Right Atrial Abnormality

Overload of the right atrium (either dilation or actual hypertrophy) may increase the voltage of the P wave. To recognize a large P wave, you must know the dimensions of the normal P wave.

When the P wave is positive, its amplitude is measured in millimeters from the upper level of the baseline, where the P wave begins, to the peak of the wave. A negative P wave is measured from the lower level of the baseline to the lowest point of the P wave. (Measurement of the height and width of the P wave is shown in Fig. 6-1.)

Figure 6-1 The normal P wave is usually less than 2.5 mm in height and less than 0.12 sec in width.

Normally, at rest, the P wave in every lead is less than 2.5 mm (0.25 mV) in amplitude and less than 0.12 sec (three small boxes) in width.

Overload of the right atrium may produce an abnormally tall P wave (2.5 mm or more). Occasionally, right atrial abnormality (RAA) will be associated with a deep (negative) but narrow P wave in lead V₁, due to the relative inferior location of the right atrium relative to this lead. This finding may cause confusion with left atrial abnormality (LAA).

However, because pure RAA generally does not increase the total duration of atrial depolarization, the width of the P wave is normal (less than 0.12 sec). The abnormal P wave in RAA is sometimes referred to as P pulmonale because the atrial enlargement that it signifies often occurs with severe pulmonary disease (Figs. 6-2 and 6-3).

Figure 6-2 Tall narrow P waves may indicate right atrial abnormality or overload (formerly referred to as P pulmonale pattern).

Figure 6-3 Tall P waves (arrow) are seen in leads II, III, aVF, and V₁ from the ECG of a patient with chronic lung disease. This finding is sometimes called the P pulmonale pattern.

The tall, narrow P waves characteristic of RAA can usually be seen best in leads II, III, aVF, and sometimes V₁. The ECG diagnosis of P pulmonale can be made by finding a P wave exceeding 2.5 mm in any of these leads. Echocardiographic evidence, however, indicates that the finding of a tall, peaked P wave does not consistently correlate with RAA. On the other hand, patients may have actual right atrial overload and not tall P waves. In other words, tall peaked P waves are of limited sensitivity and specificity in the diagnosis of right atrial enlargement (see Chapter 23).

RAA is seen in a variety of important clinical settings. It is usually associated with right ventricular enlargement. Two of the most common clinical causes of RAA are pulmonary disease and congenital heart disease. The pulmonary disease may be either acute (bronchial asthma, pulmonary embolism) or chronic (emphysema, bronchitis). Congenital heart lesions that produce RAA include pulmonary valve stenosis, atrial septal defects, Ebstein’s anomaly (a malformation of the tricuspid valve), and tetralogy of Fallot.

Left Atrial Abnormality

Enlargement of the left atrium by dilation or actual hypertrophy also produces predictable changes in the P wave. Normally the left atrium depolarizes after the right atrium. Thus, left atrial enlargement should prolong the total duration of atrial depolarization, indicated by an abnormally wide P wave. Left atrial enlargement (LAE) characteristically produces a wide P wave with duration of 0.12 sec or more (at least three small boxes). With enlargement of the left atrium the amplitude (height) of the P wave may be either normal or increased.

Some patients, particularly those with coronary artery disease, may have broad P waves without detectable enlargement of the left atrium. The abnormal P waves probably represent an atrial conduction delay in a normal-sized chamber. Therefore, rather than left atrial enlargement, the more general term left atrial abnormality is recommended to describe these abnormally broad P waves.

Figure 6-4 illustrates the characteristic P wave changes seen in LAA. As shown, the P wave sometimes has a distinctive humped or notched appearance (Fig. 6-4A). The second hump corresponds to the delayed depolarization of the left atrium. These humped P waves are usually best seen in one or more of the extremity leads (Fig. 6-5). The older term P mitrale is sometimes still used to describe wide P waves seen with LAA because these waves were first described in patients with rheumatic mitral valve disease.

Figure 6-4 Left atrial abnormality/enlargement may produce the following: A, wide, sometimes notched P waves in one or more extremity leads (formerly referred to as P mitrale pattern), and B, wide biphasic P waves in lead V₁.

Figure 6-5 Broad, humped P waves from the ECG of a patient with left atrial enlargement (abnormality).

In patients with LAA, lead V₁ sometimes shows a distinctive biphasic P wave (see Figs. 6-4B, and 6-6). This wave has a small, initial positive deflection and a prominent, wide negative deflection. The negative component is longer than 0.04 sec in duration or 1 mm or more in depth. The prominent negative deflection corresponds to the delayed stimulation of the enlarged left atrium. Remember that anatomically the left atrium is situated posteriorly, up against the esophagus, whereas the right atrium lies anteriorly, against the sternum. The initial positive deflection of the P wave in lead V₁ therefore indicates right atrial depolarization, whereas the deep negative deflection is a result of left atrial depolarization voltages directed posteriorly (away from the positive pole of lead V₁).

In some cases of LAA, you may see both the broad, often humped P waves in leads I and II and the biphasic P wave in lead V₁. In other cases, only broad, notched P waves are seen. Sometimes a biphasic P wave in lead V₁ is the only ECG evidence of LAA.

LAA by ECG, especially when marked, indicates increased risk of atrial fibrillation; conversely, patients with a history of paroxysmal atrial fibrillation not uncommonly have ECG signs of LAA when in sinus rhythm.

The patterns of LAA and RAA are summarized schematically in Figure 6-6.

Figure 6-6 Overload of the right atrium (RA) may cause tall, peaked P waves in the extremity or chest leads. An abnormality of the left atrium (LA) may cause broad, often notched P waves in the extremity leads and a biphasic P wave in lead V₁ with a prominent negative component representing delayed depolarization of the left atrium.

(Modified from Park MK, Guntheroth WG: How to Read Pediatric ECGs, 4th ed. St. Louis, Mosby/Elsevier, 2004.)

Patients with enlargement of both atria (biatrial enlargement or abnormality) may show a combination of patterns (e.g., tall and wide P waves). This finding is most likely with severe cardiomyopathy or valve disease.

Right Ventricular Hypertrophy

Although atrial enlargement (dilation or hypertrophy) may produce prominent changes in the P wave, the QRS complex is modified primarily by ventricular hypertrophy. The resultant ECG effects indicate actual hypertrophy of the ventricular muscle and not simply ventricular dilation.

You can predict the ECG changes produced by both right ventricular hypertrophy (RVH) and left ventricular hypertrophy (LVH) based on what you already know about normal QRS patterns. Normally the left and right ventricles depolarize simultaneously, and the left ventricle is electrically predominant because it has greater mass (see Chapter 4). As a result, leads placed over the right side of the chest (e.g., V₁) record rS-type complexes:

In these rS-type complexes the deep negative S wave indicates the spread of depolarization voltages away from the right and toward the left side. Conversely, leads placed over the left side of the chest (e.g., V₅, V₆) record a qR-type complex:

In this complex the tall positive R wave indicates the predominant depolarization voltages that point to the left and are generated by the left ventricle.

If sufficient hypertrophy of the right ventricle occurs, the normal electrical predominance of the left ventricle can be overcome. In this situation, what type of QRS complex might you expect to see in the right chest leads? With RVH the right chest leads show tall R waves, indicating the spread of positive voltages from the hypertrophied right ventricle toward the right (Fig. 6-7). Figures 6-8 and 6-9 show actual examples of RVH. Instead of the rS complex normally seen in lead V₁, a tall positive (R) wave indicates marked hypertrophy of the right ventricle.

Figure 6-7 The QRS patterns with left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH) can be anticipated based on the abnormal physiology. Notice that left ventricular hypertrophy exaggerates the normal pattern, causing deeper right precordial S waves and taller left precordial R waves. By contrast, right ventricular hypertrophy shifts the QRS vector to the right, causing increased right precordial R waves.

Figure 6-8 A tall R wave (as part of an Rs complex) with an inverted T wave caused by right ventricular overload is seen in leads V₁ to V₅ (also in II, III, and aVF) from a patient with right ventricular hypertrophy (RVH) that was multifactorial. Marked right axis deviation is also present because the R wave in lead III is much taller than the R wave in lead II. In fact, the RVH is so severe that the R wave progression pattern is actually reversed (rS in V₆). The negative but prominent P wave in V₁ is probably due to right atrial overload, with slightly peaked P waves in leads II, III, and aVF.

Figure 6-9 With right ventricular hypertrophy, lead V₁ sometimes shows a tall R wave as part of the qR complex. Because of right atrial enlargement, peaked P waves are seen in leads II, III, and V₁. The T wave inversion in lead V₁ and the ST segment depressions in leads V₂ and V₃ are due to right ventricular overload. The PR interval is also prolonged (0.24 sec).

How tall does an R wave in lead V₁ have to be to make a diagnosis of RVH? In adults the normal R wave in lead V₁ is generally smaller than the S wave in that lead. An R wave exceeding the S wave in lead V₁ is suggestive but not diagnostic of RVH. Sometimes a small q wave precedes the tall R wave in lead V₁ (see Fig. 6-8).

Along with tall right chest R waves, RVH often produces two additional ECG signs: right axis deviation (RAD) and T wave inversions in right to mid-precordial leads.

RVH affects both depolarization (QRS complex) and repolarization (ST-T complex). For reasons not fully understood, hypertrophy of the heart muscle alters the normal sequence of repolarization. With RVH the characteristic repolarization change is the appearance of inverted T waves in the right and middle chest leads (see Figs. 6-8 and 6-9).

These right chest T wave inversions were formerly referred to as a right ventricular “strain” pattern. Left precordial T wave inversions due to LVH were referred to as left ventricular “strain.” Preferable and more contemporary designations are T wave inversions associated with right ventricular or left ventricular overload, respectively.

With RVH the chest leads to the left of leads showing tall R waves may display a variable pattern. Sometimes the middle and left chest leads show poor R wave progression, with rS or RS complexes all the way to lead V₆ (see Fig. 6-9). In other cases, normal R wave progression is preserved and the left chest leads also show R waves (see Fig. 6-8).

Factors causing RVH, such as congenital heart disease or lung disease, also often cause right atrial overload. So, not uncommonly, signs of RVH are accompanied by tall P waves. The major exception to this rule, in which signs of RVH are, paradoxically, accompanied by marked LAA is mitral stenosis, as illustrated in Figure 23-1.

The presence of a right bundle branch block (RBBB) pattern by itself does not indicate RVH. However, a complete or incomplete RBBB pattern with RAD should raise strong consideration of a right ventricular enlargement syndrome.

In summary, with RVH the ECG may show tall R waves in the right chest leads and the R wave may be taller than the S wave in lead V_1. In addition, RAD and right precordial T wave inversions are often present. Some cases of RVH are more subtle, and the ECG may show only one of these patterns.

RVH may occur in a variety of clinical settings. An important cause is congenital heart disease,

such as pulmonary stenosis, atrial septal defect,^∗ tetralogy of Fallot, or Eisenmenger’s syndrome. Patients with long-standing severe pulmonary disease may have pulmonary artery hypertension and RVH. As noted, mitral stenosis can produce a combination of LAA and RVH. T wave inversions in leads V₁ to V₃ due to right ventricular overload may also occur without other ECG signs of RVH, as in acute pulmonary embolism (see Chapter 11).

In patients who have right ventricular overload associated with emphysema, the ECG may not show any of the patterns just described. Instead of tall R waves in the right precordial leads, very slow R wave progression is seen. RAD is also commonly present, along with low voltage QRS complexes (see Fig. 11-6).

Left Ventricular Hypertrophy

The major ECG changes produced by LVH, like those from RVH, are predictable (see Fig. 6-7). Normally the left ventricle, because of its relatively larger mass, is electrically predominant over the right ventricle. As a result, prominent negative (S) waves are produced in the right chest leads, and tall positive (R) waves are seen in the left chest leads. When LVH is present, the balance of electrical forces is tipped even further to the left. Thus, with LVH, abnormally tall, positive (R) waves are usually seen in the left chest leads, and abnormally deep negative (S) waves are present in the right chest leads.

Important note: the voltage criteria used to diagnose LVH in the chest and limb leads are by no means absolute numbers. In fact, many different criteria have been proposed, reflecting the imperfection of ECG in providing a test with both high sensitivity and specificity.

The following ECG criteria and guidelines have been proposed for the ECG diagnosis of LVH:

Figure 6-10 Pattern of left ventricular hypertrophy in a patient with severe hypertension. Tall voltages are seen in the chest leads and lead aVL (R = 17 mm). A repolarization (ST-T) abnormality, formerly referred to as a “strain” pattern, is also present in these leads. In addition, enlargement of the left atrium is indicated by a biphasic P wave in lead V₁.

Figure 6-11 Tall voltages in the chest leads (S_V1 + R_V5 = 36 mm) from a 20-year-old man represent a common normal ECG variant, particularly in athletic or thin young adults. The ST-T complexes are normal, without evidence of repolarization (ST-T) abnormalities or left atrial abnormality.

Figure 6-12 Repolarization abnormalities associated with left ventricular hypertrophy were formerly referred to as the “strain” pattern, an imprecise but still sometimes used term. Notice the characteristic slight ST segment depression with T wave inversion in the leads that show tall R waves. These repolarization changes can be referred to as “LVH-related ST-T changes” or “ST-T changes due to LV overload.”

In summary, the diagnosis of LVH can be made with a high degree of certainty from the ECG if you find high QRS voltages and associated ST-T changes with signs of LAA. Because high voltage in the chest or extremity leads can sometimes be seen in normal people, especially athletes and young adults, the diagnosis of LVH should not be made on this finding alone. ST-T changes resulting from left ventricular overload can also occur without voltage criteria for LVH.

The Ecg in Cardiac Enlargement: A Clinical Perspective

If hypertrophy is present in both ventricles, the ECG usually shows mainly evidence of LVH. Another pattern that may provide an important clue to biventricular hypertrophy is LVH with rightward axis deviation. Biventricular hypertrophy may be present, for example, in some cases of severe dilated cardiomyopathy or rheumatic valvular disease.

Always remember that in the assessment of cardiac size, the ECG is only an indirect laboratory test and not an absolute measurement. A person may have underlying cardiac enlargement that does not show up on the ECG. Conversely, the ECG may show high voltage in a normal person who does not have cardiac enlargement. When the presence or degree of cardiac chamber enlargement must be determined with more precision, an echocardiogram should be obtained. For some suspected conditions, such as arrhythmogenic right ventricular cardiomyopathy or apical hypertrophic cardiomyopathy, a cardiac magnetic resonance imaging (MRI) study may be indicated.