a common dilemma on a daily basis in adult ED's is the patient with an ECG with ST elevation - does this patient warrant urgent angioplasty or thrombolysis, or is it non-ischaemic in nature?
step 1 - could it be hyperkalaemia?
one needs to have pattern recognition of the features of potentially fatal hyperkalaemia which include ST elevation, wide QRS, etc.
step 2 - is there a LBBB pattern present?
look for a pacing spike in any broad complex rhythm - ST elevation is usually seen in inferior and precordial leads
look for P waves to help exclude a ventricular rhythm and help confirm it is a LBBB
a presumed new LBBB in the context of ischaemic chest pain is usually an indicator in itself for urgent angioplasty or thrombolysis.
a previously documented LBBB makes Mx of possible AMI and the interpretation of ST segments difficult - see Left Bundle Branch Block (LBBB) for possible solution whilst awaiting cardiac enzyme studies
not much point continuing on in this algorithm here!
step 3 - is there a RBBB present?
the ST elevation of Right Bundle Branch Block (RBBB) is usually in lateral leads (rule of discordance - ST/Twave is directed opposite to terminal portion of QRS in BBB)
one should consider the rare but potentially fatal Brugada syndrome if there is ST elevation in V1-2 as well in a young person.
step 4 - which leads is the ST elevation present in?
NB. for ST elevation to be regarded sufficient to embark on reperfusion in AMI, it must be consistent with that of an AMI and must satisfy either:
presumed new ST elevation of 1mm or more in two or more contiguous limb leads, or,
presumed new ST elevation of 2mm or more in two or more contiguous precordial leads
if it does not satisfy the above and the patient presents with possible ischaemic chest pain, then repeat ECG's looking for dynamic changes.
ST elevation mainly in aVR
think about life threatening left main coronary artery occlusion, proximal left anterior descending artery (LAD) occlusion or severe multi-vessel disease
if ST elevation in V1 but ST normal or depressed in V2, look closely at inferior leads as this could be a RV infarct - consider doing right precordial leads
if ST elevation only in V1 and V2, then if R:S amplitude ratio at least 1 then consider a posterior infarct - consider doing V7-9 leads
if ST elevation also in aVR and it is greater there than in V1, then consider infarct due to occlusion of left main coronary artery
if complete or incomplete RBBB (ie. RSR' pattern) then consider Brugada syndrome or infarct
if R waves with T wave inversion, consider potentially lethal Wellen's syndrome (critical proximal LAD stenosis)
if tall R waves, elevated J point, < 50yrs old, no reciprocal ST depression with no change over time, then consider benign early repolarisation
if deep Q waves with ST elevation then consider either:
LVH
ST elevation mainly V1-3 proportional with deep S waves
ST depression in lateral leads proportional with positive QRS
if ST changes out of proportion to QRS changes or convex then consider infarct
LV aneurysm
ratio of T wave amplitude to QRS amplitude in V1-4 is low (<0.2)
QS or Qr waves, relatively low ST elevation, some T inversion
delayed presentation of (antero)septal MI
none of the features above, then strongly consider (antero)septal MI, particularly if temporal, convex and with reciprocal ST depression.
other conditions which much less commonly cause right precordial ST elevation:
pericarditis but usually concave and ST elevation in inf/lat. leads as well