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PHRM 845: Therapeutics III > ACS > Flashcards

ACS Flashcards

1
Q

What is Acute Coronary Syndromes?

A
  • It is the IMBALANCE between the myocardial oxygen supply and demand
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2
Q

What is meant by Spontaneous MI?

A
  • The atherosclerotic plaque ruptures
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3
Q

How is the atherosclerotic plaque formed and how does it cause ischemia?

A
  • Atherosclerotic plaque is formed by monocytes entering the cell and becoming macrophages. These macrophages then eat up all the cholesterol becoming a fatty streak. That fatty streak becomes the plaque and when it ruptures is when ischemia occurs.
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4
Q

What is meant by MI secondary to ischemic imbalence?

A
  • The mismatch between the oxygen supply and demand [the heart is wanting my oxygen but cant get it]
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5
Q

What are some risk factors for ACS?

A

Smoking, sedentary lifestyle, improper diet, MALE, family history…

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6
Q

What are some precipitating factors for ACS?

A

Exertion, physical activity, weather [Hot and Cold], sexual activity, shoveling snow, large meals…

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7
Q

What are some signs and symptoms for ACS?

A

Substernal chest pain that then can radiate down the LEFT arm and also up into the lower jaw
- Also some SOB, nausea/vomiting, sweating, dizziness…
- Should go away at rest

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8
Q

How do we diagnose ACS?

A

Give the patient a ECG within 10 minutes of arrival to the ER [look at ST interval[]
- ST Elevation = STEMI [may also have Q wave changes]
- ST Depression = NSTEMI

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9
Q

What is the one Myocardial Injury Biomarkers that test for at the ER?

A

Troponin: sees how much necrotic myocytes are in the blood stream
- High Sensitivity Troponin: PREFERRED - <14 ng/L
- Conventional Troponin: <0.05 ng/mL

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10
Q

What is the difference between Stable & Unstable Angina?

A

Stable Angina:
- Chest pain that occurs during EXERTION; has a fixed stable plaque [relieved at rest and short duration]
Unstable Angina:
- Chest pain that can occur any time really; at REST, SLEEP or with LITTLE EXERTION; has a ruptured plaque [last a longer time, >30 mins]

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11
Q

What is the difference between Unstable Angina & NSTEMI?

A

Both have very similar conditions: Chest pain that can occur any time really; at REST, SLEEP or with LITTLE EXERTION; has a ruptured plaque
Unstable Angina:
- Less Ischemia [not blocked as bad]
- NO troponin
NSTEMI:
- More blocked
- Elevated Troponin

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12
Q

What is the difference between NSTEMI & STEMI?

A

NSTEMI:
- NO elevated ST Interval [ST Depression]
- Elevated Troponin
STEMI:
- ST Elevation
- Possible Q Elevation
- Elevated Troponin

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13
Q

What is a TIMI score?

A
  • Risk of experiencing either death, MI or Urgent need for revascularization within 14 days
    [Low Risk: 0-2, Medium Risk: 3-4, High Risk: 5-7]
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14
Q

How do we determine the TIMI score?

A
  1. AGE >65
  2. > risk factors for CAD [HLD, HTN DM, Smoking, Family history]
  3. Known CAD
  4. Use of Aspirin
  5. ST Depression
  6. Chest Discomfort within 24 hr
  7. Positive Biomarker
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15
Q

Other than the ECG, what is some other early hospital care we should do for ACS patients?

A

MONA

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16
Q

What is MONA?

A

DO IMMEDIATELY
- Morphine 4-8mg IV, then 2-8mg IV q15min
- Oxygen [O2 sat >90%]
- Nitrate Tab 0.3-0.4mg every 5 min x 3
- Aspirin 325mg, then 81mg indefinitely

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17
Q

What is Reperfusion?

A
  • Medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack; either procedural or medical
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18
Q

What are the Procedural reperfusion strategies?

A

PCI [Percutaneous Coronary Intervention] or CABG [Coronary Artery Bypass Graft]

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19
Q

What is a PCI?

A

A PCI is when the cardiologist goes into the arteries of the heart and puts in a stent [something to help hold the arteries open]

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20
Q

What is a CABG?

A

A CABG is basically open heart surgery [they take arteries or veins from either the radial or femoral and “bypass” the blockages in the heart]

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21
Q

What is the Medical reperfusion strategies?

A

Fibrinolytics

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22
Q

What is a Fibrinolytic?

A
  • A way to prevent clots from growing and becoming a problem [the “-plase” & SHOULDN’T be given to patients that are high risk of bleeding]
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23
Q

What is the most appropriate reperfusion strategy for STEMI patients?

A
  • The PCI is PREFERRED over the Fibrinolytic [due to less bleeding, recurrent ischemia and death]
    *Door-to-needle: 30 minutes after getting to hospital [MONA, ECG, Troponin]
    *Door-to-balloon: 90 minutes after getting to hospital [PCI + STENT]
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24
Q

If the patient arrives at a NON-PCI capable hospital, what should happen?

A
  • Transfer then to a PCI capable hospital, as long as its >120 minutes away [If <120 minutes away, then just give fibrinolytic]
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25
Q

What is the most appropriate reperfusion strategy for NSTEMI & Unstable Angina patients?

A
  • NO fibrinolytics
  • Either Ischemia Guided Strategy or Early Invasive Strategy
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26
Q

What is Ischemia Guided Strategy?

A
  • Basically just giving the patients the proper medications to help manage any symptoms or problems [the patient wants a less invasive approach]
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27
Q

What is Early Invasive Strategy?

A
  • Giving the patient that is very high risk either a CABG or PCI [patients that have new HF, High Troponin, new ST Depression]
28
Q

What are some the the Antiplatelets that we would use in ACS?

A

Aspirin, P2Y12 Inhibitors, GPIIb/IIIa Inhibitors

29
Q

How should we appropriately give the patient Aspirin for ACS?

A
  • Want to give 325mg IMMEDIATELY upon arrival [MONA] then give 81mg Once Daily Indefinitely [the higher dose literally doesn’t give an advantage]
30
Q

What are the P2Y12 Inhibitors?

A

Clopidigrel, Ticagrelar, Cangrelor, Prasugrel

31
Q

What are the LOADING dose and MAINTENANCE dose for the P2Y12s?

A
  • Clopidogrel 300-600mg LD* & 75mg daily MD
  • Ticagrelor 180mg LD & 90 BID MD
  • Praugrel 60mg LD & 10mg MD
  • Cangrelor 30mcg/kg LD & no MD
32
Q

What is important to know about Clopidogrel’s Loading Dose?

A
  • Should just give the 600mg as LD since there isn’t really about benefit about giving the 300mg
  • DON’T give 600mg during fibrinolytic
    – Fibrinolytic + >75yo = NO Loading Dose
    – Fibrinolytic + <75yo= 300mg Clopidogrel
33
Q

What is important to know about Prasugrel?

A
  • NOT recommended for Ischemia Guided Therapy
  • Has greater platelet aggregation
  • CONTRAINDICATED with stroke
  • DO NOT give to anyone >75yo, <60kg, or high bleed risk
34
Q

Which P2Y12 Inhibitor should you use in NSTEMI/UA?

A

Ischemia Gudied Therapy:
- Ticagrelor or Clopidogrel
Early Invasive Strategy [PCI]
- Any; Ticagrelor or Prasugrel are preferred

35
Q

What P2Y12 Inhibitor should you use in STEMI?

A

Fibrinolytic:
- Clopidogrel [HUGE bleeding risk]
PCI
- Ticagrelor or Prasugrel

36
Q

How should Antiplatelets be handled for someone undergoing a CABG?

A
  • Aspirin; DO NOT HOLD
  • P2Y12 Inhibitors: HOLD [Ticagrelor - 3d, Clopidogrel - 5d, Prasugrel - 7d]
37
Q

What are the GPIIb/IIIa’s?

A
  • Abciximab, Eptifibatide, Tirofiban
38
Q

What is the mechanisam of Action for the GPIIb/IIIa’s

A
  • Inhibits the platelet aggregation
39
Q

When should GPIIb/IIIa’s be given?

A
  • In ADDITION to Aspirin and P2Y12 Inhibitors [really only used when there is a NEW thrombus that has formed]
40
Q

What is the purpose of Anticoagulation in the therapy of ACS?

A
  • To improve vessel patency and prevent reocclusion
41
Q

What do Unfractionated Heparins [UFH] do?

A
  • Its a penta-saccaride that binds to AT inhibiting its activation, inhibiting thrombin [IIa] and Xa
  • Risk if HIT
  • 4T’s: Thrombocytopenia, Timing, Thrombosis, oTher
42
Q

What is Enoxaparin?

A
  • A LMWH
  • Its a smaller penta-saccaride that binds to AT inhibiting its activation, inhibiting thrombin [IIa] and Xa; BUT has a greater effect on Xa
43
Q

What is Bivalirudin?

A
  • A direct thrombin inhibitor [IIa] so it prevents the clotting ability of the blood and help prevents any harmful clots from forming
44
Q

What is Fondaparinux?

A
  • A Xa inhibitor so it helps prevent deep vein thrombosis
  • DO NOT use in PCI alone
45
Q

When should Anticoagulation be used in patients with UA & NSTEMI?

A

Ischemia Guided Therapy:
- UFH: Yes [48 hr]
- Bivalirudin: No
- Enoxiparin: Yes [8d in Hospital]
- Fondaparinux: Yes [8d in Hospital]
Early Invasive Strategy:
- UFH: Yes [Until PCI]
- Bivalirudin: Yes [Until PCI]
- Enoxiparin: Yes [Until PCI]
- Fondaparinux: No

46
Q

When should Anticoagulation be used in patients with STEMI?

A

Fibrinolytics:
- UFH: Yes [48 hr]
- Bivalirudin: No
- Enoxiparin: Yes [8d in Hospital]
- Fondaparinux: Yes [8d in Hospital[]
PCI:
- UFH: Yes [Until PCI]
- Bivalirudin: Yes [Until PCI]
- Enoxiparin: No
- Fondaparinux: No

47
Q

When should the Beta-Blockers be initiates for ACS?

A

Within 24 hours

48
Q

What would be a reason to not start a Beta-Blocker?

A
  • Bradycardia, AV Block, Asthma
49
Q

Describe the receptor selectivity of the Beta-Blockers?

A

B1: Metoprolol, Atenolol, Bisoprolol, Nebivolol
[Heart]
B2: Propranolol, Sotalol, Nadolol
[Lungs]
Mixed: Carvedilol, Labetolol
[B1, B2, Arteries]

50
Q

What are some of the Loading and Maintenance Dosages for Beta-Blockers?

A

-Metoprolol: 25-50mg q6-12h LD & 100mg BID MD
- Carvedilol: 6.25mg BID LD& 25mg BID MD
- Propranolol: 40mg BID-TID LD & 80mg QID MD
- Atenolol: 25-50mg Daily LD & 100mg Daily MD

51
Q

What is important to know about Beta-Blockers and Cocaine?

A
  • Cocaine is an Alpha and Beta receptor stimulater, so together they can cause chest pain or even MI [since the beta receptor is blocked, it all goes to the alpha receptor causing it]
52
Q

What to counsel the patient on for Beta-Blockers?

A
  • Life long medication
  • Will lower BP and HR; so it you feel dizzy maybe too low
  • If you have diabetes, may mask hypoglycemia; NO COLD SWEAT
53
Q

What are the hold parameters for Beta-Blockers?
???

A
  • Holding Parameters: if BP and HR are too low; hold the medication.
  • TOO LOW? – <90-120 SBP or < 50-60 BPM
  • HOLD FOR:
    ~ SBP < 90 & DBP < 60
    ~ SBP < 90 & HR < 60
54
Q

When should Calcium Channels Blockers be used?

A
  • Really should be used when the patient has recurrent ischemia or contraindicated to Beta-Blockers [ONLY the NON DHP: Verapamil or Diltiazem]
55
Q

What is the Mechanism of Action for the Statins?

A
  • Inhibit the conversion of HMG-CoA to Mevalonic Acid; decreasing the formation of Cholesterol and stopping the formation of plaques
56
Q

What are the statins that should be used?

A

High Intensity Statins:
- Atorvastatin: 40-80mg Daily
- Rosuvastatin: 20-40mg Daily

57
Q

What is some patient counseling for Statins?

A
  • Life long medication to prevent heart attack
  • Lower cholesterol; even if normal take it
  • Most common side effect is MUSCLE PAIN
58
Q

What is the Mechanism of Action for the ACEi?

A
  • Blocks the conversion of Angiotensin I to Angiotensin II
59
Q

What are the ACEi?

A
  • “-pril”
  • SHOULD be give to all patients as they help decrease mortality
60
Q

When should ACEi not be use?

A
  • During hypotension, renal failure, angioedema
61
Q

What are some monitoring parameters with ACEi?

A
  • Increased Creatinine [decreased pressure in glomerulus]
  • Increased Potassium [do not give to hyperkalemics]
  • Decreased BP [Hypotension]
  • Angioedema [swelling of the face]
62
Q

What is some patient counseling for ACEi?

A
  • Life long medication; helps you live longer
  • Dizziness from the decreased BP
  • Dry Cough [Switch to ARBs]
  • Angioedema [medical emergency]
63
Q

What should we do about Nirtoglyercin?

A
  • SHOULD be given to every patient
  • 0.3-0.4mg under tongue q5 mins for chest pain [max dose 3, then call 911]
64
Q

What is some counseling for NTG?

A
  • Keep on you
  • Keep stored in amber glass or airtight container
65
Q

What else should we discuss with the patient about prevention of MI?

A
  • STOP SMOKING, medication adherence, healthier diet

PHRM 845: Therapeutics III (25 decks)

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