ECG Blog #150 (J-Point - ST Elevation - Pericarditis - Myocardial Bridge - Peaked T Waves - Early Repolarization)

A previously healthy 19-year old man presented to the ED (Emergency Department) following a syncopal episode. His initial ECG is shown in Figure-1.

• Are the ST-T wave abnormalities seen in this tracing the result of Early Repolarization? Or, is this likely to represent acute pericarditis?
• A CT angiogram was performed while the patient was in the ED. It was normal. Does this alter your diagnostic considerations?

Figure-1: Initial 12-lead ECG obtained from a 19-year old man who presented to the ED with syncope. NOTE— Enlarge by clicking on the Figure.

Interpretation: We interpret the ECG shown in Figure-1 as showing sinus arrhythmia — normal intervals and axis — low voltage in the limb leads (no QRS complex >5mm in amplitude) — and no chamber enlargement. The tracing is remarkable for its ST-T wave changes ...

• QRST Changes — An rSr’ complex is present in lead III. Tiny q waves are seen in leads I, aVL, V5 and V6. R wave progression is normal, with transition occurring between leads V3-to-V4. T waves are markedly peaked in multiple leads. In addition, multiple leads show upward-sloping (ie, “smiley”-configuration) ST segment elevation. There is no reciprocal ST depression.

Diagnostic Considerations: ST segment elevation in multiple leads with T wave peaking as seen here should bring to mind several considerations. These include:

• Acute Pericarditis — Features consistent with acute pericarditis include fairly diffuse ST segment elevation, with ST segment appearance in lead II resembling lead I (whereas with inferior infarction — lead II resembles lead III much more than lead I ). In addition, there is no reciprocal ST depression (as is typically seen with acute MI ) — and the relative amount of ST elevation in lead V6 is significant, as suggested by the ST/T ratio >0.25. That said — syncope is not a typical manifestation of acute pericarditis — and — T waves appear to be significantly more peaked than is usually seen with acute pericarditis.
• Hyperkalemia — There is no obvious reason for hyperkalemia in a previously healthy 19-year old man. In addition, the shape of the peaked T waves in this tracing are asymmetric (T wave upslope in many leads is much more gradual than is T wave downslope) — whereas with hyperkalemia, T waves tend to be much more symmetric and manifest a narrow base.
• Acute STEMI — Acute ST Segment Elevation Myocardial Infarction would seem unlikely in a previously healthy 19-year old, especially in the absence of chest pain. Acute STEMI usually produces more localized changes, rather than the diffuse ST elevation seen here. And, we are told that CT Angiography was done acutely and found to be normal.
• Early Repolarization — Early repolarization should always be a diagnosis of exclusion! While unusual repolarization variants are fairly common — the amount of ST elevation and the degree of T wave peaking seen here are clearly more marked than is generally seen with a simple repolarization variant.
• Acute Myocarditis— This can’t be ruled out on the basis of this single ECG — although the history is not suggestive of acute myocarditis.
• Something Else — Could we be missing something?

The ECG was repeated a little bit later (Figure-2). For clarity — we put the original ECG on Top (BLUE border) — and the follow-up ECG below (RED border).

• What has happened since the initial tracing was done?
• How does this 2nd ECG affect your diagnostic considerations?

Figure-2: Follow-up ECG (RED border), obtained a little while after Figure-1. For ease of comparison — the original ECG is shown on top (BLUE border). What has happened in the interim? (See text).

Answer: The best way to assess serial tracings is by lead-to-lead comparison. Doing so — it should be apparent that:

• The amount of ST elevation in the follow-up tracing is clearly less in virtually all leads.
• T waves are not nearly as “peaked” as they were in the initial tracing.
• SUBTLE Finding: The terminal portion of the T wave in lead V3 appears to be turning negative in the follow-up tracing — whereas it was not negative initially. Could this reflect reperfusion?

Impression: The fact that there has been this much change in the 2nd ECG (done just a short while after the 1st ECG) means that there are dynamic ST-T wave changes. This is not something one would expect to see over the course of a few hours with acute pericarditis. As a result — the differential diagnosis in this 19-year old who presented with syncope, should be expanded to include “out-of-the-box” entities that might cause intermittent ST elevation including hyperacute changes. Think of:

• Coronary spasm.
• A myocardial bridge ...

Follow-Up: Cardiac catheterization was performed. It revealed normal left ventricular function, clean coronary arteries — and, a myocardial bridge in the mid-LAD (Left Anterior Descending) coronary artery that was felt to be causing intermittent reduced blood flow.

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What is known about Myocardial Bridging? A myocardial bridge is said to be present when instead of its usual overlying epicardial location, a part of a coronary artery takes a “tunneled” intramuscular course under a “bridge” of overlying myocardium. Myocardial bridges may be “complete” (if the tunneled segment is completely surrounded by a band of myocardial muscle) — or “incomplete” (if only partially surrounded by a myocardial band). As a result of myocardial bridging — there may be intermittent dynamic compression of the artery by the involved myocardium during cardiac contraction.

• Autopsy studies suggest that myocardial bridging may be found in as many as 1/3 of adults. In most cases, there is little or no restriction of flow. As a result, the condition is usually benign. In fact, most cases of myocardial bridging go unrecognized — unless there is occasion to perform cardiac catheterization.
• That said — myocardial bridging sometimes is clinically significant. This is more likely to occur when conditions exist that enhance the amount of coronary artery compression. Clinically significant myocardial bridging is seen more often in heart transplant recipients, and in patients with hypertrophic cardiomyopathy (HCM). In this latter condition, a greatly hypertrophied left ventricle predisposes to development of myocardial bridging that might compromise coronary flow. It has been postulated that such bridging may contribute to the increased incidence of exercise-induced sudden death in the pediatric and young adult population with HCM.
• Myocardial bridges are most often detected by cardiac catheterization. The most commonly recognized location of myocardial bridging on cardiac catheterization — is in the middle segment of the LAD. That said, any artery may be affected. The usual size of the involved artery segment is between 1-3 centimeters. Males are affected as often as females.
• Atherosclerosis may or may not be associated with myocardial bridging. If present, atherosclerosis is most commonly seen just proximal to the bridged segment (probably due to generation of excessive shear forces). In contrast, the bridged artery segment itself is often free of atherosclerotic narrowing.
• As emphasized above — the overall clinical course of most patients with myocardial bridging is benign. However, it is important to realize that myocardial bridging may cause symptoms, including: i) acute coronary syndromes due to ischemia or infarction; ii) left ventricular dysfunction; iii) exercise-induced ventricular arrhythmias; and/or iv) sudden death. 
• The mechanism of symptom production in patients with myocardial bridging is complex, and not completely understood. Symptoms sometimes appear out of proportion to the visible amount of flow reduction. Tachycardic states (including exercise or other cause of increased heart rate) may predispose to symptom production, because of disproportionate shortening of the period of diastolic ventricular filling. Whether vasoactive substances in the pre-bridged segment are involved is uncertain.
• Recent years have expanded assessment tools for detection of clinically significant myocardial bridging. In addition to cardiac catheterization — recognition of the presence and likelihood of clinical impact may now be evaluated by IVUS (IntraVascular UltraSound) — assessment of FFR (Fractional Flow Reserve) during cardiac catheterization — Cardiac CT (Computed Tomography) Angiography — and even stress echocardiography.
• TREATMENT: Medical therapy is 1st-line treatment for symptomatic myocardial bridging. Drugs of choice include ß-Blockers and non-dihydropyridine calcium channel blockers (ie, Verapamil; Diltiazem). The theoretical basis for use of these drugs is the negative chronotropic and inotropic effect that they have. In contrast, Nitrates are contraindicated — as they appear to accentuate systolic compression of bridged segments.
• If symptoms directly attributable to myocardial bridging persist despite optimal medical therapy — additional options that should be considered include surgical myotomy — coronary bypass surgery — and/or stenting of the tunneled coronary artery segment.

BOTTOM Line: Although not a common cause of acute ischemia/infarction — it is good to be aware of the possibility of myocardial bridging— especially when symptoms arise in a younger adult not expected to have coronary disease. The diagnosis in this case was not picked up by CT angiography — and would have been missed had cardiac catheterization not been performed. Recognition of dynamic ST-T wave changes on serial ECGs performed in the Emergency Department were key to pursuing a definitive diagnosis.

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References:

• Lee MS, Chen CH: Myocardial Bridging: An Up-to-Date Review: J Invasive Cardiol 27:521-528, 2015.
• Möhlenkamp S, Hort W, Ge J, Erbel R: Update on Myocardial Bridging: Circulation 106:2616-2622, 2002.
• Onan B, Onan IS, Bakir I: Left Anterior Descending Coronary Artery Muscular Bridge: Texas Heart Inst. J 39: 598-600, 2012.

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Acknowledgment: My thanks to 유영준 from Seoul, Korea for his permission allowing me to use this tracing and clinical case.

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ECG Blog #149 (ST Elevation - J-Point - Osborn - Hypothermia - Pericarditis - Acute STEMI)

A 28-year old man was found “down” in front of his house. There was a history of alcohol consumption. The patient was not lucid enough to answer questions. His initial ECG is shown in Figure-1.

• Is this acute pericarditis?
• What key piece of information is missing from the history?
• How would you interpret this ECG?

Figure-1: Initial 12-lead ECG and long lead II rhythm strip obtained from a 28-year old man who was found “down” in front of his house. NOTE — Enlarge by clicking on the Figure.

Interpretation: There is much baseline wander and significant artifact. Approaching the tracing systematically:

• Rhythm & Rhythm — The rhythm is regular at ~55/minute. The QRS complex is narrow. Regular P waves are present — although they are of very low amplitude. Rather than being best seen in lead II (as is usually the case with sinus rhythm) — P waves are probably best seen in lead I. Thus, the rhythm might be either sinus or low atrial.
• Intervals — The PR interval is upper normal (ie, ~0.20 second). As noted, the QRS is of normal duration (ie, not more 0.10 second = half a large box). However, the QT interval appears prolonged. Determination of the QTc (corrected QT interval) is always challenging when the rate is slow. It is probably easiest to assess the QT interval in the long lead II — because we have 9 consecutive beats to look at. Discounting those with significant artifact — we measure the QT = 0.52 second in this lead. Considering the reduced heart rate of ~55/minute — this corrects to a QTc ~ 480-500 msec, which is long.
• Axis — Normal (about +60 degrees).
• Hypertrophy — None.
• QRST Changes — A tiny q wave is seen in lead II. There is early transition — since the R wave becomes taller than the S wave is deep already by lead V2. Importantly, there is diffuse, upward sloping (ie, “smiley”-configuration) ST segment elevation. This is seen in virtually all leads except leads I, aVR and aVL. But rather than acute infarction or acute pericarditis — an important clue is seen just before takeoff of the ST segment (Figure-2):

Figure-2: We have added RED arrows to Figure-1, to highlight the clue seen just before the takeoff of the ST segment (See text).

Answer: The positive, notched deflections that are seen just after the QRS complex and just before the beginning of the ST segment in Figure-2 are Osborn Waves (RED arrows).

• Osborn waves were first described in 1953 by JJ Osborn. The wave is commonly linked to hypothermia — but other entities (including CNS injury and ventricular fibrillation) may also be associated with it. A number of other names have been attributed to this ECG finding (“camel-hump” sign; hypothermic wave; prominent J wave).
• Osborn waves are often not seen until the temperature drops below -32 degrees Centigrade ( = 89.6 degrees Fahrenheit).
• Other commonly associated ECG features with Hypothermia include: i) Bradycardia (which may be marked); ii) Atrial fibrillation or other arrhythmias; and iii) Artifact (from baseline undulations resulting from associated shivering).

What KEY Information was Missing from the History? No mention was made of the patient’s initial core temperature. Unfortunately, the initial temperature was not attainable — but ambient weather conditions were freezing, and the patient was “cold”.

• J waves (Osborn waves) in this case were dramatic — both in amplitude, and by their presence in virtually all leads.
• Other findings consistent with hypothermia in this case include: i) marked artifact with baseline undulations; ii) bradycardia; and iii) low amplitude atrial activity that may make it difficult to be certain of sinus origin.

The patient was intensively treated for hypothermia. He recovered. Figure-3 compares his initial ECG (top; light blue border) — with his follow-up ECG after core temperature was corrected with associated improved mental status (bottom; red border).

• What are the differences between the pre-treatment and post-treatment tracings?

Figure-3: Comparison between the pre-treatment ECG (top; light blue border) — and post-treatment ECG (bottom; red border). What changes do you see?

Answer: We note the following changes between these 2 tracings: i) the heart rate is faster after core temperature has been corrected; ii) Osborn waves are no longer seen; and iii) the diffuse ST elevation has resolved. Baseline artifact does remain.

• This patient had neither acute infarction nor acute pericarditis. Management of severe hypothermia is complex and comprehensive. Core rewarming is key. Many conditions predispose to hypothermia — including ambient cold weather exposure and alcohol consumption, as was seen in this case. Impaired mental status makes it imperative to rule out CNS injury, undetected infection or other metabolic disorders that may be contributing to his condition.

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Acknowledgment: My thanks to 유영준 from Seoul, Korea for his permission allowing me to use this tracing and clinical case.

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ECG Blog #148 (Ventricular Fibrillation - VFib - Artifact )

Is the patient whose 6 limb leads are shown in Figure-1 in VFib (Ventricular Fibrillation)?

• Can you tell from these 6 leads, even before you see the rest of his 12-lead ECG?

Figure-1: Is this patient in VFib? NOTE — Enlarge by clicking on the Figure.

If one simply looked at these 6 leads — it would be easy to think this patient had just gone into VFib. However, there is enough information on this limited tracing to tell that this is not the case.

• The presence of artifact is extremely common. Potential sources of artifact include tremor, shivering, brief seizure activity or other body movement; loose or faulty lead connection; external devices that may produce various types of interference; and application of a monitoring lead in close contact with a pulsating artery, among others. Extreme clinical conditions with acutely ill patients may at times lead to unavoidable artifact. That said, most of the time interpretation of the ECG will still be possible despite a less-than-perfect recording. However, when artifact becomes as pronounced as it is in leads III, aVL and aVF of Figure-1 — interpretation of the ECG may become extremely challenging.
• The best way to prove artifact — is to recognize persistence of an underlying spontaneous rhythm that is unaffected by any erratic or suspicious deflections that are seen. Therefore, despite close resemblance to VFib in leads III, aVL and aVF of this ECG — an underlying regular supraventricular (that is, narrow QRS) rhythm at a rate just under 100/minute can still be seen in other leads.

Figure-2 shows the remaining 6 leads for this 12-lead tracing. Do the 6 chest leads that are now seen support your answer?

Figure-2: Complete 12-lead ECG for the patient whose 6 limb leads were shown in Figure-1.

Answer: The baseline “noise” and artifact deflections continue in the chest leads. However, it is now much easier to appreciate that a regular underlying supraventricular rhythm continues throughout the entire tracing.

• Proof that the high-amplitude chaotic deflections seen in leads III, aVL and aVF constitute artifact is forthcoming from inspection of simultaneously-obtained leads (Figure-3).

Figure-3: We have dropped vertical lines (in red) from definite QRS complexes seen in leads I, II and aVR (See text). NOTE: The baseline ECG is a photograph, and was unfortunately somewhat tilted. This is why the red lines may appear with slight angulation — but they are parallel with the ECG grid lines, and therefore do correspond to simultaneously-recorded QRS complexes.

PEARL: Awareness that almost all modern ECG machines produce simultaneous recordings of at least 3 leads at a time may prove invaluable in arrhythmia interpretation.

• It allows accurate determination of QRS duration. This is especially important when part of the QRS complex lies on the baseline and appears narrow in some leads, when in fact other leads clearly demonstrate QRS prolongation.
• It tells us if atrial activity is arising from a single site or multiple atrial sites (ie, P waves from different atrial sites may look similar in some but not all leads).
• It facilitates detection of artifact — which often appears much more marked in some (but not all) leads.

Analysis of Figure-3 should remove any doubt that the chaotic deflections seen in Figure-2 are the result of artifact. Vertical RED lines should make it evident that you can clearly “walk out” a regular supraventricular rhythm at a rate just under 100/minute in virtually all leads on this tracing.

• Note that while we suspect the mechanism of the underlying narrow rhythm in this ECG is sinus (upright P waves are suggested in lead II ) — the amount of artifact prevents clear distinction between a sinus vs junctional rhythm. But we can say with certainty that a regular supraventricular rhythm is present.

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Acknowledgment: — My thanks to MG for his permission allowing me to use this tracing and clinical case.

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NOTE: For additional examples of Artifact — See ECG Blog #44 — Blog #132 — and Blog #139 —

ECG Blog #147 (AV Block - PACs - Mobitz I, II).

The long lead II rhythm strip shown in Figure-1 was diagnosed as showing 2nd-Degree AV Block, Mobitz Type II.

• Do you agree with that assessment? If not — What is your diagnosis?

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NOTE: This is a difficult arrhythmia to interpret. That said, we present numerous Pearls on arrhythmia interpretation throughout our discussion that should be of value for interpreters of any level. Are you up for the challenge?

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Figure-1: Long lead II rhythm strip that was interpreted as showing Mobitz Type II 2nd-Degree AV Block. Do you agree? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.

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KEY Clinical Points: Our systematic approach for interpreting any cardiac rhythm is to, “Watch your Ps and Qs, and the 3 Rs”. That is, systematically evaluate each and every tracing you encounter for the following 5 Key Parameters:

• i) Are there P waves? — or, if no clear P waves, then are there signs of atrial activity (such as “fib waves” or atrial flutter)?
• ii) Is the QRS wide? — for which we accept anything more than half a large box in duration (ie, >0.10 second) as qualifying as a “wide” QRS.

And the 3 Rs:

• iii) Rate? — What is the ventricular (and the atrial) rate?
• iv) Regularity? — Is the ventricular (and atrial) rhythm regular?
• v) “Related”? — Is there is a specific relationship between QRS complexes and neighboring atrial activity?

NOTE: It does not matter in what sequence you assess the Ps, Qs & 3Rs — as long as you always assess each of these 5 key parameters. We often vary the sequence in which we address the Ps, Qs and 3Rs — depending on whether atrial activity, QRS width, and/or rhythm regularity is easier or harder to evaluate in the particular rhythm we are looking at.

• PEARL: By remembering to always “Watch Ps, Qs and the 3Rs” — you have at your fingertips an easy-to-recall method to ensure that you are always systematic (as well as time-efficient) in your approach and, that you never forget to assess each of these 5 essential elements. By religiously applying the “Ps, Qs & 3R Approach” to every arrhythmia you encounter — even if the specific etiology of the rhythm remains elusive — you will have narrowed down diagnostic possibilities, and clarified which specific parts of the rhythm you are still uncertain about.

Additional Suggestions: To facilitate interpretation of more complex rhythms — we offer the following additional suggestions:

• Start with what you know! If there are easier parts to interpret in a tracing (as well as more complicated parts) — Begin with the easier parts! Is there is an underlying rhythm? If there are a number of sinus-conducted beats on the tracing — it is often easiest to first identify these sinus beats, and to leave for later interpretation of the more difficult portions of the arrhythmia.
• Use Calipers! You’ll be amazed at how much “smarter” you instantly become the moment you begin to regularly use calipers for the interpretation of challenging arrhythmias. Your colleagues will marvel at how much more focused you become by regular application of this simple measure. Even the experts do better when they use calipers! Remember: The cardiologist who does not use calipers to interpret complex arrhythmias — is a cardiologist who will not always come up with the correct interpretation.
• It often helps to label P waves on the tracing! If you are teaching others and/or if discussing a tracing with colleagues — it also often helps to number the beats, as this is the most time-efficient way to ensure that all participants in the discussion immediately know the specific part of the tracing being addressed. (Note: It is best not to mark up an original tracing — so please try to use a copy before you label.)

With these points in mind, we now proceed with our systematic interpretation of the rhythm in Figure-2:

Figure-2: We have numbered beats and labeled sinus P waves from Figure-1.

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Interpretation: Imagine the patient in question is hemodynamically stable. We begin our interpretation with assessment of the “Ps, Qs & 3 Rs”. Note the following:

• The QRS complex in Figure-2 is narrow. Although ideally we would have access to all leads on a 12-lead ECG before committing to comment on QRS duration — the QRS complexes in this tracing clearly look to be narrow and supraventricular.
• The ventricular rhythm is not completely Regular. That said, there is a pattern to this rhythm — in that “group beating” is present, with 3 groups comprised of 3 beats each in a repetitive pattern.
• Sinus P waves are evident (RED arrows) — as recognized by the presence of upright P waves with similar morphology in this long lead II rhythm strip. The P-P intervals appear to be constant, with the exception of 2 short pauses that occur at the end of each group (ie, after beat #3 and after beat #6).
• The Rate of the rhythm varies — but it is neither excessively fast, nor excessively slow.
• There does appears to be a consistent Relation between a number of sinus P waves and neighboring QRS complexes. That is, the PR interval preceding beats #2,3; #5,6; and #8,9 appears to be constant (albeit slightly prolonged).

Next Step: Now that we’ve addressed each of the 5 key parameters — Let’s see what conclusions might be drawn:

• Although this rhythm is complex — there does appear to be an underlying sinus rhythm — because an upright P wave with fixed PR interval precedes no less than 6 of the 9 beats on this tracing (ie, beats #2,3; #5,6; and #8,9).
• A much shorter, but still constant PR interval precedes the 1st beat in each of the 3 groupings. We need to explain WHY this is so. We also need to explain why the rate of sinus P waves is not constant throughout this tracing — and why short pauses punctuate each of the groups.

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Diagnostic Possibilities: Two clinical entities should come to mind as possible explanations for the ECG findings described above. These are: i) some form of AV block; and ii) Blocked PACs. Let’s consider each of these possibilities in turn.

• There is NO 2nd- or 3rd-Degree AV Block in Figure-2. Despite the apparent increase in PR interval between the 1st and 2nd beats in each grouping — the rhythm in Figure-2 is not AV Wenckebach. This is because the premise of AV Wenckebach (which is also known as the Mobitz I form of 2nd-degree AV block) — is that there should be an underlying regular sinus rhythm throughout the tracing. The PR interval with AV Wenckebach progressively increases, until one or more of the regularly occurring sinus P waves is not conducted. However, RED arrows in Figure-2 show that regular sinus P waves do not continue throughout this tracing. For similar reasons, this rhythm does not represent the Mobitz II form of 2nd-degree AV block. First, the PR interval does not remain constant (as it should if Mobitz II was present) — and second, the P-P interval of sinus P waves does not remain constant throughout the rhythm strip as it almost always does for virtually any form of AV block. Finally, this rhythm cannot be complete (ie, 3rd-degree) AV block — because there is conduction of a number of sinus beats (ie, beats #2,3; #5,6 and #8,9 are all conducted with a constant PR interval).

PEARL: The most common cause of a pause is a blocked PAC! This phenomenon occurs far more often than is generally appreciated. Blocked PACs are a much more common cause of pauses than any form of AV block. The challenge diagnostically, is that blocked PACs may be extremely subtle and easy to overlook. The secret is to look for blocked PACs whenever you encounter any unexpected pause.

• How to Look: Carefully examine at the ST segment and T wave at the onset of the pause. Compare this ST segment and T wave at the onset of the pause (ie, the ST-T wave of beats #3 and #6 in Figure-2) — with the ST-T wave of all normally conducted sinus beats on the tracing. Is there any difference?
• NOTE: We fully acknowledge that detecting blocked PACs may be challenging. One has to distinguish between minor variations that naturally occur from beat-to-beat in the ST-T wave — from notches or deflections that are the result of a premature P wave buried within (and therefore deforming) the ST-T wave.
• For Practice: We illustrate detection of blocked PACs in our ECG Blog #33 and Blog #57. Once you begin to routinely look for blocked PACs whenever you see an unexpected pause — I guarantee that you will find them with surprising frequency!

Test yourself looking for signs of blocked PACs in Figure-2. Look carefully in at the base of the T wave at the onset of each pause — paying special attention to the T wave after beat #6.

• Be sure you have magnified the tracing by clicking on it to view in a separate window!
• We illustrate our answer below in Figure-3.

Figure-3: We have added a RED-BLACK arrow at the base of the T wave near the beginning of each pause (See text).

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Answer: Note subtle angulation at the base of the T waves of beats #3 and #6 at the onset of each pause (RED-BLACK arrows in Figure-3). This subtle deformity is not present in the T waves of all other beats on this tracing.

• We strongly suspect this angulation at the base of these T waves is due to blocked PACs. These blocked PACs then reset the SA node — and this accounts for the brief pause that follows beats #3 and #6.

Final Question: Why is the PR interval at the end of each pause shorter than the PR interval of normally conducted sinus beats?
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Answer: The reason beats #1, 4 and 7 all manifest a shorter PR interval than beats #2,3; #5,6; and #8,9 — is that beats #1, 4 and 7 are junctional escape beats that occur before the sinus P waves preceding them have a chance to conduct! From the consistent-length PR interval preceeding beats #2,3; 5,6 and #8,9 — we can see that sinus conduction in this tracing requires a bit more than 0.20 second. 

• In Figure 3 — the junctional escape focus fires before the P waves preceding beats #1, 4 and 7 have enough time to conduct. 

Beyond-the-Core: Two findings support our theory that beats #1, 4 and 7 are not sinus-conducted, but are instead junctional escape beats:

• Finding #1: The R-R interval preceding the 2 junctional beats is the same! (ie, the R-R interval between beats #3-4 and between beats #6-7 is identical). The reason these 2 R-R intervals are the same, is that this R-R duration corresponds to the junctional escape rate.
• Finding #2: QRS morphology of the 3 junctional beats on this tracing (ie, beats #1,4,7) is slightly different than the QRS morphology of sinus-conducted beats. That is, the R wave of beats #1,4 and 7 is slightly taller — and the S wave slightly smaller — than the R and S waves for each of the sinus-conducted beats. Although this difference is exceedingly slight — it appears to be real, and provides an invaluable clue that beats #1, 4 and 7 are indeed junctional escape beats (and that the P waves preceding beats #1, 4 and 7 are not being conducted). This further supports our premise that this rhythm is not AV Wenckebach.

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PEARL: Sometimes (not always) the QRS morphology of AV nodal beats will look different in some slight way from the QRS morphology of sinus-conducted beats. This is because one never knows from where within the AV junction a nodal beat arises (ie, junctional beats could arise from one or another marginal edge of the AV node) — in which case the “path” that this supraventricular junctional beat travels may be just a little bit different than the path traveled by normal sinus-conducted beat. Recognition of this consistent slight difference in QRS morphology when it occurs can at times provide an invaluable clue as to which beats on a rhythm strip are sinus conducted vs which beats arise from the AV node.

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Comment: We fully acknowledge that additional monitoring of this patient would be needed to definitively prove our theory for the mechanism of this fascinating arrhythmia. And, it is true that on occasion a single definitive interpretation of a complex arrhythmia may simply not be possible from the surface ECG. That said — We feel the above discussion clearly provides a plausible explanation for all findings noted on this tracing.

• For clarification — Figure-4 offers a laddergram illustration of our theory.

Figure-4: Laddergram illustration of our theory for the mechanism of this arrhythmia. The underlying rhythm is sinus with a long PR interval. Several PACs are seen. These occur with a short coupling interval — and are therefore non-conducted to the ventricles (RED Triangles). This resets the SA node, therefore delaying the next sinus P wave. Because of the resultant brief pause — junctional escape beats (#4 and #7) arise, and are conducted to the ventricles before the sinus P waves preceding beats #4 and #7 are able to conduct to the ventricles. Therefore, this arrhythmia entails sinus rhythm (with prolonged PR interval); blocked PACs; and appropriate emergence of several junctional escape beats.

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Clinical Implications: There is no 2nd- or 3rd- AV block in this tracing. Clinical implications for this patient are the same as they would be for anyone having PACs and slight prolongation of the PR interval. This usually entails search for a cause of the PACs, with corrective measures (ie, caffeine restriction; treatment of heart failure or electrolyte disturbance, etc.) if/as clinically indicated. In the absence of other forms of heart disease — the isolated presence of 1st-degree AV block is usually of minimal clinical significance. The brief pauses terminated by junctional escape beats manifest a completely appropriate response to blocked PACs that reset the SA nodal pacemaker. In short — this is most probably a fairly benign arrhythmia.

• NOTE: Even though the precise mechanism we postulate for this rhythm is advanced — the basic principles discussed in this blog post are within grasp of any clinical provider. Use of the Ps, Qs & 3R Principle should organize your approach and narrow your differential to the entities we consider. Mobitz I and Mobitz II forms of 2nd-degree AV block can easily be ruled out — because the atrial rate is not regular. Complete AV block is ruled out because there clearly is conduction of a number of beats. Appreciation of the clinical truism that “the most common cause of a pause is a blocked PAC” should then lead you to the correct diagnosis!

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Acknowledgment: My thanks to Robert Drutel for allowing me to use this tracing and clinical case.

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Additional Material: For Review on the Basics of AV Block — See my 58-minute ECG Video on this subject at www.avblockecg.com —

• Please note that if you click on SHOW MORE on the You-Tube page under where this video appears — You’ll see a detailed linked Contents that will allow you to immediately find whatever key points you are looking for in this video.

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NOTE: For a Primer on How to Draw a Laddergram — See my ECG Blog #69 —

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For more on the recognition of Blocked PACs — Please see my ECG Blog #33 and Blog #57. With practice — you will begin to find blocked PACs with surprising frequency!