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IPCS 4 > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

What is the definition of cardiovascular disease?

A

any disorder of the heart of blood vessels

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2
Q

What is included in atherosclerotic disease?

A

Coronary artery disease
Stroke
Aortic aneurysm
Peripheral vascular disease

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3
Q

What is athero?

A

artery

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4
Q

What is sclerosis?

A

hardening

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5
Q

Coronary artery disease includes:

A

Acute coronary syndrome (CCD)
Angina

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6
Q

What is the leading cause of ischemic heart disease?

A

coronary artery disease (CAD)

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7
Q

CAD is the result of __ in coronary vessels leading to myocardial oxygen supply/demand mismatch

A

atherosclerotic plaques

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8
Q

What is ischemia?

A

deficiency of blood supply

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9
Q

What is infarct?

A

Complete cut off of blood supply leading to cell death

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10
Q

Clinical ASCVD includes:

A

Stroke, TIA
Carotid artery stenosis
Peripheral vascular disease
Aortic aneurysm

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11
Q

Atherosclerosis is a result of __ cell dysfunction, inflammation, and an increase in __

A

endothelial cell
lipoproteins

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12
Q

Plaques generally develop in the __, or the innermost layer of the arterial wall

A

intima

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13
Q

What are unmodifiable risk factors for CAD?

A

age
sex
family history
genetics

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14
Q

What are modifiable risk factors for CAD?

A

smoking
comorbidities (HTN, HLD, DM)
obesity
stress
sedentary lifestyle

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15
Q

Ischemia and angina result from a(n) INCREASE/DECREASE in oxygen demand and a(n) INCREASE/DECREASE in oxygen supply

A

increase in demand
decrease in supply

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16
Q

What are common causes of ischemia?

A

atherosclerotic plaque**
emboli
vasospasm
trauma
hypoxia
hypotension
medications

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17
Q

What is included in Acute Coronary Syndrome?

A

STEMI
NSTEMI
Unstable angina

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18
Q

What is included in Chronic Coronary Disease?

A

Chronic stable angina

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19
Q

How does the heart adapt to lack of oxygen? Can it adapt acutely?

A

Cannot adapt acutely
Extracts more oxygen from hemoglobin in RBCs
Collateral circulation (new coronary vessel formation around blockage)

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20
Q

An increase in what requires an increase in coronary flow to maintain adequate oxygen supply to the heart and leads to angina?

A

heart rate
myocardial contractility
myocardial wall tension

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21
Q

The __ of the arterial lumen determines the reduction of blood flow

A

diameter

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22
Q

Coronary plaques occupying 50-70% of the lumen are usually considered __

A

non-obstructive

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23
Q

Coronary plaques occupying 70% or more of the lumen are considered __

A

obstructive

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24
Q

Coronary plaques occupying 90% or more of the lumen are considered __

A

critical stenosis

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25
Q

Plaque build up in coronary arteries causes __ and __ blood flow

A

narrowing
decreased

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26
Q

Plaques can rupture and cause __ and __

A

thrombus
ischemia

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27
Q

Imbalance between __ and __ leads to an infarct

A

oxygen supply and demand

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28
Q

PAR-1 receptor is for __

A

thrombin

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29
Q

P2Y12 receptor is for __

A

ADP

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30
Q

Thrombin converts __ to __ which stabilizes PLT plug leading to blockage

A

fibrinogen to fibrin

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31
Q

-
-
-
-
-

A

collagen
thrombin
TXA2
ADP
serotonin
COX-1

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32
Q

Platelet activation leads to expression of __ receptors

A

GPIIb/IIIa receptors

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33
Q

GPIIb/IIIa receptors link platelets together with fibrinogen causing __

A

platelet aggregation

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34
Q

What are symptoms of acute coronary syndrome?

A

chest pain/pressure >10 min
severe dyspnea
diaphoresis
syncope
palpitations

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35
Q

What are atypical symptoms of ACS?

A

indigestion
stabbing chest pain
increasing exertion dyspnea

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36
Q

Typical ACS chest pain is described as _/3

A

3

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37
Q

Atypical ACS chest pain is described as _/3

A

2

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38
Q

What are the three factors to determine typical, atypical, or non-cardiac chest pain?

A

substernal chest discomfort
provoked by exertion or emotional stress
relieved by rest or nitro

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39
Q

Are there physical exam findings specific for ACS? If so, what are they?

A

no

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40
Q

What are signs of ACS?

A

ECG changes
Elevated troponin (I and T)
Elevated CK-MB
Elevated myoglobin
Arrythmias

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41
Q

Troponin I is related to __

A

muscle contraction

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42
Q

Troponin C is related to __

A

conformational change due to Ca

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43
Q

Troponin T is related to __

A

anchors troponin to tropomyosin

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44
Q

What is a normal Hs-cTnT?

A

<14 ng/L

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45
Q

What is a normal Troponin T?

A

0-0.04 ng/mL

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46
Q

Unstable Angina:
-ECG?
-Troponins?
-Blockage?

A

Normal, ST depression, T wave inversions
Not elevated
Partial (no myocardial injury)

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47
Q

NSTEMI:
-ECG?
-Troponins?
-Blockage?

A

ST depression, T wave inversions, nonspecific changes
Elevated
Partial (myocardial injury)

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48
Q

STEMI:
-ECG?
-Troponins?
-Blockage?

A

ST elevation, hyper acute T waves
Elevated
Complete (myocardial necrosis)

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49
Q

Ventricular remodeling happens from __ and __ activation

A

Sympathetic nervous system
Renin-angiotensin aldosterone system

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50
Q

An activated sympathetic nervous system leads to __

A

increased contractility and heart rate

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51
Q

An increase in RAAS system leads to __

A

retention of sodium and water, vasoconstriction
increased perfusion and blood volume

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52
Q

In ACS which happens first, SNS or RAAS activation?

A

SNS activation

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53
Q

What is the definition of CCD?

A

Stable angina
not an acute event
predictable chest pain exacerbated by physical exertion or emotional stress
relieved by rest or with medications

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54
Q

ACS or SIHD?
thin fibrous cap

A

ACS

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55
Q

ACS or SIHD?
Thicker fibrous cap

A

SIHD

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56
Q

ACS or SIHD?
Cholesterol-rich core more likely to erode/rupture

A

ACS

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57
Q

ACS or SIHD?
Calcified core

A

SIHD

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58
Q

ACS or SIHD?
Often 70% or greater degree of stenosis

A

ACS

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59
Q

ACS or SIHD?
Non-obstructive (<70% luminal diameter)

A

SIHD

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60
Q

What is shown on the PE of CCD?

A

No specific findings
Elevated BP
Signs of HF, + JVD, pulmonary edema, S3 gallop

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61
Q

What labs are shown with CCD?

A

troponins NOT typically elevated
Lipid panel (increased TC and LDL)

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62
Q

What are symptoms of CCD?

A

similar to ACS by predictable/resolve with rest

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63
Q

How is CCD diagnosed?

A

EKG
exercise stress test
coronary angiography
cardiac MRI
cardiac biomarkers (troponin)

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64
Q

What is the pathophysiology of peripheral artery disease?

A

plaque development and decreased nitric oxide impairs vasodilatory response and increases artery stiffness
leads to chronic occlusion

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65
Q

PAD most commonly affects which arteries?

A

medium and large arteries in the lower extremities

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66
Q

Atherosclerosis causing PAD is most commonly due to endothelial cell injury such as __ and __

A

smoking
diabetes

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67
Q

What is the clinical presentation of PAD?

A

highly variable
asymptomatic
lower extremity pain at rest
intermittent claudication
chronic limb threatening ischemia (CLTI)/critical limb ischemia (CLI)
non healing wounds/gangrene

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68
Q

What is seen on the PE to diagnose PAD?

A

Cool, dry, cyanotic extremities
bruits
hypertrophic toenails
lack of hair on calf, feet
diminished tibial, pedis pulse

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69
Q

What score is used for diagnosing PAD?

A

ABI score

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70
Q

An ABI score of what indicates PAD?

A

less than or equal to 0.9

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71
Q

ABI score is obtained while patient is in the __ position

A

supine

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72
Q

ABI score uses the SYSTOLIC/DIASTOLIC blood pressure on the arms and legs

A

Systolic

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73
Q

What are complications that can happen with PAD?

A

Impaired blood flow and vascular dysfunction
Nonhealing wounds
Skin/limb necrosis
CLTI
Amputations

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74
Q

Temporary interruption of cerebral blood flow that leads to transient focal neurological deficits

A

TIA

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75
Q

TIA has a __ onset, lasts ___, and DOES/DOES NOT have evidence of acute infarction

A

sudden onset
last seconds to minutes
no evidence of acute infarction

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76
Q

What is a TIA caused by?

A

focal spinal cord, brain, or retinal ischemia within the pertinent artery

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77
Q

What is the clinical presentation of a TIA?

A

*slurred speech or aphasia
*facial dropp
*paralysis, weakness, or *numbness of one or more limbs
Visual disturbances
ataxia
clumsiness
parasthesia
vertigo or syncope

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78
Q

TIAs are risk factors for __

A

strokes

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79
Q

Significant interruption of cerebral blood flow that generally leads to a persistent or permanent neurological deficit

A

Stroke

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80
Q

What are the three classifications of stroke neurological deficits?

A

Stable
Improving
Progressing

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81
Q

Stable, improving, or progressing?
permanent deficit will not improve or deteriorate

A

Stable

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82
Q

Stable, improving, or progressing?
Neurologic deficit is recovering, may take days to weeks

A

Improving

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83
Q

Stable, improving, or progressing?
Neurologic deficit deteriorates after its onset

A

Progressing

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84
Q

What is the clinical presentation of a stroke?

A

Similar to TIAs but to a greater magnitude and the deficits are generally permanent

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85
Q

What are the types of stroke?

A

Ischemic
Hemorrhagic

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86
Q

Which type of stroke is due to an obstruction of cerebral blood flow?

A

ischemic

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87
Q

Which type of stroke is due to bleeding into an area of the brain and surrounding structures?

A

hemorrhagic

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88
Q

Most strokes are ISCHEMIC/HEMORRHAGIC

A

Ischemic

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89
Q

Are hemorrhagic or ischemic strokes more lethal?

A

hemorrhagic

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90
Q

What are unmodifiable risk factors for cerebral infarction strokes?

A

age
men
family history of stroke
African American
Low birth weight

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91
Q

What are modifiable risk factors for cerebral infarction strokes?

A

Hypertension
DM
DLP
Smoking
AFib
Presence of carotid stenosis
Lifestyle
Sickle cell disease
Use of oral contraceptives
Post-menopausal hormone therapy

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92
Q

What is primary prevention for stroke?

A

Reduce risk factors
Antithrombotic therapy
Procedures if cardiac bruit

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93
Q

For primary prevention of stroke and patient has afib, what is antithrombotic prevention?

A

Use CHA2DS2-VASc score

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94
Q

For primary prevention of stroke and patient doesn’t have afib what is antithrombotic prevention?

A

DO NOT use aspirin

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95
Q

What procedures are used for primary prevention of stroke if carotid bruit is heard?

A

Carotid endarterectomy
Carotid angioplasty

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96
Q

What are causes of stroke due to obstructed blood flow?

A

Plaque rupture
Embolism

97
Q

How is stroke due to obstructed blood flow diagnosed?

A

PE
Brain imaging
NIH stroke scale
mRS
Differential diagnosis

98
Q

What are two approaches that have improved morbidity and mortality of cerebral infarctions?

A

Rapid initiation of acute treatment
The establishment of stroke teams and stroke units

99
Q

What should be done in all patients with cerebral infarction to see if thrombolytic therapy can be given?

A

Non-contrast CT scan or MRI of the brain
Blood glucose
Achieve blood pressure control

100
Q

What should be done for all patients with cerebral infarction soon after admission?

A

CBC
Routine coagulation tests
Routine clinical chemistries
Oxygen saturation
Cardiac markers
EKG

101
Q

If the stroke is mild and non-disabling, is thrombolytic therapy recommended?

A

No

102
Q

What is the benefit of Alteplase for stroke?

A

Decrease severity of neurological impairment

103
Q

What is a risk of using alteplase in stroke?

A

increased risk of intracranial hemorrhage

104
Q

Do not use alteplase in stroke if:

A

Symptoms are mild
Symptoms are rapidly improving

105
Q

What is the window of opportunity for alteplase in stroke patients?

A

3 hours from onset of event

106
Q

The window of opportunity for alteplase in stroke can be extended if all the following are present:

A

Age less than 80
NIH 25 or less
Does not have both DM and prior stroke
Not using oral anticoagulant
No evidence of ischemic injury associated with >1/3 of middle cerebral artery territory

107
Q

What is the goal of alteplase administration in stroke?

A

receive medication within 60 minuted of arrival to hospital

108
Q

What is the dose of alteplase for stroke?

A

0.9mg/kg max 90mg

109
Q

Can alteplase be given with heparin?

A

no

110
Q

Alteplase should be stopped Dif the patient develops:

A

severe headache
actue HTN
nausea/vomiting
worsening neurological exam

111
Q

If intracranial bleed occurs while patient is on alteplase, what should be done?

A

Stop med
Give tranexamic acid or aminocaproic acid

112
Q

What are contraindications of alteplase?

A

Bleeding
Uncontrolled HTN
BG <50
Seizure at onset of stroke
Endocarditis

113
Q

What are complications of alteplase?

A

Intracranial bleeding
angioedema
severe headache
acute HTN
worsened neurological findings
nausea/vomiting

114
Q

If agiokedema occurs while patient is on alteplase what should be dome?

A

Stop med
Stop ACEI if being used
Administer Medrol, Benadryl, Pepcid
Administer epinephrine if angioedema worsens

115
Q

When are intraarterial thrombolytics used?

A

Specialized centers
Unable/ineligible to receive IV therapy
Disorder is related to large vessel with a heavy clot

116
Q

What is the window of opportunity of intraarterial thrombolytics for stroke?

A

within 6 hours

117
Q

What is the preferred tPA if thrombectomy is being performed?

A

tenecteplase

118
Q

If stroke is due to atherosclerosis patient should be started on a __ statin

A

high-intensity

119
Q

What antiplatelet therapy is used in stroke?

A

Aspirin

120
Q

If alteplase is given, how long should you wait to give aspirin?

A

24 hours

121
Q

What antiplatelet therapy should be given in stroke for patients allergic to aspirin?

A

clopidogrel

122
Q

If anticoagulation is needed for stroke patient with low risk for hemorrhagic conversion, when should it be given?

A

2-14 days after the event

123
Q

If anticoagulation is needed for stroke patient with high risk for hemorrhagic conversion, when should it be given?

A

at least 14 days after the event

124
Q

For DVT prophylaxis in stroke patient what medications can be given and when?

A

48 hours after stroke onset
EPC cuffs
Heparin BID or TID
Enoxaparin

125
Q

What medications should not be used in stroke patients?

A

Corticosteroids for cerebral edema
Prophylactic anticonvulsant therapy

126
Q

What are complications of cerebral infarction strokes?

A

Seizures
Pneumonia
DVTs
Depression

127
Q

What is secondary prevention of cerebral infarction strokes?

A

Reduce risk factors
Blood pressure and blood glucose control
Endartectomy or stenting if >70% stenosis
Aggressive statinization
Antiplatelet therapy

128
Q

The ABCD Score determines risk for __

A

subsequent stroke

129
Q

What is secondary prevention for TIAs?

A

Reduce risk factors
Blood pressure reduction
Aggressive statinization
Antiplatelet therapy
Anticoagulation

130
Q

When is combination therapy of aspirin and clopidogrel considered?

A

TIAs (ABCD 4 or higher)
Minor stroke (NIHSS 3 or lower)

131
Q

Hemorrhagic strokes are often due to __

A

severe hypertension
arteriovenous malformations
aneurysms
trauma
medications

132
Q

Risk of bleed into cerebral tissue is increased with uncontrolled __

A

blood pressure

133
Q

Symptoms of bleed into cerebral tissue are due to __

A

blood directly irritating brain tissue

134
Q

Bleed into the subdural cavity between dura mater and arachnoid are related to __

A

head and or skull trauma

135
Q

Hemorrhagic stroke can be caused by bleeds in what three areas?

A

-Into cerebral tissue
-Into the subdural cavity between the dura mater and arachnoid
-Into space between arachnoid and pia mater

136
Q

For hemorrhagic strokes, antithrombotic therapy can be stopped in __

A

1-2 weeks

137
Q

What antithrombotic are used in hemorrhagic stroke?

A

Warfarin
Xa inhibitors
Thrombin Inhibitors
Heparin
LMWH

138
Q

When is antihypertensive therapy used in hemorrhagic stroke?

A

cerebral bleed
SBP 150-220

139
Q

Subarachnoid hemorrhage is a bleed into __

A

space between arachnoid and pia mater

140
Q

Subarachnoid hemorrhage is caused by __

A

Aneurysm (Polycystic kidney disease)
Trauma
Arteriovenous malformations

141
Q

What is the clinical presentation of subarachnoid hemorrhage?

A

“Worst headache of my life”
Feel a popping sensation at onset
Altered consciousness and/or confusion
Photophobia
Muscle aches
Nausea and/or vomiting

142
Q

What is seen in the PE for subarachnoid hemorrhage?

A

stiff neck
decreased eye movement
neurologic deficit

143
Q

How is a subarachnoid hemorrhage diagnosed?

A

Cerebral angiogram
CT angiogram
CT scan of the head

144
Q

What are complications that occur from a subarachnoid hemorrhage?

A

Rebleeding
Hydrocephalus
Delayed ischemia
Seizures

145
Q

What is hydrocephalus?

A

Accumulation of CSF within ventricular system of the brain

146
Q

How is hydrocephalus managed?

A

Surgical placement of ventriculoperitoneal shunt

147
Q

How is delayed ischemia due to subarachnoid hemorrhage prevented?

A

Volume expansion with NS
Fludrocortisone
Nimodipine

148
Q

What are the two treatment considerations for subarachnoid hemorrhage?

A

Bleeding
Control BP

149
Q

How should bleeding be managed of a subarachnoid hemorrhage?

A

Reverse anticoagulation
Surgical clipping

150
Q

What are suggested medications to control BP in subarachnoid hemorrhage?

A

Nicardipine
Clevidipine

151
Q

What is the Coronary angiography and PCI difference between a STEMI and NSTE-ACS?

A

STEMI:
-Emergent
-Preferred over thrombolytic therapy
-Primary PCI
NSTE-ACS:
-Early vs Late
-Generally early is preferred
-No mortality difference

152
Q

What is non-pharm treatment in STEMI and NSTE-ACS?

A

Heart healthy diet
A1c <7
BMI 18.5-24.9
Waist circumference <35F, <40M
Aerobic activity 150 min/wk
Smoking cessation
Limiting alcohol 1F, 2M

153
Q

What is the acronym for immediate drug therapy in STEMI/NSTE-ACS?

A

MONA-B

154
Q

What is the acronym for at hospital drug therapy in STEMI/NSTE-ACS?

A

GAP

155
Q

What is the acronym for prior to discharge for STEMI/NSTE-ACS?

A

BA2S2

156
Q

What does MONA-B stand for?

A

Morphine
Oxygen
Nitrates
Aspirin
Beta-Blocker (CCB potentially)

157
Q

What does GAP stand for?

A

GPIIb/IIIa antagonists
Anticoagulants
P2Y12 Inhibitors

158
Q

What does BA2S2 stand for?

A

Beta-blocker
Ace-Inhibitor (or ARB)
Antiplatelets (ASA and P2Y12)
Statin/Smoking cessation
SL nitro PRN chest pain

159
Q

When is should morphine be avoided?

A

Hypotension
Bradycardia
Lethargic

160
Q

What is a clinical pearl with morphine?

A

May reduce oxygen demand but increased risk of mortality and decreases absorption of other oral ACS drugs

161
Q

When should Oxygen be avoided?

A

COPD (88-92%)

162
Q

When is oxygen indicated in STEMI/NSTE-ACS patients?

A

O2 Sat <90%

163
Q

When should nitroglycerin be avoided?

A

SBP <90mmHg
PDE5 Inhibitors
RV infarct

164
Q

What is a clinical pearl associated with nitroglycerin?

A

Useful in ACS related to vasospasms (cocaine-induced)

165
Q

When should aspirin be avoided?

A

Severe bleeding
Allergy

166
Q

If pt is already on baby aspirin, should a loading dose be given for STEMI?

A

yes

167
Q

Which formulation of aspirin for loading dose should be given for STEMI/NSTE-ACS?

A

chewable

168
Q

When should beta blockers be avoided?

A

Acute decompensated HF
Cardiogenic shock
AV block

169
Q

What are clinical pearls of beta blockers for STEMI/NSTE-ACS?

A

Mortality benefit
Avoid IV (increased shock)
Can use any beta blocker

170
Q

When should CCBs be used for STEMI/NSTE-ACS?

A

If beta blockers are contraindicated
Coronary vasospasms

171
Q

When should CCBs be avoided?

A

Acute decompensated HF
Cardiogenic shock
AV block
Hypotension

172
Q

Non-DHP CCBs are contraindicated in __

A

EF <40%

173
Q

What CCB should be avoided for STEMI/NSTE-ACS?

A

IR Nifedipine

174
Q

When are fibrinolytics indicated?

A

STEMI
If cannot do PCI within 120 minutes
Symptom onset past 12 hours

175
Q

What is door-to-needle time for fibrinolytics in STEMI?

A

30 minutes

176
Q

What are relative contraindications to fibrinolysis?

A

Ischemic stroke>3 months ago
Recent major surgery <3 weeks
Trauma
Recent internal bleed <4 weeks
BP >180/110 mmHg

177
Q

What are absolute contraindications to fibrinolysis?

A

Any prior hemorrhagic stroke
Ischemic stroke <3 months
Intracranial neoplasm
Active internal bleed
Aortic dissection
Facial/head trauma <3 months
Intracranial/spine surgery <2 months
Severe hypertension

178
Q

What should be given with fibrinolytics?

A

Antiplatelets
Anticoagulation

179
Q

What anticoagulation can be given prior to PCI?

A

UFH
Bivalirudin
LMWH
Fondaparinux

180
Q

What anticoagulation should be given for STEMI patients during PCI?

A

UFH
Bivalirudin
LMWH

181
Q

If UFH or bivalirudin are to be continued after PCI when should it be stopped?

A

48 hours

182
Q

If LMWH or Fondaparinux are continued after PCI when should they be stopped?

A

8 days or at discharge

183
Q

Anticoagulation dosing for STEMI undergoing PCI is LOWER/HIGHER than for a DVT

A

lower

184
Q

What labs should be monitored for anticoagulation?

A

CBC (Hbg, HCT, PLTs)

185
Q

How should heparin be monitored?

A

aXa-UFH
aPTT
ACT

186
Q

How should Bivalirudin be monitored?

A

aPTT
ACT

187
Q

How should Enoxaparin be monitored?

A

aXa-LMWH
ACT

188
Q

During PCI the STEMI patients must have at least __ antiplatelets

A

two

189
Q

What are antiplatelet choices during PCI?

A

Aspirin and oral P2Y12 inhibitor
Aspirin and IV cangrelor
Aspirin allergy: P2Y12 inhibitor and IV GIIb/IIIa inhibitor

190
Q

What are reversible P2Y12 inhibitors?

A

Cangrelor
Ticagrelor

191
Q

What are irreversible P2Y12 inhibitors?

A

Clopidogrel
Prasugrel

192
Q

What are GIIb/IIIa inhibitor options?

A

Eptifbitide
Tirofiban

193
Q

What drug can be used to bridge patients to surgery?

A

Cangrelor

194
Q

GIIb/IIIa inhibitors are guideline recommended for __ use

A

bailout

195
Q

What is dosing for Clopidogrel?

A

75mg 3-5 days
300mg 6-8 hours
600mg 2-4 hours

196
Q

What is dosing for Prasugrel?

A

10mg 3 days
60mg 30-60 min

197
Q

What is dosing for Ticagrelor?

A

90mg 2-3 dawys
180mg 60 min

198
Q

Ticagrelor is contraindicated in __

A

intracrannial hemorrhage

199
Q

What medications can decrease concentrations of clopidogrel?

A

Esomeprazole, omeprazole
Fluconazole, voriconazole
Fluoxetine
Fluvoxamine

200
Q

Prasugrel is contraindicated in patients with history of __

A

stroke or TIA

201
Q

Prasugrel dose is reduced to 5mg QD in which patient populations?

A

> 75 yo
<60kg

202
Q

What dose of aspirin should be used with ticagrelor?

A

75-100mg

203
Q

What are the preferred P2Y12 inhibitors?

A

Prasugrel
Ticagrelor

204
Q

__ is the P2Y12 of choice in patients needing to be maintained on an oral anticoagulant

A

Clopidogrel

205
Q

__ has not been studied in patients who are medically managed (no revascularization/PCI) or in combination with fibrinolytic therapy

A

Prasugrel

206
Q

Loading dose is always needed when switching antiplatelet sin the EARLY/LATE phase

A

early

207
Q

How do you switch from Ticagrelor to Clopidogrel?

A

600mg Clopidogrel loading dose 24 hours after last Ticagrelor dose

208
Q

How do you switch from Ticagrelor to Prasugrel?

A

60mg Prasugrel loading dose 24 hours after last Ticagrelor dose

209
Q

How do you change from Clopidogrel to Ticagrelor in early phase?

A

180mg Ticagrelor loading dose

210
Q

How do you change from Clopidogrel tp Ticagrelor in late phase?

A

90mg BID Ticagrelor maintenance dose 24 hours after last Clopidogrel dose

211
Q

How do you change from Prasugrel to Ticagrelor in early phase?

A

180mg Ticagrelor loading dose 24 hours after last Prasugrel dose

212
Q

How do you change from Prasugrel to Ticagrelor in late phase?

A

90mg BID Ticagrelor maintenance dose 24 hours after last Prasugrel dose

213
Q

How do you change from Prasugrel to Clopidogrel in early phase?

A

600mg Clopidogrel loading dose 24 hours after last Prasugrel dose

214
Q

How do you change from Prasugrel to Clopidogrel in late phase?

A

75mg Clopidogrel maintenance dose 24 hours after last Prasugrel dose

215
Q

How do you change from Clopidogrel to Prasugrel in early phase?

A

60mg Prasugrel loading dose

216
Q

How do you change from Clopidogrel to Prasugrel in late phase?

A

10mg Prasugrel maintenance dose 24 hours after last Clopidogrel dose

217
Q

What is considered early phase?

A

Within first 30 days

218
Q

How do you switch from oral to IV P2Y12 Inhibitors?

A

Initiate within 72 hours from discontinuation fro a minimum of 48 hours and max of 7 days

219
Q

How do you switch from Cangrelor to Clopidogrel?

A

600mg Clopidogrel immediately after Cangrelor discotinuation

220
Q

How do you switch from Cangrelor to Prasugrel?

A

60mg Prasugrel immediately after Cangrelor discontinuation

221
Q

How do you switch from Cangrelor to Ticagrelor?

A

180mg at start of Cangrelor up to immediately after discontinuation

222
Q

What is included in DAPT?

A

Aspirin
and
Clopidogrel or Ticagrelor or Prasugrel

223
Q

What’s Clopidogrel dosing in DAPT therapy?

A

600mg load
75mg daily

224
Q

What’s Ticagrelor dosing in DAPT therapy?

A

180mg Load
90mg BID
60mg BID after 1 year

225
Q

What’s Prasugrel dosing in DAPT therapy?

A

60mg load
10mg daily
5mg daily in select patients

226
Q

When is DAPT therapy considered?

A

CABG (Clopidogrel only)
PCI
Medical Management (No Prasugrel)
Fibrinolytics (Clopidogrel preferred)

227
Q

What is the duration of DAPT therapy? In high bleed risk patients?

A

Aspirin indefinitely, P2Y12 at 12 months
P2Y12 at 6 months

228
Q

What is the duration for triple antiplatelet therapy?

A

Aspirin: 1 week
P2Y12: 12 months
OAC: indefinitelty

229
Q

A higher DAPT score indicates __

A

longer DAPT therapy

230
Q

What are the two purposes of statins post ACS events?

A

Hyperlipidemia
Plaque stabilization

231
Q

What statins should be used post ACS event?

A

Atorvastatin 40-80mg
Rosuvastatin 20-40mg

232
Q

What is the purpose of beta blocker use post ACS event?

A

Reduce likelihood of ventricular arrhythmias, recurrent ischemia/infarction, ventricular remodeling
Improve survival

233
Q

When are beta blockers contraindicated post ACS?

A

Signs/symptoms of cariogenic shock (Low BP, bradycardia)

234
Q

How long should beta blockers be continued post ACS?

A

minimum of 3 years

235
Q

How long should beta blockers be continued post ACS in patients with a preserved EF?

A

1 year

236
Q

RAAS inhibitors are suggested post ACS event in patients with which compelling indications?

A

HFrEF (<40%)
Hypertension
DM
Stable CKD

237
Q

What nitrate should be given post ACS event?

A

Nitro SL tablet
Nitro TL spray
Nitro SL powder
PRN for immediate relief

238
Q

When should nitroglycerin be avoided post ACS?

A

If recent use of PDE-5 inhibitor

239
Q
A

IPCS 4 (5 decks)

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