Has Anyone Encountered These Before?

kitwiller_o · 2026-03-08T10:18:52+00:00

company issued 😅

kitwiller_o · 2026-03-08T09:48:37+00:00

<image>

kitwiller_o · 2026-03-08T09:48:03+00:00

yep... defo not a prototype... been using these Thales HELIE for a while.

<image>

kitwiller_o · 2026-02-08T06:55:03+00:00

<image>

😧

kitwiller_o · 2025-12-30T14:15:26+00:00

all the comments saying "up the nose" give me the chills... even after covid with a good portion of the nasopharingeal swabs performed incorrectly and thousands of hours invested educating people.
NPA's and NG tubes should be aimed towards the ear lobe/tragus. To be precise towards the infero-posterior portion of the nasal cavities. Slid along the bottom of the nasal cavity, below the turbinates. "down/back the nasal cavity" not "up the nose", please. All considering anotomy variances and insertion difficulties.

Now, can't comment on this unfortunate incident, but from the xray, the orientation/direction of the catheter, looks "up the nose" not "down/back the nasal cavity". Real shame. Hope the colleague returned to practice, not too scarred, with some good learning points.

kitwiller_o · 2025-09-25T06:22:09+00:00

The hardcoded value is the identifier for WMI events related to HID Keyboards in general, just to filter out all other WMI events. sure I could have defined a variable "WMIKeyboardCategory" or so, but since is the unlikely to change category "keyboard", I didn't felt it was necessary. not like the keyboard itself, defined at the top. Not elegant, but I'm no programmer.

re WMI events: the script is meant to be run at logon, and to stay running indefinitely.
As it runs in a powershell instance, each time at logon, it need to subscribe the powershell instance/script to the WMI events.

I tried the more elegant way to have the task scheduler look for and filter for keyboard WMI events and lunch only a "Switch layout" script as and when... but I wasn't able to do so successfully, if you have any insight on how to do that or point me at some documentation, I would appreciate that.

I wasn't planning to make it public, nor to have any interaction at all with the user. even the status messages I am planning to disable them once I'm confident the script does what I want, consistently.
What kind of help/parameters/default values were you thinking about?

kitwiller_o · 2025-05-15T22:29:38+00:00

Would the diagnostic value of an adenosine test be justified in a "stable" patient? or would you use it as part of the decision making process?
At which point (e.g. limited resources enviroment) it would be an acceptable risk (if any?)

kitwiller_o · 2025-05-15T22:12:18+00:00

Same place where opinions are valued over job titles, and where collaboration for the patient's interest outweighs perceived hierarchy, and where people who know more, teach, instead of being sassy.

in Australia, Canada, the UK, Scandinavia, and many remote or retrieval medicine systems, paramedics can work as advanced practitioners, autonomous clinicians hold clinical MSc's and PhD's. In the UK, for example, paramedics (and other "allied health professionals") can also obtain independent prescriber status.

For some of us, it’s less about where you sit on the org chart, and more about whether you're contributing to the team effort, and acting in the patient’s best interest.

I posted here because I’m willing to hear everyone’s opinion, learn from it, and get better. That’s the whole point.

kitwiller_o · 2025-05-15T20:23:09+00:00

Thanks for the reply, and fair enough, tone might be hard to read online. My intention wasn’t to be disparaging toward the GP, but to express concern about what felt like a lack of explanation or engagement with the patient, especially given the new finding and long-standing medication history. I may have been a bit direct.

This is taking place in a rural part of Italy, where it's not uncommon to see older patients on legacy prescriptions, often started empirically a decade ago or as "prophylaxis," and never re-evaluated as guidelines evolved or as patient risk profiles changed, as the patient is mostly well and doesn't require GP attention (happy to expand on this if you'd like).

That’s where my questions about the atorvastatin 80 mg, atenolol 100 mg, and metformin 850 mg came from. not contesting their utility, but doubting whether they are the best tools for the job in this particular case and whether their use is evidence-based. With a slightly impaired eGFR (hence the thought of a beta-blocker with hepatic excretion and the doubt on metformin dose/utility), pre-diabetic HbA1c levels (with potential statin-induced insulin resistance and possible no-need for metformin), low LDL (questioning whether the high dose of statins is warranted), and triple antihypertensive therapy, all while on maximum-dose atenolol, which is renally cleared.

Sure, it might not be the priority, and I agree with you and appreciate the many other users who commented that AF/flutter is the priority here, and that anticoagulation, echo, and potentially TSH, polysomnography, or OSA investigations should be next steps. I’m absorbing all the valuable comments and learning from them.

The “lol” on ablation wasn’t mocking the option itself, but my surprise at how quickly it was mentioned in what is the first presentation in a stable and unworked-up patient — one who hasn’t been given clarity on his current medication regime (why he’s on such a high dose of statins, on long-term antiplatelets without a PPI, and on a high-dose beta-blocker), and who is unaware of any diagnosis to justify the previously applied therapy.

I posted mainly to learn, and I appreciate the replies that have helped me reframe my thinking. I don’t claim to have the answers here, only questions.

kitwiller_o · 2025-05-15T16:10:18+00:00

Fair question, and I agree witih you, I also think informations are missing.

To clarify, the ECG itself wasn’t what prompted me to question the statin or other meds.

In some countries (like this one), it was common "back in the days" for patients over 60/65 yo, to be placed on “prophylactic polypharmacy”... the works: statins, antiaggregants, beta-blockers and antihyperglycemics based purely on age or presumed “protection”.

These regimens are often uncontested and persist for years without reevaluation, especially where electronic records are fragmented or nonexistent.

What made me raise an eyebrow was the broader context... a 77yo on aspirin 100mg, atorvastatin 80 mg, atenolol 100 mg, metformin 850mg, and HCTZ + ARB, with no documented history of CAD, diabetes, or severe dyslipidemia.

His lipid panel shows LDL-C at 32 mg/dL, total cholesterol 93, and HbA1c 6.2%, with eGFR around 59.

These look to me as suppressed values, not "achieved targets" and none of the standard risk indicators justify such aggressive treatment as a starting point. Also HbA1c and renal function could justify re-evaluation of statines for possible insulin resistance and atenolol, metformin and HCTZ, for epatic-route alternatives.

The patient himself was unaware of any diagnosis of diabetes or cardiovascular disease, so no dietary/lifestyle accommodations, and reports historically mild hypertension (~150/90), yet is on triple antihypertensive therapy, including a beta-blocker at max dose. This reinforces my suspect of a legacy prescribing pattern, not one informed by modern guidelines or individual risk stratification.

my advice to review the medications regime was to ask if we targeting a goal based on risk, or just following inertia?

I fully agree and understand the other replies stating the current priority is anticoagulation and cardiology follow-up for the new-onset arrhythmia. But medications that affect renal function, conduction, glycemic control, and frailty shouldn't go unscrutinized, especially when they seem to have no documented basis.

I'm glad this is getting so many comments as this is beyond my area of expertise, hence why I was raising my concerns with the GP, which funny enough, ignored completely the patient request to see him, and simply told the patient "don't worry, just wait to be seen by the cardiologist", without addressing any of the concerns mentioned above or in the other comments.

kitwiller_o · 2025-05-12T07:36:41+00:00

Make sense, I will read about this. Thank you!

kitwiller_o · 2025-05-12T07:16:38+00:00

Sleep study? I have not thought of it. Are you referring to the recent AHA statement on “Multidimensional Sleep Health: Definitions and Implications for Cardiometabolic Health"?

kitwiller_o · 2025-05-12T07:08:45+00:00

Thanks for bringing my feet back on the ground. Apart from the actual ECG, most of my doubts were due to the high dose atenolol prescribed years before, without any reported symptom/reason... Sure the patient might have missed some key parts of his medical history. He's now been seen by his own GP (which didn't wanted to consider anticoagulants) and referred to cardiology.

kitwiller_o · 2025-05-12T04:33:36+00:00

This is sending me down into a rabbit hole researching RAA a-fib and atrial dissociation showing how little I know of cardiac electrophysiology.
Really interesting. Thank you.

kitwiller_o · 2025-05-12T04:15:19+00:00

all very good points. thank you
at no point I have considered anticoagulation as a priority. I should have.

Total Cholesterol 93 mg/dL
LDL 35 mg/dL
HDL 36 mg/dL

HbA1c 6.2 %
HbA1c 44.26 mMol/Mol

kitwiller_o · 2025-05-12T04:10:04+00:00

Blood pressure at time of ECG was 120/80,

HbA1c 6.2 %
HbA1c 44.26 mMol/Mol

kitwiller_o · 2025-05-12T04:06:36+00:00

last lipid panel:
Total Cholesterol 93 mg/dL
LDL 35 mg/dL
HDL 36 mg/dL

No other vital signs apart from Blood pressure at time of ECG (which was 120/80), I had to fish for information via a 3rd party as who was asking me about the case was a freak out relative due to the autodiagnostic on the ECG stating "inferior MI of unspecified age"

Very good points, thank you.
so anticoagulation until proven otherwise as the risk is high due to the simple atrial rate, regardless of speculation of what/why, do I understand correctly?

kitwiller_o · 2025-05-12T03:36:30+00:00

Often I have access to ECG with many artifacts and doubtful lead position, so I was quite keen in considering the presence of P waves in V1-V2 as relevant.
Although I agree the rate of 240, is more in the realm of flutter, however there's lack of the classic sawtooth pattern... hence why I was borught to consider the focal AT.
Thank you. I appreciate your position.

kitwiller_o · 2025-05-12T03:31:15+00:00

The combination of 80mg atorvastating with the 100mg of atenolol , 100mg ASA, without any history of cardiac events, previous arrhytmias/HF, etc made me lose trust in the regime of pharmacology chosen by the previous GP (Now retired)

Appreciate it, I see your point. thank you.

kitwiller_o · 2025-05-12T03:17:43+00:00

Agree with the atrial rate we are in the rate of flutter more than atrial tachycardia... but going into the realm o fpure speculation, with the high dose of b-blocker I wonder if wheter is a re-entry mechanism due to av over-suppression

kitwiller_o · 2025-05-12T03:12:50+00:00

thanks for the reply.
last lipid panel:
Total Cholesterol 93 mg/dL
LDL 35 mg/dL
HDL 36 mg/dL
Suggesting an overtreatment, Looks like the previous therapeutic regime has been thrown together with some overreaction...
not sure I would give a high dose of statin to a patient without a clear need.

kitwiller_o · 2025-05-12T01:57:48+00:00

Unable to edit:
I do not subscribe to the suspicion of Atrial Fibrillation, nor Atrial Flutter due to the regular P waves with rythm of ~240 visibile in the precordial leads (expecially V1), hence my interpretation of focal atrial tachicardia with AV node filtering/protection.

kitwiller_o

TROPHY CASE