This 80 year old with a history of CABG had a cardiac arrest. He was resuscitated after fairly prolonged down time, but regained consciousness, though he was confused. He did not state he had chest pain, but, then again, he couldn't remember anything. Here is the prehospital ECG at 1935:
|Sinus rhythm with left bundle branch block (LBBB). There is concordant ST elevation in all inferior leads. Remember that, in LBBB, lead II should have discordant ST depression, and the fact that it does not indicates relative ST elevation. In Sgarbossa's study, just 1 mm concordant STE in just 1 lead was 92% specific for MI and earned the ECG 5 points. There is reciprocal ST depression (excessively discordant) in I and aVL, consistent with RCA occlusion. There is proportionally excessively discordant ST elevation in V1, consistent with RV involvement. There is concordant ST depression in V2 and V3, greater than 1 mm. Just 1 mm concordant ST depression in just 1 lead of V1-V3 was 96% specific for MI and would earn the ECG 3 points. So this ECG gets 8 points PLUS has excessive discordance in V1 PLUS has the finding in many leads, not just one. 3 points gets you an MI by Sgarbossa. There are also marked Q-waves in lead III.|
We did a bedside cardiac ultrasound. Here it is:
This is a parasternal short axis view (a transverse cut through the heart; you see the left ventricle). You can see that the part of the heart closest to the transducer (top) is the anterior wall and is moving and contracting well. The part farthest (bottom) is the posterior wall and is not contracting. This is a posterior wall motion abnormality. This is consistent with MI, though one cannot tell if it is new or old. The structure at the bottom that is moving is the mitral valve, with anterior and posterior leaflets.
This is as clear a STEMI as you can get. Now, it is true that shortly after a non-ACS cardiac arrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality.
This was the initial ED ECG at 1951:
|All the same findings are there, but they have diminished, consistent with reperfusion|
There was some delay in cath team arrival since it was the middle of the night, so this right sided ECG was recorded at 2010:
|The ST segments have normalized in the limb leads and in V1R (V2) and V2R (V1). The Q-wave in lead III persists.|
As it turned out, the patient had an old inferoposterior MI that was scarred; this scar initiated primary V Fib arrest, which in turn resulted in temporary hypoperfusion of the inferior wall because of its very tenuous blood supply and resulting ST elevation on the ECG.
So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome!
This could not have been known without the angiogram. The ECG and ultrasound could not have been differentiated from acute plaque rupture with occlusion of the RCA.