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

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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Anterior-lateral M.I. With Wide QRS

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 Atrial Fibrillation or Atrial Flutter

The Patient   This ECG was obtained from a 74-year-old man who had a history of COPD. He was complaining of severe chest pain at the time of the ECG.

The ECG     The rhythm is atrial fib or flutter (the R to R intervals are irregular, but seem to repeat about 4 interals).  Flutter waves are seen during some of the longer intervals. The rate is approximately 90 beats per minute.  The ST segments are very noticeably elevated in Leads II, III, and aVF.  There is reciprocal ST depression in Leads I and aVL, and also in all the precordial leads. 

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Anterior Wall M.I. With Ventricular Bigeminy

The Patient     This ECG was obtained from a 51-year-old man who presented to EMS with acute chest pain. He had a history of hypertension, 40 pack-year smoker.

Hospital Course     He was diagnosed with anterior wall STEMI and taken to the cath lab.  He was rated Killips Class 1 (no evidence of congestive heart failure), TIMI risk score 4  (14% risk of all-cause 30-day mortality).  He underwent primary percutaneous coronary intervention (PCI) of the proximal left anterior descending coronary artery (LAD).

Ten days post PCI, the patient had ventricular arrhythmias and went into cardiac arrest, but was resuscitated. He continued to have occurrences of non-sustained ventricular tachycardia (VT), progressing to sustained VT.  Electrolytes were monitored and corrected when necessary. The patient expired before any further diagnosis was made.

ECG Interpretation    The rhythm is sinus at a rate of about 80 bpm (first two beats).  The PR interval is about .18 seconds.  The QRS duration is about .10 seconds.  After the second sinus beat, ventricular bigeminy occurs. Every other sinus beat is obscured by the PVCs.  By the end of the strip, the underlying sinus rhythm has slowed slightly.

The ECG signs that the ectopic beats are ventricular are:  lack of P waves associated with the premature beats, QRS width about .16 seconds, and compensatory pauses.  The axis of the sinus beats is around 60 degrees (normal), but the axis of the premature beats is difficult to determine due to the low voltage and biphasic QRS complexes in the frontal plane leads.  It is also difficult to determine ST and T wave changes in the PVCs for the same reason.

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Catastrophic Event With Bradycardia

The Patient:    Paramedics were summoned to the home of a 74-year-old woman who had a complaint of shortness of breath.  She was found sitting, alert and oriented, with labored respirations at 30/min. She stated that the shortness of breath came on suddenly. She denied any cardiac or pulmonary medical history, and said she took no medications. The patient was ambulatory.  Her skin was cool and moist.  Her SpO2 on room air was 85%, improving to 90% on oxygen via 15 lpm non-rebreather mask.  Her lungs sounded clear.

 

When the patient was moved to the transport vehicle, she suddenly became nonverbal, with a leftward gaze. Her pupils were noted to be unequal and non-reactive (we do not know which was larger).  Her BP was 67/43.

 

During transport, her heart rate declined into the 20’s and became apneic and pulseless.  Recorded BP was 46/25. CPR was done until and after arrival at the hospital, where efforts to resuscitate were halted after some time.

 

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Myocardial Infarction With Non-obstructive Coronary Arteries

This ECG was obtained from a 37-year-old male who was complaining of non-radiating substernal chest pain.  He offered no significant medical history.  He denied taking any medications.  He was hypertensive and bradycardic on arrival in the Emergency Dept. He was alert and ambulatory.  Approximately 20 minutes after first being seen by paramedics, he suffered an episode of ventricular fibrillation in the E.D.  He was resuscitated and sent to the cath lab.  His coronary arteries were without lesions.  We do not know the results of any lab tests, including troponins.

What does the ECG show?  The rhythm is sinus bradycardia at a rate of 48 bpm. The PR, QTc, intervals and QRS duration are normal.  The QRS frontal plane axis is normal and there is good R wave progression in the precordial leads.  There is ST segment elevation in Leads I, aVL, V2, and V3, with reciprocal ST depression in Leads III and aVF.  The ST segments that are elevated retain a relatively “normal” shape, being concave upward. There are no abnormal T wave inversions or pathological Q waves.

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Acute M.I. With Right Bundle Branch Block and Atrial Pacing

This ECG was taken from a 78-year-old man who was experiencing chest pressure in the morning, after having left shoulder pain since the night before. He has a history of hypertension and hypercholesterolemia, and has an implanted pacemaker.

What does the ECG show?  The ECG shows an atrial paced rhythm, with two premature beats, beats number 5 and 12.  These are probably PVCs.  The patient has a functioning AV conduction system, so the paced atrial beats are conducting through the AV node and producing QRS complexes.  In the interventricular conduction system, the impulse encounters right bundle branch block. This causes each QRS to have an “extra” wave attached at the end, representing slightly delayed depolarization of the right ventricle.  Instead of an “rS” pattern in V1, for example, we see “rSR’ “.  The slight delay causes the QRS to be widened, as we are measuring the two ventricles separately, rather than synchronously.

There is definite ST segment elevation in V2 and V3, and the shape of the ST segment is straight, having lost it’s normal “concave upward” appearance.  In an ECG taken three minutes later, the STE extends to V4.

Do the pacemaker or the right bundle branch block prevent us from diagnosing an ST-elevation M.I.?  The answer to that is a resounding “NO!” Pacemakers can sometimes make it difficult to assess ST elevation because ventricular pacing causes ST segment changes.  Pacing the right ventricle causes a depolarization delay in the left ventricle as the impulse travels “cell to cell” across the LV.  This means an RV-paced beat will resemble a PVC from the RV.  When LV depolarization is altered, repolarization will also be altered, causing ST elevation in leads with negative QRS complexes, and ST depression is leads with upright QRSs. These are called discordant ST changes. These changes are proportionate to the height or depth of the QRS, with very minimal or no ST changes in leads with short or biphasic QRS complexes.  We don’t have to worry about that in this situation – the pacemaker is not pacing the ventricles.

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Takotsubo Cardiomyopathy

This ECG is taken from an elderly woman with chest pressure radiating to left shoulder for 30 minutes.  She also complained of nausea with vomiting.  Her family offered a history of  unspecified cardiac disease, hypertension, hypercholesterolemia, and dementia.

The ECG shows ST elevation in Leads I and aVL, with reciprocal ST depression in Leads III and aVF.  ST segments have an abnormally flat shape in Leads aVL, II, III, aVF, V5 and V6.

She was admitted to the hospital and sent to the cath lab.  Her arteries were found to be clear, and Takotsubo cardiomyopathy was diagnosed.  See also.

 

Our thanks to Lew Steinberg and Palm Beach Gardens Fire Rescue for donating this interesting ECG.

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Simultaneous Occlusions in LAD and Diagonal

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”.

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Brugada Pattern

This patient is a 50-year-old man with a history of epilepsy and early dementia. He had a VP shunt placed in the hospital and was then discharged home.  He became extremely weak, which was not characteristic of him, and 911 was called.  He was transported to the hospital uneventfully. He was found to be afebrile.

This ECG shows a “classic” Brugada pattern. Brugada Syndrome is a hereditary disease that is associated with a high risk of sudden cardiac death. It is due to a mutation in the sodium channel gene (channelopathy). The ECG characteristics are:

·         ST elevation in V1 through V3 of at least 2 mm at the J point in the right precordial leads (V1-V3).

·         Coved upward ST segments with  negative T waves in the affected leads.

Brugada Syndrome is diagnosed when the ECG pattern exists with one of the following:

·             Polymorphic ventricular tachycardia (VT).

·             Documented ventricular fibrillation.

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