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Acute Anterior-lateral STEMI

Submitted by Dawn on Sat, 12/23/2023 - 21:15

The Patient:  A 60-year-old man at work. He experienced a sudden onset of substernal chest pain, nausea & vomiting, and dizziness.  He states the pain is a 5 on 1-10 scale.  No cardiac history or current medications. 

The ECGs:  The first ECG, taken at 12:30:05, shows a sinus rhythm with ventricular bigeminy. In some leads, you can see the sinus P waves hidden in the beginnings of the PVCs, so we know the underlying sinus rhythm is about 82 bpm.

There is obvious ST elevation in V1 through V5, which is the anterior wall, an area perfused by the left anterior descending artery.  Remember – the ST elevation sign may also show in the PVCs, but because ventricular beats have secondary ST changes of their own, we should assess only the sinus beats for ST changes. 

There is also obvious ST elevation in Leads I and aVL.  This is the high lateral wall, which is perfused by the circumflex and first diagonal arteries, both proximal branches of the left coronary artery.  So, the involvement of the high lateral wall indicates a proximal lesion in the LCA – not good.  Leads III and aVF have distinct ST depression – this is a reciprocal change reflecting the ST elevation in Leads I and aVL.

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Inferior Posterior M.I.

Submitted by Dawn on Mon, 07/24/2023 - 14:41

This is a "classic" ECG of very good quality for you to use in a classroom setting.

The Patient:  A 57-year-old man who complains of a sudden onset of "sharp" chest pain while on a long bike ride.  The pain does not radiate, and nothing makes it worse or better.  He is pale, cool, and diaphoretic.  His medical history is unknown.

The ECG:  This ECG could be considered "classic" for an inferior wall ST elevation M.I. caused by occlusion of the right coronary artery.  ECG findings include:

*   Normal sinus rhythm

*   Marked ST elevation in Leads II, III, and aVF.  The elevation is higher in Lead III than in Lead II, a reliable sign of RCA occlusion.

*   Reciprocal depression in Leads aVL and I.  ST depression in the setting of acute transmural ischemia (STEMI) is almost ALWAYS due to  reciprocal change. The fact that this STD is localized to leads that are reciprocal to the inferior wall is proof of the nature of the STD.

*   Reciprocal depression in V1 - V3.  More localized depression.  What wall is reciprocal to the anterior-septal wall?  The posterior (postero-lateral).  Since the inferior wall is really the lower part of the posterior wall, inferior wall M.I. is often accompanied by posterior wall M.I.

An additional lead, V4R, is helpful in this situation, since the right ventricle is often affected in RCA occlusions.  The EMS crew reports that V4R was negative for ST elevation, but we do not have a copy.

Small q waves have formed in Lead III, and we would watch for progression of this sign, as it can indicate necrosis.

Outcome:  The patient went to the cath lab, but we have no further followup.

 

Our thanks to Ashley Terrana for donating this tracing.

 

 

Dawn's picture

Inferior Wall M.I. In A Patient With Left Bundle Branch Block

Submitted by Dawn on Fri, 12/23/2022 - 14:24

The Patient:    A 64-year-old man complaining of chest pain and shortness of breath for 20 minutes.  Long-standing history of triple vessel disease, severe aortic stenosis, hypertension, thrombocytopenia.  Meds unknown.  He was not considered to be a candidate for valve surgery.

 

The ECG: There is normal sinus rhythm with a rate of 90 bpm.  P waves are not visualized well in all leads, so remember that the three channels of this ECG are run simultaneously.  If you see a P wave in Leads I and II, they are also present in Lead III.  The PR interval is WNL.

 

The QRS complexes are wide, at .122 seconds (122 ms).  The criteria for left bundle branch block are met. (Supraventricular rhythm, wide QRS, upright QRS in Leads I and V6, negative QRS in V1).  The frontal plane axis is within normal limits, but toward the right, at 87 degrees.  The QRS complexes transition at V4 from negative to positive, but Leads V1 – V3 have no initial r waves.  These are possibly pathological Q waves, likely from a past anterior-septal M.I.

 

Dawn's picture

Large Anterior Wall M.I. and Effect of Lead Reversal

Submitted by Dawn on Mon, 05/23/2022 - 15:52

EDIT: Please refer to the comments below this text. The second ECG in this series shows unexpected QRS and ST-T morphology changes, which I tried to explain by way of the patient's long anterior descending coronary artery. However, Dave Richley, who is a very well-known cardiac physiologist and ECG Guru took the time to analyze these morphologies and realize they can be explained by an inadvertent ECG LEAD MISPLACEMENT. This patient does have a proximal lesion of the LAD, proven and repaired in the cath lab. But the inferior wall does not have the injury it appears to have in this second ECG. Thanks to Dave for reminding us to slow down and look closely when things don't look "right".

The Patient:   These two ECGs, taken 26 minutes apart, were obtained from a 50-year-old man who complained of sudden onset of chest pain.  He denied history of coronary artery disease. He was Covid-positive, and the rest of his medical history was unremarkable.

ECG No. 1:  This ECG was obtained by paramedics enroute to the hospital.  For your beginner-level students, it will be easy to demonstrate the large ST elevations in V3 through V6. The machine’s measurements at the bottom confirm that this ECG meets any field criteria for ST elevation M.I. “STEMI”.

But there is so much more to see! Taking a methodical approach, and starting with rate and rhythm, we see sinus bradycardia at 57 bpm. Intervals and frontal plane axis are within normal limits. R wave progression in the chest leads is stalled in V1- V3 due to loss of initial r waves (narrow QS). The transition to positive deflections in V4 – V6 is abrupt.  These q waves in the V1 and V2 appear narrow, but V3 appears to have a Q wave that is almost wide enough to be considered pathological.  Narrow Q waves may be a transient sign of injury, while wide ones (>40 ms) are an ECG sign of necrosis.

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Lateral Wall M.I.

Submitted by Dawn on Tue, 02/22/2022 - 18:09

The patient:   This ECG was taken from a 66-year-old man who was complaining of chest pain at rest. He had been previously diagnosed with lung cancer with metastases to his bones.  The last ECG, taken one week ago, was normal.

The ECG:  There is mild sinus tachycardia at 101 bpm.  The rhythm is regular.  The QRS duration and PR interval are normal, as is the QTc.  The QRS voltage in the limb leads is small, and we do not know the patient’s height and weight.

There are notable ST elevations in I and aVL (high lateral wall) and in V5 and V6 (low lateral wall).  When the high and low lateral walls are similarly affected, we usually look to the circumflex artery as the culprit artery.  We also see ST depression in Leads III and aVF (reciprocal to the STE in I and aVL) and in V1 – V4.  This could indicate subendocardial damage or reciprocal changes.  This ECG meets the criteria for acute lateral myocardial infarction.

The patient was taken to the cath lab emergently.  His coronary arteries, including the left circumflex, all were free of occlusive lesions.  He had no coronary spasm during the procedure, but it was decided that spasm had been the cause of the ECG changes.  His ECG reverted to normal.

It is important to record abnormal findings, as some changes can be temporary or fleeting.  Coronary artery spasm can cause ischemia and damage to the heart, just as plaque lesions and blood clots can.

Dawn's picture

Inferior-posterior Wall M.I. and AV Dissociation

Submitted by Dawn on Mon, 12/06/2021 - 17:59

At the ECG Guru website, our main goal is to provide quality teaching materials to those who teach ECG interpretation and other cardiac topics.  This ECG offers teaching opportunities for those who teach any level of student.

The patient:   This ECG was obtained in the Emergency Department from a 54-year-old man who was complaining of severe chest pain and nausea.  His BP was 130/68.

Dawn's picture

Anterior-lateral M.I. With Wide QRS

Submitted by Dawn on Tue, 11/12/2019 - 23:56

The Patient:  An elderly man presents with chest pain, pallor, diaphoresis and weakness.

The ECG:     The rhythm is normal sinus at a rate of about 76 bpm with normal intervals. The QRS complexes are wide at about .14 seconds (140 ms).  There is ST segment elevation in all precordial leads, except for possibly V6.  The shape of the ST segments in the anterior wall range from coved upward in a “frowning” shape (V1) to very straight (V5 and V6).  There is also ST elevation in aVL with ST straightening in Lead I.  There is ST depression in the inferior leads, II, III, and aVF.  Lead II is equally biphasic while I and aVL are positive, indicating an axis that is shifted slightly to the left.  With his symptoms and this alarming ECG, he was sent promptly to the cath lab.

Interpretation:  The rather obvious ST-elevation M.I. is extensive, covering the entire anterior wall, and extending into the high and low lateral walls . This was confirmed in the cath lab, as the patient had an occlusion of the left anterior descending artery near the bifurcation of the circumflex.  The wide QRS meets the criteria for left bundle branch block (wide QRS, negative QRS in V1 and positive QRS in V6 and Lead I).  However, it doesn’t have the “look” of LBBB with the low-voltage seen in the anterior wall. After the offending artery was opened and stented, the wide complex became narrow and was considered to be an interventricular conduction delay that was due to the ischemia.  The ST depression in the inferior wall is most likely reciprocal.

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Inferior Wall M.I. With Right Ventricular M.I.

Submitted by Dawn on Sat, 10/28/2017 - 18:36

This ECG was recorded from a 75-year-old man with substernal chest pain and diaphoresis.  It shows a pretty classic picture of acute inferior wall M.I. The second ECG is a repeat tracing with the V4 wire moved to the V4 Right position, and it is positive for right ventricular M.I.  The patient was found to have a 100% occlusion of the right coronary artery, which was opened and stented in the cath lab.

There are several other examples of IWMI with RVMI in our archives, so we will confine this commentary to the ECG signs that make these tracings so typical of right coronary artery occlusion. Once you are familiar with the typical pattern of IWMI / RVMI, it is easy to see, even when the ST elevation is subtle (as this one certainly is NOT).

Signs of IWMI in these ECGs are: 

·         ST elevation in inferior leads II, III and aVF.

·         Reciprocal ST depression in leads I and aVL. 

Signs of RVMI in these ECGs are:

·         ST elevation in V4 right.

·         ST elevation in V1 without ST elevation in V2.

Dawn's picture

Simultaneous Occlusions in LAD and Diagonal

Submitted by Dawn on Sun, 07/30/2017 - 16:03

This ECG was obtained from a 35-year-old man who was complaining of crushing substernal chest pain which radiated down his left arm for the last ten minutes. He was diaphoretic, and described his pain as a “10” on the 1-10 scale. He got only modest relief from IV fentanyl.

He was transported to a full-service cardiac hospital, where he underwent angioplasty of simultaneous 100% occlusions of his proximal left anterior descending artery and diagonal artery. He was noted to have apical akinesia with a 35% ejection fraction.

He continued to improve following angioplasty, and was discharged home with an external defibrillator vest.

The ECG shows ST elevation in V2, V4, V5, and V6, which makes us suspect that the V2 and V3 wires were switched accidentally.  This reflects damage in the anterior wall of the LV. There is also very marked ST elevation in I and aVL, reflecting damage in the high lateral wall. There is reciprocal ST depression in the inferior leads aVF and III.  Fortunately, there are no pathological Q waves, which would indicate permanent damage from necrosis of the myocardium.

You can see films from his procedure in Heart Art, labeled “Simultaneous Occlusive Lesions in LAD and Diagonal”.

Dawn's picture

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

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