To understand propagation of electrical impulses throughout the heart, two types of cardiac tissue must be considered:

• Ordinary myocardium (atrial and ventricular)
• Specialized cardiac conduction system, which includes sinoatrial, or sinus node; anterior, middle and posterior internodal tracts; atrioventricular (AV) node; His bundle; right and left bundle branches; anterior-superior and posterior-inferior divisions of the left bundle and the Purkinje network

Both the ordinary myocardium and the specialized conduction system allow conduction of electrical impulses. Most cells in the specialized cardiac conduction system also depolarize spontaneously, which enables these cells to function as cardiac pacemakers. The inherent spontaneous rate of depolarization is progressively slower from the sinus node down to the Purkinje fibers. The normal rate of spontaneous depolarization in the sinus node ranges from 60 to 100 beats/min, which is faster than other cardiac pacemakers (i.e., His bundle, Purkinje network, etc.); therefore, it is the dominant pacemaker.

Depolarization of the heart from sinus impulse suppresses other potential pacemakers; their activity is normally recognized only when sinus rates fall below those of other pacemakers. The emergence of lower pacemakers to sustain a heart rate when the dominant pacemaker fails is called an escape mechanism. During an escape mechanism, the heart rate is therefore slower than the dominant pacemaker.

Sinus node automaticity (or firing) is not recorded on the surface ECG. Sinus impulse activates the internodal tracts as well as the atrial myocardium. Activation of the atrial myocardium produces the P wave on the surface ECG. During sinus rhythm, the initial part of the P wave represents right atrial activation, whereas the terminal part of the P wave represents activation of the left atrium with some overlap in the middle. The impulse then depolarizes the AV node, the His bundle, the bundle branches, the Purkinje network and the ventricular myocardium. Propagation of impulse through the AV node, His bundle branch-Purkinje system is also not recorded on the surface ECG and occurs during the isoelectric PR segment. Ventricular muscle depolarization produces the QRS complex. Atrial depolarization is followed by atrial repolarization, called Tp or Ta, but is generally not discernible. However, recovery of the ventricular myocardium, which follows the QRS complex, is clearly recorded as a T wave on the surface ECG. It should be stressed that electrical depolarization of the atrial and ventricular myocardium is not synonymous with atrial and ventricular contraction. As a rule, electrical depolarization of these structures must precede the corresponding mechanical contraction; however, mechanical contraction occasionally may not follow the electrical events, as, for example, during electrical-mechanical dissociation.

Standard signals and measurements
The ECG is generally recorded at a paper speed of 25 mm/sec. At this speed, one small square of ECG paper in the horizontal direction depicts an interval of 40 msec or 0.04 second; the large square represents a total of 200 msec or one fifth of a second. In the vertical direction, the amplitude of ECG signals is measured in millivolts; standardization of 1 mV is routine. Amplitude of 1 mV is equivalent to the height of two large squares (10 small squares or 10 mm) of ECG paper. The electrical cardiac cycle begins with the P wave, which normally has a duration of less than 120 msec and a maximum amplitude of 0.25 mV. The normal PR interval is measured from beginning of the P wave to onset of the QRS complex. The first downward deflection is called a Q or q wave, the first upward deflection an R or r wave, the second downward deflection an S or s wave, and a second upward deflection an R or r prime. Capital or lowercase letters designate the size of these deflections in relation to each other.

The electrocardiogram (ECG) is a recording of the electrical forces produced by the heart. The body acts as a giant conductor of electrical currents. Any two points on the body may be connected by electrical "leads" to register an ECG or to monitor the rhythm of the heart. The tracing recorded from the electrical activity of the heart forms a series of waves and complexes that have been arbitrarily labeled (in alphabetical order) the P wave, the QRS complex, the T wave and the U wave. The waves or deflections are separated in most patients by regularly occurring intervals.

Depolarization of the atria produces the P wave; depolarization of the ventricles produces the QRS complex. Repolarization of the ventricles causes the T wave. The significance of the U wave is uncertain, but it may be due to repolarization of the Purkinje system. It appears at a time when many ectopic (premature) ventricular complexes (PVCs) occur and is affected by a variety of factors, such as digitalis and electrolytes.

The PR interval extends from the beginning of the P wave (the beginning of atrial depolarization) to the onset of the QRS complex (the beginning of ventricular depolarization). It should not exceed 0.20 second as measured on ECG graph paper, where each small square represents 0.04 second. The QRS complex represents the electrical depolarization of the ventricles. The upper limit of normal duration of the QRS is less than 0.12 second. A QRS duration of less than 0.12 second means that the impulse was initiated from the AV node region or above (supraventricular). A wide QRS (> 0.12 second) may signify conduction that either arises from the ventricle or comes from supraventricular tissue. Prolonged conduction through the ventricle produces a widened QRS.

Right atrial enlargement
Since the initial part of the P wave is due to right atrial depolarization, enlargement of the right atrium produces a P wave prominence (peaked P waves) in leads II and aVF without necessarily increasing P wave duration. P wave voltage of more than 0.25 mV in the limb leads or V1 suggests right atrial enlargement.

Left atrial enlargement
Left atrial enlargement is suggested by P wave duration of 120 msec or more, definite notching and prominence of the terminal portion of the P wave, or prominent negativity of the terminal portion of the P wave in V1. It should be pointed out that conduction delay in the atria without hypertrophy could prolong P wave duration. However, conduction delay is secondary to hypertrophy or dilation in most instances.

Left ventricular hypertrophy
Electrical forces generated during left ventricular activation ordinarily produce the normal QRS complex. With an increase in the thickness of left ventricular myocardium (left ventricular hypertrophy) as seen with systemic hypertension and left ventricular outflow obstruction, electrical preponderance of left ventricle over right ventricle is further accentuated. The mean vector of the left ventricle becomes more posterior and leftward, increasing QRS complex voltage and ventricular activation time.

Secondary ST and T wave abnormalities are not uncommon in the later stages of left ventricular hypertrophy. On voltage criteria alone, standards have been established for different leads. Left ventricular hypertrophy may be diagnosed in the extremity leads if the sum of the R wave in lead I and the S wave in lead III equals or exceeds 25mm. An R wave of 11 mm in aVL or 20 mm in aVF is considered high voltage and adequate for diagnosis of left ventricular hypertrophy in extremity leads. For precordial leads, an S wave in V1 exceeding 24 mm, an R wave in V5 or V6 exceeding 26 mm, or a sum of R wave in V5 or V6 and S wave in V2 of more than 35 mm are generally considered sufficient for diagnosis of left ventricular hypertrophy. The presence of ST depression and T wave inversion in the presence of adequate voltage criteria improves the diagnostic accuracy of left ventricular hypertrophy by ECG. Additional ECG clues to diagnosis of left ventricular hypertrophy are left axis deviation, increased QRS duration and the presence of left atrial enlargement. Due to the increased voltage of QRS complexes, many or all leads may have to be recorded at half the usual standardization scale of mV.

Right ventricular hypertrophy
With right ventricular hypertrophy, electrical voltage generated at the right ventricular level is increased. Consequently, there is characteristic alteration in the balance of electrical forces between the ventricles. However, it should be pointed out that the increase in right ventricular forces must be sufficient to either reduce or abolish the left ventricular preponderance. Increasing hypertrophy of the right ventricle produces progressive anterior and rightward displacement of the QRS vector. These changes become more pronounced as the degree of hypertrophy increases. Progressive hypertrophy of the right ventricle causes an increase in amplitude of the R wave and a corresponding decrease in the S wave in lead V1. Therefore, the R-S ratio gradually increases. The most severe right ventricular hypertrophy is manifested by a tall R wave in lead V1.

In the extremity leads, the diagnostic criteria for right ventricular hypertrophy includes an R wave in aVR of more than 5 mm. In the precordial leads, an R wave in V1 exceeding 7 mm or an S wave in V1 of less than 2 mm suggests right ventricular hypertrophy. An R-S ratio of more than 1 in V1, or the sum of R in V1 and S in V5 of more than 10mm, or an R-S ratio in V5 or V6 of less than 1 suggest right ventricular hypertrophy. Conventionally, right ventricular hypertrophy has been classified as one of three types. Type A usually produces a tall R wave in V1 and represents concentric hypertrophy of the right ventricle, usually associated with right ventricular outflow obstruction of congenital origin. An R-S pattern is produced in type B and usually anatomically reflects a moderately severe hypertrophy of the right ventricle. Type C produces an rSr pattern that represents a moderate-to-mild hypertrophy of the crista supraventricularis and the outflow tract of the right ventricle. It is commonly seen in atrial septal defect, mitral stenosis and cor pulmanate.

Right atrial enlargement, right axis deviation and ST and T wave abnormalities in leads showing the R prominence may accompany right ventricular hypertrophy and generally support the diagnosis. Right ventricular hypertrophy can mimic posterior myocardial infarction. Changes produced by the latter are limited to the right precordial leads, and prominent S waves are seldom seen in leads I and V6. Posterior infarction is often accompanied by inferior or lateral wall infarction or both. Other conditions that produce prominent R waves in V1 include right bundle branch block and left ventricular preexcitation, which is preceded by a short PR interval. Right bundle branch block should not be diagnosed in the absence of prolonged QRS duration.

Right bundle branch block
Since the initial part of the QRS complex is inscribed as a result of left-to-right forces in the septal mass supplied by fibers of the left bundle branch, the occurrence of right bundle branch block does not alter the initial part of the QRS complex. Similarly, since the left bundle branch is intact, the remainder of the left ventricle continues to activate normally. However, soon after ventricular activation begins, transseptal muscle-to-muscle conduction from left to right generates significant electrical forces. The first 20-40 msec of ventricular activation is not altered by the presence of right bundle branch block. However, ventricular activation later becomes oriented to the right and anterior. The rightward forces become particularly prominent when left ventricular activation ceases (after 60-80 msec). Hence, the terminal vector is directed to the right and anterior. After the initial normally directed septal forces, the QRS vector is directed anteriorly and to the right, resulting in a positive terminal R pattern in V1 and a terminal S wave in leads I and V6. Because of a significant amount of muscle-to-muscle conduction, slurring is seen in the terminal portion of the QRS complex, which is a characteristic feature of right bundle branch block. As a result of unopposed right ventricular activation time in addition to normal left ventricular activation time, the QRS complex is prolonged and generally exceeds 120 msec. The term complete right bundle branch block is used when the QRS complex equals or exceeds 120 msec; the term incomplete right bundle branch block is used when QRS duration is 100-120 msec. Secondary changes in the ST and T segments usually accompany altered QRS morphology during right bundle branch block.

Left bundle branch block
During this disturbance of intraventricular conduction, septal and left ventricular activation is altered from onset. Since left septal mass cannot activate via the left bundle, septal activation occurs through the right bundle from the opposite direction, that is, to the left. This results in the absence of a q wave in leads I and V6. However, an r wave may persist in V1 because of the anterior component of right-to-left septal activation. The activation wave moves transeptally toward the left ventricle. The ventricular activation vector therefore is directed posteriorly and to the left. Due to a considerable amount of muscle-to-muscle conduction during ventricular depolarization, QRS duration frequently exceeds 120 msec. In addition to the QRS complex widening, small notching is frequently seen during R-wave inscription. Electrocardiographically, the QRS complex typically shows the absence of a q as well as a slurred R wave in leads I and V6. V1 shows a small r wave or none followed by an S wave, with total QRS duration of more than 120 msec. Secondary ST segment and T wave abnormalities are universal. In fact, the ST and T vectors are oriented in the opposite direction, compared with the QRS complex. Due to the abnormal vector throughout ventricular activation, ischemia, injury and infarction usually cannot be detected with confidence in the presence of left bundle branch block. On the other hand, since the initial part of the QRS complex is not altered in right bundle branch block, the abnormal Q waves of myocardial infarction can be accurately diagnosed in the presence of right bundle branch block.

Nonspecific intraventricular conduction defect
The term nonspecific intraventricular conduction defect is used when no characteristic pattern of right or left bundle branch block exists, although QRS duration is prolonged. Such abnormalities are frequently seen with previous myocardial infarction and scar formation. Prolonged QRS duration without a specific bundle branch block pattern can also occur due to intramyocardial conduction slowing from class I antiarrhythmic drugs, left ventricular hypertrophy and hyperkalemia.

Fascicular blocks or hemiblocks
Thus far, discussion of the left bundle branch system has been based on the assumption that it represents a single fascicle like the right bundle branch. In actuality, the left bundle branch is divided into the so-called anterior-superior division, or fascicle, and posterior-inferior division, or fascicle. These fascicles activate the corresponding portion of the left ventricular mass. Septal activation occurs from fibers of variable origin that generally arise from the left posterior division.

Left anterior-superior fascicular block or hemiblock
Like the main left bundle, a variety of conditions can produce a block in this division, including arteriosclerotic heart disease, aortic stenosis, hypertension and cardiomyopathy. Sometimes a block is not associated with obvious structural heart disease. Septal activation generally occurs in a normal left-to-right direction. However, there frequently is inferior orientation of initial forces because activation from inferior divisional fibers is unopposed by fibers from the superior fascicle. Due to the block in fibers supplying the anterior-superior portion of the left ventricle, the initial forces are directed inferiorly, producing an initial r wave in leads II, III and aVF, and a q wave in leads I and aVL. However, the mean QRS vector is directed superiorly and to the left (toward the area supplied by the anterior-superior division), resulting in a tall R wave in leads I and aVL as well as deep S waves in leads II, III and aVF. Since right and left ventricular activation proceeds simultaneously, QRS duration is generally not significantly prolonged. The main ECG abnormally produced by a left anterior fascicular block is marked left axis deviation located between -45 degrees and -75 degrees.

Left posterior fascicular block or hemiblock
Isolated block in this division is uncommon. The same diseases that produce the anterior fascicular block are frequently responsible for this abnormality as well. Interruption of the posterior fascicle causes the initial activation vector to be directed superiorly and to the left, producing an r wave in leads I and aVL and a q wave in leads II, III and aVF. The major QRS vector points to the left and inferiorly as well as posteriorly. The QRS abnormality therefore is the presence of tall R waves in leads II, III and aVF, and the presence of an S wave in lead I, the axis generally being around 120 degrees. Again, the QRS complex usually does not widen because of simultaneous activation of the ventricles. Right bundle branch block commonly coexists with either left anterior hemiblock or left posterior hemiblock, a combination also called bifascicular block.

Ventricular preexcitation
Normally, the atrial impulses conduct to the ventricles by the AV node-His-Purkinje system. Most conduction delay accounting for the normal PR interval is located in the AV node. On occasion, however, additional pathways connecting the atria with the ventricles may exist, and these are called accessory pathways. The most common of these, the Kent bundle, is a direct muscle-to-muscle bridge, anatomically separate from the normal conduction system. This type of accessory pathway forms the anatomic basis for WPW syndrome. The Kent bundle can be located anywhere around the AV junction, connecting the right atrium and right ventricle or the left atrium and left ventricle. Sometimes these bypass tracts are located within the septum. Conduction velocity is often faster in these tracts compared with the normal AV node; therefore, sinus impulses usually activate the ventricle through these pathways, resulting in a short PR interval. Initial ventricular activation by the accessory pathway is muscle to muscle; thus, the first part of the QRS complex, the delta wave, is slurred. These patients also have an intact normal pathway through which sinus impulses reach and activate the remainder of the myocardium beyond what has been depolarized via the accessory pathway. Thus, the resulting QRS is a fusion complex, which is initially activated through the accessory pathway and finally via the normal pathway. In left atrioventricular connections, ventricular activation from the accessory pathway proceeds anteriorly and produces a positive R wave in V1 (positive delta), the so-called Type A ventricular preexcitation. In right atrioventricular connection, activation is directed posteriorly, producing a predominantly negative delta wave in lead V1 (negative delta), and called type B ventricular preexcitation.

This is an oversimplification; such terminology should be abandoned since accessory pathways can be located anywhere at the AV junction, and designation of types A and B alone does not serve a useful purpose. In descending order of frequency, these accessing AV connections are located in left free wall, poster septum, right free wall and ante-osteriol regions. Depending on the relative conduction properties of the normal versus accessory pathways, the QRS complex can be normal to totally preexcited. The presence of the short PR interval and the delta wave constitutes the basic ECG abnormality. Since these patients have two potential pathways, the impulses can conduct by one and return by the other, making them prone to paroxysmal AV junctional reentrant tachycardias. The combination of ECG abnormality and a history of recurrent palpitation constitutes the WPW syndrome.

Negative orientation of the delta wave can mimic the ECG patterns of prior myocardial infarction (a Q wave) and can occur in both the anterior and inferior leads. It is not uncommon to erroneously diagnose prior myocardial infarction in patients with WPW syndrome. The presence of a short PR interval is generally the clue to correct diagnosis and should certainly raise suspicion.

• Acute pericarditis: ST elevation in acute pericarditis is generally diffuse and does not follow the pattern of blood supply. As a rule these changes are not accompanied by reciprocal depression of the ST segment in other leads.
• Early repolarization: In some patients without known heart disease, particularly young patients, early takeoff of the ST segment may be seen.
• Ventricular aneurysm: After acute myocardial infarction, the ST segment usually normalizes. However, in the presence of a persistent aneurysm in the region of infarction, ST segment elevation may persist indefinitely.

Abnormal T waves can be seen in a variety of conditions other than myocardial ischemia, including the following:

• Hyperventilation
• Cerebrovascular disease
• Mitral valve prolapse
• Right or left ventricular hypertrophy
• Conduction abnormalities (right or left bundle branch block)
• Ventricular preexcitation
• Myocarditis
• Electrolyte imbalance
• Cardioactive drugs such as digitalis and antiarrhythmic agents
• No obvious cause, particularly in women

Better understanding of certain basic anatomic and electrophysiologic concepts facilitates diagnosis of cardiac arrhythmias. Knowledge of underlying mechanisms and the site of origin of arrhythmias is particularly important.

All cardiac tissues have an inherent conduction velocity that is normally faster in the His-Purkinje system compared with the atrial and ventricular myocardium. Conduction velocity is slowest in the AV and sinoatrial nodes. Abnormally slow or ineffective propagation of atrial impulses across the AV junction can produce various degrees of AV block. Such a mechanism has also been incriminated in production of sinoatrial exit block when abnormalities exist at the sinoatrial junction.

It is difficult to recognize tachyarrhythmias that are due to slow conduction. However, slow conduction is commonly encountered during propagation of premature impulses due to incomplete recovery, where conduction may be normal during the resting state. If premature impulses block along certain fibers or pathways and conduct slowly along others, the impulse can return via fibers not previously used. If the tissue ahead of the approaching wave front has recovered excitability, propagation of the impulse can continue, starting a reentry process that produces either single beats or sustained tachycardia. In clinical settings, many reentrant arrhythmias are initiated by premature beats with abrupt onset and termination. Preentrant tachyarrhythmias can occur in structurally normal tissues such as the AV node as well as diseased tissues (ventricular tachycardia arising in diseased myocardium).

Approach
Disturbance of cardiac rhythm or arrhythmia implies a deviation from the normal pattern (sinus rhythm). Tachyarrhythmias are accelerated atrial or ventricular rates that exceed what is considered normal. Rhythms producing cardiac slowing are grouped together as bradyarrhythmias. When three consecutive complexes occur at a rate exceeding 100 beats/min, the tachycardia terminology is used. For proper ECG diagnosis of cardiac arrhythmias, particular attention should be given to the following:

• Presence or absence of atrial depolarization (P wave, flutter waves, etc.). Diagnosis of cardiac arrhythmia cannot be considered complete without accounting for atrial activity.
• Rate and regularity of atrial and ventricular depolarizations.
• Relationships between atrial and ventricular depolarization, and, if related, which one is the primary event.
• Site of origin, i.e., atrial, AV junctional or ventricular.

The heart blocks are divided into three degrees. First-degree heart blocks are characterized by PR intervals longer than 0.20 second and all of the P waves are followed by QRS complexes. Second-degree heart blocks are characterized by some P waves being blocked at the AV node. This results in some P waves occurring without following QRS complexes. Third-degree heart block is characterized by a complete dissociation between P waves and QRS complexes. A hint for separating the heart blocks into degrees is that first- and third-degree blocks usually have regular QRS rates.

Atrioventricular block
Atrioventricular block is defined as a delay or interruption in conduction between the atria and ventricles. It may be due to (1) lesions along the conduction pathway (such as calcium, fibrosis, necrosis), (2) increases in the refractory period of a portion of the conduction pathway (such as may occur in the AV node when digitalis is administered), or (3) shortening of the supraventricular cycle length, i.e., rapid atrial rates, with encroachment on the normal refractory period (as with atrial flutter, in which 2:1 AV block at the level of the AV node occurs because the normal AV node refractory period will not allow conduction at a rate of 300 beats/min but will allow it at 150 beats/min).

AV block may be classified in two ways:
According to the degree of block:

• Partial blocks
  • First-degree AV block
  • Second-degree AV block (type I and type II), 2:1, and advanced (3:1 or greater)
• Third-degree or complete AV block

According to the site of block:

• AV node
• Infranodal
  • Bundle of His
  • Bundle branches

Each degree of block may occur either at the level of the AV node or below it. This distinction is not academic, since pathogenesis, treatment and prognosis differ.

There is growing evidence that certain patients with premature ventricular complexes (PVCs) and ventricular tachycardia are at an increased risk of sudden cardiac death. In general, patients who die soon after the onset of symptoms are said to have experienced sudden cardiac death, and this is almost always due to ventricular fibrillation, which is either primary or a result of ventricular tachycardia. It is generally believed that patients with simple ventricular ectopy and no associated heart disease are not at risk for sudden cardiac death, whereas patients with more complex ventricular ectopy and associated heart disease are at risk because of the presence of the ventricular arrhythmia. Such patients may often have coronary artery disease, and the sudden death may be associated with an acute ischemic event, including myocardial infarction or angina, but it may also occur in the absence of myocardial ischemia.