Need 2 of the following:
Chest pain (typically sharp and pleuritic, improved by sitting up and leaning forward)
Pericardial friction rub (best heard at the LSB, with pt leaning forward at end-expiration)
New or worsening pericardial effusion
Suggestive ECG changes
Chest pain (typically sharp and pleuritic, improved by sitting up and leaning forward)
Pericardial friction rub (best heard at the LSB, with pt leaning forward at end-expiration)
New or worsening pericardial effusion
Suggestive ECG changes
ECG
Labs
WBC, CMP, ESR, CRP
Consider TSH, ANA based on clinical suspicion
Troponin elevation may indicate a concurrent myocarditis which predispose to risk of CHF or arrhythmia. 
CXR
Typically normal if no pericardial effusion.
Will not see increase in cardiac silhouette size until > 300mL of pericardial fluid has accumulated
Bedside Ultrasound to rule out effusion
~2/3 of cases will have pericardial effusion
Can consider CT or cardiac MRI if workup non-diagnostic and clinical suspicion persists
WBC, CMP, ESR, CRP
Consider TSH, ANA based on clinical suspicion
Troponin elevation may indicate a concurrent myocarditis which predispose to risk of CHF or arrhythmia. 
Typically normal if no pericardial effusion.
Will not see increase in cardiac silhouette size until > 300mL of pericardial fluid has accumulated
~2/3 of cases will have pericardial effusion
Must differentiate from STEMI (classical teachings are not specific enough to do that)
Classically<unk>  has diffuse ST-elevations
However,<unk>  may generate localized ST-elevations<unk>  should never produce ST-depressions (suggestive of reciprocal changes), except in V1 and aVR
Classically pericardidits has concave upwards STE
However, STEMI may have concave upwards ST-segment morphology as well
Rather, it is STE convex upwards or horizontal that favors STEMI
Classically<unk> is has PR-depression in viral<unk>  (or PR-elevation in AVR)
Less reliable in post-MI patients and those with baseline ECG abnormalities
PR-depression is often early and transient in<unk> 
In STEMI, PR-depression is associated with atrial injury, though usually not as marked as in viral<unk> 
PR-elevation in aVR may also be present in STEMI and is infrequently seen in constrictive<unk> 
However,<unk>  may generate localized ST-elevations<unk>  should never produce ST-depressions (suggestive of reciprocal changes), except in V1 and aVR
However, STEMI may have concave upwards ST-segment morphology as well
Rather, it is STE convex upwards or horizontal that favors STEMI
Less reliable in post-MI patients and those with baseline ECG abnormalities
PR-depression is often early and transient in<unk> 
In STEMI, PR-depression is associated with atrial injury, though usually not as marked as in viral<unk> 
PR-elevation in aVR may also be present in STEMI and is infrequently seen in constrictive<unk> 
Leads II and III
STE II > STE III favors<unk> 
STE III > STE II very strongly favors STEMI
STD not in aVR or V1 (reciprocol changes) suggestive of STEMI
May see low voltage/alternans if effusion present
If early repolarization confounding interpretation check ST:T ratio
If (STE)/(T height) in V6 or I > 0.25, then it is likely<unk> 
If predominantly inferior STE, ST-depression in aVL is sensitive for STEMI
Spodick's sign, purportedly in ~80% - downsloping TP segment, often best seen in lead II and lateral precordial leads
STE II > STE III favors<unk> 
STE III > STE II very strongly favors STEMI
If (STE)/(T height) in V6 or I > 0.25, then it is likely<unk> 
TWI don't invert in<unk>  until STE resolved; if TWI and STE simultaneously present, more likely ACS/MI
Stage I:
Global concave up ST elevation in all leads (especially V4-6, I, II) except aVR, V1 and III
PTa depression (depression between the end of the P-wave and the beginning of the QRS- complex)
Stage II:
"Pseudonormalisation"
ST segments return to baseline
Large T waves
PR depression
Stage III:
T wave flattening progressing to inversion
Stage IV:
Return to baseline
Global concave up ST elevation in all leads (especially V4-6, I, II) except aVR, V1 and III
PTa depression (depression between the end of the P-wave and the beginning of the QRS- complex)
"Pseudonormalisation"
ST segments return to baseline
Large T waves
PR depression
T wave flattening progressing to inversion
Return to baseline
Pericarditis
Cardiac
Constrictive pericarditis
ST-segment elevation myocardial infarction 
Myocarditis 
Post-MI 
Myocarditis
Previous MI with recurrent ischemia in same area