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, inferior orientation of initial forces often occurs 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.

This content is reviewed regularly. Last updated 11/24/2008.