ECG Blog #362 — Funny Rhythm in a 14-Year Old ...

A 14-year old boy was forced to do numerous squats as a “punishment”. He woke up the next day with severe pain in his legs — and presented to the ED (Emergency Department). 

• Renal function and serum electrolytes were normal — but CK was markedly elevated, leading to a diagnosis of Rhabdomyolysis. 
• Cardiac monitoring revealed a series of interesting (albeit asymptomatic) rhythms, 2 of which are shown below in Figure-1.

QUESTIONS:

• How would YOU interpret Rhythms A and B in Figure-1?
• Is there any evidence of AV block?
• What treatment is indicated?

Figure-1: Two of the lead II rhythm strips obtained on a 14-year old boy with acute rhabdomyolysis. Variations of this “theme” were seen on telemetry over the several days that this boy was in the hospital. How would YOU interpret these rhythms?

MY Approach to the Rhythm in Figure-1:

As always — I favor a systematic approach to rhythm interpretation — with use of the Ps, Qs, 3R Memory Aid (See ECG Blog #185 for more on the Ps, Qs, 3Rs). 

• One need not assess the Ps, Qs, 3Rs in any particular order — as long as you always remember to assess each of these 5 parameters. As a result — I usually start with whichever of the parameters is easiest to asses. For example, in Figure-1 — it is clear that the rhythm is not Regular (albeit parts of the rhythm are almost regular) — and — the coupling interval of the early beats in B is similar.
• The QRS complex in all beats seen in Figure-1 is narrow — therefore the rhythm is supraventricular.
• At least some P waves are present! That said — Assessment of the role that P waves play in today’s rhythm is the most challenging aspect of this arrhythmia.

QUESTIONS:

• Do YOU Think any of the P waves in Figure-1 are conducting to the ventricles?
• If so — Is conduction forward or backward (ie, retrograde)? That is — Is the electrical impulse moving from the SA node — then through the Atria, and finally on to reach the ventricles? — OR — Is conduction “backward” (ie, retrograde from the AV node, to return to the atria)?
• 
  
• HINT: What is the significance of the colors (RED and YELLOW) that I have chosen for atrial activity in Figure-2?

PEARL #1: As I’ve suggested many times in this ECG Blog — the most accurate (and time-efficient) way to answer the above questions is with use of calipers. Doing so allows you to instantly determine the regularity of forward-conducting P waves vs retrograde P waves.

• Without using calipers — I would have spent a lot of time guessing whether regular sinus P waves are (or are not) present. With calipers — it took me less than 5 seconds to establish the atrial rhythm!

Figure-2: I’ve added RED, PINK and YELLOW arrows to Figure-1 to highlight the relationship of P waves in these tracings to neighboring QRS complexes (See text).

MY Step-By-Step Approach in Figure-2:

The most challenging aspect of interpreting today’s rhythm — is figuring out what’s happening with atrial activity. Below is my sequential step-by-step approach:

• I first looked in front of at all 28 beats on both tracings in Figure-1 — to see IF there were any P waves that I felt were definitely conducting. The BEST example of a P wave that I could be certain was conducting is in Rhythm A. This is the RED arrow upright P wave that appears before beat #8 with a normal PR interval ( = a PR interval = 0.18 second).
• I saw a number of other places on these 2 rhythm strips in which it looked like upright P waves might be present — although it was difficult to be certain of this. So — IF there was indeed an underlying regular atrial rhythm — the best way to look for this would be by setting my calipers to the P-P interval between 2 deflections that I know represents 2 consecutive P waves. In Figure-2 — the 2nd RED arrow in Rhythm A definitely looks like it is highlighting a P wave that occurs just after the QRS of beat #9.
• Setting my calipers to the P-P interval between these first 2 RED arrows in Rhythm A — allowed me to “walk out” a fairly regular underlying sinus rhythm (Sinus arrhythmia) in Rhythm B! Some of the P waves under these RED arrows in Rhythm B are more easily seen than others (ie, some P waves are hidden within the ST-T waves — but something is seen with each "walk" of the calipers). Given that P wave deflections can be seen under all of the RED arrows in Rhythm B — it seems logical that an “on-time” P wave is also hiding within the QRS of beat #4 (and the PINK arrow in Rhythm B suggests that we do see a tiny deflection at the very end of this QRS complex — which almost certainly represents the final portion of the "hidden" on-time P wave).

What remains to interpret — is the nature of atrial activity under the YELLOW arrows in Rhythm A. 

• Since the P waves under these YELLOW arrows are negative in this lead II monitoring lead — these are retrograde (backward conducting) P waves. This is logical — since no P waves precede beats #2-thru-6 nor beats #10-thru-12 in Rhythm A — which defines these 8 QRS complexes as being junctional beats!

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Laddergram Illustration:

At this point — it might be easiest to explain details of the 2 rhythms in today's case by use of laddergrams. 

• NOTE: For readers less familiar with laddergrams — I’ll emphasize that it is EASY to learn how to read laddergrams. I bet that all it will take to become comfortable reading laddergrams  — is to review the explanations below for the 2 laddergrams from today's case.
• Learning to draw laddergrams takes more time and practice. For those interested — I review the basics for reading and/or drawing laddergrams in ECG Blog #188 (This blog post features links to more than 60 laddergrams that I’ve drawn for this ECG Blog over the years = more-than-enough practice to become comfortable drawing your own laddergrams!).

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Laddergrams for Today's Case:

In Figure-3 — I've drawn a laddergram to illustrate events in Rhythm A:

• It is often easiest to begin with a sinus-conducted beat. According to the laddergram in Figure-3 — there is only 1 sinus-conducted beat in this tracing, which is beat #8.
• We established above that beats #2-thru-6 and #10-thru-12 in Rhythm A are junctional beats — because no P wave precedes these beats — and the QRS complex of these beats is narrow (and looks identical to the QRS complex of sinus-conducted beat #8).
• We have also established that the negative deflections after these junctional beats represent P waves from retrograde conduction (which is to be expected with junctional beats — that virtually always conduct at least partially back toward the atria).
• RED circles within the AV Nodal Tier in Figure-3 — represent the imagined point origin of these junctional beats. Note that each of these junctional beats conducts both in the forward direction (ie, down through the ventricles) — as well as retrograde (the dotted lines that return to the atria).
• Beats #2-thru-6 conduct all the way back through the atria, to produce the negative deflections seen shortly after the QRS (ie, the YELLOW arrows that appear after beats #2-thru-6). 
• 
  
• KEY Point: Since the sinus P wave before beat #8 is able to conduct to the ventricles — it must be that junctional beat #7 does not conduct all the way back through the atria. As a result — whereas the 5 retrograde P waves (YELLOW arrows) before beat #7 do make it all the way back through the atria (thereby preventing the SA Node from putting out its next sinus impulse during this time) — the SA Node then has a moment to recover (because of the failed retrograde conduction of beat #7). After a brief pause — the recovered SA Node begins to fire again, putting out the sinus P wave that appears before beat #8 (RED arrow) — which results in sinus-conducted beat #8.
• 
  
• Advanced Subtlety: Note that I drew the dotted line representing retrograde conduction from junctional beat #7, with a slightly greater angle — to illustrate why retrograde conduction from beat #7 fails to conduct all the way back through the atria.

Continuing to explain the laddergram in Figure-3:

• Beat #8 in Rhythm A is sinus-conducted.
• There is no P wave before beat #9 — so this is another junctional beat.
• The P wave that occurs just after the QRS of beat #9 (3rd RED arrow in Rhythm A) is “on-time” — but this sinus P wave is not able to conduct to the ventricles because retrograde conduction from junctional beat #9 “blocks” it.
• There follows 3 junctional beats (beats #10,11,12) that do conduct all the way back through the atria to produce retrograde P waves (the final 3 YELLOW arrows in Rhythm A).
• Beat #13 is also junctional (because no P wave precedes it) — but the T wave of beat #13 is normal, because there is no retrograde P wave after this beat. In the same way that failure of retrograde conduction from junctional beat #7 allowed the RED arrow sinus P wave in front of beat #8 to conduct — the final sinus P wave in Rhythm A (ie, the last RED arrow in Figure-3) most probably would have conducted a sinus beat #14 had Rhythm A continued for 1 more beat.
• 
  
• Final Beat: I saved beat #1 in Rhythm A for last. Since no P wave precedes beat #1 — this is a junctional beat. I believe the RED arrow P wave that occurs just after the QRS of beat #1 — acts similar to the sinus P wave that occurs just after beat #9, in that this P wave occurs too soon after beat #1 to conduct.

Figure-3: Laddergram illustration for Rhythm A in today's case.

In Figure-4 — I've drawn a laddergram to illustrate events in Rhythm B:

• The principal difference between the mechanism of Rhythm A vs the mechanism of Rhythm B — is that there is no retrograde conduction in Rhythm B. Instead — RED arrows show that regular sinus P waves continue throughout the entire tracing.
• Most of these sinus P waves are unable to reach the ventricles — because their path is blocked by the underlying junctional rhythm. However — beats #3, 6, 10 and 14 are able to make it through the AV node, to be conducted to the ventricles. The laddergram in Figure-4 — illustrates the timing that is needed to allow this to happen.
• 
  
• Advanced Subtlety: Note that the PR interval before beat #6 is slightly longer than the PR interval before the other 3 sinus-conducted beats (ie, beats #3,10,14). The reason for this — is that the P wave before beat #6 occurs closer to the preceding junctional beat — thereby slightly delaying the passage of this P wave through the AV node (which I illustrate with a PINK line showing a slightly greater inclination within the AV Nodal Tier compared to the inclination of the 3 other sinus-conducted beats that manifest shorter PR intervals).

Figure-4: Laddergram illustration for Rhythm B in today's case.

QUESTION:

• Is there AV dissociation in today's rhythm?  And, if so — WHY?

ANSWER:

There is AV dissociation in today's tracing — because many of the on-time P waves in Rhythm B are not related to neighboring QRS complexes (ie, Many of these on-time P waves in Rhythm B are not conducted to the ventricles).

• In Figure-4 — None of the P waves that terminate in a butt-end (seen in the upper portion of the AV Nodal Tier) are conducted to the ventricles.

PEARL #1: Despite the AV dissociation in Rhythm B — there is no evidence of AV block. This is because none of these P waves that failed to conduct in Figure-4 had a chance to conduct!

• The P waves that appear just after the QRS of beats #1, 4, 8 and 12 — all occur too close to the preceding QRS (These P waves fall within the absolute refractory period).
• The P waves that appear just before the QRS of beats #7,11 and 15 — all occur with too short of a PR interval to allow conduction.

PEARL #2: As emphasized often in this ECG Blog — there are 3 Causes of AV dissociation. These are: i) 2nd- or 3rd-degree AV Block (in which one or more P waves that should conduct do not conduct); ii) AV dissociation by "Usurpation" (in which an accelerated junctional rhythm takes over the pacemaking function); and/or, iii) AV dissociation by "Default" (in which slowing = "default" of the SA nodal pacemaker allows a junctional escape pacemaker to emerge).

• We have already ruled out 2nd- or 3rd-degree AV block (Pearl #1).
• To determine if AV dissociation in Figure-4 is the result of "usurpation" or "default" — We need to determine and compare the atrial and junctional rates. The P-P interval of sinus P waves (RED arrows) in Rhythm B is just over 4 large boxes in duration, which corresponds to a sinus P wave rate of ~70/minute.
• The R-R interval of junctional beats in Rhythm B — is 3.4 large boxes in duration, which corresponds to a junctional rate of ~85/minute. Even accounting for the young age of today's patient — this represents an accelerated junctional rhythm.

Putting It All Together:

The principal arrhythmia in today's case is an accelerated junctional rhythm at ~85/minute. This results in AV dissociation by "usurpation". Since the junctional pacemaker is faster than the underlying sinus rhythm (~85/minute — compared to the underlying sinus rate of ~70/minute) — the junctional pacemaker takes over the rhythm, with the exception of occasional sinus P waves that occur at "just the right moment" that they are able to "capture" the ventricles (ie, Beat #8 in Rhythm A — and beats #3,6,10 and 14 in Rhythm B).

• As noted in the history for today's case — this 14-year old boy with acute rhabdomyolysis was asymptomatic from the cardiac rhythm. There is no evidence of AV block in today's tracing. Instead — the primary arrhythmia is a slightly accelerated junctional rhythm that probably is the result of this patient's acute medical problem.
• No specific treatment is needed for this arrhythmia — which will probably resolve as this patient's medical condition improves.

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Acknowledgment: My appreciation to Kianseng Ng and Leong Keen Wai (from Malaysia) for the case and this tracing. 

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
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• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 50 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #195 — Reviews the phenomenon known as Isorhythmic AV Dissociation.
• ECG Blog #192 — Reviews the 3 Causes of AV Dissociation (and emphasizes why AV Dissociation is not the same thing as Complete AV Block).
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• CLICK HERE — for an instructive review on Rhabdomyolosis.

 

ECG Blog #361 — Another WCT Rhythm ...

The ECG in Figure-1 is from a middle-aged man — who had just received thrombolytic therapy for presumed acute infarction. No other history available.

QUESTIONS:

• How would YOU interpret this ECG?
• How certain are you of your answer?

Figure-1: ECG obtained from a middle-aged man following thrombolytic therapy. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 — shows a regular WCT ( = Wide-Complex Tachycardia) at ~140/minute, without clear sign of atrial activity.

• Clinically — The 1st priority in assessing this patient would be to determine hemodynamic status. This is because IF this patient was hemodynamically unstable with this ECG — then regardless of what the rhythm happens to be — synchronized cardioversion would become immediately indicated!
• On the other hand — IF the patient is completely stable with this rhythm, then by definition — You have at least a “moment of time” to more thoroughly contemplate the etiology of this rhythm.

PEARL #1: As emphasized in many other blog posts (ie, ECG Blog #220 and Blog #196, to name just 2) — the differential diagnosis of a regular WCT rhythm without clear sign of atrial activity should be assumed to be VT (Ventricular Tachycardia) until proven otherwise.

• Taking all comers in an unselected adult population — statistical likelihood that a regular WCT without atrial activity will be VT is at least 80%.
• If the patient is at least middle-aged, and especially if there is a history of underlying heart disease — then statistical likelihood that a regular WCT without atrial activity will be VT increases to ~90%. To Emphasize — This is a 90% likelihood of VT even before you look at the ECG!
• 
  
• In today's case — Given that the patient was just treated with thrombolytic therapy for a presumed acute MI — the odds that the rhythm in Figure-1 is VT are at least 90% (even before you look at the ECG).

PEARL #2: Use of QRS morphology in the 12-lead tracing during the WCT rhythm can help to refine the statistical likelihood estimate from 80-90% — to an even more precise figure (See ECG Blog #42 for specific criteria I favor for this purpose). This is especially relevant for today’s tracing — because the QRS morphology in Figure-1 is exceedingly atypical for a supraventricular rhythm. Looking at specific ECG findings in today's case:

• There is extreme axis deviation in the frontal plane during the WCT. This is highly unlikely with a supraventricular rhythm. To Emphasize: By “extreme” axis deviation — the QRS must be entirely negative in either lead I or lead aVF. Even a small positive deflection in either of these leads negates the reliability of this criterion. The 12-lead tracing in Figure-1 satisfies this “extreme” axis deviation criterion — because the QRS is all negative in each of the 3 inferior leads! 
• 
  
• The QRS is all positive in right-sided lead aVR. This usually indicates that the origin of the WCT rhythm is from the left ventricular apex — which implies that the rhythm is VT (because supraventricular conduction does not originate from this anatomic location).
• 
  
• The QRS is all negative in leads V3-thru-V6. The finding of an all negative QRS in lead V6 — greatly increases the likelihood of VT (for a similar reason as does an all positive QRS deflection in right-sided lead aVR). Seeing an all negative QRS not only in lead V6 — but in each of the last 4 chest leads (ie, in leads V3-thru-V6) overwhelmingly favors VT.
• 
  
• Although an all positive QRS in lead V1 can be associated with RBBB-conduction — the lack of additional deflections (ie, there is no triphasic rSR’ complex in lead V1) — is more consistent with VT than with an SVT rhythm.
• 
  
• To Emphasize: There are exceptions to the above-cited morphologic criteria. These exceptions are limited to: i) If the rhythm is antidromic AVRT — in which the impulse travels forward over an AP (Accessory Pathway) in a patient with WPW, therefore resulting in a regular WCT rhythm that resembles VT (For more on the various arrhythmias in patients with WPW — See ECG Blog #18); and, ii) If the baseline ECG during sinus rhythm manifests a widened and very abnormal QRS morphology as a result of “scaring” from prior infarction(s). 
• BOTTOM Line: Other than these 2 exceptions — it’s hard to imagine how the regular WCT rhythm in Figure-1 could be supraventricular (ie, I'd estimate a 98-99% likelihood that the rhythm in Figure-1 was VT).

CASE Conclusion:

Unfortunately — I do not have follow-up on today's patient. That said — it's hard to imagine how today's rhythm could not be VT.

• Clinically — Immediate cardioversion would be indicated IF this patient was at all unstable hemodynamically. Even if stable — prompt electrical carioversion would clearly be an appropriate action for a rhythm such as that shown in Figure-1.
• Alternatively — a trial of antiarrhythmic therapy (ie, with IV Amiodarone or Procainamide) — could be appropriate IF the patient was tolerating the arrhythmia.
• Although Adenosine is used by many in selected cases for treating a regular WCT rhythm of uncertain etiology — I would not lose time by trying Adenosine in today's case. This is because today's patient by definition has underlying coronary disease (ie, He was just treated with thrombolytic therapy for presumed acute MI). Adenosine may work in the treatment of selected Idiopathic VT rhythms (as per ECG Blog #197) — but Adenosine will not work with ischemic VT.
• IF at any time during the treatment process the patient's hemodynamic status deteriorates — then immediately cardiovert! 
• 
  
• For more on evaluation and management of the regular WCT — See the ADDENDUM below.

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Acknowledgment: My appreciation to Dradam Ahmen (from Nouakchott, Mauritania) for the case and this tracing.

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ADDENDUM (2/5/2023):

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-2 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-3: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-4: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
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• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
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• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• e Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #197 — Review of Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• 
  
• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Review of criteria for distinguishing VT vs Aberration.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

 

ECG Blog #360 — The Patient has Cancer ...

The ECG in Figure-1 was obtained from an older woman. She presented with shortness of breath. The patient was known to have cancer. 

QUESTIONS:

• How would YOU interpret this ECG?
• Why is every-other-beat changing? 

Figure-1: ECG obtained from an older woman with shortness of breath. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The ECG in Figure-1 — shows a regular, supraventricular (ie, narrow-QRS) rhythm at a rate of ~90-95/minute. All intervals (PR,QRS,QTc) and the frontal plane axis are normal. There is no chamber enlargement.  ST-T wave changes do not look acute.

There are 2 “eye-catching” features on the ECG in Figure-1:

• Diffuse Low Voltage: As discussed in detail in ECG Blog #272 — a series of clinical conditions have been associated with low voltage on ECG. Clinically — the entity of “low voltage” is defined by ECG criteria as the manifestation of a QRS amplitude of ≤5 mm in all 6 limb leads. This low voltage is said to be “diffuse” — IF — in addition to satisfying limb lead criteria, QRS amplitude in all 6 chest leads fails to exceed 10 mm. Regarding the ECG shown in Figure-1 — virtually all 12 leads show diffuse low voltage.
• 
  
• Electrical Alternans: As discussed in detail in ECG Blog #83 — The phenomenon of electrical alternans encompasses a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beat — or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected. Alternating interval duration (of PR, QRS or QT intervals) may also be seen. 
• The ECG in Figure-1 is remarkable — in that further reduction of an already-reduced QRS amplitude is seen in all 12 leads with every-other-beat (The QRS becomes tiny in virtually all 12 leads for every even-numbered beat).

PEARL #1: Regarding Today’s CASE:

Although the list of clinical entities associated with diffuse low voltage and electrical alternans is long (See ECG Blog #272 and ECG Blog #83) — the occurrence of both of these ECG findings in an older patient with known cancer, who presents with shortness of breath — should immediately prompt consideration of a large pericardial effusion as the presumed diagnosis until proven otherwise. 

• Overall — the sensitivity and specificity of ECG for the diagnosis of pericardial effusion is poor. Clinically — it is rare that the ECG even enters into diagnostic deliberations — because the picture of a large, pear-shaped heart on chest x-ray usually prompts immediate consideration of a large pericardial effusion — that can then be rapidly confirmed by bedside Echo. Seeing low voltage on ECG is most often an “after-thought” to the diagnosis.
• The above said — the degree of “low voltage” and the prominence of electrical alternans of every-other-beat in Figure-1 is so extreme — that today’s tracing marks one of those truly rare occasions over my many decades of reviewing ECG cases, in which I found myself immediately thinking, “large pericardial effusion” until proven otherwise.
• 
  
• A 3rd ECG finding seen in Figure-1 consistent with the diagnosis of a large pericardial effusion — is the rapid heart rate. While not quite satisfying criteria for sinus “tachycardia” (which is a heart rate ≥100/minute) — the overall heart rate of 90-95/minute adds to our suspicion.
• 
  
• To Emphasize: Smaller pericardial effusions often do not produce noticeable ECG abnormalities — which highlights the point that the diagnosis will most often not be made from the ECG. That said, what counts clinically — is appreciation whether an enlarging pericardial effusion is evolving toward pericardial tamponade (which would be a medical emergency). 
• 
  
• PEARL #2: While in most cases, the ECG will not predict impending tamponade — an exception may be seen IF there is development of total electrical alternans (ie, of P wave, QRS complex and T wave) — as this finding suggests there may now be tamponade.
• 
  
• PEARL #3: Awareness of the above cited ECG findings may be clinically relevant in the patient with a large pericardial effusion that you are following. While definitive diagnosis of a pericardial effusion will have to be made by Echo — Be alert to the following: i) Progressive reduction in QRS amplitude; ii) Increasing heart rate; and, iii) Evolution of electrical alternans into a pattern involving not only the QRS, but also the P wave and T wave. IF you see this combination of ECG findings — Be ALERT to worsening effusion with potential impending tamponade.

Follow-Up in Today’s CASE:

In today's case — malignant metastasis was suspected in the patient whose ECG is shown in Figure-1. Her large pericardial effusion required drainage — with removal of nearly 1 liter of fluid.

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Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) for the case and this tracing. 

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #83 — Reviews the phenomenon of Electrical Alternans.
• 
  
• ECG Blog #272 — Review the Causes of Low Voltage on ECG.

ECG Blog #359 — How Many Beats in the 12-Lead?

The ECG in Figure-1 was obtained from a previously healthy older man — who complained of chest pain and “lightheadedness” while this tracing was recorded. He was not hypotensive. His chest pain had begun the night before.

• In view of this history — How would YOU interpret the ECG in Figure-1?
• A total of 12 beats are seen in the long lead II rhythm strip. How many beats are seen in the 12-lead tracing that appears above the rhythm strip?

Figure-1: 12-lead ECG and long lead II rhythm strip — obtained from an older man with chest pain and “lightheadedness. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Approach to the ECG in Figure-1:

As always when I encounter a 12-lead tracing with accompanying long lead rhythm strip — I focus first on interpretation of the rhythm (as seen in the long lead rhythm strip that appears below the 12-lead in Figure-1). Keeping in mind the Ps, Qs & 3R Approach to rhythm interpretation (as per ECG Blog #185):

• The overall rhythm in the long lead II rhythm strip shown in Figure-1 is not regular! That said — there is an underlying sinus rhythm, as determined by upright sinus P waves with fixed PR interval before beats #2,3; 5,6,7; 9,10 and 12. The QRS complex of these sinus-conducted beats is narrow. 
• 
  
• On the other hand — the QRS complex of beats #1, 4, 8 and 11 is wide. These wide beats manifest a very different QRS morphology compared to that of the sinus-conducted beats — and, these wide beats are not preceded by P waves. Therefore — these 4 beats are PVCs (Premature Ventricular Contractions).

The "Short" Answer: 

• The rhythm in ECG #1 is best described sinus with frequent PVCs.

QUESTION: 

• Why is there a short pause after 3 of the PVCs (ie, after beats #1,8,11) — but not after beat #4?
• 
  
• Advanced Point: Why is the PR interval before beat #5 slightly longer than all other PR intervals on today's tracing?

ANSWERS:

• Like the majority of PVCs that we encounter — beats #1,8,11 are PVCs that manifest a compensatory pause. That is — retrograde (backward) conduction from the PVC lasts long enough (and penetrates backward far enough) — to prevent forward conduction of the next sinus P wave.
• The reason there is no pause following beat #4 — is that this is an “interpolated” PVC (ie, this PVC is “sandwiched” between 2 sinus-conducted beats without the compensatory pause that typically follows most PVCs).  

The above concepts are best explained with the Laddergram that I made of the long lead II rhythm strip in today's tracing (Figure-2):

• NOTE: I cannot be certain from today's tracing of the extent that PVCs conduct retrograde. I therefore drew this laddergram based on what I think is happening. That said — this laddergram serves well to illustrate what generally occurs with interpolated PVCs.

Figure-2: My proposed laddergram of the long lead II rhythm strip from ECG #1. Note how the interpolated PVC ( = beat #4) slightly prolongs the PR interval of the next sinus-conducted beat (ie, slight increase in the inclination of the slanted BLUE line in the AV nodal tier).

PEARL #1: It is good to be aware that the PR interval of the sinus-conducted beat that follows an interpolated PVC may sometimes be prolonged — sometimes to a much greater extent than is seen for beat #5 in this tracing. Such PR interval prolongation is the result of concealed conduction (and not due to 2nd-degree AV block of the Wenckebach type). 

• The reason the PR interval preceding beat #5 in Figure-2 is slightly longer than all other PR intervals on today’s tracing — is that retrograde conduction from the PVC (beat #4) occurs at precisely the point in the cardiac cycle, that it slows but does not completely stop conduction of the next sinus P wave as it passes through the AV node and the ventricles (as shown by slight increase in the inclination of the slanted BLUE line in the AV nodal tier).
• The technical name for the fact that we can deduce the reason for this slight PR interval prolongation before beat #5 without actually “seeing” this delay in conduction of this next sinus P wave on the surface ECG — is called “concealed” conduction (ie, the effect of this retrograde conduction from the PVC is “hidden” from our view).
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• Note in Figure-2 — that no PR interval prolongation occurs after the other 3 PVCs. Instead, we see a compensatory pause after PVCs #1, 8 and 11.
• The slight negative deflection at the very end of the QRS of PVCs #8 and 11 most likely indicates retrograde P waves that have returned all the way to the atria (YELLOW arrows in the laddergram).
• In contrast — the occurrence of an on-time sinus P wave at the very beginning of the QRS of PVC #1 (first RED arrow in Figure-2) — prevents retrograde conduction from this PVC reaching all the way back to the atria.
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• To EMPHASIZE: The above laddergram provides an "advanced" answer to today's rhythm. The "simple" answer — is that there is sinus rhythm with PVCs, including an interpolated PVC. This simple answer is more than enough for optimal clinical assessment and management of today's patient!

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Now that we've interpreted the rhythm in today's tracing — Let's return to the 12-lead ECG. To facilitate assessment — I've reproduced Figure-1 below in Figure-3.

• As noted in my initial presentation — the patient in today's case is a previously healthy older man who complained of chest pain and "lightheadedness" while the ECG in Figure-3 was being recorded. He was not hypotensive. His chest pain had begun the night before.
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• How would YOU interpret his 12-lead ECG?

Figure-3: I've reproduced Figure-1. How would you interpret this 12-lead ECG?

MY Interpretation of the 12-Lead ECG:

Today’s ECG shows sinus rhythm with frequent uniform (ie, similar morphology) PVCs. Interpretation of ST-T wave changes in this 12-lead tracing initially depends on assessment of sinus-conducted beats in each of the 12-leads. I’ll defer interpretation of ST-T wave changes in the PVCs until later.

• Regarding Intervals — the PR interval is normal — the QRS of sinus-conducted beats is not wide — and the QTc is normal.
• Although overall QRS voltage is reduced — criteria for low voltage are not met (ie, the QRS is not ≤5 mm in all 6 limb leads).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes in sinus-conducted beats:

• Q Waves — are present in each of the inferior leads (ie, in leads II,III,aVF). QRS complexes in these leads are extremely small — with especially large and wide Q waves (considering QRS amplitude) in leads III and aVF. A small and narrow q wave is seen in lead II.
• R Wave Progression — is appropriate for the sinus-conducted beats in the chest leads. Transition (where the height of the R wave becomes taller than the S wave is deep) occurs normally here, between leads V2-to-V3.

Regarding ST-T wave Changes in sinus-conducted beats:

• In 2 of the inferior leads ( = leads III and aVF) — there is ST segment coving with slight ST elevation and fairly deep T wave inversion (relative to QRS amplitude in these leads). The ST-T wave in the 3rd inferior lead ( = lead II) is flat (Note that the long lead II rhythm strip gives us a number of additional "looks" at the ST-T wave of lead II — which confirms that it is flat).
• In high-lateral leads I and aVL — the ST segment is flat and slightly depressed. The ST-T wave in lead aVL presents the mirror-image opposite picture of the ST-T wave in lead III (See ECG Blog #184 for more on this mirror-image opposite relationship).
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• For the sinus-conducted (narrow QRS) beats in the chest leads — there is marked ST elevation in lead V1, that is totally disproportionate to the modest amplitude of the QRS complex in this lead. 
• A lesser (but still significant) amount of J-point ST elevation is seen in leads V2 and V3.
• ST-T waves are flat and slightly depressed in lateral chest leads V4,V5,V6.

Putting It All Together:

In today's patient, who presented with chest pain (that began the night before) and "lightheadedness" — the ECG in Figure-3 is diagnostic of an acute STEMI (ST Elevation Myocardial Infarction).

• The frequent PVCs (occurring every third or fourth beat in the long lead II rhythm strip) — is consistent with this diagnosis of a recent acute cardiac event (and this may account for this patient's "lightheadedness").
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• Two Questions that arise are: i) When over the past day this patient's infarct occur? — and, ii) What is the likely "culprit" artery? 
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• I initially thought the ST elevation in anterior leads V1,V2,V3 pointed to acute occlusion of the LAD (Left Anterior Descending) coronary artery as the "culprit" vessel.
• On further consideration — I suspect the "culprit" artery is the proximal RCA (Right Coronary Artery). The large Q waves in leads III and aVF, in association with a slight (residual) amount of coved ST elevation with moderate T wave inversion — suggest reperfusion T waves from an acute inferior MI that probably began the night before when the chest pain started.
• The mirror-image opposite ST-T wave picture seen in high-lateral leads I and aVL is a reciprocal change. This is consistent with spontaneous reperfusion of the "culprit" artery — that probably occurred during the hours after RCA occlusion.
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• PEARL #2: Note that the relative amount of ST elevation in the anterior leads is maximal in lead V1 — and progressively decreases as one moves to lead V2 — and then lead V3. We would generally expect the opposite progression if the "culprit" vessel was an occluded LAD. We would also expect that by this time (given onset of symptoms the night before) — that ST elevation from acute LAD occlusion would probably have extended beyond lead V3.
• In contrast — acute RV infarction is known on occasion to produce marked ST elevation that is maximal in lead V1 on a standard 12-lead tracing. (Obtaining right-sided leads on this patient could have been diagnostic — as acute RV MI with this degree of ST elevation in lead V1 would have certainly produced marked ST elevation in other right-sided leads — See ECG Blog #190 for more on acute RV MI).
• IF indeed the anterior lead ST elevation in Figure-3 is the result of acute RV MI — this would localize the "culprit" artery to the proximal RCA — because blood supply to the RV is almost always provided from the initial portion of the RCA.

PEARL #3 (Advanced Point): Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.

• That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction.
• This is the case in Figure-3. QRST morphology of the PVCs in the limb leads and in leads V4,V5,V6 — is consistent with LBBB. Although significant J-point depression is seen in the PVCs in many of these leads — this is not a specific enough finding by itself to diagnose an acute event.
• In contrast — the amount and shape of the ST elevation for the PVC that we see in simultaneously-recorded leads V1,V2,V3 in Figure-3 — is clearly disproportionate to what one would expect the ST segment of this PVC to look like. This is especially true for the coved ("tombstone"-like) ST elevation of the PVC in lead V1 — that even without the ST elevation we see in sinus-conducted beats, would strongly suggest acute infarction.
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• NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCs — See My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

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Final CHALLENGE in Today's CASE:

• A total of 12 beats are seen in the long lead II rhythm strip from today's tracing. How many beats are seen in the 12-lead tracing that appears above the long lead rhythm strip?
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• HINT: Why did I repeat the numbers 1 and 2 for each of the 3-lead groupings of simultaneously-recorded beats in Figure-4?

Figure-4: Why did I repeat the numbers 1 and 2 for each of the 3-lead groupings of simultaneously-recorded beats in today's tracing?

ANSWER to the Final Challenge:

It is important to appreciate that the long lead II rhythm strip in today's tracing is not simultaneously-recorded with each of the sets of 3 leads. This is easiest to see — if you look directly above beats #5-thru-12 in the long lead II rhythm strip.

• There are many different types of recording systems used in the too-numerous-to-count number of different ECG machine systems. The system for recording employed in today's tracing repeats beats #1 and 2 in each of the sets of 3 leads — and — in addition, provides an independent long lead II rhythm strip. (NOTE: We encountered a similar type of recording system for the case presented in ECG Blog #357).
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• Editorial Comment: This is not my favorite system for ECG recording — because I find it confusing. The advantage of this system, is that we do get to see what the first 2 beats in the long lead rhythm strip look like in all 12 leads. The decided disadvantage (in my opinion) — is that we have no idea what the other beats look like in leads other than in the long lead II.
• Another reason why this system of recording is confusing in today's tracing — is that it looks from the 12-lead ECG in Figure-4, as if the rhythm is ventricular bigeminy. On the contrary — we only see 1 PVC in the entire 12-lead tracing. This is beat #1 in the long lead II rhythm strip — that we see in simultaneously-recorded leads I,II,III. We then once again see beat #1 in simultaneously-recorded leads aVR,aVR,aVF — and again in V1,V2,V3 — and a final time in V4,V5,V6.
• Imagine how confusing this tracing might have been if instead of the 4 PVCs that we see in the long lead II rhythm strip (ie, beats #1,4,8 and 11) — if beat #1 was the only PVC that occurred. The 12-lead ECG would still look the same as it does in Figure-4 — because with this type of recording system, the first few beats are repeated in each of the 12 leads.

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• Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.
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• ECG Blog #68 — Reviews the concept of interpolated PVCs.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
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• ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare Serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves). 
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• ECG Blog #190 — Reviews the concept of acute RV MI.