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)