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Atrial and Ventricular Overload/Enlargement
The first six chapters have been devoted to the basics of electrocardiograms (ECGs). From this point on, we focus attention primarily on the recognition and understanding of abnormal ECG patterns. This chapter discusses the ECG manifestations of enlargement and related abnormalities of the four cardiac chambers.
As a prelude, we emphasize that in the detection of cardiac chamber size the ECG offers only an indirect assessment. The criteria that will be discussed—for chamber dilatation and hypertrophy—have limited sensitivity and only moderate specificity (see Chapter 24 ). A person may have underlying cardiac enlargement that does not show up on the ECG. Conversely, the ECG may show very high voltage in the healthiest of individuals (young athletes) who do not have a pathologic increase in muscle mass. When the presence or degree of cardiac chamber enlargement must be determined with more precision, an echocardiogram should be considered. For some suspected conditions, such as arrhythmogenic right ventricular cardiomyopathy or apical hypertrophic cardiomyopathy, a cardiac magnetic resonance imaging (MRI) study may also be indicated.
Cardiac enlargement describes situations in which one or more of the heart’s chambers becomes bigger because of an increase in its cavity volume, wall thickness, or both. When cardiac enlargement occurs, the total number of heart muscle fibers does not increase; rather, each individual fiber becomes larger ( hypertrophied ). With dilation, the heart muscle cells tend to become longer (termed eccentric hypertrophy ). With enlargement resulting from increased wall thickness, the cells tend to become wider (termed concentric hypertrophy ). One predictable ECG effect of advanced cardiac hypertrophy is an increase in the voltage or duration of the P wave or of the QRS complex. Increased wall thickness and chamber dilation often occur together, as with long-standing, severe hypertension.
Chamber enlargement usually results from some type of chronic pressure or volume load on the heart muscle. Classically, pressure loads (e.g., due to systemic hypertension or aortic stenosis) cause an increase in wall thickness. In contrast, volume loads (e.g., due to valve regurgitation or dilated cardiomyopathy) are associated primarily with ventricular and atrial dilation. In rarer cases, cardiac enlargement can result from genetic abnormalities or idiopathic (unknown) causes. Examples include arrhythmogenic right ventricular cardiomyopathy ( Chapter 21 ) and hypertrophic cardiomyopathy syndromes ( Chapter 9 ).
Pathologic hypertrophy resulting from increases in wall thickness or chamber dilation is often accompanied by fibrosis (scarring) and changes in myocardial geometry (remodeling), which may both worsen myocardial function and promote arrhythmogenesis (e.g., atrial fibrillation and sustained ventricular tachycardia), as well as chronic heart failure with low or preserved ejection fraction. Furthermore, pathologic alterations in the autonomic nervous system, inadequate myocardial perfusion, and disturbances in the extracellular matrix system and the renin–angiotensin–aldosterone axis may all play roles in the perturbations linking hypertrophy and fibrosis of heart muscle cells with dysfunction of other organs.
Right Atrial Abnormality/Overload
Overload of the right atrium may increase the voltage of the 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. 7.1 .)
Normally, at rest, the P wave in every lead is less than 2.5 mm (0.25 mV) in amplitude and less than 120 msec (or three small box widths). During exercise, P wave amplitude in lead II (or its equivalent) may increase transiently as a physiologic finding.
Overload of the right atrium in pathologic conditions may produce an abnormally tall P wave (2.5 mm or more), as a sustained finding. Occasionally, right atrial abnormality (RAA) a
a Note that we prefer the designations atrial abnormality or overload (right or left) to enlargement given the fact that the ECG only offers indirect evidence of anatomic size. Many electronic (and human) readouts conflate actual atrial enlargement or hypertrophy with chamber abnormality or overload. Extremely prominent P waves are the most likely to be associated with echocardiographic chamber enlargement. Thus a cautious ECG reading might be: “The very wide (140 msec) P waves in lead II, with broad (80 msec) negative components in V 1 , are consistent with left atrial abnormality and probable enlargement.” Or, in another case: “The very tall (4 mm) P waves in lead II and V 1 are consistent with right atrial overload and probable enlargement.”
will be associated with a deep (negative) but narrow P wave in lead V 1 because of the inferior location of the right atrium relative to this lead. This finding may cause confusion, sometimes leading to a false-positive identification of 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 [120 msec], or three small box lengths). The abnormal P wave in RAA has been referred to as P pulmonale because the atrial enlargement that it signifies often occurs with severe pulmonary disease ( Figs. 7.2 and 7.3 ). This term, although outmoded, is still used and most frequently encountered in older texts and articles.
The tall, narrow P waves characteristic of RAA are usually seen best in leads II, III, aVF, and sometimes V 1 . The ECG diagnosis of RAA can be made by finding a P wave exceeding 2.5 mm in any of these leads. Echocardiographic evidence, however, indicates that a tall, peaked P wave does not consistently correlate with RA overload/abnormality. On the other hand, patients may have actual right atrial overload and not show tall P waves. In other words, tall, peaked P waves are of limited sensitivity and specificity in the diagnosis of right atrial overload syndromes (see Chapter 24 ).
RAA is seen in a variety of important clinical settings. It is usually associated with right ventricular enlargement. Four of the most important are (1) acquired pulmonary disease, (2) congenital heart disease, (3) acquired tricuspid valve disease, and (4) cardiomyopathy such as arrhythmogenic right ventricular cardiomyopathy/dysplasia. The pulmonary disease may be acute (bronchial asthma, pulmonary embolism), chronic (emphysema, bronchitis, pulmonary hypertension), or combined (chronic obstructive lung disease with an exacerbation resulting from pneumonia). 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. RAA may also result from acquired disease of the tricuspid valve, including regurgitation (e.g., from endocarditis) and stenosis (e.g., with rheumatic heart disease or with carcinoid syndrome).
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