STEMI / NSTEMI Flashcards
List the ECG changes in posterior MI and the likely site of occlusion.
- Horizontal ST depression in V1-V3
- Tall, broad R waves V1-3
- Upright T-waves
- Dominant R wave in V2 (R:S >1)
- STE >0.5mm in V7-9
- Q-wave formation in V7-9
Posterior MI can be caused by either:
- Occlusion of the (L)Cx, or
- RCA/PDA
Which artery supplies the AV + SA nodes?
The RCA supplies:
- The SA node (60% of the time), and
- The AV node
List the site of occlusion in the following STEs:
- V1-2
- V3-4
- V5-6
- II, II and aVF
- STD in V2 - V3
- LAD
- LAD/Diagonal branch (D1)
- LCx/D1
- RCA/PDA
- Sub-endocardial ischaemia OR Wellens OR reciprocal change from posterior MI (Is there peaked T-waves (Wellens) or R/S ratio > 1 in V2 (Post MI)?
List the ECG findings seen in atrial infarction.
PT wave elevation w/ reciprocal PT depression.
List differential for PT depression or elevation.
- Pericarditis - PR depression (with reciprocal PR elevation in aVR and I) -> look for widespread STE with no reciprocal STE (other than STD in aVR +I)
- Atrial ischaemia - PR elevation w/ PR depression in reciprocal leads
What are the non-STE criteria for early re-perfusion?
- New LBBB or as per Sgarbossa
- New RBBB with LAFB
- Inferior wall MI - any STE in two contiguous inferior leads with any STD in aVL
- RV infarction
- Posterior MI
- High lateral MI - STE in aVL w/ STD in III
- De Winters T-waves
- Ongoing pain w/ NSTEMI
- Wellens
- Hyper-acute T waves
List the 4 criteria to define Q-waves as pathological.
- >40mm wide, or
- >2mm deep, or
- >25% QRS height, or
- Any in V1-3
List the 4 differentials for pathological q-waves.
- Old MI
- Evolving MI
- Cardiomyopathies - HOCM (NB in HOCM - Q-waves usually lateral or inf’r and <40ms -> “dagger-like”
- Rotation of the heart - extreme clockwise or counterclockwise rotation
- Lead placement errors
What are the ECG findings in acute Q-wave MI?
- Pathologic q-waves +/- STE in leads corresponding to the territory of infarct.
- Upright T-waves
What are the ECG findings in old/recent Q-wave MI?
- Pathologic Q-waves with normal ST in territory corresponding to MI.
- Inverted T-waves in region corresponding to the infarcted territory.
What is the prevalence of isolated, posterior MI (ie the % of all STEMIs)?
3-11%
What are the ECG indications of isolated posterior MI?
- ST depression in V1-3
- Lack of STE elsewhere on the normal ECG
- R:S > 1 in V1 -> these are effectively reciprocal Q-waves
- Peaked and/or upright Twaves in V2-3
What are the ECG findings of LMCA occlusion?
- Widespread ST depression
- STE in aVR
List 5 causes of ST depression in the (R) precordial leads. How can each be differentiated?
-
Posterior infarct / reciprocal change - also look for:
- look for R:S >1 (reciprocal q-waves)
- upright T-waves
- No other STE (in isolated posterior MI)
- STE in V7-9
-
Myocardial ischaemia
- Contiguous leads V1-3
- Absence of post’r infarct signs
- May be widespread STD (and STE in aVR) in LMCA occlusion
-
deWinters T-waves
- Upsloping precordial STD
- Accompanied by tall, peaked, upright T-waves
-
Hypokalaemia
- Not confined to precordium - widespread
- Presence of U-waves -> long T-U interval
-
RVH - RV strain pattern -> ST dep + TWI in V1-4 (+/- inf’r leads)
- Accompanied by RAD >+150 deg
- R:S > 1 in V1 - opposite of normal
- R:S < 1 in V6 - opposite of normal
- RBBB
- RBBB pattern: QR > 120ms + RsR’ + slurred rS in lateral leads
- STD and TWI common in V1-3
-
SVT
- Widespread STD -> rate related - not indciative of ischaemia
-
Digoxin effect
- Sagging ST segments (“Dali’s mo”)
