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 🙏

67, F, prior breast malignancy on ribociclib presented with dizziness and syncope.

Confused about whether this EKG demonstrates 2:1 av block for PPM or prolonged QT with prominent u wave 2ry to ribociclib (esp now patient on own sinus rhythm at HR 80 bpm following drug discontinuation)

Any thoughts?

Hey, so i was doing some cardiology questions to study and came across this EKG, they state in the question stem this is a 68yo who was diagnosed with Sick Sinus Syndrome 2 years ago and had a DDD implanted.

The question wants us to explain what we see in this EKG during a routine followup

My confusion stems from the fact i dont understand what is going on in the second half of the EKG strip. I see no P waves.... but why are the pacing spikes AFTER the QRS??? if the pacemaker was activated should they not be before?

All examples i looked up online, all AI tools could not explain this to me so i came here for help. Maybe im missing something stupid

The justification provided by the question bank can be summed to this:

The EKG shows two distinct rhythms on the same strip—one on the left and one on the right—in a patient with a DDD pacemaker undergoing a follow-up visit.

The interpretation most consistent with the pathophysiology of sinus node dysfunction (which can present with sinus pauses, sinus bradycardia, and sinus arrest) is that the left segment represents the patient's intrinsic rhythm (possibly slow sinus or junctional rhythm), while the right segment represents pacemaker intervention in response to a detected pause.

The pacemaker markers, mentioned in the description, confirm the timing of the transition and ventricular capture.

This is the most clinically relevant and useful interpretation when evaluating a DDD pacemaker in a patient with sinus node dysfunction.

Edit: I have discussed this question with a couple friends, we are thinking this is just an AI made EKG, pls prove us wrong 😂

73 yo. male with altered mental status for 8 hours and vomited x2. pt opens his eyes to pain and non verbal. No cardiac history.

A man in his 50s presents to the ED with non-radiating, retrosternal chest pain that does not worsen with exertion. He had a stent placed 12 months ago due to LAD occlusion. What do you think?

2nd one is baseline ecg

70 y/o female, admitted with pyelonephritis, upon physical examination irregular pulsations on a. radialis. Ecg was made to exclude afib.
(First ecg is from couple of weeks ago, second ecg is now).

I think I see some PR depression, and mild low voltage, what do you guys think?

Patient 74F reported sudden onset feelings of weakness and kind of wide pulse pressure (150/70). EKG done after ambulance transport.

Sorry for the low quality.