Main 12-Lead ECG: The Art Of Interpretation

12-Lead ECG: The Art Of Interpretation

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Welcome to the most comprehensive resource on 12-Lead ECG interpretation! This all-encompassing, four-color text, updated to the new Second Edition, is designed to make you a fully advanced interpreter of ECGs. Whether you are paramedic, nurse, nurse practitioner, physician assistant, medical student, or physician wanting to learn or brush up on your knowledge of electrocardiography, this book will meet your needs. 12-Lead ECG: The Art of Interpretation, Second Edition takes the complex subject of electrocardiography and presents it in a simple, innovative, 3-level approach. Level 1 provides basic information for those with minimal experience interpreting ECGs. Level 2 provides intermediate information for those with a basic understanding of the principles of electrocardiography. Level 3 provides advanced information for those with some mastery of the subject. The entire text is written in a friendly, easy-to-read tone. Additionally, the text contains real-life, full-size ECG strips that are integrated throughout the text and analyzed in conjunction with the concepts they illustrate.
Year:
2013
Edition:
2
Publisher:
Jones & Bartlett Learning
Language:
english
Pages:
680
ISBN 10:
0763773514
ISBN 13:
9780763773519
Series:
Garcia, Introduction to 12-Lead ECG
File:
EPUB, 27.53 MB
Download (epub, 27.53 MB)

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ST Segment and T Waves

CHAPTER 14

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Basics

It would be very difficult to discuss the ST segment and T wave separately. In this chapter, we will move back and forth between them, and occasionally talk about them together depending on the section and the topic involved. The chapter, Acute Myocardial Infarction (AMI), covers the areas related to infarction and injury of the myocardium, but the topic is introduced in this chapter.

Electrically, the ST segment represents that section of the complex in which the ventricles are between electrical depolarization and repolarization. The segment is measured from the J point, where the QRS complex and the ST segment meet, to the beginning of the T wave (Figure 14-1). In most instances, the measurement is an approximation, either because the J point is not sharp or because the beginning of the T wave is not clearly visible. The J point can be sharp and clearly identifiable, or it can be diffuse (shown in Figure 14-2).

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Figure 14-1: ST segment.

Considered together, the ST segment and T wave are one of the most important aspects of the ECG for you to master, because this is the area that reflects ischemic insult or injury to the myocardium. In general, ST depression and T waves in the opposite direction from what is normal are a sign of ischemia. ST elevation, with or without T wave changes, is a sign of myocardial injury.

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Figure 14-2: Sharp and diffuse J points.


NOTE

T waves are usually positive in leads I, II, and V3 to V6, and negative in aVR. They can be variable in appearance in the rest of the leads. (These rules do not apply in LBBB or RBBB, however.)



Where Is the J Point?

You can clearly identify the J point in Figure 14-3. There is a definite spot where the transition occurs between the QRS complex and the ST segment. You will easily be able to identify the J point on most ECGs.

Figure 14-4 presents more of a problem. Where is the exact J point? As you can see, it is very difficult to take your caliper;  leg and place it on one spot and state definitively that you have it on the J point. Because it is a slowly curving segment, you can only isolate an area where the J point should be found. We have labeled that area with a red rectangle. Narrowing it down any closer is guesswork.

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Figure 14-3: Sharp J point.

Diffuse J points are associated with early repolarization, LVH with strain, and pericarditis. AMIs sometimes have a diffuse J point, especially when there is tombstoning. We will be discussing these conditions shortly.

ST Elevation or Depression

The key thing to identify when examining an ST segment is its relationship to the baseline. This will determine the presence of ST elevation or depression, examples of which are shown in Figure 14-5. Recall that the baseline is measured from TP segment to TP segment. This is a critical determination. Using a clear ruler with hairline rules will help you greatly in identifying the baseline. In certain cases, especially tachycardias, the TP segment is difficult to identify because the T and P waves overlap. When this occurs, use your best judgment and the PR interval to determine the baseline.

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Figure 14-4: Diffuse J point.

ST elevation of less than 1 mm is considered normal in the limb leads. In V2 to V3, the upper limit of normal J-point elevation for men 40 years of age and older is 2 mm. In men younger than 40, a value of 2.5 mm is considered the upper limit of normal. In adult women, the upper limit of normal for the J point is 1.5 mm. These criteria should always be interpreted in conjunction with the patient’s clinical history, the ST-T wave morphology, and the presence or absence of reciprocal changes [to be covered in the chapter, Acute Myocardial Infarction (AMI)] in mind. In addition, you must be very careful, however, because any elevation is important if it was not there on a previous ECG, or if the history matches the presence of ischemia. Remember “the company it keeps.” If there are other signs of ischemia, any elevation can be pathological.

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Figure 14-5: Samples of the ST segment at baseline, elevated, and depressed.

ST Segment Shapes

The shape of the ST segment can be quite variable. However, certain shapes are more common than others. Because some of these shapes are found in specific conditions, they are helpful in making the diagnosis. Other shapes are just a different “normal” presentation. We’ll diagram some of these shapes for you, and list possible causes underneath each one in Figure 14-6. Each can occur with positive or negative QRS complexes. Don’t worry if you don’t know what the terms mean. You will when you finish the Level 2 sections in this chapter.

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Figure 14-6: Examples of ST segment shapes and possible causes.

The T Wave

We have already covered T wave basics in the chapter, The Basic Beat (The T Wave, page 46) and — as they relate to the blocks — in the chapter, Bundle Branch Blocks and Hemiblocks (see page 272). Take a few minutes to review those two passages. In this chapter, we will begin to explore the differing morphologies associated with T waves. They can be tall or short, broad or narrow, symmetrical or asymmetrical, and positive, negative, or biphasic. These are the three things we want you to concentrate on: shape, polarity, and height or depth.

T Wave Shape Asymmetry is the normal presentation of the T wave. Symmetrical T waves are found in pathological states including ischemia, electrolyte abnormalities, and CNS problems. Asymmetrical and symmetrical T waves are shown in Figure 14-7. T waves can also be normally symmetrical in some people, but they should be considered pathological until proven otherwise. “The company it keeps” will be your motto from now on. You must rule out the conditions listed above before you can call symmetrical Ts normal. It’s hard to believe, but we have picked up many AMIs early on by spotting symmetrical T waves. Tall, narrow Ts are common in hyperkalemia. Very broad T waves have been found in CNS events, especially intracranial hemorrhage.

To determine symmetry, place your hairline ruler vertically on the peak of the T wave as shown in Figure 14-8. If the two sides separated by the dividing line are mirror images, the T wave is symmetrical. If they are not, it is asymmetrical.

Many times, the ST segment causes difficulty in evaluating for symmetry. When this occurs, as in Figure 14-8, extend the two legs of the T wave as a straight line down to the baseline. This simple technique will make it easy to evaluate symmetry.

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Figure 14-7: T wave shape.

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Figure 14-8

Here are some additional examples:

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Figure 14-9: Additional examples of T wave shapes.

Biphasic T Waves Biphasic T waves can occur in any lead, but especially the leads transitioning between a positive and a negative T wave. If the first part of the T wave is negative, the cause is more likely to be pathological. When you look at the examples in Figure 14-10, remember that there is a spectrum of positivity to negativity.

T Wave Polarity Because repolarization is associated with its own vector, T waves can be positive, negative, or anywhere in between. The orientation of this vector in three-dimensional space will determine T wave appearance in each lead. T waves are usually positive in leads I, II, and V3 to V6, and negative in aVR. In the rest of the leads, the T wave is variable. You will see later on that there are some variations in these rules — in the BBBs, for instance.

If the T wave is negative where it should be positive, such as lead II, we say that the T wave is flipped. Flipped T waves are sometimes indicative of ischemia. They can also be found in severe ventricular hypertrophy. Remember, in bundle branch blocks, all bets are off!

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Figure 14-10: Biphasic T waves.

T Wave Height or Depth In general, T waves should not be more than 6 mm high in the limb leads and 12 mm in the precordials. A good rule to remember is that if the T wave is more than 2/3 the height of the R wave, it is definitely abnormal. Tall T waves are associated with ischemia and infarction, CNS events, and high potassium levels.

A Few Last Words on T Waves Remember, the T wave does not live in a vacuum. Its appearance can be altered by the ST segment before it. When you are looking at the T waves, remember the old adage, “Intervals are always the same in all leads.” Measure where the T waves begin and end in a lead that clearly shows the whole wave, and transfer that distance to the lead with the bizarre appearance. This will help you isolate the T wave.

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Figure 14-11: ECG ruler with ECG strip.

ECG CASE STUDIES ST Segments and T Waves

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ECG 14-1 As we have said, it is very difficult to separate ST segments and T waves in most discussions. So, in this chapter we are going to be discussing both in most ECGs.

The format of this chapter is very ECG-intensive. This is because the ST segments (and sometimes the T waves) are the most confusing parts of the ECG for most students. The distinction between normal and pathological is minor in many cases; it requires a well-trained eye. We sat down and tried to figure out how most experts develop that “eye” for pathology. We came up with a simple answer. They have seen so many thousands of ECGs that they simply know there is an abnormality present. We are going to start you down that path by showing you many examples of different kinds of abnormalities. After you finish the chapter, it will benefit you to go back and review all the ECGs covered to this point in the book.

This ECG shows scooped ST segments and tall, asymmetrical T waves. The T waves are tall but they are not pathologically tall. They need to be taller than 2/3 the height of the R wave to be considered pathological. However, if the T waves were this tall but symmetrical, they would be pathologic. Hyperkalemia, ischemia, and CNS events present with this type of symmetrical T waves in many cases. Remember, you need to put the ECG together with the patient.


REMINDER

Look at and evaluate as many ECGs as possible. Experience is your best teacher for ST and T wave issues.



ECG 14-2 This ECG also shows scooped ST segments and asymmetrical T waves. If you notice, the T waves are not as tall as in ECG 14-1. The T waves are close to symmetrical but, as the old saying goes, close only counts in horseshoes and hand grenades. These are not pathological T waves by any criteria. They are upright in leads I, II, and V3 to V6, and negative in aVR, which represents a normal T wave vector.

The ST segments are scooped out in appearance with some slight elevation and are concave upward in most cases. The ST segment in V1 is flat and concave downward, which is troubling. This is not normal. However, when you look at the surrounding leads, there is no continuation of the pathological process. In general, one isolated lead with obvious pathology is not very clinically significant. However, we once again must invoke the principle of “the company it keeps.” Look at the patient and evaluate her as well as her complaints. If she is young and is seeing you because she fractured a finger, you need go no further. The ECG would be an example of early repolarization, which we will review later this chapter. If she is visiting for chest pain, you need to evaluate further. If you take another look, there is minimal PR depression and some notching at the end of the QRS complex. This ECG could be compatible with early pericarditis. The history and physical exam are crucial in making the definitive diagnosis.

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ECG 14-1

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ECG 14-2

ECG 14-3 Let’s look at the ECG below and focus on the T waves. Can you see anything abnormal about them? They are upright in leads I and II, which is normal, right? But what about V3 to V6? They are flipped and symmetrical, as shown close-up in Figure 14-12. This is an example of abnormal T waves indicative of ischemia.

When you look at V2 to V4, it is difficult to see that the T waves are symmetrical because of slight ST elevation that is distorting the T wave. Remember to draw the extending lines from the T wave itself to see the symmetrical qualities in these waves.

In addition, notice that the T waves in the limb leads are kind of flat. This is also a sign of pathology. We would call this abnormality a nonspecific ST-T wave change (NSSTTWΔ, in abbreviated form).

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Figure 14-12: Enlargement of lead V5.

ECG 14-4 It doesn’t take an expert to notice that the T waves in the precordials of this ECG are ugly! They are flipped, and greater than 2/3 of the R or S wave with which they are associated, as shown in close-up in Figure 14-13. In addition, they are definitely symmetrical. Get used to using a clear straight edge to evaluate symmetry.

The T waves in the limb leads also show abnormalities in leads I and aVL. They, too, are symmetrical and flipped.

Do you notice anything unusual about the rhythm? Can you figure out what it is? It is an irregularly irregular rhythm with varying P waves and PR intervals. Yes, it is a wandering atrial pacemaker. This case is not associated with any obvious COPD pathology, but it may be due to ischemia, represented by the flipped, symmetrical T waves.

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Figure 14-13

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ECG 14-3

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ECG 14-4

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ECG 14-5 This is very similar to ECG 14-4 except that the T wave abnormalities are more diffuse. Note that there are abnormalities in leads II and aVF. (The T waves are markedly flattened in aVF.)

What other abnormalities are found in this ECG? Well, there are left atrial enlargement criteria in V1. In addition, the Q waves in leads II, III, and aVF are pathological. They meet both criteria: width more than 0.03 seconds, and height more than 1/3 the R wave height.

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ECG 14-5 There are definitely signs of an old IWMI in this patient. The diffuse quality of the flipped, symmetrical T waves poses a list of possible differential diagnoses: ischemia, CNS event, electrolyte abnormality, and resolving pericarditis (especially post-infarct pericarditis because of the presence of the old IWMI). Clinical correlation is needed to completely interpret this ECG.

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ECG 14-5

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ECG 14-6 Are these normal T waves? Of course not! They are flipped in leads I, II, and V3 to V6. As a matter of fact, they are upright only in aVL and aVR. (Remember, they should be flipped in aVR.) They are symmetrical. Finally, they are more than 2/3 the height of the associated R waves in many leads.

The ECG also has an abnormal R:S ratio in V2 and shows evidence of an early clockwise transition in the precordial leads. Could this be due to a large right ventricle? Probably. Are the T wave abnormalities associated with the RVH? No, they are too diffuse and symmetrical. RVH, as we will see later in the chapter, is associated with asymmetrical T waves. There is evidence for an intraatrial conduction delay (IACD), but the criteria for RAE are not met.

Lastly, there is obvious evidence of QT prolongation: The QT interval is more than 1/2 the R-R interval.

What are some of the clinical scenarios that could give rise to such an ECG? Electrolyte abnormalities are certainly a possibility. Diffuse ischemia and a CNS event are also very high on the list of differential diagnoses. You will need to obtain an old ECG, if possible, and rule these things out (or rule them in) to come up with the final answer. Remember always to put the ECG and the patient together in your mind.

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ECG 14-6

ECG 14-7 Now let’s go from deep T waves to tall ones. Look at the T waves in the mid-precordial leads. They are tall and symmetrical. We’re going to spend much more time on this topic in the chapter, Electrolyte and Drug Effects, but this is as good a time as any to introduce you to hyperkalemia. When you see tall, symmetrical T waves, especially in the mid-precordials, you should always think of hyperkalemia. It is critical that you make this association, because in many cases you will not have a great deal of time to initiate therapy before complications such as arrhythmias set in. Sometimes you have just a few minutes, sometimes hours; you just can’t tell which patient will give you the luxury of time.


REMINDER

Tall, peaked, symmetrical T waves = Hyperkalemia!



Is hyperkalemia the definitive diagnosis in this case? No, a few other things are possible, such as ischemia. However, being the astute ECG expert that you are, some other things here make you suspicious. For example, even though none of the limb leads are less than 5 mm tall, the small complexes in the limb leads may signify a small pericardial effusion. Do renal failure patients develop pericardial effusions? Yes! You also notice a prolonged QT interval that could indicate hypocalcemia. This, too, commonly appears in renal failure patients. See how experts start to put things together?

ECG 14-8 After the discussion of ECG 14-7, what should your next question be? What is the potassium level?! These T waves are more classic for hyperkalemia in that they are very tall, narrow, and pointed. (Figure 14-14)

Are the QRS complexes more than 0.12 seconds wide? Sure are. Does it match left or right bundle criteria? Neither one actually fits this ECG. This is therefore an IVCD. One of the most common causes of an IVCD is hyperkalemia.

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Figure 14-14: Sharp T wave.

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ECG 14-7

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ECG 14-8

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ECG 14-9 The T waves in this ECG, too, are peaked and symmetrical. They are also wide, and they end with some aberrancy. Notice that the T wave begins to descend and then flares out toward the next complex. This is an abnormal pattern that is rarely seen. It may be due to the main problem with the ECG, the rhythm abnormality. This ECG is extremely difficult to sort out, but let’s give it a try. Is it fast or slow? Fast; it is a tachycardia. Are the QRS complexes wider than 0.12 seconds? Yes. So, this is a wide-complex tachycardia. Are there P waves? Yes. Are they associated with the QRS complexes? Not really. Look at leads II and V1 specifically. In lead II, do you see that the P waves seem to be moving toward the QRS complexes, and actually disappear into the complexes?

This is an example of AV dissociation. It is not third-degree heart block because the P waves are not much faster than the QRS complexes. In other words, the ratio of P waves to QRS complexes is 1:1. Now, putting it together, we have a wide-complex tachycardia with AV dissociation, which by definition is ventricular tachycardia! If you have problems picking these findings up, don’t worry — you’re in good company. Experts pick them up only with very concentrated effort. This is a really tough ECG. It is a great one, though, to show you how to break down the problems into manageable chunks.

ECG 14-10 Okay, so what is the potassium level here? Once again we are faced with tall, somewhat wide T waves that are definitely pathological in appearance. The first thought that should come to mind is hyperkalemia. The rest of the differential is the same as previously mentioned: CNS event, ischemia, and other electrolyte problems. Ischemia is doubtful because the changes are quite global in nature. The most probable culprits are CNS events and electrolyte abnormalities.

The rest of the ECG shows an early counterclockwise transition with the change from negative to positive occurring slightly before V2. The axis is in the normal quadrant. There is no evidence of atrial hypertrophy.


[image: image] QUICK REVIEW

1.   ST and T wave abnormalities isolated to one lead are a sign of significant pathology. True or False.

2.   Diffuse J points are associated with a benign process in most cases. True or False.

3.   T waves are normally upright in aVR. True or False.

1. False 2. True 3. False



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ECG 14-9

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ECG 14-10

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ECG 14-11 Boy, this ECG is really chock-full of pathology! The T waves are extremely tall. Should you think about potassium abnormalities? First and always! Let’s look at the rate, which is the first thing we examine in any ECG. The atrial rate is fast, compatible with an atrial tachycardia. The QRS rate, however, is very slow at about 40 BPM. The P waves are not associated with the QRS complexes; because the atrial rate is much faster than the ventricular rate, this indicates third-degree heart block.

Now, let’s turn our attention to the QRS complexes. The complexes are wide and bizarre. The pattern of a monomorphic S wave in V1 and a monomorphic R in leads I and V6 is compatible with a left bundle branch block. The person may have an underlying LBBB or, because the QRS complexes are so bizarre, the complexes may come from an aberrant pacemaker somewhere in the ventricles (the right ventricle, to be exact, because the pattern is that of LBBB). The second option is more likely: This ECG demonstrates a third-degree heart block with atrial tachycardia and a ventricular escape rhythm.

When you are faced with a very bizarre ECG, don’t panic! Instead, break it down into its components by going through it in an organized fashion. This will make it much easier to figure out the pathology involved.

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ECG 14-12 The T waves in this ECG are pretty impressive, especially in the precordials. The ST and T waves abnormalities are indicative of a hyperacute AMI (one that is very recent in onset). It is rare to capture this finding because most patients with chest pain present late to the emergency department, after this hyperacute period. In what leads are the ST segments elevated? If you are like most people, you immediately noticed the precordials. However, there is also significant elevation in leads II, III, and aVF. There is also ST depression in I and aVL. In the chapter, Acute Myocardial Infarction (AMI), we will see that these indicate an IWMI.

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ECG 14-12 This is a textbook example of a hyperacute infarct. Is the infarct in the anterior or inferior wall? Most people state that the infarct is in the anterior wall. However, this ECG shows the classic changes of an IWMI with an associated hyperacute right ventricular infarct. The criteria that are present include: (1) an IWMI; (2) ST elevation in lead III greater than lead II; and (3) ST elevation in V1 (which can extend to V6 in some cases). Echocardiography revealed a functioning anterior wall, but also motion abnormalities of the inferior wall and changes consistent with an RV infarct.

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ECG 14-11

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ECG 14-12

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ECG 14-13 We are now moving away from tall T waves to broad ones. Notice that the ST segments in this case are diffuse and nebulous. The T wave in V1 is slightly asymmetrical, but in the other leads they are either symmetrical or flattened. These are not normal T waves; we should approach them with caution. The presence of an old ECG would be extremely helpful, but if one is not available we have to assume the worst. The worst-case scenarios are ischemia and CNS events with electrolyte abnormalities — a distant possibility as there is a very small U wave in some leads, especially V2 to V3.


[image: image] QUICK REVIEW

1.   Flipped Ts are always a sign of pathology. True or False.

2.   If a BBB is present, the T waves can be flipped and still be normal. True or False.

3.   Flat ST segments that are elevated or depressed are always secondary to benign causes. True or False.

1. False; review the criteria. They are normally flipped in aVR; they can be flipped and still be normal in III, aVL, aVF, and V1 to V2, but always be careful! 2. True 3. False




CLINICAL PEARL

Always compare your interpretation of the ECG with your patient. Use the ECG to help guide your thought process in establishing the diagnosis.



ECG 14-14 This is another tough ECG. It appears fairly normal at first glance, but start going through it in an organized fashion and you’ll see the problem. Do you see any P waves? Yes. Are they associated with the QRS complexes? No, they are not. If you look at the rhythm strip, you notice that some P waves are easy to spot, such as the one marked by the fourth star. Some of the other P waves are less obvious because they are buried inside the QRS complexes, ST segments, or T waves. When you map out the Ps using calipers, you’ll note that they are almost always the same distance apart, give or take a small amount. This is consistent with AV dissociation, which is present in this ECG. This is a normal sinus rhythm with AV dissociation and junctional escape beats.

This chapter, however, is about T waves and ST segments. We note that there are some slightly elevated ST segments in the right precordial leads of V1 to V3. These are associated with some concave, upward scooping of the segments, which appears fairly benign. The T waves, though, are wide and slightly asymmetrical. Remember to use your clear ruler to evaluate the symmetry of the wave. The asymmetry eases some of your concern about the width of the T waves. Because AV dissociation is present, you should still correlate your findings to the patient — as always — to be completely sure of the benign quality of the segments.

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ECG 14-13

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ECG 14-14

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ECG 14-15 This ECG has some pretty wide ST segments and broad T waves that are grossly abnormal. This patient was having an intracranial hemorrhage and had very high intracranial pressures. This is the classic, but very rare, electrocardiographic finding for this disorder. You need to commit it to memory because the patient with this ECG will be in coma, unable to give you a history.

What is that little spike pattern in leads I, III, and aVL? Is it a pacemaker? No, pacemakers will never fire that fast. The rate is well over 300 BPM. This is artifact caused by interference from some electrical device. Don’t worry about it.


REMINDER

Very broad, symmetrical T waves are classic for major intracranial bleeds or strokes.



ECG 14-16 This ECG also has some pretty wide ST segments and broad T waves that are grossly abnormal. This is another example of a patient with an intracranial hemorrhage. This time the T waves are not as impressive, but they are still quite wide.

Note that in leads V1 to V3, there is a second hump after the initial T wave. Is this indicative of a U wave? Well, remember we have said that intervals are always the same throughout the ECG. In comparing the QT interval in V5 to V6, we see that the second hump falls well within the QT interval and is not a U wave. Could it be the missing P wave, buried in the T wave because of first-degree heart block? Could be, and it probably is the P wave. P waves are usually best seen in V1 or V2.

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ECG 14-15

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ECG 14-16

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ECG 14-17 The ST segments are markedly elevated in this patient’s precordial leads. The T waves are flipped and symmetrical in leads I, aVL, and V2 to V6. What do you think they call this kind of ST segment, and can you imagine why? If you are having any doubts, look at Figure 14-15. These are classic tombstones. They indicate a large myocardial infarction. We have often asked you to obtain an old ECG for comparison before making a definitive diagnosis, but when you see these, you already have the definitive diagnosis. You don’t need any additional information. Can you have these changes with little or no chest pain? Yes. Patients who have altered pain sensation secondary to nerve damage or neuropathies can have silent AMIs. This occurs in normal folks sometimes, as well.

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Figure 14-15: Tombstone segment.

ECG 14-18 This is an example of a biphasic T wave that is pathological. Look at lead V2 and you will notice that it is negative and then positive. Normally, T waves are inverted first positive and then negative — the opposite of the one in the example.

The T wave accompanies a slightly elevated ST segment that is associated with some QRS complex notching in the lateral precordials. When you see notching, you can usually state with some certainty that the ST elevation is benign. In this case, though, you need to be careful because of the pathologic T wave. You will need an old ECG and some corroboration with the patient’s condition to make the definitive diagnosis.


NOTE

Pretend that the T wave is a roller coaster. You need to travel up the mountain first so that the fall will make you gain speed. This is normal. This is good. You don’t start off by going down in order to gain speed to climb the mountain. That is against the laws of theme parks. That is bad.



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ECG 14-17

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ECG 14-18

Ischemia and Injury

The most important diagnosis made with the ST segment and the T wave is that of ischemia and injury. We will spend more time on this in the chapter, Acute Myocardial Infarction (AMI). However, we cannot complete this chapter without raising the issue.

It is not only the presence of ST elevation or depression that makes the ECG ischemic. Various other things must be present. The ST segment should be flat and/or downward sloping (Figure 14-16). The T wave needs to be symmetrical or, if biphasic, it should start with a negative deflection (Figure 14-16). In addition, you should see a regional distribution of ST elevation or depression affecting these leads. Remember when we were discussing vectors and we touched on the concept of regional ECG sectors (the chapter, Individual Vectors, Localizing an Area: Inferior Wall)? To review briefly, the ECG is divided into various sectors corresponding to the septum and the inferior, anterior, lateral, and posterior walls. We will be spending much more time on this in the chapter, Acute Myocardial Infarction (AMI). For now, just remember that the changes have to be in a regional distribution.

ST depression is indicative of ischemia or a non-Q-wave infarction. (The infarction is not transmural and is therefore not associated with a Q wave.) ST elevation, which suggests injury, is usually present in infarction (Figure 14-17). More in the chapter, Acute Myocardial Infarction (AMI).

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Figure 14-16: Ischemia.

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Figure 14-17: Injury and/or infarction.

ECG CASE STUDIES Ischemia and Injury

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ECG 14-19 Look at the ST segments below and you will see quite a few leads with ST depression. The depression is definitely flat and therefore represents ischemia. Now, let’s try to figure out the location. [We will cover this in greater detail in the chapter, Acute Myocardial Infarction (AMI); this is just an exercise.] In the limb leads, the ST is depressed in II, III, and aVF. If you remember, these are the leads that face the inferior wall. In the precordials, we have ST depression in V2 to V6. Leads V5 to V6 represent the lateral wall, and these are also ischemic. V2 to V4 are an extension of the ischemic episode through additional areas. This patient, therefore, has severe inferolateral ischemia involving quite a large portion of the heart.

Why does aVR have ST elevation? Going back to the hexaxial system of the limb leads, aVR is always opposite the rest of the leads. Therefore, if the others have ST depression, then aVR — nonconformist that it is — will show ST elevation. Think of aVR kind of like your kids or your baby sibling. They will always do the opposite just for spite!

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ECG 14-19

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ECG 14-20 This is a classic ECG for an AMI. Notice the ST segments in leads II, III, and aVF. They are flat, elevated, and associated with flipped T waves. Looking at the QRS complexes, take notice of the Q waves in III and aVF. These changes are all consistent with an inferior wall AMI.

There is ST depression in leads I, aVL, and V2 to V6 (and some minimal depression in V1, as well) that is consistent with ischemia.

The ECG is also significant for LVH and a first-degree heart block.

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ECG 14-20 Once again, there is evidence of an IWMI with right ventricular involvement.

LVH is present by multiple criteria, but the ST depression in the lateral leads is not consistent with LVH with strain. This is a continuation of the lateral wall ischemia associated with the infarct. The first-degree heart block may be acutely due to increased vagal stimulation caused by the inferior MI, or it may have been present for an indeterminate amount of time.

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ECG 14-20

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ECG 14-21 This ECG is a veritable smorgasbord of ST segment changes. There is marked elevation in leads II, III, aVF, and all of the precordials. The STs in V1 to V4 are definitely tombstones.

The Q waves in II, III, and aVF are quite significant. There is also a QS wave in V1. Leads V2 to V5 have a very small r wave at the beginning of the complex so they are not truly QS waves. There is, in addition, a late clockwise transition present that could be the result of a significant loss of myocardium in the anterior wall.

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ECG 14-21 This is one of those ECGs that you just don’t want to go near without some clinical correlation. There is evidence of an AMI of indeterminate origin in the inferior leads — significant Q waves. Minimal ST elevation is also present in the inferior leads, but without reciprocal changes in I and aVL. The ST segments in leads V1 to V6 are markedly elevated, consistent with an AMI or a ventricular aneurysm. (Changes with an aneurysm usually do not extend through V5 to V6, so this is less likely.) The patient was having active pain. The only entity that can produce an AMI of both the right and left coronary arterial systems simultaneously is an aortic aneurysm, which you need to rule out aggressively in this patient.

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ECG 14-22 This ECG has some tombstone changes in leads V1 to V4 associated with flipped T waves. The Ts are symmetrical in all of the precordials, and in leads I and aVL. However, they are asymmetrical in the inferior leads of II, III, and aVF.

This is an example of an electrocardiographic pattern that develops when a patient has had a previous anteroseptal AMI that killed off enough tissue to cause a ventricular aneurysm. It is impossible, electrocardiographically, to distinguish this from an acute myocardial infarction. The only way to distinguish between the two is to be lucky enough to have an old ECG with the same findings and, naturally, to talk to the patient and find out about current complaints. There are also some physical examination findings that will help in your differential; you can consult a physical diagnosis book to search them out. Our personal experience is that the tombstoning in a ventricular aneurysm is minimal, but the QS waves cover at least V1 to V3, as in this case. The QT interval also appears normal to slightly decreased. We wish there were some magic rule to give you but, unfortunately, none exists to our knowledge. Whenever you see this pattern, assume the worst until proven otherwise. If the patient is asymptomatic, get an old ECG and contact a cardiologist right away. Remember never to give thrombolytics to an asymptomatic patient unless approved by a cardiologist!


CLINICAL PEARL

Advanced clinicians: Always compare your ECG findings to your patient’s complaints. Administration of thrombolytics for a ventricular aneurysmal pattern is not an uncommon scenario.



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ECG 14-21

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ECG 14-22

Strain Pattern

Strain pattern refers to the secondary ST-segment and T-wave configurations that arise from repolarization abnormalities found in either RVH or LVH. In recognition of the common clinical usage of this term and for the sake of simplicity, we will continue to use the term strain for now. Keep in mind, however, that the preferred nomenclature should simply state the presence of hypertrophy associated with secondary ST-T wave abnormalities.

Right Ventricular Strain Pattern

The vector in RVH is anterior and to the right. This gives rise to an increased R wave component in the right precordial leads of V1 and V2, as we saw in the axis material in the chapter, The Electrical Axis. This increased R:S ratio would be found in RVH alone. There are, however, some other characteristics that add the “strain” to the strain pattern. These are a concave, downward ST segment that is depressed, and a flipped, asymmetric T wave, as seen in Figure 14-18.

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Figure 14-18: Leads V1 to V2.

If the T wave is biphasic instead of inverted, the first part will usually be negative and the second part positive in RVH (and, as we shall see, in a posterior wall AMI). If the first part of the biphasic T wave is positive, it does not necessarily signal pathology.

Acute right ventricular strain, as occurs during a pulmonary embolus, can cause a rotation of the heart and the axis. This will give rise to a particular pattern on the ECG known as the S1Q3T3 pattern. What this means is that there is an S wave in lead I, a Q or q wave in III, and a flipped T in III. This is not, however, pathognomonic of a pulmonary embolus; it can occur in other states. However, if you suspect a pulmonary embolus in the presence of an S1Q3T3 pattern, you do have some additional support for your diagnosis.

Let’s quickly review the criteria for RVH that we have covered so far. You do not need all of the criteria in order to make the diagnosis, but you should have more than one.

1.   P-pulmonale (RAE)

2.   Right axis deviation

3.   Increased R:S ratio in V1 and V2

4.   RVH strain pattern

5.   S1Q3T3 pattern

The most important of these criteria is the increased R:S ratio. Rather than burden you with a large number of facts, we prefer to discuss the concepts. As you progress, you will be able to remember more information and criteria. When you review the book again as an advanced practitioner, which is not too far away, you will remember more of these minor criteria. Just to mention a few more now, they include an incomplete RBBB pattern, an R wave in V1 that is 7 mm or more, S wave in V1 that is 2 mm or more, and a qR pattern in V1.

Have you noticed that there are fewer Level 3 boxes in this part of the book? You are approaching that fine line that separates intermediate from advanced ECG readers. Congratulate yourself. You deserve it!

ECG CASE STUDIES Right Ventricular Strain Pattern

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ECG 14-23 This is the most picture-perfect ECG for RVH that we have ever seen. It almost looks as if it were computer generated, but it actually came from a young woman with pulmonary hypertension. All five criteria are present in this ECG: P-pulmonale (RAE), right axis deviation, increased R:S ratio in V1 to V2, RVH strain pattern, and S1Q3T3 pattern.

It is very important to remember the differential diagnosis points for an increased R:S ratio in V1 or V2. It will greatly assist with your interpretation of the ECG. Carry a flash card until you’ve committed these to memory.

1.   Right ventricular hypertrophy

2.   Right bundle branch block

3.   Posterior wall AMI

4.   WPW type A

5.   Young kids and adolescents

When you see an increased R:S ratio in V1 or V2, run through the list and see which one fits the bill.

ECG 14-24 Let’s try a little experiment. Does this ECG demonstrate RVH with strain? Go ahead and take a close look before you come back.

The answer is no. The ECG shows right axis deviation and a RBBB. If you measure the QRS complexes in V4 to V6, you will see that they are just at or slightly above 0.12 seconds. This makes it a block of some sort. There is also a slurred S in leads I and V6. Why the increased R:S ratio? Go through the differentials offered with ECG 14-23. You will see that this fits into one of the categories: RBBB. This is a tough one.

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ECG 14-24 This ECG shows RBBB with an R wave instead of a full RSR’ complex. Because it is an RBBB, the T waves in the inferior leads and precordials are abnormal. They are strongly concordant, which could indicate ischemia. An old ECG would be very helpful for comparison, and you need clinical correlation to completely interpret the ECG.

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ECG 14-25 This ECG shows a right axis deviation, P-pulmonale, and an S1Q3T3 pattern, but no increased R:S ratio in V1 to V2. The pattern is still one of RVH-with-strain. There is also some pretty significant LVH present, which may account for the absence of the increased R wave in V1 to V2. There is strong evidence of LAE, as well. So putting it all together, you have enlargement of all four chambers of the heart. This could signify cardiomyopathy.

The second beat is a PVC. There is also a borderline first-degree heart block.


[image: image] QUICK REVIEW

1.   You cannot diagnose RVH accurately in the presence of RBBB. True or False.

2.   You can diagnose LVH in the presence of RVH. True or False.

3.   S1Q3T3 pattern is indicative of right-sided strain. True or False.

1. True 2. True 3. True



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ECG 14-23

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ECG 14-24

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ECG 14-25

Left Ventricular Strain Pattern

The left ventricle can also develop a strain pattern if there is significant hypertrophy. Once again, the strain pattern is caused by repolarization abnormalities of the hypertrophied ventricle. The pattern is different from that found in RVH, however, as you would expect. In LVH with strain, we see a pattern of ST depression with downward concavity, and a flipped and asymmetric T wave in the left precordial leads of V4 to V6 (Figure 14-19). In the right precordials, there is a reciprocal change, so to speak, of the left ventricular pattern: ST elevation with upward concavity, and an upright, asymmetric T wave (Figure 14-20). The ST elevation can be 1 to 3 mm in V2 to V3, and in some cases more than that.

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Figure 14-19: Leads V4 to V6.

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Figure 14-20: Leads V1 to V3.

A key point to remember: The strain pattern is the greatest in the lead with the tallest and deepest QRS pattern. In other words, if the S wave in V2 is 15 mm and the S wave in V3 is 20, you would expect V3 to have the highest ST elevation (Figure 14-21). Conversely, if V5 has an R wave that is 20 mm tall and the R in V6 is 15 mm, V5 should have the most depression. Think of it this way: the taller or deeper the wave, the bigger the strain.

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Figure 14-21: ST elevation and depression.

More on LVH with Strain LVH with strain is one of the most problematic interpretations in electrocardiography. This is because you must distinguish it from ischemia and infarction, a potentially life-threatening distinction. As we saw in the ischemia section, ST elevation or depression that is ischemic in nature is usually flat rather than concave, and the T wave is symmetrical, not asymmetrical (Figure 14-22)! This interpretation is easy in some ECGs, but not so easy in others.

A sharp J point is also more indicative of ischemia or infarction. LVH with strain usually has a more diffuse J point in the right precordials, V1 to V3.

The strain pattern in V5 to V6 may become flat or downwardly depressed. The key thing to note is that somewhere in the V4 to V5 area, the complexes will look identical to what you would expect, with concavity downward and an asymmetric T wave (Figure 14-23). Remember, symmetric T waves are bad!

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Figure 14-22

Last but not least, remember the “company it keeps.” If your patient is visiting you because he stubbed his toe, it is more likely strain pattern. If he comes in diaphoretic and complaining of chest pain, with a blood pressure of 60 palpable and looking like he’s going to die, it may be LVH with strain — but you’d better also be treating him for the AMI he is probably having. If you are unsure of your decision, contact a cardiologist. There is nothing wrong in asking for help. Nothing is worse, in our opinion, than to let someone die because of the clinician’s vanity.

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Figure 14-23

ECG CASE STUDIES Left Ventricular Strain Pattern

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ECG 14-26 This is a typical LVH-with-strain pattern. LVH is present by multiple criteria including S in V1 to V2 plus R in V5 to V6 that is more than 35 mm, R in aVL that is 11 mm or more, and R in I that is 12 mm or more. When you first look at the ECG, you see many ST segment and T wave abnormalities. You see downwardly concave ST segment depression in V5 to V6 associated with a flipped, asymmetric T wave consistent with LVH with strain. Notice that the lead with the tallest R wave has the deepest ST depression. In addition, ST elevation in V1 to V2 is upwardly concave. Once again, the highest ST segment elevation occurs in the lead with the deepest S wave. The LVH with strain pattern is carried over to leads I and aVL, the high lateral leads. In addition, there is evidence of LAE, which occurs commonly.

ST depression is always a sign of pathology. The main problem is to decide what pathological condition is involved. Is it ischemia? Is it a strain pattern? BBB? WPW? Is it resolving pericarditis? A CNS event? When you see the abnormality, you must begin the hunt to find the definitive answer. Sometimes there are other clues on the ECG, or on an old one. Sometimes the clues come from the patient. Put on your Sherlock Holmes hat and go to work!


NOTE

A famous lawyer once said …
“If it’s flat, you’ve got to treat that!”



ECG 14-27 So what do you think is causing the ST segment and T wave changes on this ECG? It meets many criteria for LVH and also shows the changes necessary to diagnose the strain pattern. We want you to notice that the ST segments in V6, I, and aVL are flat. They are not indicative of ischemia because of the company they keep. The leads immediately preceding them show concavity downward, and the flat segments are merely a continuation of the process. Also, are the T waves symmetrical or asymmetrical? They are asymmetrical, and this pattern is not indicative of ischemia. Go back and take a look at some of the ischemic ECGs, and you will see the difference. We will be spending a lot more time on this later in the chapter.

One good thing to remember is that the greatest deviation in the ST segment is always found in the leads with the tallest or deepest complexes. Can you identify ischemic pathology in LVH-with-strain? Definitely. The ST segments will not transition through the concave pattern that we are showing you on these ECGs. Recall that the ST elevation of LVH with strain is concave upward in V1 to V3, and the ST depression is concave downward in I, aVL, and V4 to V6. You will occasionally see upwardly concave ST segment elevation in V5 to V6 associated with a small Q wave in LVH. We will show you an example soon.

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ECG 14-26

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ECG 14-27

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ECG 14-28 Now we are going to show you a few more examples of how the ST segment progresses from concave downward to flat in the lateral precordial leads. Look at V1 to V6 in this ECG. We see the ST segment changing from one that is concave upward to flat in V3, to concave downward in V4 to V5, and finally to depressed, downward sloping, and flat in V6. Figure 14-24 gives a simplified look at this progression. This represents a benign transition in a patient with obvious LVH. Note the last statement: in a patient with obvious LVH. If the patient does not have obvious LVH, then all bets are off and this could represent ischemia. That is a key point. The strain pattern is only present in obvious LVH. If you cannot diagnose LVH, you cannot diagnose LVH with strain.

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Figure 14-24: Transition of the ST segments and T waves of the precordial leads in ECG 14-28.

ECG 14-29 This is another example of LVH with strain. As in ECG 14-28, the ST segments progress to a flatter presentation in V6. The flipped, asymmetric T waves in the inferior leads are also caused by LVH. Once again, notice that they are asymmetric and the ST segments are slightly concave downward. You still need to consider other possibilities, however, such as ischemia secondary to tachycardia or CAD.

The rest of the ECG is remarkable for sinus tachycardia and LAE. The QT interval is prolonged.


[image: image] QUICK REVIEW

1.   If a large pericardial effusion is present in a patient with LVH with strain, the voltage criteria may not be obvious. True or False.

2.   You cannot diagnose AMI in LVH. True or False.

3.   You cannot diagnose LVH in LBBB. True or False.

1. True 2. False 3. True



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ECG 14-28

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ECG 14-29

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ECG 14-30 This is another example of LVH with strain. This time we have added a few other goodies to the mix by giving you one with atrial fibrillation and a PVC. It is atrial fibrillation because of the irregularly irregular rhythm with no obvious P waves. The undulating baseline in V1 is a coarse atrial fibrillation pattern. It is coarse because the undulation is very obvious (see also Figure 14-25, top). Compare that with the artifact at the beginning and the end of the ECG, which shows very fine, narrow spikes (Figure 14-25, bottom). It is important to be able to distinguish between artifact and real pathology on ECGs. That is why we have not removed artifact from the ECGs in this book.

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Figure 14-25

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ECG 14-31 A few ECGs ago, we mentioned that some examples of LVH present with small q waves in V6 and are associated with a concave, upward scooping of the ST segments. This is just such a case. The LVH is obvious in this case, but the typical strain pattern is not present. This is a type of strain pattern found in patients with large, dilated left ventricles. It is caused by volume problems (aortic regurgitation, severe mitral regurgitation, and so on), not afterload pressure problems (systolic hypertension). This is an advanced concept, just mentioned here so that you will not be shocked when you see it in a real patient.

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ECG 14-31 Dr. J. Willis Hurst describes two types of LVH patterns. The first is caused by systolic pressure overload as occurs in systolic hypertension or an outflow problem at the aortic valve. This type gives rise to the concave, downward ST depression and flipped T wave that we have already discussed. He also describes a second type, produced by diastolic pressure overload problems in ventricular hypertrophy with high volume (severe mitral or aortic regurgitation). That pattern is similar to the one below, with a small q wave and a concave, upward deflection of the ST segment. (See the Additional Readings section for further information.)

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ECG 14-30

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ECG 14-31

ECG COMPARISONS Benign Changes Versus Infarct

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The toughest thing for any intermediate student is to decide if ST and T wave changes reflect infarct or a more benign form of pathology. We are going to give you 20 examples of each, side by side, to compare. Note that, by saying “good,” we don’t mean normal, but rather the lesser of two evils when compared with an infarct. Let’s get started.

Good: ECG 14-32A These ST segments show the typical changes for LVH with strain. Note the asymmetrical T waves throughout.

Bad: ECG 14-32B These ST segments, in comparison, are flat and either elevated or depressed. Note that they are elevated in the inferior leads of II, III, and aVF, and depressed in the reciprocal areas of I and aVL. We will spend more time on reciprocal changes in the chapter, Acute Myocardial Infarction (AMI). For now, just understand that I and aVL should show changes opposite to those in II, III, and aVF, if there is an AMI present. Note the presence of a pathological Q wave starting in lead III.


CLINICAL PEARL

Always remember that ECGs, just as most medical tests, cannot be interpreted in a vacuum. What we mean is that you have to use all of the information available to you at the time of interpretation to make your diagnosis. “The company it keeps” is our motto. If an ECG looks pathological but the patient does not, question the diagnosis. Could this be a ventricular aneurysm? Could it be someone else’s ECG that was given to you by mistake? Could it be silent ischemia? Could it be an electrolyte problem? Always put your ECG and what you know about the patient together in your mind. If something does not match, there is always a reason.



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ECG 14-32A: Good

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ECG 14-32B: Bad

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Good: ECG 14-33A This is another example of LVH with strain. Notice the quality of the strain changes in A and compare them to the “bad” example in B. Also note that the flipped Ts are asymmetrical in both I and aVL and II and aVF, which could represent pathology.

Hopefully you are picking up on what we are trying to do in this section. We want you to begin to get a feel for life-threatening ST changes. This is a critical step in your development, and you should be sure you understand the differences.

Bad: ECG 14-33B These ST segments are, once again, flat in the reciprocal leads. There is no concavity, or very little, in their slopes. Nor is there any gradual transition to flat. They are just flat to start with. Notice the symmetrical quality of the Ts; they almost blend with the ST segments. This is an IWMI.

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ECG 14-33A: Good

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ECG 14-33B: Bad

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Good: ECG 14-34A This is RVH with strain. The ST segments have a definite concavity. The T waves are also asymmetrical, and there is a smooth transition from the ST segment.

Bad: ECG 14-34B This is an example of a posterior wall AMI. The ST depression is obvious and the slope is negative. Notice how the ST segments transition to horizontal and flat without going through any concave phase. Finally, look at the rhythm strip, which is lead II. The ST elevation suggests an inferior wall MI, as well. Don’t worry about the regions for now; just concentrate on the differences in appearances.

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ECG 14-34A: Good

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ECG 14-34B: Bad

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Good: ECG 14-35A Remember this ECG? It was the strange RBBB with no RSR’ wave in V1. There are diffuse ST segment changes, all concave. Notice the width of the R wave in V1 to V2. It is very wide because of the RBBB; this is an RSR’ pattern.

Bad: ECG 14-35B This ECG also has a wide R wave, greater than 0.03 seconds. There is an increased R:S ratio in V2, although it does not approach 1:1. This time it is not due to an RBBB because there is not an increased R:S ratio in V1, or a slurred S wave in V6. The ST depression in V2 to V6 is pathological. What was the differential diagnosis for increased R:S ratio in lead V1 or V2? If you review the criteria, you will note that this is another posterior wall AMI.

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ECG 14-35A: Good

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ECG 14-35B: Bad

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Good: ECG 14-36A This could be minimal pericarditis, or a variant of normal known as early repolarization. Notice how the waves are benign in appearance. The QRS complexes have some notching in the lateral leads, so the ST segment elevation is therefore associated with a benign cause. There is minimal PR depression, but it is within normal limits. All of the ST segments are concave upward, except for V1. Also note that the lead with the tallest R wave has the most ST elevation.

Bad: ECG 14-36B This ECG has a transition from ST depression to elevation, but the ST segments are always flat. The T waves are symmetrical and broad. Note the increased R:S ratio in V2. Go through your differentials for this finding. What is the most likely culprit? Posterior wall AMI. The ST elevation along the lateral leads is consistent with a lateral wall infarction. Lateral wall MIs are associated with posterior wall MIs. Don’t worry about the exact diagnoses for now; just note the MIs.

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ECG 14-36A: Good

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ECG 14-36B: Bad

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Good: ECG 14-37A This is similar to ECG 14-36A and is due to one of the same two causes. The notching is a bit more obvious, and the ST elevation a little more prominent.

Bad: ECG 14-37B The ST elevation in this ECG starts off flat, with an upward slope in lead V4. This is a sign of an injury/infarct pattern. It affects the lateral leads, and so represents a lateral infarct. Did you notice the rhythm strip at the bottom? The ST elevation in II also leads one to believe that the inferior wall is involved. Make sure you note the differences between the ST segments of the lateral leads in these two ECGs. They’re dramatic.


REMINDER

Notching is usually benign. It can, however, also occur in pericarditis and hypothermia. Once again, remember the motto, “the company it keeps.” If the person is having chest pain that is worse when lying back and eases when sitting up, it is probably pericarditis. If the person has no symptoms and is young, it is probably early repolarization. If the person is cold, has an altered mental status, and the temperature outside is 20° below zero, it is probably hypothermia.



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ECG 14-37A: Good

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ECG 14-37B: Bad

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Good: ECG 14-38A The lateral leads definitely show LVH with strain. The anterior leads are also consistent with the strain pattern, but are a little flat for our taste. We would still be very concerned about this pattern except that the patient also had this on an old ECG, and was asymptomatic. There is still some concavity to the ST segment, and the one with the tallest ST elevation is V1, which has the deepest S wave. With these findings and correlations, we can state that this is LVH with strain.

Bad: ECG 14-38B The main focus of this ECG is the lateral leads. Notice how the ST segments there are deep and flat? This is definitely lateral ischemia and not LVH with strain. LVH is present, but the depression is not indicative of strain. V1 is troublesome but, because it appears in one lead only, it is not highly significant for infarct.

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ECG 14-38A: Good

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ECG 14-38B: Bad

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Good: ECG 14-39A This is another example of a strain or early repolarization pattern. The criterion for LVH is met by adding the S wave in V2 to the R wave in V6. Once again, there is concavity of the ST segments, and the lead with the deepest S wave has the highest ST segment. The J point is quite diffuse in V2, and even in V1.

Bad: ECG 14-39B Badness, badness everywhere.… The ST segments are elevated through all of the precordial leads. The QT interval is short, so it gives the complexes a bizarre appearance. The Q waves in the lateral leads are not significant.

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ECG 14-39A: Good

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ECG 14-39B: Bad

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Good: ECG 14-40A This ECG meets multiple criteria for LVH with strain. LAE is also present. We don’t want to bore you with repetition, but repetition is the only way you can understand the comparison between good and bad. Only after seeing hundreds of ECGs with these changes will you feel comfortable making the call.

Bad: ECG 14-40B The ST segment changes are again indicative of ischemia. The ECG suggests a posterior wall AMI because of the increased R:S ratio, the flat ST segments, and the final positive deflection of the T wave. This time, however, there is no associated infarct in the inferior leads. Lead II also shows ST depression suggestive of ischemia. These diffuse ST depressions are sometimes seen in global subendocardial ischemia (ischemia of the myocardium lining the ventricles).


[image: image] QUICK REVIEW

Matching game:


	A.   Left bundle branch block

	____ 1.   QRS ≥ 0.12 seconds


	B.   Left ventricular hypertrophy

	____ 2.   R wave in aVL ≥ 11 mm


	 

	____ 3.   Monomorphic S wave in lead V1


	 

	____ 4.   Monomorphic R wave in I and V6


	 

	____ 5.   Any precordial lead ≥ 45 mm


	 

	____ 6.   R wave in lead I is ≥ 12 mm


	 

	____ 7.   R wave in lead aVF is ≥ 20 mm


	 

	____ 8.   Non-concordant T waves


	 

	____ 9.   (S in V1 or V2) + (R in V5 or V6) ≥ 35 mm




1. A 2. B 3. A 4. A 5. B 6. B 7. B 8. A 9. B



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ECG 14-40A: Good

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ECG 14-40B: Bad

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Good: ECG 14-41A This is another beautifully clear example of LVH with strain. You should be getting familiar with this pattern by now. Are you starting to feel comfortable with the difference? You should be starting to, but remembering the differences when you are faced with an ECG that doesn’t have a bad one standing next to it is a bit tougher.

Bad: ECG 14-41B This ECG was taken from a patient who had markedly elevated blood pressure and diffuse subendocardial ischemia, similar to ECG 14-40B. However, look at how pronounced the changes are in comparison. The ST elevation in lead V1 is also indicative of injury or infarction.


REMINDER

ST depression in leads V1 and V2 is always pathological in adults. It can be due to right ventricular hypertrophy, a right bundle branch block, a posterior wall MI, or WPW. Think of the differential diagnosis of the problem and see which one of the differentials best matches your patient and the ECG.



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ECG 14-41A: Good

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ECG 14-41B: Bad

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Good: ECG 14-42A Is this one an LBBB pattern? Go ahead and measure the QRS complexes out with your calipers. They don’t quite make it to 0.12 seconds, so it is just a really wide LVH with strain. The amplitude of the QRS complexes is impressive, more than meeting the 45 mm criterion.

Bad: ECG 14-42B This ECG shows the obvious ST deformities characteristic of ischemia. Once again, notice the flat, downward-sloping ST segments.

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ECG 14-42A: Good

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ECG 14-42B: Bad

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Good: ECG 14-43A Even though this ECG is obviously LVH with strain, notice how similar B at right is to leads V1 to V3. The upward concavity is a great tip-off, but this can be deceptive. What can we use to help distinguish between the two ECGs? Remember “the company it keeps.” The lateral leads show the typical changes of LVH with strain on A, but they are not present on B. In many cases, the lateral leads will help you sort out the right precordial leads.

Bad: ECG 14-43B This ECG came from a patient suffering an anteroseptal AMI. The J point is diffuse, but notice the flat ST segments, especially in V1 and V2. What appears to be concavity is actually the symmetrical, broad T wave starting off the ST segment. Draw the two legs of the T wave in V2 down to the baseline to see what we mean. The ST elevation in V4 is also very flat. (Did you notice V6? This is what happens when a lead falls off.)

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ECG 14-43A: Good

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ECG 14-43B: Bad

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Good: ECG 14-44A Are the ST segment changes caused by LVH with strain? Perhaps, but this time the strain pattern is not obvious. Could this ECG be from a young man with some early repolarization changes? Yes, the J point is diffuse and it would match the pattern. Whatever the source, we see some notching in V4 to V6 and definite asymmetry of the T waves, to make us feel comfortable in making the call that this is benign ST elevation. Clinical correlation is mandatory, however.

Bad: ECG 14-44B If you were to look just at V1 and V2, this would be a tough call because some LVH with strain looks just like these leads. However, once you get down to V3, your answer is clear. Bad. This is an anteroseptal AMI with lateral extension.

Look at the similarity between V6 on this ECG and on A. Scary, isn’t it? Remember always to look at the company it keeps — and at the patient!

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ECG 14-44A: Good

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ECG 14-44B: Bad

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Good: ECG 14-45A We are dealing with a wide LVH with strain once again, not an LBBB. There is a late intrinsicoid deflection. (Whoa, there’s something we haven’t discussed in awhile; go ahead and review it on page 45 to refresh your memory.) There is also a very pretty U wave present after the T in most leads, which is a benign finding.

Bad: ECG 14-45B This is an ugly anteroseptal infarct with lateral extension right from V1 through to V6. The ST elevation is quite marked and the T waves are symmetrical.

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ECG 14-45A: Good

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ECG 14-45B: Bad

Bad: ECG 14-46A This ECG appears very benign but there are some things that make it troubling. Can you spot them? Well, for starters, the ST segment elevation in V1 to V2 is flat. Next, the T waves are symmetrical through the entire precordium. There is definitely LVH present, but there is no classic strain pattern. Beware of this benign ECG! It could spell big trouble if you don’t get an old one or correlate it closely to the patient’s symptoms.

Worse: ECG 14-46B Notice that there are QS waves all the way to V4. These QS waves are associated with some tombstoning ST segments. This is an anteroseptal infarct that has been going on for some time and has already formed Q waves. By the way, did you notice the PR interval? Pretty wide.


[image: image] QUICK REVIEW

1.   You can always tell the difference between LVH with strain and an AMI or ischemia. True or False.

2.   The ST segment in LVH with strain is always elevated. True or False.

3.   The ST segment in RVH with strain is always elevated in V1 and V2. True or False.

4.   You can always distinguish the ST elevation of pericarditis from that of LVH with strain or AMI. True or False.

5.   A famous lawyer once said: If it’s flat …

a.   I’m OK with that!

b.   You gotta treat that!

c.   You gotta give a thrombolytic to that!

d.   You can ignore that!

e.   Who cares about that!

1. False! If there is one thing you should always remember, it is that many times you cannot tell the difference between LVH with strain and an acute infarct. You always need to clinically correlate your ECG with your patient. You should also try to obtain an old ECG whenever possible to compare with the new one. I have known many unfortunate clinicians (who have many unfortunate patients!) who have given thrombolytics for LVH with strain in asymptomatic patients. I know many, many more who have not given thrombolytics to patients with AMI because they thought it was just LVH with strain. These are experienced clinicians that have been practicing for years. It is not always clear. Remember, always interpret an ECG in the company that it keeps! 2. False. It is usually depressed in the left lateral leads of V4 to V6. 3. False. The ST segment is usually depressed in leads V1 and V2 in patients with RVH with strain. 4. False! This is another big fallacy. Remember, however, that many times an AMI patient may subsequently develop pericarditis either acutely or after a few weeks (Dressler’s syndrome). Always interpret an ECG by the company it keeps! If you are unsure, get some help! Never assume that you are correct — always make sure that you are before you treat any patient. 5. B.



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ECG 14-46A: Bad

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ECG 14-46B: Worse

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Good: ECG 14-47A Well, we’re back to our benign pattern again. ECG 14-46 was just thrown in there to keep you awake. This ECG is either early repolarization pattern or LVH with some strain in the right precordial leads.

Bad: ECG 14-47B These ST segments are obviously pathological, with flat segments and a positive slope. The T waves in the lateral leads are also flipped and symmetrical. This is an anteroseptal AMI with lateral extension.

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ECG 14-47A: Good

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ECG 14-47B: Bad

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Good: ECG 14-48A This also is benign elevation, due either to LVH or early repolarization pattern. Why do V1 to V2 look so strange? Because there is an incomplete RBBB pattern with an rSr’ pattern.

Bad: ECG 14-48B This ugly, flat ST elevation is associated with QS waves and a late transition, all markers for an anteroseptal AMI of indeterminate duration, but probably not brand new. It is at least a few hours old. There has to have been just enough time to kill off the anterior wall of the heart.

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ECG 14-48A: Good

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ECG 14-48B: Bad

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Good: ECG 14-49A We’re getting close to the end, so hang in there. Believe us, we wouldn’t be spending this much time on this if it weren’t a major problem area for most students.

This is a wide LVH-with-strain pattern with the typical features of the condition.

Bad: ECG 14-49B We have significant elevation in V1 to V2, which is consistent with injury or ischemia of the septal wall.

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ECG 14-49A: Good

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ECG 14-49B: Bad

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Good: ECG 14-50A This is an obvious LVH pattern with the T waves not completely flipped by V6. There is a late intrinsicoid deflection, best seen in V5.

Bad: ECG 14-50A We see elevation in V1 to V4 that is associated with QS waves. This could be significant for AMI of indeterminate age versus ventricular aneurysm. Clinical correlation is required for definitive interpretation.

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ECG 14-50A: Good

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ECG 14-50B: Bad

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Good: ECG 14-51A This is a perfect example of LBBB. It has all of the criteria associated with the electrocardiographic presentation of the block: wide QRS, monomorphic S in V1, monomorphic R in V6. Compare these ST segments and the T waves to those in B. Try to remember the T waves and ST segments in this example. It will help you dramatically when you are trying to determine the extent of pathology in either another block or an AMI.

Bad: ECG 14-51B This ECG shows diffuse ST elevation and flipped T waves in V1 to V5. In addition, there are QS waves in these leads. The transition, therefore, is clockwise and very late. Notice the asymmetry of the T waves.

This ECG represents an age-indeterminate anteroseptal AMI with lateral extension, or a ventricular aneurysm, or both. In the case of an aneurysm, an AMI has always preceded the aneurysm. (Scar tissue from an AMI causes the aneurysm to develop because it is weaker and non-contractile compared with normal, viable myocardium. The force within the ventricle causes the scar tissue to bulge out giving rise to the aneurysmal outpouching of the wall.) An old ECG and clinical correlation are essential to make the distinction between a ventricular aneurysm and an age-indeterminate AMI in these cases.


REMINDER

LBBB patients usually, but not always, have a small r wave at the beginning of the QRS complexes in lead V1. Patients with LVH may or may not have a small r wave; a QS wave is present when there is no small r wave at the start of the complexes in leads V1 and V2 (some authors state that it needs to extend to V3) and is a sign of an age-indeterminate anterior wall myocardial infarction. LBBB patients with no r waves in V1 are easy to diagnose because of the presence of the wide QRS complex and the presence of the rest of the LBBB criteria throughout the rest of the ECG.



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ECG 14-51A: Good

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ECG 14-51B: Bad

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Bad: ECG 14-52A This ECG was obtained when a patient first arrived in the emergency department, complaining of episodes of substernal chest pain that came on at various times during the day and awakened the patient from sleep. There was no active chest pain at the time the ECG was done. Notice the late clockwise transition with QS waves in V1 to V2. The ST segments in V5 to V6 are slightly depressed and have flattened T waves. The decision was made to admit the patient for unstable angina.

Really Bad!: ECG 14-52B Suddenly, 20 minutes later, the patient began to complain of chest pain and ECG B was obtained. Notice how the ST segments and T waves in the lateral leads (and inferiorly — look at the rhythm strip) are now sloping downward and have much more depression than before. The T waves are now pronounced and flipped. This ECG and its brother (A) are classic for the changes that occur in unstable angina. The changes are caused by ischemia of the subendocardial tissue of the ventricles.


REMINDER

ECGs and their findings are not static. The changes that are present on an ECG are only a 12-second movie clip of what is happening in the heart during any particular time period. A pathological process is a continuum of disease and you should not think of it as static. If the clinical history is highly suggestive of a pathological process but the ECG shows nonspecific or minimal abnormalities, do not hesitate in obtaining a repeat ECG in a few minutes. We had one patient who went from a benign ECG to a hyperacute infarct pattern in a matter of 3 minutes. If we had only obtained the first one, we would have been lead into a false sense of security. Obtain an ECG when the story or the symptoms change or when you see a rhythm change on a monitor.



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ECG 14-52A: Bad

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ECG 14-52B: Really bad!

Pericarditis Revisited

We began to introduce you to the concept of pericarditis in the chapter, The PR Interval, when we reviewed the PR segment. If you remember, the PR segment is depressed in pericarditis. Here is the full list of criteria:

1.   PR depression

2.   Diffuse ST elevation

3.   Scooping, upwardly concave ST segments

4.   Notching of the end of the QRS

We have covered numbers 1 and 4 above. Let’s look at the issues with the ST segments. In pericarditis, the ST segments are definitely elevated from the baseline. The amount of elevation is variable and can be quite high, up to 4 to 5 mm. The ST segments are scooped in an upwardly concave pattern; they may start at the end of the QRS notching. Tachycardia is frequently associated with these other findings.

Why are the ST segments elevated diffusely rather than just in certain leads? The entire pericardium is usually irritated. The irritation causes a net positivity of the epicardium, or outside surface of the heart, depicted in Figure 14-26. This net positivity is expressed as ST elevation.

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Figure 14-26: Irritation of the pericardium causes a net positivity in pericarditis.
When you first look at an ECG and see ST elevation in leads I and II (especially if the segments are scooped out and upwardly concave), your diagnosis of pericarditis is very likely. Next, look for the presence of PR depression and notching in these leads and in others, as shown in Figure 14-27. These criteria do not have to be found in every lead, just a lot of them. If you have all of the criteria, you will be about 80% of the way to the diagnosis. You still need one more critical aspect, however: a history and physical examination consistent with pericarditis. If they match the ECG findings, you can make the diagnosis. We suggest that you use a book on clinical medicine to review the findings in pericarditis.

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Figure 14-27: Before studying the ECGs that follow, go back and review ECG 10-1.

ECG CASE STUDIES Pericarditis

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ECG 14-53 This is an example of pericarditis. The PR depression is not very impressive in this example. We urge you to review the other ECGs with pericarditis that we have presented thus far. The ST elevation is present in leads I, II, aVF, and V1 to V6. The QRS complexes have the notching indicative of benign ST elevation. The heart rate is technically not tachycardic, but it is in the 90 BPM range. The patient’s history was consistent with pericarditis, and the ECG clinched the diagnosis.

Now, suppose the patient’s history is not classic for pericarditis but he comes in for, say, a knee injury. Could these changes be seen in another entity? Yes, as long as the PR interval is not depressed greater than 0.8 mm (just under one small block deep), it could be associated with early repolarization. Early repolarization is a benign ST elevation, usually minimal and upwardly concave, that occurs in young people. Sometimes it can be found in middle-aged individuals, but you should get an old ECG to document its prior existence before concluding that it is early repolarization. Any PR depression deeper than 0.8 mm is pathological. When diagnosing pericarditis and early repolarization, we need to remember to look at the company it keeps. You should not make either diagnosis in a vacuum, but only after obtaining a history and carefully considering the differential.

ECG 14-54 This is another example of pericarditis. Can you tell why? Well, there is diffuse ST elevation in leads I, II, III, aVF, and V1 to V6 that is upwardly concave and scooping in nature. There is some notching in the lateral leads. The patient is not tachycardic. Why, then, can it not be early repolarization instead of pericarditis? For starters, the patient’s history was consistent with the diagnosis. This is extremely important to your interpretation of the ECG. Secondly, the PR depression in lead II is 1 mm deep. This is pathological PR depression. Because the rest of the ECG and the history match the diagnosis, we have our answer.


[image: image] QUICK REVIEW

1.   PR depression should be less than 0.8 mm deep. True or False.

2.   Pericarditis patients give you a history of chest pain that hurts worse when they lie down, and is relieved by sitting forward. True or False.

3.   Pericarditis patients sometimes complain of pain when they swallow. True or False.

1. True 2. True 3. True



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ECG 14-53

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ECG 14-54

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ECG 14-55 This ECG was taken on a 24-year-old man who was being admitted to the hospital for a noncardiac problem. What do you think: Is it early repolarization (slang: early repol) or pericarditis? It’s early repol. The patient had no symptoms consistent with cardiac involvement of any kind, and the ECG is consistent with the early repol pattern.


[image: image] QUICK REVIEW

1.   All ST elevation in young patients is due to an early repolarization pattern and is not pathological. True or False.

2.   Pericarditis patients can have an underlying early repolarization pattern on an old ECG. True or False.

3.   ST elevation from early repolarization is flat. True or False.



CLINICAL PEARL

Remember that all ST elevations should be evaluated thoroughly for pathological causes. A young man having an AMI because of cocaine-induced arterial spasm can be misdiagnosed as early repolarization.

ECG 14-56 This ECG is also from a young patient, but this one was symptomatic. The changes are consistent with early repolarization. The patient had been doing some cocaine and was complaining of chest pain. Because he was young, there were no old ECGs to compare. What should you do with this patient? Send him home? Arrange outpatient follow-up?

The answer is that all chest pain in patients doing illicit drugs should be taken very seriously. We think they need to have a myocardial infarction ruled out prior to discharge. Why? Because they will fool you. The infarcts associated with many drugs are caused by spasm, not atherogenesis (plaque formation). In addition, many patients who chronically abuse drugs will develop advanced atherogenesis and heart disease.


[image: image] QUICK REVIEW

1.   Any ST elevation in a patient who is complaining of chest pain and has done cocaine or another illicit drug is benign. True or False.

2.   Any ST elevation in a patient who has taken an illicit drug and who is complaining of chest pain should be taken very seriously. True or False.

3.   Notching is always present in early repolarization. True or False.

1. False 2. True 3. False



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ECG 14-55

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ECG 14-56

STs and T Waves in Blocks

When we look at an LBBB or RBBB pattern, we are struck by the complexity of the shapes. In order to make some sense of the complexes, we need to look at how a normal heart depolarizes and repolarizes, and how a heart with a block (or any other aberrancy) does the same thing. We covered a bit of this in the chapter, The Basic Beat (The T wave), so you can go back there to review.

Under normal circumstances, the heart depolarizes from the endocardium to the epicardium (yellow arrows, Figure 14-28). Logic would dictate that the first cell to depolarize would also be the first wave to repolarize, but that would make this too easy. What really happens is that the epicardium is the first to repolarize, and the repol wave spreads inward toward the endocardium (blue arrows, Figure 14-28). This is because the pressure on the inside part of the ventricular wall is greater than the pressure on the outside.

The depolarization is a positive wave traveling toward the electrode in Figure 14-28. This creates a positive deflection of the QRS complex. The repolarization wave travels away from the epicardium, and from the electrode. Because this negative wave traveling away from the electrode is the same electrically as a positive wave traveling toward it, it results in a positive T wave (Figure 14-28).

The circumstance of a BBB or a PVC is one of pathological transmission of the action potential by cell-to-cell transmission (represented by the diagonal arrows). This will slow down the depolarization and repolarization of the cells. In turn, this produces a state in which the pressure gradient of the heart no longer alters the repolarization wave front. In these circumstances, the repolarization wave will follow the depolarization wave as you would originally expect. The result: The electrode now sees a positive wave coming toward it with depolarization (positive QRS), and a negative wave approaching it during repolarization (negative T wave; see Figure 14-29).

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Figure 14-28

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Figure 14-29

The final word is this: in a bundle branch block, the T wave is always in the opposite direction of the terminal portion of the QRS complex. This is called discordance. If the T wave travels in the same direction as the last part of the QRS, it is known as concordance (Figure 14-30). Concordance is bad, a sign of ischemia in a bundle branch block unless chronically present in old ECGs. In these chronic cases it represents an abnormal route of repolarization.

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Figure 14-30: Discordant and concordant waves.

ECG CASE STUDIES STs and Ts in Blocks

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ECG 14-57 The first thing to decide is whether this is a BBB. Is it wider than 0.12 seconds? Yes. Does it match either an LBBB or RBBB pattern? Yes, it matches an LBBB pattern except in V6. Before you label it an IVCD, let’s think about this for a minute. Remember, we mentioned to you that leads I and V6 should look identical or very nearly so, because they both represent the same area of the heart — the area both of them look at (remember the camera analogy). Then why do they look so different on this ECG? Whoever placed the precordial electrodes on the chest did not do a good job of putting them in the right places. The electrode for V6 was either too high or too anterior. The result is a very different angle than should be seen in V6. It is extremely important to place the precordial leads over exactly the right spots.

Now, imagine that V6 looks like lead I. Would that be consistent with an LBBB? The answer is yes. If you look at V3 to V6, you’ll see that the T waves are in the same direction as the last part of the QRS complex — in this case, an S wave. This makes the T waves concordant with the S wave, a sign of ischemic pathology unless it was present on an old ECG. Notice how, in the other leads, the T wave is opposite to the last part of the QRS complex (discordant). This is normal in a BBB.

ECG 14-58 This ECG shows an RBBB pattern; as a matter of fact, there is a bifascicular block. This is due to the left anterior hemiblock (LAH), which is evident from the limb leads. Which leads are concordant, and which are discordant? Well, the concordant leads are II, aVF, and V2 to V3. The rest are all discordant.


[image: image] QUICK REVIEW

1.   An easy way to remember concordance is to remember that the prefix con- means with. Therefore, concordance means that the T wave’s direction is with the last part of the QRS complex. True or False.

2.   An easy way to remember discordance is to remember that the prefix dis- means against. Discordance therefore means that the T wave’s direction is against the last part of the QRS complex. True or False.

1. True 2. True



ECG 14-59 This, once again, is an LBBB pattern. Which are the concordant leads? Leads V3 to V5 and II are definitely concordant. Leads III and aVF both have T waves that start off negative and end up positive. The negative start makes them both discordant. Notice that there is some additional ST depression in II, III, and aVF. ST depression is normal in LBBB, but because it is not found anywhere else, it is highly suspicious of ischemia. The concordance in the leads mentioned above, along with the inferior ST depressions, makes inferolateral ischemia a very strong possibility.


NOTE

It has been a very long chapter, and the next one will also be long. The reasons are worth repeating. Most of the confusion about ECGs relates to ST segments, T waves, and infarct criteria. We have therefore concentrated on these sections. We hope this has been rewarding for you and has clarified some of your questions. It is crucial that you clearly understand the concepts put forth in these chapters. A little extra effort now will pay off in the future for both you and your patients.



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ECG 14-57

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ECG 14-58

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ECG 14-59


[image: image] CHAPTER IN REVIEW

1.   The J point is the point where the QRS complex and the ST segment meet. True or False.

2.   T waves are normally positive in which leads?

A.   I

B.   II

C.   V3 to V6

D.   All of the above

E.   None of the above

3.   The baseline is a straight line from TP segment to TP segment of adjoining complexes. Any ST elevation can be significant and should be evaluated thoroughly. True or False.

4.   T waves are normally symmetrical. True or False.

5.   If the T wave is more than ______ the height of the R wave, it is considered abnormal.

A.   1/4

B.   1/3

C.   1/2

D.   2/3

E.   3/4

1. True 2. D 3. True 4. False 5. D




[image: image] CHAPTER IN REVIEW

6.   Tall, peaked, symmetrical T waves are usually found in:

A.   Myocardial infarction

B.   Ischemia

C.   Hypokalemia

D.   Hyperkalemia

E.   CNS events

7.   Very broad, symmetrical T waves are classic for:

A.   Myocardial infarction

B.   Ischemia

C.   Hypokalemia

D.   Hyperkalemia

E.   CNS events

8.   ST segment depression is classically found in:

A.   Q-wave AMI

B.   Ischemia

C.   Non-Q-wave AMI

D.   Both A and B

E.   Both B and C

9.   Which of the following is not a criterion for RVH:

A.   P-pulmonale or RAE

B.   Right axis deviation

C.   Increased R:S ratio in V1 to V2

D.   Presence of RVH with strain pattern

E.   ST segment elevation in V1 to V2

10.   Choose the incorrect answer. The differential diagnosis of increased R:S ratio in V1 to V2 includes:

A.   RVH

B.   LPH

C.   Posterior wall AMI

D.   WPW type A

E.   Young children and adolescents

11.   Strain pattern is the greatest in the lead with the tallest or deepest QRS complexes. True or False

12.   ST segment elevation or depression that is ischemic in nature is usually flat and is associated with symmetrical T waves. True or False.

13.   You can see ST segment elevation consistent with LVH with strain even if the criteria for LVH are not met. True or False

14.   LAE is always found in a patient with LVH with strain. True or False.

15.   In a BBB, the T wave always deflects in the opposite direction from the terminal portion of the QRS complex. True or False.

6. D 7. E 8. E 9. E 10. B 11. True 12. True 13. False 14. False 15. True




Putting It All Together

CHAPTER 17

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New Ground

We are entering largely uncharted territory in this chapter. Only a few books try to demonstrate the thought process involved in reading an ECG. Most authors assume that you will use your innate instincts to interpret an ECG once you understand some of the basics. Unfortunately, ECG interpretation is not an instinctual ability imprinted on our RNA or DNA by mother nature to ensure survival of our species. It takes a lot of hard work to learn how to do it. Once you get the hang of it, though, you will wonder why you were never able to. It’s kind of like riding a bike or reading.

Here is the secret of the electrocardiographic universe: Know what a normal ECG is supposed to look like. If the ECG you are looking at does not fit that pattern, then you have pathology present!

The 10 Questions of the Gram

You need a systematic approach to examining ECGs. In this block, we will be giving you a format to follow. It helps if you follow a stepwise approach to interpretation. Our system summarizes the basic steps of electrocardiography. We call it The 10 Questions of the Gram.

1.   What is my general impression?

2.   Is there anything that sticks out?

3.   What is the rate?

4.   What are the intervals?

5.   What is the rhythm?

6.   What is the axis?

7.   Is there any hypertrophy?

8.   Is there any ischemia or infarction?

9.   What is the differential diagnosis of the abnormality?

10.   How can I put it all together with the patient?

Using this approach will simplify your life tremendously. If you answer each of the questions above, you have covered the essential points the ECG can offer.

When you first start using the system, write down all of the abnormalities that you come across. Don’t rely on memory until you are comfortable with the process, because you will inevitably forget something important. When you are finished writing the answers to the questions above, synthesize the solution. The subtitle of this book, The Art of Interpretation, refers to the fact that this process is an art form, especially when you are putting it together with your patient. Keep this thought in mind: The patient is the reason that you obtained the ECG in the first place! This simple test, the ECG, can give you information about the anatomy, pathology, pathophysiology, and pharmacology of the heart. You just need to be able to tease the information out of the paper.

1. What Is My General Impression?

You start out by looking at an ECG and coming up with the main problem. Is the main problem an infarct? Is it hypertrophy? Is it an arrhythmia? Many times, you forget this general overview and you get caught up in the minutiae. This often leads to an incorrect diagnosis.

So how do we start making this initial overview? Well, we mentally compare the ECG in question to a normal example. Know what a normal ECG is supposed to look like. If the one you’re looking at does not fit that pattern, then you have pathology present! Take a look back through the book and find a normal ECG (ECG 9-4, page 92), a normal RBBB (ECG 13-5, page 263), and a normal LBBB (ECG 13-18, page 285). (There are some “normal” variations to each of these types of ECGs, which have been mentioned at various points in the book.) What we want you to do now is study these normal ECGs in great detail. Look at each lead and the general patterns presented. When you are comfortable with the normals, look at abnormal examples of each. Mentally compare the two and pick out the major differences.

Let’s start out by looking at the normal ECG. Note how the QRS complexes are nice and even. Are any of them exceptionally tall or short? Are they thin or wide? Note how the P waves interact with the QRS complexes. Look at the T waves. Are they slightly asymmetrical and not too prominent? They should all look alike. Are they upright in the leads where they should be? Look at the intervals. Do any of them seem longer or shorter than they should? Check the axis. Is it in the normal quadrant? What about the transition in the precordial leads — is it found somewhere in, or between, V3 and V4?

It may seem like a long time, but try to spend about five minutes looking at the normal ECG.

It is even more essential to understand the principles of the general impression in the bundle blocks because of their grossly abnormal appearance. Don’t get flustered by the “ugliness” of the initial gram. Remember the tale of the ugly duckling — except in this case the ugliness will turn to beauty when you make the correct diagnosis.

Now, look at the normal RBBB. Are the QRS complexes 0.12 seconds or more? Is there a slurred S wave in leads I and V6? Rabbit ears in V1? Are all of the T waves opposite the last part of the QRS complexes? Note how the QRS complexes are thin at the onset and then they get wide. What about ST elevation — is there any? Are V1 to V2, and possibly V3, normal? Are their ST segments depressed? Is there normally ST depression in these leads? Look at the complexes closely, and remember that all the intervals are the same. Is that ST segment elevation you are seeing in the inferior leads, or is part of the QRS complex causing it to appear to be ST elevation? Are there any Q waves? Are Q waves normally found in either bundle branch block?

Now, do the same for the ECG with LBBB. Are the ST segments elevated in V1 to V2? Are all the T waves discordant? Note which leads have elevation and which ones have depression. Is there ST segment elevation in V1 or V2, or is it depression? Is there ST segment depression in the left precordial leads of V5 to V6? Is that normal? What about the inferior leads — do they show ST depression? Are there prominent R waves in V1 or V2? Are Q waves anywhere except V normal in LBBB? Is this a new LBBB or was it there on a prior ECG? A new LBBB pattern signifies a possible AMI, aberrantly conducted complexes, or a ventricular rhythm. How does the patient look — stable or unstable?

Make sure you understand what we are getting at in this question. Don’t let the details overwhelm you! Form a general impression. Sometimes you can get so wrapped up in the details that you forget the big picture. Don’t make that mistake!

2. Is There Anything That Sticks Out?

We’re talking about any obvious abnormality on the ECG. In Question 1, we were looking at the whole ECG. In answering this question, we are localizing it to smaller areas. It could be one complex or a group. It may be a couple of leads that just don’t look right. Are they in a particular region of the heart, such as the inferior, lateral, or anterior wall? Are most of the complexes wide and bizarre with an occasional normal P-QRS-T cycle interspersed in the chaos? (If so, this is VTach until proven otherwise.)

If you can quickly diagnose the main pathology, it will help guide the rest of your evaluation of the ECG. Conversely, if you know the patient has some underlying pathology, you could look for related changes on the ECG. For example, if the patient came in having taken an overdose of digoxin, look for rhythm abnormalities associated with dig toxicity such as PAT with block.

Use your evaluation to guide your investigation. This confusing statement refers to the fact that an ECG may give you some clue to the patient’s underlying pathology. Suppose someone shows you an ECG. You immediately notice that it is an IVCD with no P waves. It is wide and very, very ugly. The next question out of your mouth should be: “What is the patient’s potassium level?” You then go and see the patient — who is in a coma — and you look at both arms to check for a shunt. If one is present, end-stage renal disease is probably the culprit. Now, suppose you don’t find a shunt, but instead notice that the patient’s breathing is very fast and deep, and the mental status is altered. You examine the belly, and it is tender. You immediately ask for a fingerstick glucose and a set of blood gases. You have diagnosed diabetic ketoacidosis (DKA). The people around you will be amazed at your diagnostic acumen. You, however, repeat to yourself, “the company it keeps,” and move on to your next case. Impressive!

3. What Is the Rate?

This is a simple question. We don’t just want you to come up with a simple number, though. Tie the rate to the patient. For example, suppose you have a patient breathing rapidly who is also sweaty and in distress. The heart rate should be fast because of the obvious discomfort. However, the rate is 42 BPM. Following the principles you’ve learned in this book, you ask yourself, “Why is the rate so slow?” You notice that there is some ST depression, about 3/4 millimeter sloping down in aVL. Immediately, your razor sharp mind develops the following reasoning process. Could this be high lateral ischemia? Yes, but lateral ischemia is usually not associated with bradycardia. What type of ischemia/infarct is associated with bradycardia? Well, inferior wall IWMI increases vagal tone and causes bradycardia. Could the ST segment depression be a reciprocal change — the first sign of an inferior wall AMI? You’d better believe it! You immediately ask that a cardiologist be contacted to take this patient to the cath lab. You are a hero, and the patient thanks you. Maybe the story sounds a little corny. We understand. Our stories are meant both to teach and entertain. We hope you’re picking up the concepts that they are trying to get across. Think! Put things together! It is not rocket science to come up with great diagnoses. Perhaps you don’t know all the clinical medicine yet, but you will eventually. Use every bit of information that you have learned.

4. What Are the Intervals?

The intervals are crucial to the correct diagnosis. Always measure the widest interval and use that measurement to gauge the other complexes and leads. You need to measure the PR interval, the QRS complex, and the QT interval (Figures 17-1, 17-2, and 17-3, respectively).

The PR interval will either be normal, short, or prolonged. If it is normal, so much the better. If it is prolonged and regular, it is first-degree heart block. But don’t stop there. If it is irregular but lengthening between subsequent beats, you’ve got to think about Mobitz I (Wenckebach) second-degree heart block. If it is irregularly irregular, there are various possible rhythm abnormalities.

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Figure 17-1

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Figure 17-2

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Figure 17-3

5. What Is the Rhythm?

In the chapter, Rhythms we spent considerable time going over how to evaluate the rhythm. Here we highlight certain points that relate to the interpretation of the whole ECG. Always ask yourself the following questions when evaluating the rhythm:

General:

1.   Is the rhythm fast or slow?

2.   Is the rhythm regular or irregular? If irregular, is it regularly irregular or irregularly irregular?

P waves:

3.   Do you see any P waves?

4.   Are all of the P waves the same?

5.   Does each QRS complex have a P wave?

6.   Is the PR interval constant?

QRS complexes:

7.   Are the P waves and QRS complexes associated with one another?

8.   Are the QRS complexes narrow or wide?

9.   Are the QRS complexes grouped or not grouped?

Is the rhythm fast, slow, or normal? Obviously, the differential diagnosis of a rapid rhythm is different from a slow one. We will give you some examples of each type of rhythm (Figure 17-4). You don’t have to memorize them, and keep in mind that the list is not all-inclusive.

Do I see P waves? Are they all the same? The presence or absence of P waves really helps narrow the diagnosis of the rhythm. If there are no P waves, you know that the rhythm has to originate at or below the AV node. Retrograde P waves, however, can originate in the low atrium, or at or below the AV node.

The presence of different P waves will also assist you in making the diagnosis. If there are irregular beats with differing P wave morphologies, you are looking at either premature or escape complexes, depending on whether the different P wave comes early or late. If you have more than three different morphologies, with differing PR intervals, then you have either wandering atrial pacemaker (WAP) or multifocal atrial tachycardia (MAT).

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Figure 17-4

In addition to seeing clear P waves, also think about buried P waves — those occurring at the same time as the previous complex’s QRS complex or T wave. This buried P will give the previous T wave a different morphology than its siblings; the T wave with the buried P may have a hump or be taller than the other Ts around it. Whenever you see a wave that is different than the others, stop and analyze why this is occurring! This is a very critical point. Following this advice will save you a lot of heartache.

Speaking of buried P waves, here is another crucial point. Whenever the heart rate is 150, give or take a beat, think about atrial flutter with 2:1 block. This needs to become instinctual — you shouldn’t even have to think about it. When you see a heart rate of 150 BPM, look at the lead with the smallest QRS complexes and try to find a buried P wave exactly midway between the two Ps you can see.


CLINICAL PEARL

150 BPM = Atrial flutter with 2:1 block until proven otherwise



Is the rhythm regular or irregular? This is another simple question whose answer will greatly assist your final interpretation. Regular beats have a pacemaker setting the pace. It could be atrial, junctional, or ventricular. Either the irregular beats have two or more pacemakers, or the irregularity is the result of irregular transmission through the AV node. The latter situation occurs in AFib, and AFlutter with variable block.

If the rhythm is irregular, evaluate it further by asking yourself if it is regularly irregular or irregularly irregular. In a regularly irregular rhythm, the irregularity occurs at a specified time or period, or in a predictable pattern. There is order in the irregularity. Examples of this type of rhythm include second-degree heart block and premature or escape beats. The latter may come irregularly, but the underlying baseline rhythm is regular.

There are only three true irregularly irregular rhythms: atrial fibrillation, wandering atrial pacemaker, and multifocal atrial tachycardia. This makes the decision easy once you have identified the rhythm as irregularly irregular. Look at the P waves; if you have some, it is either WAP or MAT, depending on whether the rhythm is tach