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Myocardial infarction

Inferior-lateral M.I. With QRS Fragmentation

Sat, 08/13/2016 - 23:33 -- Dawn

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.

Second-Degree AV Block, Type I

Sat, 06/13/2015 - 22:07 -- Dawn

This ECG is from an 80-year-old woman who had an acute inferior wall M.I. with a second-degree AV block.
Some people incorrectly call ALL second-degree AV blocks that are conducting 2:1 "Type II".  This is incorrect, as Mobitz Type I can also conduct with a 2:1 ratio.  The progressive prolongation of the PR interval will not be seen with a 2:1 conduction ratio, because there are not two PR intervals in a row.

This is a good example of a Type I, or Wenckebach, block which is initially conducting 2:1.  At the end of the ECG, two consecutive p waves conduct, showing the "progressively-prolonging PR interval" hallmark of a Type I block. Type I blocks are supraHisian - at the level of the AV node - and generally not life-threatening.  Blocks that are conducting 2:1 present a danger, however, in the effect they have on the rate.  Whatever the underlying rhythm is, the 2:1 block will cut the rate in half!  This patient has an underlying sinus tachycardia at 106, so her block has caused a rate of 53.  In light of her acute M.I., that rate is probably preferable to the sinus tach. This patient’s BP remained stable, and she did not require pacing. 

The ST signs of acute M.I. are rather subtle here. Note the "coving upward" shape in Lead III, and the reciprocal depressions in I, aVL, V1, and V2.  Type I blocks are common in inferior wall M.I., since the AV node and the inferior wall often share a blood supply - the right coronary artery. 

While the print quality of this ECG is not the best, it is a great teaching ECG because it starts out with 2:1 conduction, then at the end of the strip, proves itself to be a Wenckebach block.   

Inferior-Lateral M.I.

Sun, 03/29/2015 - 21:41 -- Dawn

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. 

Circumflex Occlusion with Posterior-lateral M.I.

Thu, 03/12/2015 - 13:00 -- Dawn

This ECG was obtained from a woman with chest pain who was taken to the cath lab and found to have a 100% occlusion of her circumflex artery.  

There are obvious ST segment elevations in Leads I and aVL, as well as in Lead II.  Lead II is the most leftward of the inferior wall leads, and I and aVL reflect the high lateral wall. She also has ST depressions in V1 through V3.  If you look closely at the R wave progression in the anterior leads, you will readily note that it appears that V1 and V3 wires have been reversed.  That being said, the "real" V2 and V3 have taller-than-normal R waves.  The tall R waves and ST depression are signs of "posterior wall M.I."  Recently, the actual definitions of the "lateral" wall and "posterior" wall have come into question.  However, the important thing clinically, is that this patient IS experiencing an ST elevation M.I. (STEMI), which was confirmed in the cath lab.  The locations of the ST changes were consistent with the 100% occlusion of her circumflex artery.

For our more advanced readers (and our "Gurus"), there is an interesting rhythm.  The P wave morphology changes frequently, even though the rhythm remains regular.  The rate, at 62 BPM, was adequate, and the patient did not suffer any consequential dysrhythmias during her procedure.  We don't have long-term followup information on her.


Anterior Wall M.I.

Sun, 02/08/2015 - 23:33 -- Dawn

This ECG was taken from a 60 year old man who was complaining of severe substernal chest pain, radiating to his left arm and a non-productive cough.  There was some initial discussion among the EMS crew  about the possibility of the ECG showing a "benign early repolarization" pattern because of the concave upward ("smiling") ST segments.  They also considered a diagnosis of pericarditis, because the ST segments seem widespread.  The baseline artifact makes it difficult to evaluate for PR segment depression or Spodick's Sign.

The patient's age (60 years) and troubling symptoms (chest pain radiating to the left arm) ruled out BEP for the paramedics.  The ST segment elevations are pretty widespread - Leads V3, V4, V5, V6, I and II all show some STE.  There are also "hyperacute" T waves in the leads with STE.  There are ST abnormalities ranging from flattening of the shape to depression, but the bottom line is this patient is a 60-year-old man with substernal chest pain radiating down his left arm!

The patient was treated in the ambulance with chest pain protocols, and was transferred to a hospital with an interventional cath lab.  The patient was conculusively diagnosed with an acute M.I. and underwent angioplasty.

This is a good ECG to demonstrate subtle changes when, combined with patient presentation, can help us diagnose a coronary event.  It helps us emphasize that not all STEMIs will have dome-shaped, "tombstone" ST segments, and that patient symptoms, history, and age are important to consider.

Teaching Series: Anterior Wall M.I.

Tue, 01/27/2015 - 23:31 -- Dawn

A series of ECGs can be a valuable addition to any teacher's collection.  This series follows a 75-year-old woman through three days, during which she experienced an acute anterior wall M.I., a catheterization with angioplasty and stents placement.

In the first ECG, taken at 4:09 am, the patient has presented to the Emergency Dept. with a complaint of chest pain. (Other details are no longer available).  Although there is some baseline artifact, it appears that the rhythm is sinus rhythm with one PAC (7th beat).  There is subtle but measurable ST elevation in V1, V2, and V3 (anterior-septal leads).  The shape of the STE in V1 is noticeably coved upward.  Even aVR has some STE, with coving.  There is equally subtle ST depression in Leads II, III, and aVF (inferior leads).  Fortunately, there are no pathological Q waves at this point, which would be an indication of necrotic tissue in the area of the M.I. (anterior-septal wall).

The patient was taken to the cath lab, where it was found that she had a 100% mid-left anterior descending artery occlusion, which was opened and stented.  She also was found to have widespread coronary artery disease, with the left circumflex artery 25% occluded (stented), the right coronary artery (which was dominant) proximately occluded 50% and stented, and the posterior descending artery 75% occluded (stented).

The second ECG, taken at 6:29 the same morning, after the cath procedure, shows some ST elevation with coving remaining in V1 through V3, and also aVR, but now with the loss of R waves in V1 and V2 and loss of R wave voltage in V3.  This represents the formation of pathological Q waves, and can be a permanent change in many cases.

The third ECG, taken two days later in the cardiac step-down unit, shows improvement, and progression toward healing.  The ST segments are still shaped in a slightly coved-upward shape, but they are less elevated.  The R waves have returned.  The T waves in V1-V3 are inverted.  The deeply inverted T waves of V2 and V3, especially, and classic for ischemia, and we even see the "ischemic zone" extending across the anterior-lateral wall, including V4 through V6 and Leads I and aVL.

The patient did very well to discharge, and we don't have followup after that.



Extensive Anterior-lateral M.I. With Right Bundle Branch Block

Sun, 11/16/2014 - 13:10 -- Dawn

This ECG depicts an extensive and ultimately, fatal, injury.  There is marked ST segment elevation in Leads V2 through V6 (anterior wall).  There is also ST elevation in Leads I and aVL (high lateral wall).  The ST elevation in aVR is indicative of a very proximal lesion in the left coronary artery, which supplies the anterior wall, including the anterior portion of the septum, the high lateral wall, and, in this case, the low lateral wall.  The inferior leads, II, III, and aVF, show reciprocal ST depression.

This is an old ECG - the computer readings of the rate and intervals is lost, as is the grid.  But the rate here appears to be about 80 bpm and the QRS is widened.  There is a right bundle branch block ECG pattern, which is not surprising given the extensive septal damage.  Normally, the criteria for RBBB on the ECG includes an rSR' pattern in V1 (seen here) and a small, wide s wave in Leads I and V6.  This s wave is not seen here, presumably due to the effects of the ST elevation in those leads.

What matters clinically in a patient like this is not whether there is RBBB or another type of interventricular conduction delay. This patient needs immediate restoration of blood flow through the LCA and intensive medical/nursing care.  As mentioned before, this patient did not survive, in spite of being brought to a hospital.  We do not know the exact mechanism of death or treatment course in this case.

If you are teaching students to use multiple leads in assessing rhythm, this is a great example of how one or two leads can be very misleading.  I have used this ECG's V4 in an excercise illustrating this concept.  Shown V4, many people would call this "AIVR" or "V Tach".  Seen in context with the other leads, it is obvious that we are looking at ST elevation that is as high as the R wave.  Two leads are better than one, and twelve are better than two.



Teaching Series 1113: ECG 1 of 6 - Acute Anterior Wall M.I.

Sun, 12/15/2013 - 19:16 -- Dawn

This is the first of six ECGs donated to the ECG Guru by our friend, Jenda Enis Štros. 

The patient is a man in his 60's with chest pain.  This is a pre-hospital ECG showing ST elevation across the anterior wall, beginning in V2.  Though the upwardly-concave shape "smile" appears rather benign, the amount of j-point elevation in these five related leads - in a man with chest pain - does not favor a diagnosis of early repolarization. The diagnosis is STEMI, and the cath lab is activated.

Links to the entire series of six ECGs:


Teaching Series 112213 Inferior-posterior Wall M.I. With Right Ventricular M.I.

Tue, 12/03/2013 - 21:21 -- Dawn

This series of ECGs was taken during ambulance transport of a 67 year old man with chest pain.  Earlier the same week, this man had been discharged from the hospital after having a cardiac cath, angioplasty, and stents. He was discharged the next day.  The patient stated that, until that hospital admission, he was healthy, athletic, and had no significant medical history.  He is currently taking a statin, atenolol, and "one of the new blood thinners" - he didn't know the name.

 ECG No. 3 is the first one shown here, taken at almost 39 minutes after midnight.  The patient was complaining of chest pain of 8 on a 1-10 scale.  His skin was pale, cool, and clammy.  The ECG shows acute inferior-posterior M.I., with ST elevation in II, III, and aVF and reciprocal ST depression in V2, and V3.  V1 would normally be depressed in posterior extension of an inferior wall M.I. - unless the right ventricle is also infarcted.  The message from the right ventricle to V1 would be "elevate", countering the message from the posterior wall, "depress".   The rhythm is sinus with ventricular bigeminy.  The rescue crew notified the hospital of a "STEMI Alert". The patient received I.V., O2,  nitroglycerin spray and paste, as well as aspirin.  The patient's BP was 144/92.

ECG No. 4 was taken at 12:41 a.m.  It shows a change in P waves probably reflecting a low atrial focus.  The patient has a slow underlying rhythm with ventricular bigeminy that is probably multifocal.  It is very hard to determine multifocal PVCs when there is no concurrent rhythm strip, but this is a three-channel ECG machine, and the rhythm strips are run separately from the 12-lead.  There are runs of V Tach toward the end of the ECG, and this is not a good sign in a patient with ST elevation.  In some cases, the V Tach can become persistent, in others it is transient.  The ST elevation and reciprocal depressions are still evident.

ECG No. 5, taken at 12:49 a.m., shows further development of the ST segments, and the classic "domed" shape of STEMI.  In addition, a pathological Q wave has appeared in Lead III, possibly indicating permanent damage from this M.I.  In this ECG, the paramedics have moved the V4 wire to the V4 Right position to better view the right ventricle.  V4 Right is slightly elevated, and definitely dome-shaped, like a frown.  This is an indication that the RV is injured, and medications that lower BP (especially nitroglycerin) should be avoided in the pre-hospital setting because of the danger of loss of preload of the RV and sudden drop in cardiac output. The patient's BP at this time was 138/85.

Acute Lateral Wall M.I.

Sat, 09/21/2013 - 22:45 -- Dawn

This week's ECG for your collection was kindly donated by Dr. Stasinos Theodorou, interventional cardiologist with the Limassol Cardiology Practice in Cyprus. It offers a wonderful teaching opportunity, and illustrates how valuable an ECG can be in locating a lesion during an M.I.   Dr. Theodorou previously posted this ECG and the angiograms from the same patient on FaceBook, and he has offered them to the users of the ECG Guru website  free of copyright.

Dr. Theodorou reports that the culprit lesion in this M.I. was initially very difficult to find on angiogram.  In this case the culprit was an ostially occluded second diagonal artery which, due to the anatomy, was almost impossible to spot from the initial diagnostic images.  There was no "stump" because the occlusion was in the ostium - the beginning of the artery.  The patient also had a significant right coronary artery lesion, but it was not the cause of the M.I. because the RCA perfuses the right ventricle and inferior/posterior wall of the left ventricle.  The ST elevation in this ECG is in I and aVL - the area of the high lateral wall.  Because the  ECG appeared to be inconsistent with the angiogram, Dr. Theodorou obtained further projections, allowing him to identify and treat the offending lesion.  This illustrates the importance of the ECG in locating coronary artery lesions, even in this age of high technology and cath labs.  The interventional cardiologist's proficiency in ECG interpretation enabled him to find this "invisible" lesion.

We are grateful to Dr. Theodorou for sharing this valuable learning experience with us.  You can find more from Dr. Theodorou on his website, FaceBook page, and here, on our "Ask the Expert" page.


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