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Subtle ST Changes

Submitted by Dawn on Mon, 04/11/2016 - 19:18

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. 

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Anterior-Septal M.I. With Atrial Fibrillation

Submitted by Dawn on Fri, 02/12/2016 - 19:33

This is an interesting teaching ECG on many levels.  It is obtained from a man with chest pain. No other history or follow up is available. 

Acute M.I.     Most striking is probably the clearly-seen anterior-septal wall M.I.  There is ST segment elevation in Leads V1, V2, and V3, with ST depression in the low-lateral leads, V5 and V6.  There is also ST depression in the inferior Leads II, III, and aVF.  The ST elevations have a coved-upward (frown) shape in V1 and a straight shape in V2 and V3.  Both of these ST shapes are abnormal and reflect injury.  The depressions are presumed to be due to reciprocal changes, since there is no other ST-depression producing condition apparent.  There are abnormal Q waves in V1, which could herald the onset of pathological Q waves, a sign of necrosis, in the anterior-septal wall. 

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Inferior Wall M.I. With Subtle ST Elevation

Submitted by Dawn on Mon, 01/18/2016 - 00:24

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.

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Inferior Wall M.I.

Submitted by Dawn on Tue, 11/17/2015 - 14:38

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.  

 

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Acute Inferior-Lateral M.I. In A Patient With A Dominant Circumflex Artery

Submitted by Dawn on Fri, 10/30/2015 - 22:59

This ECG was obtained from a patient who suffered an obstruction of the circumflex coronary artery.  Unfortunately, he was in the approximately 15-18% of the population in whom the circumflex artery is dominant.  That means that it connects with the posterior descending artery, perfusing not only the lateral wall of the left ventricle, but also the posterior and inferior walls.  In this case, the obstruction is in the midportion of the artery, and the high lateral wall is spared.  The large number of leads with ST elevation indicate the large amount of myocardium affected.  Leads II, III, and aVF have ST elevation, as do Leads V3 through V6.  Lead aVL has reciprocal ST depression. The T waves in the affected leads are "hyperacute", or taller than normal.  This is usually an early change in acute M.I., and disappears after the onset of ST elevation.

It is not always easy to determine from the ECG that the circumflex artery is the culprit artery, rather than the right coronary artery, which perfuses the inferior wall in the majority of people.  Some clues are:  Lead III has ST elevation equal to that of Lead II, the low lateral wall (V5 and V6) are affected, and aVL has reciprocal depression but Lead I does not.

This is a very large M.I., due to the dominance of the circumflex artery.  The patient did not survive, in spite of aggressive treatment.

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Anterior Wall M.I.

Submitted by Dawn on Sun, 07/26/2015 - 13:10

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: https://login.medscape.com/login/sso/getlogin?urlCache=aHR0cDovL3d3dy5tZWRzY2FwZS5jb20vdmlld2FydGljbGUvNTg5Nzgx&ac=401

and here:  http://content.onlinejacc.org/cgi/content/full/38/5/1355

 

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Second-Degree AV Block, Type I

Submitted by Dawn on Sat, 06/13/2015 - 22:07

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.   

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

Submitted by Dawn on Tue, 05/19/2015 - 11:10

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.

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Left Main Coronary Artery Obstruction

Submitted by Dawn on Mon, 05/11/2015 - 01:15

Today’s ECG of the WEEK comes from Sebastian Garay, Paramedic.  He presented it on his excellent website CardioCareConcepts.com, 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; ScienceDirect.com.

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Inferior-Lateral M.I.

Submitted by Dawn on Sun, 03/29/2015 - 21:41

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. 

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