In LVH, the muscle mass of the left ventricle enlarges. This tilts the main vector of ventricular depolarization more toward the left ventricle and, of course, increases its magnitude. As a result, the S wave in V1 becomes deeper, and the R wave in the lateral precordial leads (V5 and V6) becomes taller. It also follows that the electrical axis may be shifted more toward the left, often, but not always, resulting in LAD. Increased amplitude of the R wave is also frequently seen in limb leads I or aVL.
Figure 8.1 shows the ECG of a 38-year-old white male with longstanding severe hypertension. Note that the S wave in lead V1 is 31-mm-deep, and the R wave in lead V4 is 30-mm-tall.
Many different voltage criteria for LVH have been proposed, but most elec-trocardiographers would agree that LVH is likely if the S wave in V1 or V2 or
the R wave in V5 or V6, reaches 30 mm or more in magnitude. As always, there are many normal variants among humans. Individuals with thin chest walls (children in particular) and individuals who are the size of professional basketball players may have >30 mm of QRS voltage in the absence of LVH.
QRS duration in LVH is usually only mildly increased, if at all, toward the upper limits of normal, between 0.09 and 0.10 s. This is because, although the wall of the ventricle is thicker, the wall is still being depolarized by impulses spreading through the rather rapidly conducting Purkinje system. The function of the Purkinje system is the greater determining factor in QRS duration. Figure 8.1 shows a QRS duration of 0.09 s.
Certain changes in the ST and T waves can also develop in LVH, usually most prominently in the lateral precordial leads (V5 and V6), but also in those limb leads toward which the main vector of depolarization is traveling (electrical axis). As hypertrophy progresses, downsloping ST depression and T wave inversion can occur, which, in the fully developed pattern, is called left ventricular strain. Figure 8.2 shows a fully developed strain pattern in which the ST depression is typically upwardly convex, with a gentle transition into an inverted T wave. These ST and T wave changes are called secondary because they are secondary to the LVH, rather than directly reflecting
another primary myocardial abnormality. As you will learn later, the strain pattern can be confused with ST and T wave changes caused by myocardial ischemia, myocardial infarction, and other miscellaneous conditions, such as digitalis effect.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...