Figure 86.1. Normal Rate and Intervals. Provided regular rhythm, heart rate = 1500/# of small boxes between two consecutive R waves or 300/# of large boxes between two consecutive R waves; Heart rate = 60–100 bpm; PR = 0.12–0.20 sec; QRS ≤ 0.12 sec; QTc (QT/√RR) ≤ 0.45 sec in men and ≤ 0.47 sec in women.

Source: Reproduced with permission from Walker HK, Hall WD. Clinical methods: The history, physical and laboratory examinations. Chicago: Butterworth-Heinemann, 1990.

    Although it is rarely important to calculate the exact axis, recognition of an abnormal axis is important. This can be accomplished by looking at the net area under the QRS curves in leads I, aVF, and II (table 86.1).

    A normal EKG is shown in Figure 86.3. Incorrect lead placement can produce a number of variant configurations. For example, with right–left arm lead reversal, there is a negative P wave with negative QRS complexes in leads I and aVL (Figure 86.4B), although the precordial leads are unaffected. With arm–leg lead reversal, there is a far-field signal in one of the bipolar leads (II, III, or aVF) that records the signal between the right and left legs. This is seen as a lack of signal in that lead except for tiny QRS complexes (Figure 86.4C).

Table 86.1 CALCULATION OF THE QRS AXIS IN THE FRONTAL PLANE

P WAVE ABNORMALITIES

Under normal circumstances, atrial activation starts in the sinus node and spreads radially through the right atrium, interatrial septum, and left atrium. The P wave axis in the frontal plane is therefore directed inferiorly and leftward and is between 0° and 75°. The P wave is always upright in I and II and inverted in aVR. It is usually also upright in III and aVF but may be biphasic or flat. It can be biphasic in V1 and V2, with the first part reflecting right atrial depolarization and the second part reflecting left atrial depolarization. The normal P wave has a duration <0.12 seconds and an amplitude ≤2.5 mm.

RIGHT ATRIAL ENLARGEMENT

In right atrial enlargement (RAE) (Figure 86.5A), the P wave is tall and peaked in lead II (>0.25 mV), or the positive deflection in lead V1 or V2 is ≥0.15 mV. RAE is commonly seen with cor pulmonale, pulmonary hypertension, and congenital heart disease.

Left Atrial Enlargement

In left atrial enlargement (LAE) (Figure 86.5B), the P wave in lead II may be broad (≥0.12 sec) or notched (peak-to-peak interval > 0.04 sec), or the P wave in V1 has a negative component that occupies more than one small box. LAE is commonly seen in mitral valve disease, hypertension, or other causes of left ventricular hypertrophy (LVH).

CARDIAC CONDUCTION ABNORMALITIES

In normal cardiac conduction, the electrical impulse is generated in the sinus node and spreads through the atria to the atrioventricular (AV) node. In the AV node conduction slows, allowing time for the atria to contract before ventricular activation occurs. After the impulse passes through the AV node, it is conducted rapidly to the ventricles through the bundle of His, bundle branches, distal Purkinje fibers, and the ventricular myocardial cells to allow synchronized contraction of the right and left ventricles.

ATRIOVENTRICULAR CONDUCTION ABNORMALITIES

First-Degree AV Block

First-degree AV block (Figure 86.6A) represents an increase in AV nodal conduction time and is defined as prolongation of the PR interval (>0.20 msec) with a 1:1 AV ratio. Isolated first-degree AV block usually has no clinical consequences and does not require treatment.

Second-Degree AV Block

Second-degree AV block is diagnosed when there is intermittent failure of one or more of the atrial impulses to conduct to the ventricles. Second-degree AV block is divided into Mobitz type I (Wenckebach) and Mobitz type II block.

    In Mobitz type I block (Figure 86.6B), the P-P interval is constant. There is progressive prolongation of the PR interval and shortening of the R-R interval, leading to a nonconducted P wave. The R-R interval containing the nonconducted P wave is <2 (P-P) interval. If Mobitz type I block is accompanied by a narrow QRS complex, the block is usually located in the AV node. If it is associated with a wide QRS, the block may occur in the AV node (75%) or infranodally (25%) within the His bundle or one of the bundle branches. Because it is usually localized to the AV node, it does not progress to complete heart block and does not require treatment unless the patient is symptomatic.

    Mobitz type II block (Figure 86.6B) is characterized by sinus rhythm with intermittent nonconducted P waves. The PR interval in conducted beats is constant, and the R-R interval containing the nonconducted P wave is exactly 2(P-P) interval. In most instances Mobitz type II block is associated with a wide QRS complex, and the block is located below the His bundle. In a smaller proportion of cases, Mobitz type II block is associated with a narrow QRS complex, and the block is located within the His bundle or less commonly within the AV node. Patients with Mobitz type II block may be asymptomatic or may experience lightheadedness or syncope depending on the ratio of conducted to non-conducted P waves. Because the block is generally distal to the His bundle, it can progress to complete heart block and usually requires treatment with pacemaker insertion.

Third-Degree AV Block

Third-degree AV block (Figure 86.6C) or complete heart block is characterized by failure of the atrial impulses to reach the ventricles. In third-degree AV block, the atrial rate is usually greater than the ventricular rate because ventricular conduction is taken over by a subsidiary pacemaker, either within the AV node (junctional escape) or within the Purkinje fibers (ventricular escape). If the subsidiary pacemaker is located within the AV node, the QRS complex is narrow and the ventricular rate is usually between 40 and 60 beats per minute (bpm). If the subsidiary pacemaker is located within the Purkinje fibers, the QRS complex is wide, and the ventricular rate is usually <40 bpm. Third-degree AV block, especially when associated with a wide QRS, carries a poor prognosis and should be treated with a pacemaker.

AV Dissociation

AV dissociation is present when there is independent activation of the atria and ventricles from different pacemakers. Although third-degree AV block is a form of AV dissociation, AV dissociation can also occur in the presence of intact AV nodal conduction. In this case, the rate of ventricular activation, either from the AV node (junctional tachycardia or accelerated junctional rhythm) or from the ventricle (ventricular tachycardia or accelerated ventricular rhythm), exceeds the rate of atrial activation leading to AV block. This is in contrast to third-degree AV block where the atrial rate is usually greater than the ventricular rate. Occasionally, there can be simultaneous activation of the ventricle from two separate pacemakers (fusion complex) or premature activation of the ventricle by an anterograde supraventricular impulse (capture complex) that can also help exclude third-degree heart block.

Intraventricular Conduction Abnormalities

If the QRS duration is >0.12 seconds, there is usually an abnormality of ventricular conduction.

Right Bundle Branch Block

In right bundle branch block (RBBB), the electrical impulse from the bundle of His does not conduct along the right bundle branch but proceeds normally down the left bundle branch (Figure 86.7). Thus, the interventricular septum and left ventricle (LV) are depolarized in a normal fashion, and the right ventricle (RV) is depolarized later by means of cell-to-cell conduction that occurs from the interventricular septum and LV to the RV. This delayed and slower activation of the RV is manifest in the EKG by the following criteria:

1. QRS duration ≥0.12 seconds

2. A secondary R wave (R≠) in the right-sided precordial leads, with R≠ greater than the initial R wave (rsR≠ or rSR≠ pattern in V1 and V2)

3. A wide S wave in the QRS complex of left-sided leads (I, V5, and V6)

4. Delay in the onset of the intrisicoid deflection in the right precordial leads (R peak time in V1) >0.05 seconds.

    RBBB may be present in patients with hypertension, rheumatic heart disease, acute and chronic cor pulmonale, myocarditis, cardiomyopathy, degenerative disease of the conduction system, congenital heart disease, Brugada syndrome, Kearns-Sayre syndrome, ventricular pre-excitation, after cardiac surgery, and rarely in patients with coronary artery disease. The prognosis depends on the underlying disease, ranging from benign in those who have a RBBB after cardiac surgery to potentially fatal in those with Brugada syndrome.

Incomplete Right Bundle Branch Block

Incomplete right bundle branch block is often seen with RV hypertrophy (RVH) and is diagnosed when the waveforms are similar to RBBB but with QRS duration <0.12 seconds. Occasionally, an rSr≠ pattern is present in V1 as a normal variant. However, in this case, the r≠ is usually smaller than the initial r wave.

Left Bundle Branch Block

Left bundle branch block (LBBB) (Figure 86.8) occurs when there is interruption of conduction in the main left bundle branch or simultaneous disease in the anterior and posterior fascicles of the left bundle branch. The impulse then travels from the AV node down the His bundle and right bundle branch to the RV and then from the RV to the interventricular septum and LV through myocardial cell to cell conduction. This delayed and slower LV activation leads to the following EKG features:

1. QRS duration ≥0.120 seconds

2. Broad, monophasic R wave in left-sided leads I, aVL, V5, and V6

3. Absence of Q waves in I, V5, and V6

4. Delay in peak R time (intrinsicoid deflection) >0.06 seconds in V5 and V6

5. Wide, deep S waves in the right precordial leads (V1–V3)

    LBBB is most often present in patients with hypertensive heart disease, coronary artery disease, and dilated cardiomyopathy. Because the left bundle branch receives a dual blood supply from the left anterior descending artery and right coronary artery, its blockade usually implies an extensive lesion in patients with coronary artery disease.

    LBBB can also be seen in patients with aortic stenosis, degenerative disease of the conduction system, and in some cases of rheumatic heart disease involving the LV. Presence of a LBBB in patients with LV systolic dysfunction confers a poor prognosis.

Incomplete Left Bundle Branch Block

Incomplete LBBB is often seen with LVH and is diagnosed when the waveforms are similar to LBBB but with QRS duration <0.12 seconds.

Hemiblocks

The left bundle branch is divided into two divisions: the anterior and posterior fascicles. The anterior fascicle supplies the anterior and lateral walls of the LV, and the posterior fascicle supplies the inferior and posterior walls of the LV. Normally, after leaving the bundle of His, the impulse travels simultaneously down both fascicles, resulting in synchronous contraction of the LV. However, if the anterior fascicle is diseased (left anterior hemiblock, LAHB), the impulse travels down the posterior fascicle, activating the inferior and posterior walls before the anterior and lateral walls, causing asynchronous contraction of the LV. Conversely, if the posterior fascicle is diseased (posterior hemiblock, LPHB), the impulse travels down the anterior fascicle, activating the anterior and lateral walls before the inferior and posterior walls. The etiologies for LAHB and LPHB are similar to those for complete LBBB. However, isolated LAHB is much more frequent than isolated LPHB.

    In LAHB, the late QRS vectors are shifted leftward and superiorly and are manifest by the following EKG criteria: left axis deviation (–30° to –90°); qR complex in I and aVL (lateral leads) and rS complex in II, III, aVF (inferior leads); and normal or prolonged QRS duration.

    In LPHB, the late QRS vectors are shifted rightward and inferiorly and are manifest by the following EKG criteria: right axis deviation (+90° to +180°); a deep S wave in I (left-sided lead) and Q waves in II, III, and aVF (inferior leads); and normal or prolonged QRS duration.

Bifascicular Block

Bifascicular block is present when there is either (1) simultaneous RBBB and LAHB, (2) simultaneous RBBB and LPHB, or (3) simultaneous LAHB and LPHB. Patients with RBBB and either fascicular block tend to have additional disease within the conduction system and may progress to complete heart block.

Trifascicular Block

Trifascicular block is present when there is disease in the right bundle branch and in both fascicles of the left bundle branch, resulting in complete heart block.

VENTRICULAR HYPERTROPHY

LEFT VENTRICULAR HYPERTROPHY

The EKG criteria for diagnosing left ventricular hypertrophy (LVH) (Figure 86.9) derive mainly from the increased LV mass, which results in exaggeration of the leftward and posterior QRS forces. Furthermore, the increased thickness of the LV wall prolongs the time needed for LV depolarization and thus may increase the QRS duration. Because depolarization is prolonged, repolarization is often abnormal, resulting in ST-T abnormalities. The increased LV mass can also result in subendocardial ischemia, further compounding the ST-T abnormalities. If present, the ST segment and T wave are directed opposite to the dominant QRS waveform.

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