ECG Blog #552 — The Leads were Not Misplaced!

The 2 ECGs in Figure-1 were obtained from the same patient. The patient had been admitted to the hospital for evaluation of abdominal pain. The repeat ECG was recorded after admission because of the sudden onset of CP (Chest Pain).

QUESTION:

• How can it be that these 2 ECGs are from the same patient?  
• NOTE: All electrode leads were correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

Figure-1: Comparison between the 2 ECGs in today's case.

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The initial ECG in Figure-1 ...

The patient's admission ECG ( = ECG #1) is not a normal tracing.

• The rhythm in ECG #1 is sinus at a rate of ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal.
• Assuming the patient is over 35 years of age — LVH is probably present (deepest S in lead V2 + tallest R in lead V5 is very close to satisfying the 35 mm criterion, with an R wave in lead V4 that is extremely tall).
• The ST segment is coved in leads V3-thru-V6, with some ST depression and symmetric T wave inversion. There is nonspecific ST-T wave flattening in the limb leads.
• Impression: Sinus rhythm with probable LVH + ST coving and T wave inversion in leads V3-thru-V6 consistent with LV "strain" and/or ischemia. Clinical correlation is needed (and ideally finding a prior tracing for comparison).

The repeat ECG in Figure-1 ...

My 1st impression on seeing the repeat ECG was, "This is bizarre!".

• I wondered how much time had passed between the recording of ECG #1 and ECG #2?
• Seeing both tracings next to each other in Figure-1 — the differences between these 2 ECGs are striking! Not only is QRS amplitude increased in the repeat ECG — but the frontal plane axis has shifted dramatically to the right, and the QRS is now predominantly positive in lead V1 (whereas in the initial ECG — the QRS in V1 was predominantly negative). 
• This is not the result of a conduction defect — because the QRS lacks the widening of RBBB or IVCD.
• Since lead I and lead V6 are both left-sided leads — these 2 leads normally bear some resemblance to each other. Yet lead I is now predominantly negative — and left-sided chest leads V4,V5,V6 are all markedly positive.
• Yet despite this bizarre and drastic change in QRST morphology that we see between the 2 tracings in Figure-1 in both limb and chest leads — we are told that all electrode leads are correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

How Can this Be?

• Thinking "outside the box" and remembering that the reason ECG #2 was recorded was the sudden onset of CP — I wondered about physiologic events that might cause CP, and which have been known to produce bizarre positional shifts in relative cardiac anatomy (ie, abrupt onset of pneumothorax — or since this patient was admitted for abdominal pain, perhaps intestinal perforation?).
• 
  
• OR — Could this still somehow be some manifestation of a technical misadventure?
• 
  
• PEARL #1: If some kind of “lead switch” turns out to be the cause of the bizarre change in appearance between the 2 tracings in Figure-1 — it cannot be a simple extremity electrode switch. This is because mix-up of extremity electrode placement would not affect the chest leads that now show a highly unusual and unexpected predominant R wave in lead V1. 
• Instead — any type of lead mix-up to produce the abrupt change that we see between the 2 tracings in Figure-1 would have to involve misplacement (or misconnection) of electrodes from both limb lead(s) and precordial lead(s). 

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CASE Conclusion:

• 2 hs-Troponins were negative — and another repeat ECG looked the same as ECG #2. Bedside Echo was normal, without any wall motion abnormality ==> the difference between ECG #1 and ECG #2 is not the result of acute infarction.
• Both ECGs are from the same patient.
• The 4 extremity electrodes were verified to all be on the correct extremities.
• The 6 precordial lead electrodes were all correctly placed on the chest.

The Answer:

The lead connections were incorrectly attached at the cable hub ...

• The connecting cables for unipolar lead V1 and the LL (Left Leg) electrode were swapped.
• As shown in Figure-2 — it's easy to understand how the technical misadventure of misconnecting the V1 and LL cables might happen since both cables are color-coded in RED. 
• It turns out that the cable connectors were unplugged during room cleaning — and then misconnected when the cables were reattached.

Figure-2: Magnified view of the ECG cable hub.

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Discussion:

Technical misadventures produced by limb and/or precordial lead misplacement (or misconnection) — are surprisingly common in practice, with an estimated frequency between 0.4-to-4.0% of all ECGs recorded (Sukumaran and Selvaraj — Indian Pacing Electrophysiol J 24(2):119-121, 2024 - and - Rudiger et al — Am J Emerg Med 25:174-178, 2007).

• Potential consequences of errors in lead misplacement (or misconnection) are obvious — including over- and/or under-diagnosing acute coronary occlusion.
• The most common form of lead misplacement (or lead reversal) — occurs with mix-up of 2 of the 4 limb lead electrodes. By far, the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes — but any lead reversal combination is possible (See ECG Blog #479 — for a growing list of lead reversals and other technical misadventures).
• PEARL #2: Lead reversals of any 2 of the 4 limb lead electrodes are usually readily recognizable once you become familiar with the possibilities — because they generally produce characteristic patterns (as described in detail in ECG Blog #479). 
• In contrast — mix-up between limb lead electrodes and one or more of the chest lead electrodes are often unique, producing unpredictable ECG changes that complicate ECG recognition (as in today's case! ). This is because the Wilson Central Terminal is altered when there is mix-up between limb lead and chest lead electrodes.
• There is tremendous variation among ECG machines that are used worldwide. As a result — hub connections are not "standard". Fortunately — most modern ECG machines have a single cable attaching all electrodes to the machine. But some machines have 2 separate cables, providing more opportunity for lead misconnection (as seen in Figure-2).

I found the article by Paul and Jacob amazingly complete for detailing the numerous possibilities of limb lead and chest lead misplacements (Ind Pacing Electrophysiol 23(6):205-213, 2023).

• PEARL #3: Realize that although uncommon — combined mix-up between limb lead and chest lead electrodes can occur, and when it does — the resultant ECG may look bizarre with an impossible-to-explain appearance by the rules of physiology. Voltage amplitudes may be greatly increased or decreased in various leads — and unpredictable ST-T wave deviations (elevation or depression) may be seen.
• Suspect some unusual form of technical misadventure when you encounter such a bizarre tracing in a patient in whom the clinical history is not consistent with any condition likely to produce such changes (ie, normal CxR and normal Echo — especially if after verifying lead placement and repeating the ECG, the same bizarre findings are present).
• Don't forget to add checking hub lead connections to the checklist!

PEARL #4: I’ll close with reference to the primer by Lub Dub Admin — which reviews the essentials of ECG cables, including types, connectors, lead configurations and compatibility (Figure-4).

• This primer provides insight into the many ways the technical components of what goes into an ECG machine may vary. ECG machines are not all made the same. When you encounter a truly bizarre-looking ECG that does not comply with the usual predictable patterns of lead reversal — we need to put on our “detective hats” and look for unusual forms of technical misadventures.    

—  — 

Figure-3: What can go wrong with ECG Cables (by Lub Dub Admin).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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ECG Blog #551 — Are there any "Normal" Beats?

I was sent the ECG in Figure-1 — told only that it was from a middle-aged man who presented for acute CP (Chest Pain). 

QUESTIONS:

• What is going on?
• How to approach interpreting this ECG?
• What is the rhythm?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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My Approach:

As always (assuming your patient is stable and not in need of immediately cardioversion) — I favor a systematic approach, beginning with a quick look at the rhythm ==> "Watch your Ps,Qs, and the 3Rs" (as reviewed in ECG Blog #185).

• I vary which of these 5 KEY parameters I look at first — depending on particularities of the rhythm (and depending on which of these 5 parameters are easiest to recognize).
• In today's case, as I looked at the long lead II rhythm strip — I was struck by the almost beat-to-beat variability in QRS morphology. That said — many of the beats look to be narrow, suggesting the underlying rhythm is supraventricular.
• P waves are present!

PEARL #1: The simple step of labeling P waves is often surprisingly helpful in figuring out what is going on. I have done this in Figure-2 (RED arrows highlighting those P waves that I can definitely identify).

• What do we learn from Figure-2?

Figure-2: I've labeled those P waves that I can definitely identify.

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What We Learn from Figure-2:

• The underlying rhythm in today's tracing appears to be sinus — as upright P waves with a constant and normal PR interval are seen in front of beats #1,3,4,6,8,11,13 and 15.
• I look for 2 sinus-conducted beats in a row — since if the underlying atrial rhythm is regular, seeing 2 sinus-conducted beats in a row will suggest what the P-P interval is (We see this for beats #3 and 4). The R-R interval between beats #3 and 4 is just over 3 large boxes — suggesting the presence of an underlying sinus rhythm at ~90/minute.
• NOTE: Although we do not clearly see P waves throughout the entire tracing in Figure-2 — the constant P-P interval between consecutive RED arrow P waves that we do definitely see suggests that there probably is a regular underlying P wave rhythm. 

PEARL #2: By far, the most time-effective way to interpret today's complex tracing — is to use calipers! Simply stated — I could not have determined today's rhythm with any degree of certainty without using calipers. And, by using calipers — it took me literally no more than 5 seconds to establish the conclusions that become obvious on viewing the long lead II rhythm strip that I've labeled in Figure-3:

• The underlying atrial rhythm is regular. 
• In addition to the RED arrow P waves that we definitely see — the PINK arrows in Figure-3 highlight "on time" sinus P waves that partially deform some part of the QRS.
• Even though we do not see any deformation of beat #10 — it makes sense that another "on time" sinus P wave is hidden entirely within this beat ( = the WHITE arrow drawn over beat #10).
• 
  
• PEARL #3: The PR interval for all of the "on time" PINK arrow P waves is too short to conduct normally. This establishes the presence of intermittent AV dissociation — and this proves that beats #2,5,7,14 and 16 must all be ventricular beats.
• The reason for slight variation in QRS morphology for these ventricular beats is that there is some degree of fusion between sinus-conducted P waves and the ventricular beats that follow so soon thereafter that they interrupt conduction of sinus-initiated impulses through the ventricles (See ECG Blog #128 — for more on fusion beats).
• Fusion is unlikely for beat #10 — because the "on time" WHITE arrow P wave occurs too late to be able to enter the ventricles in time to conduct. The fact that the WHITE arrow P wave arrives in the ventricles too late to conduct provides insight as to what PVCs will look like in lead II — and therefore also what PVCs will look like in simultaneously-recorded leads V1,V2,V3. 

Figure-3: Using calipers — I’ve added PINK arrows and a WHITE arrow where I expect "on time" P waves to be partially or totally hiding throughout today’s long lead II rhythm strip.

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Focus for a moment on these 4 simultaneously-recorded leads ( = leads V1,V2,V3 — and lead II in the long lead rhythm strip) For clarity — I facilitate doing this in Figure-4. 

• It should now be obvious from Figure-4 — that beat #11 looks different than the 3 other beats in leads V1,V2,V3, and in the long lead II. This is because the only normal sinus-conducted impulse among these 4 beats is this beat #11.
• Beats #9,10 and 12 are ventricular (presumably with some degree of fusion for beats #9 and 12). 

Figure-4: Focus on the 4 simultaneously-recorded leads V1,V2,V3; and on the long lead II for the purpose of highlighting QRST morphology of beats #9,10,11,12).

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Putting It All Together:

Now that we know from Figure-4 that beat #11 in the long lead II rhythm strip manifests the QRST morphology of a normal sinus-conducted beat — We can go back to Figure-3 to figure out which of the 16 beats in today's ECG are sinus conducted without partial fusion from ventricular beats:

• Beats #1,3,4,6,8,11,13 and 15 are all purely sinus-conducted.
• 
  
• PEARL #4: Assessment of ST-T wave morphology for the presence of acute ischemic changes is best done from assessment of normally conducted sinus beats.

In Figure-5 — I have selected simultaneously-conducted sinus beats in each of the 4 major lead groups (within the 4 dotted BLUE rectangles).

Figure-5: Within each of the 4 dotted BLUE rectangles — are simultaneously recorded sinus beats from each of the 4 lead groups.

To facilitate visualization of QRST morphology in each of the 4 lead groups — I have modified Figure-5 by shading out the other beats in Figure-6.

• Isn't it now much easier to appreciate marked acute ST elevation in the anterior leads? ( = beat #11 as it is seen in leads V1,V2,V3 in Figure-6)?
• Completing the pattern of Precordial Swirl that is diagnostic of acute proximal LAD occlusion (See ECG Blog #380 — for more on Precordial Swirl) — is ST depression in lateral chest leads V5,V6 (beat #13). 
• Normal sinus-conducted beats #3 and #6 reveal large Q waves with slight ST elevation in inferior leads III and aVF — and ST depression in leads I,II,aVL. There is also some ST elevation in lead aVR.

Figure-6: To facilitate visualization of acute ST-T wave changes in each of the 12 leads for sinus-conducted beats — I've shaded out other beats on this tracing.

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CASE Conclusion:

Unfortunately — I lack follow-up and the results of cardiac catheterization. Nevertheless, given the history of new CP — I feel confident in concluding the following from today's initial ECG that I have once again reproduced in Figure-7.

• The underlying rhythm in Figure-7 is sinus.
• The reason for the frequently changed QRS morphology in the long lead II rhythm strip is superimposed AIVR (Accelerated IdioVentricular Rhythm) at a rate of ~115/minute. As reviewed in ECG Blog #108 — in the setting of an acute evolving OMI, AIVR is often a "reperfusion" arrhythmia that is usually short-lived, and which usually does not require specific antiarrhythmic treatment. Instead, prompt cath with PCI is needed to prevent reocclusion of the "culprit" artery.
• The reason today's ECG is so challenging to interpret — is the frequent occurrence of fusion beats that results in constantly changing QRS morphology.
• Shading out these fusion beats (as was done in Figure-6) facilitates recognition of acute proximal LAD occlusion (Precordial "Swirl" pattern — with hyperacute anterior lead ST elevation and flattened ST depression in leads V5,V6 — as described in ECG Blog #380).
• The large inferior Q waves + ST depression in leads I,II,aVL,V5,V6 in association with ST elevation in lead aVR suggests that there may be multi-vessel disease (and/or prior inferior infarction) vs extensive LAD occlusion with "wraparound". But the message is clear ==> acute proximal LAD occlusion with immediate need for cardiac cath with PCI.

Figure-7: Today's ECG with "on time" P waves labeled. 

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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ECG Blog #550 — Guess the Clinical Setting

The ECG in Figure-1 was obtained from a middle-aged man who presented with CP (Chest Pain). I was asked for my thoughts on the rhythm.

QUESTIONS:

• What is the rhythm?
• How certain are you of your answer?
• What is the probable cause of this rhythm?

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

My Approach to Today's Tracing: 

We are at a distinct disadvantage in Figure-1 for determining the rhythm. This is because we only see 9 beats, and because we lack a long lead rhythm strip. Nevertheless, a number of deductions can confidently be made.

• PEARL #1: LIfe is easier — IF we simply number the beats (as I have done in Figure-2). Doing so allows us to talk intelligently with colleagues about what is going on (as well as making it easier for us to appreciate relationships between P waves and neighboring QRS complexes).

Take Another Look in Figure-2:

• HINT:  Look first at the chest leads ...

Figure-2: I've numbered the beats in today's tracing.

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What We See in Figure-2:

P waves are present in front of beats 7,8,9 (RED arrows in Figure-3):

• The P wave in front of beat #7 is clearly too short to be normally conducted to the ventricles. Thus, at least for this one beat #7 — there is AV dissociation (which simply means that the P wave in front of beat #7 is not completely conducting this QRS complex).

Figure-3: RED arrows highlight the presence of sinus P waves.

PEARL #2: Recognizing that the PR interval in front of beat #7 is too short to be a normal sinus-conducted beat is the KEY clue to today's rhythm — as it tells us that beat #7 must be a ventricular escape beat!

• In contrast — the QRS complex in front of beats #8 and 9 is narrow, very different-looking than the QRS of beats #7,8,9 — and, the PR interval in front of beats #8 and 9 is constant and long enough to be sinus-conducted (I measure the PR interval in front of beats #7,8 to be ≥0.13-0.14 — and the PR interval might be longer if we were to see P waves in lead II).
• This tells us that beats #5 and 6 must be ventricular escape beats at the slightly accelerated rate of ~55/minute (the R-R interval between beats #5-6 and 6-7 being between 5-to-6 large boxes). 
• 
  
• PEARL #3: If we focus our attention on lead V3 — Doesn't the QRST complex of beat 7 look slightly different than the QRST of beats #5 and 6? (At least in lead V3 — the QRS and T wave of beat #7 are a little less tall than for beats #5 and 6). This tells us that beat #7 is a fusion beat, and proves that beats #5 and 6 are ventricular in origin (See ECG Blog #128 — for more on fusion beats).
• NOTE: It makes sense that beat #7 is a fusion beat — because the PR interval in front of this beat is just a little bit shorter than the PR interval of the sinus-conducting P waves in front of beats #8 and 9 (as we'll see momentarily in the Laddergram in Figure-5).

PEARL #4: That beats #5 and 6 are ventricular escape beats — is supported by another look at QRST morphology of beats #1-thru-4 in the limb leads:

• Note in lead I — that the QRS complex begins with a very deep and wide Q wave! We virtually never see such a deep and wide initial negative deflection in left-sided lead I with normal sinus conduction. Thus, this initial deep and wide Q wave in lead I strongly suggests a ventricular etiology for the 4 beats in this lead.
• PEARL #5: Note the subtle-but-real negative deflection at the end of the QRS in each of the 3 inferior leads (YELLOW arrows in Figure-4 highlighting this negative deflection in lead III — but with a similar terminal negative deflection also being seen in leads II and aVF). This terminal negative notch most likely reflects retrograde conduction of the P wave from ventricular beats #1,2,3,4.
• I suspect retrograde conduction continues in the chest leads, and is seen after beats #5 and 6 — until slight acceleration of the underlying sinus P wave rhythm allows the RED arrow P waves in front of beats #8 and 9 to recapture the ventricles with sinus-conducted beats #8 and 9 (See the laddergram below in Figure-5). 

Figure-4: YELLOW arrows suggest retrograde conduction of P waves following ventricular escape beats.

Figure-5: Laddergram suggesting the mechanism of today’s rhythm.

My Impression: I suspect the rhythm in Figure-5 begins with 7 beats of AIVR (Accelerated IdioVentricular Rhythm) at ~55-60/minute — and ends with 2 sinus-capture beats ( = beats #8 and 9).

• The first 6 ventricular beats manifest retrograde P waves (dotted RED lines in the laddergram that are headed back to the atria).
• Slight acceleration of the rate of sinus impulses allows the RED arrow P waves to recapture the ventricles with beats #8 and 9.
• The overly short PR interval and intermediate shape of the QRS complex and of the T wave for beat #7 — suggests this is a fusion beat. Early arrival of this 1st RED arrow P wave in the ventricles prevents retrograde conduction of ventricular beat #7 — which therefore makes it possible for the 2nd RED arrow P wave to “capture” the ventricles with a sinus-conducted beat.

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Putting It All Together:

• Today’s patient presented with CP.
• The underlying rhythm in the initial ECG appears to be sinus bradycardia and arrhythmia that is intermittently interrupted by AIVR at a rate of ~55-60/minute.
• 
  
• PEARL #6: The combination of AIVR in a patient who presents to the ED for CP — is commonly seen during the evolution of an acute OMI ( = Occlusion-based Myocardial Infarction). As a result — We need to go back and Take Another LOOK at the initial ECG in today's case, looking to see if there might be subtle ECG clues of a recent OMI (keeping in mind that acute ST-T wave changes of an OMI may be difficult to recognize in the presence of a ventricular rhythm such as AIVR).

PEARL #7: When AIVR is seen in association with an evolving OMI (as is especially likely when the patient presents with CP, as in today's case) — it often represents a reperfusion arrhythmia (See ECG Blog #108 — for the basics regarding AIVR).

• As a result — correlating each serial ECG with the presence and severity of CP becomes especially important for understanding the sequence of events (and for determining whether the "culprit" artery is likely to be open or closed at the time a given ECG is recorded). 
• In today's case — We would want to find out IF this patient's CP had decreased (or resolved) at the time the initial ECG was recorded. If symptoms are less at the time of this initial ECG before any treatment has been administered — this would suggest that there has been spontaneous reperfusion of the "culprit" artery (in which case ECG signs of acute infarction may be especially subtle!).

In Figure-6 — I've reproduced today's initial ECG.

• Take another LOOK at this initial ECG — with special attention looking for subtle signs of recent infarction.

Figure-6: I've reproduced today's initial ECG.

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Subtle ECG Signs of Recent Infarction:

Despite the presence of AIVR (and the likelihood of sponaneous reperfusion) — I thought there are subtle ECG signs of recent infarction in today's initial ECG (See labeled Figure-7 below):

• I focused first on the 2 sinus-conducted beats — since assessment of ST-T waves for acute changes is more reliable when seen in normally conducted beats than it is when looking at ventricular beats ( = beats #8 and 9 — within the RED rectangle in Figure-7).
• The amount of ST elevation in lead V2 for beats #8,9 looks to be disproportionately increased given modest depth of the S wave in these sinus-conducted beats.
• The ST segment takeoff in lead V3 looks to be straightened for sinus-conducted beats #8,9.
• There is ST segment straightening with slight depression in lateral chest lead V6 (BLUE arrow in this lead).   

To Emphasize: Acute ST-T wave changes can sometimes be seen in ventricular beats. It's just that these changes tend to be subtle and more difficult to recognize than when acute changes are seen in normally conducted beats:

• In the limb leads (which show 4 consecutive ventricular beats) — the overly "bulky" and depressed ST-T waves in each of the inferior leads looks disproportionate and "off" for what I'd expect given modest QRS amplitude in leads II,III,aVF (RED arrows in these leads).
• Given this inferior lead ST-T wave appearance — the elevated and overly large upright T waves in leads I and aVL manifest the mirror-image opposite picture of what we see in the inferior leads (BLUE arrows in leads I and aVL).
• In the chest leads — the ST-T wave in lead V2 looks to be disproportionately large, with an angled and overly elevated J-point for the ventricular beats. Especially in leads V4,V5,V6 — the T waves look disproportionately large given the tiny size of the QRS in these lateral chest leads (RED arrows in the above noted chest leads for ventricular beats #5,6,7).

Impression: The above noted subtle signs in multiple leads of Figure-7 in this patient with CP and intermittent AIVR are suggestive of a Precordial "Swirl" pattern from recent acute LAD occlusion (See ECG Blog #380 — for review of Precordial Swirl).

• To Emphasize: The above ECG findings are subtle! But especially IF this patient's CP was less (or resolved) at the time the ECG in Figure-7 was recorded — we are expecting less obvious ECG signs than what would probably have been seen if severe CP was still present.

Figure-7: I've labeled a series of subtle ST-T wave abnormalities present in Figure-6 that suggest there has been a recent OMI.

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The CASE Concludes:

Providers were appropriately concerned by this patient's history of new CP in association in association with today's initial ECG.

• Cardiac cath was performed in a timely manner — and revealed acute proximal LAD occlusion, amenable to PCI. 
• A repeat ECG done the next day after successful PCI is shown below in Figure-8.

QUESTIONS:

• How do you interpret the repeat ECG in Figure-8?
• How do beats #8 and 9 in ECG #2 compare with beats #8 and 9 in Figure-7?
• Why might the voltage be so low in Figure-8?

Figure-8: Repeat ECG done the day after successful PCI.

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ANSWERS:

AIVR has resolved — with reestablishment of a sinus rhythm in the repeat ECG recorded after successful PCI (RED arrows showing sinus bradycardia at ~55/minute throughout the tracing in Figure-9).

• Note that all 5 sinus-conducted beats in the chest leads of this repeat ECG look identical to sinus-conducted beats #8 and 9 in today's initial ECG.
• Note that the QRS in Figure-9 is now narrow in all beats — whereas the QRS was wide for the ventricular beats in Figure-6. The wide initial Q wave in lead I that tipped us off in the initial ECG to the presence of AIVR is no longer present.
• There is poor R wave progression in the chest leads of Figure-6 (a QS is present in leads V1,V2 — and transition to a predominant R wave never occurs). This is consistent with this patient's recent anterior MI.
• This post-PCI tracing is also remarkable for diffuse low voltage (No R wave exceeding 5 mm in the limb leads — with overall reduced QRS amplitude also in the chest leads). As highlighted in other cases on this ECG Blog — the finding of low voltage in a patient with recent infarction may be a sign of myocardial "stunning", with reduced cardiac output (See ECG Blog #272 — for more on the causes of low voltage).

Figure-9: I've labeled sinus P waves in the repeat ECG.

Final Thoughts:  

Common things are common. Recognition of AIVR in a patient who presents with CP is an important clue to the likelihood of recent infarction. This should prompt:

• Attention to the details of the patient's history — with efforts to closely correlate the presence and relative severity of CP to the timing of each ECG. Recognition of AIVR at a time when the patient's CP has decreased or resolved is an important clue that spontaneous reperfusion may have occurred.
• ECG signs of recent infarction may be especially subtle following spontaneous reperfusion — as was probably the case for today's initial ECG.
• The ECG signs of recent infarction in Figure-7 are admittedly subtle! That said — these subtle signs become much easier to recognize when you know that the combination of CP and AIVR is commonly seen following recent infarction (and when you know that ECG clues may be very subtle if the patient's CP has decreased or resolved at the time the initial ECG was recorded).

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Acknowledgment: My appreciation to Ali Ibrahim (from Tikrit, Iraq) for allowing me to use this case and these tracings. 

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