and Alwyn Scott2
(1)
School of Computer Science, University of Manchester, Manchester, UK
(2)
Cardiology High Dependency Unit, Papworth Hospital NHS Foundation Trust, Cambridge, UK
Keywords
HypertrophyAtrial abnormalityCardiomyopathyHeart failureVoltage criteriaCardiac resynchronization therapyBiventricular pacingBackground
Any physiological changes to the myocardium that cause a chamber to become enlarged or a chamber wall to become thicker than normal can cause ECG changes. There are several mechanisms that cause chamber enlargement and/or thickening to occur, including: hyperplasia, hypertrophy and dilation.
Hyperplasia is the rapid proliferation of cells that can increase the size of the heart. It is also one of the initial stages of tumor development. In contrast hypertrophy is an increase in the size of the cells. This is summarized in Table 4.1. Another cause for the increase in the size of a chamber is caused by dilation of the chamber. This manifests as an increase in the radius of the chamber.
Table 4.1
Hyperplasia and hypertrophy
What are hyperplasia and hypertrophy? |
|---|
 |
Hyperplasia: Cells reproduce rapidly causing the enlargement of an organ or other tissue |
Hypertrophy: Cells increase in size leading to the enlargement of an organ or tissue. |
Hyperplasia + hypertrophy: Both of these can occur together (a proliferation of larger cells). |
An increase in either pressure or volume can cause enlargement of a hearts chamber (Fig. 4.1). Pressure overload causing hypertrophy is due to the excess pressure required to eject blood from the chamber. This can be the result of systemic hypertension. Volume overload is often caused by regurgitation of blood into the chamber increasing its size by dilation. This is often seen in heart failure and valve regurgitation patients.
Fig. 4.1
Pressure and volume overload
An enlargement can occur in any of the main chambers of the heart. The changes in the size of the chambers can often be seen on the ECG. An abnormality in a chamber will show up differently on the ECG depending on which chamber is affected. It is also worth noting that several chambers can be affected in the same patient.
Atrial Abnormality
The morphology of the P wave gives the practitioner information about the atria.
If one were to draw a line through the center point of a normal P wave, the first half would represent depolarisation of the right atrium, the second half the depolarisation of the left atrium (Fig. 4.2). A normal P wave should be no more than 2.5 mm in height and width. The P wave should also be smooth and uniform in appearance. Any change in duration, amplitude or shape indicates the possibility of an abnormality.
Fig. 4.2
P wave showing activation of both the left and right atrium
Abnormality or Enlargement?
The terms abnormality and enlargement are often used interchangeably. Since we do not know if these morphological changes are caused by dilation, hypertrophy or an alteration in electrical activation it is more accurate to use the term abnormality than enlargement.
Right Atrial Abnormality
Right atrial abnormality (RAA) is also known as P. pulmonale and is identified on the ECG by a tall, peaked P wave >2.5 mm in amplitude (Figs. 4.3 and 4.4). P waves are often best observed in leads II, III and aVF. The term P. pulmonale derives from the fact that RAA is often seen in patients with pulmonary conditions, such as: pulmonary hypertension, stenosis and embolus.
Fig. 4.3
A normal P wave (left), tall peaked P wave with amplitude >2.5 mm (right)
Fig. 4.4
Tall P waves seen on rhythm strip of ECG (lead II)
Another clue can be seen in lead V1. As mentioned previously the first half of the P wave represents right atrial depolarization, the second half, left depolarization. Figure 4.5 shows a normal P wave in lead V1. Both halves of the P wave are fairly equally deflected positively and negatively.
Fig. 4.5
Normal P wave as seen in lead V1
If there is a RAA present, the first half of the P wave in lead V1 (representing right atrial depolarization) will increase its amplitude by 1.5 mm or more.
Left Atrial Abnormality
Left atrial abnormality (LAA) also known as P. mitrale as it is often associated with mitral valve disease. LAA is identified on the ECG by bifid (notched) P waves, best seen in leads II and V1. The notching of the P waves represents a letter ‘M’ in shape (Figs. 4.6 and 4.7).
Fig. 4.6
Normal P wave (left), bifid P wave, width >2.5 mm (right)
Fig. 4.7
Bifid (‘M’ shaped) P waves seen on the rhythm strip of and ECG (lead II)
In lead V1 the second half of the P wave (terminal negative portion) will be negatively deflected by more than 1 mm.
Bilateral Atrial Abnormality
This refers to the presence of both RAA and LAA on the same ECG. Tall and wide notched P waves are present. Table 4.2 summarises the main features of the different types of atrial abnormality.
Table 4.2
Summary of features of atrial abnormalities/enlargements
Abnormality/enlargement | Lead II | Lead V1 | Features |
|---|---|---|---|
Right atrial abnormality/enlargement |  |  | Tall peaked P waves with amplitude >2.5 mm in lead II. First half of the P wave in lead V1 >1.5 mm in amplitude |
Left atrial abnormality/enlargement |  |  | Bifid ‘M’ shaped P waves in lead II. Second half of P wave negatively deflected >1 mm in lead V1. |
Right/Left atrial abnormality/enlargement |  |  | Features of both left and right atrial enlargement seen together. Tall, wide bifid P waves. |
Left Ventricular Hypertrophy
One of the primary clues to the presence of left ventricular hypertrophy (LVH) is an increase in QRS voltage on the ECG (Fig. 4.8). This increase is due to the increased muscle mass of the hypertrophied ventricle, which increases the amount of time it takes for electricity pass through the muscle. The presence of large R waves on an ECG should alert the practitioner to the possibility of LVH. LVH is frequently caused by hypertension, cardiomyopathy and aortic regurgitation/stenosis. When documenting findings on the ECG it is better practice to state that voltage criteria for LVH are met, as an echocardiogram would be required to confirm the diagnosis. LVH can also prolong ventricular activation time.
Fig. 4.8
Voltage criteria for left ventricular hypertrophy
Athlete’s Heart/Physiological LVH
Sometimes voltage criteria exists for LVH without ST segment/T wave changes or any other normal signs or symptoms of LVH. This is a normal variant and is often seen in the young, tall thin people and athletes hence the name ‘athlete’s heart’ that is often used to describe this variant (Fig. 4.9). When presented with tall R waves practitioners should also be aware of other potential causes as well as hypertrophy. A summary of these can be seen in Table 4.3.
Fig. 4.9
‘Athletes heart’
Table 4.3
Other causes of tall R waves on the ECG
Other causes of tall R waves |
|---|
Incorrect ECG machine calibration |
Normal variant |
Right bundle branch block (RBBB) |
Ventricular rhythms originating in the left ventricle |
Posterior Myocardial Infarction (MI) |
Wolff-Parkinson-White syndrome (WPW) |
Dextrocardia |
Intrinsicoid Deflection/Ventricular Activation Time (VAT)
The intrinsicoid deflection or ventricular activation time (VAT) is often prolonged in the presence of an intraventricular conduction delay or ventricular hypertrophy. The VAT is measured from the start of the Q wave or R wave to the peak of the R wave (Fig. 4.10). This measure indicates the time it takes for an electrical impulse to reach the hearts surface below the electrode, measured in seconds.
Fig. 4.10
Intrinsicoid deflection/ventricular activation time
The normal time in seconds is around 0.02 s in V1 and 0.04 s in leads V5 or V6 (Table 4.4). Any increase means there was a delay in impulse travel time. In the case of ventricular hypertrophy this is caused by the increased time it takes for the impulse to travel through the enlarged chamber.
Table 4.4
Summary of VAT normal ranges
Ventricular activation time (normal ranges) |
|---|
Lead V1 |
< 0.03 s |
Ventricular Hypertrophy Evaluation Methods
There are numerous methods available to help clinicians evaluate ventricular hypertrophy. These methods vary in complexity and precision. The authors would recommend learning the method that is the most appropriate for their clinical role and the one they find the most practical to use and remember. The various scoring systems and criteria are summarised in Tables 4.5, 4.6 and 4.7.
Table 4.5
The Sokolow-Lyon criteria for LVH
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