm facilitates the diagnosis unless conduction abnormalities (BBB) are present during tachycardia. In the atypical form (5-10%of cases), the reentry circuit uses the fast pathway antegradely and the slow pathway retrogradely. The P' wave is negative in the inferior leads with a ratio P’R/ RP’< 1 as in atrial tachycardia from which it should be differentiated. In the normal heart, electrical signals use only one pathway to propagate through the heart. This is the atrio-ventricular or A-V node.

If there is an extra conduction pathway present, the electrical signal may arrive at the ventricle too soon. This condition is called Wolff-Parkinson-White syndrome (WPW). It is in a category of electrical abnormalities called “pre-excitation syndromes”. The electrical properties of this pathway, which is basically an abnormal muscular connection between the atrium and the ventricle, are different from those of the normal A-V conduction system and creates the conditions for a reentry circuit. The accessory pathway can conduct exclusively antegradely, in other words from the atrium to the ventricle, exclusively retrogradely, from the ventricle to the atrium or in a bidirectional manner. It can be located anywhere in the A-V groove but predominantely in the lateral region. Orthodromic tachycardia is the most common arrhythmia associated with accessory pathways. It is a macro-reentry circuit using the A-V node antegradely and the accesory pathway retrogradely. Passage through this accessory pathway delays the retrograde activation of the atrium. This manifests, on the ECG, as a time delay between the QRS complex and the next P' wave (> 100 ms). Less commonly, a shorter refractory period in the accessory tract may cause block of an ectopic atrial impulse in the normal A-V pathway, with antegrade conduction down the accessory tract and then retrograde conduction up the normal (A-V) pathway. This type of tachycardia produced is called antidromic tachycardia. The QRS complex is wide (> 140 ms), with an exaggeration of the delta wave seen during sinus rhythm (wide-QRS tachycardia). Atrial fibrillation is the third arrhythmia occuring in patients with accessory pathways. The depolarisation can reach the ventricles by both the normal A-V pathway and the accessory pathway. If the latter has a short refractory period and as conduction can be very fast over this accessory pathway, the ventricular response can be very high, up to 300 bpm and irregular. The QRS complexes are wide but with a variable width depending on the use of the accessory pathway by the depolarisation. Permanent junctional re-entrant tachycardia is a relatively uncommon form of re-entry tachycardia with antegrade conduction occurring through the atrioventricular node and retrograde conduction over an accessory pathway usually located in the postero-septal region. It is a macroreentry circuit using the A-V node antegradely and the accessory pathway retrogradely. The P' wave is negative in the limb leads with RP’>P’R.

Three or more beats that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia. If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia. If the rhythm lasts more than 30 seconds it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds). Ventricular tachycardia can be classified based on its morphology: monomorphic ventricular tachycardia means that the appearance of all the beats matches each other in each lead of a surface electrocardiogram. Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variation in morphology. The most common cause of monomorphic ventricular tachycardia is damaged or dead (scar) tissue from a previous myocardial infarction.

Ventricular fibrillation is a condition in which there is a fast un-coordinated contraction of the cardiac muscle of the ventricles in the heart. It is a chaotic dysynchronous activity of the heart without identifiable QRS complexes. If the arrhythmia continues for more than a few seconds, blood circulation will cease, and death will occur in a matter of minutes.

In this chapter, we address the basic notions of myocardial ischemia and myocardial infarction. Cardiac ischemia changes the electrical activity and the genesis of the action potential and of the resting potential. It can be divided into 3 forms; ischemia, lesion and necrosis. Modification of the QRS complex, the ST segment and T wave is observed. Ischemia is a biochemically reversible anomaly. Moreover, it is mainly ionic, notably potassium disturbances which underlie ST and T wave changes. Lesion is a more severe form of cardiac ischemia but is still reversible, with interstitial oedema and biochemical disturbances. Essentially, it is the ST segment, which is modified, in that it becomes displaced from the isoelectric baseline. The ST segment vector is determined in the same manner as that of the QRS complex: it allows for better localization of the site of the stenosis or obstruction of the culprit artey. The more leads exhibit ST changes, the bigger the territory at risk. A sum total of ST depression or elevation greater than 12 mm in the different leads implies widespread ischemia. The most severe stage of cardiac ischemia is necrosis since there is cellular death with cessation of electrical activity. Neither the action potential nor the resting membrane potential exists anymore and the conduction capability has ceased. The start of depolarisation (QRS) is modified with the apparition of an "electrical hole" (Q waves), which could progress as far as the total disappearance of the positive forces (R waves) and a QS morphology; the necrosis is transmural affecting therefore the full thickness of the myocardium. Acute coronary syndrome includes STEMI and non-STEMI. STEMI (ST Segment Elevation Myocardial Infarction) is the acute coronary syndrome with ST segment elevation and non-STEMI is associated with other ST segment changes (negative T waves or ST segment depression) but not ST segment elevation. Electrocardiographically, the electrical changes recorded in the different territories differ according to the coronary artery involved. There is a good correlation between the ischemic zone and the coronary artery affected. Ischemia is recorded by the electrode "exploring" the territory implicated. Involvement of the right coronary artery gives rise to inferior wall ischemia and this is characterized on the ECG as changes in leads II, III and aVF. Involvement of the left coronary artery gives rise to anterior wall ischemia and this is characterized on the ECG as changes in precordial leads.

In this chapter, we address the basic notions of the differential diagnosis of cardiac ischemia. Hypertrophic obstructive cardiomyopathy or HOCM is characterized on the electrocardiogram by Q waves in the inferior leads and negative T waves from V2 to V5 which is difficult to distinguish from classical ischemia due to coronary pathology.The electrocardiographic abnormalities of pericarditis are non specific and sometimes difficult to distinguish from ischemia. They are typically recognized by PR segment depression, present in the majority of the leads. The repolarisation abnormalities it causes are very similar to those of ischemia-lesion; primarily, the ST segment is elevated, with an inferior convexity, the so-called “camel hump” appearance. This segment progressively returns to the isoelectric line in the same time it takes for the amplitude of the T wave to fall, and in the end becomes negative. In V5, the amplitude of the ST elevation, compared to the amplitude of the T wave is > 0.25: a ratio < 0.25 favours early repolarisation. The electrical features of pericarditis are reputed to be diffuse, but in reality are not always so. Occasionally, acute pericarditis is the cause of an arrhythmia, almost always supraventricular (atrial fibrillation). However, there is never a pathological Q wave of necrosis. Moreover, the changes are generally diffuse and widespread without systemization of coronary abnormalities. The electrocardiographic features of pulmonary embolism are not specific: on the background of preexisting right bundle branch block, the Q waves in III and QS in V1 could be due to an inferior or an antero-septal infarct respectively. In the same vein, the raised ST segment in V1 could also be an antero-septal ischemia-lesion picture. Chatterjee phenomenon is a T wave inversion, often deep, which occurs after a period of abnormal ventricular activation (broad QRS), notably ventricular tachycardia, intermittent left bundle branch block or preexcitation, or even intermittent ventricular pacing. Early repolarisation causes in leads V2 to V5, a raised J-point and ST segment, as well as an increase in the amplitude of a symmetrical T wave, as would be expected for an ischemia-lesion but the J-point remains prominent and the convexity of the ST is inferior and not superior. Brugada syndrome is not a conduction abnormality but deserves a mention under the heading of right bundle branch block as it can mimic some aspects, notably changes in the terminal phase. There are 3 types of changes in V1 and V2 and rarely in V3. In all 3 types the J-point is raised at least 2 mm.

In this chapter, we address the basic notions of cardiac chambers hypertrophy. Hypertrophy of the left ventricle causes a significant increase in the height and depth of the QRS complex. The thickening of the wall prolongs the activation of the ventricle and as a result, the duration of the QRS complex. ST segment changes can also be present because repolarisation starts in the sub-endocardium instead of the subepicardium, or because permanent ischemia is present due to the increased left ventricular mass and reduced coronary blood flow. Typically the ST and T wave vectors have an opposite direction to that of the QRS complex. Electrocardiographic changes of right ventricular hypertrophy are seen only with severe right ventricular hypertrophy. The right electrical forces dominate the left electrical forces. Anterior forces will predominate with a tall R wave in V1 and a small S wave. In some cases the forces are posteriorly directed without changes in V1 but with a deep S wave in the left precordial leads. As with left ventricular hypertrophy, repolarisation is significantly modified with the vector of the QRS complex having an opposite direction to the vector of the ST segment (ST segment depression, T wave inversion in the right precordial leads). Left atrial enlargement prolongs the terminal portion of the P wave with an increased duration and a "double hump" or m-shaped morphology. Right atrial enlargement prolongs the initial portion of the P wave with a superimposition of its activation on the activation of the left atrium. As a consequence, the amplitude of the P wave increases in a triangular form without increasing its duration. Depolarisation of the atrium is best seen in leads II and V1. Enlargement of both atria is present when the criteria for both right and left atrial enlargement are fulfilled on the same ECG.

In this chapter, we address the basic notions of electrolytes disturbances and QT interval abnormalities. The most important abnormality of the QT interval is long QT syndrome, which provokes inhomogeneity of repolarisation with a marked tendency to induce severe ventricular arrhythmias (torsades de pointes). This long QT syndrome can be found in several clinical settings. The Jervell and Lange-Nielsen syndrome is an autosomal recessive form of long QT syndrome with associated congenital deafness and the Romano-Ward syndrome is an autosomal dominant form of long QT syndrome that is not associated with deafness. QT prolongation is associated with syncope (fainting) and sudden death due to ventricular arrhythmias (torsades de pointes). Arrhythmias are often associated with exercise or excitement. LQTS is associated with the rare, ventricular arrhythmia torsades de pointes, which can deteriorate into ventricular fibrillation and ultimately death. Several genetic mutations have been described. Syncope is usually the first manifestation of the syndrome. The acquired long QT syndrome is most often iatrogenic or associated with the following clinical situations: ischemia, subarachnoid hemorrhage, thyroid disease, electrolyte disturbances (hypocalcemia), side effects of drugs like antiarrhythmic agents (class IA, like quinidine, or class III like sotalol or amiodarone), antidepressant agents, some antihistamine drugs or even some other substances. Short congenital QT syndrome is a newly described disease characterized by a shortened QT interval, QTc, < 340 ms associated with episodes of syncope, paroxysmal atrial fibrillation or life-threatening cardiac arrhythmias. Hyperkalemia is the most dramatic and life-threatening electrolyte disorder. There appears to be a direct effect of elevated potassium on some of the potassium channels by increasing their activity and speeding up membrane repolarisation. Also, hyperkalemia causes an overall membrane depolarisation that inactivates sodium channels. The faster repolarisation of the cardiac action potential causes tenting of the T waves, and the inactivation of sodium channels causes sluggish cardiac conduction, which leads to smaller P waves and widening of the QRS complex. Hypokalemia Electrocardiographic findings associated with Hypokalemia are flattened T waves, ST segment depression and prolongation of the QT interval. U wave amplitude is slightly increased. It is rarely associated with arrhythmia. Hypercalcemia is associated with a shortening of the ST segment and consequently the QT interval. A very high Ca level broadens the T wave and may normalize the QT interval. Hypocalcemia prolongs the ST segment and the QT interval. Many drugs, especially antiarrhythmic drugs, can be implicated in QT interval prolongation. Class 1a antiarrhythmics significantly prolong the QT interval and may be responsible for ventricular arrhythmias like ``torsades de pointes''. Class 1c, mainly flecainide broadens the QRS complex by slowing conduction in the Purkinje fibres. Antidepressants may be responsible for severe arrhythmias and conduction abnormalities. Common adverse effects of digoxin include severe arrhythmias like ventricular tachycardia (fascicular origin). Conduction abnormalities and atrial tachycardia are also observed. The combination of increased (atrial) arrhythmogenesis and inhibited A-V conduction (like atrial tachycardia with A-V block) is said to be pathognomonic of digoxin toxicity, like fascicular ventricular tachycardia.