1. Is there STE of at least 1 to 2 mm in 2 anatomically oriented leads? [rules in STE]
2. Is the sum of the Q wave in lead V1/V2 + R wave in lead V5/V6 less than 35 mm? [rules out LVH]
3. Is the QRS complex less than 0.12 second in width? [rules out IVCD - BBB or PCM]
4. Is there ST-segment depression present in at least 1 lead? [rules out BER and pericarditis]
From ERCast / Amal Mattu STEMI vs. pericarditis
Step 1: Look for findings that clearly define STEMI. Is there any ST segment depression in the other leads leads (except AVR and V1-nonspecific). These are “reciprocal changes” and strongly suggest STEMI over other causes of ST elevation. Look at the ST segment elevation in Leads II and III. If the ST elevation in lead III is greater than in lead II, think STEMI. Early repolarization and pericarditis should not have more ST elevation in lead III compared to lead II. Look at the morphology of ST segment elevation. Concave upward (as in a cup holding water) does not rule out STEMI. If morphology is horizontal (tabletop) / convex upward (tombstone), think STEMI. Serial EKGs show increasing size of Q waves ( make sure they are new Q waves) = STEMI
Step 2: Look for findings that define pericarditis. PR depression in multiple leads >2mm. But be warned, PR depression is not only seen in pericarditis. It can also be seen in STEMI, so don’t hang your hang your hat on it. PR depression is also transient. It can last from a few hours up to two days and is most associated with viral pericarditis than other types of pericardial inflammation.
Step 3: If there is still a question as to what’s causing the ST elevation…Perform or order an echocardiogram. Pericarditis-may have fluid. MI-may have wall motion abnormality. Benign early repol will be normal. Serial troponins may help, but what really helps is an old EKG.