Final Test 2 Answers

Final Test 2: ECG-1

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 60 BPM	PR intervals: See discussion below
Regularity: Regularly irregular	QRS width: See discussion below
P waves: See discussion below Morphology: See discussion below Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: See discussion below

AUTHOR’S NOTE

We will ask for your patience as you read through the interpretation of Final Test 2: ECG-1. Please read the full explanation, especially the section titled Lesson for the Day. We hope this discussion will open your eyes to some of the realities of clinical medicine.

Discussion:

Let’s start off the evaluation of Final Test 2: ECG-1 by performing a quick scan of what stands out right away. Three things grab our attention:

1. The rate is not consistently regular and appears to speed up slightly from the beginning of the strip to the end (see bracketed intervals above the strip). There is a gradual acceleration without any big, sudden changes.
2. No obvious P waves are present on the strip. However, you could talk yourself into the presence of some deflections that could represent potential P waves before the first three complexes (see red arrows).
3. There appear to be pseudo-S waves at the end of the QRS complexes (see blue arrows).

Keeping these three things in mind, let’s evaluate the strip in our typical methodical fashion.

1. Is the rhythm fast or slow? As we shall see when we answer the next question, the rhythm is slightly irregular, so we can’t really use methods of calculating the rate that require exact measurements. Instead, we need to calculate the approximate rate. In this case, the ventricular rate is approximately 60 BPM (6 beats × 10 seconds = 60 BPM).

2. Is the rhythm regular or irregular? (If irregular, is it regularly irregular or irregularly irregular?) This rhythm is irregular because there appears to be a slow acceleration of the rate between each complex consistent with the type of inspiratory variation typically found in sinus arrhythmia (see R-R measurements above the strip). The gradual acceleration makes this a regularly irregular rhythm.

As a quick review, we typically see this type of rate variation occurring when the respiratory cycle causes intrathoracic pressure changes and transient blood flow fluctuations. As a response to the additional movement of blood into and out of the thoracic cavity, the heart rate changes to accommodate and maintain a constant cardiac output (CO = HR × VR [where VR is venous return]). Remember, inspiration causes a decrease in intrathoracic pressure, a resultant increase in venous return, and an increase in the heart rate to compensate for the increased volume. Expiration reverses that cycle.

Note that the fluctuating venous return affects the pacemaking functions by baroreceptor feedback loops and the autonomic nervous system. The actual pacemakers affected by this loop are not isolated strictly to the sinus node.

3. Do you see any P waves? On close examination, there appear to be a few minimal deflections before the first three complexes (see red arrows) that do not match morphologically or have the same PR intervals. This points us in the direction of baseline artifact causing the fluctuations.

4. Are all the P waves the same? See discussion below.

5. Are the P waves upright in lead II? See discussion below.

6. Are the PR intervals normal and consistent? See discussion below.

7. What is the P:QRS ratio? See discussion below.

8. Are the QRS complexes narrow or wide? The QRS complexes are narrow at 0.11 seconds, consistent with a supraventricular origin. Note that the QRS complexes would be narrower if there were no pseudo-S waves present.

For the sake of discussion, could this be a right bundle branch block (RBBB) appearance either due to an actual bundle branch block or secondary to aberrancy? Yes, since the width of the QRS complexes could appear narrower in certain leads depending on the presence of isoelectric segments. As such, since we are looking at only a single lead, we cannot rule out that possibility. To truly answer that question, you would need to get a full 12-lead ECG and obtain the true QRS interval.

9. Are the complexes grouped or not grouped? Not grouped.

10. Are there any dropped beats? No, there is no evidence of any dropped beats.

Putting It All Together. At this point, note that if there were no real P waves present, this would represent a junctional rhythm due to the narrowness of the QRS complexes. Other factors in favor of a junctional rhythm include the relatively slow rate of 60 BPM and the fact that the morphologic appearance of the terminal portion of the QRS complex looks like a pseudo-S wave (see blue arrow). (Remember, a pseudo-S wave pattern is caused by a retrogradely conducted atrial depolarization wave.) Finally, two facts serve as additional indirect proof of a junctional rhythm: (1) The last three beats in the strip do not have any possible P-wave deflections at all before the QRS complex, and (2) the respiratory cycle is not broken. Our final answer is, therefore, junctional rhythm with rate-related respiratory variation.

 

CLINICAL PEARL

In our sister textbook, 12-Lead ECG: The Art of Interpretation, we state that “intervals are intervals.” What we mean is that intervals are always the same value throughout the ECG. Certain leads have some “invisible” isoelectric segments that make the interval appear to be narrower depending on the lead. For that reason, we always promote taking the interval measurement in the lead that shows the widest value. That specific lead is the one that does not show any isoelectric “invisibility” and reflects the true value for the interval.

 

Lesson for the Day

I can still remember, as a wise teenager, confronting one of my teachers about an answer I thought I had gotten correct on a test. After I stated my case, I remember feeling embarrassed when I realized I had overlooked one simple tiny thing. I proceeded to plead, “Well, I was at least close. Could I get partial credit?” The teacher simply stated, “Son, close only counts in horseshoes and hand grenades.” Believe it or not, that simple comment proved to be a big life lesson for me, full of simple wisdom and humor at the same time.

When writing our texts, we set out with an intent to teach the reader how to read and interpret actual clinical strips and ECGs by understanding the mechanisms and principles involved—rather than creating practitioners who can identify only pristine, picture-perfect examples using strictly pattern recognition. In your daily practice, approximately 99% of all strips handed to you will not be perfect, and since strips are like fingerprints (no two are the same), pattern recognition by itself will fail you. Likewise, interpretations that are “close” are just not good enough. If you suspect or see anything abnormal or atypical, no matter how small or trivial, spend the time to figure out the cause. Don’t assume anything or ever settle for “close enough.”

If you reread our original interpretation of this strip, you’ll notice that we used a lot of qualifiers, such as “if,” “could be,” and “kind of.” When you see an interpretation that has that many qualifiers, it is a sign that the interpreter is unsure of the interpretation and is trying to hedge his or her answer. If you ever find that you are trying to convince yourself of your findings, you should stop and reassess your reasoning, because you are only trying to fool yourself. Typically, the more certain you are of your diagnosis, the less wiggle room you will need to defend your position.

Let’s go back and look at the strip again. Could those small deflections in front of the first three QRS waves be P waves? Why do they disappear in the last three complexes? Well, we talked about the respiratory changes in ECG morphology that develop in the main isoelectric limb lead due to small changes in the anatomic orientation of the heart and the main electrical axis. Those same directional changes also apply to the orientation of the main P-wave vector, the main ST-segment vector, and the main T-wave vector. Note that each one of those smaller vectors also has its own intrinsic isoelectric lead where the morphologic variations can appear exaggerated. Could lead II be the isoelectric lead for the P-wave vector, causing certain parts of the tracing to appear and reappear due to the respiratory changes? The answer is, as you can imagine, yes.

We mentioned the possibility of a pseudo-S wave at the end of the QRS complex. We failed, however, to think about alternative ideas to explain a morphologic difference similar to this one. Could the QRS complexes actually be greater than or equal to 0.12 seconds, rather than 0.11 seconds, and therefore be representative of an RBBB? Once again, the answer is yes, because there could be one or multiple isoelectric segments hiding the true width of the QRS complex.

So, once again we have rambled about possibilities but have done nothing to resolve our differential diagnosis. The bottom line is that we can make a lot of assumptions, or we can choose a simple way to arrive at the correct answer by getting a 12-lead ECG or a strip with multiple standardized leads. Remember, the monitor measures vectors, and vectors change in appearance depending on their orientation to the leads and to each other. This perspective can also change the interval widths as isoelectric segments develop and are more clearly seen or hidden in certain leads. Armed with this information and a possible solution, let’s take a look at Figure 1.

Figure 1 Notice that the obvious P waves in lead V₁ do not always translate into lead II.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

Description

Looking at just these two leads, we clearly see that there are P waves before each QRS complex. That rules out junctional rhythm. The pseudo-S wave pattern is clearly not caused by a retrograde P wave, but by an RBBB pattern within a QRS complex that measures greater than or equal to 0.12 seconds. (Note: Since we’ve mentioned about 100 times that we should never use a rhythm strip to evaluate morphology, we should definitely obtain an ECG before making a definitive diagnosis of RBBB.)

Why did we not see the possible P-wave variations on the last three complexes of our original strip? Because the orientation of the heart anatomically is shifted between being more vertical and/or more horizontal based on the diaphragmatic movement that occurs during respiration. That slight shift in anatomy also shifts the electrical axis by a few degrees. In all cases, the isoelectric lead typically shows more variation than the other because any minor change in the axis can change the amplitude of the waves from positive to negative or vice versa. In our case, those few degrees made the axis even more isoelectric in that lead, causing the disappearance of those very small deflections.

In closing, our “no horseshoes or hand grenades” diagnosis is sinus arrhythmia with a heart rate of 60 BPM in a patient with an underlying RBBB. Always focus on the unexpected; it is likely that this will be the key that opens the lock. In the words of Sean Connery in the movie The Untouchables: So endeth the lesson.

AUTHOR’S NOTE

We are aware that the original test question did not provide the second strip we show in the test answers. We did not intentionally mislead you to get the answer wrong. Instead, this reflects how the original presentation of this actual patient took place in a clinical setting. You are not always handed multiple strips right from the start and, once again, our purpose is to introduce you to problems you will encounter in the “real world.”

The true intention behind this strip is to drive home the point that a single rhythm strip can be deceptive and may even lead to misdiagnosing the rhythm. Unfortunately, scenarios such as this happen in real clinical settings all the time. The key takeaway point from this example is to remember that if there are any discrepancies at all on any rhythm strip, multiple leads or a 12-lead ECG should be immediately obtained. In our experience, by consulting on hundreds of examples similar to this one, we have adopted a clinical knee-jerk reflex to obtain a 12-lead strip or ECG the second we diagnose any clinically significant arrhythmia. We recommend that you adopt that principle early in your training.

Final Test 2: ECG-2

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 125 BPM (see discussion below)	PR intervals: 0.12 seconds
Regularity: Regular	QRS width: Wide
P waves: Present Morphology: Upright in II, humped Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: 2:1	Rhythm: Focal atrial tachycardia with block

Discussion:

The general impression when looking at Final Test 2: ECG-2 is that it is rapid and regular with wide QRS complexes of a complicated nature (lots of deflections). There appears to be a bi-humped P wave before each QRS complex with a normal PR interval. The rate is rapid and regular at about 125 BPM. For the sake of this discussion, we have labeled each of the obvious P waves with a blue arrow. So far, this strip is fairly routine, but there are many irregularities to address.

One of the first things that stands out is the strange looking ST-T–wave area. First, does anything look like an actual T wave? There is a hump after the QRS that occurs relatively early in the cycle. This is especially strange because, as we mentioned previously, the QRS complex is wide. Wide QRS complexes can occur for many different reasons, including bundle branch blocks, aberrancy, electrolyte abnormalities, and ventricular complexes. Note that almost all differentials include causes that prolong the QT, rather than shorten it as abruptly as seen in this strip.

As a side note, the appearance of the wide QRS complexes with a slurred S wave at the end in lead II is typical of an RBBB pattern. Since we can’t really give a great answer by looking at a rhythm strip because we have no standardization of the lead, we should get a 12-lead ECG to confirm.

Now, take a look at the area targeted by the red arrow. Notice anything unusual? That area appears to be double humped as well. As a matter of fact, it is almost identical to the obvious P waves found before each QRS complex. Could this be a P wave? Let’s place a small arrow on top of that (see the red arrow in Final Test: ECG-2). Do the P waves map? Yes, they definitely do! When we calculate the P-wave rate, it comes out to exactly 250 BPM, which is double the QRS rate (Figure 2). Therefore, we know that the conduction rate is 2:1 and there is an associated block of the second P wave in each complex.

Figure 2 This multilead strip demonstrates the points from the discussion more clearly. Note the mapping of the two P waves throughout the strip and the presence of blocked complexes throughout.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

Could this be an atrial flutter? The lack of a continuously undulating F-wave pattern (saw-tooth) in either of the leads is not consistent with atrial flutter. Another clue is that the P waves in this strip have identical morphologies. Flutter waves are never double humped.

The rapid rate, the return to flat baseline after each P wave, the identical morphologies of the P waves, and the block clearly point to a focal atrial tachycardia with 2:1 block. The morphology of the QRS complexes and the fact that they are positive in lead V₁ also help identify the RBBB morphology.

Final Test 2: ECG-3

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 60 BPM	PR intervals: Prolonged at 0.28 seconds
Regularity: Regularity with one PAC	QRS width: Normal
P waves: Present Morphology: Bi-humped Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Sinus rhythm with first-degree AV block with one PAC

Discussion:

Final Test 2: ECG-3 can be quite confusing when you first look at it. To be honest, a few rhythms and events crossed our minds when we first looked at it, including the possibility of a long-stringed Mobitz I second-degree AV block or Wenckebach. It is cases like these that require you to stop and break down exactly what you are seeing.

Let’s start off by isolating the P waves. Placing a marker on the first five P waves (see numbered blue circles below the strip), we see that they are the same morphology and the same PR intervals and that they map out exactly. If we continue to map the same P-P interval to the end of the strip, we see that the sixth P wave is buried inside a QRS complex (of the premature atrial contraction [PAC] discussed later) exactly on time with the other native P waves. Note that all of the blue-labeled P waves are conducted with a prolonged PR interval (first-degree AV block).

With the P waves mapping normally, let’s turn our attention to the area under the bracket labeled compensatory pause. The regular rhythm of the strip is broken by what appears to be a buried P wave in the T wave of the fifth complex. The PAC conducts normally and triggers the early beat identified by the red dot. The PAC does not reset the node, leading to a compensatory pause, and the sixth P wave arrives on schedule. However, the sixth P wave is blocked and fails to trigger any QRS (see large green QRS marker with the red X).

Final Test 2: ECG-4

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 88 BPM	PR intervals: 0.16 seconds
Regularity: Regular	QRS width: 0.12 seconds
P waves: Present Morphology: Inverted P waves Axis: Inverted P waves in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Ectopic atrial rhythm

Discussion:

The first thing we notice when we look at Final Test 2: ECG-4 is the inverted P waves in lead II. The QRS appears wide and measures exactly 0.12 seconds. The wide QRS could be due to an underlying bundle branch block, ventricular rhythm, or aberrancy. Since the rate is only 88 BPM, aberrancy would be lower on the list of possible causes.

The T waves are fairly flat but demonstrate a biphasic morphology with an initial downward deflection. The T waves and the TP segment appear to fluctuate a bit on the baseline since lead II is the isoelectric lead for those areas. Remember, the isoelectric lead tends to have slight morphologic changes since minor changes in the orientation of the electrical axis are more pronounced there.

The low voltage of the T waves makes measuring the QT interval somewhat troubling, as the slight variability present makes an accurate measurement difficult at best. Remember that taking a measurement from an area that is not a true part of the T wave can lead to errors in obtaining a true QT/QT_c interval. To obtain the true QT/QT_c interval, we need to obtain a tracing from a lead that has a well-demarcated T wave. Once again, a 12-lead ECG would clear up discrepancies caused by a hidden isoelectric segment in this lead.

Putting it all together, we have inverted P waves in lead II and an atrial rate of 88 BPM, making this an ectopic atrial rhythm (in a patient with a possible underlying bundle branch block).

Final Test 2: ECG-5

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 102 BPM	PR intervals: Normal
Regularity: Regularly irregular	QRS width: Wide
P waves: Present Morphology: Upright Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: Variable	Rhythm: Sinus tachycardia with a ventricular salvo and couplet

Discussion:

Final Test 2: ECG-5 is deceptively benign at first glance. However, it is a wolf in sheep’s clothing. The first thing you notice is the regularly irregular rhythm. Let’s start by calculating the rate. The rate in the normally conducted complexes is 102 BPM. Do we see P waves? Yes, there are obvious P waves present. Your next thought should be, do the P waves map out throughout the strip? The answer is, yes, they do (see blue arrows).

The regularity of the ventricular complexes matches the P waves where they are normally conducted and there is a 1:1 relationship of P:QRS in the narrow beats. The regularity of the rhythm is broken by the wide complexes (complexes 2, 3, 4, 5, and 10 [see green arrows]), which have their own intrinsic ventricular rate and are dissociated from the P waves. In other words, there is AV dissociation. Remember, AV dissociation is a hallmark criterion for VTach.

The second P wave on the strip fails to capture and is partly buried, fusing with the premature ventricular contraction (PVC) that initiates a salvo of four complexes. The green arrows show the salvo is regular with its own rapid rate at 120 BPM. The last two complexes are morphologically similar to the ventricular complexes found in the previous salvo. Since only two ventricular complexes are seen in this strip, we are choosing to call these a ventricular couplet.

For the sake of completeness, we would like to address some questions that you may have. You may think that the salvos could be an aberrantly conducted accelerated junctional tachycardia. A couple factors make this a viable alternative: (1) The QRS complexes are definitely wide at 0.12 seconds. QRS intervals in the 0.12- to 0.14-second range are commonly seen in the majority of uncomplicated bundle branch blocks and in aberrant conduction. In general, ventricular complexes tend to be wider since there is more area to depolarize by direct cell-to-cell conduction. (2) The initial inflections of the QRS complex (the R wave in our case) in both the native and wide complexes are similar, if not identical. Once again, this finding favors aberrant conduction.

So, is this an example of a wide-complex supraventricular tachycardia? No. VTach commonly presents with a QRS interval of 0.12 seconds. It happens all the time. In addition, the fact that AV dissociation is present during the salvos is very strong evidence that we are dealing with a unifocal, nonsustained VTach.

A Word of Clinical Advice

There is a general clinical rule that any wide-complex tachycardia is ventricular tachycardia until proven otherwise. Always keep that rule in mind, because it is there to save you from yourself and keep you from making a fatal mistake.

In clinical scenarios, you will not always be afforded the time to fully investigate a strip and you could be faced with two viable possibilities. If you find yourself in such a situation, make a quick list of the potential diagnoses involved. Then, prioritize that list into the following order:

1. What can kill my patient?
2. What can hurt my patient?
3. Other stuff

Always concentrate on and treat the things that can kill your patient first, then focus on what can hurt the patient, and, finally, worry about the rest later. Prepare yourself ahead of time for those high-stress situations, remain calm and collected, trust your gut, and make the smartest decision you can with the information you have available. Remember the sage words of Louis Pasteur, “Chance favors the prepared mind.”

Final Test 2: ECG-6

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 70 BPM	PR intervals: 0.20 seconds
Regularity: Regularly irregular	QRS width: 0.10 seconds
P waves: Present Morphology: Upright in lead II Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Sinus arrhythmia

Discussion:

In Final Test 2: ECG-6, the gradual change in R-R intervals causing a slow acceleration and deceleration pattern is consistent with a respiratory-induced sinus arrhythmia. There is a borderline first-degree AV block present with a PR interval of exactly 0.20 seconds.

Morphologically, this strip has some findings that we are bringing up only for discussion with the more advanced electrocardiographers out there. Remember that morphologic features should not be truly evaluated in a nonstandardized rhythm strip from a monitor. The features in question are PR depression, notching at the end of the QRS complex, ST elevation, and the overall broad, symmetrical appearance of the T waves. The leading contenders in our differential diagnosis for this set of findings are pericarditis from any source or pericardial involvement of a STEMI. In either case, a 12-lead ECG would prove invaluable in making a more definitive diagnosis.

Final Test 2: ECG-7

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 110 BPM Ventricular: 36 BPM	PR intervals: 0.20 seconds
Regularity: Regularly irregular	QRS width: 0.14 seconds
P waves: Present Morphology: Upright in lead II Axis: Normal	Grouping: Present
	Dropped beats: Present
P:QRS ratio: 3:1	Rhythm: High-degree AV block

Discussion:

Final Test 2: ECG-7 definitely shows a high-degree AV block with 3:1 conduction. In addition, the conducted P waves show a PR interval of 0.20 seconds, which is additional evidence for a diseased AV node. The QRS complexes are wide at 0.14 seconds, but you cannot isolate the point of origin for these complexes. For further morphologic evaluation, a 12-lead ECG should be obtained.

A quick note about terminology: Since the dropped beats occur in a consistent pattern that matches the AV block family and since the rhythm doesn’t match Mobitz II or third-degree AV block chronology, we call this a high-degree AV block. Clinically, these rhythms are dangerous and are associated with significant morbidity and mortality. These patients are usually hemodynamically unstable since the ventricular rate is slow (in our case, 36 BPM), and wide QRS complexes are fairly commonly associated with them. The relative ventricular bradycardia from the nonconducted beats and the lack of synchronized contractions of the ventricles cause a decrease in the amount of blood ejected during each systolic contraction (lower ejection fraction) and a lower general cardiac output.

 

CLINICAL PEARL

Be careful with these patients! Always have the equipment (including pacemakers) and drugs you may need to treat for a possible arrest at their bedside. Call your consultants early, if you need to. Remember the Boy Scouts’ motto: Be prepared!

 

Final Test 2: ECG-8

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 75 BPM at onset	PR intervals: 0.16 seconds at onset
Regularity: See discussion below	QRS width: 0.10 seconds at onset
P waves: Present at onset Morphology: Upright in lead II Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Torsade de pointes

Discussion:

Using Bazett’s formula of QT_c = QT/square root of R-R, we arrive at a QT_c of 0.54 seconds (QT = 0.48 seconds; QT_c = 0.54 seconds, or 540 ms). Remember, the QT_c is considered long if it is greater than 440 ms in men and 460 ms in women. Final Test 2: ECG-8 shows a very prolonged QT_c and would be associated with an overall increased risk of developing torsade de pointes. Our patient with a QT_c of 540 ms is well within the danger zone for torsade de pointes and does develop that rhythm after the first two beats.

Note the “twisting of points” pattern that is classic for torsade de pointes. The presence of the prolonged QT_c goes along with a diagnosis of torsade de pointes rather than polymorphic VTach in our patient. Further monitoring and treatment are indicated.

Final Test 2: ECG-9

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 104 BPM Ventricular: 36 BPM	PR intervals: See discussion below
Regularity: Regularly irregular	QRS width: 0.17 seconds
P waves: Present Morphology: Bi-humped, upright in lead II Axis: Normal	Grouping: None
	Dropped beats: None
P:QRS ratio: Unable to assess	Rhythm: Third-degree AV block with sinus tachycardia and an idioventricular escape rhythm

Discussion:

To come up with the correct diagnosis on Final Test 2: ECG-9, we have to break it down to its individual components. Let’s start by looking at the P waves. The P waves are bi-humped in morphology and upright in lead II, giving it a normal axis. Note that the bi-humped morphology is due to left atrial enlargement.

In addition, the P waves all map out throughout the strip (see red dots). Some of them are clearly visible and others are buried inside a QRS complex or in the ST-T–wave area (see blue arrows). Now, take a look at the buried P wave identified by the red arrow. Notice the pseudo-r′ wave at the end of that complex compared to the other QRS complexes. The buried P wave is fusing with the QRS morphology and causing that pseudo-r′ wave. The green arrow points to a bizarre peak that is caused by artifact.

The PR intervals in these beats are different and the P waves are not associated with or capturing the ventricular complexes. This is an example of complete or third-degree AV block.

Turning our attention to the ventricular complexes, we see that the QRS complexes are 0.17 seconds wide. That should give you a clue to the origin of the complexes. Remember, when a QRS complex is wider than or equal to 0.16 seconds, it is more likely originating in the ventricular tissue. Taking the width of the complexes and the ventricular rate of 36 BPM together makes this an idioventricular escape rhythm.

Final Test 2: ECG-10

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 70 BPM	PR intervals: Variable
Regularity: Irregularly irregular	QRS width: 0.10 seconds
P waves: Present Morphology: Variable (see discussion below) Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Wandering atrial pacemaker

Discussion:

When we first look at Final Test 2: ECG-10, it is obvious that there is some irregularity and that the P-wave morphologies and PR intervals appear different. As a matter of fact, there are obviously more than three P-wave morphologies, each with different PR intervals. Using our calipers, we can state with certainty that the intervals are not the same throughout the strip and the rhythm is irregularly irregular. We have taken the extra step and measured each of the PR and R-R intervals on the strip for your convenience.

Possibilities in our differential diagnosis for irregularly irregular rhythms include atrial fibrillation, wandering atrial pacemaker (WAP), and multifocal atrial tachycardia (MAT). Since there are P waves present, we know this is not atrial fibrillation. That leaves WAP and MAT, which are both associated with at least three different P-wave morphologies and different PR intervals. A rate of 70 BPM narrows our field down to the correct answer: WAP.

Final Test 2: ECG-11

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 150 BPM	PR intervals: Variable
Regularity: Irregularly irregular	QRS width: Variable but < 0.12 seconds
P waves: Present Morphology: Various morphologies present. Some nonconducted P waves. Axis: Variable	Grouping: None
	Dropped beats: Some nonconducted P waves
P:QRS ratio: See discussion below	Rhythm: Multifocal atrial tachycardia

Discussion:

The P waves on Final Test 2: ECG-11 are very difficult to visualize because the underlying tachycardia causes most of them to be buried or fused with the QRS complexes and ST-T–wave areas of the complexes. In those cases, the presence of the P waves can only be inferred.

The only irregularly irregular rhythm with at least three P-wave morphologies with varying PR intervals presenting at a tachycardic rate is MAT. The various morphologies are due to the differing P-wave vectors that are initiated by the varying ectopic foci that are scattered throughout both atria. The resulting tracings formed by the vectors create at least three different P-wave morphologies that vary between upright, flat, isoelectric, biphasic, and inverted. Due to the tachycardia, some P waves are blocked or conduction through the ventricles is aberrant, as is common in these fast MATs.

MAT typically has a rate of 100 to 150 BPM, but the rate can be as high as 250 BPM in rare cases. Our example has a calculated rate of approximately 150 BPM (15 beats in a 6-second strip = 15 complexes × 10 [number of times 6 seconds fits into a 1-minute interval] = 150 BPM).

Many patients with MAT have associated pulmonary pathology and ECG changes of RA or RV hypertrophy or pulmonary hypertension. Obtaining a 12-lead ECG would be advised to evaluate the rhythm further and to evaluate any potential evidence of pulmonary involvement. Oftentimes, rapid MAT can be found as an intermediary rhythm between sinus tachycardia and atrial fibrillation or flutter.

Final Test 2: ECG-12

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 300 BPM Ventricular: 150 BPM	PR intervals: Unable to assess
Regularity: Regular	QRS width: Narrow
P waves: F waves Morphology: F waves Axis: Upright in lead II	Grouping: 2:1 ratio
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Atrial flutter with 2:1 block

Discussion:

Final Test 2: ECG-12 is a hard strip to evaluate. The complexes are obviously small and narrow, and the rate is rapid. There appears to be an undulating baseline, and a ventricular rate of 150 BPM. Immediately, a ventricular rate of 150 BPM should reflexively make you think of atrial flutter. However, there are other rhythms that can cause a ventricular rate of 150 BPM and we need to keep those in mind.

Let’s start off by taking a look at the “T waves.” Atrial flutter is formed by a circus movement, and, as such, they are not typically notched. Instead, the circus movement leads to a smooth transition from wave to wave in a saw-tooth pattern. Examining the baseline pattern on the strip, we can talk ourselves into there being a continuously undulating pattern that would fit an atrial flutter’s saw-tooth pattern. However, the T waves in this strip show two distinct peaks at the top that are not typically seen in an atrial flutter. Since we don’t have an exact fit for our diagnosis, we need to give this a bit more thought and take a serious look at those T waves.

For the sake of discussion, let’s assume that the notches at the top of the T wave represent a buried atrial wave (either a P wave or an F wave, for now) and the top of the T wave. Which one is the atrial wave and which one is the T wave? To answer this, we have to experiment a little. Let’s start by placing the left caliper pin on the first of the two peaks of the T wave. Then, place the right pin on the same first T-wave peak of the subsequent complex. Divide that distance in half and place the left pin back on the first peak of the T wave. Does the right pin fall on anything that could represent another atrial wave? Yes, it falls on a strange little hump at the start of each QRS complex. Does that distance map throughout the entire strip? Yes, you can walk your calipers up and down, and the two humps (the one before the QRS complex and the first peak of the two on the T wave) directly map out throughout the strip.

Besides atrial flutter, can you think of any other possible rhythm that could account for the 2:1 conduction? Yes, focal atrial tachycardia with 2:1 block. This possibility could also account for the atypical undulation and notching of the waves. However, rates that high are rare.

So what is our rhythm? Unfortunately, we do not have an exact answer and, as our friends in the electrophysiology lab tell us constantly, it is often difficult, if not impossible, to differentiate between an atrial flutter and a focal atrial tachycardia on a surface ECG. The only way to prove either beyond a reasonable doubt is to take the patient to the lab and do precise intracardiac mapping and evaluation. When confronted with such a strip, the present consensus is to err on the side of calling it an atrial flutter.

We’d like to wrap up the discussion on this strip with an observation. We are constantly confronted by irate clinicians who claim we overdiagnose focal atrial tachycardia with block and that it is not clinically relevant in today’s medical environment. However, we believe many of the cases diagnosed as atrial flutter are in reality focal atrial tachycardia with block. It is, in our opinion, underdiagnosed. A leading source of contention is the belief that atrial rates over 250 BPM are not found, but this is not the case and there are exceptions to the rule.

ECG interpretation and arrhythmia recognition typically involve more than one criterion to make a diagnosis. Learn to match as many criteria as possible to the strip; do not disregard some inconvenient presentations for the sake of simplifying the identification of a rhythm disturbance. In our example, there were humps that couldn’t be easily accounted for. You need to spend the time to account for them and not simply ignore that they exist.

Final Test 2: ECG-13

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 70 BPM	PR intervals: Not applicable
Regularity: Irregularly irregular	QRS width: 0.08 seconds
P waves: None Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: None	Rhythm: Atrial fibrillation with digoxin effect

Discussion:

The first few things that stick out when we look at Final Test 2: ECG-13 is that there are no P waves, the rhythm appears irregularly irregular, and the ST segments have a scooped-out appearance. As a learned habit, when we think of the differential diagnosis of the irregularly irregular rhythms, we always think of atrial fibrillation, WAP, and MAT. Out of those, the only one that does not have P waves is atrial fibrillation.

The ventricular rate is 70 BPM (7 ventricular complexes in a 6-second strip = 7 × 10 = 70 BPM). Since there are no P waves, there are no PR intervals.

The ST-segment morphology appears to be a scooped-out or ladle-like appearance. We superimposed a ladle illustration on the last complex to illustrate that point. This pattern is typically seen in patients who take digoxin.

This rhythm, therefore, shows a compensated atrial fibrillation at approximately 70 BPM with digoxin effect.

Additional Information

Digitalis toxicity is frequently associated with focal atrial tachycardia with block. Blood levels of digitalis should always be checked in these patients to evaluate for possible toxicity. We need to keep in mind that many patients still use digitalis for various reasons (e.g., congestive heart failure). It is still frequently used due to appropriate medical indications, accessibility, lower cost, and regional or geographic practice patterns, to name a few.

Final Test 2: ECG-14

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: Approximately 80 BPM Ventricular: Approximately 60 BPM	PR intervals: Variable
Regularity: Regularly irregular	QRS width: 0.09 seconds
P waves: Present Morphology: Normal Axis: Upright in lead II	Grouping: Yes, 3:2 ratio
	Dropped beats: Yes
P:QRS ratio: See discussion below	Rhythm: Wenckebach or Mobitz I second-degree AV block

Discussion:

The grouping on Final Test 2: ECG-14 is clearly evident at first glance. The conduction ratio on the strip is 3:2 and there are certainly blocked P waves (see red circles with an X behind them). The atrial beats occur regularly (with some minor variation) and map throughout the strip. Note that every third P wave is blocked. In all cases, the blocked P waves are buried within the previous T waves. In addition, the first QRS complex after the block is slightly taller than the rest in each group, which is commonly seen in Wenckebach.

The brackets at the bottom show the increasing PR interval found in each subsequent beat within a group until the last one is blocked. The first PR interval is the shortest and the one before the blocked P wave is the longest, as is typical for Wenckebach. We are unable to show any decrease in R-R intervals because there is only one R-R interval seen in each group. These findings are all typical of Wenckebach.

The first PR interval is longer than 0.20 seconds. This leads to an interesting nomenclature issue. Remember, any PR interval longer than 0.20 seconds is a first-degree AV block. Some authors have noted this finding as a stand-alone diagnosis to go along with the diagnosis of Mobitz I second-degree AV block. Others feel that since we know the AV node is not functioning correctly, calling it both a first-degree AV block and a Mobitz I second-degree AV block is redundant. Of the two camps, the second one has won the race (at least for the moment) and is presently considered the correct nomenclature to use in these situations.

Final Test 2: ECG-15

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 250 BPM Ventricular: 84 BPM	PR intervals: See discussion below
Regularity: Regular	QRS width: 0.08 seconds
P waves: Present Morphology: Inverted Axis: Negative in lead II	Grouping: Yes, 3:1 conduction
	Dropped beats: None
P:QRS ratio: 3:1	Rhythm: Focal atrial tachycardia with block (3:1 conduction)

Discussion:

Final Test 2: ECG-15 is a tough strip, so let’s try to break it down into manageable chunks. The first thing we notice are the inverted P waves located just before the QRS complexes throughout the strip. They are classic for ectopic atrial foci since they are negative in lead II. The PR interval is prolonged at 0.28 seconds, which is a fairly wide interval. The timing of the P, QRS, and T waves appears to be equally spaced, which is highly unusual. This should automatically trigger a question in our minds: Why?

First, let’s try to figure out the issue with the inverted P waves with a prolonged PR interval. Although this doesn’t qualify as an issue that would come under the umbrella of Bix’s rule, the possibility of buried P waves remains to be clarified. To help answer that question, we whip out our handy-dandy calipers and begin to take some measurements. We begin by taking the P-P interval and moving that distance to a clear part on the ECG paper. The pins fall approximately 3½ big blocks apart—or to be exact, 0.70 seconds apart. Now, since we are trying to evaluate the strip for buried P waves, let’s try using some possible intervals and see if they fit.

Divide the 0.70-second (35 small blocks) interval in half (Figure 3). Half that distance is 0.35 seconds (17½ small blocks). When we examine that distance, can a buried P wave fall directly on that spot of the strip? Nope, there is nothing there (see the red X on Figure 3).

Figure 3 Searching for buried P waves.

© Jones & Bartlett Learning.

Description

Now let’s try dividing the 0.70-second P-P interval in thirds. Separate the pins of your calipers to 0.23 seconds (5¾ small blocks) apart. Can there be a buried P wave directly on that spot on the strip? Yes, a buried P wave could be found hidden within the QRS complex. Let’s double that distance to 0.46 seconds (11½ small blocks). Again, we see there could easily be a buried P wave within the T wave. We could easily have three P waves to every QRS complex or a 3:1 conduction of an ectopic atrial rhythm in our strip (Figure 4).

Figure 4 Location of the buried P waves within our focal atrial tachycardia with 3:1 conduction.

© Jones & Bartlett Learning.

We’ve marked all the possible P-wave locations throughout the strip with blue arrows for your convenience. The absence of flutter waves and the flat baseline within the strip point us in the direction of focal atrial tachycardia with block. As you can see, the atrial rate is 250 BPM, which is a bit fast for focal atrial tachycardia with block, but not outside the realm of possibility.

Is the low amplitude of the QRS complexes due to a low voltage problem? Is it due to a fusion between an inverted P wave and the QRS complex, which would lower the amplitude? Or is lead II simply the isoelectric lead? We will need a 12-lead ECG to evaluate those questions further. As we have mentioned many times, answers that are morphologic in nature should be evaluated by a 12-lead ECG and not a simple strip.

The negative P waves, the very rapid atrial rate of 250 BPM, and the flat baseline between the P waves narrowed down our diagnosis to a focal atrial tachycardia with block at a 3:1 conduction rate. The 12-lead ECG and the clinical course of the rhythm verified our initial diagnosis.

Final Test 2: ECG-16

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 64 BPM	PR intervals: 0.08 seconds
Regularity: Regular	QRS width: 0.09 seconds
P waves: Present Morphology: Upright, normal Axis: Positive in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Sinus rhythm

Discussion:

Final Test 2: ECG-16 shows a sinus rhythm with a short PR interval. The short PR interval is associated with a benign-looking P wave that appears to have a normal P-wave axis. A few years ago, this was thought to be a preexcitation syndrome known as Lown-Ganong-Levine (LGL) syndrome and was believed to be due to a short bypass tract within the AV node–His bundle complex known as James fibers. The James fibers were thought to provide a bypass pathway, avoiding the physiologic block. With the onset of electrophysiology studies, the tract theory has been debunked. Presently, a rhythm with a short PR interval and normal QRS morphology, though still often referred to as the LGL syndrome, is considered a variant of normal.

The term LGL syndrome is now used to identify a rhythm with a short PR interval with normal QRS morphology in a patient with sudden bouts of tachycardia. Because there is no history or evidence of bouts of tachycardia in this particular scenario, we cannot make the call of LGL syndrome. So, our final assessment of this rhythm is that this is a sinus rhythm with a short PR interval (normal variant).

If you look at the rise of the R wave on the QRS complexes (green arrow), you will note that there is some slowing or slurring of the upstroke. This is a normal variant known as the R-wave peak time or intrinsicoid deflection and represents the time it takes for the depolarization wave to travel from the endocardium to the epicardium over an isolated lead (see page 56). The deflection is considered prolonged if greater than 45 ms and is frequently seen in ventricular hypertrophy (please refer to our sister text, 12-Lead ECG: The Art of Interpretation, for more discussion on this topic). Many people confuse this finding with the delta waves typically seen in Wolff-Parkinson-White (WPW) syndrome. Note, however, that delta waves are a much more pronounced slurring of the upstroke of the R wave, which causes a widening of the QRS complex to greater than or equal to 0.12 seconds in most cases. (Please see pages 366–367 for additional information.)

Final Test 2: ECG-17

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 300 BPM	PR intervals: None
Regularity: Regular	QRS width: 0.10 seconds
P waves: None Morphology: None Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Antidromic AV reentry tachycardia

Discussion:

Final Test 2: ECG-17 is a very scary rhythm strip. It shows a ventricular rate of approximately 300 BPM that is very regular with slight variations in morphology throughout the strip. The width of the QRS complexes is around 0.10 to 0.11 seconds. So, is this a wide-complex tachycardia? If you stick to the strict criteria (which you should do), the answer is no. However, you must remember that the faster a tachycardia fires, the shorter the intervals. There is just not a lot of wiggle room for extra width. So, keep in mind that anything is possible, though it may not be possible to call everything. Keep the possibility of the wider rhythms in the back of your clinical mind.

Before we even identify the rhythm, we need to think about the fact that the heart does not like rates of 300 BPM. There isn’t enough time for rapid ventricular filling, the atrial kick, and full, coordinated ventricular contractions. These problems lead to a decrease in cardiac output and hemodynamic instability. Top that off with possible underlying cardiac disease and you are faced with a true cardiac emergency. If the patient is hemodynamically unstable, remember that “electricity is your friend.” Cardiovert or defibrillate the patient immediately to terminate this rhythm.

Let’s start our analysis by figuring out what this rhythm could be. Could this be a type of ventricular tachycardia? No, VTach typically doesn’t go anywhere near that fast. . . . But ventricular flutter does! In fact, it is quite uncommon to find rates of 300 BPM in a monomorphic VTach. Secondly, the QRS complexes are typically wider in VTach. Thirdly, there is no evidence of any atrial activity, nor is there evidence of AV dissociation. For these reasons alone, we would place VTach on our list of differentials, but not at the top.

Does a rate of 300 BPM remind you of anything? How about atrial flutter? Flutter waves love to run at a smooth 300 BPM due to the circus movement that creates them. However, ventricular rates are not typically allowed to pass through the AV node at that level. As a cardioprotective mechanism, the physiologic block slows the transmission of the flutter waves by conducting at a 2:1 rate, making 150 BPM the most common ventricular rate in atrial flutter.

In a normal heart, the only area through which AV conduction can occur is the AV node, for the reasons mentioned previously. Now, suppose the depolarization wave had a way to bypass the AV node altogether; could a ventricular rate of 300 BPM occur? The answer is yes, because there is no physiologic block along a bypass tract. Bypass tracts should make you think of WPW syndrome. The width of the complexes should actually make you think of antidromic conduction through an accessory pathway. This is, indeed, the most likely culprit in this case: an antidromic AV reentry tachycardia (AVRT) conducting an atrial flutter through an accessory pathway (Kent bundle) at a rate of 300 BPM due to the 1:1 conduction.

Clinically, the most important thing to do is to keep your patient alive. Remember, there is always the possibility of synchronized cardioversion or defibrillation in these cases. If you are going to treat with pharmaceutical agents, however, make sure you do not use any agents that slow conduction through the AV node, or you can make matters worse. (Refer to the latest advanced cardiovascular life support [ACLS] guidelines for further information on treatment protocols.)

Final Test 2: ECG-18

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: F waves: 300 BPM Ventricular: Approximately 80 BPM	PR intervals: Not applicable
Regularity: Regularly irregular	QRS width: 0.08 seconds
P waves: None Morphology: None Axis: Not applicable	Grouping: Yes, 3:1 and 4:1 conduction
	Dropped beats: Not applicable
P:QRS ratio: Variable	Rhythm: Atrial flutter with variable block

Discussion:

The flutter waves are clearly visible throughout Final Test 2: ECG-18 (see blue arrows), and they are further isolated in Figure 5. The atrial flutter is conducting at either a 3:1 or a 4:1 pattern, as can be seen on the green brackets. Therefore, our final diagnosis is an atrial flutter with variable block.

Figure 5 We have removed the QRS complexes to simplify our view of the flutter waves.

© Jones & Bartlett Learning.

Final Test 2: ECG-19

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 280 BPM Ventricular: 140 BPM	PR intervals: 0.07 seconds
Regularity: Regular	QRS width: 0.09 seconds
P waves: Present Morphology: Upright Axis: Positive in lead II	Grouping: Present
	Dropped beats: Yes
P:QRS ratio: 2:1	Rhythm: Focal atrial tachycardia with 2:1 block

Discussion:

I could see where most folks would look at Final Test 2: ECG-19 and be somewhere along the spectrum of “Huh?” and “Wow, that is VFib!” Well, we can dismiss VFib, because the pattern is repetitive. Let’s take a closer look at the original strip (Figure 6) and see what information we can get out of it.

Figure 6 Magnification of the strip in lead II. When the repetitive areas are isolated and magnified (in actuality or in our minds), we can clearly see where the corresponding areas are located.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

If you look at the strip from a distance, we can make out some areas where the undulation dies down a bit. Now, see if the pattern repeats itself. Since it repeats itself, we can begin to analyze each part and see what components are there. Let’s take one of these areas and blow it up (see green brackets). Using our imagination and knowing the morphology of the typical cardiac complexes, let’s call the first part (inside the red circle) the P wave. The last part in the complex (within the blue circle) is where the T wave would be found. Finally, assume the stuff in between (in the green circle) would be the QRS complex.

Do you see that pattern repeating throughout the strip? That is the entire cardiac beat. The problem is, that lead is a mess. Let’s try to clear up the situation by obtaining some information from other nearby leads. A 12-lead would provide us with the needed leads. Indeed, the 12-lead ECG shows that in lead V₁ (Figure 7), we can identify two P waves surrounding each QRS complex. With that information, we can calculate the ectopic atrial rate at 280 BPM, the ventricular rate of 140 BPM, and a conduction ratio of 2:1. Note that the baseline is flat between the complexes, ruling out an atrial flutter. Putting it all together, we arrive at our diagnosis: focal atrial tachycardia with 2:1 block. The next step would be to find out if the patient is digitalis toxic.

Figure 7 When we look at leads II and V₁, we can see the corresponding areas between the two leads. Note that the P waves are clearly seen in lead V₁, and, since the two strips are synchronized on this ECG, we just have to place arrows leading from V₁ to lead II to identify the appropriate P waves. See the discussion in the text for further information.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

Description

Final Test 2: ECG-20

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 90 BPM Ventricular: 45 BPM	PR intervals: 0.15 seconds
Regularity: Regularly irregular	QRS width: 0.07 seconds
P waves: Present Morphology: Upright, normal Axis: Positive in lead II	Grouping: Yes, 2:1 conduction
	Dropped beats: Yes
P:QRS ratio: 2:1	Rhythm: 2:1 second-degree AV block

Discussion:

By now, Final Test 2: ECG-20 should not prove to be much of a diagnostic challenge. This is obviously a 2:1 second-degree AV block. The real question is, which type of second-degree AV block is it: Mobitz I or Mobitz II?

Unfortunately, you will not be able to answer that question based on this strip alone, because we see only 2:1 AV blocks on this strip and cannot distinguish between the two. To designate an arrhythmia as either Mobitz I or II second-degree AV block, we need to see a grouping of at least a 3:2 conduction ratio. That is because in a 2:1 AV block, we cannot tell what happens after the second P wave. We need to see a more complete picture of the interactions between the P wave and the QRS complexes in order to identify the specific criteria that make the strip either Mobitz I or Mobitz II.

Remember, a criterion for Mobitz I is a successive lengthening of the PR interval. The shortest PR interval is typically the first one after the pause; the longest PR interval should be the one immediately before the dropped beat. There should be a slight shortening of the R-R interval as the strip progresses and a continuous regularity of the P-P interval throughout the strip. How can you make any statement about the criteria for Mobitz I if you only have two P waves and one QRS complex to evaluate? The answer is, you can’t.

The same holds for the Mobitz II second-degree AV block criteria. With only two P waves and one QRS complex, we cannot determine whether this is Mobitz II, with a regularly irregular rhythm with grouping, consistent P waves, P-P intervals, R-R intervals, and PR intervals broken up by nonconducted P waves with dropped beats.

However, if we can identify even one additional grouping anywhere along a strip as either a definitive Mobitz I or II, then we can extrapolate that the pathology involved is the same throughout the strip. In other words, a given pathology will always manifest as the same rhythm. If one grouping meets Mobitz I criteria, this means that all the 2:1 AV blocks can be assumed to be Mobitz I. What can you do if your strip only has 2:1 AV blocks on it? You can try to improve your odds by obtaining a longer strip to allow a greater chance of seeing at least a 3:2 grouping and making the right call. Paper is cheap comparatively; let the ECG paper run for a few minutes if you have to.

Final Test 2: ECG-21

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 30 BPM	PR intervals: Not applicable
Regularity: Regular	QRS width: 0.13 seconds
P waves: None Morphology: None Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Idioventricular escape rhythm

Discussion:

In Final Test 2: ECG-21, the lack of P waves and the very slow ventricular escape rhythm at 30 BPM scream out, “Emergency! Need help right now!” Note that the complexes are wide, but not as dissociated or bizarre as you would expect to see in an agonal rhythm.

We calculated an approximate rate with some simple math: 3 complexes in a 6-second strip is 3 BPM × 10 = 30 BPM (remember, there are 10 six-second strips in a minute). Using the calculation of 30 BPM, we see the QT is 0.75 seconds and the R-R interval would be 2.0 seconds. This gives us a QT_c according to Fridericia’s formula of 595 ms. The QT_c of 595 ms is very prolonged and is probably due to the severe bradycardia noted on the strip.

The QRS interval measures 0.13 seconds and starts off with a small negative Q wave (see blue arrow). The very slow heart rate of approximately 30 BPM is consistent with a distant pacemaker, probably a Purkinje cell or a ventricular myocyte. There is a small U wave present (see yellow arrow) that is not clinically relevant.

It is prudent to obtain a 12-lead ECG on this patient to further evaluate the rhythm. This patient requires emergent attention and treatment as per the ACLS bradycardia protocol. Whatever you do, do not administer anything to try to suppress this rhythm. Remember, the myocardial cells are the last pacemakers on our list of potential pacemakers. What pacemaker do you have if you suppress the last pacemaker? None; you have no other natural pacemaker.

Final Test 2: ECG-22

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: Approximately 70 BPM Ventricular: Approximately 40 BPM	PR intervals: Variable
Regularity: Regularly irregular	QRS width: Approximately 0.14 seconds
P waves: Present Morphology: Upright, normal Axis: Upright in lead II	Grouping: None
	Dropped beats: None, see discussion below
P:QRS ratio: See discussion below	Rhythm: Ventriculophasic AV dissociation with ventricular escape rhythm

Discussion:

When you first look at Final Test 2: ECG-22, it appears to be a simple 2:1 AV block. However, there is a lot more to this story. In order to figure out the rhythm, let’s see why it does not match a Mobitz I or Mobitz II second-degree AV block.

First of all, Mobitz II second-degree AV block has a regular rhythm with consistent P waves, P-P intervals, R-R intervals, and PR intervals broken up by nonconducted P waves with dropped beats. Our strip shows variability in the width of the PR and P-P intervals and no dropped beats or even the presence of association between the atrial and ventricular rhythms at all (more on this later). This rules out a Mobitz II second-degree AV block.

Now, let’s turn our attention to why this is not a Wenckebach or Mobitz I second-degree AV block. Comparing the two columns in Table 1, we see that the strip does not meet the criteria for Wenckebach, essentially ruling out that possibility.

Table 1 Analysis of Final Test 2: ECG-22 as Compared to Wenckebach

Criteria for Wenckebach	Characteristics of Final Test 2: ECG-22
1. Grouping is present. The groups occur in a P:QRS ratio of X:X – 1 (where X is the number of atrial beats). Examples are 2:1, 3:2, 4:3, and so on.	1. No grouping (discussed below).
2. P-P intervals are constant throughout.	2. P-P intervals vary with a widening–shortening recurrent pattern.
3. Shortening of the R-R interval in a group.	3. None of the “groups” have two or more QRS complexes present.
4. Progressive widening of the PR interval until there is a P wave that is nonconducted.	4. PR intervals are not associated with the QRS complexes.
5. Shortest PR interval occurs immediately after the dropped beat.	5. Location of the shortest presumed PR interval is variable.
6. Longest PR interval in a group occurs immediately before the dropped beat.	6. Location of the longest presumed PR interval is variable.
7. The largest increase in PR interval duration is usually found between the first and second complexes in a group.	7. The largest increase in PR interval duration is variable.

© Jones & Bartlett Learning.

Our rhythm is basically a combination of two separate rhythms, each occurring independent of each other. One is a normal sinus rhythm, which controls the atria. The other is an idioventricular escape rhythm. So, are we dealing with a complete heart block? Well, no. We will now attempt to discuss the long logic sequence behind the mechanisms at work in this strip.

Take a look at the red brackets and the timing of the P-P intervals. There appear to be two separate groups when it comes to the duration of the P-P intervals. There are some with “short” P-P intervals of approximately 0.83 to 0.85 seconds. The other “long” group has a longer P-P duration that measures around the 0.95- to 0.97-second range. Why are there two groups?

Remember, the occurrence of two rhythms independent of each other represents a complete, or third-degree, AV block. The occurrence of two rhythms with a minimal amount of connection to each other is more consistent with an AV dissociation. So, which one are we dealing with? Taking a closer look at the strip, we find that the “short” P-P interval group always has a QRS complex in between its two bounding P waves. In other words, the shorter group always has a QRS complex inside it. The “long” group, on the other hand, never has a QRS complex in the area between its two P waves. A rhythm must have some level of connectivity in order for the QRS complexes to influence the P-P interval, so we are dealing with an AV dissociation. In particular, this dual P-P interval characteristic is classic for a rhythm abnormality known as a ventriculophasic AV dissociation.

To use an analogy, what typically occurs in a ventriculophasic AV dissociation is that the QRS complex somehow seems to function as a “P-wave magnet,” causing the P waves around it to move closer. When there are no QRS waves, there is no “magnetic” pull toward the center, and the P waves move away from each other.

Figure 8 is a graphical representation of the fusion of the two rhythms that are found within this strip. The two rhythms fuse with each other, causing the ventriculophasic effect and some buried P waves. The grouping we see is an electrocardiographic “illusion” caused by these two factors; no grouping actually occurs on this strip. There are also no dropped beats, because you are dealing with two underlying rhythms, each paced religiously by its own pacemaking focus. Both are beating to their own drummers and there are no actual dropped or blocked beats present.

Figure 8 Final Test 2: ECG-22 is composed of a combination of a normal sinus rhythm and an idioventricular escape rhythm. Notice that there is no dropped or blocked beat in either of the two rhythms. The AV dissociation is present and so is the ventriculophasic component. The grouping effect and buried P waves are caused by fusion of the two underlying rhythms.

© Jones & Bartlett Learning.

Description

Final Test 2: ECG-23

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 140 BPM	PR intervals: Not applicable
Regularity: Regular	QRS width: 0.10 seconds
P waves: Present as pseudo-S waves Morphology: Inverted and buried in QRS complex Axis: Negative in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: AV nodal reentry tachycardia

Discussion:

Final Test 2: ECG-23 is a rapid, narrow supraventricular tachycardia at a rate of 140 BPM. There are no distinct P waves present, but pseudo-S waves are present (see red arrow). Pseudo-S waves are typically found in junctional rhythms (especially junctional tachycardias) and AV nodal reentry tachycardia (AVNRT), and represent retrogradely conducted atrial depolarization waves. The RP interval in junctional tachycardias or AVNRTs is short because the origin of the P waves is in the atria or AV node itself and the distance needed to travel prior to the start of atrial depolarization is minimal. AVNRT typically occurs between 150 and 250 BPM, but more commonly occurs at rates between 170 and 220 BPM. Rates as low as 140 BPM, as seen in this strip, also occur.

Final Test 2: ECG-24

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 84 BPM	PR intervals: 0.25 seconds, when present
Regularity: Regularly irregular	QRS width: 0.11 seconds
P waves: Present Morphology: Normal, upright Axis: Upright in lead II	Grouping: None
	Dropped beats: Yes
P:QRS ratio: See discussion below	Rhythm: Sinus rhythm with pacemaker malfunction due to oversensing

Discussion:

They say first impressions are usually correct. Final Test 2: ECG-24 shows a sinus rhythm in a patient with a malfunctioning pacemaker. If you are a beginning student and you were able to pick that up, you are doing great, especially since recognizing the presence of a pacemaker with or without malfunctions is a more advanced concept than you are expected to know!

If you feel advanced enough for further discussion, let’s move on. At first, the pacemaker senses the presence of a P wave and fires a ventricular spike to stimulate ventricular depolarization. The pacemaker spike is that very sharp deflection occurring immediately before the QRS complex. Suddenly, the pacemaker fails to fire and the only thing we see for the rest of the strip are the P waves.

With the limited information available to us, we can only state that the pacemaker is atrial sensing and ventricular pacing in this mode. The first three QRS complexes seem to have fired appropriately. The sudden termination of ventricular pacing occurs due to ventricular oversensing, ventricular output failure, or both.

Normally, the pacemaker senses stimuli from above but the ventricles fail to depolarize due to intrinsic cardiac disease. The lack of a normal ventricular response causes the pacer to discharge and assume pacing functions. Ventricular oversensing occurs when the pacemaker senses minute electrical stimuli, inappropriately preventing or inhibiting ventricular pacing. In other words, it thinks it doesn’t have to fire because the ventricles are behaving normally. The net result is that nothing fires and the ventricles sit there doing nothing. Causes of ventricular oversensing include inappropriate response to T waves and myopotential signals, like lead misplacement, inappropriate contact, lead fractures, and electromagnetic interference.

Ventricular output failure occurs when the pacer fails to fire when it should. It is essentially failing to do its job. This typically is found in cases of oversensing, lead displacement, lead fractures, or electromagnetic interference.

As you can well imagine, this type of pacemaker malfunction is a major cardiac emergency that will need emergent attention to keep your patient alive. Since the lack of electricity seems to be the problem, add some by using either an external transcutaneous pacemaker or a transvenous pacemaker on the side opposite of the already implanted pacer. These adjuncts can provide you with valuable time to initiate more definitive treatment for the malfunction itself. Typically, patients will have a card with the specifics of their particular pacemaker, and manufacturers are very helpful in helping you identify and treat the malfunction. Additional treatment of such an emergent condition is beyond the scope of this text.

Final Test 2: ECG-25

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 78 BPM Ventricular: 84 BPM	PR intervals: Variable
Regularity: Regularly irregular	QRS width: 0.13 seconds
P waves: Present Morphology: Upright, normal. Most are fusion complexes with ventricular complexes Axis: Upright in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Accelerated idioventricular rhythm with AV dissociation

Discussion:

At first glance, Final Test 2: ECG-25 shows a wide-complex rhythm with varying P-wave morphology and intervals. On closer inspection, we see a pattern develop, starting with the first and fifth complexes (see red arrows). The first complex has a normal-appearing P wave with a PR interval of 0.14 seconds. The morphology of the QRS is a bit strange with a wider-than-expected R wave and a wider-than-expected upstroke to the S wave. This complex is a fusion beat, but it is as close to a capture beat as you have on this strip. This near-normal appearance occurs because the timing of the P wave is such that it captures most of the ventricles normally, allowing more of the normal native morphologic appearance to come through. Once again, we recommend a longer rhythm strip and a 12-lead ECG to further evaluate the morphology.

The fifth complex appears to be a fusion beat as well, but the shorter PR interval makes one think of a hybrid between the capture beat morphology and the fusion morphology. In other words, the first complex is more of a true capture than the fifth. Note that both the first and fifth complexes break the underlying R-R intervals’ regularity, but the P-P intervals map through. The influence that the atrial and ventricular complexes share with each other means that the rhythm is an example of AV dissociation.

The second through the fourth complexes are fusion beats. There is less capture and more of the ventricular morphology breaking through. This causes a widening of the QRS interval and a change in the morphologic appearance of the ventricular complexes. The fusion complexes occur because the vectors creating the P wave and the QRS complex have superimposed themselves, thus altering the final morphology.

The sixth complex is, once again, a fusion complex. Here we lose the P-P interval for some reason. This could represent a change in the underlying rhythm or a change in the timing of the atrial component causing the P waves to be completely buried within the QRS complexes. The green arrow points to the presence of U waves.

If the rate of this rhythm were faster, we would call this VTach. However, the slower rate seen in our example means the underlying rhythm is an accelerated idioventricular rhythm with AV dissociation. In the past, these were called “slow VTach,” which although inaccurate, reflected the similarities with its faster cousin.

Final Test 2: ECG-26

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: Approximately 90 BPM Ventricular: monomorphic complexes at approximately 230 BPM	PR intervals: 0.13 seconds, when present
Regularity: Regularly irregular	QRS width: Variable, 0.12-second ventricular complexes
P waves: Present Morphology: Slightly biphasic in lead V1 Axis: Negative in lead V1	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Sinus rhythm with a salvo and triplet of monomorphic ventricular tachycardia

Discussion:

To start, note that Final Test 2: ECG-26 is taken in lead V₁. The P waves can be negative in that lead, and our strip shows just that scenario. The first complex shows the morphology of the native ventricular complexes. The axis and morphology quickly change in the next six beats to that of a monomorphic VTach with an underlying electrical alternans due to the rapid rates. The P waves map through with very little change in the P-P interval, as is frequently seen in VTach (see blue arrows), which represents the presence of an AV dissociation. The red arrows demonstrate notching in the ventricular complexes that are caused by the fusion with the overlying buried P waves. There is also a monomorphic triplet toward the end of the strip

Does the monomorphic VTach originate from a pacemaker in the left or right ventricles? Well, a ventricular complex that starts in the left ventricle demonstrates an RBBB appearance because the slow ventricular depolarization wave must travel from left to right. Typically, the appearance of an RBBB is a positive complex in lead V₁ with an rsR′ complex, where the first R wave is smaller than the R′. In other words, the first peak is smaller than the second. This occurs because transmission through the vast majority of the left ventricle occurs through a functioning left bundle branch to create the R wave, and the unopposed left-to-right vector is caused by a slow-moving, unopposed depolarization wave causing the taller R′. This pattern is commonly found in uncomplicated RBBBs and in aberrantly conducted beats due to a block in the right bundle.

Keep in mind, however, that the location of the ectopic pacing focus affects morphology. If the pacemaker were in the far left ventricle and did not go through a functioning left bundle branch, the slow depolarization wave heading toward the right would cause an earlier, more pronounced R wave. This would lead to the first peak appearing taller than the second (R > R′). This presentation (as is seen in our strip) is more commonly found in VTach than in uncomplicated RBBB.

If the pacemaker were in the right ventricle, then the impulse would have to travel from right to left and an LBBB pattern would emerge. The monomorphic complexes of LBBB are due to the large amounts of ventricular tissue that will need to be depolarized by slow, direct cell-to-cell conduction.

Bottom line is that this strip shows a sinus rhythm with a salvo of six monomorphic complexes and a subsequent triplet that originates in the left ventricle. AV dissociation is present.

Final Test 2: ECG-27

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 92 BPM	PR intervals: 0.26 seconds
Regularity: Regularly irregular	QRS width: 0.10 seconds
P waves: Present Morphology: Upright, normal Axis: Positive in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Sinus rhythm with a first-degree AV block and two PJCs

Discussion:

Final Test 2: ECG-27 is much less complicated than it appears at first glance. The negative QRS complexes and the presence of premature junctional complexes (PJCs) are the main source of the distraction. So, let’s approach this logically and methodically.

The P waves map out throughout the strip, as do the ventricular complexes (see blue arrows and red circles), and are regular. The ventricular complex regularity, however, is offset by two events (see green arrows). The fact that the morphology of these events is similar to the normal ventricular complexes, the lack of visible P waves associated with those beats, and the fact that they create compensatory pauses identify these as PJCs. Why do we not see a P wave on the area with the green arrows? Because the normally-occurring P waves fuse with the PJCs. That is also why the PJCs are not as deep and do not have the same morphology as the normally conducted beats. All together, the underlying regular rhythm that is broken up by the two PJCs makes the final call a regularly irregular rhythm. Finally, the PR intervals are prolonged at 0.26 seconds, making this a first-degree AV block.

Final Test 2: ECG-28

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: Approximately 330 BPM Ventricular: Approximately 166 BPM	PR intervals: 0.11 seconds (see discussion below)
Regularity: Regular	QRS width: 0.06 seconds
P waves: Present Morphology: Small, inverted Axis: Negative in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 2:1	Rhythm: Atrial flutter with 2:1 block

Discussion:

Final Test 2: ECG-28 shows a very rapid supraventricular rhythm. Many of you will ask: Is that artifact along the baseline? The answer is no. The pattern of small deflections along the baseline is repetitive. Artifact is not usually repetitive. So, if it isn’t artifact, what is it? Let’s start by identifying where one complex ends and the other begins. That spot seems to be around where the blue arrows are pointing. It is a small, negative wave that could represent a low-amplitude, inverted P or F wave. Next comes a flat segment of baseline that is consistent with the PR interval. Then, we have the obvious QRS complex followed by a small, negative wave (see green arrows).

Does that “small, negative wave” mentioned in the previous sentence sound familiar? Could this be a second inverted P or F wave with a short RP interval buried right after the QRS complex, or is this just part of the ST segment? Well, we can quickly rule out the ST segment since the morphology and orientation match the P or F wave before the QRS complex. That tells us that we are dealing with a second P or F wave.

We can verify our suspicions by using our calipers to measure the P-P interval of two known P or F waves (the ones before the QRS complexes). Now, take that distance, divide it in half, and place your caliper point on the trough of the inverted P or F wave before the QRS. Does the other presumed P or F wave map? Yes, it clearly does. Now you have verification that we are dealing with two P or F waves present for each QRS complex and the conduction ratio is 2:1.

For further evaluation, let’s get some additional leads. Lead V₁ is a great lead to evaluate atrial waves; in Figure 9, we see the clear appearance of the P or F waves in that lead. Note that the atrial waves are tall and quite peaked, which are more typical for P waves than F waves. You can, however, make a better argument for an undulating saw-tooth pattern in lead V₁. To complicate matters a bit further, the rates involved in our rhythm are very fast for an uncomplicated focal atrial tachycardia with 2:1 block, but remember, rates can be as high as 400 BPM. So, which is it? Is it a rapid atrial flutter with 2:1 block or an even faster focal atrial tachycardia with 2:1 block? Unfortunately, this is one of those times when you can’t tell on a surface ECG. As we mentioned before, in those cases, the consensus is to name it an atrial flutter with 2:1 block.

Figure 9 The blue arrows simplify the identification of the P waves in both leads II and V1 that are occurring simultaneously. The use of additional leads to clarify any inconsistencies or the individual waves is an invaluable tool in arrhythmia recognition.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

Description

Other possibilities that should be in your differential diagnosis include orthodromic and antidromic AVRT. The narrow, tall morphology of the P waves goes more for an orthodromic AVRT and against an antidromic transmission of an AVRT through an accessory pathway. Time spent reviewing old ECGs for evidence of a preexcitation pattern is never wasted.

Further evaluation should be immediately undertaken, including obtaining digitalis levels, potassium and calcium levels, toxicology screening, and further evaluation of any associated medical problems and old ECGs.

Final Test 2: ECG-29

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: Atrial: Approximately 40 BPM Ventricular: Approximately 70 BPM	PR intervals: Variable
Regularity: Regularly irregular	QRS width: 0.07 seconds
P waves: Present Morphology: Normal Axis: Upright in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Ventriculophasic AV dissociation with a PJC

Discussion:

Final Test 2: ECG-29 is similar to Final Test 2: ECG-22 in that there is a ventriculophasic AV dissociation. If you can understand the logic there, you will certainly see the same logic present on this one. The atrial depolarizations appear to be irregular, but behave as you would expect in a ventriculophasic pattern, by narrowing when a QRS complex is between the bounding P waves and separating when no QRS is found. The ventricular complexes are in a junctional bradycardia pattern with an additional PJC (see red arrow) occurring at the end.

Final Test 2: ECG-30

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 180 BPM	PR intervals: Not applicable
Regularity: Irregularly irregular	QRS width: 0.08 seconds
P waves: None Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Multifocal atrial tachycardia

Discussion:

Final Test 2: ECG-30 is an example of a very rapid irregularly irregular rhythm. So, let’s figure out which one of the three irregular rhythms it is. Recall that the three irregularly irregular rhythms are atrial fibrillation, WAP, and MAT. Which one is this?

On our strip, we see what appear to be some isolated P waves (see blue arrows). In addition, we have multiple examples of buried P waves in both the QRS complexes and the ST-T segments. The morphologies of these waves vary and so do the PR intervals. There are obviously at least three different foci involved. Since we have an obvious tachycardia here, our only viable choice among our differential diagnoses is MAT.

As an additional point, there appear to be some junctional complexes, or complexes where the P wave is completely isoelectric, on the strip as well. These are not uncommon in rapid MATs.

Keep in mind that the rapid rate could cause serious hemodynamic compromise in patients because there could easily be a loss of the atrial kick and decreased filling time of the ventricles, leading to a serious decrease in cardiac output. Patients with MAT frequently have chronic obstructive pulmonary disease with abnormal intrathoracic pressures (affecting cardiac output) and hypoxemia. Treat the underlying cause of the rapid rhythm and try to maintain stability through the use of controlled oxygen delivery and bronchodilation, as well as providing pharmaceutical or mechanical cardiac support.

AUTHOR’S NOTE

To be completely honest, we feel the evidence exists for the presence of P waves throughout the strip; however, an argument can be made for this being an uncontrolled atrial fibrillation with a coarse baseline. Clinical correlation and review of the patient’s history and old ECGs would be very helpful in evaluating this possibility.

Final Test 2: ECG-31

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 176 BPM	PR intervals: See discussion below
Regularity: Regular	QRS width: 0.12 seconds
P waves: Present Morphology: Retrograde, inverted Axis: Negative in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Antidromic AV reentry tachycardia

Discussion:

Final Test 2: ECG-31 is a rapid, wide-complex tachycardia that will require some thought to pinpoint diagnostically. Always remember that if you don’t have time to identify the rhythm due to an unstable patient, any wide-complex tachycardia is VTach until proven otherwise. Now, let’s try to identify the rhythm by looking at what we know.

We know the rhythm is regular (see red circles) and that there are no P waves before the QRS complexes that would allow capture. However, we see a notch on the upstroke of the ST segment that is caused by a retrogradely conducted P wave (see blue arrows). There is, therefore, no PR interval; instead, we have an RP interval.

The RP is typically narrower in an AVNRT because the reentry circuit is in the right atrium at the level of the AV node. In AVRT, the distance traveled by the circuit is usually longer, causing a longer RP interval. If you are unclear about these two rhythms, take a few minutes to review them in the corresponding chapters of this text. It is worth your while to truly understand the difference between these two supraventricular tachycardias, as the treatment for each is vastly different. Our strip shows a slightly longer RP interval, making it more likely that the rhythm is an AVRT. (For more information on short and long RP intervals, please refer to their respective section in Chapter 36.)

The inverted P wave that is associated with the RP interval causes a diagnostic dilemma. Here is the problem: Can you measure a clear QRS width? Where does the QRS end and the inverted P wave begin? In many cases, you may need additional leads to measure the true QRS interval. Luckily, our strip shows a QRS width of at least 0.12 seconds prior to the onset of the retrograde P wave.

Note the changes in amplitude of the QRS complexes in our strip. They become taller and shorter in a rhythmical, gentle wave pattern (see green wave). This is an example of electrical alternans that is frequently seen in rapid tachycardias and suggests no additional underlying pathology in these cases.

Finally, let’s put it together. We have a rapid, wide-complex tachycardia at 176 BPM that is associated with retrogradely conducted P waves with a wide RP interval. This is highly suggestive of an AVRT. Remember, these are usually associated with accessory pathways and WPW. Always try to get an old ECG or strip to compare. Be sure to take a thorough history and especially a family history to evaluate the presence of WPW, arrhythmias, or sudden cardiac death in a relative. Finally, make sure you obtain a 12-lead ECG after the patient is no longer tachycardic to evaluate for a possible delta wave and the other criteria of WPW.

We’re not done yet, though. We need to decide if this is an orthodromic AVRT or an antidromic AVRT. A 12-lead ECG should be obtained emergently, if possible, to make sure the QRS width is actually 0.12 seconds. Since we only have this strip, however, we have to assume the QRS is 0.12 seconds wide and that the wide complexes in this example are consistent with an antidromic circus pathway.

Which is more dangerous: an orthodromic or an antidromic AVRT? Although the rapid rates of both of these possibilities can lead to complications or death, antidromic AVRT is usually considered the more dangerous of the two. As a memory aid, you can associate the anti in antidromic AVRT with the antichrist, antipersonnel mines, and antisocial people, all of which are bad (so are wide-complex tachycardias). All in all, an antidromic AVRT is a very dangerous rhythm (that can proceed to an unchecked 300 BPM or more) that requires emergent attention and a very careful, controlled, well-thought-out treatment strategy. Consult with a cardiologist early after stabilization and be careful not to make matters worse by administering medications that could slow AV conduction. For further treatment, refer to the corresponding ACLS protocol used to treat this condition.

Final Test 2: ECG-32

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 88 BPM	PR intervals: See discussion below
Regularity: Regular	QRS width: 0.13 seconds
P waves: See discussion below Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Accelerated idioventricular rhythm

Discussion:

Final Test 2: ECG-32 is mostly composed of wide complexes that are compatible with a monomorphic ventricular complex. The rate is about 88 BPM, making this an accelerated idioventricular rhythm. There is indirect evidence of AV dissociation with a capture beat (see red arrow) and disruptions in the baseline that are made by underlying P waves (see green arrow). The only visible P wave is the one before the capture beat (see blue arrow), and the morphology or orientation is not clear; interpretation would be too subjective for us to truly use it for diagnostic purposes.

The final conclusion is that this is an accelerated idioventricular rhythm with AV dissociation and a capture beat. A 12-lead should be obtained to evaluate morphology.

On a clinical note, remember to never try to break an idioventricular rhythm. The presence of an idioventricular rhythm signifies that a large number of upper-level pacemakers have failed. If you try to break this rhythm, you may end up with an even lower-level pacemaker (and you are pretty low already), or asystole. Neither one is a great alternative. Please see the appropriate ACLS protocol for treatment. In these cases, a temporary pacemaker should be strongly considered. Pacemakers provide a highly controllable treatment strategy and can be either placed prophylactically or actively used to maintain hemodynamic control.

Final Test 2: ECG-33

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 52 BPM	PR intervals: 0.12 seconds
Regularity: Regular	QRS width: 0.08 seconds
P waves: Present Morphology: Inverted Axis: Negative in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Ectopic atrial rhythm

Discussion:

To start off our discussion, let’s take a look at the P waves on Final Test 2: ECG-33. We have seen that sinus P waves should always be positive or upright in leads II, III, and aVF. Inverted or negative P waves in those leads typically represent ectopic atrial pacemakers or junctional rhythms with retrograde conduction, since they create depolarization waves that head away from the AV node in a superior direction. Therefore, we are seeing an ectopic atrial rhythm or a retrogradely conducted junctional rhythm.

The PR intervals associated with ectopic atrial pacemakers are typically normal or slightly prolonged because they travel through the atria by direct cell-to-cell conduction. The slow cell-to-cell conduction and superiorly directed atrial depolarization vectors give the ectopic atrial pacemakers their usual negative or inverted P-wave morphology associated with normal or slightly prolonged PR intervals, as seen on our strip. Bradycardic rates are commonly found in ectopic atrial rhythms.

Short PR intervals are typically seen in junctional rhythms with retrograde conduction since the onset of the P wave is either near or directly on the AV node itself.

Now, take a look at the area around the T wave. Note that there are two low-voltage, positive waves there. The first positive deflection after the QRS complex is the T wave, by definition. The other slow, rolling positive wave is a U wave. Note, however, that the U waves typically have a much lower amplitude than the T waves that precede them. This discrepancy could lead to mistakes in the measurement of the QT/QT_c interval, which could lead to serious clinical errors. A 12-lead ECG should be obtained to help clarify the true measurement.

Final Test 2: ECG-34

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 98 BPM	PR intervals: 0.16 seconds, when present
Regularity: Regularly irregular	QRS width: 0.10 seconds, without aberrancy
P waves: Present Morphology: Upright, normal Axis: Upright in lead II	Grouping: Present
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Sinus rhythm with an aberrantly conducted premature junctional bigeminy and a unifocal ventricular couplet

Discussion:

Well, it is the final test. . . . You wouldn’t want it to all be simple, right? We will start by discussing the general concepts related to Final Test 2: ECG-34, then we’ll look at each one individually.

Let’s start by looking at the P waves. Are they present? Yes (see the blue arrows). Some of them are a bit harder to spot because they are buried in the underlying premature complexes (see red arrows) or with the T wave of complex 9 (see green arrow). They map throughout the rhythm and are undisturbed by the chaos occurring after the impulses leave the atria.

Complexes 1, 3, 5, and 7 have a measurable PR interval at 0.16 seconds. These complexes (also marked by the red dots) are regular and map out until the couplet occurs. A longer strip could have shown whether this regularity continued, but our strip unfortunately ended after three aberrant beats, so we’ll never know. For this reason, the main underlying rhythm appears to be sinus. It is important to realize that there is no evidence of AV dissociation on this strip, except over the couplet. The rest of the P waves either provide normal capture or are prevented from capture because of the premature complexes.

Note that starting with the second complex, there appears to be a junctional bigeminy pattern; every other beat appears to be an aberrantly conducted PJC (see yellow star). So, you have a native, regularly appearing complex (see red circle) and then an aberrant PJC (see yellow star). This brings us to yet another unexpected finding on this strip (as if you needed more): In bigeminy, you typically have the same interval between the two complexes (the native and the PJC). This distance is known as the coupling interval. In our strip, the coupling intervals vary slightly. Varying interpretations exist but are complex and beyond the scope of this text.

You may be asking: We can easily see that complexes 2, 4, and 6 are aberrantly conducted, but how do you know they are PJCs and not PVCs? Well, we know that PVCs and PJCs are both associated with compensatory pauses (provided there is no retrograde activation of the sinus node). This doesn’t really help differentiate between them but assures us that we are in the right ballpark. Both PVCs and PJCs are wide; however, true PVCs are usually wider than PJCs because their conduction through the entire ventricle occurs only by direct cell-to-cell contact. Aberrantly conducted PJCs typically are blocked somewhere along the path, but the conduction that occurs prior to the block is normal. They are, therefore, at the narrower end of the spectrum, typically around 0.11 to 0.12 seconds. Finally, PJCs typically start off in the same direction as the native QRS complexes (as occurs in our case; both start in a negative direction). So, in our strip we are dealing with aberrantly conducted PJCs in complexes 2, 4, and 6.

The following list breaks down what is occurring with each complex:

• Complex 1: We start with a normal P wave and PR interval. Note that the T wave is isoelectric in this lead. This appears to be the native morphology of the beats.
• Complex 2: This complex starts with fusion of the P wave with an aberrantly conducted premature complex. We know that the timing of these waves leads to more fusion than in complexes 4 and 6 because complex 2 is more isoelectric in appearance. The P wave also overlaps the premature wave to a greater degree. The T wave is discordant to the end of the QRS complex, as expected, and larger due to the aberrant conduction route that it took through the ventricles.
• Complex 3: Native complex. The P wave shows a small bump on the downstroke that appears to be of an unknown source. It is not a different P-wave morphology, because the PR interval associated with it is exactly the same as the others, 0.16 seconds.
• Complex 4: Fusion of the P wave and PJC. Here we see that the P wave is closer to the normal morphologic appearance than in complex 2. This occurs because the premature complex fired a little later, allowing less fusion of the buried P wave and the PJC.
• Complex 5: Native complex.
• Complex 6: This fusion complex is very similar to complex 4, and the same logic applies here, except that the PJC is a bit later in arriving, causing even more separation between the P wave and the PJC, and a bit less fusion.
• Complex 7: Native complex.
• Complex 8: This complex is definitely ventricular in origin. It is much wider (0.16 seconds) and more bizarre in appearance than the other aberrant beats. It is the first beat of a unifocal couplet.
• Complex 9: This is very, very similar in morphologic appearance to complex 8. Remember, in VTach or salvos, the morphology changes a bit between the first few complexes until it settles into a repeating pattern. The presence of a P wave at the tip of this T wave (see green arrow) also changes the appearance slightly.
• Complex 10: Almost identical in appearance to complex 4, this complex is a fusion between the P wave and an aberrantly conducted PJC.

Let’s move on now and look at the last three complexes and their interactions. Complexes 8 and 9 are obviously a couplet. Note that the timing of the P-P intervals is not disrupted by these events and they simply map through, undisturbed. We know this is a typical pattern in VTach when AV dissociation is present. Finally, the buried P-on-T at the end of complex 9 appears to hit during the relative refractory period, which is blocked (see crossed-out red circle).

What occurs after the end of this strip is a mystery, but in our opinion, this is a very irritable heart. It is important to search for the underlying pathology and treat it appropriately to decrease the chances of any further deterioration in the rhythm and the patient.

Final Test 2: ECG-35

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 54 BPM	PR intervals: 0.15 seconds
Regularity: Regular	QRS width: 0.10 seconds
P waves: Present Morphology: Upright, normal Axis: Positive in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: 1:1	Rhythm: Sinus bradycardia with two aberrantly conducted PACs

Discussion:

Final Test 2: ECG-35 shows a sinus bradycardia at 54 BPM. The rhythm is broken by two PACs that are associated with different P-wave morphology and PR intervals and that demonstrate an aberrantly conducted pattern with QRS widths of 0.12 seconds (see blue arrows). The appearance of the native QRS complexes is that of an incomplete RBBB, but, as you know, we should not base interpretation on morphologic findings of a rhythm strip because of lack of calibration, and we cannot rule out isoelectric segments.

Final Test 2: ECG-36

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: See discussion below	PR intervals: See discussion below
Regularity: Regular	QRS width: 0.09 seconds
P waves: Present Morphology: See discussion below Axis: Upright in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Sinus rhythm with a PAC

Discussion:

Final Test 2: ECG-36 starts off with a sinus rhythm at a heart rate of approximately 77 BPM and a PR interval of 0.18 seconds (see group A). The yellow arrow represents a PAC that falls on the last T wave of group A. This PAC resets the pacemaker and the rate of group B. Group B has a different P-wave morphology, a new rate at 88 BPM, and a different PR interval at 0.16 seconds. This shifting of the pacemaker due to a PAC is a fairly common occurrence.

Normally, the difference in the appearance of P waves caused by a reset of the pacemaker is minimal since the new pacemaker will typically be within the sinoatrial node itself. In this strip, group A shows an amplitude of 1.5 mm, and group B’s is 3 mm. That is a significant jump in amplitude. This could represent a shift in the pacemaker to the high right atrial area, rather than within the sinus node itself.

Finally, there appears to be a slight ST depression, which could be clinically relevant. This depression could be due to myocardial ischemia or could represent a reciprocal change of a lateral ST elevation. We can hear your screams of anguish as we make observations about morphology on a nonstandardized strip. We were just testing you. . . . Obtain a 12-lead to further evaluate these possibilities, and obtain some clinical correlation as well.

Final Test 2: ECG-37

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 188 BPM Ventricular: 60 BPM	PR intervals: See discussion below
Regularity: Regular	QRS width: 0.06 seconds
P waves: Present Morphology: Normal, upright Axis: Positive in lead II	Grouping: Yes
	Dropped beats: Yes
P:QRS ratio: 3:1	Rhythm: Focal atrial tachycardia with 3:1 block

Discussion:

At first glance, Final Test 2: ECG-37 appears to be a sinus bradycardia with a prolonged PR interval at 0.40 seconds. There are, however, a couple of things to make us nervous.

First, what is that little wave at the end of the third QRS complex (see red arrow)? It is the only one of its kind on the strip. For now, keep it in the back of your mind.

Secondly, a little voice inside our heads is saying: “The P waves are found near the halfway point between the two complexes. According to Bix’s rule, I need to check for buried P waves!” Using our calipers, we place one pin at point 1 (see circle labeled 1) and place the second one on the QRS where the middle of the buried P wave should be (point 2; see circle labeled 2). Now, walking the first pin over to point 3, we see it lies directly on the T wave, then on the visible P wave, then in the QRS, and so on. The distance maps throughout the strip. Based on the other two P waves, we can assume the third P wave is buried within the T wave. Final diagnosis: focal atrial tachycardia with 3:1 block.

Final Test 2: ECG-38

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 100 BPM	PR intervals: Not applicable
Regularity: Irregularly irregular	QRS width: Narrow, variable
P waves: Present Morphology: Varied Axis: Varied	Grouping: None
	Dropped beats: See discussion below
P:QRS ratio: 1:1	Rhythm: Multifocal atrial tachycardia

Discussion:

Final Test 2: ECG-38 shows an irregularly irregular rhythm with at least three P-wave morphologies associated with differing PR intervals, buried P waves, and tachycardia. The only rhythm that fits that presentation is MAT.

Indeed, our strip shows a varied array of P waves and PR intervals, including some inverted P waves. The red arrow points to a T wave that is taller and has a different shape than the other T waves on the strip. This is indicative of a buried P wave that is not conducted to the ventricles.

Note that many of the QRS complexes vary in morphology from the others. This is due to fusion with the buried P waves or varied levels of aberrancy that developed during the transmission of these impulses through the AV node and the ventricular electrical conduction system.

Final Test 2: ECG-39

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: F-waves: 300 BPM Ventricular: 150 BPM	PR intervals: Not applicable
Regularity: Regular	QRS width: Not applicable
P waves: None Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: 2:1	Rhythm: Atrial flutter with 2:1 conduction

Discussion:

Final Test 2: ECG-39 is a great example of the undulating F-wave pattern (see light blue arrows) seen in atrial flutter. The conduction ratio is 2:1 throughout. In Figure 10, we faded everything but the undulating flutter baseline itself to allow a clearer view of the saw-tooth pattern.

Figure 10 In this figure, we have faded out the QRS complex and the markers to give a clearer image of the underlying saw-tooth pattern typically found in atrial flutter.

From Arrhythmia Recognition: The Art of Interpretation, Second Edition, courtesy of Tomas B. Garcia, MD.

The QRS width cannot really be measured accurately because the ventricular morphology is, in reality, a fusion complex between the QRS complex and the F waves. If you really needed to, you could make a closer approximation of the width of the QRS complexes by extending the arms of the R waves graphically down to the baseline. It is, however, best to measure the true QRS interval during periods where there are no underlying F waves whatsoever once the rhythm has broken.

There appear to be some q waves in lead II on this strip. These small q waves are benign because they do not measure 0.04 sec. or greater. Could fusion with the F waves alter the true measurement? Yes, fusion can always interfere with the measurement of intervals. Remember, the forces from the prominent F waves could be narrowing and lessening the depth of those small q waves in our lead. This argument could be applied to a possibly hidden ST depression if the positive forces of the F waves were not present. Clinical and further electrocardiographic evaluation needs to be strongly considered to rule out an acute or age-indeterminate ischemic process in this patient.

Final Test 2: ECG-40

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 69 BPM	PR intervals: 0.16 seconds
Regularity: Regularly irregular	QRS width: 0.10 seconds in the native complexes
P waves: Present Morphology: Normal, upright Axis: Positive in lead II	Grouping: None
	Dropped beats: Yes
P:QRS ratio: 1:1	Rhythm: Sinus arrhythmia with an R-on-T PVC

Discussion:

Final Test 2: ECG-40 shows a mild sinus arrhythmia, as demonstrated by the timing difference between the actual P waves and QRS complex and the completely regular markers (see blue arrows and red circles). There is one event noted on the strip, which is an R-on-T PVC. Note the PVC is associated with a compensatory pause. The overlying P wave is blocked, since it fell at the end of the refractory period of the PVC.

Remember, R-on-T PVCs are dangerous, as they fall into either the absolute or relative refractory period of the previous complex. A PVC falling on these periods could trigger a circus movement that could lead to VTach.

Final Test 2: ECG-41

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: 83 BPM	PR intervals: 0.18 seconds
Regularity: Regularly irregular	QRS width: 0.10 seconds
P waves: Present Morphology: See discussion below Axis: See discussion below	Grouping: None
	Dropped beats: See discussion below
P:QRS ratio: See discussion below	Rhythm: Normal sinus rhythm with PAC, PJC, PVC, and atrial escape beat

Discussion:

To quickly identify the rhythm in Final Test 2: ECG-41, you need to remember the concept of events. Events occurring in a strip are abnormalities that alter the rhythmicity of the heart but are not part of the rhythm itself. Say, for example, that you are walking down the street. The cyclical rhythm of walking is the rhythm. Now, an eagle is flying by and drops a . . . fish . . . on your head. The fish smacking you on the head is the event. The fish dropping on your head will, one way or another, alter your walking pattern. Final Test 2: ECG-41 is basically a normal sinus rhythm broken up by four events.

The first event (see red arrow) is a PJC. We see that the PJC comes prior to the expected P wave (see blue arrows). In this case, the PJC did not spread retrogradely back through the atria and does not reset the sinus node, thereby creating a compensatory pause. The first red circle with an X is where the normal QRS would be if it hadn’t been interrupted by the PJC. The sinus rhythm, however, marches on. . . .

The second event (see brown arrow) is an atrial escape beat. It occurs later than the expected P wave and is associated with an inverted P wave and a different PR interval. An unexpected finding is that the inverted P wave did not reset the sinus node. This, once again, is associated with a compensatory pause.

The third event (see yellow arrow) is a PVC. It is wide and bizarre, starts in the opposite direction from the first part of the native complex, and is associated with a compensatory pause. This is pretty straightforward, so we’ll move on.

The fourth and final event (see green arrow) is a PAC caused by the premature firing of an ectopic pacemaker. Once again, the PR interval is also different from the native complexes.

Could this be a WAP? Well, the rhythm is regularly irregular and not irregularly irregular. Remember, WAP is, by definition, an irregularly irregular rhythm.

The large number of events occurring in this strip makes a unifying, simple diagnosis difficult to attain. At least, that was true until we stopped trying to identify a single cardiac rhythm that could account for the findings. When we look at them from the vantage point of individual events altering the rhythm in their own way, the diagnosis becomes simple. An understanding of rhythms and events will serve you well as you proceed in learning how to interpret arrhythmias.

Final Test 2: ECG-42

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 90 BPM	PR intervals: Not applicable
Regularity: Regularly irregular	QRS width: Variable
P waves: Present Morphology: Inverted Axis: Negative in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Accelerated idioventricular rhythm with AV dissociation

Discussion:

We decided to include Final Test 2: ECG-42 in this test because it was too classic to pass up. Note the idioventricular rhythm at the start with the typical ventricular morphology. With each passing complex, the ventricular complexes become more organized until complex 6. At this point, there is a gradual return to the idioventricular morphology seen at the start.

These slow transitions are all due to AV dissociation. As the atrial and ventricular rhythms synchronize closer, the ectopic atrial rhythm achieves more capture of the ventricular complexes. This “dance” continues until the rhythm terminates or morphs into a totally different one.

In summary:

• Complex 1: Idioventricular morphology
• Complex 2: Fusion wave, but closer to idioventricular morphology
• Complex 3: Fusion complex
• Complex 4: Fusion complex
• Complex 5: Fusion complex
• Complex 6: Native complex, capture beat
• Complex 7: Fusion complex
• Complex 8: Fusion complex
• Complex 9: Fusion wave, but closer to idioventricular morphology

Final Test 2: ECG-43

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 40 BPM	PR intervals: 0.16 seconds
Regularity: Regularly irregular	QRS width: 0.08 seconds
P waves: Present Morphology: Notched, upright Axis: Positive in lead II	Grouping: Present
	Dropped beats: Yes
P:QRS ratio: 2:1	Rhythm: 2:1 second-degree AV block

Discussion:

Final Test 2: ECG-43 is a classic example of 2:1 second-degree AV block. The P-P intervals are equal and there is no evidence of widening along any group because there is only one PR interval per group. A longer strip may show the presence of grouping of either Mobitz I or Mobitz II. Remember, if even one group matches Mobitz I or II criteria, the rest would all be assumed to be caused by the same mechanism.

Final Test 2: ECG-44

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 62 BPM	PR intervals: 0.38 to 0.41 seconds
Regularity: Regularly irregular	QRS width: 0.08 seconds
P waves: Present Morphology: P-mitrale pattern Axis: Upright in lead II	Grouping: None
	Dropped beats: Present
P:QRS ratio: 1:1 with event	Rhythm: First-degree AV block, Mobitz II second-degree AV block

Discussion:

In Final Test 2: ECG-44, the long PR interval of 0.38 to 0.41 seconds is consistent with a first-degree AV block. The dual finding of first- and second-degree AV block is a common occurrence in these patients since they typically have diffuse disease of the area involving the AV node and/or the bundle of His.

This strip has all the hallmarks of a Mobitz II second-degree AV block. As a reminder, the criteria for a Mobitz II include a P wave before each QRS complex with consistent P-P and PR intervals (except for the blocked beat), single or multiple (but not sequential) blocked P wave(s) that fail to capture the ventricles, and, finally, a pause that is a multiple of the P-P interval (see page 429).

The mild variations in the PR interval seen in this strip of less than or equal to 0.03 seconds are within acceptable limits and are not enough to make us doubt our initial assessment of Mobitz II second-degree AV block.

The P-wave morphology is classic for a P-mitrale, which is typically found in significant left atrial enlargement. However, we need to verify the morphology with a 12-lead ECG before making any definitive call.

Final Test 2: ECG-45

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: 153 BPM	PR intervals: None
Regularity: Regular	QRS width: See discussion below
P waves: See discussion below Morphology: See discussion below Axis: See discussion below	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: AV nodal reentry tachycardia

Discussion:

Final Test 2: ECG-45 shows a narrow-complex supraventricular tachycardia at 153 BPM that is extremely regular and has no directly visible P waves. The P waves are actually present but are retrogradely conducted through the atria and buried within the QRS complex, making the only visible part appear as a pseudo-S wave in lead II (see red arrow). There are no PR intervals at all since the P waves are buried within the QRS complex itself and originate instantaneously from the same focus that is triggering the QRS complex. (If there were more separation between the QRS complexes and the P waves, the interval would be an RP interval, since the atrial depolarization originates after the QRS complex.)

Since this has the appearance of a junctional tachycardia but is actually occurring at rates above 140 BPM, we are dealing with an AVNRT. We need to remember that a junctional tachycardia is not the same as AVNRT despite the similar appearance. A junctional tachycardia is caused by the firing of a single irritable junctional pacemaker. An AVNRT, on the other hand, is caused by a circus movement at the level of the AV node. Onset is acute, usually following an event such as a PAC that triggers the circus movement. Likewise, termination is abrupt when the circus movement is disrupted. Previously, these rhythms were known as one of the paroxysmal atrial tachycardias since the onset and termination were both instantaneous; however, these terms have fallen out of favor.

A word about measuring the width of the QRS interval: Make sure you do not include the width of the pseudo-S wave or pseudo-R′ waves in the measurement of the QRS complex. Remember, this additional width is actually due to the retrograde atrial depolarization wave; it is not due to the vectors that formulate the QRS complex whatsoever. In our example, the width appears to be 0.12 seconds, but if we disregard the pseudo-S wave, it is found to be actually 0.08 seconds, which is the true measurement.

Final Test 2: ECG-46

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 250 BPM Ventricular: 125 BPM	PR intervals: Not applicable
Regularity: Regular	QRS width: Unable to accurately assess
P waves: F waves Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: 2:1	Rhythm: Atrial flutter with 2:1 block

Discussion:

When we first look at Final Test 2: ECG-46, we get the impression that it is simply a sinus tachycardia at 136 BPM. We see that the voltage appears low, especially on the P waves, and that the QRS complexes appear narrow. We need to remember that strips can be used to measure intervals. However, if more accurate, true intervals are needed, you must measure them in the leads in which they are the widest, to discount the effect that isoelectric segments could have on the measurements.

At the beginning of this text, we mentioned that you need to be thorough in reviewing any abnormalities on your strip that defy a simple explanation. When we look at this strip, there appears to be a small positive deflection almost at the start of the T wave. If you notice, that deflection almost has the same morphology as the P wave. Using our calipers, we see that this is a second P wave and the intervals map throughout the strip. However, since they are occurring at a rate of 250 BPM, are these atrial waves considered P waves or F waves? Looking at the strip above, the baseline appears to be “wandering” or undulating. Therefore, these are actually F waves. The rhythm is, therefore, an atrial flutter with 2:1 block.

Remember to always formulate a list of differential diagnoses and then use it to narrow down the possibilities. The only way you can diagnose something is if you think about it.

Final Test 2: ECG-47

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Description

Rate: Atrial: Around 80 BPM Ventricular: Approximately 70 BPM	PR intervals: See discussion below
Regularity: Regularly irregular	QRS width: 0.08 seconds
P waves: Present Morphology: Normal, upright Axis: Positive in lead II	Grouping: Present
	Dropped beats: Yes
P:QRS ratio: See discussion below	Rhythm: Mobitz I second-degree AV block or Wenckebach

Discussion:

Final Test 2: ECG-47 is a great example of a Mobitz I second-degree AV block or Wenckebach. We cannot make the call on a definitive conduction rate because we do not see a complete cycle on the strip.

The typical characteristics of a Mobitz I second-degree AV block or Wenckebach are present with a widening of the PR interval until one of the P waves is blocked, progressive decrease in the R-R interval, the first PR interval after the blocked beat being the shortest, and the one prior to the dropped beat being the longest.

Final Test 2: ECG-48

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Approximately 60 BPM	PR intervals: Not applicable
Regularity: Irregularly irregular	QRS width: 0.09 seconds
P waves: None Morphology: Not applicable Axis: Not applicable	Grouping: None
	Dropped beats: None
P:QRS ratio: None	Rhythm: Atrial fibrillation

Discussion:

Final Test 2: ECG-48 shows a typical atrial fibrillation pattern at approximately 60 BPM. The rhythm is irregularly irregular with no apparent P waves. The baseline is rather coarse, which can appear to include low-voltage P waves at times, but the lack of consistent P-wave morphology rules out that possibility. Remember, the coarse baseline is created by both the haphazardness of the arrival of the f waves to the AV node, which gives rise to atypical vectors, and the summation of these atypical vectors to external artifact. We know that there is baseline artifact because the coarseness extends to the ST-T–wave area that should appear smoother.

Final Test 2: ECG-49

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 97 BPM Ventricular: 55 BPM	PR intervals: Not applicable
Regularity: Regularly irregular	QRS width: 0.14 seconds
P waves: Present Morphology: P-mitrale pattern, wide Axis: Positive in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Third-degree or complete AV block with a sinus rhythm and an accelerated idioventricular escape rhythm

Discussion:

Final Test 2: ECG-49 shows a third-degree or complete AV block with a normal sinus rhythm to depolarize the atria and an accelerated idioventricular escape rhythm to depolarize the ventricles. There is no connection whatsoever on this strip between the atrial and ventricular rhythms, as you would expect.

There are three buried P waves noted (see large arrows). The first buried P wave, marked by the green arrow, shows a slurring of the upstroke of the R wave. This complex could be confused with a delta wave, but since it appears in only that one complex, it is not a delta wave. The second buried P wave, marked by the yellow arrow, shows a slight bulging and a slight elevation of the J point. The third buried P wave, marked by the red arrow, shows the P wave peeking out in the ST-segment area. Notice that the P wave in this case is lower in amplitude due to the fusion with the underlying ST segment that is slightly depressed in the other complexes.

Final Test 2: ECG-50

From Arrhythmia Recognition: The Art of Interpretation, courtesy of Tomas B. Garcia, MD.

Rate: Atrial: 96 BPM Ventricular: 142 BPM	PR intervals: Not applicable
Regularity: Regularly irregular	QRS width: 0.18 seconds
P waves: Present Morphology: Normal, upright Axis: Positive in lead II	Grouping: None
	Dropped beats: None
P:QRS ratio: See discussion below	Rhythm: Ventricular tachycardia

Discussion:

Final Test 2: ECG-50 shows a wide-complex ventricular rhythm with obvious AV dissociation with an atrial rate of 96 BPM and a ventricular rate of 142 BPM. The ninth complex is a good example of a capture beat, while the eighth and tenth (the ones before and after the capture beat) are clearly fusion beats.

We can measure out the atrial rhythm by mapping the P waves throughout most of the strip. This is indirect evidence of AV dissociation. Quite often all we can see is this indirect evidence. Let’s discuss in a bit more detail how we typically map these out.

In this example, we are lucky to see two clear distinct P waves on the strip (see red arrows). Let’s start by placing the pins of our calipers on the tips of the P waves marked by these red arrows. Now, transfer the distance marked by the caliper pins by walking the caliper pin up toward the start of the strip. We can now clearly identify irregularities that are caused by the fusion of the P waves and the ventricular complexes. By walking the calipers throughout the entire strip, we demonstrate the entire baseline atrial rhythm. We can do the same for the ventricular complexes and notice their regularities. Note that the regularity of both rhythms remains undisturbed throughout the strip. The interaction between the two dissociated rhythms (sinus rhythm and VTach) is direct evidence of AV dissociation.

Indirect evidence of AV dissociation is also present. Note that complex 9 appears to be a capture beat (even though the PR interval is a bit wide, which could represent the patient’s baseline PR interval). Complexes 1, 4, and 10 are fusion complexes.

The R-R intervals in this strip all fall within one small block of the pin measurements if you were to map them out. That margin of error is not bad for a VTach that has evidence of an underlying AV dissociation. Remember, the P waves can influence changes in the timing of the typically very regularly occurring ventricular complexes.

Of interest, the ventricular complex 8 is very atypical and also arrives earlier than expected. The polarity of that complex and the morphology of it do not match the other ventricular complexes. This complex appears to be due to a secondary ectopic ventricular pacemaker firing off a differing PVC. The relatively slower rate of this VTach is what is probably allowing the secondary pacemaker to be out of a refractory state long enough to fire off prematurely.