Acute Coronary Syndrome Flashcards

1
Q

ACS Categorization

A

a) Unstable Angina
b) Myocardial Infarction
i) STEMI
ii) NSTEMI

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2
Q

What is the averge age of first ACS?

A

Late 60”s

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3
Q

ACS occurs more in (males/females) ration

A

Male to female ratio 3:2

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4
Q

ER Assesments of MI

A

1) Patient story
2) 12 ECG
3) Blood Tests –> Indicators of cell death

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5
Q

A normal ECG is good evidence of….

A

Strong evidence to rule OUT ACS
Physicians will investigate other possible causes of sx’s (heartburn, gallbladder attack, etc)

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6
Q

St Segment Depression Indicates

A

Strong evidence for coronary ischemia
However, ST depression is often associated with stable (fixed obstruction) angina. Further investigations will be needed to determine severity

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7
Q

ST Elevation

A

A marker of complete coronary obstruction causing cardiac myocyte death
This finding suggests a serious MI requiring urgent revascularization in most cases
If blood flow is not restored quickly, the person is at high risk for major consequences such as heart failure, arrythmias, or even death.

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8
Q

ST segment elavtion is refrred to as a

A

STEMI

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9
Q

Q-waves in normal ECG

A

Absent

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10
Q

Q waves in MI

A

Often will appear following (or during) a STEMI
Usually indicates extensive damage (transmural) to the heart wall
Often remains in the ECG for life (even after the acute event)

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11
Q

a STEMI will be confirmed if….

A

if evidence of cell death is observed

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12
Q

What are the most sensitive and specific marker of MI?

A

Tropnins

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13
Q

Cardiac tropinins in MI

A

are the most sensitive and specific biomarkers in the context of ACS

Troponins ↑ in the blood within hrs of MI and remain elevated for several days

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14
Q

The major classic presentation of STEMI is

A

ST elevation is a classic presentation of a major MI

Often leaves ECG evidence forever (Q-wave)

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15
Q

What is left-bundle branch block?

A

Conduction in the left bundle of his is slow

Results in delayed depolarization of the left ventricle

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16
Q

CRP is a test that indicates…

A

Inflammation

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17
Q

tests adminstered in the E.R. if STEMI suspected….

A

ECG
Cardiac troponins (3 – 6 hrs after symptom onset)
Natriuretic peptides (B-type or pro-B type –> Brain Naturietic Peptide elvated in MI)
CXR

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18
Q

Standard TX in ER

A

Oxygen (if O2 sats <90% or respiratory distress, etc)

ASA +/- ADP inhibitor

S/L NTG (IV NTG should be started if pain continues)
Ask about PDE5 inhibitor use!!!

Beta-blocker may be considered but onset slow and dangerous in acute setting if evidence of reduced CO, HF, or bradycardia

IV anticoagulation – recommended for all patients with suspected MI regardless of initial treatment strategy (e.g., UFH, enoxaparin, bivalirudin)

Old A** Never Beat Attacks

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19
Q

A beta-blocker should only be used once a pt is…..

A

STABLE

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20
Q

BB benfit has (increased/decreased) ove rthe years?

A

Decreased

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21
Q

Betab-blockers are highly….

A

Beta-blockers are highly protective in people who have experienced damage to myocardial cells

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22
Q

If there is more damage, a BB is….

A

More damage = higher SNS = more likely to benefit from BB

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23
Q

if there is less damage, a BB is …..

A

Less damage = lower SNS = less likely to benefit from BB

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24
Q

What is the first goal of a STEMI? Timing

A

Repurfusion

ALL patients presenting with STEMI with symptom onset within past 12 hours should receive reperfusion therapy (assuming eligibility criteria are met)

Primary PCI is the preferred method of reperfusion when done in a timely fashion

If PCI cannot be performed within 2hrs after first medical contact, fibrinolytic medications should be administered.
(tPA) –> Plasminogen to plasmin which breaks down fibrin

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25
Why is repurfusion tx benficial?
Reperfusion as quickly as possible after a STEMI has great potential to restore blood, ↓ the risk for damaged myocardium, and ↓ the risk of death
26
Before a PCI, what drugs are given....
DAPT Anticoagulant TX
27
Why are pre-PCI antiplatelet tx used?
Antiplatelets are started PRIOR to PCI procedures Helps protect against platelet activation that occurs during placement of stents Stent placement can cause endothelial damage
28
What drugs can be used in PRe-PCL antiplatlet tx? DOses? Which drug not used when?
ASA - 81-325 (325 if not taking 81 already) Loading dose of P2Y12 inhibitor (either of the following) Clopidogrel 600mg Prasugrel 60mg Ticagrelor 180mg Prasugrel should NOT be used to patients with prior history of stroke or TIA**
29
When is Pre-PCI antiplatlet tx initiated?
Administered in ED as soon as possible after decision for PCI
30
What anticoagulants can be used before PCI?
Options include: LMWH --> enoxaparin UFH Bivalirudin
31
Are IV anticoagulants always used before PCI?
YES
32
Clopidogrel is adminstered as a....
Pro-drug --> requires liver activation --> May be a disadvantage for some
33
Clopidogrel inhibits
ADP receptor
34
Clopidogrel Inhibition Type
irreversible
35
Prasurgrel MOA...
ADP receptor antagonits
36
Prasurgrel is adminstered as... Comparison to clopidogrel?
Pro-drug --> Less intra-subject variability in conversion than Clopidogrel
37
Prasurgrel Concerns for Usage
Concern regarding risk of serious bleeding in Patients >75 yrs Patients < 60kg
38
Ticagrelor administration
Not a pro-drug
39
Ticagrelor binding to ADP receptor
Reversible Inhibitor of ADP receptor (only one)
40
STEMI Meds DAY 1
ABCDEK Mechanism + angina pain ASA + Ticagrelor Bispropol ramipril Statin NTG
41
In DAPT, what is preferred over Clopidogrel?
Ticagrelor and Prasurgrel
42
DAPT is used for how long...
1 year and then re-evaluate
43
At 1 year, on DAPT, need to....
Determine bleeding risk: If not at high risk, Continue DAPT for 3 years - ASA 81 mg OD, Ticagrelor 60 mg BID or Clopidogrel 75 mg OD If high risk, SAPT --> ASA 81, or Clopidogrel 75 mg OD (1975)
44
DAPT for 1 year Combos
ASA 81 OD Ticagrelor 90 BID Prasurgrel 10 mg OD Clopidogrel 75 mg OD
45
Risk factors for bleeding...
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
46
If high bleeding risk, DAPT can be...
If bleeding risk is high, DAPT d/c can generally be considered After 1 month for a BMS After 3 months for a DES
47
Clopidogrel MOA
Irreversible P2Y12 inhbitor - Pro-drug that requires conversion by 2C19
48
Prasugrel MOA
Iireversible P2Y12 inhibitor (Pro-drug - Less intra-subject variability than clopidogrel)
49
Tocagrelor MOA
Doirect reversible inhibitor of P2Y12 (NOT A PRO_DREUG)
50
Prasugrel Comparison to Clopidogrel
Faster onset of action with increased potency in platlet inhibition compared to clopidogrel In pts with MI undegroing PCI, prasugrel reduced MACE compared to clopidogrel
51
Concerns of Prasugrel
Increased bleeding with prasugrel in patients who are olde rthan 75, hx of stroke or TIA and body weight less than 60kg Avoid prasugrel in patients with hx of stroke or TIA
52
Why is clopidogrel commonly choosen over Prasugrel and Ticagrelor?
Less bleeding risk
53
ADvers eeffect of tIcagrelor
Dyspnea
54
ASA MOA
Irreversibly inhibits COX-1 to. decraese thromboxane A2 (inyhibits platlets)
55
Indications 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
56
ACE-i in M.I. What if ACE not tolerated?
Shown to ↓ mortality in patients with recent MI – used in virtually ALL people with MI (HOPE TRIAL) - Can use an ARB
57
What ACEi to use in people with increased risk of ADR's
Short acting ACEI (captopril or enalapril)
58
if significant renal dysfunction, ACEi.....
If significant renal dysfunction, may wish to wait till kidney’s are stabilized (SCr improved)
59
ACEi are considered in all high risk pt's without HTN
TRUE
60
Speciifc s/e of ACEi
Cough, Increased K+, Angioedema
61
Drug Interactions of ACei
Anything that increases K+ Anything decreases renal perfusion
62
C.I. of ACEi
- Teratogenic - Bilateral renal artery stenosis History of angioedema - First line in renal dz --> But need to monitor
63
What other class of drugs may be prescribed?
MRA --> Eplerenone
64
Adding MRA to BB and ACEi in post MI benfit? This does not apply when...
Adding eplerenone to BB and ACEI in the post-MI setting to patients with EF<40% was associated with ↓ mortality Does NOT apply IF significant renal dysfx (Cr > 170) or high K
65
MRA is only given to people who present with....
heart failure after that heart attack
66
what revascularization technique is preferred?
PCI
67
CABG in STEMI when....
Urgent CABG indicated when coronary anatomy not amenable to PCI AND ischemia persists (or cardiogenic shock, severe HF, etc)
68
CABG risks....
much higher risk for bleeding during the procedure.
69
Before CABG, ____should be stopped and ____ should be used....
ADP inhibitors --> ASA should be used before surgery
70
Elective CABG Meds Before Surgery
In NON-URGENT situations, ADP inhibitors should be d/c for at least 5 days before surgery!!!
71
Uregent Situation - Primary CABG DAPT USe
If CABG is urgent, ADP inhibitors should be stopped at least 24hrs before surgery
72
Post CABG Anti-platlet tx depends on....
Depends on situation STEMI or NSTEMI  eligible for DAPT Elective CABG  ASA only
73
NSTEMI vs. Unstable ANgina DIagnosis
History of classic ischemic sx’s not relieved by rest ST-DEPRESSION on ECG If cell death can be proven in the context of ACS and ST depression, Jibby will be diagnosed with a NSTEMI (troponins positive – if positive, MI – if negative, unstable angina) If NO cell death can be proven in the context of ACS and ST depression, Jibby will be diagnosed with unstable angina
74
In order to be diagnosed with MI....
Cardiac cell death must be dtermined
75
What is a primary PCI? What are the features favouring PCI?
Some patients will be sent for angiography (and possible PCI) very quickly (invasive strategy) Features favouring invasive strategy STEMI Refractory angina Hemodynamic/electrical instability High risk features (Diabetes, previous MI, HF, etc)
76
BB receommended for....
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
77
Atrial Fib Define and Consequence
An arrhythmia of the atrium removing the atrial contraction altogether Clots can form in the left atrium due to pooling of blood These clots can embolize into the carotid artery and cause ischemia to the brain (i.e., stroke)
78
Atrial FIb Tx
Anticoagulants (i.e., not antiplatelets) are effective for this condition
79
ACS with Atrial FIb Tx
Makes the use of DAPT more likely to cause bleeding However, antiplatelets are still necessary for treating ACS
80
ACS and A-Fib
81
Unstable Angina TX
Similar to Fixed Obstruction --> DAPT could be avoided
82
Describe th ediagnosis of AC S
83
STE-ACS TX strategies
First Medical Contact (FMC) to needle time less than 30 minutes * FMC to balloon time less than 90 minutes
84
When are fibrinolytics used for PCI?
Rural Settings - Unable to do PCI within 2 hours
85
Fibrinolytic in ACS
Tenecteplase - Weight based dsoed - FAste rgiven, more ebenfit you get from it Most beenfit within hours of sx onset - More than 12 hours of sx, benefit quetsionable - sx 24 hours, no benefit - Do not give it Major concern —> Intracranial Hemorrhage Fibrinolytics - Follow up PCI Goals - Giving it as soon as possible
86
NST-ACS TX Strategies
87
Adjunctive RX Therapy ACS
* Anticoagulants * Antiplatelets * ACEi/ARBs * Beta-Blockers * Statins
88
Anti-coags STEMI and NSTE-ACS
89
Choice of ANti-coags in ACS
STEMI - Most clincial experience - Unfractionated Heparin, Bivalrudin (better bleed risk data - 10x price - cost imits use - option for people who cannot be on heparin), enoxaparin (less clinical experience), fondapaarinux (low bleed risk, need to give additional heparin in PCI, sub-Q formualtion) if fibrinolytic —> ENOXAPARIN --> Heparin - Also used in rural settingds Heparin CI - History of HIT NSTEMI - ENoxaparin drug of choice
90
Anti-coag Duration
Continue anticoagulation until sucessfully revascularized - If someone undergoing medical management, continue anticoagulation for atleast 48 hours Indication outside of ACS (hx of VTE, PE< a-fib), continue it after - Switch to an oral
91
Antiplatlets ACS
92
Beta-Blcokers ACS Started:
Oral beta blockers should be administered within 24 hours in all patients who do not have any of the following: 1) Signs of heart failure 2) Evidence of low-output state 3) Increased risk of cardiogenic shock 4) Other contraindications (prolonged PR, 2-3 degree AV block, reactive airway disease) (Class I; Level A/B)
93
Statin AXS
High-intensity statin therapy should be initiated or continued in all patients with STEMI or NSTE-ACS and no contraindications to its use.
94
Nitartes ACS
Reduce symptoms of myocardial ischemia – Reduce preload – Increase coronary artery blood flow * Do not attenuate myocardial injury or impact MACE Patients with NSTE-ACS with continuing ischemic pain may receive sublingual nitroglycerin (0.3 mg to 0.4 mg) every 5 minutes for up to 3 doses, after which an assessment should be made about the need for intravenous nitroglycerin if not contraindicated.
95
O2 and Morphine - ACS
No reduction in mortality, recurrent myocardial infarction, or MACE with oxygen supplementation in normoxic acute MI patients * Avoid routine prehospital administration of supplemental oxygen to STEMI patients with SaO2 90% (Weak Recommendation, Low-Quality Evidence) * Opioids (e.g. IV morphine and fentanyl) historically used for acute MI pain * No RCTs with hard clinical endpoints; may result in harm * Avoid of routine I.V. opioid administration for STEMI-related discomfort. Use may be considered for severe pain with the goal of relieving pain and reducing anxiety (Weak Recommendation, Low-Quality Evidence).
96
LMWH MOA
Enoxaparin, Dalteparin (Only ones approved for NSTEMI, stable angina, Enoxaparin Only One for STEMI) MOA: Same as heparin: Catalyzes antithrombin inactivates factor IIa and IXa, Xa, XIa, & XIIa Binds to antithrombin, but more selectively enhances inhibition of factor Xa mopre tha n Heparin Lower risk of HIT, OD Dosing, More predictable PK, Less Monitoring
97
UFH MOA
HEPARIN MOA: Catalyzes antithrombin inactivates factor IIa and IXa, Xa, XIa, & XIIa * Prolongs aPTT * Cannot bind to thrombin already in a clot * Also binds to cells and other plasma proteins  unpredictable pharmacokinetics / dynamics Works immediately after IV administration 🩺 Think: Fast-acting, broad anticoagulant effect 💡 Reversible with protamine sulfate
98
Fondaparinux MOA
Fondaparinux MOA: Glycosaminoglycan – fondaparinux Inhibits factor Xa (ONLY) Benefit: NO HIT - USE IN HIT CrCl < 30 - Do not use 🩺 Think: Pure Xa blocker via AT 💡 No reversal agent (but low bleeding risk)
99
Direct Thrombin I(nhibitors
Direct Thrombin Inhibitors (DTIs) Examples: Bivalirudin (IV) (Also dabigatran, but that’s oral) MOA: Directly bind to and inhibit thrombin (factor IIa) without needing antithrombin Prevents thrombin from converting fibrinogen → fibrin 🩺 Think: Used in HIT (heparin-induced thrombocytopenia) 💡 No antidote (except dabigatran, which uses idarucizumab)