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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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ECG Teaching Series: ST Elevation M.I. With Hyperacute T waves

Submitted by Dawn on Sat, 06/21/2014 - 13:23

This series shows the evolution of ECG changes in anterior wall M.I. secondary to occlusion of the proximal left anterior descending artery.  The patient is an 88-year-old woman with chest pain.  She was designated a "cardiac alert" from the field by paramedics.  Her proximal LAD was opened and stented in the cath lab.  We do not have follow-up information on her.

The first ECG in the series, titled "12-Lead 3", shows ST elevation at the J point in V1 through V3.  In addition, the T waves are "hyperacute" - tall, broad, and asymmetrical. This can be an early, transient sign of myocardial injury.  Slight reciprocal depressions are seen in the inferior leads.  Lead V4 has a T wave inversion that is out of place with the progression of the T waves in V3 and V5.  Lead placement may be to blame.  Hyperacute T waves in a patient with chest pain should be taken very seriously.

The second ECG, titled "12-Lead 4", shows continued elevation at the J point in Leads V1 through V3, with a lessening of T wave amplitude.  In addition, Lead aVL is showing some T wave changes. The T wave is biphasic, and may be about to become inverted.  This is not an improvement!  V1 through V3 show us the anterior-septal wall, and an M.I. here indicates occlusion in the LAD.  Leads I and aVL show the high lateral area of the anterior wall, and damage here is an indicator that the occlusion is proximal.

The third ECG, titled "12-Lead 5", shows a "maturing" of the ST segment elevation.  Even though there is some significant artifact, we can see that the ST segment in V1 is coved upward, and the ST segment in V2 is flat.  Both shapes are abnormal, and a sign of CAD.  The T waves have become less pronounced, but V2 looks as if the T wave may become inverted in the near future.  V3 looks improved in this image.

The patient's clinical symptoms did not improve during these ECG changes.  Hyperacute T waves are not a definitive sign of STEMI, but they provide a highly visible warning that may catch attention.  They definitely are an indication to run serial ECGs, as these paramedics did.

 

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Acute Anterior-Lateral Wall M.I.

Submitted by Dawn on Fri, 04/25/2014 - 14:01

This week's ECG is from a 47-year-old man who experienced a sudden onset of chest pain while mowing his lawn.  He went on to suffer a cardiac arrest and was resuscitated.  We do not have long-term followup on his outcome.

The experienced person will have no difficulty identifying a large acute antero-lateral wall M.I.  There are massive ST segment elevations in Leads V1 through V6, reflecting acute injury from the septal side of the anterior wall (patient's right) to the anterior-lateral wall (patient's left).  There are also ST elevations in Leads I and aVL, reflecting the high lateral wall.  This indicates, and was confirmed in the cath lab, that the lesion is proximal - at or above the bifurcation of the left anterior descending artery and the circumflex artery.  The ST depressions in the inferior wall leads (II, III, and aVF) likely represent reciprocal changes.  You will note that the ST depression in Lead III has a very similar shape to the ST elevation in Lead aVL.

More bad news for this patient is the presence of pathological Q waves in Leads V1 through V4, reflecting transmural death of the myocardial tissue.  This causes akinesis and poor left ventricular function.  In addition, it's not only muscle tissue that dies, but also electrical structures , such as bundle branches.   Papillary muscles can be infarcted, causing valve malfunction.  And remember, all patients who have ST elevation due to acute injury are vulnerable to ventricular tachycardia and ventricular fibrillation, due to re-entry mechanisms in injured tissue.   

This ECG will allow instructors to discuss with their students:

*  which leads reflect changes from which parts of the heart

*  what the ECG signs of acute M.I. are

*  the pathophysiology of pathological Q waves

*  the effect of damage to various parts of the heart on the patient's condition and symptoms

This "classic" M.I. pattern should be taught to all health care professionals who work in settings where ECG is used.

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Acute Inferior Wall M.I.

Submitted by Dawn on Tue, 04/15/2014 - 00:08

Another great ECG donated by Paramedic Eric Testerman.  This ECG is from a 66 year old man who was complaining of feeling dizzy, weak, and of having "minor" chest pain. He was extremely pale/ashen, had moderate cyanosis, and was very clammy and diaphoretic.  His initial heart rate was about 20 bpm.  His initial BP was 131/113 then, just before arrival at the hospital was 127/85. His HR increased to about 50 bpm (not shown). He was given 400 ml I.V. fluid, 324 gr of aspirin, and oxygen.  Transcutaneous defibrillator/pacemaker pads were applied. 

At the hospital, he was successfully treated with angioplasty for a 100% occlusion of the right coronary artery. The time from beginning of treatment to reperfusion of the artery was 47 minutes, which is very good! 

This is a "classic" inferior wall M.I., with ST elevation in leads II, III, and aVF. There are reciprocal ST depressions in I and aVL.  There are also ST depressions in V1 through V5.  This is generally considered to represent reciprocal ST changes in the posterior and lateral walls.There is a quite severe bradycardia, and the patient's skin showed signs of poor perfusion. Amazingly, the patient's BP stayed adequate during transport.  Bradycardia is common in inferior wall M.I. due to ischemic effects on the SA node and vagus nerve (sinus bradycardia) and the AV node (heart block).  In this case, the rhythm is sinus bradycardia.  The heart rate is in the 20's, and the PR interval is around .20 - .22 seconds. 

Dawn's picture

Anterior Wall M.I.

Submitted by Dawn on Wed, 03/05/2014 - 21:27

A 78-year-old woman complained of nausea and diaphoresis.  Paramedics in the field found that her 12-lead ECG showed ST elevation in V1 through V4, aVL, and aVR.  The patient denied chest pain and also denied any cardiac history.  She did not want to be transported to the hospital, but thankfully, the paramedics understood that this was not an option, and convinced her to go.

She was taken to a cardiac facility as a STEMI Alert, was evaluated in the cath lab, and sent immediately to the O.R. for coronary artery bypass surgery.  She had severe multi-vessle disease and a lesion in her proximal left coronary artery.  No other details of the cath results are known.

Some important teaching points:

  • there is subtle ST elevation in V1 and V2, but the SHAPE of the ST segment is suspect, with flattening and almost a coving upward shape in V1.  Normal ST segments are convex downward, like a smile.
  • there is nearly complete loss of r waves in V1 and V2, and V3 and V4 have very small r waves.  This signals impending pathological Q waves, a sign of necrosis of the myocardium.  Necrotic muscle does not contract.
  • there is slight ST segment elevation in aVR.  Along with STE in V1, this is a marker for proximal LCA or left main occlusion.
  • the ST elevations in V3 and V4 are more pronounced, and easily meet STEMI guidelines:  currently 1.5 mm of elevation in V3 and 1 mm of elevation in V4 for a woman.
  • there are reciprocal ST depressions in II, III, and aVF - common in AWMI.
  • aVL has slight STE, along with inverted T waves. Somewhat surprisingly, there is no ST depression in Lead I.  This indicates high lateral wall injury.
  • the patient has a "hint" of the criteria for LVH:  her S wave in V3 + her R wave in V5 = about 33 mm, and there is depression in V6.  A stretch to call it "LVH", but possibly a sign of left ventricular strain because of the acute M.I.
  • there are atrial abnormalities suggested by the tall, peaked P waves in Lead II, the "M" shaped P waves in Lead III, and the inverted P waves in V1 and V2.  Possibly bi-atrial dilation and stress brought on by the M.I.?  An echocardiogram would be a better test for this.
  • the heart rate, at about 90 bpm, reflects NSR but is a cause of more stress on an overworked, injured heart.

This is a great teaching ECG, and we hope the Gurus out there will add even more interesting points to consider.

Dawn's picture

Teaching Tips: ECG Series WO 118: STEMI With Changing ST Elevations

Submitted by Dawn on Thu, 01/23/2014 - 23:15

Continuing with our theme of using  series of ECGs for teaching, we present the case of an 83-year-old woman with weakness, chest pain, and near-syncope.  The first ECG, taken by paramedics at her home, shows a sinus rhythm with a slightly wide QRS complex.  At this point, it is unclear whether this represents left bundle branch block or a non-specific interventricular conduction delay. There is the most subtle ST elevation in Leads III and aVF. In LBBB without acute M.I., we would expect the ST segments to be discordant, or opposite, the QRS complexes.   Even more informative is the reciprocal ST depression in Leads I and aVL (and a little in V2).  This can be a sign of inferior wall injury that shows up earlier than ST elevation in the inferior leads.

ECG number 2 was taken during transport to the hospital.  The chest pain continues, and now the ST elevation in the inferior leads is pronounced, and the reciprocal depression in I, aVL, and V2 has also become much more obvious.  V1 would also normally show this depression - a sign of the injury traveling up the back of the inferior wall (posterior).  But if the right ventricle is injured, V1 will have ST elevation.    V1 in this case is probably reflecting the depression from the posterior wall AND the elevation from the right ventricle.  The ST elevation is now prominent enough that the paramedics notified the hospital of a "STEMI Alert".  The QRS remains widened at .13 sec., but the ST elevations and depressions are not opposite the QRS direction, which would be typical for LBBB without an M.I.  Therefore, even if LBBB is present, these ST elevations and depressions would be considered a sign of STEMI.  The rate is slowing in this ECG.

ECG number 3 was taken in the Emergency Department.  The patient's symptoms continued.  The bradycardia is still present, as is the QRS widening.  Now, something new has shown up:  prominent U waves in the precordial leads.  There appears to be T-U fusion.  We do not know the patient's medications or lab results, so the most likely cause for the prominent U waves is the bradycardia.  She does not have other ECG signs of hypokalemia, which is one of the many causes of U waves. 

Dawn's picture

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

Teaching Tip: A Series of ECGs Can Tell A Story

Submitted by Dawn on Fri, 12/20/2013 - 11:16

When teaching ECG, I always try to make the ECG interpretation have some practical context for the student.  Why study squiggly lines, if they don't mean something to our care of our patients?  Even putting a simple scenario (actual or invented) with an ECG can make it more relevant for your students.  A series of ECGs taken as the patient undergoes changes, is especially helpful.

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Teaching Series 1113: ECG 4 of 6 - Acute Anterior Wall M.I.

Submitted by Dawn on Sun, 12/15/2013 - 20:07

Continuing our teaching series of ECGs donated by Jenda Enis Štros, ECG 4 of 6 shows a new occurance of huge T wave inversions in the precordial leads.  Since this is the area that was stented (left anterior descending artery, anterior wall of the LV), we immediately should think of re-occlusion of the artery.  In a newly-placed stent, the danger is thrombosis (blood clot).  The patient had no chest pain at this time.

Here are links to all six of the ECGs in this series:

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-1-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-2-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-3-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-4-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-5-6-acute-anterior-wall-mi 

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-6-6-acute-anterior-wall-mi

 

Dawn's picture

Teaching Series 1113: ECG 3 of 6 - Acute Anterior Wall M.I.

Submitted by Dawn on Sun, 12/15/2013 - 19:28

This is ECG 3 in a series of 6 ECGs donated to the ECG Guru by Jenda Enis Štros. The left anterior descending artery occlusion has been confirmed in the cath lab, and angioplasty with stent placement has been performed.  Post-stent, there are T wave inversions in the precordial leads (V Leads), which is an evolutionary change during the recovery phase of acute ST elevation M.I. 

Here are the links to all six ECGs in this series:

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-1-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-2-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-3-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-4-6-acute-anterior-wall-mi

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-5-6-acute-anterior-wall-mi

 

http://www.ecgguru.com/ecg/teaching-series-1113-ecg-6-6-acute-anterior-wall-mi

 

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