12 Lead EKG in ACS
October 13th, 2009 by RH-111
Print This Post
Tim Phalen – 10/13/09
STEMI vs. Non STEMI – STEMI is ultimate candidate for reperfusion therapy – non STE-MI – much higher mortality rate.
Is the early part of the ST segment elevated – 1mm elevated at beginning – at J point only (J point elevation)
Pick one good segment – pick one where T-P matches that of T-P before it –pick a steady baseline
Notch in ST segment – not always BBB – Not STEMI
Always use the T-P segment to measure elevation
aVR – Looks from top at chamber of Left ventricle – not used because we can’t localize the injury. Also looking at endocardial tissue – wont have same meaning or significance
Evolution of AMI
Ischemia – Endocardial Hypoxia – St Depression – T wave inversion
Injury – Epicardial Hypoxia – causes ST Elevations – being that the epicardial cells have a rich blood supply – must be an occlusion.
Hyperacute Phase - T waves – Tall & peaked – first change – may give illusion of a wide based t wave (vs hyperkalemia) – Tall = in limb leads elevations of >5mm – in chest leads more >10mm – Peaked = don’t want to sit on it
Acute Phase -
Pathological Q wave – =>.04 – or greater than 1/3 of R wave. –Age undetermined
A normal 12 lead does not rule out an AMI
Reciprocal Leads
II III aVF vs. I aVL, V-Leads
Inferior wall MI – single most likely reciprocal lead is aVL
Some MIs start with reciprocals and then show elevations
More than 50% of ST Elevations are not caused by AMI – called STEMI imposters (first 3 make up 80%)
LVH – Primary cause is HTN
increased QRS amplitude – variety of formulas exist – read the interpretation – machine does the math. (Or – look at v1 – from baseline to most negative deflection – count mm – then look at v5 and v6 and count the tallest. add depth of v1 to highest of v5 or v6 – if over 35 you have LVH (if under age 35 use 53mm)
BBB – Primary cause is aging process
Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
Ventricular Rhythms including paced
Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
Benign Early Repolarization (BER)
ST elevations often in lateral leads and lead II
Tall peaked T waves – and tall QRS
Fishhook ST segment
Young healthy male (20-40 years, +African Americans)
does not typically produce reciprocal changes
Pericarditis (epicardium may be inflamed too)
May be in all leads
May be in leads not grouped anatomically
sharp pain
localize with a finger
positional – prefer leaning forward
radiates to base of neck or shoulder blade
might hear friction rub on auscultation
does not typically produce reciprocal changes
5 step analysis
Rate & rhythm
Waveform analysis
st segment
T wave
Q wave
Suspected STEMI
location
Additional considerations
voltage criteria for LVH
QRS width
Reciprocal leads
STEMI Decision
Definitely NOT a STEMI
Definite STEMI
Definite Maybe – EMS needs a plan for definite maybes – Transmit ECGs to ER for consult.
see www.ecgsolutions.com
Right and Posterior Leads
Inferior wall MI – most likely RCA – 40% of time will also have a Right Ventricular MI – Add v3r through v6r (at minimum look at v4r)
Anywhere else – Most likely LCA -
Posterior wall MI – reciprocal changes in v1- v4 (reciprocal q wave would manifest with taller R waves, sometimes)– indicative changes in V7, v8 and v9 (keep going around back – posterior axiallary mid scapular, just left of spine)
BBB Recognition
forget the notch
suspect with wide QRS
normal sinus, a-fib, or any sinus rhythm – suspect BBB
v1 – back off j point – which direction is tail end of QRS – RBBB – points up – LBBB turns down
LBBB – new onset – indication for reperfusion – (Sgarbossa criteria )
Normally BBBs produce discordant QRS-ST (direction of QRS is in opposition to ST)
Both in same direction in any one lead – infarct.
If you have LBBB with concordant (both downward) QRS & ST depressions – suspect MI if it occurs in V1 or V2 or V3
More than 5mm of elevation from baseline to j point – suspect MI in any one lead
Serial EKGs – changes are hallmark of AMI