Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 6. Atrial and Ventricular Enlargement

The basics of the normal ECG were described in the first five chapters. From this point, attention is focused primarily on abnormal ECG patterns. This chapter discusses the effects of enlargement of the four cardiac chambers on the ECG.

Cardiac enlargement refers to either dilation of a heart chamber or hypertrophy of the heart muscle:



In dilation of a chamber, the heart muscle is stretched and the chamber becomes enlarged. For example, with congestive heart failure (CHF) caused by acute aortic valve regurgitation, the left ventricle dilates.



In cardiac hypertrophy, the heart muscle fibers actually increase in size, with resultant enlargement of the chamber. For example, aortic stenosis, which obstructs the outflow of blood from the left ventricle, leads to hypertrophy of the left ventricular muscle. Other situations (described later in this chapter) can result in hypertrophy of the atria and right ventricle.

When cardiac hypertrophy occurs, the total number of heart muscle fibers does not increase; rather, each individual fiber becomes larger. One predictable ECG effect of cardiac hypertrophy is an increase in the voltage or duration of the P wave or QRS complex. Not uncommonly, hypertrophy and dilation occur together.

Both dilation and hypertrophy usually result from some type of chronic pressure or volume load on the heart muscle. The following sections discuss the ECG patterns seen with enlargement of each of the four cardiac chambers, beginning with the right atrium.


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 Figure 6-1 .)

FIGURE 6-1  The normal P wave is usually no more than 2.5 mm in height and less than 0.12 sec in width.

Normally, the P wave in every lead is less than or equal to 2.5mm (0.25mV) in amplitude and less than 0.12 second (three small boxes) in width. A P wave exceeding either of these dimensions in any lead is abnormal.

Overload of the right atrium may produce an abnormally tall P wave (greater than 2.5 mm). Because pure right atrial abnormality (RAA) generally does not increase the total duration of atrial depolarization, however, 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 ( Fig. 6-2 ). An example of RAA is presented in Figure 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 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 suggests, however, 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 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 pulmonic valve stenosis, atrial septal defects, Ebstein's anomaly (a malformation of the tricuspid valve), and tetralogy of Fallot.



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 second 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 the term left atrial enlargement, the more general term left atrial abnormality (LAA) is being used increasingly 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. 6-4 A). 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 limb 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 limb leads (formerly referred to as P mitrale pattern); and/or 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 ( Fig. 6-6 ; see Fig. 6-4 B). This wave has a small initial positive deflection and a prominent, wide negative deflection. The negative component is longer than 0.04 second 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).

FIGURE 6-6  Overload of the right atrium (RA) may cause tall peaked P waves in the limb or chest leads. An abnormality of the left atrium (LA) may cause broad, often notched P waves in the limb 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, 3rd ed. St. Louis, Mosby, 1992.)

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.

Clinically, LAA may occur in a variety of settings, including the following:



Valvular heart disease, particularly aortic stenosis, aortic regurgitation, mitral regurgitation, and mitral stenosis[*]



Hypertensive heart disease, which causes left ventricular enlargement and eventually LAA






Coronary artery disease

The patterns of LAA and RAA are summarized schematically in Figure 6-6 . Patients with enlargement of both atria (biatrial enlargement or abnormality) may show a combination of patterns (e.g., tall and wide P waves).

*  With mitral stenosis, valvular obstruction to the emptying of the left atrium into the left ventricle eventually results in a backup of pressure through the pulmonary vessels to the right ventricle. Therefore, with advanced mitral stenosis, the ECG may show a combination of LAA (or atrial fibrillation) and signs of right ventricular hypertrophy (RVH), as depicted in Figure 23-1 .



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 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 [8] [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 with an inverted T wave caused by right ventricular overload is seen in lead V1 from a patient with tetralogy of Fallot. Marked right axis deviation is also present. (The R wave in lead III is taller than the R wave in lead II.)

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 (arrow) and the ST 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 [8] [9]). These right chest T wave inversions were formerly referred to as a right ventricular “strain” pattern. A preferable term is T wave inversions associated with right ventricular overload.

Factors that cause 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 condition in which signs of RVH are accompanied by left atrial abnormality 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. A complete or incomplete RBBB pattern with RAD should, however, 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 V1.[*] 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.

The appearance of all three patterns—tall right precordial R waves, RAD, and right precordial T wave inversions—is very strong evidence of marked RVH.

RVH may occur in a variety of clinical settings. An important cause is congenital heart disease, such as pulmonic 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 V3due 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, poor R wave progression is seen. RAD is also commonly present (see Figure 11-6 ).

*  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 ).
†  Patients with right ventricular enlargement from the most common type of atrial septal defect often exhibit a right bundle branch block pattern (RSR' in lead V1) with a vertical or rightward QRS axis.



The ECG changes produced by LVH, like those from RVH, are predictable (see Fig. 6-7 ). Normally, the left ventricle, due 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 farther 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.

The following criteria and guidelines have been established to help in the ECG diagnosis of LVH:



If the sum of the depth of the S wave in lead V1 (SV1) and the height of the R wave in either lead V5 or V6 (RV5 or RV6) exceeds 35 mm (3.5 mV), LVH should be considered ( Fig. 6-10 ). High voltage in the chest leads is a common normal finding, however, particularly in athletic or thin young adults. Consequently, high voltage in the chest leads (SV1 + RV5 or RV6 > 35 mm) is not a specific indicator of LVH[*] ( Fig. 6-11 ).



Sometimes LVH produces tall R waves in lead aVL. An R wave of 11 to 13 mm (1.1 to 1.3 mV) or more in lead aVL is another sign of LVH[*] (see Fig. 6-9 ). Sometimes a tall R wave in lead aVL is the only ECG sign of LVH, and the voltage in the chest leads is normal. In other cases, the chest voltages are abnormally high, with a normal R wave seen in lead aVL.



Just as RVH is sometimes associated with repolarization abnormalities, so ST-T changes are often seen in LVH. Figure 6-12 illustrates the characteristic shape of the ST-T complex with LVH. Notice that the complex usually has a distinctively asymmetric appearance, with a slight ST segment depression followed by a broadly inverted T wave. In some cases, these T wave inversions are very deep. This LVH-related repolarization abnormality is usually best seen in leads with tall R waves (see Fig. 6-10 ).



With LVH, the electrical axis is usually horizontal. Actual left axis deviation (i.e., an axis -30° or more negative) may also be seen. In addition, the QRS complex may become wider. Not uncommonly, patients with LVH eventually develop an incomplete or complete left bundle branch block (LBBB) pattern. Indeed, most patients with LBBB have underlying LVH (seeChapter 7 ).



Finally, signs of LAA (broad P waves in the limb leads or wide biphasic P waves in lead V1) are often seen in patients with ECG evidence of LVH. Most conditions that lead to LVH ultimately produce left atrial overload as well.

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 (arrow), formerly referred to as a “strain” pattern, is also present in these leads. Similar ST-T changes may occur with ischemia, digitalis effect, and so on. In addition, enlargement of the left atrium is indicated by a biphasic P wave in lead V1 and a broad, notched P wave in lead II.

FIGURE 6-11  Tall voltages in the chest leads (SV1 + RV5 = 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 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.” Similar findings may occur with ischemia or other factors.

In summary, the diagnosis of LVH can be made with reasonable certainty from the ECG if you find high QRS voltages and associated ST-T changes. In addition, signs of LAA are often present. Because high voltage in the chest or limb 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 other evidence of LVH.

The recognition of LVH is clinically important for two reasons:



Diagnostically, LVH is a clue to the presence of a potentially life-threatening pressure or volume overload state. The two most common and important pressure overload states are systemic hypertension and aortic stenosis. The three major clinical conditions associated with left ventricular volume overload are aortic regurgitation, mitral regurgitation, and dilated cardiomyopathy. LVH patterns may also occur with hypertrophic cardiomyopathies.



Prognostically, patients with LVH from any cause are at increased risk for major cardiovascular complications, including congestive heart failure and serious atrial or ventricular arrhythmias.

*  Other LVH criteria (the Cornell voltage criteria) based on voltages in leads V3 and aVL have been suggested: for men, SV3 + RaVL > 28 mm; for women, SV3 + RaVL > 20 mm.
*  Occasionally, LVH develops with an electrically vertical axis. In this situation, a qR pattern with a tall R wave (exceeding 20 mm) may appear in lead aVF. An LVH pattern with a vertical or especially a more rightward QRS axis should suggest biventricular hypertrophy.
*  The voltage criteria used in this chapter to diagnose LVH in the chest and limb leads are by no means absolute numbers. In fact, many different criteria have been proposed (see Bibliography ).



The ECG findings associated with enlargement of each of the four cardiac chambers have been presented. In some cases, combined patterns are seen on the same tracing (e.g., LAA and RVH in mitral stenosis, LAA and LVH in systemic hypertension). If hypertrophy is present in both ventricles, the ECG usually shows mainly evidence of LVH. Another pattern that may provide an important clue tobiventricular hypertrophy is LVH with right axis deviation.

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.[*]

*  The diagnostic limitations of the ECG are discussed further in Chapter 23 .



Cardiac dilation refers to the stretching of muscle fibers, with enlargement of one or more of the cardiac chambers. Cardiac hypertrophy refers to an abnormal increase in the actual size of the heart muscle fibers. The ECG can indicate either right or left atrial dilation or hypertrophy but generally only right or left ventricular hypertrophy.

Right atrial abnormality (RAA), or right atrial overload, may be associated with tall peaked P waves exceeding 2.5 mm in height. These waves are usually best seen in leads II, III, aVF, and sometimes V1or V2.

Left atrial abnormality (LAA), or left atrial enlargement, is manifested by wide, sometimes notched P waves of 0.12 second or more duration in one or more of the limb leads. A biphasic P wave with a prominent, wide negative deflection may be seen in lead V1.

Right ventricular hypertrophy may produce any or all of the following:



A tall R wave in lead V1, equal to or larger than the S wave in that lead



Often, right axis deviation



T wave inversions in the right to middle chest leads.

With left ventricular hypertrophy (LVH), any or all of the following may occur:



The voltage of the S wave in lead V1 plus the voltage of the R wave in lead V5 or V6 often exceeds 35 mm (SV1 + RV5 or RV6 > 35 mm).



A high-voltage R wave (11 to 13 mm or more) is seen in lead aVL when the QRS axis is horizontal. (More rarely, when the axis is vertical, lead aVF may show a tall R wave exceeding 20 mm as part of a qR complex.)



Repolarization abnormalities include inverted T waves in leads with tall R waves. (Similar findings may occur with ischemia.)



Other findings often include LAA, left axis deviation, and left ventricular conduction delay (wide QRS), which may eventually progress to incomplete or complete left bundle branch block.

The diagnosis of LVH should not be made solely on the basis of high voltage in the chest leads because these high voltages may occur normally, particularly in young adults, athletes, and thin individuals. In addition, enlargement of any of the four cardiac chambers can be present without diagnostic ECG changes. Echocardiograms are more sensitive and more specific in assessing chamber enlargement than the ECG is.





Examine the ECG shown below and answer the following questions:




What is the heart rate?



Name two abnormal findings.



True or false: Echocardiography is more sensitive and specific than the ECG in assessing chamber enlargement.

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