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ST elevation

Instructors' Collection ECG of the WEEK: Acute M.I. In Patient With Pacemaker

Wed, 01/04/2017 - 21:07 -- Dawn

This ECG is taken from an elderly man who has a history of complete heart block and AV sequential pacemaker.  On the day of this ECG, he presented to the Emergency Department with chest pain and shortness of breath. His vital signs were stable and within normal limits.  We do not have information about his treatment or outcome. 

I don’t see spikes.  How do we know this is a paced rhythm?  The ECG clearly shows the presence of an AV pacemaker.  There are very tiny pacer “spikes”, probably best seen in Leads III, aVF, aVL, and most of the precordial leads.  Other ECG signs that this is a paced rhythm are:  wide QRS at about .16 seconds (160 ms); abnormal left frontal plane axis; regular rhythm with AV dissociation (there are P waves seen occasionally that have no fixed relationship to the QRS complexes).  Also, V6 is negative.  That rules out left bundle branch block unless the electrodes are misplaced.  There are no capture beats in this strip.  The patient appears to be, at least right now, 100% dependent on the paced rhythm. 

Why does the presence of a pacemaker make it harder to diagnose an M.I. from the ECG?  Wide-QRS rhythms, such as right-ventricular paced rhythms, left bundle branch block, and ventricular ectopic rhythms, usually have “discordant ST and T wave changes”.  That is, when the QRS is positive (upright), the ST and T wave are negative.  The reverse is also true:  when the QRS is negative and wide, the ST and T wave changes are positive (ST elevation).  This is not true for right bundle branch block because the conduction delay that causes the widening of the QRS is in the right ventricle, and the ST segment is reflecting the LEFT ventricle’s repolarization.  Discordant ST changes can make it difficult to determine from the ECG alone that there is an ST elevation M.I. (STEMI).  Diagnosis usually must be made from patient presentation, ECG changes over time, and cardiac enzymes – or more definitively from cardiac angiogram. Pacemakers that produce narrow QRS complexes do not cause discordant ST changes. 

 Can we see an M.I. on this ECG?   Remember that this patient was complaining of chest pain.  Fortunately, his STEMI is pretty easy to see on the ECG.  He has ST ELEVATION in leads where there should be ST depression.  That is, the wide-QRS complex paced rhythm has POSITIVE QRS complexes in Leads I and aVL – he should have ST DEPRESSION from the paced rhythm.  Instead, he has ST ELEVATION.  This is anterior-lateral STEMI. Lead III shows ST depression where we would expect to see elevation.  This is a reciprocal change caused by the M.I.   Also, Leads V2 through V6 have ST ELEVATION that is more pronounced that one would expect from a paced rhythm alone.  

Teaching Series: Acute Anterior Wall M.I.

Sun, 06/26/2016 - 15:33 -- Dawn

Intermittent chest pain.     This series of three ECG were taken from a 41-year-old man with a two-week history of intermittent chest pain.  At the time of the first ECG, 12:05 pm, he was pain-free.  We see a sinus tachycardia at 102 bpm, and has just come under the care of paramedics. There is a very subtle ST sagging and T wave inversion in Lead III, and no other ST changes. He had an uneventful trip to the hospital.

On arrival at the Emergency Department, just before he was unloaded from the ambulance (12:15), he experienced chest pain.  An ECG was obtained, which shows ST elevation in V1 through V4, as well as in Leads I and avL.  There are reciprocal ST depressions in Leads III and aVF. 

The patient was taken into the ED, where his symptoms abated, and a third ECG was obtained (12:19). The third ECG looks very much like the first one. V5 and V6 have T waves that appear flat, or even inverted, but there is some baseline artifact making it hard to see them. 

Diagnosis confirmed       Based on the patient’s presentation, and the second ECG, he was taken immediately to the cath lab. A 100% occluding lesion with a clot was discovered in the mid LAD.  The clot was removed with suction, and the lesion stented.  A 40% narrowing was discovered in the RCA. 


Repeat ECGs whenever possible       This series of ECGs offers a compelling argument for performing repeat ECGs.  This can be especially important when symptoms are waxing and waning.  Sometimes, a clot can completely occlude an artery, then “float” to another position, allowing blood flow to resume.  Sometimes, the artery constricts around the lesion, causing occlusion, then relaxes.  Had the rescue crew not repeated the ECG at 12:19, there may have been a delay in this young patient receiving interventional care.

Subtle ST Changes

Mon, 04/11/2016 - 19:18 -- Dawn

This ECG is from a 65-year-old woman who presented to the Emergency Department with a complaint of chest pain.  We have no other clinical information. 

There are several subtle, but real, abnormalities on the ECG that should be evaluated in conjuction with her clinical situation.  This is a good ECG to discuss with your more advanced students who have mastered recognition of blatant ST elevation M.I. (STEMI).  But, let’s start with what is NORMAL here. 

NORMAL FEATURES        The normal findings are:  normal sinus rhythm at about 68 bpm.  The rhythm is regular without ectopy. The intervals are within normal limits.  The frontal plane axis is normal. The T waves are all upright. 

ABNORMAL FEATURES         There is subtle ST segment elevation in Leads V1 through V3, and in I and aVL.  The shape of the ST segments is concave upward, or normal.  In a young, asymptomatic patient, we probably would not be at all concerned about this amount of ST elevation.  However, this is an older patient with chest pain. In the chest leads, the R wave progression is interrupted, as the QRS goes abruptly from negative to positive in Lead V3.  This could be due to loss of r waves ( pathological Q waves forming) in V1 and V2 lead placement, or something else. 

In addition, the inferior leads (II, III, and aVF) show ST flattening, with ST depression in Lead III.  Probably the best way to approach such subtle changes in a symptomatic patient is to repeat the ECG frequently while initiating evaluation and treatment of the chest pain.  Often, ST segments will change rapidly during an ischemic episode.  Lead aVL appears to have a pathological Q wave, but that lead sometimes has a septal q wave, which is normal. Having a prior ECG for comparison is also very helpful for differentiating acute changes. 

TEACHING OPPORTUNITIES         This tracing can help you teach students that not all cardiac patients will present with flagrant STEMIs, and we much learn to see subtle abnormalities and consider them in light of clinical features – history, symptoms, labs, and ECG changes.


Subtle ST Elevation And Left Anterior Hemiblock

Sun, 01/31/2016 - 23:11 -- Dawn

We have no clinical information about this patient, except that he was complaining of chest pain, and was initially treated by prehospital paramedics.

ST Changes      The paramedics noted a slight J point elevation in the precordial leads, specifically about one mm of elevation in Leads V2, V3, and V4.  In addition, the ST segments are curved downward like a frown in V1 and straight in the remaining precordial leads. Because of the patient’s symptoms, and the ST abnormalities, they notified the hospital that they believed this was a STEMI.  The patient was transported without complications, and the Emergency Department physician subsequently downgraded the initial assessment of STEMI Alert.  We do not have access to follow up. These ST segments are abnormal, but do not necessarily indicate an acute ST-elevation M.I. (STEMI). A flat or “frowning” ST segment DOES suggest coronary artery disease, and the patient’s symptoms are worrisome.  However, before activating the cath lab emergently, it is sometimes preferable to observe the patient, check cardiac enzymes and other lab results, and repeat ECGs. 


Are These ST Changes Due to Acute M.I.?   There are several accepted guidelines in use for evaluating ST segments for STEMI.  Some are simplified for ease of use, and some are very detailed, taking into consideration the patient’s age and gender. There are ECG features that INCREASE the chances of ST elevation being due to acute M.I.  These features include:

·        ST elevations are in related leads

·        ST segments are flat or convex upward (frowning) 

·        There are reciprocal ST depressions

·        There are associated ECG signs of M.I. such as pathological Q waves and inverted T waves

·        J points are higher than 1 mm (females have less STE requirement for M.I. diagnosis)   Leads V2 and V3 generally require 2 mm of STE for a STEMI diagnosis.

As we evaluate this ECG, we see that the subtle ST elevations are in related leads (V1 - V3).  They are flat (V2 and V3)  or convex (V1).  There is NO reciprocal depression of the ST segments.  There are NO pathological Q waves. T waves are inverted in V1 and flat in Lead III, a non-specific finding.  And the J points are minimally elevated at 1 mm or less. By most standard protocols, this ECG does not meet the criteria for acute STEMI.  This does NOT rule out the possibility of M.I.

Other Considerations    It is worth noting that strictly “normal” R wave progression is not seen in this ECG.  Leads V2 through V6 show normal R wave progression.  That is, the R waves progressively become proportionately larger, while the S waves regress.  V1, however, does not have the morphology expected, a small r wave and a deep S wave. We are not sure if this is a lead placement issue or not.  When V1 has abnormalities not shared by V2, we sometimes see similar changes in Lead III, because V1 and Lead III are both oriented toward the heart’s right side.  In this ECG, Lead III does not resemble Lead V1.  Also, there is a left axis deviation.  If no other cause for left axis deviation is readily apparent, the cause is presumed to be LEFT ANTERIOR HEMIBLOCK, also called left anterior fascicular block.  LAH is sometimes caused by anterior-septal M.I., with an incidence of about 7-15%. 

Ref.: Marriott HJL, Hogan RN. Hemiblock in acute myocardial infarction. Chest.1970; 58: 342–344.

Inferior Wall M.I. With Subtle ST Elevation

Mon, 01/18/2016 - 00:24 -- Dawn

This ECG is a good example of an inferior wall M.I. that was confirmed and treated in the cath lab.

The ST segments are elevated in Leads II, III, and aVF, but the amount of elevation may look subtle to some.   When the amount of elevation seems small, what other signs can help us recognize acute ST-elevation M.I.? 

PATIENT HISTORY AND PRESENTATION   This patient had acute chest pain, and was over the age of 50. We do not know his past medical history. His chest pain was described as substernal and epigastric, radiating to his back.  He had nausea and diaphoresis.  His past medical history is unknown, but it would be significant if he had a history of coronary artery disease, past M.I., smoking, metabolic syndrome, strong family history of heart disease, etc.

ST SEGMENT ELEVATION DISTRIBUTION   In acute STEMI, the elevation will be seen in “related leads”. That is, the leads that are affected will reflect a region of the heart that is supplied by the same artery. Some M.I.s are larger than others, affecting more leads, because some obstructions are more proximal than others in the artery.  This ECG shows STE in the inferior wall leads:  II, III, and aVF.  The culprit artery for this patient was the right coronary artery, which supplies the inferior and posterior wall of the left ventricle, the right ventricle, and the right atrium in the majority of people.

RECIPROCAL ST DEPRESSION   Finding reciprocal ST depression in the leads that are OPPOSITE the affected leads is a very reliable sign to confirm that the STEs are due to an acute M.I.  In fact, often the reciprocal depression is “stronger” or easier to see than the elevation.  It is important to teach your students how the standard leads are oriented to the heart, so they will recognize the 12-Lead ECG as a “map” of the heart.  The reciprocal ST depression in this ECG is seen in Leads aVL and I (subtle), which are across the frontal plane from Lead III.   We also note reciprocal ST depression in the precordial leads, especially notable in Leads V1 through V3.  This can reflect the injured area extending up the back of the heart from the inferior wall (posterior wall).  The R waves in V2 and V3 are a bit higher than normally expected, which could indicate a reciprocal view of pathological Q waves on the posterior wall.  Print the ECG out on paper, turn it upside down, and look at V2 and V3 through the back.  V2 and V3 will look like a “classic” STEMI.  This should be approximately the view you would get from additional posterior leads.

ST SEGMENT SHAPE   A “normal” ST segment is concave upward, like a smile.  Of course, even an ST segment with a normal shape can be abnormal if it is elevated.  But, when the shape is abnormal, even a slight amount of elevation can mean injury.  What is “abnormal”?  Convex upward, or “frowning” is abnormal, as is straight.  A straight ST segment can be horizontal or sloped.  In this ECG, you will see that the ST segments in II, III, and aVF are straight, shooting off the QRS in a straight line.  Interestingly, the reciprocal ST depressions are straight, too, as they “mirror” the STEs.

ASSOCIATED ECG SIGNS   When other abnormal ECG signs are seen with STE, it adds evidence that we are looking at an acute M.I.  ST elevation is a sign of acute injury, and it may be accompanied by T wave inversion, a sign of ischemia.  We might see pathological Q waves, an ominous sign of necrosis.  There is a Q wave in Lead III in this ECG, but Lead III often has Q waves.  They are not considered pathological unless they are also present in II and aVF.  We are happy to see no pathological Q waves, as they indicate an area of no electrical activity, like an electrical “hole” in the heart.

DYSRHYTHMIAS   The presence of dysrhythmia does not indicate an acute M.I., and the absence of dysrhythmia does not exclude M.I.  However, certain rhythms are often associated with acute M.I. due to impairment of blood supply to parts of the electrical system of the heart or to left ventricular weakening and failure.  In inferior wall M.I., for example, it is common to see sinus bradycardia and AV node blocks like second-degree AVB, Type I or third-degree AVB with junctional escape.  These reflect ischemia or damage to the SA or AV nodes, which usually have the same blood supply as the inferior wall.  AV blocks from below the AV junction, such as second-degree AVB, Type II or third-degree AVB with ventricular escape, are often attributed to interventricular septal damage.  Ventricular tachycardia and ventricular fibrillation are always a danger in acute STEMI, due to altered cellular function in the damaged tissues.


TAKE HOME POINT   When you are confronted with an ECG with subtle signs of acute ST-elevation M.I., look for associated clinical and ECG signs to help you interpret the ECG.

Inferior Wall M.I.

Tue, 11/17/2015 - 14:38 -- Dawn

This ECG shows a common manifestation with inferior wall M.I., BRADYCARDIA.  We see the signs of acute inferior wall M.I. in the inferior leads:  II, III, and aVF all have ST segment elevation.  There almost appear to be pathological Q waves in Leads III and aVF.  There are still VERY tiny r waves, and the downward deflections are not wide, but should full-blown Q waves develop in these leads, they would signify necrosis in the area.  A repeat ECG would certainly be warranted. 

Another sign that there is an inferior wall STEMI is the ST segment depression in Leads I and aVL, which are reciprocal to Lead III.  ST depression can have many meanings, but when it is localized in the leads which are opposite ST elevation, it is reciprocal.  There is also ST depression in Leads V1 and V2.  These leads are reciprocal to the POSTERIOR wall, otherwise known as the upper part of the inferior wall.  If an inferior wall M.I. is large enough, it can produce ST elevation in the posterior leads (not performed in this case), and ST depression in the anterior leads, especially V1, V2, and V3. 

The rhythm is a marked sinus bradycardia, at just under 40 beats per minute.  Sinus bradycardia is very common in inferior wall M.I., because the inferior wall and the sinus node are usually both supplied by the right coronary artery.  AV blocks can also occur because the AV node is also supplied by the RCA in most people. 

It is important to remember that bradycardia does not always need to be treated.  In patients with acute M.I., a well-tolerated bradycardia may actually be beneficial to the injured heart, reducing supply/demand ischemia.  A well-tolerated bradycardia is a rate that does not produce low blood pressure and poor peripheral perfusion.  Some people tolerate rates in the 40’s quite well.  If the patient shows signs of poor perfusion: low BP, decreased mentation, pallor, shortness of breath, the rate should be cautiously increased with medication or electronic pacing.  


Patients who present with acute inferior wall M.I. should be screened for right ventricular M.I.  Right-sided chest leads, especially V3 through V6 can reliably detect right ventricular M.I.  Other signs which may or may not be present, and have less accuracy, are:  Lead III with higher ST elevation than Lead II, aVL with ST depression of 1 mm or more, and ST elevation in V1 on the 12-Lead ECG.  For more about the prognostic implications and treatment of RVMI, we refer you to Drs. Wang and Poponick.

For a more detailed look at this ECG, and a thorough discussion of inferior wall M.I. ECG changes, please refer to the comment below from our Consulting Expert, Dr. Ken Grauer, MD.

Anterior Wall M.I.

Sun, 07/26/2015 - 13:10 -- Dawn

This is a very interesting ECG taken from an acute M.I. patient.  Your basic level students will be able to appreciate the ST elevation in V1 through V3. Although the elevations are not very high, there are plenty of other abnormalities that point to acute STEMI: the ST segments are flat and there are marked ischemic T waves in the lateral leads: V4 through V6 and I and aVL.  The patient was suffering an acute episode of chest pain.

It is also noticeable that R wave progression in the precordial leads (V1 through V6) is not optimal, as there is still a significant S wave in V6.  We do not know if this is an electrode placement issue or not.  The QT interval is just at the high limit of normal.  
For your more advanced students, aVR has ST elevation.  It is not reciprocal of an ST depression in Lead II.  Research has shown that ST elevation in aVR and V1, especially when the ST elevation is greater in aVR, is a strong indication of proximal LCA or a Left Main occlusion.  Unfortunately, we do not have cath results for this patient.  In acute M.I. patients,  higher mortality rate has been associated ST elevation in aVR.

For more information about ST elevation in aVR, click here:

and here:


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.   

Acute Inferior Wall M.I. With Right Ventricular M.I. and Atrial Fibrillation

Tue, 05/19/2015 - 11:10 -- Dawn

This 31-year-old man presented to the Emergency Dept. complaining of chest pain, shortness of breath, and nausea. His heart rate on admission was 120 - 130 bpm and irregular, and the monitor showed atrial fibrillation. His rate slowed with the administration of diltiazem. His 12-lead ECG shows the classic ST elevation of inferior wall M.I. in Leads II, III, and aVF. This patient also had JVD, bibasilar rales, orthopnea, and exertional dyspnea, signs of CHF. He had no history of acute M.I., CHF, or atrial fibrillation. He offered no history of drug use or medications.

This ECG is very useful for the basic student, in that the ST elevations are readily seen, and the atrial fib is definitely irregularly-irregular. For the more advanced student, the ST depression in V2 indicates posterior wall injury, while the flat ST segment in V1 indicates a possible right ventricular M.I.  While the posterior wall is trying to depress the ST segment, the right ventricle is trying to elevate it, resulting in flattening. Also, Lead III has a greater STE than Lead II, which has been shown to be a reliable indicator of RV infarction.  This should be confirmed with a V4 right, or all chest leads done on the right side. Right ventricular injury has been shown to increase mortality, and it also requires different management of hemodynamics.

It is unusual for a 31-year-old to experience acute M.I.  That makes it important to rule out other causes of ST elevation and chest pain.  Benign early repolarization and pericarditis should be considered.  Some of the ECG signs that FAVOR the diagnosis of STEMI are:  1) ST segments are straight, rather than curved downward like a smile.  2)  ST elevations are seen in related leads - leads oriented over the inferior wall and right ventricle (II, III, aVF, V1).  3) Reciprocal ST depressions are seen in leads known to be reciprocal to the inferior leads (I, aVL) and leads reciprocal to the "upper" inferior wall, or posterior wall.  4) There is an acute dysrhythmia (atrial fib).  Atrial fibrillation is a fairly common complication of acute M.I., and also leads to increased mortality, especially when associated with CHF.

This ECG can start a very instructive discussion on the relationship between acute M.I., acute CHF, and new-onset atrial fibrillation. That could be an entire class by itself! 

This patient was transferred to a nearby interventional cath lab, and his outcome is unknown.

Left Main Coronary Artery Obstruction

Mon, 05/11/2015 - 01:15 -- Dawn

Today’s ECG of the WEEK comes from Sebastian Garay, Paramedic.  He presented it on his excellent website, and was kind enough to share it with the ECG Guru.  It is a great example of LEFT MAIN CORONARY ARTERY lesion with ST elevation in aVR and V1.

The patient was a 68 year old man who presented with a sudden onset of chest pain, followed by cardiac arrest.  He was revived by the use of an automatic external defibrillator (AED).  The initial 12-Lead ECG shows atrial fibrillation with a rapid response of 102 bpm.  There are prominent ST ELEVATIONS in aVR and somewhat more subtle STEs in V1.  These leads reflect the base of the septum, which is the area perfused by the proximal left coronary artery.  A lesion in this area is sometimes in the LEFT MAIN coronary artery, or both the proximal LCA and the circumflex.  Both of these types of lesions carry a very high mortality rate.

The widespread ST depressions reflect the injury current, which is being directed upward and toward the patient’s right shoulder, causing a reciprocal depression in all leads except aVR, V1 and Lead III.

This patient arrived in the Emergency Dept. in grave condition and was taken to the cath lab, where an occlusive lesion was found in the LEFT MAIN coronary artery.  He later died from this severe injury.

We recommend further reading on this topic, as there has been a large body of research on ECG findings of ST elevation in aVR.  Here are some links of interest:


Dr. Smith’s Blog;   JACC Online;

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