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Inferior Wall M.I. With Wide QRS and Complete AV Block

Submitted by Dawn on Wed, 06/28/2017 - 14:13

This ECG is from a 66-year-old woman who called 911 for a complaint of chest pain for the past four hours. She also complained of nausea, vomiting, and diarrhea for that time. She was pale and diaphoretic, and her BP was 77/43 sitting up, improving to 90/54 reclining. She denied “cardiac” history.  Her medications included:  aspirin, an SSRI, cilostazol, amlodipine, umeclidinium and vilanterol inhaler, atorvastatin, levothyroid, and metoprolol. We don’t have a previous ECG.  The EMS crew followed their chest pain protocol and delivered the patient to a facility with an interventional cath lab, but they did not designate a “STEMI Alert” because of the wide QRS.  It is their protocol to use the term “STEMI Alert” only when no M.I. mimics, such as left bundle branch block, are present. 

What does this ECG show?     There is an underlying sinus rhythm at 75 bpm.  There is AV dissociation, with regular, wide QRS complexes at a rate of 44 bpm.   This meets the criteria for complete heart block (third-degree AV block).  The morphology of the QRS complexes meets the criteria for left bundle branch block (wide, upright in Leads I and V6, negative in V1).  At a rate of 44 bpm, several options for this escape rhythm are possible:  1)  junctional escape with LBBB, 2) junctional escape with intraventricular conduction delay due to AMI,  and 3) idioventricular escape rhythm.   Also, in the presence of IWMI, AV node ischemia is very likely, resulting in AV blocks at the level of the AV node.  CHB at the AV node would result in junctional escape rhythm, and CHB below that, in the fascicles of the bundle branches, would result in idioventricular escape. The issue for this patient, and ANY patient, is cardiac output, and we see several reasons for cardiac output to be lower:

·         Wide QRS

Dawn's picture

Inferior-lateral M.I. With QRS Fragmentation

Submitted by Dawn on Sat, 08/13/2016 - 23:33

SUBTLE ST CHANGES   This ECG was obtained from an 87-year-old man who was experiencing chest pain.  Due to the subtle ST elevation in Leads II, III, aVF, V5, and V6, (inferior- lateral walls) the ECG was transmitted to the hospital by the EMS crew, and the cath lab was activated.  The patient denied previous cardiac history. 

In addition to the subtle ST elevation, there is ST depression in V1 through V4, which represents a reciprocal view of the injury in the inferior-posterior-lateral wall.  Because the anterior wall is superior in its position in the chest, it is opposite the inferior/posterior wall, and can show ST depression when the inferior-posterior area has ST elevation. This ECG was the 6th one done during this EMS call.  Prior to this one, the ST segments were elevated less than 1 mm.  This is a good example of the value of repeat ECGs during an acute event.  

RIGHT VENTRICULAR M.I.?     This ECG was done with V4 placed on the right side, to check for right ventricular M.I., which is a protocol for this EMS agency. When the right coronary artery is the culprit artery (about 80% of IWMIs), RVMI is likely.  In RVMI, we would usually see reciprocal ST depression in Leads I and aVL, but the STE is very subtle here, so the depression would likely be also.  When the culprit artery is the left circumflex artery (<20%), lateral lead ST elevation is more likely, as we see here in V5 and V6. 

WHAT ABOUT RHYTHM?     The rhythm is sinus with PACs.  PACs are considered to be benign in most situations, but in a patient with acute M.I., any dysrhythmia can be concerning. The QT interval, measured as QTc (corrected to a heart rate of 60 bpm), is slightly prolonged at .458 seconds (458 ms).  Over .440 seconds is considered prolonged in men, and over .500 sec. places the patient at increased risk of developing torsades de pointes.  CAD and myocardial ischemia can lead to this modest increase in QTc.

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Acute Inferior-Lateral M.I. In A Patient With A Dominant Circumflex Artery

Submitted by Dawn on Fri, 10/30/2015 - 22:59

This ECG was obtained from a patient who suffered an obstruction of the circumflex coronary artery.  Unfortunately, he was in the approximately 15-18% of the population in whom the circumflex artery is dominant.  That means that it connects with the posterior descending artery, perfusing not only the lateral wall of the left ventricle, but also the posterior and inferior walls.  In this case, the obstruction is in the midportion of the artery, and the high lateral wall is spared.  The large number of leads with ST elevation indicate the large amount of myocardium affected.  Leads II, III, and aVF have ST elevation, as do Leads V3 through V6.  Lead aVL has reciprocal ST depression. The T waves in the affected leads are "hyperacute", or taller than normal.  This is usually an early change in acute M.I., and disappears after the onset of ST elevation.

It is not always easy to determine from the ECG that the circumflex artery is the culprit artery, rather than the right coronary artery, which perfuses the inferior wall in the majority of people.  Some clues are:  Lead III has ST elevation equal to that of Lead II, the low lateral wall (V5 and V6) are affected, and aVL has reciprocal depression but Lead I does not.

This is a very large M.I., due to the dominance of the circumflex artery.  The patient did not survive, in spite of aggressive treatment.

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Inferior-Lateral M.I.

Submitted by Dawn on Sun, 03/29/2015 - 21:41

This ECG and rhythm strip are from a 78 year old man with chest pain, but we have no other clinical data. This is a good example of inferior and low lateral injury, demonstrating the large amount of heart muscle that can be damaged when a dominant RCA or circumflex artery is occluded.  The low lateral wall is often included in an inferior wall M.I. when the RCA wraps around the left side of the heart, or the circumflex perfuses the posterior descendng artery and the inferior wall.

In this ECG, we see a sinus rhythm with obvious ST segment elevation in Leads II, III, and aVF, with reciprocal ST depression n Lead aVL.  There is reciprocal ST depression in V1 and V2, indicating that the inferior wall injury extends up the posterior wall until it is seen by the anterior leads V1 and V2 as ST depression. The term "posterior wall" has come into some scrutiny recently, but it is still commonly used, so we use it here. There is also ST elevation in Leads V4, V5, and V6, reflecting the low lateral wall.  

This is a great example of how the SHAPE of the ST segment is often altered in acute M.I. as well.   Leads II, V4, V5, and V6 have obvious "flattening" of the ST segment. Even when the ST elevation is minimal, this shape is a STRONG indicator of M.I.  Lead III has a convex-upward shape, another giveaway for an M.I. diagnosis.

Adding to the evidence for a diagnosis of acute M.I. are the associated signs:  T wave inversion in Lead III (a sign of ischemia), and poor R wave progression in V3 through V6.  Since V3, V4, V5, and V6 should all have strong R waves, this could be an ominous sign of impending pathological Q waves, a sign of myocardial necrosis.   

The rhythm strips in this case demonstrate ST elevation also.  There is artifact in Leads II and aVF.   This example can be used for beginners who are learning lead concepts.  Ask, "Which limb is the artifact coming from?"  The answer is the right arm, because Lead III doesn't use the right arm, and it is clear of artifact. 

Dawn's picture

Inferior-lateral and Posterior M.I.

Submitted by Dawn on Thu, 01/15/2015 - 23:55

This is from a Cardiac Alert patient, with chest pain, in the Emergency Department.  The ECG shows ST elevation in the inferior leads (II, III, and aVF), and in the low lateral leads (V5 and V6).  There is reciprocal depression in V1 and V2, indicating injury in the posterior wall.  One could argue that "inferior" is just the term we use for the lower part of the posterior wall - the part that faces the floor in a standing person.  So, "inferior-posterior" reflects a more proximal occlusion of the culprit artery.

The high lateral wall is represented by I and aVL.  These leads would usually show marked reciprocal ST depression when II, III, and aVF have elevation.  However, in this ECG, aVL is depressed, but not as much as expected, and Lead I almost looks elevated!  This could represent even more extensive lateral wall involvement.  A dominant right coronary artery could be the culprit, but it seems more likely that a dominant circumflex artery is to blame, as it could perfuse the entire lateral wall before joining with the posterior descending artery and perfusing the inferior wall.  Unfortunately, we do not have the cath results on this patient.

The ST elevation in this ECG has the classic appearance of acute M.I., and will be interesting to both beginner and advanced students.

Often, one ECG can provide a wealth of teaching opportunities, no matter what the level of your students.  For the student learning to monitor the rate and rhythm, you might crop this image to only show the Lead II rhythm strip at the bottom, for a good example of normal sinus rhythm with a borderline PRI of .20 sec.   For the student learning about ST elevation M.I., this is a good example of inferior-posterior and lateral injury.  Leads aVL, V1 and V2 demonstrate reciprocal ST depression.  When an observant student notices the slight ST elevation in V6, a discussion of coronary artery distribution can occur.  

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