unit 7; angina + MI Flashcards
what is acute coronary syndrome generally? how many substypes?
with insufficient flow through the coronary tree and the resultant acuteischemiaof themyocardium.
unstable angina
NSTEMI
STEMI
whats the background of ACS?
The acute plaque ruptures with the separation of the cap massive platelet and coagulation cascade activation acutely reduced coronary artery lumen diameter ischemia infarction
whats the diff between stable agina/chronic ishemic HD and ACS?
stable agina is stable plaque with trasnietn pain during activity
ACS is acute change in lumen size, no time to adjust, and sig acute ishemia!
whats the diff between unstable angina, NSTEMI and STEMI?
unstable: Ischemia that last > 30 minutes and is NOT relieved by rest
- Not significant enough to cause infarction but can lead to NSTEMI and STEMI
NSTEMI: variant angina
- ischemia that leads to endocardial infarction/necrosis with myocardial protein leaking
STEMI: artheroscletoic narrowing
- ischemia that leads to transmural infarction/necrosis with myocardial protein leaking
what will u see on the EKG for NSTEMI and STEMI?
NSTEMI (endocardial) - St depression and T inversion
STEMI (transmural) - ST elevation
where does the ishemica/infarction typically occur?
typically occurs in the subednocaridal tissue (DEEP LAYER) bc perfusion decreases as you go tot he endocaridum
what are the S/S of acute coronary syndrome?
SAME AS STABLE ANGIAN BUT WITHOUT REST/NITRATES
chest pain for more than 30 mins
*LEVINE SIGN: clutching chest feels like something put is standing on the chest
SOB, diaphoresis, nasue/vomiting
AXS/atypical population- women, obseiity, elderly, DM
which dx do you see a LEVINE sign?
acute coronary syndrome
what are the 5 complications for acute coronary syndrome?
- arrythmias - ishcemic tissues are prone to arythmias esp VFIB
- we can also get bradycardia and heart block sicne the Coronary artery supply SA/AV node - decompenstated HF - ischemic. tissue loses contractibility so SOB, JVD, edema
- cardiogenic shock - can lead to hypotension due to decrease CO
- ventricular aneursym - post STEMI
- papillary muscle dysfunction - mitral regurgitation fucked up papillary muscles
tell me the dx: EKG finding for ACS
- ST elevation in two or more continguous leads or new LEFT budle branch block = STEMI and requires urgent revascualtion
- ST depression more than 0.5mm = NSTEMI
peaked T wave = early sign usually missed
ST elevation - STEMI, transmural
Q waves - late sign indicating necrosis
T wave inversion - NSTEMI
ST depression - NSTEMI, subendocaridal injury
NSTEMI - 1/3-1/2 of wall fucked up
tell me the dx for unstable, NSTEMI and STEMI ?
Unstable
- EKG: normal or ischemic changes (ST depression/T invert)
- NO cardiac enzymes
- no relived by nitrate/rest
NSTEMI
- EKG: normal or ischemic changes
-Cardiac enzyme elevation (troponin and CK-MB)
- no relieved by rest/nitrate
STEMI
-EKG: ST-elevations
-Cardiac enzymes elevation (troponin and CK-MB)
-no relived by rest/nitrates
would you perform a stress test for someone with acute coronary syndrome ?
NO THEIR HEART IS ALWAYS ISHCEMIC WE DONT WANAN ADD MORE STRESS
what testing and how long would YOU do if someone came w ACS?
- EKG every 10 mins and troponin levels every 3-4 hours (since unstable can lead to nstemi or stemi)
what is the best lab test for ACS and explain.
troponin 1 is best lab test. its the most sensitive for MI
troponin increases within 3-5 hours and gets normal 5-14 days. it peaks at 24-48 hours
what are exception to using troponin to test for ACS?
1 - elevated troponin is seen in chronic kidney diesase/ESRD
2- elevated troponin is seen in heart failure
what lab testing is less sensitive for MI
CK-MD lelves
how long does CK-MD last in the blood?
CK-MD increases for 4-8 hours and returns normal in 48 hours. it peaks at 24 hours
what is better use to indicate re-infarction with second MI
CK-MD due to it shorter half life
what is the initial management as a provider for ACS?
- EKG is INITAL TEST OF CHOICE
- draw blood to test troponin levles and CK-MD
- chest xray will show cardiomegalay of effusion and kuerly B lines in HF
MONA HEP B
morphine, oxygen, nitrates, asprin, heparin, beta blocker
what are the three therapies?
anti-ishchemic, anti-thrombotic, reperfusion revascularization therapy