ACS 2 - Quiz 3 Flashcards
(110 cards)
1
Q
goals of ACS therapy
A
- restore epicardial coronary blood flow
- limit myocardial damage
- minimize risk for complications
2
Q
general therapies
A
- bed rest
- supplemental oxygen
- analgesia
- anti-ischemic therapies
- Anti-platelet and Antithrombotic therapies
3
Q
purpose of bed rest
A
- minimize oxygen demand
4
Q
purpose of supplemental oxygen
A
- improves oxygen supply
5
Q
purpose of analgesia
A
- reduce anxiety and chest pain
- minimize oxygen demand
6
Q
treatment for ST segment elevation
A
- open artery emergently
7
Q
treatment for no ST segment elevation
A
- antiplatelet therapy
- anti-ischemic therapy
- anticoagulant therapy
- invasive versus conservative
8
Q
goals of anti-ischemic medications
A
- restore balance between oxygen demand versus supply
9
Q
goals of anti-thrombotic therapy
A
- prevent further growth of thrombus
- enhance resolution
10
Q
drugs for anti-ischemic therapy
A
- beta blockers
- nitrates
- non dihydropyridine calcium channel blockers
11
Q
sympathetic effect of beta blockers
A
- decrease sympathetic drive
- reduce O2 demand
12
Q
electrical stability effect of beta blockers
A
- enhance electrical stability
13
Q
mortality effect of beta blockers
A
- reduce mortality
14
Q
contraindications of beta blockers
A
- marked bradycardia
- severe bronchospasm
- hypotension
- acute heart failure
15
Q
when do you start beta blockers
A
- orally within first 24 hours
16
Q
target HR on beta blockers
A
- below 60
17
Q
do you continue beta blockers?
A
- yes, indefinitely
18
Q
nitrates purpose
A
- venodilation
- coronary vasodilation
19
Q
result of venodilation
A
- decreases preload
- less wall stress
- lower O2 demand
20
Q
what is pre-load
A
- venous return to the heart
21
Q
coronary vasodilation result
A
- improve blood flow
- reduce vasospasm
- improved O2 supply
22
Q
nitrates given how
A
- sublingual (underneath the tongue)
23
Q
nitrates contraindications
A
- patients with RV infarction
24
Q
why we don’t use nitrates in patients with RV infarction
A
- these patients are preload dependent
- nitrates cause hypotension
25
non-dihydropyridine calcium channel blockers result
- vasodilation
- decreased myocardial O2 demand
- increased supply
26
non-dihydropyridine calcium channel blockers - mortality effect
- no mortality benefit
27
non-dihydropyridine calcium channel blockers - when to use
- refractory ischemic symptoms
| - contraindication to beta blocker
28
non-dihydropyridine calcium channel blockers - contraindications
- patients with LV systolic dysfunction
| - increases their mortality
29
Anti-platelet therapies
- aspirin
- clopidogrel
- IV glycoprotein IIB/IIIA inhibitor
30
aspirin effect
- inhibits platelet synthesis of TxA2
| - inhibits platelet activation
31
aspirin mortality effect
- reduces mortality
32
when to give aspirin
- give immediately
33
clopidogrel effect
- P2Y12 inhibitor
| - give to aspirin-allergic patients
34
best way to reduce mortality in patients with NSTEMI-ACS
- give aspirin and plavix
35
which is the most potent Anti-platelet agent
- IV glycoprotein IIB/IIIA inhibitor
36
result of IV glycoprotein IIB/IIIA inhibitor
- block final common pathway of platelet activation
37
use of IV glycoprotein IIB/IIIA inhibitor
- adjunctive therapy with PCI
38
anticoagulant therapies
- unfractionated heparin
- low molecular weight heparin
- fondaparinux
- bivalirudin
39
result of unfractionated heparin
- enhance antithrombin effects
- impedes thrombus development
- improves cardiovascular outcomes
40
UFH versus LMWH
- reduced death and ischemic rates with LMWH
41
problem with LMWH
- hard to monitor during procedures
42
fondaparinux inhibits
- factor Xa
43
fondaparinux result
- reduces CV events
| - less bleeding risk
44
fondaparinux used for
- when no PCI is planned
45
bivalirudin inhibits
- thrombin
46
bivalirudin result
- reduced clinical events
| - less bleeding risks
47
bivalirudin used for
- in Cath lab for PCI
48
what do we use now for PCI
- drug eluting stent
49
how does a drug eluting stent work?
- anti proliferative agent elutes from Bare metal stent platform
50
approach for unstable angina
- conservative
51
approach for NSTEMI
- early invasive
52
process for early invasive therapy
- urgent coronary angiography
| - followed by coronary revascularization
53
process for conservative therapy
- medical management
54
when do you do a cardiac Cath in conservative therapy
- only with recurrent ischemia
| - positive stress test
55
most important factors from TIMI score
- ST change
| - elevated cardiac markers
56
reperfusion strategies with STEMI
- fibrinolysis
| - PCI
57
result of fibrinolysis
- accelerates clot lysis
- restore blood flow
- salvage myocardium
58
MOA of fibrinolysis
- transforms plasminogen to plasmin
| - lysis fibrin clot
59
major complication of fibrinolysis
- bleeding
60
when do we give fibrinolysis
- within 120 minutes of onset of symptoms
61
contraindications for fibrinolysis
- active ulcer disease
- bleeding disorder
- recent CVA or surgery
- uncontrolled HTN
- elderly
62
what do we usually give with fibrinolysis
- aspirin
- heparin
- clopidogrel
63
when does PCI need to be performed
- within 90 minutes of hospital presentation
64
adjunctive therapies with PCI
- aspirin
- P2y12 inhibitor
- bivalirudin or heparin
- IV GP IIB/IIIA inhibitor
65
when do we give fibrinolytics over PCI
- if time taken to PCI is longer than one hour
66
complications of MI
- recurrent ischemia
- arrhythmias
- heart failure
- right ventricular infarction
- ventricular aneurysm
- pericarditis
- thromboembolism
67
recurrent ischemia may represent problem with
- malplacement of stent
- acute thrombosis
- repeat cardiac cath
68
mechanisms of why you get arrhythmias after MI
- impaired perfusion to conduction system
- accumulation of toxic metabolic products
- autonomic stimulation
- arrhythmic drugs
69
what is the most common cause of death within first 48 hours after an MI
- Vtach or Vfib
70
early Vtach or Vfib after MI due to
- electrical instability
71
late Vtach or Vfib after MI due to
- structural disease
72
AV node supplied by
- RCA
73
bundle of His supplied by
- LAD
74
right bundle branch supplied by
- proximal portion by LAD
| - distal portion by RCA
75
left bundle branch anterior fascicle supplied by
- LAD
| - most susceptible to ischemia
76
left bundle branch posterior fascicle supplied by
- LAD
| - PDA
77
conduction block arrhythmias development from
- ischemia
| - necrosis of conduction tracts
78
post MI heart failure caused by
- impaired contractility from ischemia
| - increased myocardial stiffness
79
signs/symptoms of post MI heart failure
- dyspnea
- rales
- S3
- peripheral edema
- SOB when lying flat
80
how to treat HF
- revascularization
| - ace inhibitors, beta blockers, diuretics
81
cardiogenic shock due to
- severely decreased cardiac output
| - hypotension
82
physiologic effects of intra-aortic balloon pump
- enhanced coronary blood flow
- left ventricular unloading
- improved cardiac output
83
EKG for right heart fialure
- ST elevation in lead II, III, and aVF
- more III than II
- also check V4R
84
signs of right heart failure
- elevated JVP
- hypotension
- clear lungs
85
treatment of right heart failure
- volume and reperfusion
86
mechanical complications of MI
- papillary muscle rupture
- ventricular septal rupture
- ventricular free wall rupture
87
when does papillary muscle rupture occur
- 3-5 days post MI
88
papillary muscle rupture results in
- acute, severe mitral regurgitation
| - holosystolic murmor
89
when does ventricular septal rupture occur?
- 3-7 days post MI
90
ventricular septal rupture results in
- form in inter ventricular septum
- shunt from LV to RV
- holosystolic murmor
91
diagnosis of ventricular septal rupture
- EKG
92
ventricular septal rupture leads to
- heart failure
93
ventricular free wall rupture occurs when
- 14 days post MI
94
ventricular free wall rupture result
- blood fills pericardial space
| - causes cariogenic shock
95
when would a ventricular aneurysm occur
- weeks to months after an MI
96
when does a ventricular aneurysm develop
- as well weakens with phagocytic process used to clear necrotic tissue
97
how to check for ventricular aneurysm
- persistent ST segment elevation weeks after STEMI
98
acute pericarditis symptoms
- sharp, pleuritic pain
- fever
- pericardial friction rub on auscultation
99
how to treat acute pericarditis
- aspirin
| - avoid anticoagulants
100
Dressler syndrome
- immune process directed against necrotic myocardium
101
Dressler syndrome treatment
- aspirin
| - NSAIDS
102
thromboembolism due to
- stasis of blood in regions of impaired LV wall contractility
103
thromboembolism can be seen with
- LV aneurysm
104
thromboembolism requires
- anticoagulation
105
other therapies for ACS
- ACE inhibitors
| - statins
106
purpose of ACE inhibitors
- reduce incidence of heart failure
- reduce recurrent ischemia
- reduce mortality
107
ace inhibitors greatest benefit with which patients
- those with LV dysfunction
| - high risk patients
108
statins effects
stabilize endothelium
109
standard post discharge therapy following MI
- aspirin
- P2Y12 inhibitor
- beta blocker
- statins
- ACE inhibitors
- aldosterone antagonists
- risk factor modification
110
why do we give aldosterone antagonists
- for patients with LV dysfunction
