Atrial and Ventricular Enlargement

Published on 02/03/2015 by admin

Filed under Cardiovascular

Last modified 02/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3448 times

Chapter 6 Atrial and Ventricular Enlargement

Please go to expertconsult.com for supplemental chapter material.

The basics of the normal ECG have been described in the first five chapters. From this point, attention is focused primarily on abnormal ECG patterns. This chapter discusses the effects on the ECG of enlargement (and related types of overloads) of the four cardiac chambers.

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

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. In rarer cases, cardiac enlargement can result from genetic abnormalities. Examples include arrhythmogenic right ventricular cardiomyopathy (“dysplasia”) (Chapter 19) and hypertrophic cardiomyopathy syndromes (Chapter 8).

Pathologic hypertrophy and dilation are often accompanied by fibrosis (scarring) and changes in myocardial geometry (remodeling) that may worsen myocardial function and lead to arrhythmias and chronic heart failure (CHF). The autonomic nervous system, inadequate myocardial perfusion, the nitric oxide system, and the renin-angiotensin axis may all play roles in the complicated perturbations linking hypertrophy and fibrosis of heart muscle cells with axis and dysfunction of other organs.

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.)

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).

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.

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