Cap 8 Elevacion Del St

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This chapter and the next (forming one unit)examine one of the most important topics in clini-cal electrocardiography and clinical medicinethediagnosis of myocardial ischemia and infarction*(ischemic heart disease), including ST segmentelevation myocardial infarction (STEMI). Basicterms and concepts are briey discussed rst.

MYOCARDIAL ISCHEMIA

Myocardial cells require oxygen and other nutri-ents to function. Oxygenated blood is supplied bythe coronary arteries. If severe narrowing or com-plete blockage of a coronary artery causes theblood ow to become inadequate, ischemia of theheart muscle develops. Ischemia means literally tohold back blood.

Myocardial ischemia may occur transiently. For

example, patients who experience angina pectoriswith exercise are having transient myocardial isch-emia. If the ischemia is more severe, necrosis of aportion of heart muscle may occur. Myocardialinfarction (MI) refers to myocardial necrosis (or, innontechnical parlancea heart attack).

This discussion focuses primarily on ischemiaand infarction of the left ventricle, the predomi-nant pumping chamber of the heart. The impor-tant clinical topic of right ventricular infarction isalso discussed briey.

TRANSMURAL AND SUBENDOCARDIALISCHEMIA

A simplied cross-sectional diagram of the leftventricle is presented in Figure 8-1. Notice that the

*The terms infarction and infarctare used interchangeably in this bookand clinically.

CHAPTER 8

Myocardial Infarction andIschemia, I: ST SegmentElevation and Q WaveSyndromes

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left ventricle consists of an outer layer (epicardor subepicardium) and an inner layer (subendodium). This distinction is important because mcardial ischemia may be limited to just the inlayer, or it may affect virtually the entire thicknof the ventricular wall (transmural ischemia).

MYOCARDIAL BLOOD SUPPLY

The cardiac blood supply is delivered by the thmain coronary arteries and their branches (8-2). The right coronary artery supplies both inferior (diaphragmatic) portion of the heart the right ventricle. The left main coronary arter

Left ventricular

chamber

Transmural

infarction

}E

picardium

}S

ubendocardium

Subendocardial

infarction

Figure 8-1. Cross section of the left ventricle showing thference between a subendocardial infarct, which involvesinner half of the ventricular wall, and atransmuralinfarct, winvolves the full thickness (or almost the full thickness) owall. As discussed in the text, pathologic Q waves may marker of transmural infarction. However, not all transmmyocardial infarctions produce abnormal Q waves; in scases, subendocardial (nontransmural) infarctions are asated with Q waves.
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66 PART I Basic Principles and Patterns

short and divides into the left anterior descendingcoronary artery, which generally supplies the ven-tricular septum and a large part of the left ventric-ular free wall, and the left circumex coronaryartery, which supplies the lateral wall of the left

ventricle. This circulation pattern may be variable.

Sometimes, for example, the circumex artery alsosupplies the inferoposterior portion of the left ven-tricle. MIs tend to be localized to the region (e.g.,anterior or inferior) of the left ventricle supplied byone of these arteries or their branches.

The serial, typical effects involving STEMI and Qwave MI on the ECG are examined in this chapter.Chapter 9 discusses the diversity of ECG patternsassociated with nonST segment elevation isch-emia and nonQ wave infarctions.

ST SEGMENT ELEVATION,TRANSMURAL ISCHEMIA, AND

ACUTE MYOCARDIAL INFARCTIONTransmural MI is characterized by ischemiaand ultimately necrosis of a portion of the entire

(or nearly the entire) thickness of the left ventric-ular wall. Most patients who present with acuteMI have underlying atherosclerotic coronaryartery disease. The pathophysiology of acuteSTEMI and subsequent evolving Q wave MI mostoften relates to occlusion of one of the coronary

arteries by a ruptured atherosclerotic plaque,followed by the formation of a clot at this site.The clot in the culprit artery is composed ofplatelets and brin, blocking the blood owdownstream.

Other factors can cause or contribute to acuteSTEMI, including cocaine, coronary artery dissec-tions (spontaneous or induced during interventionalprocedures), coronary emboli, and other factors.

Not surprisingly, large transmural MIs generallyproduce changes in both myocardial depolarization(QRS complex) and myocardial repolarization (ST-Tcomplex).

The earliest ECG changes seen with an acutetransmural ischemia/infarction typically occur inthe ST-T complex in sequential phases:

Figure 8-2. The three major coronaryarteries that supply blood to the heart.

Aorta

Rightcoronary

artery

Left anterior descendingcoronary artery

Left circumflexcoronary artery


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CHAPTER 8 St Segment Elevation, Transmural Ischemia, and Acute Myocardial Infarction

1. The acute phase is marked by the appearance ofST segment elevations and sometimes tall posi-tive (hyperacute) T waves in multiple (usually twoor more) leads. The term STEMI refers to thisphase.

2. The evolvingphase occurs hours or days later and

is characterized by deep T wave inversions in theleads that previously showed ST elevations.Transmural MIs can also be described in terms

of the location of the infarct. Anteriormeans thatthe infarct involves the anterior or lateral wall ofthe left ventricle, whereas inferiorindicates involve-ment of the inferior (diaphragmatic) wall of theleft ventricle (Fig. 8-3). The anatomic location ofthe infarct determines the leads in which the typi-cal ECG patterns appear. For example, with an

acute anterior wall MI, the ST segment elevatiand tall hyperacute T waves appear in one or mof the anterior leads (chest leads V1 to V6extremity leads I and aVL) (Fig. 8-4). With an irior wall MI the ST segment elevations and hyperacute T waves are seen in inferior leads II,

and aVF (Fig. 8-5).An important (but not always present) featof the ST-T changes seen with STEMI is their

procity. The anterior and inferior leads tend to shinverse patterns. Thus in an anterior infarctwith ST segment elevations in two or more of le

V1 to V6, I, and aVL, ST segment depression is ofseen in leads II, III, and aVF. Conversely, withacute inferior wall infarction, leads II, III, and show ST segment elevation, with reciprocal depressions often seen in one or more of leadsto V3, I, and aVL. Reciprocal changes are illustrain Figures 8-4 and 8-5.

The ST segment elevation seen with acute Mcalled acurrent of injury and indicates that damhas occurred to the epicardial (outer) layer of heart as a result of severe ischemia. The exact sons that acute MI produces ST segment elevatare complex and not fully understood. Normthe ST segment is isoelectric (neither positive negative) because no net current ow is occurrat this time. MI alters the electrical charge on myocardial cell membranes in a number of w

As a result, current ow becomes abnor(current of injury) and produces ST segm

deviations.

A B

LVLV

Figure 8-3. Myocardial infarctions are most generally local-ized to either the anterior portion of the left ventricle (A) or the

inferior (diaphragmatic) portion of the walls of this chamber (B).

aVFaVRI II III aVL V2 V4 V6

A

B

C

ECG Sequence with Anterior Wall Q Wave Infarction

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


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The ST segment elevation seen with acuteMI may have different shapes and appearances

(Fig. 8-6). Notice that the ST segment may be pla-teau-shaped or dome-shaped. Sometimes it isobliquely elevated.

The ST segment elevations (and reciprocal STdepressions) are the earliestECG signs of infarction,and are generally seen within minutes of bloodow occlusion. Tall, positive (hyperacute) T wavesmay also be seen at this time (Figs. 8-7 and 8-8).

These T waves have the same signicance as the STelevations. In some cases, hyperacute T waves actu-ally precede the ST elevations.

Guidelines for assessing whether ST segment(and usually J point) elevations are due to acuteischemia have been suggested. However, strictcriteria are limited because of false-positives(due to normal variants, left ventricular hyper-trophy, etc., as described in Chapter 9) and false-negatives (e.g., T wave positivity may precede STelevations or the ST elevations may be less than1-2 mm).

Clinicians should be aware that ST changes inacute ischemia may evolve with the patient underobservation. If the initial ECG is not diagnostic ofSTEMI but the patient continues to have symp-toms consistent with myocardial ischemia, serialECGs at 5- to 10-minute intervals (or continuous12-lead ST segment monitoring) should beperformed.

After a variable time lag (usually hours to a fewdays) the elevated ST segments start to return tothe baseline. At the same time the T waves becomeinverted in leads that previously showed ST seg-

ment elevations. This phase of T wave inversions iscalled the evolving phase of the infarction. Thus withan anterior wall infarction the T waves becomeinverted in one or more of the anterior leads (V1 to

V6, I, aVL). With an inferior wall infarction the Twaves become inverted in one or more of the infe-rior leads (II, III, aVF). (These T wave inversions areillustrated in Figs. 8-4 and 8-5.)

aVFaVRI II III aVL V2 V4 V6

A

B

C

ECG Sequence with Inferior Wall Q Wave Infarction

Figure 8-5. A, Acute phase of an inferior wall myocardial infarction: ST segment 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 andB,notice the reciprocal ST-T changes in the anterior leads (I, aVL, V2, V4).

Figure 8-6. Variable shapes of ST segment elevations seenwith acute myocardial infarctions.


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CHAPTER 8 St Segment Elevation, Transmural Ischemia, and Acute Myocardial Infarction

Figure 8-7. Chest leads from a patientwith acute anterior ST segment eleva-tion myocardial infarction (STEMI). A,In the earliest phase of the infarction,tall, positive (hyperacute) T waves areseen in leads V2 to V5. B, Several hourslater, marked ST segment elevation ispresent in the same leads (current ofinjury pattern), and abnormal Q wavesare seen in leads in V1 and V2.

V2V1 V3 V4 V5

V2V1 V3 V4 V5

A

B

V2V1 V3

V5V4

APB

V6

aVFaVR aVL

IIII II

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


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QRS Changes: Q Waves of InfarctionMI, particularly when large and transmural,often produces distinctive changes in the QRS(depolarization) complex. The characteristic depo-larization sign is the appearance of new Q waves.

Why do certain MIs lead to Q waves? Recall thata Q wave is simply an initial negative deection ofthe QRS complex. If the entire QRS complex isnegative, it is called aQS complex:

A Q wave (negative initial QRS deection) inany lead indicates that the electrical voltages aredirected away from that particular lead. With atransmural infarction, necrosis of heart muscleoccurs in a localized area of the ventricle. As aresult the electrical voltages produced by this por-tion of the myocardium disappear. Instead of posi-tive (R) waves over the infarcted area, Q waves areoften recorded (either a QR or QS complex).

As discussed in the next chapter, the commonclinical tendency to equate pathologic Q waves

with transmural necrosis is an oversimplication.Not all transmural infarcts lead to Q waves, and not all Qwave infarcts correlate with transmural necrosis.

In summary, abnormal Q waves are characteris-tic markers of infarction. They signify the loss ofpositive electrical voltages caused by the death ofheart muscle.

The new Q waves of an MI generally appearwithin the rst day or so of the infarct. With an

anterior wall infarction these Q waves are seen inone or more of leads V1 to V6, I, and aVL (see Fig.8-4). With an inferior wall MI the new Q wavesappear in leads II, III, and aVF (see Fig. 8-5).

ECG LOCALIZATION OF INFARCTIONS

As mentioned earlier, MIs are generally localized toa specic portion of the left ventricle, affectingeither the anterior or the inferior wall. Anteriorinfarctions are sometimes designated as anteroseptal,

strictly anterior, or anterolateral/anteroapical, depend-ing on the leads that show signs of the infarction(Figs. 8-9 to 8-11).

Anterior Wall Q Wave InfarctionsThe characteristic feature of an anterior wall Qwave infarct is the loss of normal R wave progression inthe chest leads. Recall that normally the height of theR wave increases progressively as you move fromlead V1 to lead V6. An anterior infarct interruptsthis progression, and the result may be pathologicQ waves in one or more of the chest leads. In clini-cal practice cardiologists often subdivide anteriorMIs into a number of subsets depending on theleads showing Q waves. Clinicians should be awarethat these ECG localizations may not correspondexactly with imaging or postmortem ndings andthat different authors may not use exactly the samedenitions.

Anteroseptal Q Wave InfarctionsRemember from Chapter 4 that the ventricular sep-tum is depolarized from left to right and that leads

V1 and V2 show small positive (r) waves (septal rwaves). Now consider the effect of damaging the sep-tum. Obviously, septal depolarization voltages arelost. Thus the r waves in leads V1 and V2 may disap-pear and an entirely negative (QS) complex appears.

The septum is supplied with blood by the leftanterior descending coronary artery. Septal infarc-tion generally suggests that this artery or one of itsbranches is occluded.

Strictly Anterior Q Wave InfarctionsNormally leads V3 and V4 show RS- or Rs-typecomplexes. If an infarction occurs in the anteriorwall of the left ventricle, the positive R waves thatreect the voltages produced by this muscle areaare lost. Instead, Q waves (as part of QS or QRcomplexes) are seen in leads V3 and V4. A strictlyanterior infarct generally results from occlusion ofthe left anterior descending coronary artery.

Key Clinical Correlates

n O major importance is the fnding thatacute reperusion therapieswithpercuta-neouscoronaryinterventions(angioplastyprocedures) or intravenous thrombolytic

medicationshavebeenshownconsistentlyto improve mortality rate only or acuteSTEMI.

n Furthermore, the earlier such therapy isgivenater the onseto the acuteSTEMIthemorelikelyitistoreducethesizeotheinarctandtheriskomajorcomplications,includingheartailureanddeath.

n SuccessulreperusiontherapyorSTEMIis generally associated with a promptdecreaseintheamplitudeotheischemicSTelevations.


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CHAPTER 8 ECG Localization of Infarctions

Anterolateral or AnteroapicalQ Wave Infarctions

An infarction of the anterolateral or apical wall ofthe left ventricle produces changes in the morelaterally situated chest leads (V5 and V6). With such

infarctions, abnormal Q waves, as part of QS orcomplexes, appear in leads V5 and V6 (see Fig. 7The infarcts are often caused by occlusionthe left circumex coronary artery, but they malso result from occlusion of the left ante

V2V1 V3 V4 V5 V6

aVFIIIIII aVR aVL

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

V2

V1

V3

V5V4 V6

aVFaVR aVL

IIII II

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


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descending coronary artery or even a branch of adominant right coronary artery.

ST elevations and pathologic Q waves localizedto leads I and aVL are often ascribed to a high lat-eral MI. The culprit artery in such cases is usu-ally an occluded diagonal branch of the leftanterior descending or branch of the left circum-ex coronary.

Differentiating Anterior Wall Infarctions:General Comments and Caveats

As noted, the foregoing classication of anteriorinfarctions is not absolute, and infarct types oftenoverlap. To avoid ambiguity, you can simplydescribe Q wave MIs by simply referring to anyinfarct that shows ECG changes in one or more of

leads I, aVL, and V1 to V6 as anteriorand then speci-fying the leads that show Q waves and ST-Tchanges.

Not surprisingly, anterior infarctions associatedwith large Q waves in leads V1 to V5 or V6 usuallyrepresent extensive damage and substantiallyreduced left ventricular function (ejection frac-tion) (see Fig. 8-11).

Inferior Wall InfarctionsInfarction of the inferior (diaphragmatic) portionof the left ventricle is indicated by changes in leadsII, III, and aVF (Figs. 8-12 to 8-14). These threeleads, as shown in the diagram of the frontal planeaxis, are oriented downward or inferiorly (see Fig.5-1). Thus they record voltages from the inferior

V2V1 V3

V5V4 V6

aVFaVR aVL

IIII II

Figure 8-11. Evolving extensive anterolateral wall infarction. The infarct occurred 1 week earlier. Notice the poor R wave progres-

sion 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 deviationis the result of loss of lateral wall forces, with Q waves seen in leads I and aVL.


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CHAPTER 8 ECG Localization of Infarctions

portion of the ventricle. An inferior wall infarctionmay produce abnormal Q waves in leads II, III, and

aVF. This type of infarction is generally caused byocclusion of the right coronary artery. Less com-monly it occurs because of a left circumex coro-nary obstruction.

Posterior InfarctionsInfarctions can occur in the posterior (back) sur-face of the left ventricle. These infarctions may bedifcult to diagnose because characteristic abnor-mal ST elevations may not appear in any of the 12conventional leads. Instead, tall R waves and STdepressions may occur in leads V1 and V2 (recipro-

cal to the Q waves and ST segment elevations thatwould be recorded at the back of the heart). Dur-ing the evolving phase of these infarctions, whendeep T wave inversions appear in the posteriorleads, the anterior chest leads show reciprocallytall positive T waves (Fig. 8-15).

In most cases of posterior MI the infarct extendseither to the lateral wall of the left ventricle,

producing characteristic changes in lead V6, othe inferior wall of that ventricle, producing ch

acteristic changes in leads II, III, and aVF (see8-15). Because of the overlap between inferior,eral, and posterior infarctions, the more genterms inferoposterior or posterolateral are udepending on which leads are involved.

Right Ventricular InfarctionsA related topic is right ventricular infarction. Cical and autopsy studies have shown that patiewith an inferoposterior infarct not uncommohave associated right ventricular involvementone postmortem study, right ventricular inf

tion was found in about one of four cases of infposterior MI but not in cases of anterior Clinically, patients with a right ventricular infmay have elevated central venous pressure (tended neck veins) because of the abnormally hdiastolic lling pressures in the right side of heart. If the damage to the right ventricle is sevhypotension and even cardiogenic shock m

I

II

II

III

aVR

aVL

aVF

V1

V2

V4

V5

V3 V6

Acute Infero-Lateral STEMI

Figure 8-12. Acute inferolateral wall ST segment elevation myocardial infarction (STEMI). Notice the prominent ST elevatioleads II, III, and aVF, as well, more subtly, in V5 and V6. The reciprocal ST depressions are in leads I and aVL, and V1 to V2. The lnding may be reciprocal to lateral or posterior ischemia. (Used with permission from Nathanson LA, McClennen S, Safran C, Gberger AL: ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu.)
http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./


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result. Atrioventricular conduction disturbancesare not uncommon in this setting. The presence of

jugular venous distention in patients with acuteinferoposterior wall MIs should always suggestthis diagnosis. Many of these patients also have STsegment elevations in leads reecting the right

ventricle, such as V1 and V3R to V5R, as shown inFigure 8-16 (see also Chapter 3).Recognition of right ventricular infarction is of

major clinical importance. Careful volume expan-sion may be critical in improving cardiac output inpatients who are hypotensive and have a low ornormal pulmonary capillary wedge pressuredespite elevated central venous pressure.

CLASSIC SEQUENCE OF ST-T CHANGESAND Q WAVES WITH STEMI

To this point the ventricular depolarization (QRScomplex) and repolarization (ST-T complex)changes produced by an acute MI have been dis-cussed separately. As shown in Figures 8-4 and 8-5,

these changes often occur sequentially.Ordinarily, the earliest sign of transmural ischemiais ST segment elevations (with reciprocal ST depres-sions). The ST elevations (current of injury pat-tern) usually persist for hours to days. During thissame period, Q waves often begin to appear in theleads that show ST elevations. Once these changeshave occurred, the ST segments start to return to

V2V1 V3

V5V4 V6

aVFaVR aVL

IIII II

Figure 8-13. Inferior wall infarction. This patient sustained a myocardial infarction 1 month previously. Notice the abnormal Qwaves and symmetrical T wave inversions in leads II, III, and aVF. In addition, T wave attening is seen in lead V6. After infarction, Qwaves and ST-T changes may persist indenitely or may resolve partially or completely.


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CHAPTER 8 Classic Sequence of St-T Changes and Q Waves with Stemi

the isoelectric baseline and the T waves becomeinverted during the evolving phase.

In the weeks or months after an infarct, whatshould you expect to happen to the Q waves and

the ST-T changes just described? The answer isthat you cannot make any certain predictions. Inmost cases the abnormal Q waves persist formonths and even years after the acute infarction.Occasionally, however, the abnormal Q wavesdiminish in size and even disappear entirely. Insome cases, abnormal T wave inversions persistindenitely. In others, improvement occurs, but

minor nonspecic ST-T abnormalities suchslight T wave attening may persist (see Figs. and 8-5).

Normal and Abnormal Q Waves:A Brief OverviewA frequently encountered diagnostic problemdeciding whether Q waves are abnormal. Not awaves are indicators of MI. For example, a Q wis normally seen in lead aVR. Furthermore, smseptal q waves are normally seen in the left chleads (V4 to V6) and in one or more of leads I, a

V3V1 V5V4V2 V6

aVFaVR aVLIIII II

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

V3V1 V5V4V2 V6

aVFaVR aVLIIII II

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


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II, III, and aVF. Recall from Chapter 4 the signi-cance of these septal q waves. The ventricular sep-tum depolarizes from left to right. Left chest leadsrecord this spread of voltages toward the right as asmall negative deection (q wave) that is part of aqR complex in which the R wave represents thespread of left ventricular voltages toward the lead.

When the electrical axis is horizontal, such qRcomplexes are seen in leads I and aVL. When theelectrical axis is vertical, qR complexes appear inleads II, III, and aVF.

These normal septal q waves must be differenti-ated from the pathologic Q waves of infarction.Normal septal q waves are characteristically nar-row and of low amplitude. As a rule, septal q waves

are less than 0.04 sec in duration. A Q wave is gen-erally abnormal if its duration is 0.04 sec or morein lead I, all three inferior leads (II, III, aVF), orleads V3 to V6.

What if Q waves with duration of 0.04 sec ormore are seen in leads V1 and V2? A large QS com-plex can be a normal variant in lead V1 and rarely in

leads V1 and V2. However, QS waves in these leadsmay be the only evidence of an anterior septal MI.An abnormal QS complex resulting from infarc-tion sometimes shows a notch as it descends, or itmay be slurred instead of descending and risingabruptly (see Fig. 8-9). Further criteria for differen-tiating normal from abnormal Q waves in theseleads lie beyond the scope of this book.

V3V1 V5V3R V2

aVFaVR aVLIIII II

V3V1 V5V3R V2

aVFaVR aVLIIII II

A

B

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 segment elevations (arrows) in the right precordial leads (V3R and V1). The ST-T changes in lead V6are consistent with lateral wall ischemia. The ST segment depressions in leads I and aVL are probably reciprocal to inferior lead STelevations. B, Follow-up tracing obtained the next day, showing diminution of the ST changes. (From Goldberger AL: MyocardialInfarction: Electrocardiographic Differential Diagnosis, 4th ed. St. Louis, Mosby, 1991.)


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CHAPTER 8 Ventricular Aneurysm

What if a wide Q wave is seen in lead aVL, or Qwaves are present in leads III and aVF? These wave-forms can also occur normally. Although a discus-sion of the precise criteria for differentiatingnormal from abnormal Q waves in these leads isalso beyond the scope of this book, the followingcan be taken as general rules:

An inferior wall MI should be diagnosed withcertainty only when abnormal Q waves are seenin leads II, III, and aVF. If prominent Q wavesappear just in leads III and aVF, the likelihood of

MI is increased by the presence of abnormalST-T changes in all three inferior extremity leads.

An anterior wall MI should not be diagnosedfrom lead aVL alone. Look for abnormal Q wavesand ST-T changes in the other anterior leads (Iand V1 to V6).Furthermore,just as not all Q waves are abnormal,

all abnormal Q waves are not the result of MI. Forexample, slow R wave progression in the chestleads, sometimes with actual QS complexes in theright to middle chest leads (e.g., V1 to V3), mayoccur with left bundle branch block (LBBB), left

ventricular hypertrophy, amyloidosis, and chroniclung disease in the absence of MI, in addition tomultiple other factors. Prominent noninfarctionQ waves are often a characteristic feature in theECGs of patients with hypertrophic cardiomyopa-thy (Fig. 8-17). Noninfarction Q waves also occurwith dilated cardiomyopathy (see Fig. 11-4). Asmentioned previously, the ECGs of normal people

sometimes have a QS wave in lead V1 and rarelleads V1 and V2. Prominent Q waves in the abseof MI are sometimes referred to as apseudoinf

pattern (see Chapter 24).

VENTRICULAR ANEURYSM

After a large MI a ventricular aneurysm developsome patients. An aneurysm is a severely scarportion of infarcted ventricular myocardium tdoes not contract normally. Instead, during vtricular systole the aneurysmic portion bulges o

ward while the rest of the ventricle is contractVentricular aneurysm may occur on the anterioinferior surface of the heart.

The ECG may be helpful in making the diagsis of ventricular aneurysm subsequent to an Patients with ventricular aneurysm frequenhave persistent ST segment elevations afterinfarct. As mentioned earlier, the ST segment

vations seen with acute infarction generally reswithin several days. The persistence of ST segmelevations for several weeks or more is suggestiva ventricular aneurysm (Fig. 8-18). However,

absence of persisting ST segment elevations dnot rule out the possibility of an aneurysm.

Ventricular aneurysms are of clinical imptance for several major reasons. They may leadcongestive heart failure. They may be associawith serious ventricular arrhythmias. A thrommay form in an aneurysm and break off, resultin a stroke or some other embolic complication

V3 V1 V5V4 V2 V6

aVFaVR aVLIIII II

Figure 8-17. Hypertrophic obstructive cardiomyopathy (HOCM). Notice the prominent pseudoinfarction Q waves, which arresult of septal hypertrophy. (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagnosis, 4th edLouis, Mosby, 1991.)


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MULTIPLE INFARCTIONS

Not infrequently, patients may have two or moreMIs at different times. For example, a new ante-rior wall infarct may develop in a patient with aprevious inferior wall infarction. In such casesthe ECG initially shows abnormal Q waves inleads 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 multi-ple infarcts [anterior and inferior] is presented inFig. 8-19.)

SILENT MYOCARDIAL INFARCTION

Most patients with an acute MI have symptoms.They may experience the classic syndrome ofcrushing substernal chest pain, or they may have

atypical pain (e.g., a sensation like indigestion,upper back pain, or jaw pain). Sometimes, how-ever, patients may experience few if any symptoms(silent MI). Therefore, it is not unusual for anECG to show abnormal Q waves that indicate aprevious infarction in a patient without a clinicalhistory of denite MI.

DIAGNOSIS OF MYOCARDIALINFARCTION IN THE PRESENCEOF BUNDLE BRANCH BLOCK

The diagnosis of infarction is more difcult whenthe patients baseline ECG shows a bundle branchblock pattern or a bundle branch block develops asa complication of the MI. Then the ECG picturebecomes more complex.

V2V1 V3

V5V4 V6

aVFaVR aVL

IIII II

Figure 8-18. Anterior wall aneurysm. The patient had a myocardial infarction several months before this ECG was taken. Noticethe prominent Q waves in leads V1 to V3 and aVL, the persistent ST elevations in these leads, and the reciprocal ST segment depres-

sions in the inferior leads (II, III, and aVF). The persistence of ST elevations more than 2 to 3 weeks after an infarction suggests thepresence of a ventricular aneurysm.


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CHAPTER 8 Diagnosis of Myocardial Infarction In the Presence of Bundle Branch Block

V2V1 V3 V4 V5 V6

aVFIIIIII aVR aVL

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

Right Bundle Branch Block withMyocardial InfarctionThe diagnosis of an MI can be made relatively eas-ily in the presence of right bundle branch block(RBBB). Remember that RBBB affects primarilythe terminal phase of ventricular depolarization,producing a wide R wave in the right chest leadsand a wide S wave in the left chest leads. MI affectsthe initial phase of ventricular depolarization, pro-ducing abnormal Q waves. When RBBB and aninfarct occur together, a combination of these pat-terns is seen: The QRS complex is abnormally wide

(0.12 sec or more) as a result of the bundle branchblock, lead V1 shows a terminal positive deection,and lead V6 shows a wide S wave. If the infarctionis anterior, the ECG shows a loss of R wave pro-gression with abnormal Q waves in the anteriorleads and characteristic ST-T changes. If the infarc-tion is inferior, pathologic Q waves and ST-Tchanges are seen in leads II, III, and aVF. (An ante-rior wall infarction with a RBBB pattern is shownin Fig. 8-20.)

Left Bundle Branch Block with

Myocardial InfarctionThe diagnosis of LBBB in the presence of MI isconsiderably more complicated and confusingthan that of RBBB. The reason is that LBBB inter-rupts both the early and the late phases of ventric-ular stimulation (see Chapter 7). It also producessecondary ST-T changes. As a general rule, LBBBhides the diagnosis of an infarct. Thus a patient with

a chronic LBBB pattern who develops an acute MI mnot show the characteristic changes of infarction descrin this chapter.

Occasionally, patients with LBBB manifest mary ST-T changes indicative of ischemia or actinfarction. The secondary T wave inversionsuncomplicated LBBB are seen in leads V4 to V6 (wprominent R waves). The appearance of T winversions in leads V1 to V3 (with prominent S wais a primary abnormality that cannot be ascribethe bundle branch block itself (Fig. 8-21).

The problem of diagnosing infarction w

LBBB is further complicated by the fact that LBBB pattern has several features that resemthose seen with infarction. Thus an LBBB pattcan mimic an infarct pattern. As discussedChapter 7, LBBB typically shows slow R wave pgression in the chest leads because of the reverway the ventricular septum is activated (i.e., frright to left, the opposite of what happens nmally). Consequently, with LBBB a loss of the nmal septal R waves is seen in the right chest leaThis loss of normal R wave progression simulathe pattern seen with an anterior wall infarct.

Figure 7-5 shows an example of LBBB with sR wave progression. In this case, anterior winfarction was not present. Notice that the ST ment elevations in the right chest leads resemthe pattern seen during the hyperacute or acphase of an infarction. ST segment elevation inright chest leads is also commonly seen with LBin the absence of infarction.


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V2V1 V3 V4 V5 V6

A

B

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

I

II

II

III

aVR

aVL

aVF

V1

V2

V4

V5

V3 V6

Acute Anterior STEMI and RBBB

Figure 8-20.Acute anterior wall ST segment elevation myocardial infarction (STEMI) and right bundle branch block (RBBB). Thewide QRS (about 120 msec) complexes with terminal R waves in leads V1 and V2 and a prominent S wave in lead V5 indicate the pres-ence of RBBB. The concomitant pattern of acute anterior myocardial infarction (MI) is indicated by the ST segment elevations inleads V1 to V4 (also slightly in leads I and aVL) and Q waves in leads V1 to V3. Reciprocal ST depressions are seen in the inferior limbleads. Borderline left axis deviation is present. This combination points to a very proximal occlusion of the left anterior descendingartery, with a large amount of ischemic/infracting myocardium. This nding indicates increased risk of abrupt high-degree atrioven-tricular (AV) heart block with infranodal conduction block (see Chapter 17). (Used with permission from Nathanson LA, McClen-nen S, Safran C, Goldberger AL: ECG Wave-Maven: Self-Assessment Program for Students and Clinicians.http://ecg.bidmc.harvard.edu.)
http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./http://ecg.bidmc.harvard.edu./


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CHAPTER 8 Diagnosis of Myocardial Infarction In the Presence of Bundle Branch Block

As a general rule, a patient with an LBBB pat-tern should not be diagnosed as having had an MIsimply on the basis of poor R wave progression inthe right chest leads or ST elevations in those leads.However, the presence of Q waves as part of QRcomplexes in the left chest leads (V5 and V6) withLBBB generally indicates an underlying MI (Fig.8-22). In addition, the appearance of ST segment

elevations in the left chest leads or in other lewith prominent R waves suggests ischemia Fig. 8-22, lead V5), as do ST segment depressionthe right leads or other leads with an rS or a morphology. (The discussion of the ECG wischemia and infarction continues in Chaptewhich focuses onsubendocardialischemia and nQ wave MI patterns.)

V2V1 V3 V4 V5 V6

aVFIIIIII aVR aVL

Figure 8-22. Chronic (prior) anterior wall infarction with left bundle branch block. Notice the prominent Q waves in the left c

leads as part of QR complexes (see text). (From Goldberger AL: Myocardial Infarction: Electrocardiographic Differential Diagn4th ed. St. Louis, Mosby, 1991.)

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