Thursday, January 26, 2023

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 12The 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.

  • 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?

  • 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).

  • 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.

  • 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!

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.

  • 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).

  • 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").

  • Two Questions that arise are: i) When over the past day this patient's infarct occur? — and, ii) What is the likely "culprit" artery? 

  • 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.

  • 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.

  • 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 PVCsSee My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.


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?

  • 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).

  • 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.


  • Acknowledgment: My appreciation to Arron Pearce (from Manchester, UK) 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 — Reviews the Ps, Qs, 3R Approach to Arrhythmia Interpretation.

  • ECG Blog #68 — Reviews the concept of interpolated PVCs.

  • 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 #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 #258 — How to "Date" an Infarction based on the initial ECG.

  • 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.

  • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves)

  • ECG Blog #190 — Reviews the concept of acute RV MI.