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Inferior Wall M.I. and Right Bundle Branch Block

Submitted by Dawn on Fri, 10/24/2014 - 15:36

This ECG shows two obvious abnormalities, right bundle branch block AND inferior wall M.I.  It is also a good teaching example of how the terminal wave of RBBB can be mistaken for the ST elevation of M.I.

First, check this ECG to see if it meets the criteria for right bundle branch block:

1)  The QRS will be wide. That is, it will be greater than or equal to .12 seconds (120 ms).  In this case, the QRS is 134 ms.

2)  The rhythm will be supraventricular.  Supraventricular rhythms originate from above the ventricles.  This ECG has P waves before each QRS.  Even though the rhythm is irregular, slowing down during this recorded period, it is a sinus rhythm.

3)  The QRS will have a terminal wave after the "normal" part of the QRS.  This represents the right ventricle depolarizing late.  It is very easily seen in V1, which normally has an rS pattern, and with RBBB has an rSR' pattern, making it appear upright.  V6 and Lead I will show this terminal wave as a wide little s wave.

As mentioned, there is also an acute inferior wall M.I. here.  The ST segment elevation in Leads II, III, and aVF are actually quite subtle.  The flat top of the ST segments gives them away as abnormal, along with the associated ST elevations in V5 and V6, and the reciprocal ST depressions in V1 through V3.  Normally, in IWMI, there will be reciprocal ST depressions in Leads I and aVL, but the elevations they are reflecting are very subtle, and so, therefore, are the depressions. 

The tricky thing about this ECG is that you must look carefully at the inferior wall leads to see the true ST elevation, which, as mentioned, is subtle.  The RBBB terminal wave of the QRS complexes in Leads III and aVF is upright, and is often mistaken for ST elevation.  Remember, ST segments are smooth from the end of the QRS to the peak of the T wave.  See the detail illustration.

This ECG is suitable for your classes from beginner level (rate variation in sinus rhythm) through advanced (clinical significance of RBBB in acute M.I.).  It also offers an example of reciprocal ST changes, and of a situation where the inferior leads II, III, and aVF are related to the low lateral leads V5 and V6 by a shared blood supply.

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Extensive Anterior Wall M.I. With Recent Inferior Wall M.I.

Submitted by Dawn on Fri, 08/29/2014 - 17:15

This 88-year-old woman was brought to the Emergency Department in cardiogenic shock.  Very little is known of her past medical history, but it was relayed to the EMS responders that she had been ill for about four days, when she became much worse.

This ECG shows a large, acute anterio-lateral wall M.I., as evidenced by the ST ELEVATIONS in V2 through V6, Leads I and aVL.  To make matters worse, there are PATHOLOGICAL Q WAVES in Leads V2 through V6.  Pathological Q waves indicate areas of necrosis.  Because the myocardium facing the positive electrode is not electrically active, we "see through" the dead tissue to the myocardium on the opposite side of the heart.  Pathological Q waves could be thought of as "reciprocal R waves".  This represents a great deal of dead myocardium, which will be akinetic - not moving.

To make matters worse, she has pathological Q waves in the INFERIOR WALL as well, in Leads II, III, and aVF.  Her ST segments in those leads are flattened and possibly slightly elevated, but not much.  There are no reciprocal ST depressions in I and aVL, because they are affected by the anterior - lateral wall M.I., and are elevated.

The accompanying photos show her left coronary artery angiogram indicating severe coronary artery disease and a "missing" left anterior descending artery.  This is due to a proximal lesion that occurred around the area of the first diagonal artery, cutting off blood flow to a very large part of her anterior-lateral wall.  The photo of the right coronary artery shows a very tight lesion which is allowing some blood to pass.  The Interventionalist felt that this represented a resolving 100% occlusion (remember, she had been sick for four days).  As the blood clot broke up, blood flowed again, lowering the ST segments.  Unfortunately, permanent damage had already been done, and she had Q waves in the inferior wall also.  This leaves very little of her heart beating, and it is easy to understand why she presented in shock.  She suffered cardiac arrests several times during the procedure, and was managed with a balloon pump and ventilator.

Unfortunately, this type of injury is not survivable, and she died in the CVICU a few hours after her procedure. She contributes to our education by demonstrating the cumulative effects of M.I., especially when permanent damage occurs.  For a look at her ventriculogram, to understand the devastating effects of these injuries, go to our You Tube channel.

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Artifact on an ECG With Inferior, Posterior, Lateral M.I.

Submitted by Dawn on Sat, 07/05/2014 - 00:01

If you are an ECG instructor, it is important that you address the subject of artifact on the ECG.  Artifact has many causes, and it is important eliminate it whenever possible.  We should strive for the "cleanest" ECG possible.  As you can see in this example, the presence of artifact has caused the machine's computer rhythm interpretation to be incorrect.  The noisy baseline has caused the computer to call this rhythm "atrial fibrillation", but we clearly see P waves in all leads, especially in Lead II.  We recognize these P waves as authentic because they are regular, they  all look alike, and they have the same relationship to the QRS complexes each cycle (PR interval is the same).  

The patient is suffering a very large M.I., showing as ST segment elevation in Leads II, III, aVF, with slight elevation in V5 and V6.  In addition, Leads V1 through V3 have definite  ST depression, indicating extension of the inferior wall injury up the posterior wall of the heart.  There has been quite a bit of discussion lately in the literature about whether to call this a "posterior" M.I, or "high lateral", or just "inferior".  Semantics aside, the involvement of so many leads tells us that this  is a large M.I.  The patient was in the Emergency Dept. complaining of chest pain.

It is fortunate that the artifact did not affect our ability to see the ST elevation, but it could have.  And, of course, we would not want to treat this patient's "atrial fib" based on the machine interpretation.  But, it is always prudent to try to get rid of artifact.  In this example, Lead III has no artifact, so it could be assumed that the right arm electrode is the culprit, as Lead III does not utilize the RA electrode, and the other leads do.  

Troubleshoot for the cause of the artifact, and then retake the ECG.  Some common causes of baseline  artifact of this nature include:  patient movement, loose electrode, dried electrode, something touching the electrode, faulty or broken lead wire, and poor skin contact due to substances on the skin.  The electrodes should be fresh from the package, and applied to skin that is clean and dry.  The patient should be encouraged to relax and hold still (not so easy for a patient in distress).  Others at the bedside should avoid touching or manipulating the limbs of the patient during acquisition of the ECG data.  This only takes about 10 seconds.  I have seen artifact many times when a patient's blood was being drawn during the ECG, and the patient was squeezing his fist for the phlebotomist.

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Acute Inferior Wall M.I.

Submitted by Dawn on Tue, 04/15/2014 - 00:08

Another great ECG donated by Paramedic Eric Testerman.  This ECG is from a 66 year old man who was complaining of feeling dizzy, weak, and of having "minor" chest pain. He was extremely pale/ashen, had moderate cyanosis, and was very clammy and diaphoretic.  His initial heart rate was about 20 bpm.  His initial BP was 131/113 then, just before arrival at the hospital was 127/85. His HR increased to about 50 bpm (not shown). He was given 400 ml I.V. fluid, 324 gr of aspirin, and oxygen.  Transcutaneous defibrillator/pacemaker pads were applied. 

At the hospital, he was successfully treated with angioplasty for a 100% occlusion of the right coronary artery. The time from beginning of treatment to reperfusion of the artery was 47 minutes, which is very good! 

This is a "classic" inferior wall M.I., with ST elevation in leads II, III, and aVF. There are reciprocal ST depressions in I and aVL.  There are also ST depressions in V1 through V5.  This is generally considered to represent reciprocal ST changes in the posterior and lateral walls.There is a quite severe bradycardia, and the patient's skin showed signs of poor perfusion. Amazingly, the patient's BP stayed adequate during transport.  Bradycardia is common in inferior wall M.I. due to ischemic effects on the SA node and vagus nerve (sinus bradycardia) and the AV node (heart block).  In this case, the rhythm is sinus bradycardia.  The heart rate is in the 20's, and the PR interval is around .20 - .22 seconds. 

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Teaching Tips: ECG Series WO 118: STEMI With Changing ST Elevations

Submitted by Dawn on Thu, 01/23/2014 - 23:15

Continuing with our theme of using  series of ECGs for teaching, we present the case of an 83-year-old woman with weakness, chest pain, and near-syncope.  The first ECG, taken by paramedics at her home, shows a sinus rhythm with a slightly wide QRS complex.  At this point, it is unclear whether this represents left bundle branch block or a non-specific interventricular conduction delay. There is the most subtle ST elevation in Leads III and aVF. In LBBB without acute M.I., we would expect the ST segments to be discordant, or opposite, the QRS complexes.   Even more informative is the reciprocal ST depression in Leads I and aVL (and a little in V2).  This can be a sign of inferior wall injury that shows up earlier than ST elevation in the inferior leads.

ECG number 2 was taken during transport to the hospital.  The chest pain continues, and now the ST elevation in the inferior leads is pronounced, and the reciprocal depression in I, aVL, and V2 has also become much more obvious.  V1 would also normally show this depression - a sign of the injury traveling up the back of the inferior wall (posterior).  But if the right ventricle is injured, V1 will have ST elevation.    V1 in this case is probably reflecting the depression from the posterior wall AND the elevation from the right ventricle.  The ST elevation is now prominent enough that the paramedics notified the hospital of a "STEMI Alert".  The QRS remains widened at .13 sec., but the ST elevations and depressions are not opposite the QRS direction, which would be typical for LBBB without an M.I.  Therefore, even if LBBB is present, these ST elevations and depressions would be considered a sign of STEMI.  The rate is slowing in this ECG.

ECG number 3 was taken in the Emergency Department.  The patient's symptoms continued.  The bradycardia is still present, as is the QRS widening.  Now, something new has shown up:  prominent U waves in the precordial leads.  There appears to be T-U fusion.  We do not know the patient's medications or lab results, so the most likely cause for the prominent U waves is the bradycardia.  She does not have other ECG signs of hypokalemia, which is one of the many causes of U waves. 

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Previous Inferior Wall M.I. and Left Axis Deviaton

Submitted by Dawn on Fri, 01/17/2014 - 21:39

If you are teaching frontal plane axis to your students, you will need to teach them HOW to determine the axis - usually beginning with the QRS axis and then adding the P and T waves.  But, you also need to teach them WHY we measure axis, to provide relevance to something that may seem challenging to beginners.  There are many ECG interpretations that rely heavily or are dependent upon the determination of the axis.  

This ECG is a great example of left axis deviation.  The cause is readily discernible, if your students know the ECG signs of myocardial infarction. This patient had an inferior wall M.I. in the distant past, and now has pathological Q waves in Leads II, III, and aVF.  Pathological Q waves in related leads in a patient with history of M.I. are a sign of necrosis, or permanent damage, in that part of the heart.  The inferior wall has lost an extensive amount of tissue, which is now electrically inactive as well as mechanically inactive.  (You may also find it helpful to show students videos of ventriculograms showing normal LV function and hypokinesis of the LV due to M.I.)  Because of the loss of electrical activity in the inferior wall, the "mean" electrical direction (or axis) is AWAY from the inferior wall.  That is, the electricity travels AWAY from II, III, and aVF and TOWARD I and aVL.

Many of the blogs and webpages listed in our "Favorites" address the subject of axis determination.  Here is one from Cardio Rhythms Online if you would like a review.

 

 

 

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Inferior Wall M.I. With Junctional Rhythm

Submitted by Dawn on Fri, 01/10/2014 - 15:07

We do not have a patient history for this ECG, other than that it was an 81-year-old woman with chest pain.  The classic signs of acute ST-elevation inferior wall M.I. are there:  ST segment elevations in Leads II, III, and aVF.  There are the expected reciprocal ST depressions in Leads I and aVL.   The ST depression in V2 suggests posterior wall injury, and would normally be seen in V1 as well, unless something else is causing ST elevation in V1 at the same time.  That "something" would be right ventricular injury, and it can be confirmed by performing a V4Rt (or full set of right-sided V leads).  The slight elevation in V3 and V4 don't seem to "fit" with the IWMI - one might expect V5 and V6 to have ST elevation, reflecting injury in the low lateral wall.  We don't have the cath lab results, so we do not have an explanation for this (lead placement issues, perhaps?).

The rhythm here is interesting, but not unexpected with IWMI.  The rhythm is junctional, as reflected by the regular, narrow QRS complexes at a rate of about 54/min.  IWMI often causes blocks of the AV node, which has the same blood supply as the inferior wall in most people.  Even though there appear to be some "PR intervals", they are not consistent, and also do not meet the criteria for second-degree AVB Type I, so we are left with an interpretation of complete heart block.  The P waves here are also inconsistent.  They are regular at times, then disappear.  The SA node can be affected in IWMI also, and develop rate irregularities and exit blocks.  The IMPORTANT thing to consider is how the patient is handling the rate.  If this rate is not causing perfusion problems, that is - the patient has enough rate to maintain her blood pressure and level of consciousness, the rate is not harmful, and the junctional rhythm is not harmful.  In fact, one could argue that this junctional rhythm is more beneficial to the injured heart than a faster sinus rate would be.

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Anterior Wall M.I. With Previous Inferior Wall M.I.

Submitted by Dawn on Mon, 11/04/2013 - 13:40

This ECG illustrates an acute anterior wall M.I. in a patient with a previous history of inferior wall M.I.  The anterior wall M.I. can be seen in the classic signs in V1 through V6:  ST elevations with coved upward shape (tombstones), T waves inverting beginning around V2 and continuing through V6, and pathological Q waves in V1 through V6.

The patient had a history of previous inferior wall M.I., unknown age.  This is normally seen in Leads II, III, and aVF.  The first two complexes on the strip are wide QRS complexes without associated P waves, presumably ventricular.  It is impossible to know from this ECG whether the first complex is a PVC or escape beat, but the second appears to be escape.  So, to evaluate the ST segments, T waves, and pathological Q waves in the inferior wall, all we have are aVF and the Lead II rhythm strip at the bottom.  These show pathological Q waves (necrosis), and some slight elevation of ST, with coving or horizontal flattening.  From this, we know there is damage in the inferior wall, but the age of the M.I. is undetermined.

This patient went to the cath lab, and received angioplasty with stenting of the proximal left anterior descending branch of the left coronary artery.

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Inferior Wall M.I. Due To Circumflex Artery Occlusion

Submitted by Dawn on Fri, 10/25/2013 - 21:26

This ECG is from an 81 year old woman with an extensive history of coronary artery disease.  She was experiencing chest pain at the time of the ECG.  We can clearly see ST elevation in Leads II, III, and aVF, indicating an inferior wall ST-elevation M.I. (STEMI).  There are reciprocal ST depressions in Leads I and aVL.  There are subtle and less specific ST changes in V1 (flat ST and T), V2 (ST depression), V3 (ST elevation and inverted T wave), and V4 through V6 (slight ST elevation).  The flat, horizontal shape of most of the ST segments is another clue to her CAD.  What coronary artery do you think is the culprit for the ST elevation?

This patient received coronary angiography, so we do not have to guess at where her lesions are.  She was found to have an occluded left internal mammary artery (LIMA) graft.

The left anterior descending coronary artery (top of view) is very diseased, with some extremely narrow areas.  The circumflex artery is large and covers a lot of area, but it, too, is very diseased, with a critical occlusion (marked with arrow).  On this day, the circumflex artery received angioplasty and stents.  The patient's right coronary artery was patent.

In approximately 85% of the population, the RCA supplies the inferior wall of the heart.  In most of the rest, a branch of the circumflex supplies the posterior/inferior wall.

This patient also has a very interesting arrhythmia.  We see P waves (numbered) that appear regular for three beats, then we see no P waves for a pause.  Then, three more P waves appear.  There is no readily-seen "hidden" P wave in the ST segments or T waves.  Even though there appear to be "progressively prolonging PR intervals", the PR intervals of each group of three do not match the other group of three.  The first "PRI" - P wave number 1- and the last one - P wave number 7 - appear too short to be normal PR intervals.  The ventricular rate is regular, and the QRS complexes are slightly wide at  .10 sec.  The rate is 54 bpm.  This suggests junctional rhythm.

We are eager to hear your comments regarding this rhythm.

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Inferior Wall M.I.

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.

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