The only EKG book. 9th Ed

Chapter 2. Hypertrophy and Enlargement of the Heart

In this chapter you will learn:

1

what happens to a wave on the EKG when an atrium enlarges or a ventricle hypertrophies

2

the meaning of electrical axis and its importance in diagnosing hypertrophy and enlargement

3

the criteria for the EKG diagnosis of right and left atrial enlargement

4

the criteria for the EKG diagnosis of right and left ventricular hypertrophy

5

about the cases of Mildred W. and Tom L., which will test your ability to recognize what happens to the EKG with hypertrophy and enlargement, and why this matters

A Few Introductory Remarks

The EKG can diagnose many important and urgent problems—things that can really get your heart pumping! Hypertrophy and enlargement, alas, are—with a few exceptions—not among them. Don’t misunderstand—recognizing atrial enlargement or ventricular hypertrophy can have important clinical implications for your patients (you’ll encounter some of these in this chapter), but for genuine soul-stirring excitement it does not compare to diagnosing an evolving heart attack or a potentially lethal rhythm disturbance.

So why start here? First, because hypertrophy and enlargement are easy to understand. Second, their EKG manifestations build logically from what we have discussed so far. And third, any good book should have an appealing narrative arc, building slowly to a thrilling climax. Starting high and finishing low would not leave you at the end with that shiver down the spine, that feeling that you can’t wait to get out there into the real world and save some lives!

So, here we go—our first foray into how we can use the EKG to diagnose abnormalities of the heart.

Definitions

The terms hypertrophy and enlargement are often used interchangeably, but they are not really the same thing. Hypertrophy refers to an increase in muscle mass. The wall of a hypertrophied ventricle is thick and powerful. Most hypertrophy is caused by pressure overload, in which the heart is forced to pump blood against an increased resistance, as in patients with systemic hypertension or aortic stenosis. Just as weight lifters develop powerful pectoral muscles as they benchpress progressively heavier and heavier weights, so the heart muscle grows thicker and stronger (at least for a while) as it is called on to eject blood against increasing resistance.

Enlargement refers to dilatation of a particular chamber. An enlarged ventricle can hold more blood than a normal ventricle. Enlargement is typically caused by volume overload; the chamber dilates to accommodate an increased amount of blood. Enlargement is most often seen with certain valvular diseases. Aortic insufficiency, for example, may cause left ventricular enlargement, and mitral insufficiency may result in left atrial enlargement.

Enlargement and hypertrophy frequently coexist. This is not surprising, because both represent ways in which the heart tries to increase its cardiac output.

(A) A hypertrophied left ventricle caused by aortic stenosis. The wall is so thick that the chamber size is significantly diminished. (B) An enlarged left ventricle. The chamber is bigger, but the wall thickness is normal.

The EKG is not very good at distinguishing between hypertrophy and enlargement. However, it is traditional to speak of atrial enlargement and ventricular hypertrophy when reading EKGs.

The term atrial enlargement has been supplanted in the minds of some by the term atrial abnormalities. This change in terminology reflects the recognition that a variety of electrical abnormalities can cause the changes on the EKG characteristically associated with atrial enlargement. However, we will continue to use the term atrial enlargement in this book, both because the term is more rooted in tradition (and traditional values still matter as we race headlong through the 21st century) and because the vast majority of cases of P-wave changes are due to enlargement of the atria.

Because the P wave represents atrial depolarization, we look at the P wave to assess atrial enlargement. Similarly, we examine the QRS complex to determine whether there is ventricular hypertrophy.

Hypertrophy and enlargement can represent healthy and helpful adaptations to stressful situations, but because they often reflect serious underlying disorders affecting the heart, it is important to learn how to recognize them on the EKG. In addition, over time, the increase in muscular thickness and/or size can compromise the heart’s ability to adequately pump blood to the rest of the body, causing heart failure. Hypertrophied myocardium demands more blood supply for the overgrown heart muscle, but it has a reduced density of capillaries and is therefore more susceptible to ischemia than is normal myocardium.

How the EKG Can Change

Three things can happen to a wave on the EKG when a chamber hypertrophies or enlarges:

1. The chamber can take longer to depolarize. The EKG wave may therefore increase in duration.

2. The chamber can generate more current and thus a larger voltage. The wave may therefore increase in amplitude.

3. A larger percentage of the total electrical current can move through the expanded chamber. The mean electrical vector, or what we call the electrical axis, of the EKG wave may therefore shift.

Because the concept of axis is so important for diagnosing hypertrophy and enlargement, we need to digress for just a moment to elaborate on this idea.

(A) A normal wave. (B) The same wave when the chamber has enlarged or hypertrophied. The amplitude and duration of the wave have increased. A third alteration, a shift in the electrical axis, is discussed in the following pages.

An increase in amplitude is the most dramatic change that occurs when a chamber enlarges, and is critical to all criteria for diagnosing enlargement and hypertrophy as you will shortly see. However, be aware that very thin people, particularly those with pectus excavatum, a common congenital deformity of the anterior thoracic wall, can have abnormally large EKG waves in the precordial leads simply because the chest electrodes are so much closer to the heart and not dampened by overlying tissue.

Axis

Earlier, we discussed how the EKG records the instantaneous vector of electrical forces at any given moment. Using this idea, we can represent the complete depolarization (or repolarization) of a chamber by drawing a series of sequential vectors, each vector representing the sum of all the electrical forces at a given moment.

Because it is easier to visualize, let’s first look at ventricular depolarization (the QRS complex) before turning to atrial depolarization (the P wave) and ventricular repolarization (the T wave).

Ventricular depolarization is represented by eight sequential instantaneous vectors, illustrating how the electrical forces normally move progressively leftward. Although, for the sake of clarity, we have shown only eight instantaneous vectors, we could just as well have shown 80 or 8000.

The first vector represents septal depolarization, and each successive vector represents progressive depolarization of the ventricles. The vectors swing progressively leftward because the electrical activity of the much larger left ventricle increasingly dominates the EKG.

The average vector of all of the instantaneous vectors is called the mean vector.

The direction of the mean vector is called the mean electrical axis.

A single vector summarizes all of the instantaneous vectors. This summation vector is called the mean vector, and its direction is the axis of ventricular depolarization. Axis is defined in the frontal plane only.

The mean QRS vector points leftward and inferiorly, representing the average direction of current flow during the entirety of ventricular depolarization. The normal QRS axis—the direction of this mean vector—thus lies between +90° and 0°. (Actually, most cardiologists extend the range of normal from +90° to -30°. In time, as you become more comfortable with the concept of axis, you should add this refinement to your electrical analysis, but for now, +90° to 0° is satisfactory.)

If the QRS axis lies within the shaded quadrant, between 0° and 90°, it is normal.

We can quickly determine whether the QRS axis on any EKG is normal by looking only at leads I and aVF. If the QRS complex is predominantly positive in leads I and aVF, then the QRS axis must be normal.

Why is this?

Determining Whether the QRS Axis Is Normal

We have already discussed how any lead will record a positive deflection if the wave of depolarization is moving toward it. Lead I is oriented at 0°. Thus, if the mean QRS vector is directed anywhere between -90° and +90°, lead I will record a predominantly positive QRS complex.

Any mean QRS vector oriented between -90° and +90° will produce a predominantly positive QRS complex in lead I. Three different QRS mean vectors are shown. All three are oriented between -90° and +90°; hence, they will all produce a predominantly positive QRS complex. The three QRS complexes depicted here illustrate what lead I would record for each of the three vectors.

Lead aVF is oriented at +90°. Therefore, if the mean QRS vector is directed anywhere between 0° and 180°, lead aVF will record a predominantly positive QRS complex.

Any mean QRS vector oriented between 0° and 180° will produce a predominantly positive QRS complex in lead aVF. Three different mean QRS vectors are shown, all oriented so that lead aVF will record a predominantly positive deflection as illustrated.

You see where this is going: If the QRS complex is predominantly positive in both lead I and lead aVF, then the QRS axis must lie in the quadrant where both are positive, that is, between 0° and +90°. This is the normal QRS axis.

Another way to look at this is to take the converse approach: If the QRS complex in either lead I or lead aVF is not predominantly positive, then the QRS axis does not lie between 0° and +90°, and it is not normal.

Six different QRS axes are shown (A). Only an axis directed between 0° and +90° (shaded quadrant) will produce a predominantly positive QRS complex in both lead I and lead aVF. (B) The QRS complexes in leads I and aVF associated with each of the six axes are shown. Only axis 2 is normal and associated with a predominantly positive QRS complex in both leads, although most cardiologists would consider axis 1 and axis 3 to be normal as well.

Many electrocardiographers believe that a normal axis can extend from +90° all the way to -30°. Using this criterion, QRS complexes that are predominantly negative in lead aVF can still be normal if the QRS complexes in lead I and lead II are positive. If you can’t intuitively see this, take a colored pencil and shade in the various quadrants as we did in the preceding figure, and you’ll soon see that this criterion extends the range of a normal axis out to -30°. In point of fact, however, very rarely does a clinical decision turn on a variation of a few degrees of axis, so if you are more comfortable with the simpler definition, you are in good company and should not feel at all embarrassed. We’re going to stick with the simpler definition from here on out, just to show you that we can be good sports about it.

Defining the Axis Precisely

Although it is usually sufficient to note whether the axis is normal or not, it is possible to be more rigorous and to define the actual angle of the axis with fair precision. All you need to do is look for the limb lead in which the QRS complex is most nearly biphasic, that is, with positive and negative deflections extended equally on both sides of the baseline (sometimes, the deflections are so small that the wave appears flat, or isoelectric). The axis must then be oriented approximately perpendicular to this lead because an electrode oriented perpendicularly to the mean direction of current flow records a biphasic wave.

Thus, for example, if the QRS complex in lead III (orientation, +120°) is biphasic, then the axis must be oriented at right angles (90°) to this lead, at either +30° or -150°. And, if we already know that the axis is normal—that is, if the QRS complex is positive in leads I and aVF—then the axis cannot be -150°, but must be +30°.

QRS complexes are shown for leads I, III, and aVF. Determining the axis is easy. The QRS complex in lead III is biphasic. The axis therefore must be either +30° or -150°. However, because the QRS complex is positive in both leads I and aVF, the axis must be normal; that is, it must lie within the shaded quadrant. The axis therefore can only be +30°.

Axis Deviation: Getting More Specific About Defining Abnormal Axes

The normal QRS axis is between 0° and 90°. If the axis lies between 90° and 180°, we speak of right axis deviation. Will the QRS complex in leads I and aVF be positive or negative in a patient with right axis deviation?

The QRS complex in lead aVF will still be positive, but it will be negative in lead I.

Right axis deviation. The QRS complex is negative in lead I, whereas it is positive in aVF.

If the axis lies between 0° and -90°, we speak of left axis deviation. In this case, the QRS complex in lead I will be positive, but it will be negative in lead aVF.

Left axis deviation.

In rare instances, the axis becomes totally disoriented and lies between -90° and 180°. This is called extreme right axis deviation. The QRS complex in both lead aVF and lead I will be negative.

-90°

The axis of extreme right axis deviation is sometimes called a superior axis or a northwest axis.

Extreme right axis deviation.

SUMMARY

Axis

1. The term axis refers to the direction of the mean electrical vector, representing the average direction of current flow. It is defined in the frontal plane only.

2. To determine the axis of any wave, find the lead in which the wave is most nearly biphasic. The axis must lie approximately perpendicular to that lead.

3. A quick estimate of the axis can be made by looking at leads I and aVF:

Axis

Lead I

Lead aVF

Normal axis

Positive

Positive

Left axis deviation

Positive

Negative

Right axis deviation

Negative

Positive

Extreme right axis deviation

Negative

Negative

On the EKG below, the waves recorded by the six leads of the frontal plane are shown. Is the QRS axis normal, or is there axis deviation?

This patient has left axis deviation; the QRS complex is predominantly positive in lead I and negative in lead aVF.

Now, can you define the axis more precisely by finding the lead with a biphasic QRS complex?

The QRS complex in lead aVR is approximately biphasic; therefore, the electrical axis must lie nearly perpendicular to it, that is, at either -60° or +120°. Because we already know that the axis falls within the zone of left axis deviation (i.e., between 0° and -90°), the correct axis must be -60°.

Just as we have done for the QRS complex, so we can define an axis for the P wave and T wave on every EKG. The normal P-wave axis lies approximately between 0° and 70° in adults (between 0° and 90° in children). The T-wave axis is variable, but it should approximate the QRS axis, lying within 50° to 60° of the QRS axis.

Can you identify the axis of the QRS complex, P wave, and T wave on the following EKG?

The QRS complex: the QRS axis is about 0°. It is nearly biphasic in aVF, implying an axis of 0° or 180°. Because the QRS complex in lead I has a tall R wave, the axis must be 0°. The P wave: in lead aVL, the P wave is virtually invisible (isoelectric), so the P-wave axis must lie perpendicular to this lead and is either 60° or -120°. Since the P wave is positive in leads I and aVF, the axis must be 60°. The T wave: all of the leads with tall R waves have positive T waves. The T waves are flat in lead III, indicating an axis perpendicular to lead III (either +30° or -150°). Because there is a tall T wave in lead I, the axis must be about +30°.

Axis Deviation, Hypertrophy, and Enlargement

Why does axis deviation have anything to do with hypertrophy and enlargement? Because the concept of axis deviation is most successfully applied to ventricular hypertrophy, let’s consider what happens to the flow of electricity when a ventricle hypertrophies.

In the normal heart, the QRS axis lies between 0° and +90°, reflecting the electrical dominance of the much larger left ventricle over the right ventricle. Imagine, now, a 65-year-old man who has allowed his hypertension to go untreated for many years. He comes to see you for headaches and shortness of breath, and you discover a greatly elevated blood pressure of 190/115 mm Hg. This sustained and severe hypertension has forced the left ventricle to work too hard for too long, and it has hypertrophied. Its electrical dominance over the right ventricle has therefore become even more profound. The mean electrical vector is drawn even further leftward, and the result is left axis deviation.

With left ventricular hypertrophy, the electrical axis moves further leftward, resulting in left axis deviation.

Right ventricular hypertrophy is far less common and requires a huge change in the proportions of the right ventricle in order to overcome the electrical forces generated by the normally dominant left ventricle. It can occur, however, in patients with chronic obstructive pulmonary disease sufficiently severe to cause pulmonary artery hypertension or in patients with uncorrected congenital heart disease associated with profound volume or pressure overload of the right ventricle. If the right ventricle greatly hypertrophies, it can be detected on the EKG as a shift in the QRS axis. The mean electrical axis of current flow is drawn rightward, and the result is right axis deviation.

With right ventricular hypertrophy, the electrical axis moves rightward, resulting in right axis deviation.

This is a good time to restate the three things that can happen to a wave on the EKG with enlargement or hypertrophy:

1. The wave can increase in duration.

2. The wave can increase in amplitude.

3. The electrical axis of the wave can deviate from normal.

Specific EKG criteria for the diagnosis of atrial enlargement and ventricular hypertrophy have been devised, and these are discussed in the following pages.

Atrial Enlargement

The normal P wave is less than 0.12 second in duration, and the largest deflection, that is, voltage, whether positive or negative, should not exceed 2.5 mm. The first part of the P wave represents right atrial depolarization and the second part left atrial depolarization.

Virtually all of the information you need to assess atrial enlargement can be found in leads II and V1. Lead II is useful because it is oriented nearly parallel to the flow of current through the atria (i.e., parallel to the mean P-wave vector). It therefore records the largest positive deflection and is very sensitive to any perturbations in atrial depolarization. Lead V1 is useful because it is oriented perpendicularly to the flow of electricity and is therefore biphasic, allowing easy separation of the right and left atrial components.

(A) Normal atrial depolarization. (B) The normal P wave in leads II and V1. The first part of the P wave represents right atrial depolarization, and the second part represents left atrial depolarization.

Right Atrial Enlargement

With right atrial enlargement, the amplitude of the first portion of the P wave increases. The width does not change because the terminal component of the P wave is left atrial in origin, and this remains unchanged.

Enlargement of the right atrium may also cause the right atrium to dominate the left atrium electrically. The vector of atrial depolarization may swing rightward, and the P-wave axis may move rightward toward or even beyond +90°. The tallest P wave may therefore appear no longer in lead II, but in lead aVF or lead III.

The classic picture of right atrial enlargement is illustrated in leads II and V1, below, and has been called Ppulmonale because it is often caused by severe lung disease.

(A) The normal P wave in leads II and V1. (B) Right atrial enlargement. Note the increased amplitude of the early, right atrial component of the P wave. The terminal left atrial component, and hence the overall duration of the P wave, is essentially unchanged.

Right atrial enlargement is diagnosed by the presence of P waves with an amplitude exceeding 2.5 mm in at least one of the inferior leads II, III, and aVF.

Left Atrial Enlargement

With left atrial enlargement, the second portion of the P wave may increase in amplitude. The diagnosis of left atrial enlargement requires that the terminal (left atrial) portion of the P wave should drop more than 1 mm below the isoelectric line in lead V1 (remember that lead V1 overlies the right heart, so when an enlarged left atrium depolarizes, the result will be a larger negative deflection in lead V1).

However, a more prominent change in the P wave is an increase in its duration. This occurs because left atrial depolarization represents the terminal portion of the P wave, and prolonged depolarization can be readily seen (with right atrial enlargement, prolonged depolarization of the right atrium is hidden by the left atrial portion of the P wave). The diagnosis of left atrial enlargement, therefore, also requires that the terminal portion of the P wave should be at least 1 small block (0.04 second) in width.

The electrocardiographic picture of left atrial enlargement has been called P mitrale because mitral valve disease is a common cause of left atrial enlargement.

(A) Again, the normal P wave in leads II and V1. (B) Left atrial enlargement. Note the increased amplitude and duration of the terminal, left atrial component of the P wave.

SUMMARY

Atrial Enlargement

To diagnose atrial enlargement, look at leads II and V1.

Right atrial enlargement is characterized by the following:

1. P waves with an amplitude exceeding 2.5 mm in the inferior leads

2. No change in the duration of the P wave

3. Possible right axis deviation of the P wave

Left atrial enlargement is characterized by the following:

1. The amplitude of the terminal (negative) component of the P wave may be increased and must descend at least 1 mm below the isoelectric line in lead V1.

2. The duration of the P wave is increased, and the terminal (negative) portion of the P wave must be at least 1 small block (0.04 second) in width.

3. No significant axis deviation is seen because the left atrium is normally electrically dominant.

It should be stressed that electrocardiographic evidence of atrial enlargement (especially left atrial enlargement) sometimes has no pathologic correlate and in these cases may merely reflect a nonspecific conduction abnormality. Abnormalities of the P-wave axis can also be seen when the heart rhythm arises from a source other than the sinus node, something we shall discuss later. Interpretation of atrial enlargement on the EKG must therefore be tempered by knowledge of the clinical setting (a good idea in any circumstance!).

Ventricular Hypertrophy

The diagnosis of ventricular hypertrophy requires a careful assessment of the QRS complex in many leads.

Right Ventricular Hypertrophy

Looking at the Limb Leads

In the limb leads, the most common feature associated with right ventricular hypertrophy is right axis deviation; that is, the electrical axis of the QRS complex, normally between 0° and +90°, veers off between +90° and +180°. This reflects the new electrical dominance of the usually electrically submissive right ventricle.

Many cardiologists feel that the QRS axis must exceed +100° in order to make the diagnosis of right ventricular hypertrophy. Therefore, the QRS complex in lead I (oriented at 0°) must be more negative than positive.

Right ventricular hypertrophy shifts the axis of the QRS complex to the right. The EKG tracings show right axis deviation. In addition, the QRS complex in lead I is slightly negative, a criterion that many believe is essential for properly establishing the diagnosis of right ventricular hypertrophy.

Looking at the Precordial Leads

The precordial leads can also be helpful in diagnosing right ventricular hypertrophy. As you might expect, the normal pattern of R-wave progression, whereby the R-wave amplitude enlarges as you proceed leftward from lead V1 to V5, is disrupted. Instead of the R-wave amplitude increasing as the leads move closer to the left ventricle, the reverse may occur. There may be a large R wave in lead V1, which lies over the hypertrophied right ventricle, and a small R wave in leads V5 and V6, which lie over the normal, but now electrically humble, left ventricle. Similarly, the S wave in lead V1 is small, whereas the S wave in lead V6 is large.

These criteria have been expressed in the simplest possible mathematics:

 In lead V1, the R wave is larger than the S wave.

 In lead V6, the S wave is larger than the R wave.

In lead V1, the R wave is larger than the S wave. In lead V6, the S wave is larger than the R wave.

The most common causes of right ventricular hypertrophy are pulmonary disease and congenital heart disease.

Left Ventricular Hypertrophy

The diagnosis of left ventricular hypertrophy is somewhat more complicated. Left axis deviation beyond -15° is often seen, but by and large, this is not a very useful diagnostic feature. Instead, increased R-wave amplitude in those leads overlying the left ventricle forms the basis for the EKG diagnosis of left ventricular hypertrophy.

Unfortunately, there are almost as many criteria for diagnosing left ventricular hypertrophy on the EKG as there are books about EKGs. Nevertheless, all the criteria reflect a common theme: There should be increased R-wave amplitude in leads overlying the left ventricle and increased S-wave amplitude in leads overlying the right ventricle. The various criteria vary in their sensitivity and specificity. Those listed here are not the only ones, but they will serve you well.

Looking at the Precordial Leads

In general, the precordial leads are more sensitive than are the limb leads for the diagnosis of left ventricular hypertrophy. The most useful criteria in the precordial leads are as follows:

1. The R-wave amplitude in lead V5 or V6 plus the S wave amplitude in lead V1 or V2 exceeds 35 mm.

2. The R-wave amplitude in lead V5 exceeds 26 mm.

3. The R-wave amplitude in lead V6 exceeds 20 mm.

4. The R-wave amplitude in lead V6 exceeds the R-wave amplitude in lead V5.

The more criteria that are positive, the greater the likelihood that the patient has left ventricular hypertrophy.

It is, sadly, worth your while to memorize all of these criteria, but if you want to be selective, choose the first because it probably has the best predictive value.

Note: These criteria are of little value in individuals younger than 35 years of age, who frequently have increased voltage due, in many cases, to a relatively thin chest wall. They are particularly unreliable in young children.

Left ventricular hypertrophy in the precordial leads. Three of the four criteria are met. The R-wave amplitude in V5 plus the S-wave amplitude in V1 exceeds 35 mm, the R- wave amplitude in V6 exceeds 20 mm, and the R-wave amplitude in lead V6 slightly exceeds the R-wave amplitude in lead V5. The only criterion not met is for the R wave in lead V5 to exceed 26 mm.

Looking at the Limb Leads

The most useful criteria in the limb leads are as follows:

1. The R-wave amplitude in lead aVL exceeds 11 mm.

2. The R-wave amplitude in lead aVF exceeds 20 mm.

3. The R-wave amplitude in lead I exceeds 13 mm.

4. The R-wave amplitude in lead I plus the S-wave amplitude in lead III exceeds 25 mm.

Again, if you aspire to electrocardiographic nirvana, learn them all. If you must pick one, pick the first; it is the most specific for left ventricular hypertrophy. In other words, if this criterion is present, there is a good chance the patient has left ventricular hypertrophy, but relying on this criterion alone will sometimes lead you to miss the diagnosis (i.e., it is not very sensitive).

Left ventricular hypertrophy in the limb leads. Criteria 1, 3, and 4 are met; only criterion 2, regarding the R-wave amplitude in lead aVF, is not met.

There is another criterion that is generally regarded as the most accurate of all, and it combines one limb lead and one precordial lead:

The R-wave amplitude in aVL plus the S-wave amplitude in V3 exceeds 20 in women and 28 in men.

The leading causes of left ventricular hypertrophy are systemic hypertension and valvular disease.

You may have noticed that, in our discussion of ventricular hypertrophy, unlike atrial enlargement, no comment has been made about the duration of the QRS complex. Both right and left ventricular hypertrophy may slightly prolong the QRS complex, but rarely beyond 0.1 second.

When Both Ventricles Are Hypertrophied

What happens when both the right ventricle and left ventricle are hypertrophied? As you might expect, there may be a combination of features (e.g., criteria for left ventricular hypertrophy in the precordial leads with right axis deviation in the limb leads), but in most cases, the effects of the usually dominant left ventricle obscure those of the right ventricle.

Now Test Yourself: Is There Ventricular Hypertrophy in the Tracing Below? The Patient is a 50-Year-Old Female

Yes. This patient has aortic stenosis and has left ventricular hypertrophy on the EKG. She meets the criteria in both the precordial and limb leads.

Secondary Repolarization Abnormalities of Ventricular Hypertrophy

Something else may happen with hypertrophy of a ventricle that can dramatically alter the EKG, specifically the ST segment and the T wave. As we know, the ST segment plus the T wave represent the time from the end of ventricular depolarization to the end of ventricular repolarization. Therefore, these changes are called secondary repolarization abnormalities and include the following:

1. Downsloping ST-segment depression

2. T-wave inversion (i.e., the T wave changes its axis so that it is no longer closely aligned with the QRS axis)

Note how the depressed ST segment and the inverted T wave appear to blend together to form a single asymmetric wave. The downward slope is gradual; the upward slope is abrupt.

Several theories have been advanced to explain the cause of these abnormalities, ranging from inadequate blood flow in the capillary beds of the subendocardium (the inner layer of the myocardium lying just beneath the endocardial lining of the ventricle) to an overlapping of depolarization and repolarization forces in the region of thickened muscle. No one knows for sure. Until recently, these changes were referred to as strain, but the implication that these changes necessarily reflect the straining of an overworked and hypoxic muscle has proven to be more simplistic than true, and the term should rightly be discarded.

Repolarization abnormalities are not at all uncommon. They are most evident in those leads with tall R waves (reasonably so, because these leads lie over, and most directly reflect, the electrical forces of the hypertrophied ventricle). Thus, right ventricular repolarization abnormalities will be seen in leads V1 and V2, and left ventricular repolarization abnormalities will be most evident in leads I, aVL, V5, and V6. Left ventricular secondary repolarization abnormalities are far more common than right ventricular abnormalities.

Repolarization abnormalities usually accompany severe hypertrophy and may even herald the onset of ventricular dilatation. For example, a patient with aortic stenosis and no clinical symptoms may show a stable pattern of left ventricular hypertrophy for years. Eventually, however, the left ventricle may fail, and the patient will develop severe shortness of breath and other symptoms of congestive heart failure. The EKG may then show left ventricular hypertrophy with secondary repolarization abnormalities. This progression is illustrated in the two EKGs below.

(A) Lead aVL in a patient with aortic stenosis and left ventricular hypertrophy. Note the tall R wave, meeting the criteria for left ventricular hypertrophy. The ST segment is flat, and the T wave is upright. (B) One year later, the same lead shows the development of secondary repolarization abnormalities, reflecting the onset of left ventricular failure. The ST segment is depressed, and the T wave is inverted. Note, too, that the amplitude of the R wave has increased.

It is important to recognize the asymmetric contour of the ST- segment and T-wave changes that occur with secondary repolarization abnormalities. The descent is gradual and is followed by a more abrupt ascent. In Chapter 6, we will see that ST-segment depression and T-wave inversion can also occur with cardiac ischemia, and one of the key ways to tell ischemia from secondary repolarization is by their differing configurations—asymmetric with secondary repolarization abnormalities and symmetric with cardiac ischemia.

SUMMARY

Ventricular Hypertrophy

Right ventricular hypertrophy is characterized by the following:

1. Right axis deviation is present, with the QRS axis exceeding +100°.

2. The R wave is larger than the S wave in V1, whereas the S wave is larger than the R wave in V6.

Left ventricular hypertrophy is characterized by voltage criteria and, not infrequently, secondary repolarization abnormalities. The most useful criteria are the following:

1. The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35 mm.

2. The R wave in aVL is 11 mm.

3. The R wave in aVL plus the S wave in V3 exceeds 20 in women and 28 in men.

4. Left axis deviation exceeding -15° is also often present.

Secondary repolarization abnormalities include asymmetric, T-wave inversion and downsloping ST-segment depression.

Although the EKG pattern of left ventricular hypertrophy is easily recognized, it is present in only about 50% of patients whose echocardiograms demonstrate a thickened left ventricle. The sensitivity of the EKG criteria for left ventricular hypertrophy is thus fairly low. However, when the EKG pattern of left ventricular hypertrophy does appear, there is a 90% likelihood that a thickened ventricle will be seen on an echocardiogram. The specificity of the EKG criteria for left ventricular hypertrophy is thus quite high.

CASE 1.

Mildred W., a 53-year-old widow (her husband died of cerebral anoxia induced by his futile efforts to memorize all of the EKG criteria for left ventricular hypertrophy), comes to your office for a routine checkup. She is new to your practice and has not seen a doctor since her last child was born, which was more than 20 years ago. She has no specific complaints other than an occasional headache. Routine physical examination is unremarkable, except that you find her blood pressure is 170/110 mm Hg. She is unaware of being hypertensive. You would like to know if her hypertension is long-standing or of recent onset. Your laboratory assessment includes measurement of serum electrolytes, creatinine, and blood urea nitrogen; a urinalysis; a chest x-ray; and the EKG shown below. Is the EKG helpful?

Mildred’s EKG is essentially normal, which is not at all surprising. Most patients with hypertension have normal EKGs (and hopefully you recognized that this EKG is normal!). Nevertheless, had you found left ventricular hypertrophy, with or without repolarization abnormalities, you would have had at least one piece of evidence suggesting that her hypertension may be long-standing. In this particular case, an echocardiogram could be done to exclude hypertrophy, but it is certainly not necessary for deciding that Mildred’s hypertension should be treated.

CASE 2.

Tom L. is a 23-year-old marathon runner. Nearing Central Park at about the 20-mile mark of the New York Marathon, he suddenly turns pale, clutches his chest, and drops to the ground. Another runner, although on pace for a personal best, stops to help. Finding Tom pulseless and apneic, he begins cardiopulmonary resuscitation. The timely intervention proves lifesaving. Tom responds, and moments later, the following EKG is taken as he is being rushed to the nearest hospital. Why did Tom collapse?

Hint: If you get this, you already know too much.

Tom L. collapsed because of a hypertrophic disease of his heart muscle. A leading cause of sudden death in young, healthy athletes is hypertrophic cardiomyopathy, of which one variant is hypertrophic obstructive cardiomyopathy, or HOCM (also called idiopathic hypertrophic subaortic stenosis, or IHSS). More than half of cases are familial, with men affected slightly more often than women. Approximately 1 out of every 500 people is affected, and it is the leading cause of sudden cardiac death in young adults in the U.S. (see Chapter 7 for more about using the EKG to identify the various different causes of sudden death). In this disorder, disorganized proliferation of muscle fibers in the interventricular septum can cause significant septal hypertrophy. The resultant clinical repercussions can range from severe and life threatening to virtually none. Death can result from (1) obstruction to left ventricular outflow by the hypertrophied muscle; (2) impaired filling of the stiff, hypertrophied left ventricle during diastole; or (3) an abnormal ventricular rhythm (see the next chapter).

EKG abnormalities are present in at least 90% of patients with HOCM. The classic features on the resting EKG are the following:

1. Ventricular hypertrophy

2. Repolarization abnormalities in those leads with the tallest R waves

3. Narrow, deep Q waves, of uncertain etiology, most often in the inferior and lateral leads

Although this case was patently unfair, you may have recognized some of the features we have been talking about in this chapter, namely, the presence of criteria for left ventricular hypertrophy, especially in the precordial leads. Repolarization abnormalities are evident in all the left lateral leads (I, aVL, V5, and V6). Note, too, the deep Q waves in leads II, III, and aVF.

The timely intervention of his fellow runner saved Tom’s life. It turned out that Tom had experienced similar, albeit less severe, episodes in the past, characterized by light-headedness and chest pain. He was subsequently advised to avoid strenuous and competitive exercise (mild to moderate aerobic activity is fine) and was placed on verapamil, a calcium channel blocker, which prevented any recurrence of his symptoms. Verapamil reduces the strength of ventricular contraction, thereby decreasing the obstruction from the hypertrophied muscle, and improves the compliance of the stiffened ventricle. Beta-blockers are also used in this condition; they also lessen the risk for significant ischemia and may prevent arrhythmias. Placement of an implantable cardioverter defibrillator (ICD) should be considered in any patient with hypertrophic obstructive cardiomyopathy who has recovered from an episode of sudden cardiac death.

 
If you find an error or have any questions, please email us at admin@doctorlib.info. Thank you!