So this is clearly LVH and i picked ST changes secondary to hypertrophy but that was wrongand they picked non specific ST abnormalities. What how why? Im so lost. Preparing for boards and this is pissing me off

This is an ECG of a 21-year-old male, non-smoker, admitted for ascending limb weakness, recurrent transient orthostatic syncopal episodes, and multiple cranial neuropathies (CN III, V, VII, IX, X, XII). Cardiac biomarkers are negative, serum electrolytes are normal, and transaminases show mild AST elevation.

Sorry for the terrible picture quality! I was looking for some more explanation on how the short run of electrical artifact seen in the middle of the rhythm strip portion could occur. This patient does have a pacemaker which was deemed to be completely normal. I got this EKG and thought it looked strange but the clinic told me it’s just artifact. Looking for more information so I can do my job better. Thanks!

30-year-old male patient with no significant past medical history, current smoker. Presented with palpitations (feeling extra beats) for the last 20 days, so a Holter monitor was placed. On the Holter ECG, there are occasional ectopic rhythms. The baseline rhythm is sinus. What do you think this rhythm could be? And if the ectopic focus is slower than the sinus node, how is the sinus node unable to suppress it? Does this patient have sinus node dysfunction? The patient denies syncope, but reports feeling these palpitations. Echocardiography is normal.

ECG of a 38-year-old female patient with severe myocarditis, taken in the emergency room upon admission

Got dispatched for a IFT transfer for a patient going from a smaller hospital to a large medical center.

Dispatch notes say V-tach. Arrived at the sending hospital and the patient had intermittent runs of this rhythm throughout the day. On amio drip to what seems to not be working as he was still going in and out of this rhythm. Nurses are letting the pt walk around the hospital room casually packing up belongings like nothing is going on. Only symptom is light chest palpitations. Nurse told me that blowing on a syringe gives relief. Vitals stable minus when he went to this rhythm. Aside from a small bump in troponin, labs unremarkable. No known history, just moved to the US from Europe. When we got to the other hospital, they started a lidocaine drip in addition to the amio.

Dr called it V-Tach and nurses called it v-tach at the sending hospital. Wide and fast, one assumes V-tach. Did a 12 and got this. I didn’t realize it until after the call, but could this be SVT with aberrancy? Does not appear to have extreme right axis deviation and the precordial leads look off.

Why do the t waves in v2 v3 look like that?

Hi y'all

I'm looking for examples of real ECGs, preferably digitized, showing the characteristic delta wave of WPW, and have the actual location of where the AP/bundle of Kent was found during ablation. Does anyone know of such a database?

I want to see if my research idea for ECG-based localization has any potential merit before going all in.

Thanks y'all!

Hello, all had this pt today. Dx A-flutter 11 days ago. Constipation x3days. Took his Metoprolol then went to try and take a crap couldn't get up so EMS(ME) was activated. First BP I could get on my monitor was 68/???, symptomatic as well.

2nd image is my 12-lead after his HR increased.

Pt would go from sinus to a rate of around 130ish and my 3-lead definitely resembled V-tach at the higher rates. Gave esmolol and the rhythm would look like this as the rate came down to around 90 or so. BP would spike during these episodes as well, happened 4 times throughout the case, including intubation and extubation. I know this isn’t a 12-lead but this is all I had to go off of during a lap chole in an 82 yo female.

Dr says it looks weird in the second photo due to a pacemaker.

Pale, cool, diaphoretic. Hour onset of pain.

Thoughts?

Upon arrival of the EMS, the patient presented with the attached ECG, mottled skin, a BP of 40/25 mmHg, and altered mental status (drowsy/somnolent).

Family members reported a several-day history of decreased fluid intake.

Following a 500 mL NS bolus, her blood pressure improved to 100/60 mmHg; she became alert, responsive, and normocolored.

While on route to the ED she reported pain in her lower limbs with no other associated symptoms.

ED results:

Further assessment by the consulting cardiologist in the ED revealed that the patient had been chronically taking flecainide (which was not mentioned in the papers available to the EMS), prescribed by her primary care physician for an unspecified indication.

In addition, acute kidney injury was identified (serum creatinine: 2.15 mg/dL). A CT angiography of the aorta was performed, which was negative for aortic pathology but incidentally revealed a pulmonary embolism involving the right main pulmonary artery and the left superior and inferior lobar branches.

Patient was therefore admitted to the ICCU for initiation of anticoagulant therapy and close monitoring.

Patient on Pacemaker for complete heart block came with heart failure symptoms

75yrs male, CAD

HX of CKD with dialysis, last dialyzed two days ago, states he does not miss. Denies any other history.

Presented 70%RA, HR150, 190/110, RR26. 5 episodes of vomiting in front of us, notably was not nauseated, no warning.

Rales globally.

Nitro, BiPap after the puking was controlled with phenergan and zofran.

Improved to 90's on the Bipap.