ACS 2 - Quiz 3 Flashcards

1
Q

goals of ACS therapy

A
  • restore epicardial coronary blood flow
  • limit myocardial damage
  • minimize risk for complications
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2
Q

general therapies

A
  • bed rest
  • supplemental oxygen
  • analgesia
  • anti-ischemic therapies
  • Anti-platelet and Antithrombotic therapies
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3
Q

purpose of bed rest

A
  • minimize oxygen demand
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4
Q

purpose of supplemental oxygen

A
  • improves oxygen supply
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5
Q

purpose of analgesia

A
  • reduce anxiety and chest pain

- minimize oxygen demand

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6
Q

treatment for ST segment elevation

A
  • open artery emergently
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7
Q

treatment for no ST segment elevation

A
  • antiplatelet therapy
  • anti-ischemic therapy
  • anticoagulant therapy
  • invasive versus conservative
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8
Q

goals of anti-ischemic medications

A
  • restore balance between oxygen demand versus supply
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9
Q

goals of anti-thrombotic therapy

A
  • prevent further growth of thrombus

- enhance resolution

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10
Q

drugs for anti-ischemic therapy

A
  • beta blockers
  • nitrates
  • non dihydropyridine calcium channel blockers
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11
Q

sympathetic effect of beta blockers

A
  • decrease sympathetic drive

- reduce O2 demand

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12
Q

electrical stability effect of beta blockers

A
  • enhance electrical stability
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13
Q

mortality effect of beta blockers

A
  • reduce mortality
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14
Q

contraindications of beta blockers

A
  • marked bradycardia
  • severe bronchospasm
  • hypotension
  • acute heart failure
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15
Q

when do you start beta blockers

A
  • orally within first 24 hours
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16
Q

target HR on beta blockers

A
  • below 60
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17
Q

do you continue beta blockers?

A
  • yes, indefinitely
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18
Q

nitrates purpose

A
  • venodilation

- coronary vasodilation

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19
Q

result of venodilation

A
  • decreases preload
  • less wall stress
  • lower O2 demand
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20
Q

what is pre-load

A
  • venous return to the heart
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21
Q

coronary vasodilation result

A
  • improve blood flow
  • reduce vasospasm
  • improved O2 supply
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22
Q

nitrates given how

A
  • sublingual (underneath the tongue)
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23
Q

nitrates contraindications

A
  • patients with RV infarction
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24
Q

why we don’t use nitrates in patients with RV infarction

A
  • these patients are preload dependent

- nitrates cause hypotension

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25
Q

non-dihydropyridine calcium channel blockers result

A
  • vasodilation
  • decreased myocardial O2 demand
  • increased supply
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26
Q

non-dihydropyridine calcium channel blockers - mortality effect

A
  • no mortality benefit
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27
Q

non-dihydropyridine calcium channel blockers - when to use

A
  • refractory ischemic symptoms

- contraindication to beta blocker

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28
Q

non-dihydropyridine calcium channel blockers - contraindications

A
  • patients with LV systolic dysfunction

- increases their mortality

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29
Q

Anti-platelet therapies

A
  • aspirin
  • clopidogrel
  • IV glycoprotein IIB/IIIA inhibitor
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30
Q

aspirin effect

A
  • inhibits platelet synthesis of TxA2

- inhibits platelet activation

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31
Q

aspirin mortality effect

A
  • reduces mortality
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32
Q

when to give aspirin

A
  • give immediately
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33
Q

clopidogrel effect

A
  • P2Y12 inhibitor

- give to aspirin-allergic patients

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34
Q

best way to reduce mortality in patients with NSTEMI-ACS

A
  • give aspirin and plavix
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35
Q

which is the most potent Anti-platelet agent

A
  • IV glycoprotein IIB/IIIA inhibitor
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36
Q

result of IV glycoprotein IIB/IIIA inhibitor

A
  • block final common pathway of platelet activation
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37
Q

use of IV glycoprotein IIB/IIIA inhibitor

A
  • adjunctive therapy with PCI
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38
Q

anticoagulant therapies

A
  • unfractionated heparin
  • low molecular weight heparin
  • fondaparinux
  • bivalirudin
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39
Q

result of unfractionated heparin

A
  • enhance antithrombin effects
  • impedes thrombus development
  • improves cardiovascular outcomes
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40
Q

UFH versus LMWH

A
  • reduced death and ischemic rates with LMWH
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41
Q

problem with LMWH

A
  • hard to monitor during procedures
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42
Q

fondaparinux inhibits

A
  • factor Xa
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43
Q

fondaparinux result

A
  • reduces CV events

- less bleeding risk

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44
Q

fondaparinux used for

A
  • when no PCI is planned
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45
Q

bivalirudin inhibits

A
  • thrombin
46
Q

bivalirudin result

A
  • reduced clinical events

- less bleeding risks

47
Q

bivalirudin used for

A
  • in Cath lab for PCI
48
Q

what do we use now for PCI

A
  • drug eluting stent
49
Q

how does a drug eluting stent work?

A
  • anti proliferative agent elutes from Bare metal stent platform
50
Q

approach for unstable angina

A
  • conservative
51
Q

approach for NSTEMI

A
  • early invasive
52
Q

process for early invasive therapy

A
  • urgent coronary angiography

- followed by coronary revascularization

53
Q

process for conservative therapy

A
  • medical management
54
Q

when do you do a cardiac Cath in conservative therapy

A
  • only with recurrent ischemia

- positive stress test

55
Q

most important factors from TIMI score

A
  • ST change

- elevated cardiac markers

56
Q

reperfusion strategies with STEMI

A
  • fibrinolysis

- PCI

57
Q

result of fibrinolysis

A
  • accelerates clot lysis
  • restore blood flow
  • salvage myocardium
58
Q

MOA of fibrinolysis

A
  • transforms plasminogen to plasmin

- lysis fibrin clot

59
Q

major complication of fibrinolysis

A
  • bleeding
60
Q

when do we give fibrinolysis

A
  • within 120 minutes of onset of symptoms
61
Q

contraindications for fibrinolysis

A
  • active ulcer disease
  • bleeding disorder
  • recent CVA or surgery
  • uncontrolled HTN
  • elderly
62
Q

what do we usually give with fibrinolysis

A
  • aspirin
  • heparin
  • clopidogrel
63
Q

when does PCI need to be performed

A
  • within 90 minutes of hospital presentation
64
Q

adjunctive therapies with PCI

A
  • aspirin
  • P2y12 inhibitor
  • bivalirudin or heparin
  • IV GP IIB/IIIA inhibitor
65
Q

when do we give fibrinolytics over PCI

A
  • if time taken to PCI is longer than one hour
66
Q

complications of MI

A
  • recurrent ischemia
  • arrhythmias
  • heart failure
  • right ventricular infarction
  • ventricular aneurysm
  • pericarditis
  • thromboembolism
67
Q

recurrent ischemia may represent problem with

A
  • malplacement of stent
  • acute thrombosis
  • repeat cardiac cath
68
Q

mechanisms of why you get arrhythmias after MI

A
  • impaired perfusion to conduction system
  • accumulation of toxic metabolic products
  • autonomic stimulation
  • arrhythmic drugs
69
Q

what is the most common cause of death within first 48 hours after an MI

A
  • Vtach or Vfib
70
Q

early Vtach or Vfib after MI due to

A
  • electrical instability
71
Q

late Vtach or Vfib after MI due to

A
  • structural disease
72
Q

AV node supplied by

A
  • RCA
73
Q

bundle of His supplied by

A
  • LAD
74
Q

right bundle branch supplied by

A
  • proximal portion by LAD

- distal portion by RCA

75
Q

left bundle branch anterior fascicle supplied by

A
  • LAD

- most susceptible to ischemia

76
Q

left bundle branch posterior fascicle supplied by

A
  • LAD

- PDA

77
Q

conduction block arrhythmias development from

A
  • ischemia

- necrosis of conduction tracts

78
Q

post MI heart failure caused by

A
  • impaired contractility from ischemia

- increased myocardial stiffness

79
Q

signs/symptoms of post MI heart failure

A
  • dyspnea
  • rales
  • S3
  • peripheral edema
  • SOB when lying flat
80
Q

how to treat HF

A
  • revascularization

- ace inhibitors, beta blockers, diuretics

81
Q

cardiogenic shock due to

A
  • severely decreased cardiac output

- hypotension

82
Q

physiologic effects of intra-aortic balloon pump

A
  • enhanced coronary blood flow
  • left ventricular unloading
  • improved cardiac output
83
Q

EKG for right heart fialure

A
  • ST elevation in lead II, III, and aVF
  • more III than II
  • also check V4R
84
Q

signs of right heart failure

A
  • elevated JVP
  • hypotension
  • clear lungs
85
Q

treatment of right heart failure

A
  • volume and reperfusion
86
Q

mechanical complications of MI

A
  • papillary muscle rupture
  • ventricular septal rupture
  • ventricular free wall rupture
87
Q

when does papillary muscle rupture occur

A
  • 3-5 days post MI
88
Q

papillary muscle rupture results in

A
  • acute, severe mitral regurgitation

- holosystolic murmor

89
Q

when does ventricular septal rupture occur?

A
  • 3-7 days post MI
90
Q

ventricular septal rupture results in

A
  • form in inter ventricular septum
  • shunt from LV to RV
  • holosystolic murmor
91
Q

diagnosis of ventricular septal rupture

A
  • EKG
92
Q

ventricular septal rupture leads to

A
  • heart failure
93
Q

ventricular free wall rupture occurs when

A
  • 14 days post MI
94
Q

ventricular free wall rupture result

A
  • blood fills pericardial space

- causes cariogenic shock

95
Q

when would a ventricular aneurysm occur

A
  • weeks to months after an MI
96
Q

when does a ventricular aneurysm develop

A
  • as well weakens with phagocytic process used to clear necrotic tissue
97
Q

how to check for ventricular aneurysm

A
  • persistent ST segment elevation weeks after STEMI
98
Q

acute pericarditis symptoms

A
  • sharp, pleuritic pain
  • fever
  • pericardial friction rub on auscultation
99
Q

how to treat acute pericarditis

A
  • aspirin

- avoid anticoagulants

100
Q

Dressler syndrome

A
  • immune process directed against necrotic myocardium
101
Q

Dressler syndrome treatment

A
  • aspirin

- NSAIDS

102
Q

thromboembolism due to

A
  • stasis of blood in regions of impaired LV wall contractility
103
Q

thromboembolism can be seen with

A
  • LV aneurysm
104
Q

thromboembolism requires

A
  • anticoagulation
105
Q

other therapies for ACS

A
  • ACE inhibitors

- statins

106
Q

purpose of ACE inhibitors

A
  • reduce incidence of heart failure
  • reduce recurrent ischemia
  • reduce mortality
107
Q

ace inhibitors greatest benefit with which patients

A
  • those with LV dysfunction

- high risk patients

108
Q

statins effects

A

stabilize endothelium

109
Q

standard post discharge therapy following MI

A
  • aspirin
  • P2Y12 inhibitor
  • beta blocker
  • statins
  • ACE inhibitors
  • aldosterone antagonists
  • risk factor modification
110
Q

why do we give aldosterone antagonists

A
  • for patients with LV dysfunction