Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)

Part I. BASIC PRINCIPLES AND PATTERNS

Chapter 8. Myocardial Ischemia and Infarction

Section I ST segment elevation ischemia and Q wave infarct patterns

This chapter and the next examine one of the most important topics of clinical electrocardiography: the diagnosis of myocardial ischemia and infarction (ischemic heart disease). Basic terms are discussed first.

MYOCARDIAL ISCHEMIA

Myocardial cells require oxygen and nutrients to function. Oxygenated blood is supplied by the coronary arteries. If severe narrowing or complete blockage of a coronary artery causes the blood flow to become inadequate, ischemia of the heart muscle develops. Ischemia means literally to hold back blood.

Myocardial ischemia may occur transiently. For example, patients who experience angina pectoris with exercise are having transient myocardial ischemia. If the ischemia is more severe, necrosis of a portion of heart muscle may occur. Myocardial infarction (MI) refers to myocardial necrosis (“heart attack”), which is usually caused by severe ischemia.

This discussion focuses primarily on ischemia and infarction of the left ventricle, the predominant chamber of the heart. Right ventricular infarction is also discussed briefly.

 

TRANSMURAL AND SUBENDOCARDIAL ISCHEMIA

A cross-sectional diagram of the left ventricle is presented in Figure 8-1 . Notice that the left ventricle consists of an outer layer (epicardium) and an inner layer (subendocardium). This distinction is important because myocardial ischemia may be limited to just the inner layer, or it may affect virtually the entire thickness of the ventricular wall (transmural ischemia).

FIGURE 8-1  Cross section of the left ventricle showing the difference between a subendocardial infarct, which involves the inner half of the ventricular wall, and a transmural infarct, which involves the full thickness (or almost the full thickness) of the wall. As discussed in the text, pathologic Q waves may be a marker of transmural infarction. Not all transmural myocardial infarctions, however, produce abnormal Q waves; in some cases, subendocardial (nontransmural) infarctions are associated with Q waves.

 

MYOCARDIAL BLOOD SUPPLY

Certain basic facts about the blood supply to the left ventricle are also important. The cardiac blood supply is delivered by the three main coronary arteries ( Fig. 8-2 ). The right coronary artery supplies both the inferior (diaphragmatic) portion of the heart and the right ventricle. The left anterior descending coronary artery generally supplies the ventricular septum and a large part of the left ventricular free wall. The left circumflex coronary artery supplies the lateral wall of the left ventricle. This circula- tion pattern may be variable. Sometimes, for example, the circumflex artery also supplies the inferior-posterior portion of the left ventricle. MIs tend to be localized to the region (anterior or inferior) of the left ventricle supplied by one of these arteries or their branches.

FIGURE 8-2  The three major coronary arteries that supply blood to the heart.

 

TRANSMURAL ISCHEMIA WITH MYOCARDIAL INFARCTION

This chapter examines the effect of a classic transmural MI on the ECG. Chapter 9 discusses the ECG patterns of subendocardial ischemia and non–Q wave infarction.

Transmural infarction is characterized by ischemia and ultimately necrosis of a portion of the entire (or nearly entire) thickness of the left ventricular wall. Not surprisingly, large transmural infarctions generally produce changes in both myocardial depolarization (QRS complex) and myocardial repolarization (ST-T complex).

The earliest ECG changes seen with an acute transmural infarction usually occur in the ST-T complex in two sequential phases. The acute phase is marked by the appearance of ST segment elevations and sometimes tall positive (hyperacute) T waves in certain leads. The evolving phase occurs hours or days later and is characterized by deep T wave inversions in the leads that previously showed ST elevations.

Transmural MIs can also be described in terms of the location of the infarct. Anterior means that the infarct involves the anterior and/or lateral wall of the left ventricle, whereas inferior indicates involvement of the inferior (diaphragmatic) wall of the left ventricle ( Fig. 8-3 ). The anatomic location of the infarct determines the leads in which the typical ECG patterns appear. For example, with an acute anterior wall MI, the ST segment elevations and tall hyperacute T waves appear in one or more of the anterior leads (chest leads V1 to V6 and limb leads I and aVL) ( Fig. 8-4 ). With an inferior wall MI the ST segment elevations and tall hyperacute T waves are seen in inferior leads II, III, and aVF ( Fig. 8-5 ).

FIGURE 8-3  Myocardial infarctions are generally localized to either (A), the anterior portion of the left ventricle (LV) or (B), the inferior (diaphragmatic) portion of the walls of this chamber.

FIGURE 8-4  A, Acute phase of an anterior wall infarction: ST elevations and new Q waves. B, Evolving phase: deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A and B, notice the reciprocal ST-T changes in the inferior leads (II, III, and aVF).

FIGURE 8-5  A, Acute phase of an inferior wall myocardial infarction: ST elevations and new Q waves. B, Evolving phase: deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, and V2).

One of the most important characteristics of the ST-T changes seen with MI is their reciprocity. The anterior and inferior leads tend to show inverse patterns. Thus in an anterior infarction with ST segment elevations in leads V1 to V6, I, and aVL, ST segment depression is often seen in leads II, III, and aVF. Conversely, with an acute inferior wall infarction, leads II, III, and aVF show ST segment elevation, with reciprocal ST depressions often seen in one or more of leads V1 to V3, I, and aVL. (These reciprocal changes are illustrated in Figures 8-4 and 8-5 [4] [5].)

The ST segment elevation seen with acute MI is called a current of injury and indicates that damage has occurred to the epicardial layer of the heart with a transmural ischemia. The exact reasons acute MI produces ST segment elevation are complex and not fully understood. Normally, the ST segment is isoelectric (neither positive nor negative) because no net current flow is occurring at this time. MI alters the electrical charge on the myocardial cell membranes. As a result, current flow becomes abnormal (current of injury) and produces ST segment deviations.

The ST segment elevation seen with acute MI may have different shapes and appearances ( Fig. 8-6 ). Notice that the ST segment may be plateau shaped or dome shaped. Sometimes it is obliquely elevated.

FIGURE 8-6  Variable shapes of ST segment elevations seen with acute myocardial infarctions.

The ST segment elevations (and reciprocal ST depressions) are the earliest ECG signs of infarction, and are generally seen within minutes of the infarct. Tall positive (hyperacute) T waves may also be seen at this time (Figs. 8-7 and 8-8 [7] [8]). These T waves have the same significance as the ST elevations. In some cases, hyperacute T waves actually precede the ST elevations.

FIGURE 8-7  Chest leads from a patient with acute anterior wall infarction. A, In the earliest phase of the infarction, tall positive (hyperacute) T waves are seen in leads V2 to V5B, Several hours later, marked ST segment elevation is present in the same leads (current of injury pattern), and abnormal Q waves are seen in leads in V1 and V2.

FIGURE 8-8  Hyperacute T waves with anterior wall infarction. This patient was complaining of severe chest pain. Notice the very tall (hyperacute) T waves in the chest leads. In addition, slight ST segment elevations are present in lead aVL and reciprocal ST depressions are seen in leads II, III, and aVF. Notice the atrial premature beat (APB) in lead V4.

After a variable time lag (hours to days), the elevated ST segments start to return to the baseline. At the same time, the T waves become inverted in leads that previously showed ST segment elevations. This phase of T wave inversions is called the evolving phase of the infarction. Thus, with an anterior wall infarction, the T waves become inverted in one or more of the anterior leads (V1 to V6, I, aVL). With an inferior wall infarction, the T waves become inverted in one or more of the inferior leads (II, III, aVF). (These T wave inversions are illustrated in Figures 8-4 and 8-5 [4] [5].)

Clinical correlate: Of major importance is the finding that emergency reperfusion with percutaneous coronary intervention or with thrombolytic therapy has only been shown to be efficacious for acute MI associated with ST segment elevations. The earlier such therapy is given after the onset of the acute ST segment elevation MI (STEMI), the more likely it is to reduce the size of the infarct and the risk of major complications, including heart failure and death. Furthermore, successful reperfusion therapy for STEMI is generally associated with a prompt decrease in the amplitude of the ischemic ST elevations.

QRS CHANGES: Q WAVES OF INFARCTION

MI, particularly when large and transmural, often produces distinctive changes in the QRS (depolarization) complex. The characteristic depolarization sign is the appearance of new Q waves.

Why do certain MIs lead to Q waves? Recall that a Q wave is simply an initial negative deflection of the QRS complex. If the entire QRS complex is negative, it is called a QS complex:

 

A Q wave (initial negative QRS deflection) in any lead indicates that the electrical voltages are directed away from that particular lead. With a transmural infarction, necrosis of heart muscle occurs in a localized area of the ventricle. As a result, the electrical voltages produced by this portion of the myocardium disappear. Instead of positive (R) waves over the infarcted area, Q waves are often recorded (either a QR or QS complex).

As discussed in the next chapter, the common clinical tendency to equate pathologic Q waves with transmural necrosis is an oversimplification. Not all transmural infarcts lead to Q waves, and not all Q wave infarcts correlate with transmural necrosis.

In summary, abnormal Q waves are characteristic markers of infarction. They signify the loss of positive electrical voltages caused by the death of heart muscle.

The new Q waves of an MI generally appear within the first day or so of the infarct. With an anterior wall infarction, these Q waves are seen in one or more of leads V1 to V6, I, and aVL (see Fig. 8-4 ). With an inferior wall MI, the new Q waves appear in leads II, III, and aVF (see Fig. 8-5 ).

 

LOCALIZATION OF INFARCTIONS

As mentioned, MIs are generally localized to a specific portion of the left ventricle, affecting either the anterior or the inferior wall. Anterior infarctions are sometimes designated as anteroseptal, strictly anterior, or antero-lateral/apical, depending on the leads that show signs of the infarction (Figs. 8-9 to 8-11 [9] [10] [11]).

FIGURE 8-9  Anterior wall infarction. The QS complexes in leads V1 and V2 indicate anteroseptal infarction. A characteristic notching of the QS complex, often seen with infarcts, is present in lead V2 (arrow). In addition, the diffuse ischemic T wave inversions in leads I, aVL, and V2 to V5 indicate generalized anterior wall ischemia or non–Q wave myocardial infarction.

FIGURE 8-10  Evolving extensive anterior Q wave infarction. The patient sustained the infarct 1 week earlier. Notice the abnormal Q waves (leads I, aVL, and V2 to V5) with slight ST segment elevations and deep T wave inversions. Left axis deviation resulting from left anterior fascicular block is also present (see Chapter 7 ).

FIGURE 8-11  Evolving anterior wall infarction. The infarct occurred 1 week earlier. Notice the slow R wave progression in leads V1 to V5 with Q waves in leads I and aVL. The T waves are slightly inverted in these leads. In this ECG, right axis deviation is the result of loss of lateral wall forces, with Q waves seen in leads I and aVL.

ANTERIOR WALL Q-WAVE INFARCTIONS

The characteristic feature of an anterior wall Q-wave infarct is the loss of normal R wave progression in the chest leads. Recall that normally the height of the R wave increases progressively as you move from lead V1 to lead V6. An anterior infarct interrupts this progression, and the result may be pathologic Q waves in one or more of the chest leads. In clinical practice, cardiologists often subdivide anterior MIs into a number of subsets depending on the leads showing Q waves.

Anteroseptal Infarcts

Remember from Chapter 4 that the ventricular septum is depolarized from left to right and that leads V1 and V2 show small positive (r) waves (septal r waves). Now consider the effect of damaging the septum. Obviously, septal depolarization voltages are lost. Thus the r waves in leads V1 and V2 may disappear and an entirely negative (QS) complex appears.

The septum is supplied with blood by the left anterior descending coronary artery. Septal infarction generally suggests this artery or one of its branches is occluded.

“Strictly” Anterior Infarcts

Normally, leads V3 and V4 show RS- or Rs-type complexes. If an infarction occurs in the anterior wall of the left ventricle, the positive R waves that reflect the voltages produced by this muscle area are lost. Instead, Q waves (as part of QS or QR complexes) are seen in leads V3 and V4. A strictly anterior infarct generally results from occlusion of the left anterior descending coronary artery.

Anterolateral or Anteroapical Infarcts

An infarction of the anterolateral or apical wall of the left ventricle produces changes in the more laterally situated chest leads (V5 and V6). With such infarctions, abnormal Q waves, as part of QS or QR complexes, appear in leads V5 and V6 (see Fig. 7-7 ). The infarcts are often caused by occlusion of the left circumflex coronary artery, but they may also result from occlusion of the left anterior descending coronary artery or even a branch of a dominant right coronary artery. ST elevations and pathologic Q waves localized to leads I and aVL are often ascribed to a “high lateral” MI.

Differentiating Anterior Wall Infarcts: Some Cautions

The foregoing classification of anterior infarctions is not absolute, and infarct types often overlap. Q wave MIs may be most usefully described by simply referring to any infarct that shows ECG changes in one or more of leads I, aVL, and V1 to V6 as anterior and then specifying the leads that show Q waves and ST-T changes.

Of note, anterior infarctions associated with large Q waves in leads V1 to V5 or V6 usually represent extensive damage and substantially reduced left ventricular function (ejection fraction) (see Fig. 8-11).

INFERIOR WALL INFARCTIONS

Infarction of the inferior (diaphragmatic) portion of the left ventricle is indicated by changes in leads II, III, and aVF (Figs. 8-12 to 8-14 [12] [13] [14]). These three leads, as shown in the diagram of the frontal plane axis, are oriented downward or inferiorly (see Fig. 5-1 ). Thus, they record voltages from the inferior portion of the ventricle. An inferior wall infarction may produce abnormal Q waves in leads II, III, and aVF. This type of infarction is generally caused by occlusion of the right coronary artery. Less commonly, it occurs because of a left circumflex coronary obstruction.

FIGURE 8-12  Acute inferior wall ST elevation infarction. Notice the ST elevations in leads II, III, and aVF and the reciprocal ST depressions in leads I and aVL. Abnormal Q waves are also present in leads II, III, and aVF.

FIGURE 8-13  Inferior wall infarction. This patient sustained a myocardial infarction 1 month previously. Notice the abnormal Q waves and symmetric T wave inversions in leads II, III, and aVF. In addition, T wave flattening is seen in lead V6. After infarction, Q waves and ST-T changes may persist indefinitely or may resolve partially or completely.

FIGURE 8-14  Old inferior wall infarction. Notice the prominent Q waves in leads II, III, and aVF from a patient who had a myocardial infarction 1 year previously. The ST-T changes have essentially reverted to normal.

POSTERIOR INFARCTIONS

Infarctions can occur in the posterior (back) surface of the left ventricle. These infarctions may be difficult to diagnose because characteristic abnormal ST elevations may not appear in any of the 12 conventional leads. Instead, tall R waves and ST depressions may occur in leads V1 and V2 (reciprocal to the Q waves and ST segment elevations that would be recorded at the back of the heart). During the evolving phase of these infarctions, when deep T wave inversions appear in the posterior leads, the anterior chest leads show reciprocally tall positive T waves ( Fig. 8-15 ).

FIGURE 8-15  Posterior infarction. Notice the tall R waves in leads V1 and V2. This patient had a previous inferior infarction (Q waves in leads II, III, aVF) and probably a lateral infarction as well (T wave inversions in leads V4 to V6). Notice also the reciprocally tall positive T waves in anterior precordial leads V1 and V2.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.)

In most cases of posterior MI, the infarct extends either to the lateral wall of the left ventricle, producing characteristic changes in lead V6, or to the inferior wall of that ventricle, producing characteristic changes in leads II, III, and aVF (see Fig. 8-15 ). Because of the overlap between inferior and posterior infarctions, the more general term inferoposterior can be used when the ECG shows changes consistent with either inferior or posterior infarction.

RIGHT VENTRICULAR INFARCTIONS

A related topic is right ventricular infarction. Clinical and autopsy studies have shown that patients with an inferoposterior infarct not uncommonly have associated right ventricular involvement. Right ventricular infarction in 30% or more of cases of inferoposterior MI but not in cases of anterior MI. Clinically, patients with a right ventricular infarct may have elevated central venous pressure (distended neck veins) because of the abnormally high diastolic filling pressures in the right side of the heart. If the damage to the right ventricle is severe, hypotension and even cardiogenic shock may result. Atrioventricular (AV) conduction disturbances are not uncommon in this setting. The presence of jugular venous distension in patients with acute inferoposterior wall MIs should always suggest this diagnosis. Many of these patients also have ST elevations in leads reflecting the right ventricle, such as V1 and V3R to V6R, as shown in Figure 8-16 (see also Chapter 3 ).

FIGURE 8-16  Acute right ventricular ischemia with inferior wall infarction. A, Q waves and ST segment elevations in leads II, III, and aVF are accompanied by ST elevations (arrows) in the right precordial leads (V3R and V1). The ST-T changes in lead V6 are consistent with lateral wall ischemia. The ST depressions in leads I and aVL are probably reciprocal to inferior lead ST elevations. B, Follow-up tracing obtained the next day, showing diminution of the ST changes.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.)

Recognition of right ventricular infarction is of major clinical importance. Careful volume expansion may be critical in acutely improving cardiac output in patients who are hypotensive and have a low or normal pulmonary capillary wedge pressure.

 

SEQUENCE OF Q WAVES AND ST-T CHANGES WITH EVOLVING MYOCARDIAL INFARCTIONS

To this point, the chapter has discussed the ventricular depolarization (QRS complex) and repolarization (ST-T complex) changes produced by an acute MI separately. As shown in Figures 8-4 and 8-5 [4] [5], these changes often occur sequentially.

Ordinarily, the earliest sign of transmural ischemia is ST segment elevations (with reciprocal ST depressions). The ST elevations (current of injury pattern) usually persist for hours to days. During this same period, Q waves often begin to appear in the leads that show ST elevations. Once these changes have occurred, the ST segments start to return to the isoelectric baseline and the T waves become inverted during the evolving phase.

In the weeks or months after an infarct, what should you expect to happen to the Q waves and the ST-T changes just described? The answer is that you cannot make any certain predictions. In most cases, the abnormal Q waves persist for months and even years after the acute infarction. Occasionally, however, the abnormal Q waves diminish in size and even disappear entirely. In some cases, abnormal T wave inversions persist indefinitely. In others, improvement occurs, but minor nonspecific ST-T abnormalities such as slight T wave flattening may persist (see Figs. 8-4 and 8-5 [4] [5]).

NORMAL AND ABNORMAL Q WAVES

A frequently encountered diagnostic problem is deciding whether Q waves are abnormal. Not all Q waves are indicators of MI. For example, a Q wave is normally seen in lead aVR. Furthermore, small “septal” q waves are normally seen in the left chest leads (V4 to V6) and in one or more of leads I, aVL, II, III, and aVF. Recall from Chapter 4 the significance of these septal q waves. The ventricular septum depolarizes from left to right. Left chest leads record this spread of voltages toward the right as a small negative deflection (q wave) that is part of a qR complex in which the R wave represents the spread of left ventricular voltages toward the lead. When the electrical axis is horizontal, such qR complexes are seen in leads I and aVL. When the electrical axis is vertical, qR complexes appear in leads II, III, and aVF.

These normal septal q waves must be differentiated from the pathologic Q waves of infarction. Normal septal q waves are characteristically narrow and of low amplitude. As a rule, septal q waves are less than 0.04 second in duration. A Q wave is generally abnormal if its duration is 0.04 second or more in lead I, all three inferior leads (II, III, aVF), or leads V3 to V6.

What if Q waves with duration of 0.04 second or more are seen in leads V1 and V2? A large QS complex can be a normal variant in lead V1 and rarely in leads V1 and V2. QS waves in these leads may be the only evidence of an anterior septal MI, however. An abnormal QS complex resulting from infarction sometimes shows a notch as it descends, or it may be slurred instead of descending and rising abruptly (see Fig. 8-9 ). Further criteria for differentiating normal from abnormal Q waves in these leads lie beyond the scope of this book.

What if a wide Q wave is seen in lead aVL or Q waves are present in leads III and aVF? These waveforms can also occur normally. Although a discussion of the precise criteria for differentiating normal from abnormal Q waves in these leads is beyond the scope of this book, the following can be taken as general rules:

 

   

An inferior wall MI should be diagnosed with certainty only when abnormal Q waves are seen in leads II, III, and aVF. If prominent Q waves appear only in leads III and aVF, the likelihood of MI is increased by the presence of abnormal ST-T changes in all three inferior limb leads.

 

   

An anterior wall MI should not be diagnosed from lead aVL alone. Look for abnormal Q waves and ST-T changes in the other anterior leads (I and V1 to V6).

Furthermore, just as not all Q waves are abnormal, all abnormal Q waves are not the result of MI. For example, slow R wave progression in the chest leads, sometimes with actual QS complexes in the right to middle chest leads (e.g., V1 to V3), may occur with left bundle branch block (LBBB), left ventricular hypertrophy, and chronic lung disease in the absence of MI. Prominent noninfarction Q waves are often a characteristic feature in the ECGs of patients with hypertrophic cardiomyopathy ( Fig. 8-17 ). Noninfarction Q waves also occur with dilated cardiomyopathy (see Fig. 11-4 ). As mentioned previously, the ECGs of normal people sometimes have a QS wave in lead V1 and rarely in leads V1 and V2. Prominent Q waves in the absence of MI are sometimes referred to as apseudoinfarct pattern (see Chapter 22 ).[*]

FIGURE 8-17  Hypertrophic obstructive cardiomyopathy (HOCM). Notice the prominent pseudoinfarction Q waves, which are the result of septal hypertrophy. Leads V2 to V4 are recorded at ½, the usual voltage calibration.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.)

*  For a more complete discussion of this subject, see Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.

 

VENTRICULAR ANEURYSM

After a large MI, a ventricular aneurysm develops in some patients. An aneurysm is a severely scarred portion of infarcted ventricular myocardium that does not contract normally. Instead, during ventricular systole, the aneurysmic portion bulges outward while the rest of the ventricle is contracting. Ventricular aneurysm may occur on the anterior or inferior surface of the heart.

The ECG may be helpful in making the diagnosis of ventricular aneurysm subsequent to an MI. Patients with ventricular aneurysm frequently have persistent ST segment elevations after an infarct. As mentioned earlier, the ST segment elevations seen with acute infarction generally resolve within several days. The persistence of ST segment elevations for several weeks or more is suggestive of a ventricular aneurysm ( Fig. 8-18 ). The absence of persisting ST segment elevations, however, does not rule out the possibility of an aneurysm.

FIGURE 8-18  Anterior wall aneurysm. The patient had a myocardial infarction several months before this ECG was taken. Notice the prominent Q waves in leads V1 to V3 and aVL, the persistent ST elevations in these leads, and the reciprocal ST depressions in the inferior leads (II, III, and aVF). The persistence of ST elevations more than 2 to 3 weeks after an infarction suggests the presence of a ventricular aneurysm.

Ventricular aneurysms are of clinical importance for several major reasons. They may lead to congestive heart failure. They may be associated with serious ventricular arrhythmias. A thrombus may form in an aneurysm and break off, resulting in a stroke or some other embolic complication.

 

MULTIPLE INFARCTIONS

Not infrequently, patients may have two or more MIs at different times. For example, a new anterior wall infarct may develop in a patient with a previous inferior wall infarction. In such cases the ECG initially shows abnormal Q waves in leads II, III, and aVF. During the anterior infarct, new Q waves and ST-T changes appear in the anterior leads. (The ECG of a patient with multiple infarcts [anterior and inferior] is presented in Figure 8-19 .)

FIGURE 8-19  Multiple myocardial infarctions. This ECG shows evidence of previous anterior wall and inferior wall infarcts. Notice the slow R wave progression and QS complexes in chest leads V1 to V5, as well as the QS waves in leads II, III, and aVF.

 

“SILENT” MYOCARDIAL INFARCTION

Most patients with an acute MI have symptoms. They may experience the classic syndrome of crushing substernal chest pain, or they may have atypical pain (e.g., a sensation like indigestion, upper back pain, or jaw pain). Sometimes, however, patients may experience few if any symptoms (“silent” MI). Therefore it is not unusual for an ECG to show abnormal Q waves that indicate a previous infarction in a patient without a clinical history of definite MI.

 

DIAGNOSIS OF MYOCARDIAL INFARCTION IN THE PRESENCE OF BUNDLE BRANCH BLOCK

The diagnosis of infarction is more difficult when the patient's baseline ECG shows a bundle branch block pattern or a bundle branch block develops as a complication of the MI. Then the ECG picture becomes more complex.

RIGHT BUNDLE BRANCH BLOCK WITH MYOCARDIAL INFARCTION

The diagnosis of a Q wave MI can be made relatively easily in the presence of right bundle branch block (RBBB). Remember that RBBB affects primarily the terminal phase of ventricular depolarization, producing a wide R′ wave in the right chest leads and a wide S wave in the left chest leads. MI affects the initial phase of ventricular depolarization, producing abnormal Q waves. When RBBB and an infarct occur together, a combination of these patterns is seen: The QRS complex is abnormally wide (0.12 second or more) as a result of the bundle branch block, lead V1 shows a terminal positive deflection, and lead V6 shows a wide S wave. If the infarction is anterior, the ECG shows a loss of R wave progression with abnormal Q waves in the anterior leads and characteristic ST-T changes. If the infarction is inferior, pathologic Q waves and ST-T changes are seen in leads II, III, and aVF. (An anterior wall infarction with the RBBB pattern is shown in Figure 8-20 .)

FIGURE 8-20  Acute anterior wall infarction and the right bundle branch block (RBBB) pattern. The wide QRS complexes with an rSR′ wave in lead V1 and a qRS pattern in lead V5 indicate the presence of RBBB. A pattern of acute anterior wall infarction is indicated by the Q waves and ST elevations in leads I and aVL and the marked reciprocal ST depressions in leads II, III, and aVF. Finally, notice the left axis deviation caused by the left anterior fascicular block. This combination—left anterior fascicular block and RBBB—is an example of bifascicular block and may herald complete (trifascicular) heart block in patients with an acute anterior wall infarction (see Chapter 17 ).

LEFT BUNDLE BRANCH BLOCK WITH MYOCARDIAL INFARCTION

The diagnosis of LBBB in the presence of MI is considerably more complicated and confusing than that of RBBB. The reason is that LBBB alters both the early and the late phases of ventricular stimulation (see Chapter 7 ). It also produces secondary ST-T changes. As a general rule, LBBB hides the diagnosis of an infarct. Thus a patient with a chronic LBBB pattern who develops an acute MI may not show the characteristic changes of infarction described in this chapter.

Occasionally, patients with LBBB manifest primary ST-T changes indicative of ischemia or actual infarction. The secondary T wave inversions of uncomplicated LBBB are seen in leads V4 to V6 (with prominent R waves). The appearance of T wave inversions in leads V1 to V3 (with prominent S waves) is a primary abnormality that cannot be ascribed to the bundle branch block itself ( Fig. 8-21 ).

FIGURE 8-21  A, Typical left bundle branch block (LBBB) pattern. Notice the slow R wave progression in the right precordial leads and the discordance of QRS and ST-T vectors reflected by the ST elevations in the right precordial leads and the ST depressions with T wave inversions in the left precordial leads. B, LBBB with ischemia. Subsequently, the ECG from this patient showed the development of primary T wave inversions in leads V1 to V3 (arrows) caused by anterior ischemia and probable infarction.  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.)

The problem of diagnosing infarction with LBBB is further complicated by the fact that the LBBB pattern has several features that resemble those seen with infarction. Thus LBBB patterns can mimic infarct patterns. As discussed in Chapter 7 , LBBB typically shows slow R wave progression in the chest leads because of the reversed way the ventricular septum is activated (i.e., from right to left, the opposite of what happens normally). Consequently, with LBBB, a loss of the normal septal R waves is seen in the right chest leads. This loss of normal R wave progression simulates the pattern seen with an anterior wall infarct.

Figure 7-5 shows an example of LBBB with slow R wave progression. In this case, anterior wall infarction was not present. Notice that the ST segment elevations in the right chest leads resemble the pattern seen during the hyperacute or acute phase of an infarction. ST segment elevation in the right chest leads is also commonly seen with LBBB in the absence of infarction.

As a general rule, a patient with an LBBB pattern should not be diagnosed as having had an MI simply on the basis of slow R wave progression in the right chest leads or ST elevations in those leads. The presence of Q waves as part of QR complexes in the left chest leads (V5 and V6) with LBBB, however, generally indicates an underlying MI ( Fig. 8-22 ). In addition, the appearance of ST elevations in the left chest leads or in other leads with prominent R waves suggests ischemia (see Fig. 8-22 , lead V5), as does the appearance of ST segment depressions in the right leads or other leads with an rS or a QS morphology. (The discussion of the ECG with ischemia and infarction continues in Chapter 9 , which focuses on subendocardial ischemia and non–Q wave MI patterns.)

FIGURE 8-22  Anterior wall infarction with left bundle branch block. Notice the prominent Q waves in the left chest leads as part of QR complexes (see text).  (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th ed, St. Louis, Mosby, 1991.)

 

REVIEW

Myocardial ischemia occurs when the blood supply to the myocardium is not adequate. Myocardial infarction (MI) refers to necrosis of the myocardium caused by severe ischemia.

Myocardial ischemia or infarction may affect the entire thickness of the ventricular muscle (transmural injury) or may be localized to the inner layer of the ventricle (subendocardial ischemia or infarction). Transmural MI, especially when large, often (but not always) produces a typical sequence of ST-T changes and abnormal Q waves. The ST-T changes can be divided into two phases:

 

1.   

The acute phase is marked by ST segment elevations (current of injury pattern) and sometimes tall positive T waves (hyperacute T waves).

 

2.   

The evolving phase is characterized by the appearance of deeply inverted T waves in leads that showed the hyperacute T waves and ST elevations.

These ST-T changes occur during a period of hours or days and usually resolve over weeks or months. During the first day or so after an MI, new abnormal Q waves may appear in one or more leads.

Thrombolytic therapy has only been found efficacious in the treatment of acute ST segment elevation MI (STEMI).

The persistence of ST segment elevations for more than 2 or 3 weeks after an acute MI may signify that a ventricular aneurysm has developed. The abnormal Q waves tend to persist, but may become smaller with time and, rarely, may even disappear.

A Q wave MI can also be described in terms of its location. With an anterior infarction, ST segment elevations and abnormal Q waves occur in one or more of leads V1 to V6, I, and aVL. Reciprocal ST depressions may be seen in leads II, III, and aVF. With an inferior infarction, ST elevations and Q waves appear in leads II, III, and aVF, and reciprocal ST depressions may be seen in one or more of the anterior leads.

Right ventricular MI is a common complication of inferoposterior infarcts. In acute cases, the ECG may also show elevated ST segments in the right chest leads.

The pathologic Q waves of infarction must be distinguished from normal Q waves. For example, small normal “septal” q waves as part of qR complexes may be seen in the left chest leads (V4 to V6), in leads II, III, and aVF (with a vertical electrical axis), and in leads I and aVL (with a horizontal axis). These septal q waves are normally less than 0.04 second in width.

A QS wave may be seen normally in lead V1 and occasionally in leads V1 and V2. Q waves may also be seen as normal variants in leads aVF, III, and aVL.

Multiple MIs can occur. In such cases, the ECG may show old Q waves from the preceding infarct and new Q waves and/or ST-T changes from the current infarct.

When right bundle branch block (RBBB) complicates an acute MI, the diagnosis of both conditions is possible. The RBBB prolongs the QRS width, and lead V1 shows a tall positive final deflection. In addition, abnormal Q waves and ST segment elevations resulting from the acute MI are present in the chest leads with an anterior MI and in leads II, III, and aVF with an inferior MI.

When left bundle branch block (LBBB) complicates an acute MI, the infarction may be difficult to diagnose because the LBBB may mask both the abnormal Q waves of the infarction and the ST segment elevations and T wave inversions of the ischemia. In addition, LBBB may produce QS waves in the right chest leads with ST segment elevations and slow R wave progression across the chest withoutMI. The presence of QR complexes in the left chest leads with LBBB is suggestive of underlying MI. Ischemia with underlying LBBB is suggested by the presence of T wave inversions in the right chest leads, ST segment elevations in the left chest leads (or in other leads with prominent R waves), or ST segment depression in the right precordial leads (or other leads with rS or QS waves).

 

QUESTIONS

See the end of Chapter 9 .