EKG in Tox


80 year old demented female, unresponsive, BP 55/20, blood glucose 24

1. What’s the rhythm?  2. What’s the differential for bradycardia?  3. Think tox – now narrow your differential. What do the vitals suggest?  4. How do you want to treat this patient?

1. What’s the rhythm?

2. What’s the differential for bradycardia?

3. Think tox – now narrow your differential. What do the vitals suggest?

4. How do you want to treat this patient?


21 year old male, suicidal, intentional overdose

1. Rate, rhythm, axis, intervals – you can glean a lot of information from these pieces alone  2. What’s the suspected overdose?  3. Treatment?

1. Rate, rhythm, axis, intervals – you can glean a lot of information from these pieces alone

2. What’s the suspected overdose?

3. Treatment?


41 year old female, sent from methadone clinic for nausea. Given Zofran at the clinic. Was acting belligerent at triage and required Haldol. Records show she is currently on azithromycin outpt for recent pneumonia.

You get this EKG right before she goes into cardiac arrest.

1. What the hell happened?  2. How you gonna treat?

1. What the hell happened?

2. How you gonna treat?


92 year old demented man, wife found him unresponsive near an open medicine cabinet

1. This is a classic dysrhythmia secondary to  which  toxicity?  2. What is a classic, more subtle finding you can see when the patient in normal sinus rhythm?

1. This is a classic dysrhythmia secondary to which toxicity?

2. What is a classic, more subtle finding you can see when the patient in normal sinus rhythm?


EKGotW #4 – Tox Edition


Brown and University of Cincinnati have amazing reference websites for this topic!


Here are some reference tables from their sites with links that you should totes check out!


Beta Blocker Overdose

1.     What’s the rhythm?

a. Junctional bradycardia.

These are QRS complexes without P waves – no P waves means the ventricles are either being triggered from the AV node or more distally (in the actual ventricles).

The complexes are narrow, which means the AV node is likely triggering the impulses, conducting electricity down the bundle of his through the normal conduction pathway.

If the complexes were wide, these might be ventricular escape rhythms – not only do the SA and AV node have their own automaticity, but the actual myocytes themselves may trigger impulses as well.

1.     What’s the differential for bradycardia?

a.     H.I.D.E.

                                               i.     Hypothyroid/Hypothermia

                                             ii.     Ischemia/Increased ICP

                                           iii.     Drugs

                                            iv.     Electrolytes (K, Ca, Mag)

2.     Think tox – now narrow your differential. What do the vitals suggest?

a.     Several toxidromes may cause severe bradycardia. Commonly we talk about calcium channel blockers and beta blockers. (Don’t forget digoxin from David Elkin’s M&M a few weeks ago!)

Classically, hypoglycemia + bradycardia = beta blocker overdose.

Beware of bronchospasm as a clue as well.

3.     How do you want to treat this patient?

a. Glucagon – increases intracellular cAMP and calcium

                      i.   Give with Zofran!

b. Calcium – increase inotropy

c. Epi Drip – for cardiogenic shock

d. High Dose Insulin – 1u/kg/hr, 30-60 min to take effect

e. Lipid Emulsion Therapy – uncertain mechanism

f. Atropine / Pacing can be considered – atropine often ineffective. (Remember, atropine counteracts excessive vagal stimulation, but this is not the etiology of bradycardia in BB OD patients!)
My fave article on this:


TCA Overdose

1.     Rate, rhythm, axis, intervals

a.      Rate = QRS x 6 = 21 x 6 = 126

b.     Rhythm – You can see P waves hiding in I, V5/V6, and maybe small irregularities in the T waves of V3/V4 that hint at presence of P waves. This is sinus.

c.      Axis - Downward deflection in I, upward in aVF = RIGHT AXIS

d.     Intervals

                                               i.     PR < 200msec

                                              ii.     QRS > 120msec

                                            iii.     QTc = QT/Ö(RàR’) = 0.312 / Ö0.48 = 450msec

^^^(I used V2 for this)

Sinus tachycardia with RIGHT AXIS deviation and WIDE QRS complex

2.     What’s the suspected overdose?

a. Hallmarks of TCA Overdose EKG

                 i.  Widened QRS

                ii.  Big-ass R wave in aVR

              iii.  New right axis

iv. Deep slurred S waves, I & aVL

3.     Treatment?

a. Sodium Bicarb pushes

                      i.   Until the QRS narrows

b. Lidocaine for refractory arrythmia

Read about TCA -- http://www.emdocs.net/ecg-pointers-tca-overdose/

Video about TCA -- https://emin5.com/2015/12/22/tca-toxicity/


Long QT

1.     What the hell happened?

a. Haldol, azithromycin, methadone are all QT prolonging agents, which predispose to Torsades de Pointes, or Polymorphic Ventricular Tachycardia

b.     Using V5…
QTc = QT / (Square root of R->R’) = 0.74 / (SqRt(1.08) = 711msec

2.     How you gonna treat?

a. Defibrillate if in arrest

b. 2g Mag Sulfate slow IV push

c. Isoproterenol +/- pacer if super brady

This case: http://hqmeded-ecg.blogspot.com/2014/06/acquired-long-qt-do-not-trust.html

Torsades overview: https://wikem.org/wiki/Torsades_de_pointes


Digoxin Toxicity

1.     Classic Findings

a. This is Bidirectional V-Tach, classic for digoxin toxicity

b. Like David Elkin talked about a few weeks ago in M&M, lots of different arrhythmias possible with digoxin

c. Beware of atrial arrythmias and dangerous bradycardias

d. Classic EKG finding of scooped, down-sloping, Salvador Dali moustache ST segment

Screen Shot 2019-09-27 at 3.17.25 PM.png

Remember the theoretical phenomenon of stone heart – dig tox may give you hyperK. When you treat with calcium, the theory is that it may cause tetany of the myocardium and precipitate cardiac arrest. Digifab (antidote) will treat hyperK, so consider your options.


Dig Toxicity EKG - https://litfl.com/digoxin-toxicity-ecg-library/

Treatment - https://www.wikem.org/wiki/Digoxin_toxicity







EKG in Syncope

Why did each of these patients pass out?



EKG #2

EKG #3

EKG #4


EKG #5


EKG #6



This week’s theme was EKG in syncope!


Third Degree Heart Block

Screen Shot 2019-09-20 at 9.22.55 AM.png


Hypertrophic Cardiomyopathy

Screen Shot 2019-09-20 at 9.24.59 AM.png


Wolff Parkinson White

Screen Shot 2019-09-20 at 9.25.19 AM.png


Arrhythmogenic Right Ventricular Dysplasia (ARVD)

Screen Shot 2019-09-20 at 9.25.36 AM.png




Prolonged QT

Screen Shot 2019-09-20 at 9.26.21 AM.png

Here’s how you can think through your EKG in syncope!

Start from the left side and
work systematically through the rhythm.

Screen Shot 2019-09-20 at 9.38.37 AM.png

Irregular Rhythms

EKG #1

What’s the rhythm?


EKG #2

Dude, what’s the rhythm?


EKG #3

Home skillet, what’s the rhythm?


BONUS QUESTION: What is a Lewis Lead?

EKG #1 - Atrial Fibrillation

·      Super irregular! This is probably the most common irregularly irregular rhythm we see

·      You may have confused this with atrial flutter because of the coarse fib waves in V1

o   First, you’re not alone: 1999 study showed high frequency of incorrect diagnosis, even by cardiologists: https://www.ncbi.nlm.nih.gov/pubmed/10549907

o   It may not matter, since aflutter and afib are treated same way in the ED


But since you’re all nerds like me, here’s how to differentiate…

1.     The waves in atrial flutter are much more uniform than the ones above.

2.     Flutter waves are classically sawtooth morphology

3.     Remember atrial flutter can be regular. It is only irregular when you have variable conduction.

I.e. when you have two flutter waves and a QRS, then three flutter waves and a QRS, then four, then two again…

Screen Shot 2019-09-13 at 5.25.55 PM.png

EKG #2 - Multifocal Atrial Tachycardia (MAT)

·      Multiple foci in the atria triggering the AV node. Look at all the different P wave shapes!

·      Three separate P wave morphologies = diagnostic of MAT

·      The slow version of MAT is a wandering pacemaker (MAT without the T)

·      Classically presents in a patient with COPD or CHF

·      Note that this EKG has R axis deviation, perhaps from cor pulmonale

EKG #3 - Premature Atrial Contractions, Normal Sinus Rhythm

·      So this is yet another irregularly irregular EKG, and at first glance you may call this atrial fibrillation.

·      However, note all the well defined p waves – this is sinus tach

·      So why is it irregular?

·      Before those irregularly occurring QRS complexes, there is a p wave, and it looks exactly the same as all the other p waves (in height, width, and axis)

·      The SA node is firing early, depolarizing the ventricles, and creating an irregular rhythm

What is a Lewis Lead?

Ohmygod, great question, so glad you asked!

From Wikipedia: “A Lewis Lead is a modified ECG lead used to detect atrial [activity] when [it] is suspected… but is not definitively demonstrated on the standard 12 lead ECG.”

So you think someone has atrial flutter (sustained HR of 145 perhaps?) but you can’t see any p waves or sawtooth activity. 

Maybe you’re trying to discern SVT from fast sinus tach?

How can you solve this conundrum?

Lewis Lead!

1. You can do this on the monitor,  you don’t need a 12lead   2. Arrange the leads as seen here.  ( The green one can go anywhere, it’s just an electrical ground )  3. Check for atrial activity

1. You can do this on the monitor, you don’t need a 12lead

2. Arrange the leads as seen here. (The green one can go anywhere, it’s just an electrical ground)

3. Check for atrial activity

Before the Lewis Lead… (where the p waves at?)

After the Lewis Lead! (Retrograde p waves, mostly upright at the end of the QRS. No p waves prior to the QRS. This is SVT.)

Tachydysrhythmia Algorithm

Tachydysrhythmia Algorithm

ST Elevation - Scary or Not?


EKG #1

36 year old, swole, healthy male, sharp diffuse anterior chest pain after pumping mad weights at the gym yesterday. He has a snake tattoo on his shoulder.
Like, what? Why?

  1. How would you describe this EKG over the phone to a consultant?

  2. What's the most likely EKG diagnosis? Anything else on your ddx?

  3. Name two EKG findings that support your diagnosis.

  4. Are you getting a troponin on this patient? If so, how many?

EKG #2

28 year old female, recent fever/cough, now with pleuritic/central/sharp chest pain. Kind of whiney. She’s on her phone.


1.     What’s the most likely diagnosis?

2.     Name two findings that support your diagnosis.

3.     Is this EKG different from the previous? If so, how?

EKG #3

46 year old male with chest pain


1.     What is the diagnosis? What about the EKG supports your diagnosis?

2.     Is this EKG different from the previous two? If so, how?


EKG #1

Benign Early Repolarization

·      BER is a super common EKG pattern, so be familiar!

·      Two main findings:

Screen Shot 2019-08-19 at 9.42.20 AM.png

o   Diffuse concave ST elevation, more-so in the precordial leads (usually < 2mm)

o   Elevation & notching at the J-point.

§  Notching best seen in V4 – may look slurred in other leads

·      Importantly, there are NO RECIPROCAL CHANGES

·      Be suspicious of this diagnosis in patients over 50yo, consider ischemia

·      With regards to the troponin, this is probably a style point, and I’m not sure there’s a right answer. Some attendings probably won’t get one. Most will just order one at the onset and call it a day. Some will argue that you can’t rule out ACS without serial troponins.

EKG #2


·      Like BER, pericarditis also has diffuse concave ST elevation!

So how do we distinguish between BER and pericarditis??

Screen Shot 2019-08-19 at 9.46.27 AM.png
Screen Shot 2019-08-19 at 9.49.44 AM.png

EKG #3

Anterior STEMI

THIS IS AN IMPORTANT EKG. Our job isn’t to diagnose BER – it’s to see if our patient is having a heart attack.


Why is this an AMI and not benign early repolarization?

1.     ST segments are nearly linear and lack the obvious concavity of the other EKGs

2.     There is reciprocal change in lead III (look to inferior leads in anterior STEMI)

3.     Leads V2-V4 have scary (pathologic) Q waves

4.     There is poor R wave progression (there should be at least 3mm in V3 – here it’s 0mm)


Finally, for those of you who want to take it to the next level…


·      This is actually an anterior MI, which is super frightening.

·      It’s concave, there aren’t Q waves, there’s not reciprocal depressions (?III is inverted), though there is poor R wave progression and the T waves look big.

·      There is a crazy formula you can use to distinguish BER from an AMI.

 (1.062 x STE at 60 ms after the J-point in V3 in mm) + (0.052 x computerized QTc) - (0.151 x QRSV2) - (0.268 x R-wave Amplitude in V4 in mm)

·      >18.2 is likely an LAD occlusion.

·      More important than knowing this formula is knowing…

o   Just because you don’t see a STEMI doesn’t mean they’re not infarcting

o   If you’re suspicion is high enough, get a repeat EKG


Benign Early Repol - https://litfl.com/benign-early-repolarisation-ecg-library/

Pericarditis - https://litfl.com/pericarditis-ecg-library/

Anterior STEMI vs BER - http://www.emdocs.net/ber-vs-anterior-stemi/

Anterior STEMIs - https://litfl.com/anterior-myocardial-infarction-ecg-library/


For a super crazy next level anterior STEMI lesson…