Left Ventricular Hypertrophy

Left ventricular hypertrophy causes several changes on the EKG. The enlarged ventricle causes increased R wave amplitude in the leftward leads (and increased S wave amplitude in the rightward leads), prolonged depolarization leading to prolonged R wave peak time (time from beginning of QRS complex to peak of R wave), and delayed repolarization (ST/T abnormalities-'LV strain') in the lateral leads. The repolarization abnormalities should be discordant to the QRS complex (ST elevation in rightward leads and ST depression in leftward leads). The QRS amplitude and 'strain' changes are often relative to the patient's blood pressure at the time of EKG capture and are the primary exception to ischemia being the sole cause of dynamic changes. if the patient has significant hypertension while the first EKG is being obtained, the QRS amplitude and ST/T changes will be more significant. If the patient's blood pressure decreases during their course, the amplitude and ST/T changes will be decreased (you will see dynamic changes with changes in blood pressure). These usually lead to left axis deviation as well.

Voltage Criteria

There have been numerous criteria that have been developed over the years. Ultimately, the criteria are not very sensitive, though are fairly specific, for the presence of LVH. I do not have all of these memorized, but a select few.

Limb leads:

R wave in aVL>11mm
R wave in aVF>20mm
S wave in aVR>14mm
R wave in I + S wave in III>25mm

Precordial leads:

R wave in V4, V5, or V6>26mm
R wave in V5 or V6 + S wave in V1>35mm
largest R wave + largest S wave>45mm

Examples:

Ischemia Evaluation in the Setting of LVH

Ischemia can be very difficult to evaluate in the setting of LVH. As mentioned above, LVH naturally produces discordant ST/T changes that can be dynamic with the patient's blood pressure. At this time, there are no absolute criteria to be able to detect NOMI in the presence of LVH. The best advice would be to use old EKG's (if available) and the patient's presentation to evaluate the possibility of acute myocardial infarction.

However, concordant changes should not be present and do strongly suggest OMI. The ST elevation is usually concave in patients without ischemia. Additionally, the degree of ST deviation relative to the QRS amplitude should be used to evaluate for AMI. ST deviation>25% of the R or S wave (whichever is larger) amplitude is concerning for ischemia. The ST depression in the lateral leads usually has a downsloping morphology in LVH; if the ST segment is flat, that is also a potential sign of ischemia. Furthermore, 'normal' ST segments in the setting of LVH may be concerning ('pseudonormalization') as one would expect to have repolarization abnormalities. Lastly, terminal T wave inversion is a good sign of acute MI.

Examples:

This EKG shows LVH by voltage criteria. Although some of the leads have repolarization abnormalities typical of this (ie V6), some of the leads have pseudonormalization (V2 and V3). This pseudonormalization in V2 and V3 is essentially ST depression (as the ST segments are isoelectric but normally are elevated).

This EKG shows LVH. There is very slight/borderline ST elevation in V5 and V6 that is convex and into a pure TWI. The ST depression in V4 is flat, which is a concerning morphology. Additionally, the ST segments in V1-V3 are isoelectric or slightly depressed.