ECG Blog #375 — At Least 3 Major Findings ...

The ECG in Figure-1 was obtained from a 50-year old man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain).

QUESTIONS:

• There are at least 3 principal findings on this ECG — some of which deal with a possible “culprit” artery and/or the location of whatever is going on. How many of these findings can YOU identify?
• 
  
• HINT: Is the rhythm sinus?

Figure-1: The initial ECG in today's case — obtained from a 50-year old man with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always — I like to start my interpretation of 12-lead ECGs with assessment of the rhythm (as per my systematic approach in ECG Blog-205). Since there is no long lead rhythm strip — I focus my attention on the 3 beats that we see in lead II from the 12-lead ECG shown in Figure-1.

• The QRS complex is narrow. As a result — the rhythm is supraventricular.
• Although we lack a long lead rhythm strip — it appears that the overall rhythm in Figure-1 is Regular — at a Rate between ~80-85/minute (ie, with an R-R interval of between 3-4 large boxes in duration).
• Upright P waves are present in lead II — but there is something unusual about these P waves in lead II. Did you notice this unusual finding that is not typically seen with a normal sinus rhythm?

PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as it passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II in the frontal plane (lead II being located at +60 degrees in the frontal axis plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).

• Note in Figure-1 — that the upright P wave in lead II is clearly smaller than the upright P wave in lead I. While possible that this discrepancy in relative P wave size between leads I and II could be seen with either an ectopic atrial rhythm or certain forms of dextrocardia — this P wave size discrepancy should prompt consideration of the most commonly overlooked form of lead reversal, which is a mix-up of the LA (Left Arm) and LL (Left Leg) electrodes.

What Happens with LA-LL Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
• 
  
• By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).
• 
  
• In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal in Figure-2.

Figure-2: LA-LL Lead Reversal (adapted from LITFL).

What Should the Initial ECG in Today's Case Look Like?

For clarity — I've taken the limb leads from the initial ECG in today's case ( = ECG #1) — and inverted lead III — switched leads I and II — and switched leads aVL and aVF. The result is ECG #1a — which is seen in the righthand portion of Figure-3. 

• Note that the chest leads in ECG #1a of Figure-3 — are unchanged from what they were in Figure-1.

QUESTIONS:

Looking at ECG #1a in Figure-3:

• Is the P wave in lead II of ECG #1a now larger than the P wave in lead I (as it should be with a normal sinus rhythm)?
• 
  
• Now that we've established that the 1st KEY finding in today's case is that there was LA-LL Lead Reversal — How would YOU interpret ECG #1a, which shows what today's 12-lead ECG would look like IF lead placement was correct?

MY Interpretation of ECG #1a:

Having accounted for what today's initial tracing would have looked like had lead placement been correct — I see the following in ECG #1a:

• The rhythm is sinus at ~80-85/minute.
• There is dramatic ST elevation in each of the inferior leads. A Q wave is forming in lead II.
• There is equally dramatic reciprocal ST depression in lead aVL (which manifests the mirror-image opposite ST-T wave picture as seen in lead III).
• Significant reciprocal ST depression is also seen in the other high-lateral lead ( = lead I).
• 
  
• In the chest leads — there is significant ST elevation, with a straightened ST segment takeoff in lead V1.
• There is abrupt transition to a surprisingly tall R wave (of ~10 mm) already by lead V2. There is significant ST depression with a positive "Mirror" Test for acute posterior infarction in lead V2. Chest lead ST depression is limited to lead V2.
• There is marked overlap of QRS complexes in virtually all chest leads. The deep anterior S waves and tall lateral chest lead R waves suggest significant LVH.

Putting It All Together: 

After correcting for LA-LL lead reversal — ECG #1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement.

• PEARL #2: The "culprit" artery in today's case — is almost certain to be the proximal RCA (Right Coronary Artery). As discussed in ECG Blog #141 — ECG features in Figure-3 that strongly support the likelihood of the RCA as the "culprit artery" are: i) ST elevation in lead III>II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement. 

PEARL #3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx (Left Circumflex) coronary occlusion. The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the culprit artery. 

• ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI. That said — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. 
• Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changess due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement. This is precisely what we see in lead V1 of ECG #1a.

Figure-3: Comparison of the limb leads from the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal. (To improve visualization — I've digitized the original ECG using PMcardio).

==========================================

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

==========================================

==================================

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.
• 
  
• ECG Blog #190 — When to suspect acute RV Infarction?
• ECG Blog #141 — On acute RCA Occlusion (with RV MI).
• ECG Blog #80 — More on the "culprit" artery.
• 
  
• 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).
• 
  
• ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis). 
• ECG Blog #317 — reviews use (or not) of Posterior Leads.
• 
  
• 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.
• 
  
• ECG Blog #264 — For review of another limb lead reversal (ie, LA-RA lead reversal in a patient with an acute MI).

OTHER Examples of Lead Reversal (from Dr. Smith's ECG Blog):

Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — it's important to familiarize ourselves with how best to recognize the various forms of these "misadventures". For review — Check Out My Comment — at the bottom of the page in the following posts on Dr. Smith's ECG Blog:

• The June 4, 2018 post (LA-LL reversal).
• The July 29, 2018 post (LA-RA reversal).
• The November 4, 2018 post (Leads V1,V2 misplacement).
• The February 11, 2020 post (LA-RA reversal).
• The March 18, 2020 post (LA-RA reversal).
• The August 28, 2020 post (LA-LL reversal).
• The November 19, 2020 post (LA-LL reversal).
• The November 27, 2021 post (LA-RA reversal).
• The April 17, 2022 post (Leads V1,V2 misplacement).
• The May 24, 2022 post (LA-LL reversal).
• The May 26, 2022 post (LA-LL reversal).
• The August 17, 2022 post (LA-RA reversal).

================================== 

ECG Blog #374 — Do You Know the "Culprit"?

The ECG in Figure-1 was obtained from a 90-year old woman — who presented with a 2-to-3 day history of chest pain, that became worse on the day of admission.

• How would YOU interpret the ECG in Figure-1?
• Is there acute coronary occlusion? If so — What is the "culprit" artery?

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

MY Thoughts on the ECG in Figure-1:

There is significant baseline artifact in a number of leads in ECG #1. That said — the rhythm is sinus, at a rate just under 100/minute. The PR interval is normal — but the QRS is wide:

• The reason for QRS widening is bifascicular block: i) The all upright and notched R wave in lead V1 — in association with wide terminal S waves in lateral leads I and V6 is consistent with RBBB (Right Bundle Branch Block); and, ii) Predominant negativity in each of the inferior leads is consistent with LAHB (Left Anterior HemiBlock).
• 
  
• A small q wave is seen in lead aVL. A tiny initial negative deflection (q wave) is also seen in lead V2. I suspect these small q waves are not clinically significant.
• What is clinically significant, especially in view of new chest pain over the past 2-3 days that this patient reports — are the significant ST-T wave deviations in multiple leads (Figure-2).

Figure-2: I've labeled today's ECG to highlight ischemic findings. The vertical RED lines mark the end of the QRS complex in each of the 12 leads — and the "Ts" highlight hyperacute T waves. (See text).

Looking Closer at Today's ECG:

The most challenging part of assessing ST-T wave deviations in today's tracing — is distinguishing between the end of the QRS complex — and — the beginning of the ST-T wave. To facilitate this distinction — I've added vertical RED lines to mark the end of QRS complex in each of the 12 leads.

• NOTE: Although the end of the QRS is not well seen in many of the leads in today's tracing — it is clearly delineated in leads II and aVR in the limb leads — and especially in lead V1 in the chest leads.
• To facilitate assessment of ST depression and/or elevation — I focused my attention on the relative position of the J-point (located just to the right of the vertical RED line) in each of the 12 leads — with respect to the short dotted RED lines that mark the ST segment baseline in each lead.

ST-T Wave Abnormalities in Figure-2:

• ST depression is most marked in the chest leads (clearly beginning in Lead V2 — and extending through to lead V6).
• The J-point also appears to be depressed in lead V1 — though this J-point depression with T wave inversion that we see in lead V1 is not necessarily abnormal given the RBBB.
• ST depression is also marked in lead I — and seen (albeit to a lesser extent) in limb leads II, aVL and aVF.
• 
  
• ST elevation is marked in lead aVR. It is not seen in other leads.
• 
  
• Hyperacute T waves (ie, being taller, "fatter"-at-their-peak and wider-at-their-base than expected given QRS amplitude in each respective lead) — are seen in multiple leads (ie, in leads II,III,aVF; and in leads V3-thru-V6 — as suggested by the "Ts" in these leads).

Putting It All Together: 

In view of the 2-3 day history of chest pain, that became worse at the time the ECG in Figure-2 was recorded — My thoughts were the following:

• The relatively rapid sinus heart rate (just under 100/minute) is potentially worrisome — since sinus tachycardia is usually not seen with acute MI unless there is hemodynamic compromise.
• There is bifascicular block (ie, RBBB/LAHB) — with fragmentation of the QRS complex. These 2 findings strongly suggest significant underlying heart disease in this 90-year old patient — although without a prior tracing for comparison, we can not tell what is "new" vs "old".
• 
  
• There is marked and diffuse ST depression in multiple leads (with ST elevation in lead aVR). This ECG pattern suggests coronary disease that may be acute — but which does not localize to any particular anatomic lead area. The underlying pathophysiologic process responsible for this ECG pattern is "supply-demand mismatch". The terminology favored to describe these ECG findings is diffuse subendocardial ischemia (See ECG Blog #271 — for more on diffuse subendocardial ischemia).
• 
  
• In addition to diffuse ST depression — there are hyperacute-looking T waves in multiple leads (that I've labeled with a Ts in Figure-2). This pattern of J-point ST depression rising to hyperacute-looking T waves in multiple chest leads in a patient with new chest pain — suggests deWinter-like T waves as a result of ongoing LAD (Left Anterior Descending) occlusion (See ECG Blog #183 — for more on deWinter T Waves).
• 
  
• NOTE: As stated a moment ago — without a prior tracing, we don't know if the RBBB/LAHB is "new" or "old". That said — this combination of conduction defects is very commonly seen with acute proximal LAD OMI (Occlusion-based MI).
• 
  
• BOTTOM Line: Looking at this single tracing — I wasn't sure about what the acute lesion might be, or when it may have happened. The patient's symptoms had been ongoing for "2-3 days" — and at 90 years of age with significant QRS fragmentation of her bifascicular conduction defect — much of what we see may have happened in the past. Other than lead aVR — there is no ST elevation in Figure-2. That said — the important point is her ongoing (and increasing) chest pain. Pending more data (ie, repeat ECG; troponins, Echo, etc.) — an extensive acute ongoing event must be assumed until proven otherwise.

CASE Follow-Up:

The patient's chest pain was controlled. Initial troponin was only minimally elevated. Echo revealed a localized apical wall motion abnormality. 

• Cardiac Cath — revealed a 90-99% LMain (Left Main) — and — a 90-99% proximal LAD narrowing. There was no significant disease in the LCx or RCA. 
• 
  
• PCI was successful — and this 90-year old patient did surprisingly well!
• Subsequent troponin values rose markedly — with a peak value = 77000.

Acute LMain Disease:

Emergency providers rarely encounter patients with acute LMain occlusion. The reason for this is simple — Most such patients die quickly, usually before they reach the hospital.

• There is no “single” ECG presentation for patients with acute LMain occlusion. Quite literally — You can see almost anything!
• As shown in Figure-3 — the reason for the highly variable ECG presentation with LMain occlusion — is that multiple territories may be involved to varying degrees — making it impossible to predict how much ST elevation you will see — and how much opposing (reciprocal) ST depression will attenuate (if not completely cancel out) these initial ST segment vector forces.
• The ST-T wave appearance in lead aVR can be anything when there is acute LMain occlusion.
• 
  
• To Emphasize: We don't know for certain whether the LMain or the proximal LAD was the "culprit" vessel in today's case — as the patient's symptoms were ongoing for several days, and neither vessel was 100% occluded at the time of cath. It's almost certain there was at least some spontaneous reperfusion of one or both vessels. What was certain in today's case — was the need for prompt cath and PCI, that fortunately was accomplished.

Figure-3 (I updated this Figure on 5/11/2026 — so as to include additional data): Reasons for the varied ECG presentation of acute LMain occlusion — with this summary synthesized from Dr. Smith’s 8/9/2019 post in his ECG Blog. I discussed the findings of acute LMain occlusion further in My Comment in the January 16, 2020 post of Dr. Smith's ECG Blog — and I have now updated this Figure from my December 18, 2025 post of Dr. Smith's ECG Blog.

==========================================

Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and this tracing.

==========================================

==================================

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.
• 
  
• ECG Blog #271 — Reviews the concept of diffuse subendocardial ischemia.
• 
  
• ECG Blog #316 — The patient died. Was the LMain coronary artery the "culprit"?

Additional Relevant ECG Blog Posts

• ECG Blog #193 — Reviews a case with a dominant LCx as the "culprit" artery (with ECG AUDIO Pearl on the concept of "OMI" and on Predicting the "Culprit" Artery).
• 
  
• ECG Blog #184 — That magical inverse relationship between leads III and aVL.
• ECG Blog #167 — More on that "magical" lead III-aVL relationship.
• ECG Blog #183 — deWinter-like T waves.
• 
  
• ECG Blog #56 — Posterior MI; Mirror Test.
• ECG Blog #80 — What’s the Culprit Artery? + the Mirror Test
• ECG Blog #82 — What’s the Culprit Artery?
• ECG Blog #162 — What’s the Culprit Artery?
• ECG Blog #193 — What's the Culprit Artery?
• ECG Blog #222 — What's the Culprit Artery? 

ECG Blog #373 — 86yo and this Rhythm ...

The 12-lead ECG and long lead II rhythm strip in Figure-1 was obtained from an 86-year old man — who presented to the ED (Emergency Department) with presyncope. No chest pain. The patient was hemodynamically stable in association with this rhythm.

• How would YOU interpret the ECG in Figure-1?
• What is the rhythm?

Figure-1: The initial ECG in today's case — obtained from an 86-year old man with presyncope, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

The overall rate of the rhythm in Figure-1 is not fast. Knowing that this patient is hemodynamically stable provides us with some time to carefully consider the etiology of the rhythm before turning our attention to findings on the 12-lead ECG.

• PEARL #1: When your patient is stable in a rhythm that is not overly fast — I favor starting with assessment of the long lead rhythm strip before going into detail about findings on the 12-lead ECG. As will soon become apparent — the reason for this is that knowing which beats are ventricular vs supraventricular will be critical for assessing the likelihood of acute ST-T wave changes.

The Long Lead II Rhythm Strip:

As always — I favor a systematic approach to rhythm interpretation, using the Ps, Qs, 3R memory aid (See ECG Blog #185).

• Regarding QRS width — there are 2 different QRS shapes in the long lead II rhythm strip in Figure-1: i) Beats #1,2,3,4; and beats #8,9,10 are wide; and, ii) The remaining QRS complexes are narrower.
• P waves are present in today’s tracing! In Figure-2 — I’ve highlighted with RED arrows those P waves that I can be certain about. 
• Note that each of the 4 RED arrows in Figure-2 — appear with a constant (and normal) PR interval before narrow-QRS complex beats that manifest a similar morphology. This tells us that there is an underlying sinus rhythm in today's tracing, here with a heart rate of ~70/minute (ie, the R-R interval between beats #5-6; 6-7; and between beats #11-12; and #12-13 — is just over 4 large boxes in duration, which corresponds to a rate of ~70/minute).

Are there Additional P Waves?

• The easiest way to find out if there are additional P waves in Figure-2 — is to use calipers. Setting your calipers to the P-P interval defined by 2 consecutive P waves about which I am certain (ie, I set my calipers to the P-P interval between beats #6-7) — it can be seen that the “next walk” of the calipers using this P-P interval will fall right on the PINK arrow in Figure-2.
• 
  
• PEARL #2: Identifying additional atrial activity is the KEY to interpreting today’s rhythm. Note that the very small initial triangular deflection under the PINK arrow in Figure-2 — is wider than the small initial r wave in front of all other beats in this tracing. This confirms that after the first 2 RED arrows in Figure-2 — the next on-time sinus P wave lies directly under the PINK arrow.
• 
  
• PEARL #3: The fact that the PR interval that begins from the PINK arrow (and extends until the QRS of beat #8) is too short to conduct — indicates that at least for this beat, there is AV dissociation (because this PINK arrow P wave is not Related to its neighboring QRS). This very short PR interval means that "something else" must have occurred before the PINK P wave has a chance to conduct — which confirms that the wide and different-looking beat #8 must be a ventricular beat!

PEARL #4: Is Beat #8 a PVC or an “Escape” Beat?

It is important to clarify distinction between a "PVC" vs an "escape" beat. By definition — a PVC is “Premature" (ie, occurs earlier-than-expected). In contrast — an "escape" beat occurs later in the cycle. 

• Instead of occurring “early” — beat #8 in Figure-2 occurs relatively late in the cycle. As a result — beat #8 is best classified as a ventricular "escape" beat.
• 
  
• Since beats #1-thru-4; and #9,10 all look the same in QRS morphology as beat #8 — these are all ventricular beats. And since each of these ventricular beats is separated by a similar R-R interval (that is ~4 large boxes in duration) — these beats constitute 2 short runs of AIVR (Accelerated IdioVentricular Rhythm) at a rate of ~75/minute.
• 
  
• NOTE: As discussed in detail in ECG Blog #108 — "AIVR" is an "enhanced" ventricular ectopic rhythm that occurs faster than the intrinsic ventricular escape rate (which is typically between 20-40/minute) — but slower than hemodynamically significant Ventricular Tachycardia (ie, VT at rates >130-140/minute).

Putting It All Together:

To emphasize — It should take you no more than seconds to complete the above rhythm analysis steps. These steps strongly suggest the following regarding the rhythm in Figure-2:

• That there is an underlying sinus rhythm at ~70/minute.
• This underlying sinus rhythm is interrupted by short runs of AIVR that occur at a slightly faster rate (ie, of ~75/minute).

Figure-2: I've highlighted with RED arrows the 4 P waves in today's rhythm that I can be certain about.

Remaining Questions about Today's CASE:

A few questions remain regarding the ECG in today's case:

• Are there more "hidden" P waves?
• What is the etiology of beats #5 and #11 in Figure-2?
• Is the overall rhythm in today's case related to the presyncopal episode that prompted this 86-year old man to present to the ED?

What about Beats #5 and #11?

For clarity — I show only the long lead II rhythm strip in Figure-3. Note that I have now added 3 additional PINK arrows (ie, over the small "hump" that appears just after the QRS of ventricular beat #9 — and at the peak of the T waves that precede beats #5 and 11).

• Isn't it logical to propose that the PINK arrow I have added just after the QRS of beat #9 must represent another on-time sinus P wave?
• And — Aren't the T waves that precede beats #5 and #11 in Figure-3 ever-so-slightly taller than T waves of the other ventricular beats in this tracing?
• Isn't it logical to therefore propose that the PINK arrows I have added before beats #5 and #11 — are likely to represent additional on-time sinus P waves that are conducted to the ventricles (albeit with a slightly prolonged PR interval) to produce beats #5 and #11?

Figure-3: For clarity — I focus on the long lead II rhythm strip. Note that I've added 3 additional PINK arrows since Figure-2 (ie, over the small "hump" that appears just after the QRS of ventricular beat #9 — and at the peak of the T waves that precede beats #5 and #11).

What is the Clinical Significance of AIVR in this Case?

As discussed in ECG Blog #108 — AIVR generally occurs in one of the following Clinical Settings: i) As a rhythm during cardiac arrest; ii) In the monitoring phase of acute MI (especially with inferior MI); or, iii) As a reperfusion arrhythmia (ie, following thrombolysis, acute angioplasty, or spontaneous reperfusion). It may also occur in patients with underlying coronary disease, cardiomyopathy, and/or with digoxin toxicity. 

• On rare occasions — AIVR may occur intermittently in otherwise healthy subjects without underlying heart disease. If such subjects are asymptomatic during episodes — then no treatment is needed.
• 
  
• Regarding Today's CASE: The patient is elderly (86 years old) — and he presented following a presyncopal episode. The patient may have SSS (Sick Sinus Syndrome) as the reason for presyncope. The other main consideration — is to take another look at the 12-lead ECG, and assess this for recent ischemia or infarction.
• Assessment for QRST morphology is best accomplished by looking at sinus-conducted beats — since Q waves and ST-T wave changes are often difficult to evaluate for ventricular beats. To facilitate this assessment in Figure-4 — I've enclosed within dotted RED rectangles the QRST complexes to be evaluated within various leads on the 12-lead tracing for sinus-conducted beats #5,6,7; and #11,12,13. These suggest that there is some QRS widening for these sinus-conducted beats (ie, a nonspecific IVCD), with some nonspecific ST-T wave flattening — but nothing that looks acute.

Figure-4: Taking another look at the 12-lead tracing in today's case. I've enclosed within dotted RED rectangles — the QRST complexes to be evaluated within various leads on the 12-lead tracing for sinus-conducted beats #5,6,7; and #11,12,13 (See text).

========================================

LADDERGRAM Illustration:

Clarification of the mechanism in today's arrhythmia is best explained by laddergram illustration (Figure-5).

• As I have often emphasized — it takes a little time to get good at drawing laddergrams (See ECG Blog #188). In contrast — It is not difficult to learn how to read laddergrams!
• 
  
• In Figure-5 — Regular sinus P waves are seen conducting in the Atrial Tier, except for the first 4 beats for which I don't see evidence of atrial activity.
• The wider beats in Figure-5 that are not preceded by P waves  are ventricular. In the laddergram — these beats originate from the Ventricular Tier — and conduct to some degree beyond the AV node. These ventricular beats constitute 2 short runs of AIVR (ie, beats #1,2,3,4; and #8,9,10).
• Retrograde conduction from ventricular beats #8 and 9 prevents forward conduction of the on-time sinus P waves that are seen just before the onset of beat #8 — and just after the QRS of beat #9.
• Retrograde conduction from ventricular beats #4 and #10 results in "concealed" conduction — and slows forward conduction of the next on-time sinus P waves that are hidden within the T waves of beats #4 and #10 (dotted RED lines seen within the AV Nodal Tier).
• Beats #6,7; and 12,13 — are normally conducted sinus beats.
• Presumably — the run of AIVR from beats #1-thru-4 inhibited the SA node from firing during this period.

Figure-5: Laddergram illustration of today's arrhythmia.

==================================

Acknowledgment: My appreciation an anonymous clinician for the case and these tracings.

==================================

Relevant ECG Posts to Today's Case:

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #210 — Reviews the every-other-beat Method for estimating the rate of regular rapid rhythms.
• 
  
• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.
• 
  
• ECG Blog #108 — Reviews the concept of AIVR.
• Riera ARP, et al: AIVR: Chronology and Main Discoveries: Indian Pacing and EP Journal 10: 40-48, 2010.
• 
  
• ECG Blog #68 — Reviews the concept of "concealed" conduction.