PE-classification massive, submassive, non massive
This was a tough session today with some difficult cases and questions. PE classification based on clinical shock, uss evidence rv dysfunction or tn leak indicating damage or dysfunction. Check out Dunn or UTD on this topic
HIV and fistula
Very low CD counts = Cell mediated immunity severely affected = viral infection, fungal infection, then TB and microbes. See the document on UTD regarding immune deficient patients such as HIV or chemotherapy patients. Also review Harrisons for a good review of the subject. Pertinent as a disease modifier on the floor and in exams.
Risk factors - esp alcoholic patients / boerhaves
present with chest pain and sepsis
cxr findings can be subtle - cardiac borders outlined sharply, continuous diaphragm sign etc - check radiopedia or Rabi et al.
polymicrobial - needs broad spectrum management of sepsis - NGT / enteric tubes for feeding
This is not an easy thing to do. The source of the wct is from outside the normal Sa- avn - his purkinje system. In both VT and wpw avrt anti d, the source is from a nidus outside this system and in the ventricle.
The following rules were developed knowing that it is an imperfect science. Wpw avrt ant d occurs in 6% of wct. It should be considered in patients without structural
Heart disease or the common risk factors for VT ie ischemia and cmo.
Look at V4-V6
If all qrs complexes r negative = VT likely
If positive , look for qR in V2-6 , if present = likely VT
If not - look for av dissociation - If present = likely VT
If none of above is present, consider wpw avrt antidromic circuitry
Do not give adenosine or any drug that could block the av node.
DC cardio version synchronized in a well patient 100J or unsychronised in a ALOC patient is the treatment option if wpw antidromic avrt is considered.
Many em doctors have asked what is the best way to prepare or practice MCQ’s.
I suggest the following :
Join ACE the ACEM ! We will cover about 100 MCQ’s in detail over 6 months during the course !
Have a look at
MCQ’s will be released on that sister site focusing on PEM topics with discussion of answers during the course.
An excellent text to review is
Emergency Medicine MCQ’s
by Waruna de Alwis and Yolande Weiner
It has a range of contributors ( including me 😁 - no financial interest though) and really covers the breadth of EM well.
It has a large bank of mcq’s Written by facems who are involved in acem exam teaching. The commentary and references are pretty good.
A review of the MCQ packages attached with one of the main texts :
Is a good way of covering all the syllabus. Because time is short - I suggest just going thru 1 of these packages combined with the above resources first.
We completed a very important session today - Resuscitation and shock.
Review the documents published by Ilcor - these are vital to review.
Download the resus booklet published by Ilcor.
Review the documents published by Australian Resuscitation Council.
Areas for specific review include neonatal and paediatric resuscitation.
Post cardiac arrest hypothermia also important.
Inotropes, aortic balloon pumps, LV assist devices and ECMO are receiving increasing attention from acem.
Classification of shock and the surviving sepsis campaign 3 for Australia are further areas we reviewed.
The first session of cardiology 2 has just wrapped up. It was a tough session with some tricky subjects covered. The team doing the session actually did very well considering the difficulty of the questions.
Takotsubo syndrome - review uptodate
- mimics acs, no CAD on angio, modest rise of trop too small for the level of distress and pain and cardiomyopathy present, apical hyokinesis on bedside echo,
mayo clinic criteria
bnp pro / tn I ratio most sensitive marker
physical stressors more prevalent then emotional stressors
VT - review uptodate
VT vs SVT vs WpW AVRT
VT - concordance, av dissociation, NW axis, fusion or capture beats
VT vs wpw avrt - v4-v6 - ? negative ? qR - if not - consider wpw
Aortic Dissection - review uptodate or emedicine
clinical features - risk stratification - complications - ecg findings - classifications - compare the tests - management
- aortic vlave leaf malcoaptation
- ant impulse therapy in ed
- learn infusion doses for esmolol / labetolol / metoprolol / SNIP
- know to read a cross section CTA
Key concepts covered in the cardiology webinar today:
Chest pain stratification scores :
ED ACS ( accelerated chest pain pathways)
Aus cardiology society cp guide - high intermediate and low risk
Approach to an ECG:
PR / elevation - depression / P Ta elevation
QRS - rule out BBB / LVH / hocm / ER / brugada first
Then consider ST segment for stemi or nonstemi
Drugs / dig / electrolytes / toxin
STEMI patterns on the ECG, localization of the lesion eg anterolateral stemi, correlation with specific coronary vessels involved
STEMI differential - note not all stemi has reciprocal change
Early depolarization ( low medium high risk)
Ventricular hypertrophy / hocm
Arrhythmia eg brugada
Takotsubo - 💔 broken heart syndrome
Inflammation - pericarditis / myocarditis
Osbourne waves / hypothermia
Vasospasm - prinzmetal angina
AVR - ‘the death lead’ - elevation > 1mm and more than V1 with widespread Sr depression = Left main stem equivalent lesion.
Posterior STEMI diagnosis - look for V1-2 st depression r/s ratio > 1 and upright T waves
Right ventricular STEMI diagnosis
Atrial infarction with PTa elevation - increased mortality
RBBB - acs and STEMI diagnosis is complicated.
AF and flutter guidelines - rate vs rhythm control, drugs to use, chadsvasc2, hasbled score
MJA AF guideline.
Still another 150 ecg’s to go !
Happy studying ! 💔 🖤😎