Dawn's picture
Submitted by Dawn on Sun, 08/18/2013 - 22:34

This ECG was obtained from a 78-year-old woman who had been experiencing intermittant chest pain for two days.  When she finally presented to the Emergency Department, her ECG showed ST elevation in the inferior leads II, III, and aVF.  She also has ST depression in I and aVL, which represents reciprocal changes seen in the high lateral leads, which are opposite the inferior wall.  In addition, V1 and V2 show some ST depression, with early transition of the R waves (taller than normal for V2 and V3).  This is a common finding in IWMI, and indicates posterior wall involvement.  The injury is continuous from the inferior wall of the left ventricle, up the posterior wall, because both were supplied in this case by the right coronary artery.

This ECG has three rhythm strips.  The more rhythm strips you have, the easier it is to determine the rhythm.  In this case, the rhythm is normal sinus rhythm.  But the extra rhythm strips would allow you to compare P wave morphology in three views if the rhythm was in question.  Instructors:  ask your students what they think about this rate (78 per minute) in the setting of acute M.I.   Is it within normal range? Is it optimal for the injured heart?   Another good point to bring up is the use of additional right-side leads to assess the right ventricle.  V3R and V4R can be very useful in determining whether right ventricular M.I. is also present.  Some practitioners skip this step and evaluate the RV using echocardiography.  In the emergency setting, however, it can be very helpful to know the condition of the RV.  RVMI is always a possiblity in RCA occlusion, and RVMI can increase mortality significantly.  BP must be protected, since the injured right ventricle is very dependent on preload to function adequately as a pump, providing preload for the left side of the heart.

This patient was lost to followup.

Related Terms: 
Inferior Wall M.I.
STEMI
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Submitted by susan on Mon, 08/19/2013 - 18:43

If it is a high RCA lesion in the RCA, then yes it is RV failure. The RV marginal feeding the Right Ventricle is a vessel that originates about 1/3 to 1/2 the waydown on the RCA from the ostium of the vessel. If it is  a high closure, then RV failure is inevitable. However, if the lesion is low, the RV is spared. More importantly, look at this patient clinically,If in failure, RV pressures will be high, PAWP will be low,  what do his lungs tell you? and, what does is blood pressure tell you.

Susan Elwell RN, MSN - ED

ekgpress@mac.com's picture

Submitted by [email protected] on Tue, 08/20/2013 - 05:26
     This week's ECG Guru Instructor's Collection is as classic as they come for illustrating proximal RCA (Right Coronary Artery) occlusion with resultant acute infero-postero MI. That said - there are a number of additional points worthy of mention about this specific case.
 
  • The history is chest pain for 2 days in this 78 year old woman. Despite that duration of symptoms - there are no more than tiny q waves in the inferior leads - and there is still dramatic ST segment deviations (elevation and depression). This leaves us wondering WHEN did this patient's infarct occur? This ECG clearly doesn't look like it is "2 days old". Bottom Line: Acute cath may be indicated despite the 2 day duration of her symptoms to define the anatomy - as a coronary artery occlusion much more recent than by history may be present.
  • Inferior MIs most often are due to acute RCA occlusion. About 15% of patients have a "left-dominant" system - in which the LCx (Left Circumflex) coronary artery is a larger vessel that continues after supplying the lateral free wall of the left ventricle along the back and undersurface of the heart. In patients with a left-dominant system - the inferior wall is not supplied by the RCA. Instead - the LCx supplies the infero-postero-lateral walls. That said - this case is almost certainly the result of proximal RCA occlusion. There is no ST elevation in V5,V6 (note slight ST depression in these leads! ). Proximal RCA occlusion is strongly suggested whenever there is acute inferior MI with ST elevation in lead III > II - especially when there is marked reciprocal ST depression in lead aVL (and ST depression in aVL > lead I as seen here).
  • This tracing provides an EXCELLENT illustration of what is meant by "reciprocal ST depression". In "your mind's eye" - you get a mirror image reflection with reciprocal changes. It is easy in your "mind's eye" to see how the ST-T wave picture in leads I and aVL is the true "mirror image" of what we see in leads II, III, aVF. Seeing reciprocal changes (esp. when marked as is the case here) - is powerful indication that coronary occlusion is acute.
  • There are 3 possible causes of the ST depression we see in leads V1 and esp. in V2. These are: i) Acute posterior involvement; ii) Reciprocal ST depression (in response to the acute inferior MI ); and iii) concomitant anterior ischemia (there could be narrowing in the LAD as well as occlusion of the RCA). While we cannot be sure which of these 3 causes is operative (or if perhaps there is contribution from all 3 potential causes) - given strong ECG evidence of acute proximal RCA occlusion - this tracing is virtually diagnostic of acute posterior involvement. We say this because of the postive "mirror test" (flip the tracing over and hold it up to the light - and the taller-than-expected R waves in V2,V3 become Q waves, while the ST segment depression shape in V2 becomes ST elevation). While some advocate for posterior leads to diagnose posterior MI (leads V7,V8,V9) - they are really not essential given what we already see on these 12 leads (See MIRROR TEST)
  • As per Dawn - there is often also right ventricular involvement in patients with acute inferior MI from proximal RCA occlusion. That said - I am less suspicious of RV involvement from this tracing. Definitive diagnosis of acute RV (Right Ventricular) MI is made by use of right-sided leads. Peak ST elevation is most often seen in V4R - and there should be progressive increase in ST elevation amount as one moves from V2R-toward-V4R. That said - standard lead V1 is a "right-sided" lead. In most cases of acute RV involvement - the ST segment in V1 will either be flat or slightly elevated. Instead - there is no elevation and T wave inversion in this tracing. So unless, blood pressure was low or the patient had a disproportionately large drop in BP in response to low-dose nitroglycerin - significant RV involvement is less likely to be present here.

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

Dave Richley's picture

Submitted by Dave Richley on Tue, 08/20/2013 - 07:57

I agree with Dawn and Ken that this an RCA occlusion, but is it necessarily proximal as Ken suggests? My understanding is that proximal occlusion is often associated with ST elevation in V1, presumably because of RV invlovement, and that ST depression in V1 suggests a more distal occlusion. Of course, I may be wrong!

Dave R

Dawn's picture

Submitted by Dawn on Thu, 08/22/2013 - 20:28

Hi

I did enjoy your blog. The last case, however, contains some mistaken
information. The "old concept" of posterior MI (and indeed posterior wall)
due to changes in leads V1 and V2 (either ST depression or early R
transition) were removed from current guidelines, after the publications from
Bayes de Luna et al. Using MRI, Bayes de Luna convinced us that the psoterior
wall of the heart does not exists. It is inferior and basal. The old
parameters to refer to Posterior MI correspond actually to the lateral wall.
This info was collected in the latest guidelines.
However, it will take years until we change our mid set and start calling
this properly.

I have recently released an Atlas of Advanced of ECG Interpretation
(www.ecgatlas.com) that could be of interest to you, In the Atlas you will
find 100 cases described by all the ECG Masters around the world. You can
download the ECGs as PPT for your own teaching.
You will notice that I did the same mistake you did in this ECG, because I
completed the Atlas at the same time that Dr Bayes de Luna (from Barcelona,
google him or Pumed him!) was releasing this interesting concept.

Again, congratulations on a great Blog, that I will recommend to my students.

Adrian BAranchuk MD FACC FRCPC
Associate Professor of Medicine
Director, EP Training Program
Queen's University

 

Dawn Altman, Admin

Dawn's picture

Submitted by Dawn on Thu, 08/22/2013 - 20:32

Thank you so much, Dr. Baranchuk, for your comments.  I am aware of Dr. Bayes de Luna's work (not well-versed in it).  I am guilty of hanging onto the "old" ways, accidentally.  It is so hard to change people's thinking.  How many times have people tried to change the classification of AV blocks?  

 

I am never offended by dissenting opinions - I am not the "ECG Guru" - the site itself is.  It is meant to provide resources for ECG instructors, and your references are just such a resource.  By people like yourself providing this information, the ECG Guru becomes like a "wiki" site - it constantly updates and improves.  I purposely keep my comments rather simple, and rely on the comments from people like yourself for added value.



 

Dawn Altman, Admin

Dave Richley's picture

Submitted by Dave Richley on Sat, 08/24/2013 - 00:58

 

Dr Baranchuk makes a very interesting point. The International Society for Holter and Noninvasive Electrocardiography in 2006 (http://circ.ahajournals.org/content/114/16/1755.full?ijkey=7391a9707e270bc0a9628b266af71d6d24b48923&keytype2=tf_ipsecsha)     did indeed recommend new terminology, based on MRI findings, to describe the relationship between ECG changes and location of myocardial infarction and, as Dr Baranchuk says, that group did state that there is no posterior LV wall and that the ECG changes traditionally ascribed to posterior wall MI are actually due to lateral wall infarction. However, the AHA in its 2009 recommendations for the Standardization and Interpretation of the Electrocardiogram in acute ischemia and infarction (http://circ.ahajournals.org/content/119/10/e262.full)  specifically state that the recommendations of the ISHNE should not be adopted. They say, ‘It is the opinion of the committee that for the present, and not withstanding the recommendation of the International Society for Holter and Noninvasive Electrocardiography, the current ECG terminology of posterior be retained to describe ST depression in leads V1 and V2 and the subsequent development of broad R waves in these leads’.

Therefore we have two conflicting recommendations. I find it interesting that Galen Wagner was a member of both groups and a co-author of both papers!

I teach my students both sets of recommendations and try not to confuse them. This also serves the purpose of illustrating that many things in medical science are not settled, that knowledge continues to evolve and that often there are competing theories and recommendations. This is real life!

Dave R

Dawn's picture

Submitted by Dawn on Sat, 08/24/2013 - 15:27

My students are mostly basic-level, a few are intermediate.  I have always taught them that the "posterior wall" is really just the basilar part of the inferior wall - in other words, the inferior wall faces the patient's back and left side near the base.  This is variable due to position of the heart in the chest.  The reason I teach it this way is that so many beginner-level students want to diagnose inferior wall M.I. AND "anterior septal wall ischemia" when they see the ST depression in V1 and V2.  I am mainly trying to teach the concept of reciprocal changes, and keeping my students focused on the ST elevation, since most of my students are in the emergency field.  When they see the signs of "posterior wall M.I.", they should know that the injured area is likely to be large, and the patient does not have two separate M.I.s going on.  Since the LV is oval or rounded, I think it is difficult to define "walls" as separate entities.  There are no corners, or even dividing lines, between the walls.

Dawn Altman, Admin

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