60’s male, short of breath, copd, nausea vomiting, denies chest pain, no reported cardiac issues. Vitals otherwise stable. I’m still learning so looking for more perspective or maybe an explanation as to how, if it truly is, this is a STEMI.

79yo PT witnessed arrest by family. Family on scene states that PT fell out of their wheelchair and was “having trouble breathing.” Call time to ACLS start roughly about 6 minutes with no CPR performed prior. PEA the whole time, 2 rounds of EPI pushed. ROSC achieved at 8 minute mark after arriving on scene and then lost about 1 minute after. Second ROSC achieved at 15 minute mark, with this 12 lead being obtained shortly after. ROSC sustained to hospital, CATH activated (obviously)

1st EKG

Disclaimer : I don't live in an english speaking country so some terminology might be wrong

So I needed some external validation, approximately a year ago I was seeing patients in a physical rehabilitation unit for geriatric patients, this is from a 70-something male with dementia, no physical complaints. As I auscult him I seem to hear an irregular rythm, so I did this EKG which I interpreted at the time as a 3:2 Mobitz 2 ABV. Later in the day I redid the EKG which showed a seemingly normal EKG apart from bradycardia.

2nd EKG

So I called cardiology for advice with those 2 pictures, the cardiologist who answered was very skeptical as to how I could hear an AVB, and very sternly concluded with a simple bradycardia before hanging up. So 3 questions here :
- Is it possible to hear a Mobitz 2 AVB? I don't know why you wouldn't be able to but apparently the question must either be very obvious or very stupid because I can't find a conclusive answer online.
- Is my interpretation correct on the first EKG?
- Is an AVB typically self-limiting?

Howdy all, current paramedic, year 3 med student looking for help on my interpretation process.

Disclaimer: Shown 12 lead is after 300 Amio, but morphology is unchanged, initial rate was just closer to 200.

Background: 80s y/o M Pt CC 2/10 chest “tightness” onset 1 hour PTA while eating dinner. Pt began taking Rx nitro q10 till EMS arrival [2.4 mg/1hr]. PMH includes “few silent heart attacks”, hypertension, CHF, T2DM; Rx Carvedilol, Furosemide.

On EMS arrival, Pt asymptomatic, no complaints of chest pxn or SOB. Attempted refusal but was convinced. Received aspirin 324, 150amio/10min x2 during transport; remained asymptomatic, hemodynamically stable.

My interpretation: wide complex, monomorphic tachycardia, with RAD. No previous ecg to compare for lbbb, cannot rule out SVT or AVNRT with aberrancy.

I have read this article [ https://litfl.com/vt-or-not-vt/ ] but when following brugada criteria, struggle to differentiate RS complexes (with the exception of V2) in the precordial leads. Any advice on further reading to help with interpretation?

From my interpretation the corrected QT is 402ms . A 40s male came in complaining of light dizziness

Rate: ~60; Rhythm: Regular, seems to have 2 missed qrs complexes after p waves. Increased PR interval. Possible Mobitz II block? Ntot sure what to make of the T/U waves in antyerior precordial leads.

Very confusing to me. Ventricular rate is regular at ~ 27, atrial rate ~85. Seems independence between p waves and qrs complexes. QRS complexes seem wide, possible low voltage? There is a progression through the precordial leads, but haven't really seen such small r waves before, so not sure how to interpret this. Inverted t waves across precordial leads. I would call this complete heart block, but flying blind really.

We were called to our pt c/o SOB. Upon arrival pt was diaphoretic, very anxious, denied chest pain. I heard bilateral rales, had 1 Stent placed a year ago. Did not tolerate CPAP, while moving pt to stretcher pt became pulseless. Started CPR, initially PEA, no shocks, after 2 epi pt had strong femoral pulses with this rhythm with a BP of 110/60. Pt did not wake up, assisted ventilation with igel.

Was this a STEMI? PARTICALLY WITH V1-V3, even with the QRS 138ms? I'm a newer Medic and I'm looking to learn more, thank you.

Hello! A friend of mine that is farther along in med school received a bundle of EKGs from faculty at her school w/ a plan to meet and discuss them, and she sent them along to me to use for my own learning. Obviously I don't have access to the discussion, so I'm flying blind and won't ever get an explanation. Was hoping I could post here and people might chime in. I will say in advance, I am terrible at this and just starting to learn, so apologies in advance for my stupidity! I will post each EKG and my own interpretation; would appreciate any feedback on any of them, even just to tell me how off I am lol.

#1:

Rate: ~50, bradycardic Rhythm: Regular rhythm. No clear p wave, possible p wave buried inside QRS, visible on lead II. Axis: Upright in I, II, and AVF. NormalIntervals: No P waves. QT approximately 400 ms.Waveforms: P wave not visible. QRS: Narrow complex. No hypertrophy. ST: No elevation or depression. T/U wave: T waves upright, no U wave. DDx: Possible junctional rhythm caused by beta blocker or calcium channel blocker.

#2:

Rate: ~46, bradycardic Rhythm: Regular rhythm. Sinus rhythm.Axis: Upright in I, II, and AVF. Normal Intervals: Normal PR interval. QT interval ~500 ms. Waveforms: P waves: Normal QRS: Narrow complex RSR’ pattern in V1. Slurred S wave in V6. Consistent with RBBB. ST: ST segment depression in V3-V6. T/U wave: Upright t waves. Prominent U waves visible in II, V3-V6 DDx: Possible RBBB. Possible acute ischemia given ST depression. Prominent U waves and prolonged QT interval possible electrolyte derangement or medication or substance toxicity.

#3:

Rate: Bradycardic at ~37 bpm.Rhythm: Regular rhythm. P wave before every q qrs. Sinus rhythm, no ectopy or conduction block.Axis: Upright in I, II, and AVF. Normal Intervals: Normal PR interval. Prolonged QT interval. Waveforms: P wave: Normal QRS: Narrow complex. ST: Possible ST elevation in V2+V3. T/U wave: Inverted T waves in V2-V6. DDx: Possible recent myocardial infarction. Unsure the role opioids might play here.

#4:

Rate: ~60Rhythm: Regular rhythm. P waves not visualized. P waves present? Sinus P wave before every qrs? Ectopy QRS after every p? If no, blockAxis: Upright in I, Down in 2, Down in AVF. Left axis deviation. Intervals: No p waves for PR interval. Normal QT interval. Waveforms: P wave: upright in I II, inverted aVR, Biphasic V1 QRS: Wide complex. ST: No ST elevation or depression. T/U wave: Peaked T waves in V2-V6. T waves abnormally upright in V1. DDx: Possible hyperkalemia with peaked T waves and flattening of p waves?

#5:

5.Rate: ~42 Rhythm: Regular rate. Narrow complex. Sinus rhythm. Axis: upward in I + II, downward in aVF. Normal Intervals: Greatly increased PR interval, although variable throughout ECG. Waveforms: P wave: upright in I II, inverted aVR, Biphasic V1 QRS: Narrow complex. No hypertrophy. RSR’ morphology present throughout precordial leads V1-v5. ST: No elevation or depression. T/U wave: Inverted T waves throughout anterior precordial leads. DDx: no real idea on this. Because of prolonged PR, was thinking heart block, but don’t see dropped beats or progressive prolongation of PR.

Sorry for such a long post!

41 y/o male, known drugs and alcohol abuser. Chest pain, intermittent, since 6 hours. Awake for 3 days, used cocaine and amphetamines and ghb and weed besides alcohol the last few days. Was in heavy crushing chest pain at the moment I did this ECG.

Elderly female with unspecified cardiac history. Patient experienced sudden chest pain that felt like an elephant on their chest with difficulty breathing. The EKG was considered insignificant by ER doc.

Hello,

so I need help understanding why the T wave is positive in ALL precordial leads…For example V1: P wave is positive or bi phasic because positively charges ions travel towards V1 which is a positive electrode, bi phasic cause V1 is positioned somewhere in the upper region of the right ventricle but the depolarisation current also must spread to the left atrium so it goes a “a little away” from V1

• all in all a positive current moved toward a positive electrode so we have a positive deflection, hence the P wave which id also positive in all precordial leads.

Next we have a QRS komplex which is “reversed” in V1 (and V2,V3) cause the positive current moves away from the positive electrode creating a negative deflection, hence the “negative” QRS komplex

I also understand why the T wave is positive in leads I,II, III, aVL and aVF and negative in aVR- repolarisation moves from epi to endocardium, so repolarisation moves towards the heart basis…That means we have a NEGATIVE current moving toward a negative electrode (or away from a positive one) and therefore a positive deflection….

So WHY is it that in lead V1 (and all precordial leads) the T wave is positive??? Shouldn’t it be logical that a negative current (ventricle repolarisation) is moving up where the positive V1 electrode is placed creating a negative deflection? At leats in precordial leads where also the QRS is negative (V1 to V3)?

Would appreciate if someone could help with a thorough explanation :)

Thank you in advance!

60 yo post surgery. HR 130

No cardiac hx and no medications. This began this morning without any exacerbating or alleviating factors

I’m a relatively new paramedic that had this patient recently.

50’s male, sudden onset of SOB, diaphoresis, nausea, and dizziness while watching TV. He was also wearing a holter monitor with a potential a-fib diagnosis coming down the pipeline. He initially denied chest pain but had some moderate central pain come on upon arrival at the hospital.

I called the interventionalist, was accepted into the cath lab, and had a pretty unremarkable ~20 minute drive in. Things became a bit less smooth from there. The doc took a look at the above 12 and said “yeah I don’t know about this one”, and said that I had oversold things on the phone. The patient was hit a bit harder by the fentanyl than anticipated and had to be given some naloxone, which also worked a little more effectively than we thought, so now we had a patient that was having a tough time holding still. The RCA proved to be a bit elusive, and after ~40-50 minutes or so on the table and still being unable to find the right coronary, the doc said “forget it, you’re just gonna have open heart surgery instead”.

Given the patient presentation (he looked quite unwell) and the (admittedly small) elevation and reciprocal changes on the 12, I feel good about the decision to call this a STEMI in the field. That said, given the inconclusive cath experience and the skepticism of the doctor I’m second guessing things a little bit.

Would anyone else feel comfortable calling this a STEMI, or am I just looking for something to be there? For what it’s worth, Queen of Hearts feels confident this is an OMI, so at least I have a blurb on my phone that says I did okay lol

Ran a heart alert with inferior STEMI the other week. Patient was diaphoretic with SOB. Pulse was 35-45. BP was hypertensive at 180s/120s the whole time. What is the patho of hypertension with a slow heart rate?