Cardiac Hypertrophy & Enlargement
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Chapter 1: Atrial and ventricular enlargement: hypertrophy and dilatation on ECG
Cardiac chamber enlargement refers to abnormally large atria or abnormally large ventricles. These conditions are referred to as atrial enlargement and ventricular enlargement. From a hemodynamic standpoint, there are two types of enlargement, namely hypertrophy and dilatation. Both hypertrophy and enlargement may reduce atrial and ventricular function as well as predispose to significant arrhythmias. Typically, atrial enlargement predisposes to atrial fibrillation/flutter and ventricular enlargement predisposes to ventricular tachycardia. The ECG is a useful tool for detecting hypertrophy/dilatation but echocardiography and magnetic resonance imaging (cardiac MRI) are superior to the ECG in terms of sensitivity and specificity.
Nevertheless, to detect hypertrophy/dilatation using the ECG, a wide range of criteria and algorithms have been developed over the years. Most of them are easy to use and require very little calculation. Sensitivity and specificity vary markedly, as discussed in detail in the articles on left ventricular enlargement, right ventricular enlargement and atrial enlargement. Below follows a discussion on the principles and differences of dilatation and hypertrophy, as well as typical ECG changes seen in atrial and ventricular enlargement.
Dilatation is caused by volume (diastolic) overload
Volume overload (diastolic overload) causes increased pressure within the chamber and this leads to dilatation. The most common cause is valvular regurgitation (insufficiency). For example, aortic regurgitation causes the flow of blood from the aorta back into the left ventricle during diastole. The flow of blood into the ventricle causes volume overload, which exhausts the ventricle and ultimately leads to dilatation.
Hypertrophy is caused by pressure (systolic) overload
Pressure overload (systolic overload) implies that there is increased resistance across the aortic valve, making it more challenging to pump blood into the aorta. The most common causes are hypertension (in which the pressure in the aorta is increased) and aortic stenosis (in which the narrowing of the opened aortic valve orifice makes it difficult for blood to flow from the ventricle to the aorta). Hypertension and aortic stenosis result in increased afterload.
ECG changes in hypertrophy and dilatation
Increased QRS amplitudes
Hypertrophy manifests on the ECG as increased amplitudes of the QRS complexes. The explanation is straightforward: myocardial muscle mass is increased and therefore it generates greater electrical potentials. However, a dilated chamber may also bring about increased QRS amplitudes. This is because large chambers may be positioned closer to the electrodes (chest leads) which therefore observe stronger electrical potentials. However, severe dilatation (late stages) is usually associated with poor ventricular function and lower QRS amplitudes.
Hypertrophy and dilatation may coexist. Moreover, the ECG cannot distinguish whether large QRS amplitudes are due to dilatation or hypertrophy. Because the majority of the literature in the field of electrocardiology has focused on hypertrophy, the remainder of this discussion will only concern hypertrophy.
QRS duration
Hypertrophy may cause a slight prolongation of the QRS duration because it takes longer to depolarize the large ventricular mass. It does not, however, reach 0.12 s (such significant prolongation is due to intraventricular conduction defects).
Hypertrophy may also shift the electrical axis (to the right in right ventricular hypertrophy, and to the left in left ventricular hypertrophy).
ST-T segment
Significant hypertrophy may result in abnormal depolarization of the ventricular myocardium. This is presumably due to a mismatch between the expansion of contractile cells as compared with conduction cells. Therefore it is very common to observe secondary ST-T changes, characterized by ST-segment elevations and ST-segment depressions. These elevations and depressions are discordant with the QRS complex (a negative QRS is followed by a positive ST-T segment and vice versa).
The ECG may provide strong, but never conclusive, indications of hypertrophy. It is important to be able to recognize these ECG changes because hypertrophy is associated with adverse cardiovascular outcomes (increased risk of heart failure and arrhythmia), even though the patient may be asymptomatic for several years. Whenever the ECG shows signs of hypertrophy (atrial or ventricular) it is recommended that the patient be referred to echocardiography in order to elucidate cardiac function and structural characteristics.
Several ECG criteria (which, in the context of hypertrophy, are referred to as an index) have been developed and validated over the years. All these indexes have low sensitivity (virtually all <50%) but very high specificity (many around 90%). This implies that the ECG index will only detect less than 50% of patients with hypertrophy, but whenever the criteria are fulfilled it is very likely that the patient actually has hypertrophy.
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Chapter 2: ECG in left ventricular hypertrophy (LVH): criteria and implications
The following figure shows characteristic ECG changes in left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). Note that ventricular hypertrophy is primarily evident in the chest leads (V1, V2, V5 and V6), although leads aVL and I may show changes similar to those in V5 and V6.
Figure 1. ECG changes in left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). The electrical vector of the left ventricle is enhanced in LVH, which results in large R-waves in left-sided leads (V5, V6, aVL and I) and deep S-waves in right-sided chest leads (V1, V2). Right ventricular hypertrophy causes large R-waves in right-sided chest leads and deeper S-waves in left-sided leads.
Left ventricular hypertrophy (LVH)
The most common causes of left ventricular hypertrophy are aortic stenosis, aortic regurgitation, hypertension, cardiomyopathy and coarctation of the aorta. There are several ECG indexes, which generally have high diagnostic specificity but low sensitivity. These indexes were developed several decades ago but they are still in use in clinical practice. It should be noted that there are newer, more complicated, indexes that are utilized in modern ECG machines but the sensitivity and specificity are only negligibly better than the old indexes.
Figure 2. ECGs showing left and right ventricular hypertrophy.
ECG criteria (index) for left ventricular hypertrophy (LVH)
Sokolow-Lyon criteria
(RV5 or RV6) + (SV1 or SV2) > 35 mm or
RaVL > 11 mm
Sokolow-Lyon’s index is the most used index, despite having the lowest sensitivity (20%) of all indexes. The specificity is high (>85%).
Cornell-voltage criteria
Men: S(V3) + R(aVL) > 28mm
Women: S(V3) + R(aVL) > 20 mm
Sensitivity 42%, specificity 95%
Cornell product criteria
(RaVL+ SV3) • QRS duration > 2440 mVms
Presumably the best index. Sensitivity 51%, specificity 95%.
Romhilt-Este’s index
Romhilt-Este’s index, which is point-based, has been reported to have a sensitivity of 60%. 4 points make LVH probable. 5 points make LVH very likely.
| Romhilt-Este’s score system | Points |
|---|---|
| Any of the following: R or S in any limb lead ≥20 mm SV1 or SV2 ≥30 mm RV5 or RV6 ≥30 mm | 3 |
| Discordant ST-T change in a patient not on digoxin treatment | 3 |
| Discordant ST-T change in a patient on digoxin treatment | 1 |
| ECG signs of left atrial enlargement | 3 |
| Left axis deviation | 2 |
| QRS duration ≥90 milliseconds | 1 |
| Prolonged R-wave peak time: V1-V2 (right ventricle): ≥35 milliseconds V5-V6 (left ventricle): ≥45 milliseconds | 1 |
ECG changes in left ventricular hypertrophy (LVH)
Large R-waves in left-sided leads (V5, V6, I and aVL) and deep S-waves in right-sided leads (V1, V2) indicate that the vector of the left ventricle is amplified.
Secondary ST-T changes in left-sided leads – Left ventricular hypertrophy is often accompanied by J point depression, downsloping ST segment and inverted (asymmetric) T-waves in the left-sided leads. It is typical that the ST-segment bulges upwards (Figure 1 and 2) in these leads. These ECG changes were previously referred to as strain pattern because it was believed that they indicated left ventricular exhaustion. However, this term is not in use anymore because it has been shown that such ECG changes also occur in conditions where the left ventricle is not overloaded (e.g. dilated cardiomyopathy, hypertrophic cardiomyopathy). Therefore, the term secondary ST-T changes should be preferred.
Secondary ST-T changes in right-sided leads – ST-segment elevation is common in leads V1 and V2. The ST segment is typically slightly concave (Figures 1 and 2).
Prolonged QRS duration – Because it takes a longer time to depolarize a larger myocardial mass, the QRS duration may be slightly prolonged. For the same reason, R-wave peak time may also be prolonged. This prolongation may also be due to myocardial fibrosis which is typical in hypertrophy. Finally, the QRS complex may be notched.
P mitrale – Left atrial enlargement (P mitrale) may develop because LVH affects the hemodynamics of the left atrium.
Left axis deviation – is common in LVH.
QT prolongation – A slight prolongation of the QT (QTc) interval is frequently seen.
QRS amplitude is not reliable to detect left ventricular hypertrophy
All indexes are based partly on QRS amplitudes which may appear logical but it is actually a rather unreliable variable because it is affected by a range of factors not related to ventricular mass. Body configuration is the most obvious factor. Lean individuals tend to have a shorter distance between the heart and the electrodes, which therefore record the signals as stronger (as compared with an obese individual). The distance between the heart and the electrodes is greater in obese individuals, as well as those with chronic obstructive pulmonary disease (COPD, due to hyperinflation of the chest). Age is also important because QRS amplitudes diminish naturally with increasing age. Hence, young individuals have greater QRS amplitudes and some experts suggest that no index should be used in individuals aged less than 35 years. Moreover, athletes will often have large QRS amplitudes due to their ventricular remodeling, but they do not have pathological hypertrophy. Finally, women have lower QRS amplitudes than men.
Next chapter
Right Ventricular Hypertrophy
Related chapters
Overview of Hypertrophy and Dilatation
Biventricular Hypertrophy
Atrial Hypertrophy and Dilatation (P-mitrale, P-pulmonale)
Chapter 3: Right ventricular hypertrophy (RVH): ECG criteria & clinical characteristics
Figure 1. ECG changes seen in left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). The electrical vector of the left ventricle is enhanced in LVH, which results in large R-waves in left-sided leads (V5, V6, aVL and I) and deep S-waves in right-sided chest leads (V1, V2). Right ventricular hypertrophy causes large R-waves in right-sided chest leads and deeper S-waves in left-sided leads.
Right ventricular hypertrophy (RVH)
During normal circumstances, the left ventricle is many times larger than the right ventricles, which is why the QRS complex is dominated completely by left ventricular vectors. Hence, right ventricular hypertrophy must be pronounced in order to come to the expression on ECG. Moderate right ventricular hypertrophy may not alter the ECG significantly. The ECG is particularly helpful in RVH because echocardiography is less sensitive with respect to RVH, because the right ventricle is difficult to visualize clearly with trans thoracic echocardiography.
Causes of right ventricular hypertrophy
Lung disease (with increased pulmonary vascular resistance), congenital heart disease (transposition of the great arteries, pulmonary valve stenosis, atrial septal defect, ventricular septal defect), tricuspid valve regurgitation are the most common causes.
ECG changes in right ventricular hypertrophy
V1 and V2 shows larger R-waves and smaller S-waves. The R-wave may be larger than the S-wave. R-wave peak time is typically prolonged (35 to 55 milliseconds) in V1–V2. Hence, the QRS duration is slightly prolonged (but it does not reach 120 milliseconds, unless there is concomitant bundle branch block).rSR’ pattern is occasionally seen in V1–V2. This resembles, but is not, right bundle branch block (RBBB).Secondary ST-T changes are common in V1–V3. The ST-T segment is usually discordant to the QRS complex.V5, V6, I and aVL displays smaller R-waves than normal. Along with larger R-waves in right sided leads, the R-wave progression may be opposite.The electrical axis is virtually always shifted to the right. Right axis deviation is almost mandatory.S-waves are occasionally seen in leads I, II and III (SISIISIII pattern).P pulmonale is very common.
Figure 2. Two ECGs showing left and right ventricular hypertrophy.
Next chapter
Biventricular Hypertrophy
Related chapters
Overview of Hypertrophy and Dilatation
Left Ventricular Hypertrophy
Atrial Hypertrophy and Dilatation (P-mitrale, P-pulmonale)
Chapter 4: Biventricular hypertrophy ECG and clinical characteristics
Simultaneous hypertrophy of the left and right ventricle is rather common. The ECG has low sensitivity with respect to detecting biventricular hypertrophy. This is because the strong and oppositely directed forces tend to cancel each other out. However, the ECG may show features characteristic of biventricular hypertrophy.
Biventricular hypertrophy ECG
In case the ECG or other examinations suggest left ventricular hypertrophy (LVH), one should suspect concomitant right ventricular hypertrophy (RVH) if the following ECG criteria are presented:
Right axis deviation (>90°) – This never occurs in LVH.
Deep S-wave in V5 or V6 (>6 mm)
Large RS complexes in multiple leads
P pulmonale
Figure 1. ECG changes seen in left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). The electrical vector of the left ventricle is enhanced in LVH, which results in large R-waves in left sided leads (V5, V6, aVL and I) and deep S-waves in right sided chest leads (V1, V2). Right ventricular hypertrophy causes large R-waves in right sided chest leads and deeper S-waves in left sided leads.
Chapter 5: Left atrial enlargement (P mitrale) & right atrial enlargement (P pulmonale) on ECG
The atria may become dilated and/or hypertrophic during pathological circumstances. As for ventricular enlargement, the ECG cannot differentiate dilatation from hypertrophy, which is why some experts have suggested that the term atrial abnormality be used instead of enlargement. Atrial enlargement/abnormality often accompanies ventricular enlargement. The ECG has, as one could expect, low sensitivity but high specificity with respect to detecting atrial enlargement. Left atrial enlargement is also referred to as P mitrale, and right atrial enlargement is often referred to as P pulmonale. The reasons for this are explained below.
The normal P-wave contour on ECG
The normal P-wave (Figure 1, upper panel) is typically smooth, symmetric and positive. The P-wave in lead II may, however, be slightly asymmetric by having two humps. This is often (but not always) seen on ordinary ECG tracings and it is explained by the fact that the atria are depolarized sequentially, with the right atrium being depolarized before the left atrium. The first half of the P-wave is therefore a reflection of right atrial activation and the second half is a reflection of left atrial activation. This is shown in Figure 1 (upper panel). Moreover, the P-wave may be slightly biphasic (diphasic) in lead V1, implying that the terminal part of the P-wave is negative (Figure 1, upper panel). This negative deflection is generally <1 mm deep. The amplitude of the normal P-wave does not exceed 2.5 mm in any limb lead.
Reference values for the P-wave
The negative deflection of biphasic (diphasic) P-waves is generally <1 mm deep.
P-wave duration ≤0,12 seconds.
P-wave amplitude in limb leads <2,5 mm.
Figure 1. The ECG contour of the normal P-wave, P mitrale (left atrial enlargement) and P pulmonale (right atrial enlargement)
Abnormal P-waves: atrial enlargement
If an atrium becomes enlarged (typically as a compensatory mechanism) its contribution to the P-wave will be enhanced. Enlargement of the left and right atria causes typical P-wave changes in lead II and lead V1 (Figure 1, second and third panel).
P pulmonale: right atrial enlargement (hypertrophy, dilatation)
Enlargement of the right atrium is commonly a consequence of increased resistance to empty blood into the right ventricle. This may be due to pulmonary valve stenosis, increased pulmonary artery pressure etc. The right atrium must then enlarge (hypertrophy) in order to manage to pump blood into the right ventricle. Right atrial enlargement (hypertrophy) leads to stronger electrical currents and thus enhancement of the contribution of the right atrium to the P-wave. The P-wave will display higher amplitude in lead II and lead V1. Such a P-wave is called P pulmonale because pulmonary disease is the most common cause (Figure 1). The P-wave amplitude is >2.5 mm in P pulmonale.
P mitrale: left atrial enlargement (hypertrophy, dilatation)
If the left atrium encounters increased resistance (due to mitral valve stenosis, mitral valve regurgitation, hypertension, hypertrophic cardiomyopathy) it becomes enlarged (hypertrophy) which enhances its contribution to the P-wave. The second hump in lead II becomes larger and the negative deflection in V1 becomes deeper. This is called P mitrale, because mitral valve disease is a common cause (Figure 1). The duration of the P-wave will exceed 120 milliseconds in lead II.
Biatrial abnormality/enlargement
Biatrial abnormality implies that the ECG indicates both left and right atrial enlargement; i.e a large P-wave in lead II and a large biphasic P-wave in lead V1.