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In this chapter you will learn:
1 | 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)
2 | how to distinguish normal Q waves from the Q waves of infarction
3 | how the EKG can localize an infarct to a particular region of the heart
4 | the difference between the various acute coronary syndromes, particularly ST-segment elevation myocardial infarctions (STEMIs) and non–ST-segment elevation myocardial infarctions (non-STEMIs)
5 | the value of stress testing in diagnosing coronary artery disease
6 | 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?
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.
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.
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.
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.
During an acute STEMI, the EKG evolves through three stages:
- T-wave peaking followed by T-wave inversion (A and B, below)
- ST-segment elevation (C)
- The appearance of new Q waves (D)
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.
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.
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.
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.
ST-segment elevation is the second change that occurs acutely in the evolution of a STEMI.
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!
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.
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.
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||Men < 40||Men > 40||Women of all ages|
Leads V2 or V3
>2.5 mm STE
> 2.0 mm STE
>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:
- 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.
- 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.
The appearance of new Q waves indicates that irreversible myocardial cell death has occurred. The presence of Q waves is diagnostic of myocardial infarction.
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.
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.
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:
- The Q wave must be greater than 0.04 seconds in duration.
- The depth of the Q wave must be at least 25% the height of the R wave in the same QRS complex.