Acute Coronary Syndrome Flashcards

1
Q

What causes ACS?

A

the build up of plaque in arteries and then they rupture, leading to thrombus

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2
Q

duration and severity of ACS?

A

occurs at rest, increasing in severity and can last longer for example > 20 minutes

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3
Q

ECG readings in ACS

A

S-T elevation if STEMI
S-T depression in NSTEMI or T-wave inversion

In someone who has MI, they will always have a Q-wave. (Rules in/out past MI)

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4
Q

cardiac biomarkers

A

troponin
creatinine kinase
-they are high within a few hours of chest pain in MI, it shows sign of myocardial necrosis (cell death) = ACS

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5
Q

when does chest pain occur in STEMI or NSTEMI?

A

at rest

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6
Q

Goals of therapy

A

-restore blood flow in occluded artery
-prevent re-occlusion, complications, and death
-treat chest pain

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7
Q

Early therapy for STEMI

A
  1. Oxygen
  2. Nitroglycerin (SL)
  3. Morphine
  4. ASA
  5. Second antiplatelet agent
  6. Anticoagulant (IV unfractionated heparin)
  7. Reperfusion: PCI or fibrinolytic
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8
Q

For reperfusion, what is the preferred strategy?

A

PCI - more effective than fibrinolytic therapy but PCI needs to be done in a timely way and its not always available

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9
Q

Indication for fibrinolytic therapy

A

STEMI < 12 hrs of symptom onset

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10
Q

What are the contraindications of fibrinolytic therapy?

A
  1. prior intracranial hemorrhage or ischemic stroke within 3 months
  2. intracranial malignant neoplasm
  3. facial trauma within 3 months
  4. active bleeding

Fib tx = increased risk of intracranial hemorrhage, so avoid if pt is already at risk of bleeding

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11
Q

example of fibrinolytic therapy

A

tPA (alteplase)
TNK (tenecteplase)

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12
Q

Dosing for ASA in acute MI

A

162-325 mg to chew x 1, then 81 mg daily INDEF

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13
Q

Ticagrelor vs. Clopidogrel comparison

A

efficacy: T> C
side effects: T> C
DDI: T = cyp3a4 interactions, C = 2c19 interactions
T = quicker onset

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14
Q

What is the benefit of using DAPT post-ACS?

A

to avoid stent thrombosis and future recurrent plaque rupture

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15
Q

How long should DAPT be used with ASA + ticag or clopidogrel?

A

atleast 1 year

*A+T = if bleeding risk is not high x 1 year
*A+C = if pt had fibrinolytic treatment in acute STEMI (bc lower bleeding risk) x 1 year

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16
Q

Total time from FMC to first device
activation (for primary PCI)

A
  • within 90 minutes of first medical contact (FMC) at a PCI-capable hospital.
  • within 120 minutes of FMC if the patient must be transferred from a non-PCI hospital.
17
Q

What happens if PCI can not be performed in time?

A

If PCI cannot be performed within these time frames, fibrinolytic therapy should be initiated within 30 minutes of arrival, and PCI can follow later if needed.

18
Q

AEs of antiplatelets

A

bleeding
dyspepsia (ASA)
diarrhea, rash (clopido)
dyspnea (ticagrelor)

19
Q

AEs of anticoagulants (UGH, enoxa, fondaparinux)

A

bleeding
heparin-induced thrombocytopenia (heparin & enoxaparin)

20
Q

What are the clinical signs of bleeding?

A

-CBC (hemoglobin)
-melena
-hemoptysis hematemesis
-bruising

21
Q

Other drugs to start after ACS?

A

ACEi, BB, statins

22
Q

how long to space apart PDE5 inhibitors from nitrates?

A

sildenafil and vardenafil - 24 hours
tadalafil - 48 hrs

23
Q

contraindications of beta blockers?

A
  • reactive airway disease
  • bradycardia (HR< 50)
  • 2nd or 3rd degree heart block without a functioning pacemaker
  • hypotension (SBP < 100)
24
Q

What is the role of CCBs in NSTEMI?

A

-used if BB and nitrate max dose reached + need further symptom relief
- or used if pt can not tolerate BB and has variant angina (coronary spasm)
-non DHP CCB - use with caution if also using BB

25
Q

What is the interaction between non-DHP CCB and BBs?

A

heart block
-left ventricular dysfunction
-severe bradycardia
-increased AV nodal block

26
Q

Efficacy of ace inhibitors

A

reduce mortality in pts with LV systolic dysfunction, HF, diabetes, or recent MI
-ideally start within 24 hours of presentation

27
Q

optimal duration of heparin therapy in NSTEMI?

A

2-5 days

28
Q

T/F - heparin is usually not administered after successful PCI.

A

true

29
Q

Amongst anticoagulants, when is enoxaparin vs, UFH used?

A

enoxaparin- preferred in NSTEMI, used in CrCl > 30 mL/min
UFH - appropriate if CrCl </= 30 mL/min

30
Q

what are the advantages of LMWH?

A

-easy of administration
-no need to monitor anticoagulant effect.
-predictable response

31
Q

which population of patients have increased bleeding events with Prasugrel?

A

> 75 y/o
body weight < 60 kg
history of stroke or TIA

32
Q

how many days prior to surgery should prasugrel be held?

A

7 days prior

33
Q

prasugrel vs ticagrelor

A

same risk of bleeding
P = lower risk of death, MI, and stroke

34
Q

what genetic polymorphism affects the efficacy of clopidogrel?

A

cyp2c19 - requires activation

35
Q

clopidogrel should be held for a minimum of __ days before non-urgent bypass surgery

A

5 days

36
Q

what is a side effect of ticagrelor that may require switching to a thienopyridine (clopido, prasu)

A

dyspnea (SOB)

37
Q
A