The only EKG book. 9th Ed

Chapter 6. Myocardial Ischemia and Infarction

In this chapter you will learn:


the three major things that can happen to the EKG during a myocardial infarction (T-wave peaking and inversion, ST-segment elevation or depression, and the appearance of new Q waves)


how to distinguish normal Q waves from the Q waves of infarction


how the EKG can localize an infarct to a particular region of the heart


the difference between the various acute coronary syndromes, particularly ST-segment elevation myocardial infarctions (STEMIs) and non-ST-segment elevation myocardial infarctions (non- STEMIs)


the value of stress testing in diagnosing coronary artery disease


about the cases of Joan L., a woman with an acute infarction and a number of complications requiring your acute attention, and Saul S., who feels fine, but what is that we see on his EKG?

Stable Angina and Acute Coronary Syndromes

Let’s start by defining a few key terms:

Angina is the classic symptom of cardiac ischemia. Patients most often describe it as diffuse chest pain or pressure that may radiate to the neck, arms, or back and may be accompanied by shortness of breath, nausea, vomiting, dizziness, or diaphoresis (sweating). The underlying pathophysiology in most patients is progressive narrowing of the coronary arteries by atherosclerosis, which impedes blood flow to the heart muscle (other less common causes of angina include aortic stenosis and hypertrophic cardiomyopathy). With physical exertion, the limited blood supply is inadequate to meet the increased demands of the heart. Although there is variability among patients, blockage of about 70% of the lumen is typically sufficient to cause exertional angina. Patients whose chest pain is brought about only by a given level of exertion (e.g., walking up stairs) and relieved with rest have what is called stable angina. These patients are not at immediate risk of a myocardial infarction.

The term acute coronary syndrome is used to describe urgent situations when the blood supply to the heart is acutely compromised. Acute coronary syndromes are most often caused by acute rupture or erosion of an atherosclerotic plaque which in turn prompts the formation of a thrombus in the coronary artery, further limiting or completely blocking blood flow. The result can be either what is called unstable angina or a myocardial infarction (aka heart attack).

Patients with unstable angina experience the same type of symptoms as those with stable angina, but they can occur with much less—or even no—exertion and are typically more severe and last longer. Many of these patients will have a history of stable angina, and a change in their typical pattern of symptoms is what marks it as unstable.

Myocardial infarctions occur in two basic varieties. If blood flow through a coronary artery is totally occluded, the result can be what we call an ST-segment elevation myocardial infarction or STEMI. As you might suspect from the name, its most characteristic feature is elevation of the ST segments on the EKG. A STEMI is a true emergency, because the heart muscle is starved of blood supply.

If, however, blood flow is reduced but not totally blocked, the result can be either unstable angina or a non-ST-segment myocardial infarction (non-STEMI or NSTEMI). In non-STEMIs and unstable angina, the ST segments do not elevate, may remain normal, but most often are depressed (in the morphologic, not emotional, sense).

So what’s the story with these ST segments? They clearly are a key diagnostic feature in diagnosing ischemic heart disease, and we will be spending a lot of time with them in this chapter. Now is therefore a good time to ask why they sometimes elevate and sometimes depress in response to impaired blood flow. The answer is complex and not fully understood, but depriving myocardium of blood flow and oxygen alters the electrical properties of the myocardial cells, leading to voltage gradients between normal myocardium and ischemic myocardium. These gradients create injury currents within the heart tissue, and it is these that move the ST segments one way or another.

Predicting which plaques will rupture is the holy grail of cardiology. Plaques with lots of inflammatory cells, a thin fibrous cap, and a large pool of lipids are most prone to rupture. Small plaques are actually often more unstable than large plaques, so the size of the underlying plaque is a poor predictor of a future heart attack.

Occlusion of a coronary artery can lead to infarction of the region of myocardium that is dependent on that artery for its blood supply. (A) The coronary artery is gradually narrowed by atherosclerotic plaque. (B) Infarction can be caused by an acute thrombus superimposed on the underlying plaque.

Not all myocardial infarctions occur because of obstruction of one of the coronary arteries. Some happen when the oxygen demand of the myocardium exceeds the body’s ability to deliver the necessary blood supply. These patients may or may not have obstructive coronary artery disease. Causes include extreme tachycardias and severe hypotension due to blood loss (shock). The EKG cannot distinguish between the different causes of heart attack, although the changes on the EKG—as well as the patient’s symptoms—tend to be less dramatic when the primary cause is not coronary artery occlusion.

How to Diagnose a Myocardial Infarction

There are three components to the diagnosis of a myocardial infarction: (1) history and physical examination, (2) cardiac enzyme determinations, and (3) the EKG.

History and Physical Examination. When a patient presents with the typical features of infarction—the sudden onset of prolonged, crushing substernal chest pain radiating to the jaw, shoulders, or left arm, associated with nausea, diaphoresis, and shortness of breath—there can be little doubt about the diagnosis. However, many patients may not have all of these symptoms, or their symptoms may be atypical, described instead as burning, a knot in the throat, or a sensation of fullness in the neck. Patients with diabetes, women, and the elderly are most likely to present with atypical chest pain. In fact, they often present without angina at all but with just one or several of the associated symptoms. It is estimated that up to one-third of all myocardial infarctions are “silent”; that is, they are not associated with any overt clinical manifestations whatsoever. When angina is present, its severity is not an accurate predictor of either the likelihood of a myocardial infarction or the size of the infarct.

Sublingual nitroglycerin, a nitrate which acts as a vasodilator, is used to treat patients with ischemic symptoms, and it remains a very important component of our management. A patient’s symptoms will often quickly disappear with a single sublingual tablet. However, the response to nitroglycerin is a very poor predictor of the cause of a patient’s symptoms, since patients with various other conditions, such as esophageal spasm, can respond to nitroglycerin just like those with cardiac ischemia. Thus, although sublingual nitroglycerin can be an excellent therapeutic intervention, it is a very poor diagnostic tool.

Cardiac Enzymes. Dying myocardial cells leak their internal contents into the bloodstream. Elevated blood levels of creatine kinase (CK), particularly the MB isoenzyme, have long been used as a diagnostic tool for infarction. Today, elevated levels of the cardiac troponin enzymes occupy a more prominent role in the laboratory diagnosis of myocardial infarction. Troponin enzyme determinations are the go-to blood test to help rule in or rule out a myocardial infarction. Troponin levels rise earlier than the CK-MB isoenzyme (within 2 to 3 hours) and may stay elevated for several days. CK levels do not usually rise until 6 hours after an infarction and return to normal within 48 hours.

Intracellular enzymes are released by the dying myocardial cells after complete coronary occlusion resulting in acute infarction.

Although testing for cardiac troponins has increased our ability to diagnose a myocardial infarction, they have by no means supplanted the EKG as an equally valuable tool. In emergency settings, if the EKG shows changes of a myocardial infarction in a patient with a consistent history, no one waits around for the enzyme levels to come back-that patient is off to the catheterization lab!

Cardiac troponins can be elevated in conditions other than an infarction, for example, with pulmonary embolism, sepsis, respiratory failure, and renal impairment. They can also rise from other disorders associated with myocardial injury, such as congestive heart failure, myocarditis, or pericarditis. Thus, although normal troponin levels make it very unlikely that the patient is having a myocardial infarction, false positives are not uncommon. Depending on where you define your cutoff, some patients with an elevated troponin level will prove to have something other than a myocardial infarction.

The EKG. In most infarctions, the EKG will reveal the correct diagnosis. Characteristic electrocardiographic changes accompany a myocardial infarction, and the earliest changes occur almost at once with the onset of myocardial compromise. An EKG should be performed immediately on anyone in whom an infarction is even remotely suspected. However, the initial EKG may not always be diagnostic, and the evolution of electrocardiographic changes varies from person to person; therefore, it is important to obtain serial cardiograms, often within minutes of each other, if the first EKG is not diagnostic.

ST-Segment Elevation Myocardial Infarctions (STEMIs)

During an acute STEMI, the EKG evolves through three stages:

1. T-wave peaking followed by T-wave inversion (A and B, below)

2. ST-segment elevation (C)

3. The appearance of new Q waves (D)

(A) T-wave peaking, (B) T-wave inversion, (C) ST-segment elevation, and (D) formation of a new Q wave.

One caveat before we proceed: although the EKG typically evolves through these three stages during an acute STEMI, it does not always do so, and any one of these changes may be present without any of the others. Thus, for example, it is not at all unusual to see ST-segment elevation without T-wave inversion. Nevertheless, if you learn to recognize each of these three changes and keep your suspicion of myocardial infarction high, you will almost never go wrong.

The T Wave

With the onset of infarction, the T waves become tall, nearly equaling or even exceeding the height of the QRS complexes in the same lead. This phenomenon is called peaking. These peaked T waves are often referred to as hyperacute T waves. Shortly afterward, usually a few hours later, the T waves invert; that is, positive peaked T waves will become negative.

(A) T-wave peaking in a patient undergoing acute infarction. (B) The same lead in a patient 2 hours later shows T-wave inversion.

These T-wave changes reflect myocardial ischemia, the lack of adequate blood flow to the myocardium.

Ischemia is potentially reversible: if blood flow is restored or the oxygen demands of the heart are eased, the T waves will revert to normal. On the other hand, if actual myocardial cell death (true infarction) has occurred, T-wave inversion may persist for months to years.

T-wave inversion by itself is not diagnostic of myocardial infarction. It is a very nonspecific finding. Many things can cause a T wave to flip; for example, we have already seen that both bundle branch block and ventricular hypertrophy with repolarization abnormalities are associated with T-wave inversion. Hyperventilation, which is a common and understandable response to being hooked up to an EKG machine and having folks in white coats telling you they are worried about your heart, is itself sufficient to flip T waves!

One helpful diagnostic feature is that the T waves of myocardial ischemia are inverted symmetrically, whereas in most other circumstances they are asymmetric, with a gentle downslope and rapid upslope.

(A) The symmetric T-wave inversion in a patient with ischemia. (B) An example of asymmetric T-wave inversion in a patient with left ventricular hypertrophy and repolarization abnormalities.

In patients whose T waves are already inverted, ischemia may cause them to revert to normal, a phenomenon called pseudonormalization. Recognition of pseudonormalization requires comparing the current EKG with a previous tracing.

It is normal to see inverted T waves in leads V1, V2, and V3 in children and young adults; in some people, particularly African American athletes, these T waves may remain inverted into adulthood, a finding referred to as persistent juvenile T-wave pattern. An isolated inverted T wave in lead III is also a common normal variant seen in many individuals. And, of course, inverted T waves are to be expected in lead aVR, that extreme right-sided outlier.

The ST Segment

ST-segment elevation is the second change that occurs acutely in the evolution of a STEMI.

Two examples of ST-segment elevation during an acute STEMI: (A) without T-wave inversion and (B) with T-wave inversion.

ST-segment elevation often signifies myocardial injury. Injury probably reflects a degree of cellular damage beyond that of mere ischemia, but it, too, is potentially reversible, and in some cases, the ST segments may rapidly return to normal even without treatment. In most instances, however, ST-segment elevation is a reliable sign that true infarction has occurred and that the complete electrocardiographic picture of infarction will evolve unless there is immediate and aggressive therapeutic intervention.

A logical question to ask is: ST-segment elevation in relation to what? In other words, what is the reference baseline? There are two obvious candidates—the TP segment and the PR segment. And the best answer is the TP segment. The reason for this is that the PR segment can be depressed in patients with pericarditis, a condition which can clinically mimic ischemia (and which we will discuss in the next chapter). A depressed PR segment will make the ST segment look artificially elevated, so to be on the safe side, use the TP segment as your reference.

Even in the setting of a true infarction, the ST segments usually return to baseline within a few hours. Persistent ST-segment elevation often indicates the formation of a ventricular aneurysm, a weakening and bulging out of the ventricular wall.

Like T-wave inversion, ST-segment elevation can be seen in a number of other conditions in addition to an evolving myocardial infarction—the most common of these are discussed and summarized in Chapter 7. There is even a very common type of ST-segment elevation that can be seen in normal hearts. This phenomenon has been referred to as J point elevation. The J point, or junction point, is the place where the ST segment takes off from the QRS complex. Let’s stress again: J point elevation is very, very common, so pay close attention to what follows!

Two examples of J point elevation.

J point elevation is often seen in young, healthy individuals, particularly in leads V1, V2 and V3. Sometimes, along with an elevated J point, you will see a small notch or slur in the downslope of the R wave, and this combination of findings is referred to as early repolarization. J point elevation by itself appears to have no pathologic significance and carries no risk to the patient. But there is ongoing debate as to whether early repolarization, especially when seen in the inferior leads, may slightly (very slightly) increase the risk of ventricular tachycardia.

Early repolarization. Note the J point elevation and the notching at the terminal portion of the R wave.

How can the ST-segment elevation of myocardial injury be distinguished from that of J point elevation? With myocardial injury, the elevated ST segment has a distinctive configuration. It is bowed upward (convex downward) and tends to merge imperceptibly with the T wave. In J point elevation, the T wave maintains its independent waveform.

ST-segment elevation during a STEMI. Note how the ST segment and T wave merge into each other without a clear demarcation between them.

Specific criteria have been devised to help distinguish the ST elevation of true cardiac ischemia from J point elevation, which is benign. The table below summarizes the criteria for the diagnosis of a STEMI that are best supported by evidence:

Leads with ST elevation

Leads V2 or V3

Men < 40

>2.5 mm STE

Men > 40

> 2.0 mm STE

Women of all ages

>1.5 mm STE

All other leads

>1 mm STE

>1 mm STE

>1 mm STE

Plus the ST elevation much be present in at least two contiguous leads

The following point cannot be overstressed: these criteria are guidelines, not axioms carved in granite. If you see ST-segment elevation that fails to meet these criteria, but the clinical context is worrisome for an evolving myocardial infarction, don’t waste time dithering over electrocardiographic subtleties—get your patient the urgent care he or she needs ASAP!

A couple of other simple steps can help you decide what to do when you are unsure if the ST-segment elevation on a patient’s EKG is concerning:

1. If you have access to a previous EKG, just compare the old one to the new one—if the ST elevation is new, you are most likely dealing with an acute coronary syndrome.

2. If the patient is stable and in a monitored environment where emergency care is available, obtain serial EKGs. Any increase in the ST-segment elevation over the ensuing 15 to 60 minutes is indicative of cardiac ischemia. J point elevation will not change.

Q Waves

The appearance of new Q waves indicates that irreversible myocardial cell death has occurred. The presence of Q waves is diagnostic of myocardial infarction.

(A) Lead III in a healthy patient. (B) The same lead in the same patient 2 weeks after undergoing an inferior STEMI. Note the deep Q wave.

Q waves usually appear within several hours of the onset of a STEMI, but in some patients, they may take several days to evolve. The ST segment usually has returned to baseline by the time Q waves have appeared. Q waves usually persist for the lifetime of the patient.

Why Q Waves Form

The genesis of Q waves as a sign of infarction is easy to understand. When a region of myocardium dies, it becomes electrically silent—it is no longer able to conduct an electrical current. As a result, all of the electrical forces of the heart will be directed away from the area of infarction. An electrode overlying the infarct will therefore record a deep negative deflection, a Q wave.

(A) Normal left ventricular depolarization with the arrow showing the electrical axis. Note the tall R wave in lead I. (B) The lateral wall of the left ventricle has infarcted and, as a result, is now electrically silent. The electrical axis therefore shifts rightward, away from lead I, which now shows a negative deflection (Q wave).

Reciprocal Changes

Other leads, located some distance from the site of infarction, will see an apparent increase in the electrical forces moving toward them. They will record tall positive R waves.

These opposing changes seen by distant leads are called reciprocal changes. The concept of reciprocity applies not only to Q waves but also to ST-segment and T-wave changes. Thus, a lead distant from an infarct may record ST-segment depression.

Reciprocal ST-segment and T-wave changes in an inferior infarction. The acute ST elevation and T-wave peaking in lead II are echoed by the ST depression and T-wave inversion in lead V3.

Normal Versus Pathologic Q Waves

Some Q waves are perfectly normal. Small Q waves can often be seen in the left lateral leads (I, aVL, V5, and V6). These Q waves are caused by the early left- to-right depolarization of the interventricular septum. Q waves, good-sized Q waves, are also commonly seen in lead III and, when present in that lead but in no other inferior lead, are a normal variant.

Pathologic Q waves signifying infarction are wider and deeper. They are often referred to as significant Q waves. The criteria for significance are the following:

1. The Q wave must be greater than 0.04 seconds in duration.

2. The depth of the Q wave must be at least 25% the height of the R wave in the same QRS complex.

An example of a significant Q wave. Its width (A) exceeds 0.04 seconds, and its depth (B) exceeds one-third that of the R wave.

Note: Because lead aVR occupies a unique position on the frontal plane, it normally has a very deep Q wave. Lead aVR should not be considered when using Q waves to look for possible infarction.

Pathologic Q waves are almost never isolated to a single lead but are present in two or more contiguous leads, that is, leads that look at the same geographic region of the heart such as the inferior leads considered as a group, the anterior leads, or the left lateral leads. As stated above, isolated deep Q waves in lead III are a particularly common normal variant that almost never signifies a myocardial infarction. If you remember this point, it will save you a lot of unnecessary agita in the future.

When you see significant Q waves meeting the above criteria on the EKG of a patient in whom you have no reason to suspect a myocardial infarction, take a closer look. You will be surprised how often you will detect tiny R waves preceding the negative waves, so that what at first glance appears to be Q waves are in fact S waves and therefore of no concern.

Are the following Q waves significant?

Answers: The Q waves in leads I and aVF are significant. The Q wave in lead V2 is too shallow and narrow to qualify (don’t confuse the tiny Q wave with the large S wave). The Q wave in lead aVR is immense, but Q waves in aVR are never significant!


The EKG Changes of an Evolving STEMI

1. Acutely, the T wave peaks and then inverts. T-wave changes reflect myocardial ischemia. If true infarction occurs, the T wave may remain inverted for months to years.

2. Acutely, the ST segment elevates and merges with the T wave. ST-segment elevation reflects myocardial injury. If infarction occurs, the ST segment usually returns to baseline within a few hours.

3. New Q waves appear within hours to days. They signify myocardial infarction. In most cases, they persist for the lifetime of the patient.

Diagnosing a STEMI early in its evolution is one of the most important things you can do. Therapy is widely available that— delivered within the first few hours of the onset of the event—can prevent completion of the infarct and improve survival. Thrombolytic agents can lyse a clot within the coronary arteries and restore blood flow before myocardial death has occurred. In hospitals with catheterization and angioplasty capabilities, emergency angioplasty within the first several hours—ideally within the first 90 minutes—of the onset of infarction offers superior survival to thrombolysis alone, both acutely and in long-term follow-up.

Once angioplasty has been successfully carried out, the placement of stents coated with antiproliferative drugs to prevent reocclusion (which usually occurs as a result of cell proliferation) at the site of the original lesion prevents restenosis. The administration of both oral and intravenous platelet-inhibiting agents (glycoprotein Ilb/IIIa inhibitors) has further improved patient outcomes.

Whichever intervention is chosen, the key to successful therapy is timing: you must intervene quickly. The lives of patients are being saved every day by alert and informed health care providers. The recognition of the acute changes of a threatened or evolving myocardial infarction on the EKG is a critical diagnostic skill.

Localizing the Infarct

The region of myocardium that undergoes infarction depends on which coronary artery becomes occluded and the extent of collateral blood flow. There are two major systems of blood supply to the myocardium, one supplying the right side of the heart and one supplying the left side.

The right coronary artery runs between the right atrium and right ventricle and then swings around to the posterior surface of the heart. In most individuals, it gives off a descending branch that supplies the atrioventricular (AV) node.

The left main artery divides into a left anterior descending (LAD) artery and a left circumflex artery. The LAD runs between the two ventricles and supplies the anterior wall of the heart and most of the interventricular septum. The circumflex artery runs between the left atrium and left ventricle and supplies the lateral wall of the left ventricle. In about 10% of the population, it gives off the branch that supplies the AV node.

The main coronary arteries.

Localization of an infarct is important because the prognostic and therapeutic implications are in part determined by which area of the heart is affected.

Infarctions can be grouped into several general anatomic categories. These categories include inferior, lateral, anterior, and posterior infarctions. Combinations can also be seen, such as anterolateral and inferoposterior infarctions.

The four basic anatomic sites of myocardial infarction.

Almost all myocardial infarctions involve the left ventricle. This should not be surprising because the left ventricle is the most muscular chamber and is called on to do the most work. It is therefore most vulnerable to a compromised blood supply.

The characteristic electrocardiographic changes of infarction occur only in those leads overlying or near the site of infarction:

1. Inferior infarction involves the diaphragmatic surface of the heart. It is often caused by occlusion of the right coronary artery or its descending branch. The characteristic electrocardiographic changes of infarction can be seen in the inferior leads II, III, and aVF.

2. Lateral infarction involves the left lateral wall of the heart. It is most often due to occlusion of the left circumflex artery. Changes will occur in the left lateral leads I, aVL, V5, and V6.

3. Anterior infarction involves the anterior surface of the left ventricle and is usually caused by occlusion of the left anterior descending (LAD) artery. Any of the precordial leads (V1 through V6) may show changes. Occlusion of the left main artery will characteristically cause an extensive anterolateral infarction with changes in the precordial leads plus leads I and aVL.

4. Posterior infarction involves the posterior surface of the heart and is usually caused by occlusion of the right coronary artery. Posterior infarctions rarely occur in isolation, but usually accompany an inferior infarction or, less commonly, a lateral infarction. There are no leads directly overlying the posterior wall. The diagnosis must therefore be made by looking for reciprocal changes in the anterior leads, for example, a tall R wave in leads V1, V2, or V3.

A note of caution: Coronary anatomy can vary markedly among individuals, and the precise vessel involved may not always be what one would predict from the EKG.

Inferior Infarcts

Inferior infarction typically results from occlusion of the right coronary artery or its descending branch. Changes occur in leads II, III, and aVF. Reciprocal changes may be seen in the anterior and left lateral leads.

T-wave inversion in lead aVL is a particularly common reciprocal change during an inferior infarction, and it may even be the first sign, appearing before the inferior ST-segment elevation and T-wave inversion we associate with an acute inferior infarction. Serial EKGs will soon—usually within minutes—show the expected inferior changes.

Although in most infarctions significant Q waves persist for the lifetime of the patient, this is not necessarily true with inferior infarcts. Within half a year, as many as 50% of these patients will lose their criteria for significant Q waves. The presence of small Q waves inferiorly may therefore suggest an old inferior infarction. Remember, however, that a small Q wave in a single inferior lead, particularly lead III, also may be seen in normal hearts. The clinical history of the patient must be your guide.

A fully evolved inferior infarction. Deep Q waves can be seen in leads II, III, and aVF.

Lateral Infarction

Lateral infarction may result from occlusion of the left circumflex artery.

Changes may be seen in leads I, aVL, V5, and V6. Reciprocal changes may be seen in the inferior leads.

An acute lateral wall infarction. ST elevation can be seen in leads I, aVL, V5, and V6. Note also the deep Q waves in leads II, III, and aVF, signifying a previous inferior infarction. Did you also notice the deep Q waves in leads V3 through V6? These are the result of yet another infarction, this one affecting another portion of the left ventricle that occurred years ago.

Anterior Infarcts

Anterior infarction most often results from occlusion of the LAD. Changes are seen in the precordial leads (V1 through V6). If the left main artery is occluded, an anterolateral infarction may result, with changes in the precordial leads and in leads I and aVL. Reciprocal changes are seen inferiorly.

The loss of anterior electrical forces in anterior STEMI is not always associated with Q-wave formation. In some patients, there may be only a loss or diminishment of the normal pattern of precordial R-wave progression. As you already know, under normal circumstances, the precordial leads show a progressive increase in the height of each successive R wave as you look from lead V1 to V5. In normal hearts, the amplitude of the R waves should increase at least 1 mV per lead as you progress from V1 to V4 (and often V5); the amplitude of the R wave should normally exceed that of the S wave by lead V4. This pattern may vanish with anterior infarction, and the result is called poor R- wave progression. One simple criterion for the diagnosis of poor R-wave progression is if the R wave in lead V3 is not larger than 3 mV. Even in the absence of significant Q waves, poor R-wave progression may signify an anterior infarction.

Poor R-wave progression is not specific for the diagnosis of anterior infarction. It also can be seen with right ventricular hypertrophy, in patients with chronic lung disease, in patients who are obese, and—perhaps most often—with improper placement of the leads on the chest wall.

An anterior infarction with poor R-wave progression across the precordium.

Anterior STEMIs can have devastating clinical consequences, since they can compromise the bulk of the left ventricular myocardium.

Recognizing them early is critical for your patients. It is therefore important to point out two special types of T-wave abnormalities that can herald occlusion of the left anterior descending artery and an anterior myocardial infarction:

1. deWinter’s T waves: In a patient with chest pain, upsloping ST depression leading into tall, symmetric, hyperacute T waves in the precordial leads can be the first sign of an anterior infarction. These peaked T waves are called deWinter’s T waves and should be considered every bit as concerning for occlusion of the left anterior descending coronary artery as ST-segment elevation. Approximately 2% of acute LAD occlusions present with deWinter’s T waves rather than with ST-segment elevation.

2. Wellens’ waves: Deeply inverted or biphasic T waves in leads V2, V3 and sometimes V4 predict a proximal occlusion of the left anterior descending artery and are cause for concern. When you see biphasic T waves in these leads, a tip-off that these may be Wellen’s waves is that the upright portion of the T wave occurs first, followed by inversion of the terminal portion. There may or may not be ST-segment elevation.

Posterior Infarction

Posterior infarction typically results from an occlusion of the right coronary artery, the same artery responsible for most inferior infarctions. Therefore, as mentioned above, posterior infarction rarely occurs in isolation, but usually accompanies inferior, and sometimes lateral, infarctions. Of the various types of myocardial infarction, this is the one most often misdiagnosed, particularly in those uncommon cases when it occurs in isolation (at most 10% of all posterior infarctions). Because none of the conventional leads overlie the posterior wall, the diagnosis requires finding reciprocal changes in the anterior leads. In other words, because we can’t look for ST-segment elevation and Q waves in nonexistent posterior leads, we have to look for ST-segment depression and tall R waves in the anterior leads, notably lead V1. Posterior infarctions are the mirror images of anterior infarctions on the EKG.

The normal QRS complex in lead V1 consists of a small R wave and a deep S wave; therefore, the presence of a tall R wave, particularly with accompanying ST-segment depression, should be easy to spot. In the appropriate clinical setting, the presence of an R wave of greater amplitude than the corresponding S wave in lead V1 is highly suggestive of a posterior infarction.

Because in most posterior infarctions you will also see evidence of an inferior infarction, the complete EKG picture will often show clear-cut evidence of inferior ST elevation and anterior ST depression.

There is one other way to recognize a posterior infarction. It is a very simple matter to put electrodes on a patient’s back to get a good look at the posterior electrical forces. When this is done (and, unfortunately, it is done only rarely), the ability of the EKG to diagnose a posterior myocardial infarction is greatly enhanced. These so-called 15-lead EKGs, which include two V leads placed on the back (V8 and V9) and one on the right anterior chest wall (V4R), can often detect ST-segment elevation in patients with a suspected posterior STEMI in whom the standard 12-lead EKG is not diagnostic.

One caveat before we leave the subject of posterior infarctions. You will recall that the presence of a large R wave exceeding the amplitude of the accompanying S wave in lead V1 is also one criterion for the diagnosis of right ventricular hypertrophy. The diagnosis of right ventricular hypertrophy, however, also requires the presence of right axis deviation, which is not present in posterior infarction.

A posterior infarction. In lead V1, the R wave is larger than the S wave. There is also ST depression and T-wave inversion in leads V1 and V2.

Right Ventricular Infarctions

Because the left ventricle is so much more powerful than the right ventricle, it demands much more from its blood supply and therefore is far more susceptible to infarction when its blood supply is compromised. However, right ventricular infarctions do occur, virtually always accompanying inferior infarctions. What you will typically see are the expected changes of an inferior infarction (i.e., ST elevation and so forth in leads II, III and aVF) plus T-wave changes and ST- segment elevation in the most rightward anterior lead, V1. If there is also ST elevation in lead V2, it will be of smaller magnitude than that in V1, and often V2 will show ST depression. In the limbs leads, one tipoff that an inferior infarction is accompanied by a right ventricular STEMI is that the ST elevation in lead III is greater than that in lead II (why?—because lead III lies far to the right of lead II).

An evolving inferior STEMI with a right ventricular STEMI. Note the inferior changes, with the ST elevation greater in lead III than lead II, plus the ST elevation in lead V1 and ST depression in lead V2.

Another way to recognize a right ventricular infarction is to place electrodes over the right chest wall as shown in the picture below. Because these electrodes will overlie the right heart, they will most often show the characteristic features of infarction.

The figure on the left shows the proper alignment of right ventricular leads. The tracing on the right show the resultant ECG in a patient with a right ventricular STEMI; ST-segment elevation is most notable in leads V3R through V6R.

Does it make any difference clinically whether or not an infarction of the inferior wall of the left ventricle is accompanied by right ventricular infarction? Yes, indeed it does. Patients with right ventricular infarctions are “preload sensitive,” that is, they require high fluid volumes to maintain an adequate cardiac output and blood pressure, and they can become extremely hypotensive if they are treated with nitrates, such as nitroglycerin, which are vasodilators.

Where is the infarct? Is it acute?

This is an example of an anterior infarction. There is ST-segment elevation in leads V2 and V3 as well as poor R-wave progression.

Where is the infarct? Is it acute?

This tracing shows an acute posterior and inferior infarction (remember how we said that most posterior infarctions are accompanied by evidence of inferior infarction?). ST-segment elevation can be seen in leads II, III, and aVF, indicating an acute inferior infarction. There is also evidence of posterior wall involvement, with a tall R wave, ST- segment depression, and T-wave inversion in lead V1.

Non-ST-Segment Myocardial Infarctions


Not all myocardial infarctions are associated with ST-segment elevation. These infarctions, or non-STEMIs, also do not lead to the evolution of deep Q waves. Most often they are caused by either nonocclusive thrombosis of a major coronary artery or complete occlusion of a small offshoot of one of the major coronary arteries. Unlike STEMIs, these infarctions involve less than the entire thickness of the heart muscle. They can be localized to a particular region of the heart supplied by a single coronary vessel just the same as STEMIs. The only EKG changes seen with non-STEMIs are T-wave inversion and ST-segment depression (not elevation).

Non-STEMIs are actually more common than STEMIs. They behave much like small, incomplete infarctions and have a lower initial mortality rate but a higher risk for further infarction and mortality than STEMIs. They are initially treated medically, but cardiologists take a very aggressive stance with these patients, in particular those patients at high risk for further infarction and death, often sending them for coronary angiography and proceeding with revascularization right away.

A non-STEMI. ST-segment depression is most prominent in leads V2, V3, and V4, and T-wave inversion can be seen in leads V2 through V6. This patient never evolved Q waves, but his cardiac enzymes soared, confirming occurrence of a true infarction.

Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy is a condition that can closely mimic an acute STEMI on the EKG, complete with T-wave inversions and ST-segment elevations. As many as 2% of patients, most often postmenopausal women under extreme psychological stress (such as the death of a loved one or watching their grandchild play in a tense soccer match), who have what appears to be an acute infarction on their EKG will prove to have this syndrome instead. The EKG changes reflect ballooning of the left ventricle, and the condition has therefore also been referred to as apical ballooning syndrome. It acquired the name Takotsubo because the bulging ventricle reminded one of the original investigators of the shape of an octopus trap, for which the Japanese term is takotsubo.

The cause is usually psychological or emotional stress; therefore, yet another name for this syndrome is broken heart syndrome. The pathologic mechanism is not fully understood. One of the leading theories posits a state of excessive catecholamine stimulation. There may or may not be underlying atherosclerosis, but in any case, it is not responsible for the syndrome. In most patients, the coronary arteries appear perfectly normal. Because takotsubo cardiomyopathy has also been found to occur more commonly in persons with migraine headaches and Raynaud’s syndrome, generalized vasomotor dysfunction may play a role in its genesis.

Troponin levels can be elevated, although rarely as high as in an acute infarction, and there is no evidence of underlying coronary artery disease should the patient be brought to the catheterization lab. As many as 50% of these patients may develop transient heart failure and rarely can even go into shock. Patients generally improve over several weeks.

There are no electrocardiographic criteria that can reliably distinguish takotsubo cardiomyopathy from a STEMI caused by coronary artery occlusion. The distinction is made in the cath lab; patients with takotsubo cardiomyopathy will not show the occluded coronary arteries seen with a STEMI.

Limb leads in a patient with takotsubo cardiomyopathy. The ST-segment elevation looks for all the world like a typical inferior wall STEMI.

Takotsubo cardiomyopathy is one of several disorders grouped under the heading Myocardial Infarction With Normal Coronary Arteries (MINOCA; yes, there had to be an acronym!). In addition to takotsubo cardiomyopathy, other causes include small vessel coronary artery disease and myocarditis).

Angina Without Infarction

During an attack of angina, the EKGs of patients with both stable and unstable angina may demonstrate T-wave inversion and often ST-segment depression. In between attacks, the EKG is usually normal. Since the EKGs of patients with non-STEMIs also typically show these changes, how can you determine whether a patient is suffering from an anginal attack with or without infarction? The answer is simple: measure the cardiac enzymes. If they are significantly elevated, the patient is having a non-STEMI; if they are normal, infarction is highly unlikely.

Three examples of the EKG changes that can accompany angina without infarction: (A) T-wave inversion, (B) ST-segment depression, and (C) ST-segment depression with T-wave inversion (the ST-segment and T waves merge seamlessly).

Prinzmetal Angina

There is one type of angina that is associated with ST-segment elevation (Yes, I know— nothing is ever as easy as it first seems). Whereas typical angina is usually brought on by exertion and is the result of progressive atherosclerotic cardiovascular disease, Prinzmetal’s angina can occur at any time and results from coronary artery spasm in the absence of significant coronary artery disease. Presumably, the ST-segment elevation reflects reversible transmural injury. The contours of the ST segments often will not have the rounded, domed appearance of true infarction, and the ST segments will return quickly to baseline when the patient is given antianginal medication (e.g., nitroglycerin).

Sorting Out the Different Ischemic Syndromes

Are you having trouble trying to remember what the various ischemic symptoms and syndromes do to the EKG? T-wave changes are not particularly helpful since ischemia of any type can cause T-wave inversion. The key therefore is to focus on the ST segments and to measure the cardiac enzymes. Whether or not Q waves evolve is generally not helpful in the acute setting. The following table should help you get your thoughts in order:

Symptom or Syndrome

ST-Segment Changes

Cardiac Enzymes

Stable angina without infarction

ST depression


Unstable angina without infarction

ST depression



ST elevation



ST depression,


Takotsubo cardiomyopathy

ST elevation,


Prinzmetal’s angina

ST elevation


*Stable and unstable angina are distinguished by the clinical history as described earlier.

**Patients often have to undergo cardiac catheterization to distinguish this from infarction.

Recognizing elevated ST segments is critical to quickly diagnosing a STEMI, but it is important to remember that—as we mentioned when discussing J point elevation—there are other things that can elevate the ST segment. The clinical context is always helpful in sorting these out, but there are accompanying features on the EKG that can be helpful as well. Some of these we have already mentioned, and we will discuss many of these other confounding entities in the next chapter, so for now just take a good look at the following list so you can start to get this differential diagnosis into your head:

Causes of ST-Segment Elevation

An evolving STEMI

Prinzmetal’s angina

J point elevation/early repolarization

Takotsubo cardiomyopathy

Acute pericarditis

Acute myocarditis

Pulmonary embolism

Brugada pattern

Hypothermia (Osborne waves)

Ventricular aneurysm

CNS catastrophes


Left bundle branch block

Left ventricular hypertrophy

Paced rhythms

There are also several causes of ST-segment depression, but you will be happy to know that there aren’t quite so many of these:

Causes of ST-Segment Depression

Stable and unstable angina without infarction


Supraventricular tachycardias—ST depression in this setting does not imply coexisting ischemic disease

Typically seen in leads V1-V3 with right bundle branch block


Limitations of the EKG in Diagnosing an Infarction

Because the electrocardiographic picture of an evolving myocardial infarction typically includes T-wave changes, ST-segment changes, and sometimes Q-wave formation, any underlying cardiac condition that masks these effects by distorting the T-wave, ST-segment, and QRS complex will render electrocardiographic diagnosis of an infarction extremely difficult. We’ve already discussed several of these entities, including Wolff-Parkinson-White (WPW), left ventricular hypertrophy, and left bundle branch block, all of which can distort the EKG in ways that make recognizing an infarction by the criteria we’ve just discussed quite problematic. Right bundle branch block is generally of less concern because most infarctions involve the left ventricle.

Various criteria and algorithms have been devised and tested to aid in the EKG assessment of myocardial infarction in patients with left bundle branch block. We’re getting in a bit deep here, but if you are interested, here are the critical points: in a patient with left bundle branch block the presence of ST- segment elevation of at least 1 mm in any lead with a predominant R wave or ST-segment depression of at least 1 mm in leads V1-V3 if deep S waves are present is strongly suggestive of an evolving infarction.

One important point that you should not overlook: the appearance of a new left bundle branch block may signify infarction and should be treated with the same urgent attention as a STEMI.

In patients with WPW, the delta waves are often negative in the inferior leads (II, III, and aVF). This pattern is therefore often referred to as a pseudoinfarct pattern because the delta waves may resemble Q waves. The short PR interval is the one remaining clue that can distinguish WPW from an infarction on the EKG.

Stress Testing

Stress testing is a noninvasive method for assessing the presence and severity of coronary artery disease. It is by no means flawless (false-positive and falsenegative results abound), but it can be useful in patients who have or are suspected of having underlying atherosclerosis in order to help determine if their hearts, when stressed, show evidence of inadequate blood flow to parts of their myocardium.

Stress testing is usually done by having the patient ambulate on a treadmill, although stationary bicycles have been used just as effectively. The patient is hooked up to an EKG monitor, and a rhythm strip is monitored throughout the test. A complete 12-lead EKG is taken every minute or so and at the peak of exercise. Every few minutes, the speed and angle of incline of the treadmill are increased until (1) the patient cannot continue for any reason; (2) the patient’s maximal heart rate is achieved; (3) symptoms, such as chest pain, supervene; or (4) significant changes are seen on the EKG.

The physiology behind stress testing is simple. The graded exercise protocol causes a safe and gradual increase in the patient’s heart rate and systolic blood pressure. The product of the patient’s blood pressure multiplied by his heart rate, called the double product, is a good measure of myocardial oxygen consumption. If cardiac oxygen demands exceed consumption, electrocardiographic changes and even symptoms of myocardial ischemia may occur.

Significant coronary artery disease of one or several coronary arteries limits blood flow to the myocardium and hence limits oxygen consumption. Although a patient’s resting EKG may be normal, the increased demands of exercise may bring out evidence of subclinical coronary artery disease.

With a positive test for coronary artery disease, the EKG will reveal ST- segment depression. T-wave changes are too nonspecific to have any meaning in this setting.

There is a wealth of literature looking at precisely what constitutes significant ST-segment depression during an exercise test. It is generally acknowledged that ST-segment depression of greater than 1 mm that is horizontal or downsloping and persists for more than 0.08 seconds after the J point is suggestive of coronary artery disease. If a depression of 2 mm is used as the criterion, the number of false-positive results is greatly reduced, but the number of falsenegative results increases. Occasionally, upsloping ST segments may signify coronary artery disease, but the number of false-positive results is very high.

You may be wondering: what if I see ST-segment elevation during a stress test? Fortunately, this is a very rare occurrence, because this indicates the high likelihood of an unstable plaque and impending infarction. If you see ST- segment elevation in any lead other than aVR during a stress test, get your patient right to the catheterization lab!

(A) Downsloping ST depression. (B) Upsloping ST depression. (C) Horizontal ST depression. Only A and C are highly suggestive of coronary artery disease.

The earlier in the test that ST segment depression occurs—particularly, if the changes persist several minutes into the recovery period—the greater the likelihood that coronary artery disease is present and the greater the possibility that the left main coronary artery or several coronary arteries are involved. On the other hand, rapid resolution of ST-segment changes at the conclusion of the test is a hopeful prognostic indicator. The onset of symptoms (e.g., chest pain or dizziness) and falling blood pressure are particularly poor prognostic signs, and the test must be stopped immediately and further workup initiated.

The incidence of false-positive and false-negative results is dependent on the patient population that is being tested. A positive test in a young, healthy individual with no symptoms and no risk factors for coronary artery disease is likely to be a false test. On the other hand, a positive test in an elderly man with chest pain, a prior infarction, and hypertension is much more likely to be a truepositive result. In no one does a negative test result absolutely exclude the possibility of coronary artery disease.

(A) A patient’s resting EKG. (B) The same lead in the same patient 12 minutes into an exercise test. Note the prominent ST-segment depression associated with the increased heart rate.

Indications for stress testing may include the following:

1. The differential diagnosis of chest pain in someone whose baseline EKG is normal

2. The evaluation of a patient who has recently had an infarction, in order to assess his or her prognosis and need for further invasive testing, such as cardiac catheterization

3. The evaluation of individuals over 40 years of age who have risk factors for coronary artery disease, particularly diabetes mellitus, peripheral vascular disease, a history of a prior myocardial infarction, or a family history of premature heart disease

4. Suspicion of silent ischemia, such as in patients without chest pain but who may complain of shortness of breath, fatigue, or palpitations with exertion

Contraindications to stress testing include any acute systemic illness, severe aortic stenosis, uncontrolled congestive heart failure, severe hypertension, angina at rest, and the presence of a significant arrhythmia.

Mortality from the procedure is very low, but resuscitation equipment should always be available.

Both the sensitivity and specificity of the exercise stress test can be increased by (1) doing an echocardiogram before and after the procedure, looking for exercise-induced changes in wall motion that might signify myocardium in jeopardy, or (2) injecting the patient with radioactive imaging agents during the test and then recording images of the heart. In the latter procedure, termed myocardial scintigraphy, the myocardium extracts the radiotracer from the coronary circulation, but regions of compromised blood flow will be unable to extract the radiotracer. Films are obtained at rest and during stress. In a normal test, myocardial scintigraphy will reveal uniform uptake of the isotope by the left ventricle at both rest and under stress, but in a patient with coronary stenosis, a large perfusion defect may evolve during stress

In patients who are unable to exercise, there are alternatives to the traditional stress test. These include adenosine stress testing and dobutamine stress testing.

Adenosine, given intravenously, produces transient coronary vasodilatation, increasing coronary blood flow up to 400%. Vessels with significant stenosis, however, are already maximally vasodilated at rest and are unable to expand any further, so that the territory of the heart they supply will not show increased coronary flow. Typically, there are no diagnostic EKG changes during this test.

A dobutamine stress test mimics the stress of exercise on the heart. Dobutamine is an adrenaline-like agent that is given in incremental doses over several minutes. In patients with coronary artery disease, EKG changes just like those induced by exercise may be seen, and transient wall motion abnormalities will be seen on an accompanying echocardiogram.

Stress testing is not the only noninvasive way to assess the coronary circulation and the extent of any underlying atherosclerosis. Coronary artery calcium scoring utilizes rapid CT scanning of the heart. It can provide a measure of the patient’s overall atherosclerotic burden, but it does not reliably predict the degree of blockage at any one specific site. It is most useful in helping establish the risk of a future coronary event and guide decision-making about starting preventive therapy (e.g., should the patient be treated with a statin to lower LDL cholesterol levels?) and help determine the need for further work-up in patients whose risk of coronary artery disease is neither low (in which case further intervention is probably not needed) nor high (in which case aggressive evaluation, including stress testing and cardiac catheterization, are probably already on the table). CT angiography and MRI angiography, which can identify stenosed coronary vessels without the invasiveness of cardiac catheterization, are also being used more and more.

CASE 10.

Joan L. is a 62-year-old business executive. She is on an important business trip and spends the night at a hotel downtown.

Early the next morning, she is awakened with shortness of breath and severe chest pressure that radiates into her jaw and left arm. She gets out of bed and takes Pepto-Bismol, but the pain does not go away. Feeling dizzy and nauseated, she sits down and phones the front desk. Her symptoms are relayed by phone to the doctor covering the hotel, who immediately orders an ambulance to take her to the local emergency room. She arrives there 2 hours after the onset of her symptoms, which have continued unabated despite three sublingual nitroglycerin tablets given to her during the ambulance ride.

In the emergency room, a 12-lead EKG reveals the following: Is she having an infarction? If so, can you tell if it is acute and what region of the heart is affected?

The EKG shows ST-segment elevation in leads V2 through V5. There are no Q waves. Joan is in the throes of an acute anterior STEMI.

Joan’s prompt arrival in the emergency room, the elevated ST segments, and the absence of Q waves on the EKG mean that she is an excellent candidate for either thrombolytic therapy or acute coronary angioplasty. Unfortunately, she relates that only 1 month ago, she suffered a mild hemorrhagic stroke, leaving her with some weakness in her left arm and leg, making the risks of thrombolytic therapy prohibitive. In addition, acute angioplasty is not available at this small community hospital, and the nearest large medical center is several hours away. Therefore, doing the best they can under the circumstances, the medical staff have Joan admitted to the cardiac care unit (CCU) to be monitored. Her pain is controlled with morphine and intravenous nitroglycerin. Aspirin is also given, but all other anticoagulant agents are withheld because of her stroke history. Her first troponin level comes back elevated.

Late on the first night of her hospital stay, one of the nurses notices peculiar beats on her EKG:

The patient’s normal sinus rhythm is being interrupted by a run of three consecutive premature ventricular contractions (PVCs). In the setting of an acute infarction, these can be concerning. Her clinicians decide to start her on a beta-blocker to lessen sympathetic stimulation to her heart.

The next morning, Joan’s EKG looks like this. What has changed?

Joan’s EKG shows that all ventricular ectopy has been suppressed. It also shows new Q waves in the anterior leads, consistent with full evolution of an anterior infarct.

Later in the afternoon, Joan again begins to experience chest pain. A repeat EKG is taken. What has changed?

Joan is extending her infarct. New ST elevations can be seen in the left lateral leads.

A few hours later, she complains of light-headedness, and another EKG is performed. Now what do you see?

Joan has gone into third-degree AV block. Serious conduction blocks can develop during a myocardial infarction. Her light-headedness is due to inadequate cardiac output in the face of a ventricular escape rhythm of approximately 35 beats per minute. Pacemaker insertion is mandatory.

A pacemaker is placed without difficulty, and Joan suffers no further complications during her hospital stay. One week later, ambulatory and pain free, she is discharged. The morning after returning home, she again awakens short of breath and is taken to the emergency room. There, she is found to be in congestive heart failure. A cardiac echogram reveals markedly diminished left ventricular function as a result of her large myocardial infarction. She is treated in the hospital and is discharged after 3 days. No further problems develop, and she is able to return to her normal life at home and at work.

This case is very typical of the sort of thing you can see over and over again in hospitals across the country. It emphasizes how critical the EKG is in diagnosing and managing patients with acute myocardial infarctions. With Joan, an EKG confirmed the initial suspicion that she was having an infarct. In the CCU, electrocardiographic surveillance permitted the diagnosis of further infarction and accompanying rhythm and conduction disturbances and guided major therapeutic decisions.

CASE 11.

Sam S., a 45-year-old florist, is referred to you for a preoperative evaluation prior to an elective cholecystectomy. His medical history is unremarkable, and his physical exam is normal. He is on no medications. The surgeon has requested a preop EKG and lab work. You move on to your next patient, and the technician in your office draws the patient’s blood and runs a 12-lead EKG before letting the patient go home.

Later that day, before leaving the office, you check his EKG. Let’s look at just the precordial leads. What do you see?

Note the Q wave (actually a QS wave) in lead V2. It looks like Sam may have had an anterior myocardial infarction sometime in the past.

You call Sam at his flower shop (he keeps very late hours, like you), and he assures you he is fine and has never experienced a moment of chest pain in his life. Nevertheless, you are concerned and ask him to come back the next day. He does, and you repeat the EKG, this time running it yourself. Now what do you see?

You heave a sigh of relief; the Q wave has magically disappeared; what first looked like a Q wave in lead V2 turns out to be a small R wave followed by a deep S wave, a normal QRS complex! Or maybe not so magically. As you suspected, the first EKG was an error, in this case a common error of lead placement. Attaching leads V1 and V2 too high on the chest wall (toward the head) is common and can cause precisely this sort of confusion. With this mistake in lead placement, the view of the heart can be altered just enough so that, during the initial stage of ventricular depolarization, the current appears to be moving away from the electrodes, generating Q waves. In the hands of someone less astute, this mistake could have had important repercussions, leading to a delay in the patient’s surgery and to unnecessary testing (e.g., a stress test or even cardiac catheterization).

Happy ending: Sam had his gallbladder removed without complication and is back at work feeling just fine!

If you find an error or have any questions, please email us at Thank you!