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.
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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 V2); and, ivless ST elevation in lead V6 than is seen in lead III. None of these features is seen in this case.
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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.
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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.
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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.
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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:
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Figure-3: Comparison of the 2 ECGs in this case (See text). 
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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!
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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.
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Acknowledgment: My thanks to Rory Prevett from Dublin, Ireland for his permission allowing me to use this tracing and clinical case.
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NOTE: For more on how to determine the Culprit Artery” — Please CLICK HERE.
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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)

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NOTE: The complete write-up of this case with my detailed ANSWER is found on the ECG Guru— CLICK HERE — 
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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:

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.

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NOTE: My complete ANSWER to this case is found in the ECG Guru — CLICK HERE for the link — 
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Thursday, January 31, 2019

ECG Blog #160 (AV Block - AV Dissociation - Isorhythmic)

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NOTE: My complete write-up of this case is found on the January 31, 2019 post on Dr. Smith's ECG BlogCLICK HERE — 
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The Case: A previously healthy young man presented to the ED for shortness of breath and chest pressure that occurred ~3 hours earlier, when he suddenly felt his heart “skip a beat”, and then begin “racing”. He felt “lightheaded” (presyncopal) during the episode — with the “strong sensation of his heart beating”. He did not feel better until ~45 minutes later. Similar episodes had occurred over the past month — but none lasted as long. Of note, the patient is an active athlete. Figure-1 shows his initial ECG that was obtained in the ED.

P.S. There is a family history of a “junctional or other abnormal rhythm”.

Questions:
  • What is the rhythm in Figure-1?
  • Why is this not “isorhythmic” AV dissociation?
  • Might the fact that this patient’s mother is known “to have a junctional rhythm” have anything to do with this case?
  • Clinically — What would you do for this patient?

Hint:
  • Use of calipers is strongly advised for interpreting the rhythm!

Figure-1: The initial ECG in this case.
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NOTE: My complete write-up of this case is found on the January 31, 2019 post on Dr. Smith's ECG Blog — CLICK HERE — 
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Friday, December 28, 2018

ECG Blog #159 (Bradycardia – AV Block – AV Dissociation – Junctional)

The lead II rhythm strip in Figure-1 was obtained from a middle-aged woman who presented to an out-patient clinic with non-cardiac chest pain.
  • What do you see?
  • Does this patient have a cardiac problem?
Figure-1: ECG obtained from a middle-aged woman with non-cardiac chest pain. What do you see? NOTE — Enlarge by clicking on the Figure.
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NOTE: The rhythm strip was recorded at the standard speed of 25mm/second. There is slight distortion (slanting) of the tracing. This is unfortunate — because it makes it much more difficult to assess differences in interval duration, which turns out to be very important in this case. That said, the “good news” is that despite this technical shortcoming — we still are able to determine what is going on with this tracing.
  • We outline our step-by-step process of analysis below.

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Interpretation: The QRS complex is narrow in this single monitoring lead — so the rhythm appears to be supraventricular. At first glance — the rhythm in Figure-1 looks to be fairly regular. P waves are present — but it looks like the PR interval does not remain constant throughout the tracing.
  • PEARL #1: When confronted with a difficult-to-interpret rhythm strip — 2 simple measures greatly facilitate both interpretation, as well as explanation of your approach to others: iNumber the beats in the tracingand, ii) Label atrial activity with arrows. Numbering the beats saves time and effort — because without this, one is never certain as to which beat is being referred to. Labeling P waves allows you to determine IF there is an underlying sinus rhythm (RED arrows in Figure-2). I have been amazed at how often (and how quickly) simply labeling sinus P waves makes underlying relationships obvious.
  • NOTE: Please do not mark up the original rhythm strip with arrows or other notations. The rhythm strip is an official medical record — and if your initial theory turns out to be wrong — then you can’t erase ink markings … So best to make a COPY of the tracing — and then feel free to write on that copy as much as desired.
Figure-2: We have numbered the beats and labeled P waves (RED arrows). How would you describe the relationship between P waves and QRS complexes in this rhythm strip?
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QUESTION: Take a good look at Figure-2. A fairly (but not completely) regular atrial rhythm is evident (RED arrows).
  • How would you describe the relationship between P waves and QRS complexes in Figure-2?
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ANSWER: As noted above — there appears to be a fairly regular supraventricular (ie, narrow QRS) rhythm in Figure-2:
  • PEARL #2: When dealing with a complex rhythm — Start with what you KNOW! We know the PR interval preceding beat #3 is too short to conduct. The PR interval preceding beats #2 and #6 also appears to be too short to conduct.
  • Next  Ask yourself IF there is an underlying sinus rhythm? Note that the PR interval preceding all other beats on this tracing (ie, the PR interval before beats #1; 4,5; 7,8,9) is longer than the PR interval preceding beats #2,3,6 (Figure-3). As alluded to earlier — P waves in this tracing are slightly irregular. But because the PR interval is equal and normal (~0.14 second) preceding beats #1; 4,5; and 7,8,9 — and since P waves are all upright in this lead II monitoring strip — the underlying rhythm is sinus arrhythmia. Since the overall heart rate is under 60/minute — there is also bradycardia.
  • Since the 3 beats that are preceded by a PR interval too short to conduct all have a narrow QRS and look similar in morphology to the 6 sinus-conducted beats on this tracing — these 3 beats (ie, beats #2,3,6) must be junctional escape beats.
Figure-3: The PR interval preceding beats #2, 3 and 6 is too short to conduct (WHITE arrows). In contrast — the PR interval preceding all other beats on this tracing is equal and normal (RED arrows) — which tells us that the underlying rhythm is sinus (technically sinus bradycardia and arrhythmia — See text).
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QUESTION: Look at Figure-3.
  • Is there AV dissociation?
  • If so — Is there AV block?
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ANSWER: By definition — there is transient AV Dissociation in Figure-3. That’s because, at least for some brief period of time — there are some P waves that are not related to neighboring QRS complexes!
  • PEARL #3: Just because there is transient AV dissociation does not necessarily mean there is AV block! It is important to realize that there are 3 potential Causes of ADissociationiAV dissociation due to some form of 2nd or 3rd degree AV Block; iiAV dissociation by “Usurpation” — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over the pacemaking function (because it is faster than the underlying sinus rhythm); and/or, iiiAV dissociation by Default” — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing).
  • PEARL #4: The term, “AV Dissociation” — should never be used as a “diagnosis” per se. Instead — optimal rhythm diagnosis indicates there is AV dissociation because of whichever one or two of the 3 potential causes of this phenomenon is (are) operative. For example, there may be “AV dissociation by usurpation” with Digitalis toxicity — because an overly high dose of Digoxin commonly results in an accelerated junctional rhythm, that then “usurps” control of the underlying sinus rhythm (that is beating at a slower rate).
  • PEARL #5: There is no evidence of AV block in Figure-3. In order for there to be 2nd or 3rd-degree AV block — at least some atrial impulses must fail to conduct to the ventricles despite having adequate opportunity for conduction to occur. This never happens in Figure-3. That’s because the P waves preceding beats #2, 3 and 6 never have a chance to conduct, since the PR interval preceding these beats is clearly too short to allow conduction. The only way to determine if some form of AV block might be present in this patient — would be to see a much longer period of monitoring. One needs to see P waves occurring at all points in the cycle at a slow enough rate (usually under 50-60/minute) — before one can judge if some of these P waves are not being conducted despite having adequate opportunity to do so.
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QUESTION: Take another look at Figure-3.
  • Why is there AV dissociation?
  • What are the clinical implications of this finding?
  • And — What is the rhythm in Figure-3?

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ANSWER: To address these final questions — we measure all R-R intervals on the tracing (Figure-4).
  • PEARL #6: You cannot accurately interpret complex arrhythmias unless you regularly use Calipers. IF you have not yet incorporated regular use of calipers into your practice — You will be amazed at how doing so instantly makes you not only “smarter” — but much faster in your assessment of complex arrhythmias.
Figure-4: Using calipers — we have measured all R-R intervals on this tracing (See text).
  • PEARL #7: When confronted with a rhythm strip in which there is transient AV dissociation, and you are not certain as to which beat(s) may be conducting — Look for unexpected shortening of the R-R interval. Such shortening usually indicates which beat(s) is being conducted.
  • Most of the time, such shortening will be obvious. However, it is not at all obvious in Figure-4. That said, we can see from our measurements that all sinus-conducted beats in Figure-4 (ie, all beats preceded by P waves with RED arrows) have a shorter preceding R-R interval (ie, between 6.1-to-6.5 large boxes) than the R-R interval preceding the 3 junctional escape beats.
  • The R-R interval preceding all 3 junctional escape beats on this tracing = 6.6 large boxes, which corresponds to a junctional escape rate of about 45/minute (ie, 300 ÷ 6.6). This is appropriately within the 40-60/minute normal range for a junctional rhythm.
  • The R-R interval preceding the sinus-conducted beats in Figure-4 is between 6.1-to-6.5 large boxes. This corresponds to a sinus bradycardia and arrhythmia with a rate between 46-49/minute.
  • PEARL #8: The above measurements tell us that what we are seeing in Figure 4 is ADissociation by Default” (ie, whenever the sinus pacemaker slows to a rate below 46/minute — the junctional escape rhythm takes over at the appropriate junctional escape rate = 45/minute).
  • NOTE: The rhythm in Figure-4 is not “AV dissociation”. Instead, the rhythm is sinus bradycardia and arrhythmia. It is because of this sinus bradycardia that AV dissociation occurs. And, since we never see P waves that fail to conduct despite having a chance to conduct — there is no evidence on this tracing of any form of AV block ...
  • PEARL #9: The clinical implications of the rhythm in Figure-4 depend on the reason for sinus bradycardia. The cause might be iatrogenic — if for example the patient was taking a medication such as a ß-blocker that may overly slow the sinus rate. If this were the case — all that might be needed could be to stop the drug (or reduce the dose). If this resulted in a slightly faster underlying sinus rate — there might no longer be need for a junctional escape rhythm to take over the pacemaking function.
  • Another potentially benign cause for the rhythm in Figure-4 could be that the patient is a completely healthy endurance athlete, with a “normal-for-her” rhythm of sinus bradycardia and arrhythmia. An intermittent junctional rhythm under such circumstances may be a normal response in a patient without any pathology.
  • On the other hand — the reason for sinus bradycardia and arrhythmia might be SSS ( = Sick Sinus Syndrome) — and, perhaps with a longer period of monitoring, evidence of AV block (or more profound sinus rate slowing) might be seen ...
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BOTTOM Line: Clinical correlation and a longer period of monitoring is essential for determining IF the rhythm in Figure-4 is pathologic or not. This rhythm might represent a normal, physiologic response in this middle-aged woman with non-cardiac chest pain. Potentially, no other interventions might be needed for such a rhythm. On the other hand — further evaluation might reveal this rhythm to be pathologic and mandate a pacemaker.
  • Optimal interpretation for the rhythm in Figure-4 should be: “Sinus bradycardia and arrhythmia, that results in AV dissociation by default — but without evidence of AV block on this tracing”. Optimal management to determine what (if anything) need be done — will depend on clinical correlation.
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Acknowledgment: My thanks to Dr. Wai Shein from Kyaukpadaung, Myanmar, for his permission allowing me to use this tracing and clinical case.
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NOTE: For more on the Basics of AV Block — Please CLICK HERE. My discussion on AV Dissociation begins at 49:25 in this hour-long ECG video.
  • For written material regarding the difference between AV Dissociation vs AV Block — See also ECG Blog #21 and/or Section 20 in our ACLS-2013-ePUb.