Coronary artery disease

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Instructors' Collection ECGs: Complete AV Block

Submitted by Dawn on Sun, 03/30/2025 - 15:56

This is an interesting case for your students who want to delve into dysrhythmias with an eye on detail. It is also a good teaching case for discussing treatment options when the diagnosis may be uncertain or controversial. I will start the discussion by admitting that I am not an expert of electrophysiology or complex dysrhythmias. My approach has always been more clinical - how is this rhythm affecting the patient and what are the chances it will deteriorate? I hope some of our dysrhythmia Gurus will delve into the rhythm and maybe even provide laddergrams.

The patient: This is a man in his seventies who complains of light-headedness for several days, and feeling worse today, prompting an emergency call. He offers no cardiac history. BP 116/62 and 116/58. Blood glucose 220 mg/dL. Physical exam unremarkable.

12-Lead ECG : I will admit that, on first quick glance, I thought I was looking at a 2:1 AV block. But on closer inspection, I noted that the "PR intervals" varied, becoming shorter as the strip progressed. Another 12-lead on the same patient showed even more pronounced variations. The atrial rate is about 76 bpm (measured with a digital caliper). The atrial rhythm is fairly regular (allowing for slight variations in sinus rhythm). The ventricular rate is around 39 bpm, almost exactly half that of the atrial rate. This rhythm is also regular. Because of the PRI interval changes, I believe this is complete AVB with an escape rhythm that is just about half the atrial rate. If that is correct, the ventricular rhythm originates in the AV junction, because the QRS complexes are narrow, and the rate is very near 40 bpm. The frontal plane axis is slightly leftward, within normal range, and the R wave progression in the chest leads shows a late transition, with patholoogical Q waves in V1. There are also Q waves in III and aVF.

There are ST and T wave changes in Leads I, aVL, V1, V2, and V3. I do not know if this patient has a history of cardiac disease or a recent complaint of chest pain, but T wave inversion and some biphasic T waves makes me think of reperfusion changes, reflecting a recent M.I. The ST segments in leads with T wave changes are also uncomfortably straight. We do not have followup on this patient's hospital course or treatment.

I have included a rhythm strip with some markup for those who would like to really get into the mechanism of this rhythm. For myself, as a retired ER RN and paramedic, I think of the clinical ramifications of such a rhythm.

1) Is this rhythm the result of OMI? This would demand further investigation, probably with a temporary transvenous pacemaker as a safeguard measure.

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Subtle ST Elevation And Left Anterior Hemiblock

Submitted by Dawn on Sun, 01/31/2016 - 23:11

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

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Deep, Symmetrical T Wave Inversions

Submitted by Dawn on Tue, 12/15/2015 - 21:20

This ECG is from a 50-year-old man with chest pain. Unfortunately, we don’t have any other clinical information. This tracing is a good example of widespread, symmetrical inverted T waves. Inverted T waves are present in Leads I, aVL, II, and V3 through V6. (The anterior-lateral leads). There are ST segment elevations in Leads V1 and V2.

Many conditions can cause inverted T waves, and bedside assessment is necessary to make a certain diagnosis. Some T wave inversions are benign, such as in persistent juvenile T wave pattern. Some can be due to life-threatening problems like pulmonary embolism, CNS injury, and cardiac ischemia. T wave inversions can be secondary to conditions like left ventricular hypertrophy, left bundle branch block, and ventricular rhythms. When T waves are deep and symmetrical as they are here, they may be a sign of acute coronary syndrome, or cardiac ischemia. Since we know this patient had chest pain, and there is some ST elevation, this should be considered as a cause for his T wave changes.

In addition to the dramatic T waves, he also has P waves suggestive of “P mitrale”, or left atrial enlargement. The P waves in Lead II are wide (about 10 or 11 ms) and just over 1 mv tall. This is “borderline” for most LAE criteria. The P waves in Lead V1 are biphasic, with the second portion negatively deflected and over 1 mv deep. Acute myocardial infarction can cause left ventricular dysfunction, which can cause backup pressure to the left atrium.

Inverted T waves, like all ST and T wave changes, should always be assessed in the context of the patient presentation, history, and previous ECGs, if available.

References: Consultantlive.com, Dr. Ken Grauer

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Inferior Wall M.I. Due To Circumflex Artery Occlusion

Submitted by Dawn on Fri, 10/25/2013 - 21:26

This ECG is from an 81 year old woman with an extensive history of coronary artery disease. She was experiencing chest pain at the time of the ECG. We can clearly see ST elevation in Leads II, III, and aVF, indicating an inferior wall ST-elevation M.I. (STEMI). There are reciprocal ST depressions in Leads I and aVL. There are subtle and less specific ST changes in V1 (flat ST and T), V2 (ST depression), V3 (ST elevation and inverted T wave), and V4 through V6 (slight ST elevation). The flat, horizontal shape of most of the ST segments is another clue to her CAD. What coronary artery do you think is the culprit for the ST elevation?

This patient received coronary angiography, so we do not have to guess at where her lesions are. She was found to have an occluded left internal mammary artery (LIMA) graft.

The left anterior descending coronary artery (top of view) is very diseased, with some extremely narrow areas. The circumflex artery is large and covers a lot of area, but it, too, is very diseased, with a critical occlusion (marked with arrow). On this day, the circumflex artery received angioplasty and stents. The patient's right coronary artery was patent.

In approximately 85% of the population, the RCA supplies the inferior wall of the heart. In most of the rest, a branch of the circumflex supplies the posterior/inferior wall.

This patient also has a very interesting arrhythmia. We see P waves (numbered) that appear regular for three beats, then we see no P waves for a pause. Then, three more P waves appear. There is no readily-seen "hidden" P wave in the ST segments or T waves. Even though there appear to be "progressively prolonging PR intervals", the PR intervals of each group of three do not match the other group of three. The first "PRI" - P wave number 1- and the last one - P wave number 7 - appear too short to be normal PR intervals. The ventricular rate is regular, and the QRS complexes are slightly wide at .10 sec. The rate is 54 bpm. This suggests junctional rhythm.

We are eager to hear your comments regarding this rhythm.

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Anterior Wall M.I.

Submitted by Dawn on Tue, 08/27/2013 - 15:03

This series of three ECGs is from a 75-year-old woman who came to the Emergency Dept. with chest pain. The first ECG shows ST elevation in V1, V2, and V3, with generally low voltage in the QRS complexes. There is some coving upward of the ST segment in aVR, which can suggest a very proximal lesion of the left coronary artery (LCA). She was taken to the cath lab, where it was discovered that she had a 100% occlusion of the midportion of the anterior descending branch of the left coronary artery, which was repaired and stented. The second ECG, taken after the angioplasty, shows some Q waves in V1 and V2, with poor R wave progression in the V leads. A 25% occlusion of the obtuse marginal branch of the circumflex artery was stented two days later. The third ECG was obtained after that procedure. It shows that the Q waves have disappeared in the anterior leads (possibly due to different technicians performing the ECGs with different lead placement). It also shows marked T wave inversion in I and aVL, representing ischemia in the lateral wall, and in all the chest leads, representing ischemia in the anterior wall. The QTc is prolonged in this third ECG at 479 ms. It is not known what medications the patient was on. This patient also had a 50% proximal occlusion in the RCA and a 75% occlusion in the posterior descending artery. This is a good example of a patient with extensive coronary artery disease who finally presented for treatment when she developed ST elevation M.I.