Too busy studying for the inservice to be Bored Review

ECG STEMI Basics

Please describe: 1. What and where the pathology is 2. Where you would see reciprocal changes 3. Which artery is blocked, and 4. What other ECG’s are indicated.

ST elevations in II, III, AVF.

1. Inferior MI 2. ST depressions in Lateral Leads, 3. Most commonly RCA (especially if right sided infarction too). Less often LCx. Rarely LAD. How straightforward is that? 4. Do a RIGHT Sided ECG to look for right ventricular infarction

ST elevations in I, AVL, V5, V6

1. Lateral MI 2. ST depressions in inferior leads 3. LAD/LCx 4. none

ST elevations in V1, V2

1. Anterior MI (V3-V4 are septal) 2. ST depressions in inferior leads 3. LAD 4. none

No ST elevations, but ST depressions in V1 and V2

1/2. Posterior MI! (V1, V2 are the reciprocal leads to a posterior MI – whose ST elevations aren’t evaluated on a normal 12 lead ECG). 3. Circumflex, maybe branch of RCA (posterior descending) 4. If you see these, do a posterior ECG!!!

ST elevation in aVR alone...

You may think this isn’t an MI because it’s not “greater than 1mm ST elevation in contiguous leads”, but, in fact, lead aVR has no contiguous leads. ST elevation in aVR on it’s own is concerning for Left Main Artery occlusion. If this elevation has reciprocal st depressions in the rest of the leads, it may also be secondary to high stress – severe anemia, sepsis, PE, head bleeds that cause a lower flow state to someone with triple vessel disease.

Issue: Due to its location + the fact that it sometimes gives redundant information (reciprocal information covered by leads aVL, II, V5 and V6), we often ignore it

Studies show that ST segment elevation in aVR strongly predicted proximal LAD

aVR ST segment elevation greater than the ST segment elevation in V1 predicts acute left main coronary artery (LMCA) occlusion with a sensitivity of 81% and a specificity of 80%

What else is aVR on it's own good for?

1. TCA/sodium channel blocker Poisonings (Terminal R wave) 2. PE (acute right ventricular overload is often reflected in the EKG as ST-segment elevation in lead aVR) 3. Arrythmias (a dissociated, negative P-wave in lead aVR is useful in the wide QRS tachycardia in diagnosing a ventricular origin of the arrhythmia)

By Dr. Brenda Oiyemhonlan, Dr. Andrew Grock, and Dr. Sally Bogoch

References:

Gorgels, A., Engelen, D., & Wellens, H. (2001). Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. Journal of the American College of Cardiology, 1355-1356.

Vorobiof, G., & Ellestad, M. (2011). Lead aVR: Dead or Simply Forgotten? JACC: Cardiovascular Imaging, 187-190.

uptodate.com

rivers

life in the fast lane http://lifeinthefastlane.com/ecg-library/

Bio
Latest Posts

andygrock

Latest posts by andygrock (see all)

Levamisole Toxicity - May 26, 2015
Of Course, US Only for Kidney Stones… - May 18, 2015
Case of the Month 11: Answer - May 12, 2015

2 Comments

Nathan Reisman · February 10, 2015 at 11:24 am

ST elevation in aVR is a little more complicated than that. It can be a sign of transmural ischemia at the base of the septum, which can be from LMCO as you said, but also from very proximal LAD as long as it is proximal to the first septal perforater which supplies the basal septum. It can also be seen in severe triple vessel disease.

But STE in aVR can also be a reciprocal change from diffuse ischemia when associated with ST depression in multiple leads. This pattern is not specific to coronary occlusion and is seen in subarachnoid hemorrhage, severe hypothermia, seizures, and ischemic stroke.

Reference:

Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. Journal of the American College of Cardiology. 1999;34(2):389-95.

Kim E, Birnbaum Y. Acute coronary syndromes presenting with transient diffuse ST segment depression and st segment elevation in lead aVR not caused by “acute left main coronary artery occlusion”: description of two cases. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2013;18(2):204-9.

Wang H, Hollingsworth J, Mahler S, Arnold T. Diffuse ST segment depression from hypothermia. International journal of emergency medicine. 2010;3(4):451-4.

Mitsuma W, Ito M, Kodama M, Takano H, Tomita M, Saito N, et al. Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest. Resuscitation. 2011;82(10):1294-7.

Ian deSouza · February 10, 2015 at 3:19 pm

Good point Reisman. When their is ST elev. in aVR, remember to consider diffuse myocardial ischemia as a result of global hypoperfusion/shock and treat this accordingly. Once you call your “code H”, your “cardiologist” will not.