EKGenie March 2018

Case:

63 yo female with PMH of HTN, HLD presets with pleuritic chest pain for 4 days.Pain is substernal, radiates to R shoulder and R neck, worse with deep inspiration and laying backward. 

Vital Signs: BP 158/71, HR 83, RR 17, Temp 98.2, O2 sat 98% RA

Exam: regular rate and rhythm, no murmur, no rub 

EKG1.jpg

+ Rate

80

+ Rhythm

Sinus, regular

+ Intervals

WNL

+ Pathology

o Diffuse ST Elevation o Look at aVR – you see ST depression and PR elevation

+ Diagnosis

Pericarditis

Key features include:

  1. Diffuse ST elevation with PR depression
  2. PR elevation and ST depression in aVR
  3. Concave ST segments
  4. ST elevation in lead II > lead III

+ Why is this important?

As an EM physician we have to know the difference between pericarditis and STEMI. This can sometimes be very challenging. Below is a table comparing the two. We also highly recommend checking out the life in the fast lane link below for Amal Mattu's lecture on this!

+ What should be your next step in mangement

Once you've been the BOSS EM Doc that we know you are and determined that this is NOT a STEMI and is pericarditis, treatment includes: • Aspirin 650-975 mg TID-QID for 1-2 weeks • NSAIDs o Ibuprofen 400-800 mg TID for 1-2 weeks o Indomethacin 50 mg TID for 1-2 weeks • Colchicine 0.5 or 0.6mg BID up to 3 months o in studies comparing colchicine + either aspirin or NSAID vs aspirin or NSAID alone, pts who received colchicine had lower rates of recurrence, quicker alleviation of symptoms and decreased hospital stay. o Contraindications to colchicine use = pericarditis 2/2 to malignancy, TB or bacterial infection/ pregnancy/ significant liver of kidney disease • Steroids – only use in pts who cannot tolerate NSAIDs + colchicine tx • PPI – this is a stylistic point! Remember you're giving your patients high dose NSAIDs or aspirin plus colchicine, or steroids, all of which can cause GI upset. To minimize the GI side effects don’t forget about a PPI

+ Additional resources

• Great LITFL segment on pericarditis vs STEMI http://lifeinthefastlane.com/heres-the-rub-stemi-vs-pericarditis/http://lifeinthefastlane.com/ecg-library/basics/pericarditis/ • L. Lilly, Treatment of Acute and Recurrent Idiopathic pericarditis http://circ.ahajournals.org/content/127/16/1723.full.pdf+html#sec-3 • M. Imazio et al. A Randomized trial of colchicine for acute pericarditis http://www.nejm.org/doi/full/10.1056/NEJMoa1208536 • REBEL EM colchicine for acute pericarditis http://rebelem.com/colchicine-treatment-pericarditis/

Dr Smith’s EKG Blog: http://hqmeded-ecg.blogspot.com.au/search/label/Wellens%27%20syndrome

REBEL EM: http://rebelem.com/r-e-b-e-l-ecg-week-wellens-syndrome-stemi/

Amal Mattu: Wellens? Maybe? https://www.youtube.com/watch?v=5UfPqNL2DaY

EKGenie February 2018

Case:

Case: 71 yo male with PMH of CAD, HTN, STEMI w/ complete occlusion of LAD 1 month prior presents with 3 weeks of bilateral lower extremity edema w/ associated dyspnea.

Initial Vital signs: BP 118/62, HR 100, RR 20, O2 sat 97%, Temp 97.2

Exam: Remarkable only for bilateral pitting edema 

EKG1.jpg

+ Rate

90

+ Rhythm

Sinus, regular

+ Intervals

WNL

+ Pathology

a. ST elevation in V1-V4 b. Q waves most noticeable in V2-V4 c. T wave inversions in precordial leads

+ Diagnosis

Left ventricular aneurysm (LVA)

Key Features of LVA:

  1. ST elevation >2 weeks after a STEMI
  2. Q waves a. LVA in anterior wall can produce a Qr wave = deep Q followed by small R wave or a QS wave = single deep negative wave in V1-V4. b. NOTE** - Q waves can occur within the 1st hour of a STEMI
  3. T wave amplitude is small compared to QRS a. Twave/QRS ratio <0.36 data-preserve-html-node="true" in all precordial leads think LVA b. STEMI's more commonly have hyperacute T waves c. Dr. Smith's blog talks about this in more detail (see link below). He found this was the best way to differentiate between LVA and STEMI
  4. Lack of reciprocal ST depression
  5. Lack of dynamic changes on repeat ECG

+ Why is this important?

Aside from the obvious STEMI vs not a STEMI conundrum, recognizing LVA is important for several different reasons. LVA increases a pt's risk of developing cardiac arrhythmias and subsequent death. It also increases the risk of developing CHF and mural thrombus.

+ What should be your next step in mangement

Call cardiology and admit the patient. These patients will ultimately need an ECHO for official diagnosis. In discussion with cardiology consider giving patient an antiplatelet and/or anticoagulant.

+ Additional resources

Dr Smith's Blog: http://hqmeded-ecg.blogspot.com/2008/11/ecg-review-2_10.html

http://hqmeded-ecg.blogspot.com/2012/01/left-ventricular-aneurysm-morphology.html

LITFL: https://lifeinthefastlane.com/ecg-library/left-ventricular-aneursym/

EKGenie January 2018

Case:

73 yo M PMH of CAD, HFpEF, HTN, cocaine abuse presented with a single episode of chest pain and sob which began 3 days prior while walking after using cocaine that day. CP was R sided, non radiating, lasted seconds, sob lasted about 20 min.

Vital Signs: BP 159/93HR 84   RR 19O2sat 98   Temp98.4        

Exam: unremarkable

EKG1.jpg

+ Rate

90

+ Rhythm

Sinus, regular

+ Intervals

PR 248msec QRS complex 170msec

+ Pathology

o rS complex in V1 o Broad dominant S wave in V1 and V2 o "M" shaped QRS complex in aVL

+ Diagnosis

Left Bundle Branch Block (LBBB)

Key Features of LBBB:

• Broad QRS >120 • Broad R waves in I, aVL, V5, and V6 (Depolarization moving toward these leads) o R waves can be monomorphic, "M" shaped, rS complex, or notched • Broad, dominant, S wave in V1 and V2 (Depolarization moving away from these leads)

+ Why is this important?

According to 2013 ACC/AHA guidelines NEW LBBB ALONE is no longer a STEMI equivalent and NOT a criteria for cath lab activation. However, as EM physicians we must recognize if ST elevation in the presence of LBBB (new or old LBBB) is due to infarction or not.

So how do you recognize this?!

SGARBOSSA CRITERIA!!!!!

Original Sgarbossa criteria: 1) ST-segment elevation ≥1 mm concordant (points in same direction) with the QRS complex in any lead (5 points) 2) ST-segment depression ≥1 mm in lead V1, V2, or V3 (3 points) 3) ST-segment elevation ≥5 mm discordant (opposite direction) with the QRS complex in any lead (2 points) (This finding is less specific than 1 or 2)

+ What should be your next step in mangement

If a patient has a score of ≥ 3 activate the cath lab for PCI or give thrombolytics

+ Additional resources

http://rebelem.com/bundle-branch-blocks101/

http://lifeinthefastlane.com/ecg-library/basics/left-bundle-branch-block/

GREAT Amal Mattu video at the end explaining sgarbossa's criteria worth the ~20 min to watch! http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/

http://www.emdocs.net/left-bundle-branch-block-myocardial-infarction-update/

http://rebelem.com/modified-sgarbossa-criteria-ready-primetime/

http://www.emdocs.net/left-bundle-branch-block-myocardial-infarction-update/

http://rebelem.com/r-e-b-e-l-ecg-week-lbbb-stemi/

EKGenie December 2017

Case:

Your patient is a 27 yo M with no past medical history presents with a chief complaint of intermittent palpitations for the last 10 days.

Vital signs: HR 87 BP 124/84 RR 14 O2 97%RA Temp 98.7

Exam: unremarkable

EKG1.jpg

+ Rate

80

+ Rhythm

Regular, wide complex, sinus

+ Intervals

PR: 100msec QRS: 120msec QTc: wnl

+ Pathology

This EKG is full of many outstanding nuggets of information. However, most importantly, there is a short PR interval, wide QRS, slurred R waves (aka delta waves) This EKG suggests there is an accessory pathway outside of the AV node that allows unfiltered electrical flow through the atria and ventricles. This is why the normal AV nodal pause, represented by the PR interval on an EKG, is dramatically shortened.

+ Diagnosis

Wolff-Parkinson White syndrome

WPW should always cross your mind when evaluating patients complaining of palpitations or syncope. This is especially true with younger patients, as in this case

+ Why is this important?

WPW should always cross your mind when evaluating patients complaining of palpitations or syncope. This is especially true with younger patients, as in this case

+ What should be your next step in mangement

As always, the treatment algorithm begins with the evaluation of “stable vs unstable.” Stable patients, like in this case, should be admitted for expedited cardiac evaluation and ablation. For unstable patients, the treatment of choice is cardioversion or procainamide 20-50mg/min or 100mg Q5min until controlled.

+ Additional resources

Amal Mattu covers the basics: http://www.mededmasters.com/wpw.html

Dr Smith’s ECG Blog: http://hqmeded-ecg.blogspot.com/2013/03/wide-complex-tachycardia.html

Amal Mattu again: https://www.youtube.com/watch?v=3Opx1XMA-yo

EKGenie November 2017

Your patient is a 63 yo F with past medical history remarkable for smoking and HTN presenting with chief complaint of chest pain and diaphoresis. Her symptoms began as she was walking up her stairs and resolved upon rest. She chewed 4 aspirins and came straight to your ED for evaluation. She has no symptoms at this time

 

Vital Signs: Temp 98.6 BP 167/92 HR 90 SpO2 93% RA

Exam: Calm, cooperative; HR regular without murmurs, lungs CTA, extremities and abd unremarkable

EKG1.jpg

+ Rate

70

+ Rhythm

Sinus, regular

+ Intervals

PR ~120msec QRS complex – ~80msec QT interval – 320msec

+ Pathology

Biphasic T waves in V1-3 with inverted, symmetrical T wave inversion (TWI) V4

+ Diagnosis

Wellen's Syndrome

2 types of Wellen’s Syndrome EKG Patterns o Type A (more common): Deeply and symmetrically inverted T-waves in V2-3 o Type B: Biphasic T-waves with initially positive and terminal negativity

Usually V2-3, can extend V1-6

+ Why is this important?

This finding is described as a “reperfusion pattern” as it demonstrates restoration of blood flow after a STEMI involving the left anterior descending coronary artery (LAD). Likely from aspirin in this case.

+ What should be your next step in mangement

IV, O2, monitor, advanced airway equipment ready. Call cardiology, as this is a STEMI equivalent!

+ Additional resources

Dr Smith’s EKG Blog: http://hqmeded-ecg.blogspot.com.au/search/label/Wellens%27%20syndrome

REBEL EM: http://rebelem.com/r-e-b-e-l-ecg-week-wellens-syndrome-stemi/

Amal Mattu: Wellens? Maybe? https://www.youtube.com/watch?v=5UfPqNL2DaY

EKGenie October 2017

70 y.o female with past medical history of hypothyroidism and COPD, presenting with chief complaint of “heart racing”. Symptoms began earlier that day. Patient denies any chest pain or shortness of breath.

Initial Vital Signs: HR 112, BP 112/74, RR 18, O2 Sat 100%

Exam: Remarkable only for tachycardia and irregular rhythm

EKG1.jpg

+ Rate

~140-150

+ Rhythm

Irregular, no clear P waves

+ Intervals

PR – do you see any P waves? QTc – normal ~ 400ms

+ Pathology

  1. Irregularly irregular rhythm
  2. No P waves
  3. Irregular “fibrillatory” waves – best seen in V1

+ Diagnosis

Atrial Fibrillation with rapid ventricular rate

+ Why is this important?

Atrial Fibrillation increases your risk of thrombus formation and of embolic stroke!

+ What should be your next step in mangement

Is the patient Stable or Unstable?

Unstable = Cardioversion!

Stable? o Diltiazem: dose = 0.25 mg/kg IV over 2 min followed by a 2nd bolus of 0.35mg/kg IV over 2 min o OR 5mg slow push (max of 50mg) followed by a drip 5-15mg/hr o Metoprolol: dose 5mg IV Q5min up to 15mg

Recent prospective randomized double blinded study by Fromm C et al comparing diltiazem vs metoprolol in decreasing HR <100 data-preserve-html-node="true" in w/in 30 min showed diltiazem had a more rapid rate control

Other drugs o Esmolol: dose = 0.5mg/kg bolus over 1 min, followed by a drip 0.05-0.2mg/kg/min o Digoxin: loading dose of 0.5mg then repeat
o Amiodarone: dose = 150mg IV over 10 min followed by drip

+ Additional resources

EMCrit: http://emcrit.org/emnerd/the-case-of-the-irregular-irregularity/ o Tips on what to do when cardioversion doesn’t work http://emcrit.org/podcasts/crashing-a-fib/

Life in the Fast Lane: http://lifeinthefastlane.com/ecg-library/atrial-fibrillation/

EBM Medicine: http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=53

Rebel EM: http://rebelem.com/journal-update-beta-blocker-vs-calcium-channel-blocker-for-rate-control-in-atrial-fibrillation/

Diltiazem vs. Metoprolol in the Management of Atrial Fibrillation or Flutter with Rapid Ventricular Rate in the Emergency Department. http://www.ncbi.nlm.nih.gov/pubmed/25913166

EKGenie September 2017

Case:

Your patient is a 56 yo F with past medical history remarkable for CKD, HTN presenting with chief complaint of progressive diffuse weakness, malaise and fatigue over the last 3 days

Vital Signs:

Exam: T 98.6 BP 148/92 HR 102 RR 16 SpO2 97% Glucose 99

Alert, conversive but fatigued. No pallor or jaundice

CV/lung/abd: slightly tachy but regular, no murmurs, otherwise unremarkable

Ext: Well healing surgical incision Lt upper arm                                                             

What is your impression of the EKG?

+ Rate

~105

+ Rhythm

Regular wide complex rhythm without associated P-waves

+ Intervals

PR: n/a QRS: 154msec
QTc: 472msec

+ Pathology

T waves appear relatively peaked along septal leads

Regular, wide complex tachycardia without associated P waves should ALWAYS inspire the thought of Vtach…then Vtach…then Vtach again. This, however, is going a little slow for Vtach, which is usually >120bpm. Generally, QRS complexes are wide for 2 reasons: either aberrant conduction (bundle branch blocks, accessory pathways) or rhythms originating below AV node, aka idioventricular rhythms.

+ Diagnosis

Without a previous EKG, this patient has either an accelerated junctional rhythm with LBBB or accelerated idioventricular rhythm (AIVR).

+ Why is this important?

Differentiating from VTach is ALWAYS important. Some etiologies of AIVR include electrolyte abnormalities, ischemia/infarction, structural disease, medications (i.e., digoxin toxicity). Interestingly, this patient was found to be hyperkalemic! Do not forget: hyperkalemia is the great masquerader (aka the syphilis of EKGs)

+ What should be your next step in mangement

Ensure stability of the patient, identify and treat the cause.

+ Additional resources

Amal Mattu ECG Weekly: http://www.mededmasters.com/bizarre--hyperkalemia.html

Life in the Fast Lane: http://lifeinthefastlane.com/ecg-library/aivr/ Medscape: http://emedicine.medscape.com/article/150074-overview#a4

Dr Grauer’s Rhythm Diagnosis Review: https://www.youtube.com/watch?v=Xoju_l0OYFE

EKGenie August 2017

HPI:

Your patient is a 42 yo M with past medical history of HTN presents for medication refill, denying any complaints. Did smoke marijuana about 1 hr prior to arrival. Found to have HR 144, his EKG is below

Vital Signs: T 98.7 137/89 144 RR 14 SpO2 99%RA

Exam: Mildly injected conjunctiva bilaterally, exam is normal otherwise

What is your impression of the EKG?

+ Rate

~140 bpm

+ Rhythm

P-waves present for every QRS

+ Intervals

PR 200 msec QRS <100 data-preserve-html-node="true" msec QTc normal

+ Pathology

P waves in lead II are inverted and they are upright in aVR. The rate here is supraventricular, as there is clear p wave-QRS complex association. However, sinus rhythms, including sinus tachycardia, originate from the SA node. This is located in the right atrium, where the SVC empties into the right atrium. Waves of depolarization that originate from here should create p waves that are upright in lead II and inverted in aVR. This EKG does not demonstrate this typical atrial depolarization pattern, meaning that the pace is being set from an ectopic focus within the atrium.

+ Diagnosis

Ectopic atrial tachycardia

+ Key features

  1. Widespread concave ST elevation <2mm data-preserve-html-node="true"

  2. J-point elevation with notching (often best seen in V4)

  3. Prominent T waves that are concordant (point in same direction) as QRS complex

  4. Normal R wave progression

  5. No reciprocal changes

  6. Stable appearance on serial EKG

+ Why is this important?

Clinically, you should always be wary of tachycardia that does not respond at all to any intervention, especially when it is in the 125-150 range, as this should spark consideration of atrial flutter or other atrial tachycardias. While an astute clinician would have noticed this is not a sinus pattern, it takes an equally aware physician to recognize that the patient is not responding appropriately and the initial impression should be reassessed.

+ What should be your next step in mangement

Ectopic atrial tachycardia has several causes. Structural (i.e., heart failure, valvular disorders), ischemia, electrolyte abnormalities, sympathomimetics (cocaine, caffeine, amphetamines). Identify and treat any obvious, correctable etiologies. Because this is not an AV nodal dependent rhythm, adenosine will not help. Sometimes beta blockers are used but in general, this tends to self resolve. Caution, as persistently elevated heart rates can lead to tachycardia induced heart failure. Overall this is a relatively rare arrhythmia and consultation with a cardiologist in recommended. Admission to assess for structural disease should be considered

Additional resources

Ken Grauer: (start at 8:35 mark) https://www.youtube.com/watch?v=Xoju_l0OYFE&feature=youtu.be&t=8m35s

Life in the Fast Lane: https://lifeinthefastlane.com/ecg-library/atrial-tachycardia/

EKGenie July 2017

HPI:

41 y.o male with no significant PMH, presents with 2-3 months of intermittent, non-exertional chest pain, lasting a few seconds. No other associated symptoms.

Initial Vitals:

BP 126/83, HR 63, RR 16, Temp 97.8, O2Sat 100%

Exam:

unremarkable

What is your impression of the EKG?

+ Rate

~60 bpm

+ Rhythm

NSR

+ Intervals

WNL

+ Pathology

ST elevation in leads V1-V6, II, III, AVF J point elevation with notching (look at V4) Concavity to ST segments

+ Diagnosis

Early repolarization

+ Key features

  1. Widespread concave ST elevation <2mm data-preserve-html-node="true"

  2. J-point elevation with notching (often best seen in V4)

  3. Prominent T waves that are concordant (point in same direction) as QRS complex

  4. Normal R wave progression

  5. No reciprocal changes

  6. Stable appearance on serial EKG

+ Why is this important?

Early Repolarization is a common EKG pattern to recognize, seen in young (< 50 y.o), healthy people. It can mimic pericarditis or acute MI. Be careful of diagnosing early repol in pts over 50 as ST elevation is more commonly due to acute MI. Also remember when calculating a pt's HEART score early repolarization counts as an EKG abnormality!

Is early repolarization truly benign? – A 2009 cohort study showed increased risk of death from cardiac causes in pts with early repolarization in inferior leads (Tikkanen et al, NEJM). Another study showed that in pts with idiopathic V fib there was an increased prevalence of early repolarization (Haissaguerre et al, NEJM)