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
Q

what is PCI and firbinolytic therpay for reperfusion therapy?

A

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
Q

what are the absolute contradindication for fribinolytic therpay?

A

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
Q

what is ischemic heart disease and whats the eitology?

A
  • 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
Q

whats the RF for ischemic heart disease ?

A

HTN, DM, dyslipidemia, obesity, smoking, age, family hx

29
Q

what is stable angina/chronic ischemia heart diease ?

A
  • 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
Q

easy way to tx stable angina?

A

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
Q

explain the s/s of chest pain and C8-T3 afferent innervation?

A

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
Q

what are the s/s of stable chronic angina and the M/C for ax/ayptical people?

A
  • 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
Q

whats the #1 dx for stablie angina ?

A

EKG W STRESS TEST!!! you will see S-T depression!!!!

34
Q

how can u add stress to EKG for stbale angina?

A

treadmil - M/C

meds - dobutamiine which will increase HR or adenosine or dipyridamole which are vasodialtors

35
Q

what else can you do to dx stable angina?

A

you can do myocaridal perfusion scanning to see where the ischemia is located using SPECT tomography

36
Q

what is the GOLD STANDARD for dx stable angina?

A
  • Coronary Angiography: GOLD STANDARD
    if theres more than 70$ occulusioon in 1 or more vessels!!
37
Q

how would you tx stable angina? many rx!

A

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
Q

when should you NOT GIVE nitrate for stable angina?

A

if there is INFERIOR WALL MI

39
Q

explain tachphylaxix with nitrate med

A

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
Q

what are some contraindication for giving nitrate to those with stable angina?

A
  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
Q

whats the TWO defintivie mangemnte for stable angina?

A

-Revascularization with percutaneous coronary intervention (PCI)

Revascularization with coronary artery bypass graft (CABG)

42
Q

what is Revascularization with coronary artery bypass graft (CABG)

A

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
Q

what is Revascularization with percutaneous coronary intervention (PCI)

A

PCI is use when theres 1-2 VESSEL DAMANGE!!

it is when you put a stent and do ballooning to dialte the vessel

44
Q

whats hospital overview medication for untable angina, NSTEMI and STEMI?

A

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
Q

whats outpateint overview medication for untable angina, NSTEMI and STEMI?

A
  • 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
Q

benefits of BB

A

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
Q

benefits of nitrates

A

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
Q

beenfits of ACEi

A

Decrease afterload, lowers BP
Decrease O2 consumption
Improve mortality after MI
Prevent adverse cardiac remodeling after an AMI

49
Q

what is prinzmetal’s angina? whats the RF?

A

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
Q

whats the dx and tx for prinxmetal’s angina?

A

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
Q

what is cocacine induced MI? and its manifestation?

A

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
Q

whats the dx and tx for cocaine induced MI?

A

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