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Spring 2024 Therapeutics 3 > Exam 1: Acute Coronary Syndromes > Flashcards

Exam 1: Acute Coronary Syndromes Flashcards

1
Q

What is Acute Coronary Syndrome (ACS)?

A

Heart Attack

(an imbalance in demand of oxygen by heart tissue and the supply of oxygen the heart is getting)

(AKA: not enough oxygen for heart)

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2
Q

What are the worst arteries for ischemia to happen in and why?

A

-Right Coronary artery
Left main coronary artery

-These coronary arteries are high up in the heart and have other coronary arteries feeding off of them
-Therefore, if ischemia happens here, the heart attack will be larger because oxygen will also be cut off to the vessels downstream from it

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3
Q

What is the most severe acute coronary syndrome?

A

STEMI

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4
Q

What causes ischemia?

A

-An atherosclerotic plaque forms

-The plaque ruptures

-Platelets adherence is activated, they aggregate and activate the clotting cascade at the area

-Fibrin and platelets form a clot that blocks blood/oxygen flow

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5
Q

What is a Type 1 ACS?

A

Spontaneous MI

(from atherosclerotic plaque rupture)

*what we mainly talk about

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6
Q

What is a Type 2 ACS?

A

MI Secondary to Ischemic Imbalance

(oxygen supply/demand mismatches to the heart, not getting enough blood flow)

-Ex: vasospasm, anemia, hypotension

*Not necessarily due to plaque

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7
Q

What is the median age of ACS presentation?

A

68 years old

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8
Q

What gender is more likely to have ACS?

A

Males

(3 Males : 2 Females)

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9
Q

What are the risk factors for ACS?

A

-Older age
-Male
-Family history of CAD
-Peripheral artery disease
-Diabetes
-Renal insufficiency
-Prior MI
-Smoking

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10
Q

What are some precipitating factors for ACS?

A

-Exercise
-Weather (cold or warm)
-Diet (large meal)
-Emotions (fright, anger, stress)
-Coitus (sexual activity)
-Walking against wind
-Smoking

(these increase oxygen demand)

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11
Q

What are the signs of Acute Coronary Syndrome?

A

-Retrosternal chest pain
(can radiate to shoulder, down left arm, to back, or to jaw)

**Mostly occurs at rest

*Crushing, radiating pain

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12
Q

What are the symptoms of Acute Coronary Syndrome?

A

-Nausea
-Vomiting
-Diaphoresis (cold sweat)
-SOB
-Anxiety
*Chest pain

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13
Q

What are the atypical symptoms of ACS?

A

-Epigastric pain
*Indigestion
-Stabbing or pleuritic pain
-Dyspnea (SOB) without chest pain

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14
Q

Who is more likely to experience atypical ACS symptoms?

A

-Elderly
-Females
-Diabetics
-Impaired renal function
-Dementia

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15
Q

When should a patient call 911?

A

If they are experiencing chest pain and high risk features like:
-Continuing chest pain
-Severe dyspnea
-Syncope/presyncope (fainting)
-Palpitations

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16
Q

Why should patients experiencing ACS be transported to the hospital by ambulance instead of driving themself?

A

-Treatment/testing can be initiated on the way to the hospital

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17
Q

Upon arriving at the hospital for a suspected ACS, how soon should a patient have an ECG?

A

Within 10 minutes!

Note: all patients with acute chest pain should receive this

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18
Q

What does the P wave on an ECG show?

A

Atria contracting

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19
Q

What does the QRS wave on an ECG show?

A

Ventricle contracting

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20
Q

What does the T wave on an ECG show?

A

Ventricle relaxing

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21
Q

Note*

A

See lecture 1 slide 24 for ECG waves, know which is which

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22
Q

What is the order of the waves on an ECG?

A

P-Q-R-S-T

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23
Q

What changes can be seen on an ECG when a patient experiences a STEMI?

A

ST elevation

Q wave changes
(not present on initial ECG, develops over hours to days)

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24
Q

Why is the Q wave often not present initially on an ECG with a STEMI?

A

An ‘electrical hole” is there
(scar tissue cannot conduct electricity)

-Not acute damage, it is from old damage that accumulates over time from scar tissue

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25
Q

What may be seen on an ECG for NSTEMI or Unstable Angina?

A

-May be normal

-May have:
-ST depression
-ST elevation
-T wave inversion (upside down)

*Unlikely to have Q wave change
*No ST segment elevation

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26
Q

Note:

A

See lecture 2 slide28 for NSTEMI and UA ECG picture

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27
Q

What patients should have their troponin levels measured?

A

-All patients presenting to the ED with acute chest pain and suspected ACS

*measure ASAP

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28
Q

What is troponin?

A

A myocardial injury biomarker

(released from injured heart cells into blood stream)

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29
Q

What is the gold standard for ACS detection?

A

Troponin

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30
Q

What are the two troponin tests and which one is preferred?

A

High sensitivity troponin (*preferred)

Conventional troponin

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31
Q

Why is high sensitivity troponin preferred?

A

-Greater sensitivity and negative predictive values

-Shorter time from onset of chest pain to a detectable concentration

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32
Q

What units are high sensitivity and conventional troponin measured in?

A

High sensitivity: ng/L

Conventional: ng/mL

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33
Q

What is sensitivity vs specificity?

A

Sensitivity: Likelihood of detecting a disease when it exists (true positive rate)

Specificity: Likelihood of not detecting a disease when it does not exist (true negative rate)

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34
Q

What does troponin detect?

A

Myocardial injury

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35
Q

What value for HIGH SENSITIVITY TROPONIN indicates damage to the heart?

A

> 14 ng/L

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36
Q

What value for CONVENTIONAL TROPONIN indicates damage to the heart?

A

> 0.05 ng/mL

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37
Q

When we check troponin, how many times do we check it?

A

Check 3 levels over 12 hours

*because damage is currently happening and there may not be much at the first level but it will trend upwards

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38
Q

Does elevated troponin levels immediately mean a patient is having an MI?

A

NO

-could also be a pulmonary embolism
-have to use multiple factors to diagnose

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39
Q

What are the differences between Stable Angina and Unstable Angina?

A

Stable Angina
-Chest pain occurs during physical exertion
-Predictable
-Relieved by rest
-< 5 minutes

Unstable Angina
-Chest pain occurs at rest, while sleeping, or with little exertion
-Surprise
-More severe, longer (can be >30mins)
-Does not go away with rest

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40
Q

What are the differences between unstable angina and NSTEMI?

A

UA:
Less ischemia
Does not elevate troponin

NSTEMI
-Elevated troponin

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41
Q

What are the differences between NSTEMI and STEMI?

A

Both:
-Chest pain
-Elevated troponin

NSTEMI:
-No ST segment elevation
(may have ST depression or T wave inversion)

STEMI:
-ST elevation!!!

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42
Q

What does a thrombolysis in myocardial infarction (TIMI) risk score tell us?

A

Risk of experiencing either death, MI, or urgent need for revascularization within 14 days

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43
Q

What range of points indicates “low risk” on the TIMI risk score?

A

0-2

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44
Q

What range of points indicates “medium risk” on the TIMI risk score?

A

3-4

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45
Q

What range of points indicates “high risk” on the TIMI risk score?

A

5-7

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46
Q

What are the complications of ACS?

A

-Heart failure
-Valvular dysfunction
-Arrhythmias
-Bradycardia/heart block
-Pericarditis (swelling of sack around heart)
-Stroke secondary to LV thrombus
-Cardiogenic shock (BP cannot keep up to profuse organs)
-Death

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47
Q

What is ventricular remodeling?

A

Changes in shape, size, and function of left ventricle after ACS

**leads to heart failure

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48
Q

What 3 things are usually included in MACE?

A

-Stroke
-MI
-Cardiovascular death

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49
Q

What are the two initial recommendations for patients presenting to the ED with symptoms of ACS?

A

ECG within 10 minutes

Serial troponin levels

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50
Q

If the initial ECG a patient receives is not diagnostic but they are still experiencing symptoms of ACS what should be done?

A

Perform serial ECGs

*Every 15-30 minutes for the first hour

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51
Q

Who should receive MONA?

A

UA, NSTEMI, and STEMI patients

*immediately upon arrival!

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52
Q

What are the 4 components to MONA?

A

Morphine
Oxygen
Nitroglycerin
Aspirin

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53
Q

What is the initial dose of morphine given to patients?

A

4-8 mg IV, followed by 2-8mg IV every 5-15 mins

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54
Q

What are the side effects of morphine?

A

-Sedation
-Respiratory depression
-Nausea/vomiting

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55
Q

Why should NSAIDs be discontinued and avoided during hospitalization for ACS patients?

A

They lead to sodium and water retention

*This increases risk of MACE

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56
Q

When is oxygen initiated and what is its saturation goal?

A

Initiate when saturation < 90%

Goal: Maintain saturation >90%

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57
Q

What dose should sublingual NGT be initiated at?

A

0.3-0.4 mg every 5 minutes x 3
(for ischemic pain)

*NOTE: Give this first, then start IV dosing if needed

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58
Q

What dose should IV nitroglycerin be given at?

A

Start: 10 mcg/min

Titrate: By 5 mcg/min every 5 mins

Max: 200mcg/min

**NOTE: give this after the SL dose if needed

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59
Q

Can we use transdermal NTG for ACS?

A

NO

-onset of action is not rapid enough
-takes a longer time to absorb in skin

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60
Q

What is tachyphylaxis?

A

When a drug loses part of or its entire efficacy over time as the body develops tolerance to it

(seen in nitrates)

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61
Q

Why are nitrates contraindicated with phosphodiesterase inhibitors?

A

Both medications cause vasodilation

-this leads to severe hypotension

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62
Q

What dose of aspirin should be given to all ACS patients presenting to the hospital?

A

162-325mg chewable aspirin x 1 dose immediately

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63
Q

Can enteric coated aspirin be given to patients presenting to the ED?

A

YES
*it has to be chewed so it will absorb quickly

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64
Q

If the patient already takes a baby aspirin and took their dose that morning, do you still give them a loading dose of aspirin (325mg)?

A

YES
-If they just took their dose, you can give an additional 81mg tablets x 3

(makes a total dose of 324mg with the baby aspirin)

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65
Q

What are the 3 reperfusion strategies?

A

Percutaneous Coronary Intervention (PCI)

Coronary Artery Bypass Graft (CABG)

Fibrinolytic therapy

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66
Q

What is a coronary angiography and what does it show?

A

A catheter inserted into the radial + femoral artery and fed up to the heart

Dye gets injected into the coronary arteries

X-ray is taken and shows the blocked arteries (areas where dye does not reach)

Stent is placed in blocked arteries

OVERALL: shows which arteries in the heart have blockages

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67
Q

What is a PCI?

A

Procedure where a small balloon is used to reopen a blocked artery to increase blood flow

*A stent is placed if needed to keep artery open

ASSOCIATE PCI WITH A STENT

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68
Q

What is a CABG?

A

Open-heart surgery

-a vein or artery from another part of the body is removed and attached to the heart to “bypass” the blocked artery/arteries

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69
Q

How does a fibrinolytic work?

A

Changes plasminogen to plasmin

Plasmin breaks down fibrin into fibrin degraded products

70
Q

What are the 3 fibrinolytics?

A

Tenecteplase (TNK-tPA)
Reteplase (rPA)
Alteplase (tPA)

71
Q

What fibrinolytic is preferred?

A

No preference for one over the other

72
Q

Who should receive reperfusion therapy?

A

All eligible STEMI patients whose symptoms began in the last 12 hours

73
Q

What is preferred: a PCI or a Fibrinolytic?

A

PCI (STENT or CABG)

*if hospital is able to perform these procedures, they should do it

74
Q

Upon arriving at the hospital, how quickly should a patient receive a fibrinolytic?

A

within 30 minutes

75
Q

Upon arriving at the hospital, how quickly should a patient receive a STENT?

A

within 90 minutes

76
Q

When is fibrinolytic therapy recommended?

A

For STEMI patients at non-PCI-capable hospitals that are at least 120 mins away from a PCI-capable hospital

77
Q

Are fibrinolytics used for NSTEMI or UA?

A

NO

78
Q

What reperfusion strategies are used for NSTEMI/UA?

A

Early Invasive: (Coronary Angiography +/- Revascularization)

Ischemia Guided: (Medical Management)

79
Q

When is early invasive reperfusion therapy (Coronary Angiography +/- Revascularization) used in NSTEMI/US patients?

A

Preferred for patients with high risk features:

-Refractory angina
-New-onset Heart Failure
-Rising troponin
-New ST-segment depression

80
Q

What is ischemia-guided reperfusion therapy (Medical Management)?

A

Treatment with evidence-based medications

*No heart catheterization unless the patient becomes high risk

81
Q

What are the 3 options you may find when performing a heart cath?

A
  1. It wasn’t a blockage, misdiagnosed
  2. You see a blockage and put a STENT in
  3. You find profuse disease with lots of blockages, pull the cath out, and schedule a CABG
82
Q

What is the standard dose of aspirin to give a patient immediately upon presentation to the hospital?

A

325mg

83
Q

What is the maintenance dose of aspiring that patients should be on the rest of their lives?

A

81 mg

(preferred dose but could be up to 325mg)

84
Q

What is one counseling point for aspirin?

A

Take with food

85
Q

How long is DAPT recommended for STEMI, NSTEMI, and UA?

A

12 months

86
Q

When would we use Cangrelor for antiplatelet therapy (IV only)?

A

*Option for LOADING DOSE ONLY

-Use during PCI if patient did not already receive loading dose because it works really fast

87
Q

What is the preferred loading dose of clopidogrel (Plavix)?

A

600 mg

(over 300mg)

*Unless you used a fibrinolytic, then use 300mg due to bleeding risk

88
Q

What is the loading dose of Cangrelor?

A

30mcg/kg, followed by 4mcg/kg/min for 2 hours

89
Q

When would we not use a loading dose of a P2Y12 inhibitor?

A

Already took a fibrinolytic + > 75 years old

90
Q

When would we use a 300mg loading dose of Clopidogrel instead of 600mg?

A

Already took a fibrinolytic + 75 years old or YOUNGER

91
Q

What is the most commonly used P2Y12 inhibitor?

A

Clopidogrel

*Prodrug
-Common due to insurance coverage

92
Q

True or False: Clopidogrel is a prodrug

A

True

93
Q

True or False: Ticagrelor is more effective than Clopidogrel

A

True

-greater inhibition of platelet aggregation

94
Q

What trial showed the effectiveness of Ticagrelor vs Clopidogrel?

A

PLATO trial

(showed ticagrelor decreased the endpoint slightly more)

95
Q

How does ticagrelor affect aspirin dosing?

A

Max dose of Aspirin should be 81 mg when used in combination with ticagrelor

96
Q

What are the side effects of ticagrelor?

A

Dyspnea (SOB)

Ventricular pauses

97
Q

Why is prasugrel not commonly used?

A

It inhibits platelet aggregation more than clopidogrel

**This gives it a high bleeding risk

**Highest bleeding risk of all

98
Q

When is Prasugrel contraindicated?

A

Patients with history of TIA/stroke

99
Q

What patients is prasugrel not recommended in?

A

75 years old or older

<60kg

High bleeding risk

100
Q

What PSY12 inhibitors are prodrugs/ not prodrugs?

A

Clopidogrel: Prodrug
Prasugrel: Prodrug
Ticagrelor: Not a prodrug

101
Q

Why would we switch from Clopidogrel to Ticagrelor/Prasugrel?

A

Inadequate response

102
Q

Why would we switch from Ticagrelor to Clopidogrel?

A

Bleeding
Cost
Dyspnea*
Adherence*

103
Q

Why would we switch from Prasugrel to Clopidogrel?

A

Bleeding
Cost
Stroke/TIA***

104
Q

For an STEMI or NSTEMI/ UA with PCI (early invasive strategy) what P2Y12 is preferred?

A

Any could be used

*Ticagrelor or Prasugrel preferred

105
Q

For an NSTEMI/UA with Ischemia Guided Therapy, what P2Y12 is preferred?

A

Clopidogrel or Ticagrelor

106
Q

For a STEMI with a fibrinolytic used, what P2Y12 inhibitor is preferred?

A

Clopidogrel

107
Q

Which type of stent is associated with a higher rate of late STENT thrombosis?
(bare metal or DES)?

A

Drug eluting stent (DES)

*may not be preferred if patient cannot comply with prolonged DAPT

108
Q

What drug is released from a Drug Eluting Stent (DES)?

A

Anti-rejection drug

-Everolimus, Zotarolimus, Ridaforolimus

*prevents body from rejecting the stent

109
Q

What are 2 counseling points for Ticagrelor?

A

Take BID dosing 12 hours apart (morning and night)

Tell doctor if you experience shortness of breath

110
Q

When should aspirin be held before underrgoing a CABG?

A

DOES NOT NEED TO BE HELD

111
Q

When do the P2Y12 inhibitors need to be held before a CABG?

A

Ticagrelor- 3 days
Clopidogrel- 5 days
Prasugrel- 7 days

**If emergency CABG, try to hold for 24 hours

112
Q

What are the 3 GP IIb/IIIa inhibitors?

A

Abciximab
Eptifibatide
Tirofiban

*potent IV antiplatelets

113
Q

When are GP IIb/IIIa inhibitors given?

A

*In addition to aspirin and P2Y12i

At time of PCI

*no benefit to giving it before hand

*NOTE: not routinely used

114
Q

What cases would warrant use of a GP IIb/IIIa inhibitor?

A

NSTEMI: high risk features (such as positive troponin)

STEMI: large thrombus burden

*inadequate P2Y12i loading

**As “bail out”: if thrombus develops during procedure or low blood after stenting

115
Q

What is the bolus dose of Abciximab?

A

0.25 (mg/kg IV)

116
Q

What is the bolus dose of Eptifibatide?

A

180 x2 (mcg/kg IV)

117
Q

What is the bolus dose of Tirofiban?

A

25 (mcg/kg IV)

118
Q

What is the brand name of Abciximab?

A

ReoPro

119
Q

What is the brand name of Eptifibatide?

A

Integrilin

120
Q

What is the brand name of Tirofiban?

A

Aggrastat

121
Q

When is anticoagulation therapy recommended?

A

In addition to antiplatelet therapy

-Improve vessel patency
-Prevent re-occlusion

122
Q

What factors does unfractionated heparin (UFH) affect?

A

Anti-Xa

Anti-IIa

*note: enoxaparin also affects these two factors

123
Q

What is heparin induced thrombocytopenia (HIT)?

A

-Drop in platelet count
-Increased thrombosis

*Caused by the formation of antibodies that activate platelets

124
Q

What are the 2 screening tests used if HIT is suspected?

A

Enzyme-linked immunosorbent assay (ELISA)
*quick, high false positive, re-
check if positive

Serotonin release assay (SRA)
*gold standard

125
Q

Should a patient with a history of HIT be re-challenged with unfractionated Heparin or LMWH?

A

NO

-if a patient experiences HIT, never give heparin again

126
Q

What are 2 benefits of using Unfractionated Heparin (UFH?)

A

Quick onset

Short half life

127
Q

How is unfractionated heparin (UFH) dosed?

A

Given as a continuous infusion (IV drip)

*Dosed based on the:

-Activated partial thromboplastin time (aPTT)

-Activated clotting time (ACT)

128
Q

How is Enoxaparin (Lovenox) eliminated?

A

By the kidneys

accumulates in renal impairment

*CALCULATE CrCl FOR THIS DRUG

129
Q

Which factor is affected most by Enoxaparin?

A

Factor Xa

(also has anti-IIa properties but higher ratio of Xa)

130
Q

What type of drug is Bivalirudin?

A

Direct thrombin inhibitor

131
Q

What drug class should we not use Bivalirudin with?

A

GPIIa/IIb inhibitors

except for “bail out”!

132
Q

How does Bivalirudin compare to UFH?

A

-Conflicting results

-May not be as effective for MACE and stent thrombosis

-May have lower bleeding risk

133
Q

What type of drug is Fondaparinux?

A

Factor Xa inhibitor

134
Q

When do we use Fondaparinux?

A

**Not commonly used
*Use in patients with history of HIT

DO NOT USE ALONE FOR PCI

135
Q

Why do we not use Fondaparinux alone for PCI?

A

High rates of thrombosis

*if patient is already receiving fondaparinux and needs a PCI, give UFH or bivalirudin as well

136
Q

When is Fondaparinux contraindicated?

A

CrCl < 30ml/min

137
Q

What is a benefit of UFH for renal dosing?

A

UFH can be used in all degrees of renal function!

-dose not adjusted

138
Q

What anticoagulants are used with PCI?

A

UFH and Bivalirudin

ONLY THESE 2
-no enoxaparin or fondaparinux

139
Q

When is Bivalirudin preferred leading up to a PCI?

A

When there is a high bleeding risk

140
Q

What 4 long-term medications (maintenance) should a patient with ACS be started on?

A

-Beta blockers
-Statins
-ACEi/ARB
-Nitroglycerin prn

141
Q

How soon after an ACS should a patient be started on a beta blocker?

A

Within the first 24 hours

142
Q

What are some reasons not to start a beta blocker?

A

-Bradycardia

-Heart failure or other low-output state
(beta blockers will make it worse)

-Risk for cardiogenic shock

-PR interval > 0.24s

-Second or third degree heart block

-Active asthma or reactive airway disease

143
Q

What are the 4 commonly used beta blockers post-MI?

A

Metoprolol
Carvedilol
Propranolol
Atenolol

144
Q

If a patient has HFrEF, what beta blockers can be used?

A

Sustained release:

-Metoprolol succinate
-Carvedilol
-Bisoprolol

145
Q

When would we consider IV beta blockers?

A

Only with hypertension or ongoing ischemia

*use Metoprolol tartrate 5mg IV q5min
(up to 3 doses)

146
Q

What are the 4 selective beta blockers?

A

Atenolol
Metoprolol
Bisoprolol
Nebivolol

147
Q

Why is there controversy over using a beta blocker in patients who abuse cocaine?

A

-Cocaine stimulates both alpha and beta receptors
-Giving a beta blocker allows all of the cocaine to stimulate alpha receptors

(causes unopposed alpha effects)

-can cause hypertensive complications or increased troponin

148
Q

In patients who abuse cocaine, what type of beta blocker is best to use?

A

Non-selective BB

*such as carvedilol that blocks some alpha receptors too

NOTE: do not use BB if cocaine is in their system, only after

149
Q

When should we avoid starting or increasing a beta blocker?

A

During an acute heart failure exacerbation

(fluid overload, SOB)

150
Q

Why do we avoid beta blockers during acute heart failure exacerbations?

A

-Slow down the heart rate and decrease cardiac output

-Can cause pulmonary edema

151
Q

If a patient with an acute heart failure exacerbation is already taking a beta blocker, can they continue their maintenance dose?

A

YES
-better outcomes observed

152
Q

Why are beta blockers used for ACS?

A

To prevent future heart attacks and help the patient live longer

(typically used for BP, important to make distinction)

153
Q

What are the “hold parameters” for beta blockers?

A

HR < 60 consider, definitely if < 50

BP <90/60

154
Q

What ejection fraction is considered HFrEF?

A

39% or less

155
Q

When are calcium channel blockers used in ACS patients?

A

Non-DHP given to patients with recurrent ischemia and CONTRAINDICATIONS TO BB

(diltiazem or verapamil)

156
Q

What patients should Non-DHP CCBs not be used in?

A

LV dysfunction (HFrEF)**

Increased risk for cardiogenic shock

PR interval >0.24s

2nd or 3rd degree AV block without a cardiac pacemaker

157
Q

What statins should ACS patients receive?

A

High intensity

Atorvastatin 40-80mg
Rosuvastatin 20-40mg

158
Q

True or False: Statins help lower cholesterol but should be taken with ACS even if your cholesterol is normal

A

True

*lifelong treatment

159
Q

Which high intensity statin tends to have less problems with muscle pain?

A

Rosuvastatin

160
Q

What patients should receive ACE inhibitors?

A

All ACS patients

*Especially with:
-HFrEF
-DM
-CKD

161
Q

When should ACEi be started after an ACS?

A

Use cautiously within first 24 hours
-may cause hypotension or renal dysfunction

*Best to add them after 24 hours due to the large amount of other drugs added during this period

162
Q

What 4 ACEi and 1 ARB are used in ACS?

A

Captopril
Lisinopril
Ramipril
Trandolapril

Valsartan (ARB)

163
Q

When do we not want to use an ACEi?

A

-Hypotension/shock

-Bilateral renal artery stenosis or history of worsening renal function with ACEi/ARB use

-Acute renal failure

-Drug allergy/angioedema

164
Q

What needs to be monitored with ACEi?

A

Serum creatinine
(will increase a bit, >30% is a problem)

Potassium (increases)

BP (decreases)

Angioedema (rare)

165
Q

If a patient experiences angioedema while on an ACEi, what should be done with their dosing?

A

STOP the drug, seek medical attention

166
Q

What medications are included in triple antithrombotic therapy?

A

Oral anticoagulant
Aspirin
P2Y12 inhibitor

167
Q

For patients with Afib, how long should they receive triple antithrombotic therapy after ACS?

A

Discontinue aspirin after 1-4 weeks after PCI

Continue P2Y12i and anticoag (warfarin) for 1 year

After year, restart aspirin

168
Q

Who should receive nitroglycerin?

A

All ACS patients

(0.3-0.4 mg SL)

169
Q

How often do nitroglycerin tablets need to be replaced once opened?

A

Every 3-6 months

170
Q

What is an important counseling point for sublingual NTG spray?

A

It needs to be PRIMED

Nitrolingual: spray first 5 sprays into air

Nitromist: Spray first 10 sprays into air

Spring 2024 Therapeutics 3 (24 decks)

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