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ECG tutorial: Chamber enlargement and hypertrophy

ECG tutorial: Chamber enlargement and hypertrophy
Literature review current through: Jan 2024.
This topic last updated: Jun 08, 2022.

INTRODUCTION — This topic will discuss electrocardiographic (ECG) manifestations of cardiac chamber enlargement or cardiac muscular hypertrophy.

LEFT ATRIAL ABNORMALITY/ENLARGEMENT — Atrial activation occurs after impulse formation from the sinus node. Normally, activation of the right atrium occurs first, followed by left atrial activation, sometimes leading to slight physiologic notching of the P wave. Left atrial enlargement is manifested as the P wave on the surface ECG becoming broadened and often substantially notched, with an interpeak interval >0.04 s (figure 1 and waveform 1). The voltage of the terminal portion of the P wave is increased if there is left atrial enlargement ("P mitrale"), reflecting left atrial depolarization.

Causes include:

Left atrial hypertrophy

Left atrial dilation

Left atrial distention

Left atrial scarring

Intraatrial conduction delay

Interatrial block (see 'Interatrial block' below)

These ECG changes of left atrial enlargement are most apparent in the inferior leads. Leads V1 and V2 show a deeply inverted or negative portion of the P wave (reflecting left atrial activation, which is directed posteriorly) with an area that is greater than that of the initial upright portion of the P wave (reflecting right atrial activation, which is directed anteriorly). The negative portion of the P wave in V1 is >1 mm wide and >1 mm deep at normal voltage and sweep speed settings. If the P wave in V1 is completely negative, this usually reflects left atrial abnormality, but may be normal or indicate an ectopic atrial focus or lead malposition. In lead II, the P wave is ≥0.12 s. The left atrial vector may also increase toward the left (-30° to -90°) if left atrial enlargement progresses and becomes more pronounced, resulting in a negative terminal deflection of the P wave in leads III and aVF.

As noted below, a narrow but prominent, entirely negative P wave in lead V1 may also, paradoxically, occur in certain cases of right atrial abnormality, especially when the right atrium is located below the level of the V1 electrode. In such cases, tall, peaked P waves are usually seen in the inferior leads, more typical of right atrial abnormality ("P pulmonale").

The following criteria suggest left atrial enlargement/abnormality when correlated with echocardiographic data:

Negative phase of P in V1 >0.04 s – sensitivity 83 percent; specificity 80 percent

Negative phase of P in V1 >1 mm – sensitivity 60 percent; specificity 93 percent

P-terminal force >0.04 mm/s – sensitivity 69 percent; specificity 93 percent

Notched P, interpeak interval >0.04 s – sensitivity 15 percent; specificity 100 percent

P wave duration >0.11 s – sensitivity 33 percent; specificity 88 percent

P wave/PR duration >1.6 – sensitivity 31 percent; specificity 64 percent

Interatrial block — Interatrial block reflects delay of conduction to the left atrium, usually at the level of the Bachmann bundle. Diagnosis of interatrial block versus left atrial abnormality can be difficult or impossible from the surface ECG. First degree interatrial block is recognized by a P wave ≥0.12 s, which is usually bimodal in leads I, II, or III (waveform 2). This common finding in older adults may be seen in those with no evidence of left atrial enlargement on imaging. Second degree interatrial block is defined by a pattern of changing P wave morphology from normal to interatrial block or from first to third degree interatrial block, usually after a premature atrial or ventricular contraction. It is infrequently seen. Third degree interatrial block, also infrequently seen, is due to absent conduction through the interatrial septum where conduction to the left atrium occurs through the coronary sinus musculature. The ECG criteria are a P wave ≥0.12 s, usually with a bimodal P wave in leads I and aVL, and a biphasic P wave (positive, then negative) in leads II, III, and aVF, and frequently also in V1 to V2 (waveform 3).

First degree interatrial block with a prolonged P wave duration, especially with a P wave >0.123 s, has been associated with an increase in all-cause and cardiovascular mortality [1]. Third degree interatrial block has been associated with supraventricular arrhythmias [2].

RIGHT ATRIAL ABNORMALITY/ENLARGEMENT — Delayed activation of the right atrium as a result of dilatation, hypertrophy, scarring, or a conduction abnormality leads to simultaneous activation of the right and left atria. This synchronous electrical activity has an additive effect upon the surface ECG, resulting in a relatively narrow P wave that is of increased amplitude ("P pulmonale") (figure 2 and waveform 4). The most common finding is a P wave >2.5 mm in lead II. In addition, a P wave >1.5 mm in V1 or V2 or a P wave that has a rightward axis may be seen. The amplitude of the P wave may become significantly increased in the presence of right atrial hypertrophy/overload, and it becomes peaked due to the increase in amount of depolarized tissue. If the right atrium becomes sufficiently large, it may extend toward the left, causing P waves in V1 to be inverted and giving the illusion of left atrial enlargement. In contrast to left atrial abnormality or interatrial block, the P wave duration is usually normal.

Causes include:

Right atrial hypertrophy

Right atrial dilation

Right atrial distention

Right atrial scarring

Intraatrial conduction delay

LEFT VENTRICULAR HYPERTROPHY — Pathologic left ventricular hypertrophy (LVH) is present when there is substantially increased LV muscle mass associated with concentric, eccentric, or asymmetric patterns. LVH is usually the result of an increase in systolic pressure generated by the LV in response to increased resistance to contraction; this type of pressure load most commonly occurs with long-standing hypertension or aortic outflow obstruction, particularly aortic stenosis. LVH can also be due to sustained mitral or aortic regurgitation (volume loads), dilated cardiomyopathy, or hypertrophic cardiomyopathy and its variants.

It takes longer for an electrical impulse to traverse the hypertrophied ventricular muscle, and the amplitude of the impulse is increased since there is a greater muscle mass. Thus, the QRS complex has an increased amplitude and is often slightly widened, reflecting an intraventricular conduction delay (waveform 5A-B) (see "Left ventricular hypertrophy: Clinical findings and ECG diagnosis"). The widening is primarily observed as an initial slowing in the inscription of the QRS complex to >0.04 s (the time to reach the peak of the R wave is delayed); this is known as a delay in the intrinsicoid deflection. A similar pattern of tall QRS voltage may be seen in young people who have thin chest walls; however, in these patients, the intrinsicoid deflection is normal and there is no hypertrophy or delay in activation or conduction.

The changes of LVH are often associated with other ECG abnormalities, including:

Left atrial abnormality

Left axis deviation due to the increased mass of left ventricular muscle

ST segment and T wave abnormalities (downsloping ST segment depression and T wave inversion)

The ST-T wave abnormalities have often been termed a "strain pattern," though are now more frequently described as "LVH with associated ST-T wave abnormalities." They probably represent either subendocardial ischemia, which results from a relative lack of blood and oxygen supply to the hypertrophied muscle as demand is greater than supply, or repolarization abnormalities of the hypertrophied cardiac muscle. The changes are most frequently seen in the left lateral leads (I, aVL, V5 to V6); they may also occur in the inferior leads when a vertical heart is present.

ECG criteria — There have been multiple ECG criteria proposed for diagnosing LVH. The most popular include:

Sokolow and Lyon – Amplitude of S wave in lead V1 + amplitude of R wave in V5 or V6 (whichever is the tallest) ≥35 mm.

Cornell – Amplitude of R wave in aVL + amplitude of S wave in V3 >28 mm for men, or >20 mm for women.

Roberts – QRS voltage in all leads >175 to 225 mm.

Scott

Limb leads:

R in I + S in 3 more than 25 mm

R in aVL more than 11 mm or >18 mm if left axis is present

R in aVF more than 20 mm

S in aVR more than 14 mm

Chest leads:

S in V1 or V2 + R in V5 or V6 more than 35 mm

R in V5 or V6 more than 26 mm

R + S in any V lead more than 45 mm

Romhilt-Estes scoring system – This index gives different weights to specific findings (table 1). A score of 5 or more indicates "definite" LVH; a score of 4 indicates "probable" LVH.

Among the most specific (although not sensitive) criterion is the amplitude of the R wave in lead aVL; LVH is present when this is greater than 11 mm (or 18 mm in the presence of left axis deviation).

RIGHT VENTRICULAR HYPERTROPHY — Right ventricular hypertrophy (RVH) is present when there is a pathologic increase in muscle mass of the right ventricle. This may be seen with pulmonary hypertension, pulmonic stenosis, or severe lung disease and cor pulmonale. There are multiple criteria for the diagnosis of RVH that have been proposed [3]. However, no one set of criteria has sufficiently high sensitivity and specificity to allow it to be used to screen for RVH [4].

The RV forces become predominant in patients with RVH (especially due to a pressure load as with pulmonic outflow obstruction or severe pulmonary hypertension), producing tall R waves in the right precordial leads (V1 and V2), and deep S waves in the left precordial leads (V5 and V6) (waveform 6). Because of the increase in the amplitude of the R wave and decrease in the depth of the S wave, the R:S ratio in V1 >1 is suggestive of RVH. However, there are other causes of an increased R:S ratio in adults that must be excluded before a diagnosis of RVH can be definitively established (table 2):

Right bundle branch block

Posterior wall myocardial infarction

Wolff-Parkinson-White pattern (especially due to lateral or posterolateral left-sided pathways)

Hypertrophic cardiomyopathy (septal hypertrophy)

Early precordial transition (counterclockwise rotation)

Normal or positional variant

Obtaining an R:S ratio >1 from a right sided precordial lead (V3R or V4R) may be a more reliable indicator of RVH.

Right axis deviation (axis >+90º-100º) is often present with RVH. There also may be associated right atrial overload and ST segment and T wave abnormalities in the right precordial leads (formerly called “RV strain”), reflecting subendocardial ischemia or repolarization abnormalities of the right ventricular myocardium.

Thus, reported clues to the diagnosis of right ventricular hypertrophy include:

Right axis deviation (>+90)

R in V1 >6 mm

R in V1 + S in V5 or V6 >10.5 mm

R/S ratio in V1 >1

S/R ratio in V6 >1

Late intrinsicoid deflection in V1 (>0.035 s)

Incomplete right bundle branch block

ST-T wave abnormalities ("strain") in inferior leads

Right atrial hypertrophy/overload ("P pulmonale")

S>R in leads I, II, III, particularly in children (S1S2S3 pattern)

Clinicians should also be aware that apparent limitations in the accuracy of RVH criteria, and conflicting results in the literature, may reflect the fact that different pathophysiologic substrates give rise to very different ECG findings. Tall (normal duration) right precordial R waves (as part of R, RS, or qR morphologies) with right axis deviation, as noted above, are most likely to be associated with severe RV pressure overloads due to pulmonic stenosis (and its variants) or pulmonary hypertension from causes other than chronic obstructive pulmonary disease (COPD) (eg, primary pulmonary hypertension or recurrent pulmonary emboli). Pulmonary hypertension due to severe COPD (emphysema) may be associated with very slow R wave progression, delayed precordial transition zone, and right axis deviation. In contrast, RVH due to a classic volume load state (eg, ostium secundum atrial septal defect) may be associated with RV conduction delay and right axis deviation.

BIVENTRICULAR HYPERTROPHY — Biventricular hypertrophy is suggested on the ECG if there are voltage criteria for left ventricular hypertrophy, combined with right axis deviation, prominent R wave in V1 to V2, prominent S wave in V5 to V6, tall biphasic R/S complexes, and/or right atrial abnormality (waveform 7). In some cases, there will be evidence of left atrial enlargement or tall R wave and deep S waves in V2 to V4 (>60 mm combined) combined with criteria diagnostic of right ventricular hypertrophy, including R/S ratio >1 in V1 to V2 or S/R ratio >1 in V5 to V6, a deep S wave in V5 to V6, or right axis deviation. The latter may also be seen with mitral stenosis.

SUMMARY

There is no single best ECG criterion for diagnosis of hypertrophy or enlargement of any of the cardiac chambers. Several different sets of criteria have been used with various sensitivities and specificities.

Left atrial abnormality/enlargement is characterized by P waves that are broad and often notched, with an interpeak interval >0.04 s (figure 1 and waveform 1). The voltage of the terminal portion of the P wave may be increased, especially if there is left atrial enlargement (classical "P mitrale"), reflecting left atrial depolarization. These ECG changes are most apparent in the inferior leads and V1. (See 'Left atrial abnormality/enlargement' above.)

Right atrial abnormality/enlargement is characterized by P waves that are relatively narrow but of increased amplitude (classic "P pulmonale") (figure 2 and waveform 4). (See 'Right atrial abnormality/enlargement' above.)

Left ventricular hypertrophy is characterized by the QRS complex having increased amplitude and usually slight widening, reflecting an intraventricular conduction delay (waveform 5A-B). There are often associated ST segment and T wave abnormalities. Evidence of left atrial abnormality and left axis deviation is commonly seen. (See 'Left ventricular hypertrophy' above.)

Right ventricular hypertrophy, especially due to right ventricular pressure loads from pulmonic stenosis or pulmonary hypertension not due to chronic obstructive pulmonary disease, may be characterized by an increase in the amplitude of the R wave and a decrease in the depth of the S wave in the right precordial leads, causing an increase in the R:S ratio (waveform 6) usually with a vertical or frankly rightward QRS axis. Evidence of right atrial abnormality may be present. (See 'Right ventricular hypertrophy' above.)

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