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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.

Dawn's picture

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.

Dawn's picture

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.

Dawn's picture

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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Inferior-posterior Wall M.I.

Submitted by Dawn on Sat, 06/15/2013 - 21:40

This 66-year-old man presented with a complaint of chest pain.  His ECG shows a "classic" inferior wall ST-elevation M.I. (STEMI).  The ST elevation is apparent in Leads II, III, and aVF, which are the leads that reflect the inferior wall of the left ventricle.  In addition, this ECG shows ST elevation in Leads V5 and V6, the low lateral wall.  The ST depression in V1 and V2 are reciprocal changes caused by acute injury in the posterior wall. In the majority, the RCA supplies the inferior-posterior wall, the right ventricle, the right atrium (including the SA node and the AV node), and in some, the low lateral wall.  The proximal location of this man's occlusive lesion has caused damage in all these areas.  The relatively slow rate is common in IWMI and can be caused by SA node injury, vagal stimulation, or medications.  Clinical data is not available for this patient.  

Dawn's picture

ST Elevation in aVR and Proximal Arterial Occlusion

Submitted by Dawn on Sun, 02/19/2012 - 03:07

This ECG is from a patient with chest pain.  We have no other information about the patient.  The rythm is atrial fibrillation with a ventricular response of about 113/min.  There is  ST elevation in aVR, with ST depression in all other leads, except V1 and aVL.  V1 is probably caught between showing us ST elevation from the base of the heart (like aVR) and ST depression from the anterior wall (like V2).  Therefore, the ST is flat.  aVL is often elevated in proximal LCA lesions, as well.

This pattern in a person with chest pain is associated with severe acute coronary syndrome (ACS), often with conditions that cause cardiogenic shock.  Proximal left coronary artery obstruction or severe triple vessle disease are likely.

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