Chi non ha mai avuto dubbi sull’interpretazione dell’ECG pediatrico?
Frequenza, ritmo, morfologia sono completamente diversi da quello dell’adulto, ed alcuni aspetti a prima vista molto “pericolosi” sono in realtà assolutamente normali nel bambino.
In questo breve video-podcast Amal Mattu rivede alcuni concetti base dell’ECG pediatrico.
Non un compendio completo di elettrocardiografia pediatrica ma alcuni utlissimi concetti che possono migliorare la pratica quotidiana.
68 years old male referring dizziness and lighthead. Denies chest pain.
Pale cold sweating is laying on bed. Chest and abdominal examination are negative. Cardiac examination reveals arrithmiyc tones and free pauses. No smoking no diabetes.
His past history is positive for cardiac amyloidos (proteinuria Bence Jones k) triple A surgically corrected many years ago. Hypertension and AFib farmacologiccally cardioverted 1 year ago. He is in treatment with Propafenone 150×4, Ramipril and Warfarin. No smoking no diabetes.
This morning ha did a routine control ECG and echo. All the parameters where fine. The documentation is not with him right now so is not possible a proper confrontation with the actual findings.
Vital signs:
BP is 70/50, satO2 room air 98%.
The 12 leads EKG is shown below
and a longer monitor recording….
Which are the EKG findings?
When the patient is invited to stand refers presyncopal signs and tends to faint. BP drops and the skin become pale and sweaty
Which is the racommended management?
Blood exams are normal except TnI tha is slightly elevated (0,23) and the INR is 3
Which is your diagnosis?
Ok I know Amal Mattu already said that: Lead aVR gets no respect!
And to make a long story short, let’s go to the point!
Yesterday morning a very good friend of mine, 60 year old male, send me a photo of the EKG he did as routine control, after a week or so of ongoing non specific (GERDS for his GP) symptoms
Precordial leads
Limb leads
His doctor said he had to do some other tests due to of EKG signs of LVH but my friend said I’m still not well so he called and sent me the photo of his EKG. 9.20 am.
I immediately referred him to the local hospital (where I worked for over 10 years) where he arrived almost 1 hour later.
I called my coll on duty that morning and told him: have you seen ST in aVR? He answered me a little fuzzy and said let’s wait for the Troponin. First sign of no respect . Here is the EKG in ED.
Troponin arrived in 1 hour and the result was 0,02 (normal for our standards).
But what about aVR!!??
So I begged for a bedside echo that showed left ventricular hypertrophy and normal wall motion with good EF (my friend has a mild hypertension on BBlock). So aVR and ST depression were interpreted as sign o LVH.
Second Troponin 5 hours later still negative and still no symptoms. So I called the cardiologist (always on the phone I was on HEMS shift that day) with my “story” about aVR, and he finally gave me credit, but he said: unfortunately no Troponin no symptoms no cath lab.
He was really concerned about the clinical history and the EKG and admitted my friend in ICU for follow up. 17,00 pm
At 17.49 pm my friend called the nurse cause of a chest discomfort, a bedside EKG was recorded and shown below
This time aVR became really important and the cath lab did his job more than 6 hours later: triple vessel disease, 3 STENT placed no complications good angiographic result.
Take home message: always lissen to the Guru, even in Florence!
Thanks Amal.
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Do You…..Torsade?
13 Mag26 yrs old female with PM/ICD implanted for conenital Long QT Syndrome referring one syncopal episode before our arrival.
3 more consecutive episodes occurred during the observation.
EKG records during syncopal episodes (click to enlarge)
The 12 Leads EKG is also shown.
12 leads EKG of the case (click to enlarge)
The symptoms (and the EKG findings ) stopped after Amio 150 mg. The patients was asyntomatic until the arrival in ED.
If the ryhthm during syncopal episodes is pretty clear, the 12 L EKG analysys is really intriguing.
The PM is in VVI mode, but it looks like the atrial sensing is not working and so the ventricle is contracting at his own pace resulting in a rate of 45 bpm. At this rate, as shown on the 12 leads EKG, the QTc is 552 ms (normal value <460 ms in women). This increases the probability of torsade.
It looks like even the ICD is not working properly cause of the absence of shock despite the duratio of Torsade.
In conclusion, malfunctioning PM inducing bradycardia and Torsade. (Very)Suspected malfunctioning ICD.
Amio is not the appropriate therapy (but still an option) in this case.
Magnesium 2 mg is the first choice therapy for Torsade. Lido and isopreterenolo are other reasonable options.
To learn more:
Congenital Long QT Syndrome
Torsade de pointes
Further readings:
The Mechanism of Pause-Induced Torsade de Pointes in Long QT Syndrome
Pediatric Long QT Syndrome
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Tag:ecg, EKG case, Long QT, QT prolongation, Torsade