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unit 7; angina + MI Flashcards

1
Q

what is acute coronary syndrome generally? how many substypes?

A

with insufficient flow through the coronary tree and the resultant acuteischemiaof themyocardium.

unstable angina
NSTEMI
STEMI

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2
Q

whats the background of ACS?

A

The acute plaque ruptures with the separation of the cap  massive platelet and coagulation cascade activation  acutely reduced coronary artery lumen diameter  ischemia  infarction

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3
Q

whats the diff between stable agina/chronic ishemic HD and ACS?

A

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!

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4
Q

whats the diff between unstable angina, NSTEMI and STEMI?

A

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

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5
Q

what will u see on the EKG for NSTEMI and STEMI?

A

NSTEMI (endocardial) - St depression and T inversion

STEMI (transmural) - ST elevation

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6
Q

where does the ishemica/infarction typically occur?

A

typically occurs in the subednocaridal tissue (DEEP LAYER) bc perfusion decreases as you go tot he endocaridum

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7
Q

what are the S/S of acute coronary syndrome?

A

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

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8
Q

which dx do you see a LEVINE sign?

A

acute coronary syndrome

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9
Q

what are the 5 complications for acute coronary syndrome?

A
  1. 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
  2. decompenstated HF - ischemic. tissue loses contractibility so SOB, JVD, edema
  3. cardiogenic shock - can lead to hypotension due to decrease CO
  4. ventricular aneursym - post STEMI
  5. papillary muscle dysfunction - mitral regurgitation fucked up papillary muscles
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10
Q

tell me the dx: EKG finding for ACS

A
  • 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

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11
Q

tell me the dx for unstable, NSTEMI and STEMI ?

A

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

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12
Q

would you perform a stress test for someone with acute coronary syndrome ?

A

NO THEIR HEART IS ALWAYS ISHCEMIC WE DONT WANAN ADD MORE STRESS

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13
Q

what testing and how long would YOU do if someone came w ACS?

A
  • EKG every 10 mins and troponin levels every 3-4 hours (since unstable can lead to nstemi or stemi)
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14
Q

what is the best lab test for ACS and explain.

A

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

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15
Q

what are exception to using troponin to test for ACS?

A

1 - elevated troponin is seen in chronic kidney diesase/ESRD

2- elevated troponin is seen in heart failure

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16
Q

what lab testing is less sensitive for MI

A

CK-MD lelves

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17
Q

how long does CK-MD last in the blood?

A

CK-MD increases for 4-8 hours and returns normal in 48 hours. it peaks at 24 hours

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18
Q

what is better use to indicate re-infarction with second MI

A

CK-MD due to it shorter half life

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19
Q

what is the initial management as a provider for ACS?

A
  • 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

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20
Q

what are the three therapies?

A

anti-ishchemic, anti-thrombotic, reperfusion revascularization therapy

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21
Q

when should u use anti-ishchemic, anti-thrombotic, reperfusion revascularization therapy

A

UA AND NSTEMI AND STEMI = anti-ishchemic, anti-thrombotic

ONLY STEMI
reperfusion revascularization therapy

22
Q

what medication would you give for anti ishcemic therapy?

A
  1. NITRATE: vasodialtion to increase blood supply
    • decrease preload so decrease contractile
    • vasodilation increases perfusion
      - do not give nitrate for inferiro MI or sidafil use
  2. BB: within 24 hours. decreases contractile and increase perfusion
    - dont use if decompenstated HF present since you shouldnt decrease HR
  3. STATIN - decreased lipid atheroscleoriss
  4. MORPHINE - for pain
  5. OXYGEN - if hypoxic < 95%
23
Q

what medication would you give for anti-thrombotic therapy?

A
  1. ASPRIN 325mg - reduce aggregation which decreases thrombosis
  2. Antiplatelete drugs P2t12 inhibitors (clopidogrel, ticagrelor) –> reduce platelet activation via P2Y12 blockade

*RECOMMENDED TO GIVE BOTH ASPRIN AND P2Y12 TG. After acute phase, pt can take asprin 81mg +/- clopidrogel

  1. HEPARIN** - reduce thrombosis by targeting cascade
  • LMWH (enoxaparin/lovenox)–> better to use over unfractioned heparin
  • unfractioned heparin –> better than LMWH in reducing mortality in high risk pt
24
Q

whehn to do reperfusion therapy for STEMI pt? what are the two types

A

must od reperufsion therpy in STEMI pt within 12 hours of symptoms

PCI - percutaneous coronary intervention

fibrinolytic therapy

25
what is PCI and firbinolytic therpay for reperfusion therapy?
PCI is when you add a stent, should be done within 90 mintues fribinolytic therapy is when plasmin degrades the clots for better perfusion (plasmin such as streptokinase, alteplase, TPA - should be done within 30 mins for best results but u can do it up to 24 hours but bettter within 6 hours
26
what are the absolute contradindication for fribinolytic therpay?
since the plasmin are preventing clot formation you need to be careful if the pt is alreayd bleeding or if its necessayr for them to make clots - uncontrolled HTN - prev intracrnal hemorrhage - ischemic stroke within 6 months - intracranial mass - arotic dissection - surgery, trauma, peptic ulcer dx
27
what is ischemic heart disease and whats the eitology?
- inadequate supply of blood/O2 to the myocardium in relation to an increased demand on the myocardium M/C coronary artery atherosclerosis, CAA but could also be vasospastic disroder like prinzmental angina or cocacine induced MI
28
whats the RF for ischemic heart disease ?
HTN, DM, dyslipidemia, obesity, smoking, age, family hx
29
what is stable angina/chronic ischemia heart diease ?
- Stable lumen plaques leading to chronically decrease myocardial perfusion - NO SX AT REST!!!! - worse when u exercise due to high demand and low supply ***transeient chest pain sx also bad when u wake up
30
easy way to tx stable angina?
REST and NITRATE within 5-30 mins will resolve nitrate will vasodialtion which will increase perfusion and it will decrease preload which will decrease contractile
31
explain the s/s of chest pain and C8-T3 afferent innervation?
s/s chest pain w viserceral innervation will be dull and diffusion but w somatic innfernation till be sharp and localized pain will go to left arm and shoulder since they same the same c8-t3 innervation pain will also go to jaw due to irritation of pericardium and phrenic nerve
32
what are the s/s of stable chronic angina and the M/C for ax/ayptical people?
- Chest pain with exertion, RELIEVED by REST (5-30mins) - substernal, achy, dull, pressure like, “someone sitting on my chest” o +/- radiation to jaw or left arm - Shortness of breath with exertion - Acute myocardial ischemia  decrease myocardial contractility  backed up pressure/blood to pulmonary vessels/lungs - Diaphoresis, anxiety, nausea - Sympathic overdrive! Body tries to stimulate heart to work harder - AXS or atypical presentation (epigastric pain) - M/C in DM, ELDERLY, OBSEITY, FEMALE-
33
whats the #1 dx for stablie angina ?
EKG W STRESS TEST!!! you will see S-T depression!!!!
34
how can u add stress to EKG for stbale angina?
treadmil - M/C meds - dobutamiine which will increase HR or adenosine or dipyridamole which are vasodialtors
35
what else can you do to dx stable angina?
you can do myocaridal perfusion scanning to see where the ischemia is located using SPECT tomography
36
what is the GOLD STANDARD for dx stable angina?
- Coronary Angiography: GOLD STANDARD if theres more than 70$ occulusioon in 1 or more vessels!!
37
how would you tx stable angina? many rx!
the main goal is to increase perfusion and decrease demand 1. BETA BLOCOCKERS - METROPROLOL: will slow HR and increase perfusion, will also slow contractilibty and decrease demand 2. ASPRIN - reduce plateltly aggregation 3. NITRATE - vasodilators which will improve supply, venodilation which will decrease preload and decrease demand *last for 30 mins can be sublingual, patch, paste RAPID!!!! 4. CCB - wroks like BB but not the best 5. Ranolazine - O2 consumption helper
38
when should you NOT GIVE nitrate for stable angina?
if there is INFERIOR WALL MI
39
explain tachphylaxix with nitrate med
nitrate should be given for 16 with a 8 hour free nitrate break not good to use it for 24 hours it will decrease effifacy
40
what are some contraindication for giving nitrate to those with stable angina?
1. hypotension --> will make it worse 2. inferiro wall MI - the right ventricle is pre load dependant and nitrate decreases preload so the heart will get more fucked uo 3. SIDENAFIL USE - sidenafil also vasodialtes so tis too much all at once can lead to hypothension
41
whats the TWO defintivie mangemnte for stable angina?
-Revascularization with percutaneous coronary intervention (PCI) Revascularization with coronary artery bypass graft (CABG)
42
what is Revascularization with coronary artery bypass graft (CABG)
CABG is when you use spahenous vein to connect ascending arota to coranary artery to bypass occlusion or u can use internal throacici artery but youll lose it so not the best use this tx if others dont work ONLY USE THIS IF THERES MORE THAN 3 VESSEL DAMANGE!!! pt must be put on asprin or P2Y12 inhibiotor like clopidogrel to prevent thrombossi
43
what is Revascularization with percutaneous coronary intervention (PCI)
PCI is use when theres 1-2 VESSEL DAMANGE!! it is when you put a stent and do ballooning to dialte the vessel
44
whats hospital overview medication for untable angina, NSTEMI and STEMI?
if ACS is suspected: - EKG within 10mins of arrival - ASPRIN 325mg immedaitly - troponin levles drawn now then 3-4 hours later if ACS is confirmed: - intiaite anti-ischemic therpay, anti-thrombotic therpay - Asprin +clopidogrel, BB within 24 hours, statin, heparin (LMWH or UH) - nitrate or morphine or O2 as needed
45
whats outpateint overview medication for untable angina, NSTEMI and STEMI?
- asprin 81 + clopidogrel - decreases thombogensis by slowing aggregation - BB: decreases HR contractilies and increases purfusion - ACEi and SATIN to decrease afterload nad lipid induced plaques
46
benefits of BB
Lower heart rate Lowers angina threshold Improve mortality after MI Caution in cardiogenic shock – BP is already low bc of HTN, can also lead to organ failure
47
benefits of nitrates
Dilate Coronaries- Improve coronary perfusion Lower angina threshold Decrease preload, lower BP Decrease O2 consumption DO NOT improve mortality Main side effect headache, tachyphylax(taking it for 24hour which decrease efficacy and u have tachyphylacis, then u put pt on nitrate take a break for 8 then go back on normal mesd) is
48
beenfits of ACEi
Decrease afterload, lowers BP Decrease O2 consumption Improve mortality after MI Prevent adverse cardiac remodeling after an AMI
49
what is prinzmetal's angina? whats the RF?
Focal spasm of coronary arteries  decreased arterial luminal size myocardial ischemia - MI with NO ATHEROSCLEROSIS happens in young pt w recccurent ACS sx -not ass w exertion
50
whats the dx and tx for prinxmetal's angina?
EKG: transient ST segment elevation - coronary angiography - defifntive dx to see vasospams - THIS DX CANNOT BE CONFIEMD WITHOUT CATH LAB tx: - CCB: (diltiazem and amlodipine) - will decrease vasospams via vasodilation - nitrates as needed: casue vasodialtion
51
what is cocacine induced MI? and its manifestation?
cocacine binds to a1 receptors on coronary artery --> vasospams --> ishcmeia --> MI MI WITH NO ATEHROSCLEORSIS EITHER ! note that cocaoien can also bind to b1 recpetror and increase HR/contraction which will increase demand !!! - ACS sx and NOT ASS W EXCERTION
52
whats the dx and tx for cocaine induced MI?
EKG: transient ST segment elevation - coronary angiography - defifntive dx to see vasospams BUT if pt is on cocaine DO NOT DO THIS tx: - CCB: (diltiazem and amlodipine) - will decrease vasospams via vasodilation - nitrates as needed: casue vasodialtion - AVOID BETA BLOCKERS

Clin med 2 (7 decks)

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