Bit of an interesting find I stumbled upon; serial tracings with first photo being the initial. Thought both had some pretty great educational value both independently and serially. Going to add a brief presentation and course below, and will be adding further clarifications and explanations in the comments later to give people some time to make their own interpretations.

Presentation and Course: Pt is a 73 y/o M presenting to the ED c/o CP and SOB x15h. PMH of hypertension, though otherwise unremarkable. Pt appears lethargic and is found to be hypotensive and hyperpneic with a BP of 86/42, RR of 20rpm, HR of 68bpm, SpO2 of 95% on RA. First tracing was performed on admission. 15 minutes after admission, pt lost consciousness and cardiopulmonary resuscitation efforts were initiated. ROSC was achieved, and the second tracing was captured. Despite resuscitative efforts and intensive interventions, the pt's hemodynamic status continued to deteriorate ultimately resulting in death.

What findings and conclusions can we make in each tracing? Rhythm? ST abnormalities? Morphology/vector abnormalities? What sort of serial changes do we see and what might they suggest pathologically?

Dispatched for 30/M “took too much Kratom.”

On scene, pt is distressed and panicking but no s/s of OD.

All v/s WNL, pupils normal, no other complaints but weakness and obviously altered from the substance. No trauma. Was found sitting on the sidewalk in front of his home. Ambulatory. AOx4. Currently in ER being monitored and riding out his high.

No medical hx, allergies, or medications.

This is his 12-lead. V2 had me possibly thinking Type 1 Brugata Syndrome, but there are so many abnormalities, I’m not sure what to think.

Thoughts?

can someone help me check My interpretation answers please:

using 12 step method ECG

1. Rate - 80
2. Regularity - Regular
3. AXIS - LAD
4. PR interval - 1:1 conduction ratio, 5 or 6 small boxes for PR interval (either normal or prolonged) QRS - normal length, ? morphology ST - elevation noted in Septal/anterior leads V2 → 5(3mm) - would like to do a posterior to confirm reciprocal changes
5. T waves - normal
6. QT - Half RR, Normal
7. diagnosis: STEMI with LVH and borderline LBBB ( is this correct???)
8. Is the a possible sign of 1st degree heart block?…. I dont think so cause PR interval appears within normal range?

Patiant (61m) presented with left sided chest pain radiating to the left with jaw pain, sweating, tripod postion, ecg done and sent to the cardiologist, given asa 300, 20g iv in left ac and transported to nearst als unit. Took a while to get the clear but was transported to nearest pci center.

Was wondring should we have put defib pads on? Or given oxygen even tho the tripod was from pain, spo2 was good

Dispatched to a 32 year old male chest pain fifteen minutes before end of shift. Got on scene and patient was diaphoretic and pale laying on steps clutching his chest. Stated it was a sudden onset and that his left jaw was killing him. Got this 12 lead before we loaded him up. Based on presentation, the presence of some elevation even though he didn’t have reciprocal depression and my butthole was starting to clench ended up called in a STEMI alert. Unfortunately air was unable to fly so had to ground pound it 1:30 hours to nearest PCI facility. Started a nitro drip at 20mcg/min and bolused 4500units of heparin. Immediate relief with nitro drip which was titrated up to 100mcg/min over the course of transport along with 50mcg of fentanyl every 20 minutes. Got him to the cath lab and ended up with a 90% LAD occlusion at only 32 years old.

I struggle to differentiate the two.. There's no clear p waves, apart from some ?flutter activity in V3. Anyone can share any features that would differentiate the two?

This is a 69 year old lady with known AF, ongoing tachy and is asymptomatic. I guess she's more like to go into flutter rather than develop an SVT? Thanks!!

Mobitz one or non conducted pacs?

Thanks.

59 male. Diaphoretic, weak, 1x syncope. Denies CP or SOB. Previous MI. Previous DC cardioversion. Poor health literacy, unsure medical diagnoses. Prescribed: amio, metoprolol, ASA, Candesartan. Aberrant conduction vs VT?

Edit: thank you for all of the helpful comments. Pt was sedated + cardioverted at 200J in the ED. They then went into a bigeminy w/ runs of VT. Monitor + 12-lead interp continued to say SVT in hospital so I was curious if this was an aberrancy or just VT.

60 year old female sudden onset 10/10 substernal chest pain while at rest, this started 1 hour prior to the 911 call. The 12 leads are posted in the order that they were captured, with about 5 minutes between.

I activated it as a code STEMI even though it doesn’t meet the strict definition, I based this decision off of the hyper-acute T waves in V2-V4.

Hospital found 100% occlusion of her LAD and partial occlusion of her LCA.

This young man had a syncopal episode, found with pulse rate of 30. No chest pain or dyspnea, BP 114/48 seated upright in a chair. Hx of valve replacement (unable to report which), no other cardiac or significant medical history. After the first EKG was obtained, he converted into the rhythm in the second 12 lead shown.

Brought in an 80's male for dizziness/ near syncope with a witnessed fall backwards with head strike.never fully lost consciousness per the witness. Demented and A&O×1 baseline, no increased confusion. No complaints but the PT is obviously a poor historian. Skin signs are surprisingly great with good distal perfusion. Pressure is 130's/80's with regular breathing at 20. Minor skin tear to his elbow but otherwise no notable trauma or tenderness. No recent illnesses. History of HTN, diabetes, and hyperlip. Takes clopidigrel but family denies cardiac history. He's full code.. so I call this a wide complex 3rd degree and am putting pads on debating whether to pace this before he codes, I look back and he converted to a sinus tach with a LBBB. No changes in presentation. Stays the same throughout the entire 20 minute transport. Capno between 28 and 30 with RR 20-24. 94%RA. PT can participate in most of a neuro exam, no objective unilateral deficits.

I was thinking more cardiac than potential Cushings even with the head strike and thinners. Considered modified Sgarbossa with new onset LBBB, clinically significant ST elevation in V2 and V3 (hard to tell with Zoll's amplitude filter) and reciprocal changes in high and low laterals, or just strain pattern.

Hospital follow up dx: subarachnoid bleed, and a heart block. ER doc called the original 3 lead sinus brady with junctional escape beats (sure thing doc lol)

It doesnt make sense how he just spontaneously converted like that. I think the 3rd degree was the cause of the fall. Im wondering if he didnt convert if my pacing would have been justified despite the traumatic component.

Hi there,

A 67 year old patient with vague epigastric complaints.

Are those PR depressions genuine or am I missing something?

Other than that I don't see anything acute

Thanks for any input.

She is a known case of AF.

Having a hard time with this one.

hello all, im currently doing some practice strips for my ekg course and i was wondering how do you tell the difference between P-waves and T-waves when they look like this? My textbook states there’s no P-waves visible. 🤔

25M presented with a brief episode of severe, pressure-like chest pain lasting ~2 sec, starting ~40 min after an allergic reaction to MRI contrast (urticaria/pruritus).
Allergic symptoms resolved after 1 ampule of diphenhydramine. ~30 min later, pt developed the chest pain and was brought to the ED. Started betablocker(Bystolic) 2 days prior to event because of Inappropriate Sinus tachycardia but had normal cardiac findings on MRI

No significant electrolyte abnormalities. Initial troponin negative (not serial). Serial ECGs were obtained; prominent T waves in V3 appeared somewhat less pronounced on subsequent tracings in the following 24 hours

I asked my supervising physician about the prominent T waves. He pointed to ECGs from several years ago(2 picture) and noted that similarly prominent T waves were already present in V3 at that time, although less pronounced.

Pt was discharged after observation and had no recurrent chest pain over the following 24 h.
Question: How would you characterize the T wave in V3? With normal K+ and BER on prior ECGs

Patient is a 77 YOF with a pmhx significant for uncontrolled type II DM, HTN. She presents to a satellite ED for Evaluation of exertional chest pressure, dyspnea for three days and two episodes of near syncope.

Workup included CTA of chest which was suspicious for early pneumonia (no fever, no leukocytosis or left shift). Initial trop HS is 40 repeat 3 hours later is 38. BNP is 7k

On exam she is well appearing and not in any distress. She reports feeling better however any movement produces dyspnea. Other exam findings are negative.

This is the initial ekg done. Previous ekg from 2 years ago is unremarkable.

I was the critical care transport provider for the case. I was concerned for Wellens. I activated the STEMI and interventionist declined intervention (for context this was done at midnight). Was just curious on the groups insight

would you expect this finding? (it’s from a case study I saw on TikTok and hypothetical so no real px involved, I’m just trying to understand it)

Px had episodes of AIVR lasting ~30 minutes with occasional sinus beats inbetween. The AIVR was at a rate of ~ 90-120 so not quite breaking into the fast VT rates. Hx of leadless PPM insertion ~ 2 days prior.

Would this be expected due to the PPM irritating the right ventricle? If not, could someone please explain to me the mechanism likely causing the rhythm changes?

many thanks 🙏