ACS Flashcards

1
Q

Presentation of Coronary Atherosclerosis

A

Silent disease
chronic, stable angina
acute coronary syndromes (ACS)
- unstable angina, NSTEMI, STEMI

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2
Q

What are the type of ACS?

A

unstable angina and myocardial infarction

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3
Q

What are the types of MI?

A

STEMI
NSTEMI

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4
Q

What are the classic signs of ACS?

A

pressure/pain behind the sternum
pain radiates to arms, neck and jaw
persisted for over 5 minutes despite trying to rest

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5
Q

What are some symptoms for women getting ACS?

A

sweating
dyspnea
nausea
abdominal pain
fainting

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6
Q

What are the main assessments that determine treatment at ER?

A

the story and the pt
12 lead ECG
blood test for biomarkers of cardiac cell death

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7
Q

What are the major indications of MI?

A

in the blood tests will show increased troponins
have to have evidence of cardiac cell death

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8
Q

What does a normal ECG mean?

A

strong evidence to rule out ACS
will investigate other possible causes

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9
Q

What does a ST segment depression mean in the ECG?

A

strong evidence for coronary ischemia
ST depression is often associated with stable angina too

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10
Q

What does a ST segment elevation mean in the ECG?

A

a marker of complete coronary obstruction causing cardiac myocyte death
suggests a serious MI requiring urgent revascularization
STEMI (ST elevation MI)

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11
Q

What could happen in severe cases of ST segment elevation on a ECG?

A

major consequences if blood flow is not restored is heart failure, arrhythmias or even death

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12
Q

What does a Q wave show?

A

often will appear following a STEMI
usually indicates extensive damage
often remains in the ECG for life

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13
Q

T/F Healthy people have no Q wave appear during an ECG

A

True

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14
Q

What is needed to confirm STEMI

A

Must have evidence of cell death

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15
Q

what is the biomarker of myocardial necrosis

A

troponins (most sensitive and specific)

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16
Q

How long is troponins levels elevated after MI?

A

increase within hours and remain for several days

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17
Q

What is the definition of STEMI?

A

ST elevation is a classic presentation of a major MI
often leaves ECG evidence forever

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18
Q

What is LBBB?

A

left bundle branch block
conduction in the left bundle of his is slow
results in delayed depolarization of the left ventricle

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19
Q

What are some factors that will be there if diagnosed with STEMI

A

history of classic ischemic sx’s not relieved by rest
ST segment elevation on ECG
evidence of Cardiac cell death

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20
Q

What are some tests adminstered in ER?

A

ECG
Cardiac troponins
natriuretic peptides
CXR

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21
Q

Standard treatment in the ER

A

oxygen
ASA (might add ADP inhibitor if PI is choosen)
S/L NTG
BB
IV anticoagulation

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22
Q

What are the takeaways from BHAT?

A

several post MI trials showing similar benefits on lowering risk of death
recent years the management of STEMI has improved dramatically in other areas
most BB studies in the post MI setting are old

we didnt have surgery
very helpful in severe

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23
Q

Why the benefit of BB have decreased over the years?

A

post MI risk is lower today due to mechanical revascularization and medication use
therefore people are likely to have less damage

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24
Q

What level of troponin is in a healthy person?

A

zero

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25
What is the first goal of STEMI treatment is? Within how many hours?
reperfusion within 12 hours
26
What is preferred method of reperfusion?
Primary PCI
27
What if you cannot do a PCI within 2 hours, what do you do?
fibrinolytic medication should be given
28
Why is it important to reperfusion as quickly as possible after a STEMI?
has the greater potential to restore blood lowering the risk for damaged myocardium lower risk of death
29
What is needed prePCI?
antiplatelets and anticoagulants specific --> ADP receptor antagonists probably LMWH or UFH
30
Why have antiplatelets prior to PCI?
helps protect against platelet activation that occurs during placement of stents as it causes endothelial damage
31
What is the loading dose for ADP inhibitors?
Clopidogrel 600 mg Ticagrelor 180 mg
32
What is the major difference between ticagrelor and other ADP inhibitors?
it is reversible vs irreversible it is not a prodrug
33
What is the acronym for the meds given in a heart meds?
ABC CKD BE CAD
34
What is given if pt has already had 81 ASA?
they give 325 mg ASA
35
Why is ACEi given if there is no hypotension?
it can help lower the chance of death (HOPE)
36
What is DAPT?
dual antiplatelet therapy taking a ADP inhib and ASA this is used for a set amount of time after ACS
37
List some factors that increase bleeding risk on DAPT
Need for OAC, NSAIDs, or prednisone Age > 75 Frailty Anemia with Hb < 110 CrCl < 40ml/min Body weight < 60kg Bleeding hosp within previous year Prior stroke/intracranial bleed
38
List some issues pertaining to DAPT
increase bleeding risk (compared to mono) optimal duration in unclear not sure if it is helpful in low risk pt
39
Current Recommendations for BB post MI
LVSD / Heart failure – absolute indication (not in acute phase) Arrhythmia – absolute indication STEMI – absolute indication STEMI without residual dysfunction – 3 years and re-evaluate (AHA) NSTEMI without residual dysfunction – “consider” BB
40
What is the caution with ACEI?
caution in first 24 hrs of MI because risk of hypotension or renal dysfunction
41
Efficacy of ACE inhibitors
Mechanism↓ RAAS First line in HTN when: ACVD, CKD, HF Considered in all high risk pts even without HTN (HOPE) Protects against CV events and renal disease progression (through BP mechanism for CV events, glomerular mechanism for CKD, uncertainty whether it has other protective benefits such as tissue specific effects)
42
Safety of ACE inhibitors
General BP related side effects Renal specific effects: drop in GFR expected after starting ACEI (up to 25% is safe) Cough (can be quite common) Increased K (through RAAS effect) Angioedema (rare swelling reaction… often around mouth/lips)
43
DI of ACEI
Anything that ↑ K (all other RAAS blockers) Anything that decreases renal perfusion (NSAIDs, Diuretics, etc)
44
Convenience of ACEi
Most are once (or twice daily) Many single pill combinations available (these are important)
45
CI of ACEi
Teratogenic Bilateral renal artery stenosis History of angioedema First line in renal dz – BUT need caution in renal dz!!!
46
What is the purpose of aldosterone blockade?
adding eplerenone to BB and ACEi in the post mI setting to pt with EF<40% was associated with lower mortality
47
When is CABG used for a STEMI?
when coronary anatomy not amenable to PCI and ischemia persists
48
What is the danger in CABG?
poses a much higher risk for bleeding during the procedure
49
If possible what should not be used before CABG?
should not have used ADP inhibitors within the last 5 days at least 24 hours if urgent
50
What is the post antiplatelet therapy CABG?
just ASA if elective possibility if STEMI or NSTEMI for DAPT
51
What is the condition if ST depression and ischemia is seen with cell death?
This is a NSTEMI
52
What is the condition if ST depression and ischemia is seen without cell death?
unstable angina
53
When is 325 ASA given?
If they have already taken 81 ASA that day before
54
What is a primary PCI used for?
STEMI refractory angina hemodynamic/electrical instability high risk features (DB, previous MI, HF)
55
When is beta blockers recommended?
LVSD/HF Arrhythmia STEMI STEMI without residual dysfunction (for 3 years then see)
56
What is the specific time that BB are consider but not automatically used?
NSTEMI without residual damage
57
Why are ACEi recommended?
it has been shown to decrease mortality after recent MI
58
What are the strong indications to use ACEi after MI?
EF < 40% HTN CKD
59
Why does A Fib complicate the use of DAPT?
because there is an increase in risk of bleeding
60
What is A Fib?
Atrial fibrillation an arrhythmia of the atrium removing the atrial contraction altogether clots can form due to pooling blood in the left atrium
61
What is recommended for AFIB instead of DAPT?
anticoagulants
62
What is the medical treatment after UA?
Many get a scheduled for a elective PCI to remove the blockage