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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.

Dawn's picture

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

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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