Search our site 
 
Advanced Search
 
Home | Exam dates | Contact us | About us | Testimonials |
 
 

map
You are in Home >> Resources >> Clinical anaesthesia >> ECG interpretation


Hypertrophies

Created: 29/8/2006
Updated: 11/6/2007
 

Ventricular hypertrophy

In general, the limb leads are less useful in diagnosing ventricular hypertrophies. Lesser degrees of hypertrophy (especially right ventricular hypertrophy) may be present without any ECG changes or with non-specific changes only.

The left ventricular wall thickness is about three times greater than the right ventricular free wall. This results in the left ventricular muscle mass generating a voltage that is 10 times greater than the right ventricular voltage. Thus, left ventricular hypertrophy (LVH) produces an exaggeration of the normal QRS complex, whereas right ventricular hypertrophy (RVH) alters the QRS pattern in the various ECG leads. Secondary ST-T segment and T wave changes follow the primary QRS changes in both RVH and LVH.


Left ventricular hypertrophy (LVH)

In addition to the higher voltage contribution made by the bulky left ventricle, the thicker LV wall also results in prolongation in the time taken for the depolarisation wave to travel from endocardium to epicardium. This time, called the "ventricular activation time" or the "intrinsicoid deflection time" is measured from the onset of the QRS complex to the peak of the R wave. It is measured only in left precordial leads showing a qR complex.

Criteria for left ventricular hypertrophy (LVH):
(assuming normal calibration)

1) The R waves in any one or more of the leads V4, V5 or V6 exceeds 27 mm.
2) The tallest R wave in any of the leads V4, V5 or V6 plus the deepest S wave in any of the leads V1, V2 or V3 exceeds 40 mm.
3) The S waves in one or more of the leads V1, V2 or V3 exceeds 30 mm.
4) The R wave in aVL exceeds 13 mm.
5) The ventricular activation time (e.g. in V6) = 0.05 s.
6) Abnormal ST segment depression (>1 mm below the isoelectric line) in any lead facing the left ventricle (i.e. V4, V5 or V6 and in leads I and aVL when the heart is horizontal or in leads II and aVF when the heart is vertical).
7) T wave inversion in leads facing the left ventricle (as in point 6 above).

In general, the greater the number of criteria listed above that are fulfilled, the more likely is the diagnosis of LVH.


Click here for a larger image

In this example of LVH, the precordial leads do not meet the usual voltage criteria or exhibit significant ST segment abnormalities. The frontal plane leads, however, show voltage criteria for LVH and significant ST segment depression in leads with tall R waves. The voltage criteria include: 1) R in aVL >11 mm; 2) R in I + S in III >25 mm; and 3) (RI+SIII) - (RIII+SI) >17 mm (Lewis Index).


Associated features in LVH:

1) Left ventricular complexes ("qR" complexes) may appear further to the right in the precordial leads than the usual V4 –V6 - i.e. there is often counterclockwise cardiac rotation. This is because of an increase in the physical size of the left ventricle, resulting in more of the LV lying beneath the chest leads.
2) Usually, LVH results in a slight shift of the mean QRS axis towards the left. However, the axis usually remains within the normal range and typically between +30° and -30°.
3) ECG evidence of left atrial hypertrophy usually accompanies that of LVH.
4) Prominent U waves are often seen in the right and mid-precordial leads.


Left ventricular "strain" patterns:

Hypertrophy of the left ventricle can occur due to conditions causing a systolic overload - e.g. aortic stenosis or conditions causing a diastolic overload, such as aortic regurgitation.
 
The so-called "s"ystolic overload pattern is one in which the "S"T segment and T wave changes are relatively more prominent than the QRS changes.

Conversely, in the so-called diastolic overload pattern, the QRS changes are relatively more prominent than the ST-T wave changes. These are ill-defined concepts and not very reliable.

Clinical significance:

Systemic hypertension is the most common cause of recognisable LVH. Other causes include aortic stenosis, aortic incompetence, coarctation of the aorta, mitral incompetence and hypertrophic cardiomyopathy.



Click here for a larger image

Right ventricular hypertrophy (RVH)

The most obvious consequence of RVH is an increase in the voltage of the R wave in the right precordial leads. The most diagnostic feature is a "dominant R wave" in V1. The term "dominant R wave" (seen in V1) means that, whatever the configuration of the QRS complex in V1, the largest wave in that QRS complex is an R wave. Thus, the most readily understood configuration of the QRS complex in V1 is an "Rs" complex.

Unlike LVH, RVH is accompanied by deviation of the axis beyond the normal range, resulting in right axis deviation.

Diagnostic criteria for right ventricular hypertrophy (RVH):

1) Mean QRS axis more positive than +90°.
2) Dominant R wave in V1 (Rs, R, RR’, qR or qRS).
3) Absence of evidence of anterolateral infarction.
4) QRS duration must be less than 0.12 s.




Note the qR pattern in the right precordial leads. This suggests right ventricular pressures greater than left ventricular pressures. The persistent S waves in lateral precordial leads and the right axis deviation are other findings in RVH.


Additional features frequently present in RVH:

1) ST segment depression and T wave inversion in some of the leads V1-V4.
2) Deep S waves in V5, V6 and also in leads I and aVL.
3) Evidence of right atrial hypertrophy.


Clinical significance:

RVH is predominantly caused by conditions that produce a RV systolic overload. These include pulmonary stenosis, pulmonary hypertension and Fallot’s tetralogy. Chronic cor pulmonale gives rise to RVH relatively rarely.

Diastolic overload of the right ventricle occurs in atrial septal defect, anomalous pulmonary venous return and tricuspid incompetence. The ECG changes of RV diastolic overload are indistinguishable from those in complete or incomplete RBBB.

Biventricular hypertrophy

This may be impossible to diagnose from an ECG because of the increased electrical forces, due to RVH and LVH cancelling each other (being directed in opposite directions). If they both are enlarged to different extents, the pattern may be that of the more dominant ventricle.

Essential features of biventricular hypertrophy are:

1) It may exist without any ECG changes.
2) Total QRS duration may be prolonged to 0.10 or 0.11 s.
3) T wave inversion may be present in the precordial leads.
4) The combination of signs of LVH with an axis more positive than +90° is suggestive of biventricular hypertrophy.
5) Occasionally, the combination of signs of RVH with an axis more negative than -30° is present.


Atrial hypertrophies

Important normality to be remembered:

a) In lead V1, the right atrial phase of depolarisation gives rise to a positive wave and the left atrial phase gives rise to a negative wave.

This results in a biphasic P wave in V1, in which the initial part of the P wave is the right atrial component and the latter part is due to the left atrial component.

b) In lead II, both the right and the left atrial phases of depolarisation give rise to positive waves. This results in an upright P wave in lead II.

Right atrial hypertrophy (RAH)

In RAH, the right atrial component of the P wave is increased in both voltage and duration. This component being a positive deflection in leads II and V1, the P wave height is increased in both of these leads.

However, because right atrial depolarisation is normally complete well before left atrial depolarisation is completed, the delay in completion of right atrial depolarisation is not sufficient to prolong it beyond the end of left atrial depolarisation. Hence, the P wave duration is not increased.


Criteria for right atrial hypertrophy:

P wave height = 3 mm in leads II, III or aVF.

An additional feature is that the positive part of the "P" wave in V1 is usually >1.5 mm in height and there is usually also evidence of RVH.


Click here for a larger image

RAH is recognised by the tall (>2.5 mm) P waves in leads II, III, aVF. RVH is likely because of right axis deviation (+100°) and the Qr (or rSR') complexes in V1-2.


Left atrial hypertrophy (LAH)

In LAH, the left atrial component of the P wave is increased in voltage and duration. Since the terminal part of the normal P wave is produced by left atrial depolarisation, it follows that the total P wave duration is prolonged in LAH.

Criteria for LAH:

Either (more likely, both) of the following criteria suggest the diagnosis:
1) The P wave is notched and exceeds 0.12 s in duration in leads I, II, aVF or aVL.
2) The P wave in V1 has a dominant negative component (i.e. either it is entirely negative or, alternatively, the terminal negative component exceeds the initial positive component).


Click here for a larger image

The P wave is notched, wider than 0.12 s and has a prominent negative (posterior) component in V1 - all criteria for left atrial abnormality or enlargement. The PR interval is >0.20 s. Minor ST-T wave abnormalities are also present.


Bi-atrial hypertrophy

Even the presence of only one of the criteria listed below suggests the diagnosis:

1) P waves in limb leads which are both = 3 mm in height AND >0.12 s in duration.
2) Large biphasic P wave in V1 with an initial upright portion = 2 mm in height AND a terminal negative portion at least 1 mm deep and 0.04 s in duration.
3) Tall peaked P waves = 2 mm in height in V1 in combination with wide, notched P waves (> 0.12 s in duration) in the limb leads or in the left precordial leads.


ArticleDate:20060829
SiteSection: Article
 
   
    
                                            
  Posting rules

     To view or add comments you must be a registered user and login  




Login Status  

You are not currently logged in.
UK/Ireland Registration
Overseas Registration

  Forgot your password?








 
All rights reserved © 2020. Designed by AnaesthesiaUK.

{Site map} {Site disclaimer} {Privacy Policy} {Terms and conditions}

 Like us on Facebook 

vp