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ST Elevation

Instructors' Collection ECG of the WEEK, April 15, 2014 __ Acute Inferior Wall M.I.

Tue, 04/15/2014 - 02:08 -- Dawn

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. 

This patient's unstable condition and close proximity to the hospital prevented the EMS crew from getting a second ECG, but when there is time, a repeat ECG with a V4R lead can be helpful in deciding how much I.V. fluid is safe to give.  This patient's heart rate improved spontaneously during transport, but had it not, the transcutaneous pacemaker could have been used.  In some protocols, a trial of Atropine is advised.  In others, treatment goes straight to the pacemaker or to I.V. epinephrine.  During the angioplasty, a transvenous pacemaker is often inserted into the right ventricle to support the patient's rate if necessary.  

This patient was fortunate to be in an area with advanced paramedics and an interventional cath lab close by.  It is notable that he never developed pathological Q waves, and hopefully had an uneventful recovery.  



Anterior Wall M.I.

Wed, 03/05/2014 - 22:27 -- Dawn

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.

Stroke and ST Elevation

Thu, 02/13/2014 - 00:59 -- Dawn

A 77-year-old man was brought to the Emergency Department with stroke symptoms.  He had less than one hour since symptom onset.  He presented with extreme weakness of his right side and slurred speech.   He has a history of coronary artery disease and previous acute M.I.  His BP was 188/80, P 46/min., and resp. 16/min.  He denies chest pain, N&V, and shortness of breath.  The E.D. physician called in the stroke team, and a diagnosis of CVA was made.   What does his ECG show?

This ECG shows clear ST elevations in V1 and V2, with abnormally flat ST segments in nearly all leads.  In addition, there are ischemic T wave inversions in Leads V3, V4, V5, I, and aVL.   A diagnosis of anterio-lateral M.I. is made in addition to stroke.

Ischemic changes, like ST elevation and T wave inversions have been demonstrated frequently in patients with strokes.  Stroke symptoms have also been recorded in patients who are having M.I.s.  Ischemic stroke has been shown to be a complication of acute myocardial infarction.  Hemorrhagic stroke can follow anticoagulation or thrombolysis.   Also, acute M.I. has been shown to be a complication of stroke. Artery disease is a common denominator in both conditions. 

Needless to say, this can be a very complex problem, and the patient with stroke symptoms requires a CT scan to rule out hemorrhage before the M.I. is treated with anticoagulants or thrombolytics. 

References:  MI After Stroke, The Heart.orgIncidence of Stroke After Acute M.I., Witt, et al ; Ischemic Stroke After Acute Myocardial Infarction, Mooe, et al.



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

Fri, 01/24/2014 - 00:15 -- Dawn

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. 

The patient was taken to the cath lab for angioplasty.  In the cath lab, her right coronary artery was found to have several serious lesions, one of which was almost 100%.  These lesions were stented.  Often, when lesions are not completely occluding the artery, ST elevation can come and go. Arteries dilate and constrict, allowing more or less blood to flow past the partial occlusion.  Changing arterial diameter, fluctuant thrombi, or increased/decreased myocardial oxygen demand can cause the ST segments to rise and fall. Changes in the nature of the chest pain can occur as well.

This ECG shows a continuing bradycardia (which may be affected by her medications), but her QRS has narrowed to .108 seconds (108 ms).   Her inferior leads show a very slight coving upward of the ST segment, with T wave inversion, signs of evolution of the M.I.  Unfortunately, pathological Q waves have formed in Leads III and aVF, which probably reflect permanent damage to the inferior wall.  Followup ventriculograms or echocardiograms can establish LV function as time goes on.  The good news is that the patient received good relief of her symptoms from the angioplasty procedure, and she did well to hospital discharge.  We do not know about her condition post discharge.  

To see images from this patient's RCA angioplasty, click HERE.

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

Sun, 12/15/2013 - 21:25 -- Dawn

This ECG is the last in a series of 6 that were donated by Jenda Enis Štros showing the evolutionary changes of an M.I. from onset, through spontaneous reperfusion, angioplasty, re-occlusion by thrombus, and recovery.  This ECG shows deep precordial T wave inversions, an expected evolutionary change after reperfusion of an occluded artery - in this case, the left anterior descending.  The patient has lost some of his QRS amplitude (viable heart muscle), but has not developed pathological Q waves.  Pathological Q waves would indicate full-thickness necrosis of the wall, which is usually a permanent injury.  

The patient was discharged home with a 45% ejection fraction (60% is ideal), and he had akinesis of part of his anterior wall.  This can be permanent or temporary, and followup studies would be needed to evaluate the ongoing health and function of the left ventricle.

Here are links to all six ECGs from this series:



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

Sun, 12/15/2013 - 21:07 -- Dawn

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:


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

Sun, 12/15/2013 - 20:28 -- Dawn

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:


Teaching Series 1113: ECG 2 of 6 - Acute Anterior Wall M.I.

Sun, 12/15/2013 - 20:23 -- Dawn

To continue the series donated by Jenda Enis Štros, ECG 2 shows spontaneous resolution of the ST elevation, coinciding with relief of the patient's chest pain.  Spontaneous reperfusion can occur when the artery diameter is increased, the offending clot shifts position to allow blood flow, or other reasons.  This does not mean, however, that the lesion has disappeared.

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


Anterior Wall M.I. With Previous Inferior Wall M.I.

Mon, 11/04/2013 - 14:40 -- Dawn

This ECG illustrates an acute anterior wall M.I. in a patient with a previous history of inferior wall M.I.  The anterior wall M.I. can be seen in the classic signs in V1 through V6:  ST elevations with coved upward shape (tombstones), T waves inverting beginning around V2 and continuing through V6, and pathological Q waves in V1 through V6.

The patient had a history of previous inferior wall M.I., unknown age.  This is normally seen in Leads II, III, and aVF.  The first two complexes on the strip are wide QRS complexes without associated P waves, presumably ventricular.  It is impossible to know from this ECG whether the first complex is a PVC or escape beat, but the second appears to be escape.  So, to evaluate the ST segments, T waves, and pathological Q waves in the inferior wall, all we have are aVF and the Lead II rhythm strip at the bottom.  These show pathological Q waves (necrosis), and some slight elevation of ST, with coving or horizontal flattening.  From this, we know there is damage in the inferior wall, but the age of the M.I. is undetermined.

This patient went to the cath lab, and received angioplasty with stenting of the proximal left anterior descending branch of the left coronary artery.

Acute Lateral Wall M.I.

Sun, 09/22/2013 - 00:45 -- 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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