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