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How to miss left ventricular hypertrophy in ECG ?

Posted May 29 2011 8:04am

LVH can be diagnosed with fair degree of  accuracy  by surface ECG . We have a set criteria .The Estes  scoring is  the most popular. Very rarely we have all  the classical features of LVH in a given ECG .

With the advent of echocardiography ECG diagnosis of LVH has become redundant . Still , it is essential to  build the  foundations  in cardiology  for the current generation cardiologists.

The following are the  magnified views from the above   ECG

High Voltage

High voltage QRS is a hall mark of LVH .It increases in both chest  and  limb leads .In chest leads , both R and S wave gets amplified , while in limb leads only the R wave  is taller . We have to sum up R  from lead  V 5 and S from V2  (Practically any deep S and tall R can be added . LVH is diagnosed  if  sum qrs voltage  is  >35 mm . Voltage criterias in limb leads do not require these  addition business . An  R wave amplitude > 11mm  in limb leads by itself  would indicate an LVH (In the absence of bundle blocks )

Pit falls in voltage  criteria

It is our belief    qRS voltage  would faithfully   reflect the   quantum of cardiac muscle mass ,  but in general  to equate qRS voltage  to myocardial  mass  is   a  huge error we make ! (Of course  It  may be true in  some cases  following MI )  .

The qRS  voltage is determined by   numerous  factors (Important ones are :  chest wall thickness , age , LV cavity size ,  amount of blood inside LV cavity,  heart rate , conduction delays  etc ) This is the reason a 10-year-old boy’s   ECG will  satisfy the criteria of LVH  by 100 % .Do not ever report a ECG without knowing the age of the patient .

At high heart rates R wave amplitude increases (Broddy effect ) due to high conductance of blood

Chest lead always balances RV and LV forces .One can mask the other .So be ready for surprises when you find a perfectly normal ECH in bi-ventricular  hypertrophies ) A balancing act !

Mini summary : Never diagnose LVH with high voltage alone

Left axis deviation

The axis deviation is again non specific  . The LV mass shifts the mean axis to left (Beyond -15 degrees) .The axis shift would also be contributed by mild forms of LAFB . This  fascicle  which criss crosses the LVOT  easily gets injured to hemodynamic stress ( or rather insulted ) and  lose its function . So its job is  transferred to  the posterior fascicle  which  shoots  towards  anterior and superior and left , hence the  left axis deviation) .The LAFB is generally a benign defect unless it occurs in an acute fashion as a response to ischemia.

Mini summary : Never diagnose LVH on the basis of left axis alone

Left Atrial  abnormality

This need not be present in every one with LVH . It happens only  if  LVH  is associated with relaxation defect , when   it calls for  LA’s  assistance .(In other words , presence  of LAE in hypertensive  patients is  a  sure and simple way to confirm diastolic dysfunction ) . Similarly absence of  LAE (  with a   significant LVH )  is a good sign as the LV is able to tackle the hypertensive stress in solo fashion in all likely hood free from significant diastolic dysfunction.

Apart from LAE , note also the p wave encroaches good part of PR interval .

Mini summary : LAE can be very useful parameter to diagnose LVH . (Is it not ironical  to note   LAE is more reliable to diagnose LVH ! . This is because qrs morphology is unreliable as it influenced by many factors  while p wave  changes are  not subjected to such influence )

Secondary repolarization changes

We know ventricular depolarization and repolarization are interlinked phenomenon .Both  occur in  opposite directions still  , able to  record   ECG deflection  in same direction  (positive QRS/positive T)  . This is due to the fact  the epicardium and endocardium has  action potential with different velocities . At times of   LVH this epicardial  , endocardial heterogeneity in repolarization becomes void. (Note : This is a simplified statement of a complex repolarization process)

Because of this the repolarization is recorded opposite to that of depolarization .Hence we get all sorts of secondary ST /T changes. (The  term secondary is used to denote secondary to alteration  in depolarisation ).

Many times  all of the following  could   mean the same  in the bed side clinical parlance !

  • Secondary ST/T changes
  • Non specific ST/T ,
  • LV strain
  • LV systolic over load etc .

Note : Primary ST depression occurs in true ischemia without any alteration in LV Mass or conduction defect.

*** For advanced readers  only : Some of the ST depression that occur in ischemia could again be secondary changes. This  needs further reading.

Echo is the gold standard for diagnosing LVH .There are two definitions .

  1. Based on septal thickness
  2. Based on LV mass*

LV mass > 200mg in men and 175mg in women is considered LVH . LVH based on LV mass is  ideal . But can be misleading in a dilated heart where the mass may be increased with a  relatively   thinned  out IVS .

Final message

There are numerous  ways to miss    LVH in ECG,  But the definite way  for not missing  is by echocardiogram !

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