QUESTION 5
MMC Prac fellowship exam, June 2015. Papers marked by: Michaela Mee
Background re: Posterior STEMI
Often missed dx
15-21% of STEMis
strict/ ‘true’ posterior AMI : 3-10%
22% of ‘true’ posterior STEMI have mod-severe mitral regurg
often accompanied by inferior/lateral stemi
Usually due to to occlusion of RCX, but may also be due to RCA occlusion
In 10% of pt, RCX is the dominant vessel
Classic post stemi includes ST dep in ant leads, and also prominent R waves in anterior leads
(equivalent of Q ie once evolving) and prominent T waves too. However the latter ECG changes
not required.
Below is just a guide as to how I marked the question. I am not an examiner
and I have likely been kinder than an examiner would, so beware! Look out
especially for unsafe (non-judicious) use of IV fluids/ certain drugs, given
patient is (1) likely APO and (2) cardiogenic shock. Examiners might give
auto mark of 0 for that section if unsafe dosing.
Pass rate was 81% using my marking system and assuming pass mark
17/30
Part 1 max grade 8/8
Part 2 max grade 12/12
Part 3 max grade 10/10
Part1:
Best answers: (2 pt each)
Best answers give info relevant to the diagnosis, or help exclude differential
+: ST dep V1-4 1-2mm
-: No prominent T waves
-: No prominent R wave in V1-3 (equiv of Q in post leads)
-: No significant inferior/lateral STE (<1mm)
-: Normal SR
..other appropriate
Dx: (Early) (isolated/true) Posterior STEMI
Can add: possible evolving high lateral/inf stemi (not yet meeting criteria), but had to get
posterior to pass question
Can add: in patient with likely cardiogenic shock and APO
Acceptable; (0.5-1.5) but not as useful in deciding diagnosis
Eg Normal axis
Use of term ‘infarct’ rather than STEMI
Wrong/not good/no points: (0)
Put three dx (which do I choose?)
RV infarct
Inferior stemi (STE is not significant in these leads, <0.5mm))
NSTEMI
Incorrect ECG interpretation
Unsafe answer, or missed posterior STEMI: (auto fail this part, get 4/8 max)
Part 2:
Best answers: (2 pt each to max 12)
General:
-Resus, full cardiac monitoring, defib pads, team approach
A/B:
-PPV/CPAP/BIPAP/NIV 100%O2, while prepare to intubate
C:
-IV inotropes eg adrenaline eg 5mcg/min IV infusion, eg 10mcg boluses
-IV, Send bloods GpH, trop, vbg, fbe euc coag
-Cautious IV fluid (eg 250ml bolus NS), careful as likely APO
Rx:
-Referral: cardiology interventionist, for PCI/cath lab urgent
-Antiplatelet: aspirin 300mg
-clopidogrel 600mg, pre cath lab, dosing included
-Analgesia eg fentanyl cautious dosing eg 25mcg increments
Other:
-Confirm dx: posterior ECG V7-9, STE >0.5mm confirms, BUT NOTE: normal post leads doesn’t
exclude posterior STEMI!
Acceptable: (0.5-1.5 each)
IV fluid 500ml NS, but must mention caution/titration/look for response
Notify NOK
Consider mitral valve rupture (TTE) +/- surgical referral
GTN/frusemide if BP corrected
Attach defib pads/ full cardiac monitoring
Remove GTN patch
?check for signs of Aortic Dissection
CXR (1)
Bedside cardiac echo if available quickly (1.5)
Not so great:
GTN infusion given acutely in hypotension (need clarifying statement)
-morphine analgesia ‘2.5-10mg’ (careful how you write drug doses, can be interpreted as 10mg
stat)
?norad upper range 70 mcg/min (this upper range you wouldn’t go to with this pt) need end
points/aims here
atropine 150-300mcg (low dose, and why?)
‘atropine 1mg for bradycardia’ (I wouldn’t do this in STEMI with HR 60)
Unsafe: (auto fail score 0 for that part)
Incorrect dose inotrope eg Adrenaline 5mg/min (likely due to messy writing/rushed writing) =
UNSAFE
-IV fluid 20ml/kg stat (usually people who thought it was RV infarct) NB in APO?
Part 3:
‘Timing’ has been interpreted in different ways. Best to think of as time in relation to induction
drug or order of drugs and time between. Some people made intervals between drug x as per if
you repeated same drug x (ie ‘frequency’) which doesn’t make sense for RSI
1 point for acceptable drug
1 point for appropriate dose
0.5pt for correct timing. Remember this is emergent! 5 min wait between fentanyl and induction
doesn’t make sense!
Best (2.5 each max):
1. Analgesic
eg Fentanyl 100mcg, given pre induction approx 1-2 min prior
2. Induction
-high dose fentanyl would have been good choice (but no one did this)
-Ketamine 2mg/kg approx
3. Neuromuscular blockade :
-Sux 1-1.5mg/kg/150mg,
-or Roc ~1.2mg/kg
4. Circulatory support:
-adrenaline eg infusion 1-200 mcg/min, or 10-50mcg boluses acceptable
-OR metaraminol eg 0.5-1mg boluses IV
OK/acceptable
2. Induction:
Propofol cautiously dosed eg 0.5mg/kg
Midaz cautiously dosed eg 2mg
Not good:
Induction:
-ketamine dose <1mg/kg (too low), or 3-5mg/kg IV (too high)
-2 agents given for induction (cant give points for alternate drugs
Inotrope/circ support:
-metaraminol dose too high, or too low!
-Norad dose too high
-500ml-1L pre induction (that candidate may have thought RV infarct)
-atropine 1mg as bradycardic
Neuromuscular blockade: 2 RSI agents given
Timing:
Eg small doses of fentanyl 25-50 mcg ‘titrated every 4-5 min until total 150-200mcg’: this is not
great in emergent RSI for cath lab
‘Ketamine for sedation’ (sedation is not the same as induction, induction dose given by
candidate)
Unsafe:
-midazolam dose 0.1mg/kg (eg ?10 mg if 100kg??!!)
stat 2 L NS
Unsafe doses --> auto reduction in mark for that section to max 5/10
Examiners likely to be harsher
APPENDIX: to Q5
Appendix 1: from Dr Smith’s ECG Blog
Some ways to differentiate subendocardial ischemia from
posterior STEMI
First, you should know that when there is precordial ST depression due
to subendocardial ischemia, it is not necessarily due to anterior wall
ischemia. Data from stress testing shows that subendocardial ischemia
DOES NOT LOCALIZE on the ECG, and usually is in leads II, III, aVF
and V4-V6. But, again, this does not tell you which artery is involved.
Second, ST depression in V1-V3, vs. V4-V6, is much more likely to be
posterior than subendocardial ischemia.
Third, patients at higher risk of NSTEMI (older, more risk factors, h/o
angiogram with multivessel disease) are much more likely to have
subendocardial disease (vs. younger smoker).
Fourth, patients with reasons to have demand ischemia (tachycardia,
sepsis, GI Bleed, etc.) are much more likely to have subendocardial
ischemia (like in a stress test); those with posterior MI are much more
likely to present with onset of chest pain and with normal vital signs.
Fifth, look for tall R-waves in V1-V3 (the analog of Q-waves in other
locations).
Sixth, placement of posterior leads (take leads V4-V6 and place them
at the level of the tip of the scapula, with V4 placed at the posterior
axillary line ("V7"), V6 at paraspinal area ("V9"), and V5 ("V8") between
them. At lease 0.5 mm of ST elevation in just one lead is very sensitive
and specific for posterior MI.
Seventh, an immediate echocardiogram can make the
distinction. These are very difficult and it is very hard to detect a
posterior wall motion abnormality unless you are very experienced. I
recommend a formal study with Definity before concluding there is no
posterior wall motion abnormality.
Eighth, see above. Whether or not it is STEMI, the cath lab should be
activated if the ischemia cannot be controlled medically: aspirin, nitro,
beta blockers, clopidogrel, heparin/enoxaparin, GP IIb/IIIa inhibitor.