Friday, April 19, 2019

ECG Blog #163 (Escape-Capture - Wenckebach - SA Block - Sinus Bradycardia - Bigeminy - PACs - Laddergram - Calipers)

You are asked to interpret the ECG that appears in Figure-1 without the benefit of clinical information.
  • How do you interpret the rhythm?
  • Along the way to arriving at an ECG diagnosis — there are a bunch of interesting observations that should be made. How many can you come up with?
  • Realizing that you have not been told the clinical story — What are likely to be the most important management considerations?
Figure-1: 12-lead ECG + simultaneously-obtained long lead rhythm strips in 3 leads (V1, II and V5). How do you interpret the rhythm? NOTE — Enlarge by clicking on the Figure.
NOTE: The 12-lead ECG and accompanying rhythm strips in Figure-1 were recorded at the standard speed of 25mm/second. Because the ECG grid is faded — I have indicated the size of a large box in GRAY, as well as showing the duration of 5 large boxes ( = 1.0 second) in small BLACK numbers that appear just above the long lead V5 recording at the bottom of Figure-1.
MApproach: This is a complex tracing! I believe there is more than a single possible interpretation. In the hope that My Approach may prove insightful — I list my step-wise Thought Process below:
  • I began by looking at the long-lead rhythm strips at the bottom of the tracing. I daresay that you will not be able to interpret the cardiac rhythm in this case from simply looking at the 12-lead ECG. Instead — attention to one or more of the long-lead rhythm strips is essential!
  • Observation #1: There appears to be group beating for at least a portion of the tracing. That is — there are 3 groups of 2-beats each (beats #1-2; #3-4; and #5-6) — before the rhythm becomes irregular for the last 3 beats in the tracing. Recognition of group beating is helpful — because it tells you at the outset that some type of Wenckebach conduction may be present. Alternatively, since there are several groups of coupled beats each in a “short-long” pattern — there could also be some form of bigeminal rhythm.
  • Before going any further — find a pair of CalipersI daresay that you will not be able to appreciate (or interpret) the fine points of this complex arrhythmia unless (until) you use calipers.
  • All QRS complexes in this tracing are narrow! You may have noted that beat #4 looks slightly different than the other 8 beats in this tracing (especially in the long lead V1 rhythm strip). As an advanced point (that does not alter our final interpretation of the rhythm here) — this difference in the QRS appearance of beat #4 most probably reflects a certain amount of aberrant conduction (that manifests with LAHB/incomplete RBBB morphology) — But, the Bottom Line from our initial inspection of the rhythm in Figure-1 — is that this is a supraventricular rhythm.
Once we have established that the rhythm in Figure-1 is supraventricular (in which there is group beating for parts of the tracing) — the KEY becomes selection of that long-lead rhythm strip that offers the best visualization of waves. This is challenging — because P wave amplitude is very small (if P waves are visible at all) in virtually all leads in this tracing.
  • When I first looked at Figure-1 — I had NO idea if there was an underlying sinus rhythm — or, if P waves were irregular — or, if there were premature beats — or, if only some P waves were conducting to the ventricles, and other P waves were being conducted in retrograde fashion — or, if there was partial or complete AV dissociation.
  • Although most of the time, lead II is the best lead for identification of normal sinus P wave activity — this is not the case in Figure-1. That’s because, with the exception of the P wave that appears just before beat #9 — potential P wave deflections are just too small (and too distorted) by the preceding ST segment in lead II to be identified with any certainty.
  • Observation #2: Atrial activity is best seen in the long-lead V1 rhythm strip! (RED arrows in Figure-2). 
Figure-2: We have added RED arrows to Figure-1 to illustrate that there are regularly-occurring sinus P waves (See text).

We emphasize the following points about Figure-2:
  • The reason we know the small amplitude biphasic (positive-then-negative) P wave deflections in lead V1 are coming from the SA node — is that the P wave in lead V1 that occurs just before beat #9 corresponds to the upright sinus P wave with normal PR interval that is seen to occur in lead II just before this beat #9.
  • Using calipers — we can walk out a surprisingly regular (with minimal variation) P-P interval between each of the RED arrows in Figure-2. This P-P interval measures just under 10 large boxes in duration — which corresponds to a sinus P wave rate of ~32/minute.
Continuing our assessment with several additional observations about What we Know to be true:
  • Observation #3: Beats #1, 3, 5, 7 and 8 are all junctional escape beatsWe know this — because: iNone of these supraventricular beats are preceded by any P wave in lead II; iiThe R-R interval preceding each of these junctional escape beats is virtually identical (ie, the R-R interval between beats #2-3; between beats #4-5; and between beats #6-7 and 7-8 = just over 7 large boxes). This corresponds to a junctional escape rate ~300 ÷ 7+ ~41/minute (which fits perfectly within the usual junctional escape rate range between 40-60/minute)andiiiThe R-R interval preceding the sinus-conducted beat at the end of the tracing ( = the R-R interval before beat #9) is clearly shorter than the R-R interval preceding each of the junctional escape beats. The best clue that the upright P wave in lead II that precedes beat #9 is being conducted — is that beat #9 occurs earlier-than-expected considering the timing of the junctional escape beats.
  • Observation #4: Looking specifically at the long lead V1 rhythm strip — beats #2, 4 and 6 are each preceded by a P wave (RED arrows) — and each of these beats occur earlier-than-expected. This made me suspect that each of these beats (#2,4,6) are somehow being conducted! This relationship = a junctional beat followed by a P wave that then “captures” (ie, conducts to) the ventricles, brings to mind the phenomenon of an Escape-Capture” Rhythm, which narrows diagnostic possibilities ...
  • Observation #5: Using calipers — the PR interval preceding beats #2, 4 and 6 is not the same! So, if beats #2, 4 and 6 are being conducted — there must be some reason why the PR interval preceding these beats is changing ...
  • Observation #6: No QRS complex follows that P wave (RED arrow) that occurs just after beat #7. It seems most likely that this is because the RP interval of this particular P wave (ie, the distance from the QRS of beat #7 until this P wave that follows it) is shorter than the RP interval after beats #2, 4 and 6 — therefore falling within the absolute refractory period after beat #7.
BOTTOM Line: The mechanism of the rhythm in Figure-2 is complex. Although my 40+ year experience in arrhythmia interpretation has enabled me to very quickly interpret the overwhelming majority of all rhythms I encounter by simple inspection — on occasion, I need to construct a laddergram in order to reasonably postulate (and demonstrate) what I believe is going on. The beauty of drawing a Laddergram — is that “a picture tells 1,000 words” (Figure-3).
Figure-3: Laddergram of the long lead V1 rhythm strip (See text).
Laddergram Interpretation: The underlying rhythm in Figure-3 is sinus bradycardia. As stated earlier — the P-P interval between the RED arrows in lead V1 of Figure-3 is just under 10 large boxes in duration — which corresponds to a sinus bradycardia at a rate of ~32/minute.
  • As a result of this marked sinus bradycardia — the junctional escape pacemaker at a set rate of ~41/minute (See Observation #3is able to take over the rhythm (beats #1, 3, 5, 7 and 8) — until the last sinus P wave in the rhythm strip fortuitously occurs at a point (just before beat #9) in the cycle when it is able to capture (conduct to) the ventricles.
  • I postulate in the Laddergram (Figure-3) — that junctional beats ( = the small RED circles in the AV nodal tier) do not conduct all the way back to the atria (dotted lines ending in a dotted butt within the AV nodal tier). It has been shown that the degree of anterograde block for impulses entering the AV node can be different than the degree of retrograde AV block for impulses being conducted back to the atria. I chose to draw the laddergram in Figure-3 postulating the existence of complete AV block in the retrograde direction out of the AV node.
  • P waves following the first 3 junctional escape beats do conduct to the ventricles — but with a progressively increasing PR interval (that increases from 0.30 -to- 0.36 – to 0.38 second) — until the next P wave (that occurs just after beat #7) fails to conduct. This progressive increase in PR interval after junctional escape beats until a P wave fails to conduct is an unusual form of Wenckebach, because it follows a series of junctional escape beats. Consistent with Wenckebach — the next on-time P wave (that occurs just before beat #9) is conducted with a shorter and normal PR interval ( = 0.18 second).

QUESTION: Could there be another explanation for why the rate of sinus P waves in Figure-3 is so slow (ie, ~32/minute)?
  • HINT: What if the rate of SA nodal discharge in Figure-3 was twice as fast as what we see in Figure-3 ( ie, ~64/minute)?

ANSWER: Perhaps instead of the overly slow P wave rate of 32/minute — the SA nodal discharge rate was 64/minute — with only one out of every two SA nodal impulses being able to "get out" of the SA node because of the presence of 2:1 SA Block?
  • I will emphasize that we cannot prove that there is 2:1 SA block from the single ECG that we have been given. But it would seem logical to postulate a more reasonable sinus rate ~64/minute in this patient who seems to manifest multiple conduction disturbances (ie, SA block, Wenckebach conduction when passing through the AV node + complete AV block when conducting retrograde out of the AV node).
Figure-4: Addition of the SA nodal tier to the laddergram drawn in Figure-3 — in which we postulate the presence of 2:1 SA block (See text).

Management Considerations: The primary problem with the ECG in Figure-1 is bradycardia — either due to marked sinus bradycardia at ~32/minute, or 2:1 SA block. In addition — there is Wenckebach conduction of captured sinus impulses. Finally — there is junctional escape at ~42/minute, in response to the overly slow rate of sinus P waves on this ECG.
  • It is likely that the junctional escape rhythm will go away — IF a reasonable sinus rhythm rate could be restored. If so — the Wenckebach conduction might also go away.
Realizing that we have not been told any clinical history on this patient — the usual causes of marked bradycardia + AV and/or SA nodal conduction disturbances in adults include:
  • Recent ischemia/infarction (albeit there is NO evidence of this on the 12-lead ECG shown in Figure-1).
  • Sleep apnea.
  • Rate-slowing medications (ie, beta-blockers, verapamil/diltiazem, digoxin, amiodarone).
  • Hypothyroidism.
  • SSS ( = Sick Sinus Syndrome) — which is a diagnosis of exclusion, to be made only after the other causes listed have been ruled out.
BOTTOM Line: If a potentially correctable cause of the marked bradycardia is not found — then a pacemaker will probably be needed.

Acknowlegment: My thanks to Robert Drutel for allowing me to use this tracing and clinical case.
NOTE: Among the important concepts touched upon in this ECG Blog are: iDiagnosis of AV BlocksiiSA BlocksandiiiUse of Calipers and Laddergrams. We offer some sources of additional information on these subjects below.
  • For Review on the Basics of AV Block — See my 58-minute Video on this subject at
  • Please note that if you click on SHOW MORE on the You-Tube page under where this video appears — You'll see a detailed linked Contents that will allow you to immediately find whatever key points you are looking for in this video.
  • For a Primer on How to Draw a Laddergram — See my ECG Blog #69
  • For More on SA Blocks — Click on Figure-5:

Figure-5: Essentials of SA Block.

Sunday, March 3, 2019

ECG Blog #162 (STEMI – Coronary Circulation – Culprit – BBB)

The ECG in Figure-1 was obtained from an older woman who called EMS because of new-onset chest pain.
  • How would you interpret this tracing?
  • Which coronary vessel is likely to be acutely involved?
Figure-1: Initial ECG obtained from an older woman with new-onset chest pain. NOTE — Enlarge by clicking on the Figure.
Interpretation: There is baseline artifact, especially in the inferior leads — as this ECG was obtained in the ambulance in route to the hospital. That said — the tracing is still interpretable. The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the axis are normal. There is no chamber enlargement. Regarding Q-R-S-T Changes:
  • There are no Q waves.
  • R wave progression is normal — with transition (where the R becomes taller than the S wave is deep) occurring between lead V3-to-V4, which is normal.
  • There is 1-2 mm of J-point ST elevation in leads V4-thru-V6. Although marred by artifact — the T waves in each of the inferior leads (II, III, aVF) appear to be larger, wider at their base, and more-peaked-than-expected — consistent with hyperacute T wave changes. There is subtle-but-real ST-T wave depression in leads aVL, V1 and V2.
IMPRESSION: In a patient with new-onset chest pain — the ECG in Figure-1 is strongly suggestive of an acute lateral STEMI (ST Elevation Myocardial Infarction). In addition, there is most probably posterior and inferior wall involvement.
  • Although the vast majority (~80-90%) of acute inferior Mis are the result of acute RCA (Right Coronary Arteryocclusion — the culprit” artery in this case is much more likely to be the LCx (Left Circumflex Artery). This is because the most prominent area of ST elevation is in the lateral chest leads (V4,V5,V6— rather than in the inferior leads.
  • When the LCx is a dominant vessel — it supplies the lateral, posterior and inferior walls of the left ventricle. These are precisely the areas of the heart that appear to be affected in this initial ECG.
  • Because of the anatomic location of the RCA  acute occlusion of this vessel typically results in: iST elevation in lead III > lead II; iimarked reciprocal ST depression in lead aVL, that is characteristically the “mirror-image” of the ST elevation seen in lead III; iiiECG evidence suggesting acute RV involvement (ie, much less ST depression in right-sided lead V1 compared to lead V2 — or sometimes even ST elevation in V1); and, ivless ST elevation in lead V6 than is seen in lead III. None of these features is seen in this case.
Comment: Although relatively modest in amount — it is the composite of ST-T wave changes in virtually all leads in this patient with new-onset chest pain that makes the diagnosis of an acute STEMI.
  • Lack of any J-point notching — and, the shape of the ST elevation in lateral chest leads V4-thru-V6 that looks hyperacute — is what suggests acute lateral infarction.
  • In support that these findings are real (and not the result of early repolarization) — is the subtle-but-real ST-T wave depression in leads V1, V2 that suggests associated posterior infarction. Reasons why the amount of anterior ST depression is modest might include either multivessel disease, and/or attenuation of ST depression by the ST elevation in other chest leads.
  • In the setting of acute postero-lateral MI — we look extra close at the inferior leads. As noted earlier — the ST-T waves in each of the inferior leads appear to be hyperacute — with reciprocal ST depression in lead aVL.
  • Finally, the ST segment in lead V3 appears to be straighter-than-expected — consistent with what one might anticipate for a “transition lead” between ST depression in V1,V2 and ST elevation in V4-6.
  • Putting This Together — While none of these changes are marked, a “story” is clearly being told in this patient with new chest pain, in which 10 out of the 12 leads in this ECG are consistent with acutely evolving infero-postero-lateral STEMI. Another ECG should be obtained shortly in an attempt to clarify the picture.
A 2nd ECG was obtained 12-minutes later, as the ambulance arrived at the hospital. 
  • What does this 2nd ECG show (Figure-2)?
  • What has happened since the 1st ECG?
  • Why might this change in QRS appearance have occurred?
  • If you had not seen the 1st ECG in Figure-1 — Would you be able to make a definite diagnosis of acute STEMI from this 2nd ECG alone?
  • How does knowing what the 1st ECG looked like, help interpreting this 2nd ECG?
Figure-2: The 2nd ECG on this patient — obtained just 12-minutes after the initial ECG that was shown in Figure-1.
ANSWERS: The rhythm for the 2nd ECG that is shown in Figure-2 is again sinus. However, since the 1st ECG was done — the heart rate has increased slightly (up to ~85/minute — compared to ~70/minute for the ECG in Figure-1).
  • The QRS complex has widened. QRS morphology is now fully consistent with complete LBBB (Left Bundle Branch Block— in that there is a monophasic R wave in left-sided leads I and V6 — and a predominantly negative QRS complex in right-sided lead V1.
  • Although diagnosis of acute MI is often more difficult in the setting of complete LBBB — definitive diagnosis of an acute STEMI is possible in Figure-2because there is clearly abnormal coved ST elevation that should not be there in lateral chest leads V5 and V6!
  • There are 2 reasons why this patient may have developed complete LBBB since the 1st ECG was done: iThis may be a rate-related BBB — since the heart rate is now faster (~85/minute) than it was at the time the 1st ECG was done (~70/minute); and/oriiAcute ischemia from ongoing acute infarction, with compromised perfusion to the bundle branch system. Regardless of which cause(s) is operative — development of new LBBB implies a more significant lesion.
COMMENT: From a teaching perspective — Comparison of the 2 ECGs in this case is a “golden opportunity” to appreciate how to recognize some of the some of the subtleties of acute ischemia/infarction in association with complete LBBB. For clarity — We put both tracings together in Figure-3:
Figure-3: Comparison of the 2 ECGs in this case (See text). 
What WSee in Figure-3: As mentioned — the presence of clearly abnormal ST elevation (in leads V5 and V6) in association with LBBB in this patient with new chest pain is diagnostic of an acute STEMI.
  • The ST-T wave in lead V4 of the LBBB tracing is also clearly abnormal, and represents a hyperacute ST-T wave. Note how unexpectedly tall, wide-at-its-base, and fat-at-its-peak this T wave in lead V4 is.
  • Similarly, the T wave in lead V3 of the LBBB tracing is unexpectedly tall with an inappropriately wide base. This also reflects a hyperacute change. We know these findings in leads V3 and V4 of the LBBB tracing are real — because we saw ST-T wave abnormalities in these same leads in the initial ECG when the QRS complex was narrow.
  • PEARL: Keep looking at neighboring leads when assessing to see if subtle changes are likely to be abnormal. We did this in Figure-1 — when we looked at lead V3. The ST segment flattening in V3 was extremely subtle, and recognized as abnormal primarily because it occurred as a “transition lead” between the ST depression we saw in neighboring lead V2 — and the hyperacute ST-T wave we saw in lead V4. Similarly, the flat “shelf” for the ST segment in lead V2 of the LBBB tracing can be recognized as abnormal, given its proximity to clearly abnormal leads V3-thru-V6.
  • Finally, the ST-T waves in each of the inferior leads in the LBBB tracing are hyperacute. In addition to their appearance in the LBBB tracing (wider-than-expected base + fat-at-their-peak) — we know that these inferior lead changes are real — because we saw similar hyperacute changes in these same leads in the initial ECG when the QRS was narrow.
  • Note that although there is ST-T wave depression in both leads I and aVL in the LBBB tracing — even in retrospect, it’s difficult to know if this finding is marked enough to qualify as "abnormal" in the setting of LBBB. But even without counting what we see in leads I and aVL — we see clearly abnormal ST-T wave findings in 8 of the 12 leads in the LBBB tracing!
BOTTOM Line: This patient is in process of a large acute infero-postero-lateral STEMI — with development of new LBBB just 12 minutes after the initial ECG.
  • The patient was taken to the cath lab soon after arrival at the hospital. The “culprit” artery was the Obtuse Marginal Branch of the LCx.
Acknowledgment: My thanks to Rory Prevett from Dublin, Ireland for his permission allowing me to use this tracing and clinical case.
NOTE: For more on how to determine the Culprit Artery” — Please CLICK HERE.
For quick review on ECG Basics of BBB — Please CLICK HERE.
  • NOTE: If you click onSHOW MORE just below the video on the YouTube page — You’ll see a linked Contents of everything in this 17-minute video.
For written review on ECG Basics of BBB — Please CLICK HERE.
  • NOTE: For more on how to diagnose acute ischemia/infarction in association with underlying BBB — See Sections 05.24-thru-05.29 in the above pdf.
  • For more on Rate-Related BBB — Please CLICK HERE.

Tuesday, February 26, 2019

ECG Blog #161 (Acute STEMI - Abnormal Rhythm)

NOTE: The complete write-up of this case with my detailed ANSWER is found on the ECG Guru— CLICK HERE — 
The Case: A 74-year old man presented to the ED with new-onset chest pain and the ECG shown in Figure-1. Of note — the patient had a history of severe COPD. For teaching purposes — I'll spotlight a number of interesting findings in the form of questions:


  • 1) What is the rhythm?
  • 2) What is the probable “culprit” artery of this STEMI?
  • 3) Which areas of the heart are affected? (HINT: Your answer should list at least 3 different areas! ).
  • 4) Why do you think there is so much ST depression?
  • 5) Is there any finding on this ECG that may be the result of this patient's severe pulmonary disease?

Figure-1: The initial ECG in this case.


NOTE: My complete ANSWER to this case is found in the ECG Guru — CLICK HERE for the link —