PE-classification massive, submassive, non massiveThis 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 fistulaVery 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. PneumomediastinumRisk 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
0 Comments
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. References Many em doctors have asked what is the best way to prepare or practice MCQ’s. I suggest the following : 1. Join ACE the ACEM ! We will cover about 100 MCQ’s in detail over 6 months during the course ! 2. Have a look at www.apemaustralia.com.au/ apemaustralia.com.au MCQ’s will be released on that sister site focusing on PEM topics with discussion of answers during the course. 3. 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. 4.
Check out Emcq practice 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. 5. A review of the MCQ packages attached with one of the main texts : Dunn Tintinalli Rosen’s EM 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 remember - 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 : TIMI HEART ED ACS ( accelerated chest pain pathways) Aus cardiology society cp guide - high intermediate and low risk Approach to an ECG: Rate Rhythm Axis PR / elevation - depression / P Ta elevation QRS - rule out BBB / LVH / hocm / ER / brugada first Then consider ST segment for stemi or nonstemi Qtc 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 ELEVATION mnemonic Electrolytes Early depolarization ( low medium high risk) LBBB Ventricular hypertrophy / hocm Aneurysm Arrhythmia eg brugada aortic dissection Takotsubo - 💔 broken heart syndrome Intracranial haemorrhage 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 Increased mortality 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 ! 💔 🖤😎 |
Archives
June 2020
Categories |