Case: A 56 yo male with a history of T2DM, atrial fibrillation (on metoprolol 50 mg XL q daily, not on AC), presents with 3 days of worsening chest pain, epigastric discomfort, and shortness of breath. Today, he had significantly worsening dyspnea on exertion and persistent chest pressure radiating to the left arm. He states that he took his metoprolol today as prescribed.
Initial vitals:
HR: 38 beats/minute
BP: 90/55
RR: 20 breaths/minute
O2: 97% on room air
T: 37°C.
Triage EKG shown below:
Computer Interpretation: atrial flutter with slow ventricular response (ventricular rate of 39). Inferior myocardial infarction, of indeterminate age.
Physician Interpretation: coarse atrial fibrillation with slow ventricular response (heart rate of ~39), 3rd degree AV block with a junctional escape rhythm. Inferior occlusion myocardial infarction (OMI) with posterior extension.
Why this EKG? This ECG highlights several important points:
1) The identification of inferior ischemia:
An inferior myocardial infarction (MI) is suggested by [1]:
ST elevation in leads II, III, aVF
Reciprocal ST depression in aVL
Progressive development of Q waves in II, III, aVF
In this ECG, we see:
Well formed Q waves in leads III and aVF with small Q waves visible in lead II
ST segment elevation of 1mm in lead III
Subtle ST segment depression and T wave inversion in leads I and aVL
These findings are suggestive of inferior ischemia and in the presence of active chest pain and electrical instability, must be treated as an acute process. This combination of findings raises suspicion for an occlusion myocardial infarction (OMI).
Lead aVL is an important lead when evaluating for inferior ischemia. Since it is facing the superior parts of the left ventricle, it is the only lead that is truly reciprocal to the inferior wall.
Moreover, ST depression in aVL has been shown to be more prevalent than ST elevation in inferior leads among patients with inferior MIs [2].
2) The identification of posterior ischemia:
A posterior MI is suggested by the following changes in V1-V3 [1]:
Horizontal ST depression
Tall, broad R waves
Upright terminal portion of the T waves
Dominant R wave (R/S ratio > 1) in V2
Posterior wall MI accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction [6].
Why do we see these changes?
Leads V1-V3 are directed from the anterior precordium towards the internal surface of the posterior myocardium. Since electrical activity from the posterior aspect of the heart is being recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:
ST elevation will appear as ST depression, Q waves will appear as R waves, and the terminal T wave inversion typically seen in ischemia will appear as a terminal upright T wave.
These findings are highlighted when lead V2 in our ECG is flipped, showing the more typical injury pattern of ischemia described above.
In our patient’s ECG, we see:
Prominent R waves (early R wave progression) in leads V1 and V2 (the R/S ratio in V2 is >1).
Mild horizontal ST segment depression <1mm in V2.
Upright terminal portion of the T wave in lead V2.
All of these findings suggest a posterior wall MI.
Image from: Hollander JE, Diercks DB. Acute Coronary Syndromes. In: Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, et al., eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 8th ed. New York, NY: McGraw-Hill; 2016:(Ch) 49.
3) Identification of the culprit artery
Inferior MIs primarily result from occlusion of the following two coronary arteries [3]:
Dominant right coronary artery (RCA) in 80% of cases
Dominant left circumflex artery (LCx) in 18% of cases
The RCA territory covers the medial part of the inferior wall, including the inferior septum. An RCA occlusion typically produces ST elevation in lead III > lead II (as lead III is more rightward facing), as well as possible reciprocal ST depression in lead I and aVL.
The LCx territory covers the lateral part of the inferior wall and the left postero-basal area. A LCx occlusion produces ST elevation in the lateral leads I, aVL, and V5-6 (in addition to ST elevation in the inferior leads).
In our case, ST elevation in lead III is greater than in lead II, without associated ST elevation in lateral leads, suggesting occlusion of the RCA.
4) The identification of complete heart block in the setting of atrial fibrillation
In atrial fibrillation, fibrillatory waves may be present and can be fine (amplitude <0.5mm) or coarse (amplitude >0.5mm).
Coarse fibrillatory waves, as seen in our patient, can mimic P waves, and may appear very similar to flutter waves, often leading to misdiagnosis. We can differentiate these from atrial flutter waves due to their constant variation in the wave morphology (as compared to the identical morphology of the flutter waves throughout).
An example of these differences is shown in the figure below [5]:
Image from: Hoevelmann J, Viljoen C, Chin A. Irregular, narrow-complex tachycardia. Cardiovasc J Afr. 2018 May/Jun;29(3):195-198. PMID: 30067274; PMCID: PMC6107807.
Our patient also has a regular rhythm, and moreover - there is no relationship between the QRS complexes and the preceding fibrillatory waves. The combination of atrial fibrillation with a regular rhythm (“Regularised Atrial Fibrillation”) indicates that none of the atrial impulses are conducted to the ventricles. This is diagnostic of a complete (3rd degree atrioventricular) heart block.
This patient also has a narrow QRS complex in the setting of a complete heart block, indicating that the escape rhythm is originating from above the ventricles, suggestive of a junctional escape rhythm.
This is an important finding because up to 20% of patients with inferior STEMIs will develop high-grade AV block [3]. This is thought to primarily occur due to ischemia of the AV node from impaired blood flow from the AV nodal artery, which arises from the RCA in 80% of patients.
Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia or sinus pauses, since the SA node is supplied by the RCA in 60% of people [3].
Bradyarrhythmias in the setting of inferior STEMI, however, are usually transient (lasting hours to days), typically respond well to atropine, and do not usually require permanent pacing.
What happened next?
Aspirin 325 mg PO was immediately given, the pacer pads were applied on the patient with atropine at the bedside. A bedside echocardiogram demonstrated bradycardia with an estimated ejection fraction of 50%, as well as akinesis of the inferior myocardium.
Cardiology service was quickly consulted, and in the setting of ongoing chest pain and regional wall motion abnormalities on the echocardiogram, also had a high suspicion for an OMI of the inferoposterior region. The catheterization lab was activated and the patient was started on a heparin drip.
Labs returned, demonstrating a troponin I of 46.44ng/mL, and an acute kidney injury, but no other lab abnormalities.
Repeat ECG was obtained, and was largely unchanged:
The patient was emergently taken to the catheterization lab, where he underwent coronary angiography that revealed a 100% thrombotic occlusion of the distal RCA. He had percutaneous coronary intervention (PCI) and mechanical thrombectomy with a drug eluting stent (DES) placed. A temporary transvenous pacemaker was also placed in the catheterization lab.
He was admitted to the CCU, where he had an uncomplicated recovery.
The Heart of the Matter:
Inferior myocardial infarctions are frequently associated with infarction of the posterior myocardial wall
Among patients with inferior MIs, ST depression in aVL has been shown to be more prevalent than ST elevation in inferior leads
Inferior MIs primarily result from occlusion of the RCA or LCx
Coarse atrial fibrillatory waves can be differentiated from atrial flutter waves by
their constantly changing morphologies
The combination of atrial fibrillation with a regular rhythm is suggestive of
complete heart block
Up to 20% of patients with inferior STEMIs will develop high-grade AV block
Written by:
Rayyan Kadi, MD - PGY 4 | Cook County Health
Twitter: @RayyanKadi
Ishmael Avery, MD - PGY4 | Cook County Health
Reviewed by:
Tarlan Hedayati, MD
Chair of Education | Department of Emergency Medicine |Cook County Health
Twitter: @HedayatiMD
For more reading:
https://litfl.com/posterior-myocardial-infarction-ecg-library/ https://litfl.com/atrial-fibrillation-ecg-library/
https://litfl.com/digoxin-toxicity-ecg-library/
References:
Morris F, Brady WJ. ABC of clinical electrocardiography: Acute myocardial infarction-Part I. BMJ. 2002 Apr 6;324(7341):831-4. PMID: 11934778.
Bischof JE, Worrall C, Thompson P, Marti D, Smith SW. ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med. 2016 Feb;34(2):149-54. Epub 2015 Oct 3. PMID: 26542793.
Berger PB, Ryan TJ. Inferior myocardial infarction. High-risk subgroups. Circulation. 1990 Feb;81(2):401-11. PMID: 2404629.
Hollander JE, Diercks DB. Acute Coronary Syndromes. In: Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, et al., eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 8th ed. New York, NY: McGraw-Hill; 2016:(Ch) 49.
Hoevelmann J, Viljoen C, Chin A. Irregular, narrow-complex tachycardia. Cardiovasc J Afr. 2018 May/Jun;29(3):195-198. PMID: 30067274.
Lizzo JM, Chowdhury YS. Posterior Myocardial Infarction. 2020 Nov 29. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 31985961.