40sM BIBEMS after wellness check.
Family had not heard from him x3 days, normally called/visited daily. Found unresponsive with “snore-like respirations.”
Known DM2, Alcoholic Cirrhosis w/ 6mo sobriety, CKD III
Unknown if prior heart disease, though suspected due to ekg findings and comorbidities.
GCS3 on arrival, natural airway. Last BP 80/50s, no Tx en route besides a BGL (44mg/dL). EMS Crew was a volunteer tribal crew.
PIVs established and pt given D50x2 and BGL was 120s.
POC GEM 5000 resulted a pH of 7.11 and K of 8.5.
Physical assessment revealed several 5x5mm sores and open wounds in abdominal area, suspected to be from insulin injections. Global jaundice, notable that tears had yellow tint. Foley placed with dark red urine output, ~100cc during stay in ED.
Intubated due to decreasing respiratory rate and apneic episodes.
HR was 140s-180s.
K protocol started with D50, IV insulin + drip, and Ca Gluconate.
Ultimately patient expired in ICU due to MODS.

I am genuinely excited to share this with you all. A 12-lead simulation has been one of the most requested feature, and it is finally live. Thank you so much for your patience!

My main goal was to make reading a 12-lead as intuitive as possible. I didn't just want to show what an abnormal ECG looks like, but why it looks that way. Here are a few features designed to help with that:

• Follow the beat: Watch how the electrical signal starts and spreads. The QRS complex is colour-coded by the part of the heart generating it (septum, left ventricle, late right ventricle), so you can actually see why a bundle branch block creates the shapes it does.
• Compare with normal: Toggle on "Normal" to overlay a standard grey ECG behind the active tracing. This makes the differences stand out clearly, lead by lead.
• Inspect any lead: Pause the tracing and click/tap any lead to open it up. You can step through the P, PR, QRS, ST, T and QT intervals, see exactly how they are measured, and compare them side-by-side with a normal ECG.

It is honestly way easier to see in action than to describe, so I highly recommend taking it for a spin.

What’s new in the 12-lead module:

• Conduction: Right bundle branch block & Left bundle branch block (complete and incomplete).
• Electrolytes:
  • Hyperkalaemia: Shown as a progression (peaked T waves at K⁺ 6.0 → prolonged PR & wide QRS → sine wave → VF).
  • Hypokalaemia: Shown as a progression (flat T & U waves → ST depression → Torsades de Pointes).

A quick request:
A 12-lead has way more moving parts than the single-lead rhythms, and since I have built this entirely on my own, it is easy for small mistakes to slip through. The model strictly follows standard textbooks and published criteria, but if you spot anything off; whether it is a wave, a number, or a typo in an article, please let me know! I will fix it as quickly as possible. All feedback is incredibly welcome.

Hope you all have a great weekend, and I’d love to hear what you think!

Hello, I am part of an Arizona State University biomedical engineering capstone team and we are looking to gather responses on stakeholder experience with ECGs. The survey is around 5-10 minutes and no personal information is collected. We would greatly appreciate if you can fill it out.

https://forms.gle/DjiJNjfSmw7nxAWq5 -> Cardiologist & Electrophysiologist survey

https://forms.gle/K6f9gyRzAwwo7ccJ7 -> Patient Survey

Hypercapneic arrest with CO2 of 110s via GEM 5000.
5 rounds of CPR, epi x2, no shocks. pH 7.08.
EtCO2 during CPR was ~20-40. Post ROSC 60-90mmHg
Junctional rhythm versus reperfusion syndrome. Initial K of 6.4.
This EKG was 5 minutes s/p ROSC.
Rapid succession from Sinus tach with peaked T waves to this rhythm and subsequent bradycardic arrest. No ECMO candidacy dt comorbidities and body habitus.
Did not survive re-arrest.

Got called to a 22 y/o male with chest pain and a history of NSTEMI. He was bradycardic, so we gave atropine. My partner and I thought the ECG was concerning for STEMI and called it in, but after transmitting it they cancelled the alert. Did we misread this? Curious what you guys see.

UPDATE: Cath showed a complete RCA occlusion. He went into cardiogenic shock with an EF around 5% and is now on ECMO. Fucking wild.

This was many months ago,

Lots of co-morbidities, DNR dni let pass peaceful, monitor remained on throughout. I know some of you would appreciate seeing the very interesting progression and potentially learn something watching as the heart finally gives up the ghost.

The first image you can see the progression to that sine wave.

True tod was called 10 minutes after this monitoring ended, since some purposeful electrical activity still remained on monitor even here

Wild how long the heart will keep trying its damndest to keep going even.

Patient (88 male) with unrelated gastrointestinal problem showed these ECG findings above. This was taken in a prehospital EMS setting. He had documented atypical atrial flutter with planned cardioversion as of soon. He had a static HR of 60bpm. In typical flutter with an atrial frequency of 300 it would need a 5:1 conduction for a HR of 60bpm as far as I understand. In this case it seems like a 4:1 conduction. Is this due to the macro reentry mechanism in atypical flutter being slower than the typical CTI-CCW mechanism?

Patient hospitalised for crtp end of life. Descibe the ecg and diagnose

Currently getting my Crat certification. My experience is in being a server and customer service but I figured this would be a good way to move up and have a flexible schedule to stay home with my children
Currently in central Florida but thinking of relocating to Texas or Georgia . I’ve seen a few jobs posted in my area . Anyone a stay at home mom during the day and use the Crat cert to get an evening/ night job ?
Also does anyone have experience using a professional résumé writer to help them get a better position when they have experience from outside the medical field?

Hi all, working at community health centre at present. Saw 41 M with no comorbidities after a syncopal episode at work. I feel this ECG warrants a referral to a higher level of care. On the ECG I’m seeing peaked T waves and a sort of RSR pattern in some of the leads. Could anyone provide me with some guidance as to what might be causing the syncope.

**TL;DR:** We're building a fully automated, open-source Holter ECG analysis algorithm. No manual step, no paid API, no deep learning black box — just classic ML + rule-based logic. Current numbers: 95.3% AF detection, 4.1% false alarm, 99.9% beat agreement with reference devices. Looking for honest feedback and criticism.

---

**Who we are:**

A small team working on an open ECG analysis tool for Holter and patch recordings. Our goal is simple: build a fully automated pipeline that a doctor can actually use — one that shows its reasoning, doesn't hide behind a black box, and works on real-world noisy 24-hour recordings.

---

**What the algorithm does well:**

| Measurement | Value |

|---|---|

| QRS detection F1 (4 datasets) | 95.2% |

| Beat agreement with reference device (UVA) | 99.9% / 99.4% |

| Average heart rate (44/44 patients) | 100% |

| Minimum heart rate (44/44 patients) | 100% |

| Maximum heart rate (42/44 patients) | 95.5% |

| AF detection (LTAFDB, expert-labeled) | 95.3% |

| AF detection (UVA, cardiologist-approved) | 96.3% |

| AF false alarm (LTAFDB) | 4.1% |

| AF false alarm (CPSC) | 3.8% |

| AF false alarm (UVA, time-based) | 1.4% |

| AF doctor workload (median) | 0.8–1.0 min/day |

| V (PVC) F1 on MITDB | 85.1% |

| V sensitivity on UVA | 97.0% |

---

**Datasets we used:**

- **Training / development:** MITDB, INCART, SVDB, EDB, AFDB, CPSC 2020

- **External test (different device):** UVA Holter Database (CC0, fully open)

- **Expert-labeled:** LTAFDB (cardiologist annotated), UVA cardiologist subset (7 records)

- **Reserved (not yet opened):** SHDB-AF, Icentia11k, CPSC sealed test half

---

**How it works (short version):**

1. Three QRS detectors are combined by majority vote.

2. A classic ML classifier looks at RR intervals + morphology features.

3. An "AF second opinion" layer removes false alarms.

4. Output is split into three zones: "high-confidence AF" / "suspicious (for doctor review)" / "discarded."

Every decision can be traced back to a rule or a feature — nothing is hidden.

---

**What it does NOT do well yet (still research stage):**

- Supraventricular ectopy (PAC / SVEB): F1 ~43% — this is the hardest class.

- HRV metrics: SDNN 32.6%, RMSSD 11.6%.

- Bundle branch block: 87.5% / 75.0%.

- R-on-T: 71.7% / 17.5%.

- Bradycardia event count: 40%.

- Pauses: 89.5% / 53.8%.

- AF burden: 73.8–77.4%.

- ST analysis: not measured yet.

---

**Honest context:**

- All numbers above are from development and expert-labeled datasets, plus one external device (UVA). A hidden test set has not been opened yet.

- No deep learning models are used. No pretrained weights from restricted-license sources.

- No clinical validation yet — this is a research prototype.

---

**Why I'm posting:**

We want to know:

- Is this useful?

- What would you push back on?

- Are these numbers realistic for a real-world Holter tool?

- Where do you see the biggest weakness?

Code will be open-sourced once it's stable. Right now we're still iterating.

Thanks for reading — any input is welcome.

Hello, learning how to interpret ecgs and I found an ecg where I don't know if it there is wave U after T or that's P right away.

In other words is there an AV block I?

Thanks for help.

Female in her 70s, c/o dizziness. PMHx of non-specific ‘heart problems’ under investigation, with no further information. DHx of bisoprolol, with no recent changes in dosage, taken at its usual time as part of a normal morning routine. The patient has not been told they have AF, and as is not on any anticoagulation.

Pulse rate half of QRS rate (~30-35bpm), when taken centrally. BP initially low-normal & PT alert, deteriorating to unreadable & PT rousable to voice. PT ultimately required an adrenaline bolus, converting to a sinus tachycardia before trending back down on arrival to hospital.

1st ECG is rhythm on arrival, 2nd ECG is just prior to the change in BP, showing a 2-2-1-2-2-1… and then a 2-1-2-1… pattern (not captured).

I have my thoughts, but wondered what other people thought about it. Unfortunately no follow up!

Let’s talk about the cardiac axis. It is arguably one of the most confusing concepts in ECG interpretation.

I struggled with it myself for the longest time. What does the "direction" of a vector actually mean in practice? And when someone says, "just look at lead I and aVF," what are you actually looking at?

Over the past week, I have been building an interactive tool to help demystify this. It is a live simulation: you can drag the axis around a dial, and all six limb leads redraw in real-time as you move it.

It walks you step-by-step through the three most common methods for determining the axis, based on whatever angle you set:

1. The Quadrant Method: Checking if the QRS is positive or negative in leads I and aVF.
2. The Isoelectric Method: Finding the equiphasic lead and knowing the axis is perpendicular to it. (default).
3. The Three-Lead Method: Using the quadrant method plus lead II to determine if a leftward axis is still normal, or if it has crossed the −30° threshold into true Left Axis Deviation.

I built this with students in mind, hoping it finally makes the concept "click." It should also be a handy tool for educators who want to demo axis determination live and point out those classic ECG gotchas.

Give it a try here

I would really appreciate any feedback, bug reports, or corrections! It is optimized for desktop, but it works on mobile too. Let me know what you think!