1
Q
signs and symptoms of ACS is generally
A
non-sensitive and non-specific
2
Q
typical symptoms of ACS
A
chest, arm, jaw/neck, or epigrastric pain/discomfort with exertion or at rest
3
Q
atypical symptoms of ACS
A
SOB, jaw/back pain, N/V, dizziness, “cold sweat”, dyspepsia-like sensation or anorexia, hypotension, crackles in lung fields
4
Q
women atypical ACS symptoms
A
SOB, jaw/back pain, nausea
5
Q
DM ACS atypical symptoms
A
symptoms may be reduced due to autonomic neuropathy
6
Q
elderly ACS atypical symptoms
A
symptoms may also include altered mental status
7
Q
what does MONA stand for
A
morphine, oxygen, nitrate, aspirin
8
Q
ER based aspirin
A
- 162-325mg CHEWED PO once
- give additional ASA if pt takes a lower dose at home
- decreases mortality**
9
Q
ER based oxygen
A
- prn to maintain O2 sats>90%
10
Q
what agents are used in ER to manage chest pain?
A
SL NTG
morphone
IV NTG
11
Q
ER based SL NTG
A
- 4mg SL Q5min prn chest pain up to 3 doses
- avoid if exposed to PDE-5 inhibitors
12
Q
ER based morphine
A
- 2-5mg IV q5min prn chest pain NOT relieved by SL NTG
- analgesia+ vasodilation + decreased sympathetic tone
- hold for sedation & hypotension
13
Q
ER based IV NTG
A
- to relive chest pain if NOT relieved by SL NTG &/or morphine
- hold for hypotension, tachycardia, bradycardia, arrhythmia
- do not immediately DC, must titrate down if possible
14
Q
ER based beta blockers
A
oral BB’s should be initiated w/in the first 24 hours
15
Q
what is the only agent that decreases mortality?
A
aspirin!
16
Q
definition of acute MI
A
- rise or fall of a cardiac toponin w/ one value >99th percentile w/ one of the following:
- symptoms of new angina (angina)
- new ST changes or left bundle branch block on EKG
- new onset Q waves
- imaging evidence of loss of myocardium/wall motion abnormality
- ID of coronary thrombus by angiography or autopsy
17
Q
ECG helps distinguish
A
NSTEMI from STEMI
- NSTEMI can be ST elevation <20 minutes*
18
Q
STEMI is either managed with
A
percutaneous coronary intervention (PCI/stenting) or fibrinolysis
19
Q
goal of STEMI therapy
A
restoration of complete blood flow to occluded artery w/in 90 min of arriving at the hospitals
20
Q
after____ of symptoms STEMI interventions are unlikely beneficial since ischemic tissue cannot be salvaged
A
24 hours
21
Q
PCI
A
involves angioplasty &/or stenting
22
Q
goal of PCI
A
- w/in 90 minutes of medical contact
- preferred method due to 90+% coronary patency after procedure
23
Q
fibrinlysis
A
pharmacological dissolution of the clot occluding the coronary artery
24
Q
goal of fibrinolysis
A
- w/in 30 minutes of arriving at hospital (if PCI cannot be performed)
not preferable to PCI (50-60% patency) - typically transferred to PCI-capable hospital for angiography after administration
25
NSTE-ACSI can be classified as
high risk or low-medium risk
26
high risk NSTE-ACSI should be managed
early
| - angiography +/- PCI w/in 12-24 hours
27
moderate risk NSTE-ACSI are managed with
an ischemia guided strategy
28
low risk NSTE-ACSI are
frequently sent home for our patient workup
29
goal of NSTE-ACSI treatment
identification & appropriate management of high & moderate risk pts to minimize loss of myocardium, prevent death & control chest pain & related symptoms
30
NSTE-ACSI risk stratification- candidates of early invasive management
- GRACE score >140
- elevated troponin
- ST depression (>1mm)
31
early invasive management
- high risk pts
- start antithrombotics, coronary angiography
+/- PCI should be performed w/in 24 hours
32
delayed invasive management
- medium risk pt
- start on antithrombotics, coronary angiography
+/- PCI w.in 24-72 hours
33
ischemia guided management
- low risk pt
| - initial antithrombotics therapy & will have further diagnostics to determine if angiography/PCI is required
34
medical management
- pt/physician preference
- some pts do not wish or have blockages that are not amenable to catherization w/PCI.
- they will be placed on standard antithrombotics & secondary preventable measures
35
what does CABG stand for?
coronary artery bypass grafting
36
antiplatelets
aspirin
P2Y12 inhibitors
glycoprotein IIb/IIIa inhibitors
37
anticoagulants
heparinoids
direct thrombin inhibitors
factor Xa inhibitors
38
fibrinolyteics
alteplase
reteplase
tenecteplase
39
in general each patient will receive
ASA, a P2Y12 inhibitor and an anticoagulant
| - everyone needs (MON)A-PA!**
40
those with NSTE-ACS undergoing ischemia guided therapy/medical management
- are generally at low risk of ischemic events and do not require multiple, expensive, highly potent agents
41
those undergoing PCI
- are at high risk of thrombosis
- need highly potent antithrombotic therapy
- GP2b/3a inhibited may be added for PCI
42
those undergoing fibrinolysis
- only STEMI
- high risk of bleeding
- use less potent agents (plavix instead of effient, arixtra inctead of heparin, no 2b3a inhibitors)
43
absolute CI to effient use
history of stroke (CVA) or TIA
44
P2Y12 inhibitor drugs
clopidogrel (Plavix)
prasugrel (effient)
ticagrelor (brilinta)
45
aspirin therapy
started in the ER and continued for EVERYONE
46
plavix is an option for
all NSTE-ACS and STEMI PCI and fibrinolysis
47
effient is an option for
PCI ONLY!
- mod-high risk NSETMI & STEMI
- too potent for fibrinolysis
- fewer ischemic events but more major bleeding than plavix
- do not give loading dose until pts has angiography that shows need for stening
48
brillinta is an option for
all NSTE-ACS (incl. ischemic guided & medical management) as well as STEMI
- NOT with fibrinolysis
- fewer ischemic events & similar bleeding to plavix
- reduced mortality compared to plavix
- may cause dyspnea or ventricular pauses
49
GP IIb/IIIa inhibitors
abciximab (reopro)
tirofiban (aggrastat)
eptifibrate (integrillin)
50
GP IIb/IIIa inhibitors are used
when planning/performing PCI
51
GPIIb/IIIa inhibitors are omitted when
bivarlirudin (angiomax) is used as the anticoagulant for PCI
52
GPIIb/IIIa inhibitors have virtually the time CI as
fibrinalytics
53
monitor bleeding with GPIIb/IIIa
platelets at baseline/2/4/12 hours
54
how long can abciximab (reopro) be used for
up to 12 hours
55
how long ca tirofiban (aggrastat) be used for
up to 18-24 hours
56
how long can eptifibatide (integrillin)be used for
up to 18-24 hours
57
heparinoid drugs
heparin (UFH)
| enoxaparin (Lovenox)- LMWH
58
factor Xa inhibitor
fondaparinux (Arixtra)
59
direct thrombin inhibitor
bivalirudin (Angiomax)
60
HIT
- heparin-induced thrombocytopenia
- heparin and enoxaparin can lead to thrombocytopenia from an immune-mediated activation of platelets
- activation of platelets leads to increased risk of blood clots in the legs & lungs despite plts ebing low
- risk of HIT: heparin>enoxaparin>fondaparinux(~0%)> bivalirudin(0%)
61
heparin titration
- heparin dosing is very individualized due to variable PD
| - aPTT used to characterize degree of anticoagulation by heparin
62
enoxaparin
- similar rates of thrombosis & less bleeding than heparin
- **for NSTEMI PCI: give additional 0.3mg/lg IV if going to PCI & nearing next dose
- in fibrinolysis: complicated dosing based on age & capped for overweight pts
63
fondaparinux
- typically used in those not going to cath lab
- lower dose= less bleeding
- for PCI, is insufficient & heparin will be added
64
bivalirudin
- used for PCI
- not GP2b/3Ai's
- fibrinolysis: when used at normal doses, caused increase in intracranial hemorrhage & bleeding
65
rt-PA agent
alteplase (activase)
| 1 bolus= continuous infusion
66
rPA agent
reteplace (ratavase)
| 2 bolus
67
TNK-tPA agent
tenecteplase (TNKase)
| 1 bolus
68
fibrinolytics are only
fibrin-specific & should be combined with ASA(162-325 once in ER), clopidogrel(300mg loading dose) & and anticoag(heparin, enoxaparin or fondaparinux)
69
before fibrinolytic use
patients should ALWAYS be screened for contraindications!!
70
absolute CIs to fibrinolytics
```
active internal bleeding
intracranial bleed (ever)
intracranial tumor or aneurym or AV malformation
aortic dissection
head/facial trauma (3mo)
prior ischemic stroke (3mo)
```
71
relative CI to fibrinolytics
```
severe HTN (>180/110)
dementia
current warfarin use
bleeding diathesis
active peptic ulcer
prior ischemic stroke (>3mo)
major surgery (3wks)
prior internal bleeding (2-4wks)
traumatic or prolonged CPR (>10min)
```
72
fibrinolytics are only used in people with
STEMI
73
secondary preventio of ACS: includes control of
- hypertension/prevention of HF
- dyslipidemia
diabetes
lifestyle
74
life style modification for secondary prevention of ACS
- obesity/diet/alcohol
- exercise at least 30-60 min of mod-intensity at least 5/wk
- medical rehab recommended after ACS
75
secondary ACS prevention: beta blockers
- prefer to initiate w/in 24 hours but caution in thsoe with risk factors or displaying cadiogenic shock/acute HF
- gradually titrated in pts with mod-severe HF or < LVEF
76
secondary ACS prevention: ACEI/ARB
- prefer to initiated w/in 24 hours but do not initiate early IV ACEI due to risk of hypotension
77
secondary ACS prevention: aldosterone antagonists
- eplerenone or spironolactone
| - for those with LVEF 5mEq/dL
78
secondary ACS prevention: dyslipidemia
- high dose statin in ALL ACS pts regardless of baseline LDL
- recommended w/in 24 hours
- plaque stabilizing effect-> decreased mortality
79
stents placed during PCI are
"platelet-philic" and require some duration of dual antiplt therapy for minimum of 1 year
80
antithrombotic therapy for those in medical management or fibrinolysis
- significantly benefit from 2-4 wks of dual antiplt therapy & probably from 12 months of DAPT
81
prevention of GI bleeding in those with increased risk of GI bleeding
1. history of GI bleeding or chronic anticoag- give PPI
2. advanced age, steroid or NSAID use- PPI is reasonable
3. all others are unlikely to benefit
82
triple antithrombotic therapy
ASA+ P2Y12I+ anticoagulant
- e.g someone with ACS & AFib
- risk of bleeding goes up significantly
- target warfarin INR 2-2.5
- ASA <81mg
- minimal safety datd for prasugrel, ticagrelor, dabigatran, rivaroxaban, apixaban
Cardio Exam 2
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