Timeline:

• Divide learners into 4 groups at different tables (this approach is suggested for groups of 8 or more learners and should be modified to 1 or 2 groups so sites with lower numbers of learners)

• 5 min large group review of the Unit II Summary “Approach to Ischemia: Ischemia Mimics”

• Give each group 2 copies of the Unit 2 EKG Challenges Packet (merged challenge EKG content for EKGs 5-8), this allows learner groups to all review content and record their group's answers to the interpretation and questions for each EKG

• Allow 20 minutes for groups to complete the 4 challenges (give updates at 5min increments)

• 20 minutes large group discussion of answers to challenges. May consider asking each group to present their responses to a different EKG

Meeting Resources:

• Notify learners in advance of the session that they need to review the unit summary and challenge EKGs

• Before the session, have a few copies of the unit summary (pages 2-7 of this document) printed to give to learners who forgot their copies/devices and copies of the Unit 2 EKG Challenges Packet to give to groups

• Before the session, make sure to print this document for your own reference during the group discussion

• After the meeting, send out the answer document to learners for independent review

Foundations EKG I

Unit 2 Instructor—Ischemia Mimics

Foundations EKG I Unit 2 Instructor—Ischemia Mimics

Unit 2, Case 5—36yM with HTN c/o intermittent CP that lasts for 3-4 hours at a time.

No exertional pain, diaphoresis, family history of early MI/dissection. PERC negative.

Challenge Questions: Would you expect the EKG abnormalities to be more or less

pronounced if the patient’s heart rate increased to 110?

HR: 60 BP: 160/110

RR: 18 O2 Sat: 96%

Unit 2, Case 8—20yM with hx of asthma c/o severe substernal chest pain. He thinks his

father had his first MI at 48.

Challenge Question: What treatment options do you have for this patient?

HR: 130 BP: 120/80

RR: 20 O2 Sat: 98%

Unit 2, Case 7—63yF with hx of CAD sent to the ED from clinic for 1-2 weeks of severe

diarrhea

Challenge Question: What treatment options do you have for this patient and how

do they work?

HR: 78 BP: 140/90

RR: 18 O2 Sat: 97%

Unit 2, Case 6—65 y/o M with a history of a STEMI 3 weeks ago presents to the ED

from his cardiologists office because an outpatient echo this morning showed a “clot in

my heart”. He has had not chest pain since his MI 3 weeks ago.

Challenge Questions: Putting the EKG together with the clinical history, what do you

think is going on with this patient?

How should this patient be managed?

HR: 65 BP: 118/66

RR: 12 O2 Sat: 98%

Although STEMI diagnosis is critical not all ST elevation represents STEMI. There are many possible harms

of a false positive STEMI activation or transfer including but certainly not limited to the risks of receiving

anti-platelet agents or even tPA in the setting of a transfer, complications of angiography (bleeding,

dissection, etc), as well as operational issues of the cath lab team being activated overnight or cancelling a

scheduled case.

An EKG with a STEMI pattern must be considered in the context of the patient’s past medical history, HPI,

and exam. This summary will provide an overview of common STEMI mimics including left ventricular

aneurysm, hyperkalemia, pericarditis, Brugada syndrome, elevated intracranial pressure, and left ventricular

hypertrophy.

LV Aneurysm is defined by EKG criteria as ST elevation that persists for more than 2 weeks after an MI. It is

important to note that it is considered normal for ST elevation to slowly resolve after MI and it may not

immediately return to normal. Distinguishing LV aneurysm from STEMI can be difficult, however typically

there are clear Q waves and a lack of hyperacute T waves. Additionally, the patient should not have pain or

active anginal equivalent symptoms. LITFL Review

Foundations EKG I

Unit 2 Summary - Ischemia Mimics

Brugada syndrome is the result of an inherited or

spontaneous mutation in cardiac sodium channels that

predisposes patients to ventricular tachyarrhythmias

and sudden cardiac death. To be diagnosed with the

syndrome, one must have ECG features and symptoms

consistent with ventricular tachyarrhythmia (syncope,

palpitations, etc). LITFL Review

The image above is an example of Type 1 Brugada

with coved ST-elevation in V1-2 sloping into an

inverted T-wave.

Large and particularly rapid increase in intracranial pressure (a

good example would be a large subarachnoid hemorrhage) can

cause EKG changes that are often confused with ischemia.

Most frequently the changes are deep T wave inversions (aka

cerebral T waves) however sometimes there can be associated

ST elevation and depression. The history and exam are critical

in this situation because normal therapies for ischemia like an-

tiplatelet agents could be devastating if there is a concurrent

intracranial hemorrhage. As an example it is atypical for a

STEMI patient to be altered or obtunded which can be a clue

that there is another or concurrent process. The image above

is an example of cerebral T waves. LITFL Review

Courtesy of Edward Burns of Life in the Fast Lane

Creative Commons License

Osbourne or J Waves are upward deflections of the J point that are typically caused by hypothermia,

but may also be the result of hypercalcemia or elevated intracranial pressure. The elevated J point

creates the appearance of significant ST elevation. Consider getting a core temperature in patient’s

with abnormalities of the J point.

Courtesy of NYU Emergency Care Electrocardiogram (ECG) Database

Left Ventricular Hypertrophy is frequently the result of untreated hypertension and aortic valve dysfunc-

tion. It causes characteristic EKG abnormalities including massive QRS amplitudes (typically large S waves

in V1-3, III, aVR and large R waves in V4-6, I, and aVL) as well as prolonged QRS duration and ST segment

changes like ST elevation and ST depression. LITFL Review

Courtesy of Edward Burns of Life in the Fast Lane Creative Commons License

Hyperkalemia is a common electrolyte derangement that can cause significant changes to a patient’s

EKG. Classically, hyperkalemia progressively leads to peaking T waves, PR prolongation, loss of P waves,

QRS widening, bundle or fascicular block morphology, sine wave, and ventricular dysrhythmia or asysto-

le as the potassium rises. The bizarre appearance of the EKG in hyperkalemia can be easily confused

with STEMI and it is important to keep hyperkalemia in your differential particularly in patients with

known renal dysfunction/failure, patients undergoing chemotherapy, patients using ACE inhibitors or

potassium sparing diuretics, and all patients receiving potassium supplementation. LITFL Review

Pericarditis frequently causes diffuse ST elevation that can be confused with STEMI. However, it is

important to recognize that the ST elevation of pericarditis should also be associated with PR depres-

sion (except in aVR which has PR elevation) and NOT be associated with ST depression in leads other

than aVR and V1. Patients with pericarditis often have pain that improves when sitting forward and

is exacerbated by laying back. The clinical history and exam is very important with this diagnosis as

well as it can sometimes be difficult or impossible to distinguish pericarditis and STEMI. The EKG

above is an example of diffuse STE and STD in aVR/V1 with diffuse PR depression and PR elevation in

aVR and V1. LITFL Review

Created by William Burns, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd

aVR

aVR I V1 V4

aVL II V2 V5

aVF III V3 V6

36yM with HTN c/o intermittent CP that lasts for 3-4 hours at a time.

No exertional pain, diaphoresis, family history of early MI/dissection.

PERC negative.

HR: 60 BP: 160/110

RR: 18 O2 Sat: 96%

What is your interpretation of the EKG?

History/Clinical Picture

Rate

Rhythm

Axis

P Waves

Q/R/S Waves

T Waves

U Waves

PR Interval

QRS Width

ST Segment

QT Interval

Would you expect the EKG abnormalities to be more or less

pronounced if the patient’s heart rate increased to 110?

Foundations EKG - Unit 2, Case 5

Triage EKG—Unit 2, Case 5

What is your interpretation of the EKG? History/Clinical Picture—young age and intermittent chest pain Rate—84 (14 x 6) or ~80 (just under 4 large boxes) Rhythm—Sinus Rhythm Axis—Normal (positive in I, II, III, aVF) P Waves—normal Q, R, S Waves—No pathologic Qs T Waves—V2-5 have concordant, tall, asymmetrical T waves. U Waves—no U waves PR Interval—normal, ~160ms. QRS Width—narrow, ~80ms ST Segment—0.5-1.0mm ST elevation V1-6 that is less than 25% the height of the T wave in V6 (4mm). No reciprocal ST de-pression. Notching of the J-point that is most prominent in leads V3-5. QT Interval—not prolonged Diagnosis—Most consistent with benign early repolarization. Benign Early Repolarization is characterized by:

- Diffuse STE that is most pronounced in the precordial leads (typically V2-5) but typically not very significant in comparison to QRS. STE in V6 should be less than 25% the height of the QRS - Notching/Slurring of the J-point - Prominent, concordant (same direction as QRS) T waves - No reciprocal changes (ST depression, T wave inversion)

Would you expect the EKG abnormalities to be more or less pronounced if the patient’s heart rate increased to 110? The STE and notching/slurring of early repolarization actually become less noticeable as the heart rate increases.

Resource Links: Life in the Fast Lane Dr. Steve Smith’s Blog

Created by William Burns, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd

Unit 2, Case 5—Early Repolarization

65 y/o M with a history of a STEMI 3 weeks ago presents to the ED from

his cardiologists office because an outpatient echo this morning showed a

“clot in my heart”. He has had not chest pain since his MI 3 weeks ago.

HR: 65 BP: 118/66

RR: 12 O2 Sat: 98%

What is your interpretation of the EKG?

History/Clinical Picture

Rate

Rhythm

Axis

P Waves

Q/R/S Waves

T Waves

U Waves

PR Interval

QRS Width

ST Segment

QT Interval

Putting the EKG together with the clinical history, what do

you think is going on with this patient?

How should this patient be managed?

Foundations EKG I - Unit 2, Case 6

Triage EKG—Unit 2, Case 6

EKG courtesy of Robert Cooney, MD, MS

What is your interpretation of the EKG?

History/Clinical Picture— 65yoM presents for evaluation of intracardiac thrombus 3 weeks after MI.

Rate— 72

Rhythm— sinus with PACs (beats 5 and 9)

Axis— normal

P Waves— normal. PAC most obvious in V1 with change in P wave morphology from negative to biphasic

Q, R, S Waves— pathologic Q-waves in V1, V2

Any Q wave meeting the following criteria are suggestive of prior myocardial infarction

All leads except V2-3: ≥ 0.03s (3/4 of a small box) and ≥ 0.1mV deep (1 small box)

Leads V2-3: ≥ 0.02s (1/2 of a small box)

It is important to note that Q waves that are < 25% the height of the R-wave may be normal

T Waves— inverted in aVL

U Waves— not present

PR Interval— normal

QRS Width— borderline at 110ms

ST Segment— 1mm STE in V1, 1.5mm STE in V2 and V3

QT Interval— normal

Diagnosis: Sinus rhythm with PACs and STE consistent with LV aneurysm

Discussion: This patient recently had a large anteroseptal STEMI and the EKG findings of large q-waves in V1 & V2 with

persistent ST-elevation suggests left ventricular (anterior wall) aneurysm. The aneurysmal segment is likely hypokinetic or

dyskinetic and, in conjunction with a reduced ejection fraction, may contribute to blood stasis in the ventricle. This patient’s

history is most suggestive of intra-cardiac thrombus, possibly within the aneurysm itself. This patient is at high risk for em-

bolic events and should be initiated on anticoagulation, and admitted to the hospital.

Created by Duncan Wilson, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd

Resource Links: Life in the Fast Lane

Unit 2, Case 6—LV Aneurysm

63yF with hx of CAD sent to the ED from clinic for 1-2 weeks of

decreased PO intake

What is your interpretation of the EKG?

History/Clinical Picture

Rate

Rhythm

Axis

P Waves

Q/R/S Waves

T Waves

U Waves

PR Interval

QRS Width

ST Segment

QT Interval

What treatment options do you have for this patient and

how do they work?

Foundations EKG - Unit 2, Case 7

HR: 78 BP: 140/90

RR: 18 O2 Sat: 97%

Triage EKG—Unit 2, Case 7

What is your interpretation of the EKG?

History/Clinical Picture—age and known CAD, decreased PO intake concerning for AKI and electrolyte derangements

Rate—78 (13 x 6) or ~75 (4 large boxes)

Rhythm—Sinus Rhythm

Axis—Normal, I positive, aVF positive

P Waves—normal

Q, R, S Waves—Q present in III but no other Q’s in contiguous leads

T Waves—Very tall, peaked T waves with narrow bases that are most prominent in V4-6

U Waves—no pathologic U waves noted

PR Interval—approximately 160ms, no PR depression or elevation

QRS Width—narrow, ~90ms

ST Segment—no ST elevation or depression

QT Interval—not prolonged

Diagnosis—Most consistent with hyperkalemia.

What treatment options do you have for this patient and how do they work?

Stabilize Myocardium—Calcium is the only option that stabilizes the cardiac membrane

Intracellular Relocation—Insulin/Dextrose, Bicarb, & Albuterol work to activate Na/K pump to move K into the intracellular space

Elimination—Dialysis (most effective), Normal Saline with/without Furosemide (increased urinary excretion), Kayexylate (unclear

efficacy but thought to trap K in the gut)

Resource Links: Life in the Fast Lane Dr. Steve Smith’s Blog

Created by William Burns, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd

Unit 2, Case 7—Hyperkalemia

20yM with hx of asthma c/o severe substernal chest pain. He

thinks his father had his first MI at 48.

What is your interpretation of the EKG?

History/Clinical Picture

Rate

Rhythm

Axis

P Waves

Q/R/S Waves

T Waves

U Waves

PR Interval

QRS Width

ST Segment

QT Interval

What treatment options do you have for this patient?

Foundations EKG - Unit 2, Case 8

HR: 130 BP: 120/80

RR: 20 O2 Sat: 98%

Triage EKG—Unit 2, Case 8

What is your interpretation of the EKG?

History/Clinical Picture—young age and family history of early CAD

Rate—132 (22 x 6) or ~130-140 (>2 large boxes)

Rhythm—Sinus Tachycardia

Axis—Normal, I positive, aVF positive

P Waves—normal

Q, R, S Waves—No pathologic Qs

T Waves—Flattening V3-6, Inversion III & aVF

U Waves—no clear U waves however possibly present in V4-6

PR Interval—approximately 120ms, significant PR elevation in aVR, significant PR depression in V4-6, I, II, aVL

QRS Width—narrow, ~90ms

ST Segment—ST segment elevation is defined in relation to the T-P segment during which the heart is electrically inactive.

ST elevation: ~1mm above T-P segment in Lead I, < 1mm above T-P segment in Leads II and aVL

QT Interval—not prolonged

Diagnosis—Most consistent with pericarditis

The EKG manifestations of pericarditis have classically been described in 4 stages but it is important to note that less than 50% follow this pattern. The first 2 weeks are characterized by diffuse ST elevation, PR depression, and the opposite (STD and PR elevation) in aVR. Then over several weeks the ST elevation resolves and the T waves flatten. Next the T waves flatten. Finally, over several weeks the EKG returns to the patient’s baseline.

What treatment options do you have for this patient and how do they work?

Colchicine—First line in patients without contraindications as it reduces rates of recurrent pericarditis

NSAIDS/Aspirin—First line, typically 2 week course at a therapeutic dose (ex. Ibuprofen 600-800 q8 hrs)

Corticosteroids—treatment option for patients with Colchicine/NSAID/Aspirin contraindication (increases recurrence)

EKG Resource Links: Life in the Fast Lane Dr. Steve Smith’s Blog Pericarditis Treatment: Rebel EM

Created by William Burns, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd

Unit 2, Case 8—Pericarditis