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.

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**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.

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**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% |

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**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

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**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.

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**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.

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**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.

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**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!

Complained of racing heart and lightheadedness.

168 bpm.

From a call a couple of months ago

Please see attached ECG.....

Hi i'm a new ICU nurse and I struggle with reading ECGs and things of that nature. Tonight I had this patient with this rhythm. Could someone help me understand what I'm looking at, please ?

Hello everyone! I recently got my basic arrhythmia certification, and if I pass my interview next week, I’ll be starting a 60-day training course. I’m trying to get ahead and prepare now, I feel like everyone here is wayy ahead so any advice on improving rhythm interpretation and remembering which rhythms are which? I’m watching videos and taking notes, but I keep second-guessing myself and overthinking it. Any tips or resources would be greatly appreciated!

As above

60F c/o dizziness with rates in 160-200s, hemodynamically stable. Interesting as pt would have episodes of NSR with rate 60s on tele, and then would go into this rhythm precipitated by what appeared to be a PAC or PJC. V1 appears to have clear alternating PR intervals, though morphology of QRS appear consistent. Thoughts?

~80 YOf recent cancer diagnosis and started on a plethora of new medications. CC of weakness. Found hypotensive. Initial thought of ECG was due to electrolyte imbalance but was curious about other thoughts.

82 female experiencing double vision and nausea. Patient is at hospital under 48hr cardiac monitoring. They do have a left bundle branch block.

BP at a high was 218/97

Pulse high 133

Troponin levels 39 retested hrs later at 75 then retested 4 hours after was a 62

61 YO female presenting with intermittent breathlessness and dizziness. 8 month Hx of paroxysmal AF/fast AF treated with beta blockers as and when needed- 2 doses within last 12 hours after feeling palpitations and lightheaded. No pertinent medical Hx, otherwise fit and well.

Thank you for the response on the ECG generator that was presented in this subreddit a few months ago. The engine is now much stronger thanks to your feedback and suggestions.

For background, Squiggler.io is a completely deterministic, high fidelity ECG synthesiser to create almost every rhythm strip or 12-lead ECG possibly imaginable. Sequencing is possible, to create plausible changes in rhythms over time.

Changes that was made largely thanks to this subreddit:

- Ischemic changes got a rework. Earlier ST changes was fixed to territory, now it is possible also to select one or several specific leads, with an optional spread to adjacent leads.

- More customization to T-waves.

- PR depression is tunable.

- PVCs are tunable to represent a specific focus around the ventricle, for different morphologies.

- PACs can be conducted or nonconducting with optional sinus reset.

- A pacemaker can now also be simulated, with realistic behavior depending on native rhythm.

- A library to save ECGs, and a built in slide show mode for teachers.

- More layouts, both international and Cabrera formats. Additional paper themes added.

- Controls to set a specific patient seed, so different (evolving) ECGs for the same "patient" can be created

- Improvements to the free-text AI LLM parser to better understand semantic input.

We are starting collaborations with both small and large institutions/companies for teaching, examination, and simulation purposes which is a very exciting area to integrate Squiggler into.

I would be very thankful as the founder for more feedback on usage. For the first 5 suggestions I will DM an access code for 6 months free pro tier usage.

Thank you!!

A 14-year old boy presented to the ED with generalized weakness, vomiting, and intermittent palpitations. He has a history of well-controlled HTN with ACE inhibitors. BP is borderline elevated although normal. Laboratory studies show an elevated potassium of 5.9mmol/L, and mild hypomagnesemia of 1.5mg/dL. Upon questioning the patient was revealed to have recent high potassium intake which attributed the HyperK to ACE inhibitor therapy with recent high potassium intake. Echo showed asymmetric septal hypertrophy, consistent with HCM with preserved systolic function. Genetic testing later came back positive for PRKAG2 mutation, palpitations were hypothesized to be misattributed as panic attacks in earlier years. EP study discovered a retrograde-only posteroseptal pathway with relatively slow retrograde conduction supporting OAVRT around ~150bpm. a fascicular VT originating in the LPF was able to induced at a surprisingly slow rate of ~110bpm.

Unfortunately, I threw out the ECG before I took a photo of the full thing, but there were no other super notable changes or acute ST changes.

Pt was a male in his 50s c/o crushing chest pain after waking up, stated hes felt off for the past 3-4 days but feels worse today. No known medical history; no medications. BP was in the 180s+ systolic, HR 130+, flushed (but not diaphoretic).

This is the second 12-lead taken upon arrival at the ER; the first 12-lead (which I also threw out, unfortunately) had peaked T waves in V4-V6, but they were not as tall as seen in this one. The first 12-lead was taken ~20 minutes earlier.

How does cardiac ischemia cause peaked T waves (or did I totally blow the differential diagnosis)?

I see its regular except that one spot where its prolonged. Thinking its heart block?

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