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Cardio Exam 2 > lecture 10 > Flashcards

lecture 10 Flashcards

1
Q

signs and symptoms of ACS is generally

A

non-sensitive and non-specific

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2
Q

typical symptoms of ACS

A

chest, arm, jaw/neck, or epigrastric pain/discomfort with exertion or at rest

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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

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4
Q

women atypical ACS symptoms

A

SOB, jaw/back pain, nausea

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5
Q

DM ACS atypical symptoms

A

symptoms may be reduced due to autonomic neuropathy

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6
Q

elderly ACS atypical symptoms

A

symptoms may also include altered mental status

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7
Q

what does MONA stand for

A

morphine, oxygen, nitrate, aspirin

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8
Q

ER based aspirin

A
  • 162-325mg CHEWED PO once
  • give additional ASA if pt takes a lower dose at home
  • decreases mortality**
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9
Q

ER based oxygen

A
  • prn to maintain O2 sats>90%
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10
Q

what agents are used in ER to manage chest pain?

A

SL NTG
morphone
IV NTG

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11
Q

ER based SL NTG

A
  1. 4mg SL Q5min prn chest pain up to 3 doses

- avoid if exposed to PDE-5 inhibitors

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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
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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
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14
Q

ER based beta blockers

A

oral BB’s should be initiated w/in the first 24 hours

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15
Q

what is the only agent that decreases mortality?

A

aspirin!

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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
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17
Q

ECG helps distinguish

A

NSTEMI from STEMI

- NSTEMI can be ST elevation <20 minutes*

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18
Q

STEMI is either managed with

A

percutaneous coronary intervention (PCI/stenting) or fibrinolysis

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19
Q

goal of STEMI therapy

A

restoration of complete blood flow to occluded artery w/in 90 min of arriving at the hospitals

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20
Q

after____ of symptoms STEMI interventions are unlikely beneficial since ischemic tissue cannot be salvaged

A

24 hours

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21
Q

PCI

A

involves angioplasty &/or stenting

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22
Q

goal of PCI

A
  • w/in 90 minutes of medical contact

- preferred method due to 90+% coronary patency after procedure

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23
Q

fibrinlysis

A

pharmacological dissolution of the clot occluding the coronary artery

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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
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25
Q

NSTE-ACSI can be classified as

A

high risk or low-medium risk

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26
Q

high risk NSTE-ACSI should be managed

A

early

- angiography +/- PCI w/in 12-24 hours

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27
Q

moderate risk NSTE-ACSI are managed with

A

an ischemia guided strategy

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28
Q

low risk NSTE-ACSI are

A

frequently sent home for our patient workup

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29
Q

goal of NSTE-ACSI treatment

A

identification & appropriate management of high & moderate risk pts to minimize loss of myocardium, prevent death & control chest pain & related symptoms

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30
Q

NSTE-ACSI risk stratification- candidates of early invasive management

A
  • GRACE score >140
  • elevated troponin
  • ST depression (>1mm)
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31
Q

early invasive management

A
  • high risk pts
  • start antithrombotics, coronary angiography
    +/- PCI should be performed w/in 24 hours
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32
Q

delayed invasive management

A
  • medium risk pt
  • start on antithrombotics, coronary angiography
    +/- PCI w.in 24-72 hours
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33
Q

ischemia guided management

A
  • low risk pt

- initial antithrombotics therapy & will have further diagnostics to determine if angiography/PCI is required

34
Q

medical management

A
  • 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
Q

what does CABG stand for?

A

coronary artery bypass grafting

36
Q

antiplatelets

A

aspirin
P2Y12 inhibitors
glycoprotein IIb/IIIa inhibitors

37
Q

anticoagulants

A

heparinoids
direct thrombin inhibitors
factor Xa inhibitors

38
Q

fibrinolyteics

A

alteplase
reteplase
tenecteplase

39
Q

in general each patient will receive

A

ASA, a P2Y12 inhibitor and an anticoagulant

- everyone needs (MON)A-PA!**

40
Q

those with NSTE-ACS undergoing ischemia guided therapy/medical management

A
  • are generally at low risk of ischemic events and do not require multiple, expensive, highly potent agents
41
Q

those undergoing PCI

A
  • are at high risk of thrombosis
  • need highly potent antithrombotic therapy
  • GP2b/3a inhibited may be added for PCI
42
Q

those undergoing fibrinolysis

A
  • only STEMI
  • high risk of bleeding
  • use less potent agents (plavix instead of effient, arixtra inctead of heparin, no 2b3a inhibitors)
43
Q

absolute CI to effient use

A

history of stroke (CVA) or TIA

44
Q

P2Y12 inhibitor drugs

A

clopidogrel (Plavix)
prasugrel (effient)
ticagrelor (brilinta)

45
Q

aspirin therapy

A

started in the ER and continued for EVERYONE

46
Q

plavix is an option for

A

all NSTE-ACS and STEMI PCI and fibrinolysis

47
Q

effient is an option for

A

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
Q

brillinta is an option for

A

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
Q

GP IIb/IIIa inhibitors

A

abciximab (reopro)
tirofiban (aggrastat)
eptifibrate (integrillin)

50
Q

GP IIb/IIIa inhibitors are used

A

when planning/performing PCI

51
Q

GPIIb/IIIa inhibitors are omitted when

A

bivarlirudin (angiomax) is used as the anticoagulant for PCI

52
Q

GPIIb/IIIa inhibitors have virtually the time CI as

A

fibrinalytics

53
Q

monitor bleeding with GPIIb/IIIa

A

platelets at baseline/2/4/12 hours

54
Q

how long can abciximab (reopro) be used for

A

up to 12 hours

55
Q

how long ca tirofiban (aggrastat) be used for

A

up to 18-24 hours

56
Q

how long can eptifibatide (integrillin)be used for

A

up to 18-24 hours

57
Q

heparinoid drugs

A

heparin (UFH)

enoxaparin (Lovenox)- LMWH

58
Q

factor Xa inhibitor

A

fondaparinux (Arixtra)

59
Q

direct thrombin inhibitor

A

bivalirudin (Angiomax)

60
Q

HIT

A
  • 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
Q

heparin titration

A
  • heparin dosing is very individualized due to variable PD

- aPTT used to characterize degree of anticoagulation by heparin

62
Q

enoxaparin

A
  • 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
Q

fondaparinux

A
  • typically used in those not going to cath lab
  • lower dose= less bleeding
  • for PCI, is insufficient & heparin will be added
64
Q

bivalirudin

A
  • used for PCI
  • not GP2b/3Ai’s
  • fibrinolysis: when used at normal doses, caused increase in intracranial hemorrhage & bleeding
65
Q

rt-PA agent

A

alteplase (activase)

1 bolus= continuous infusion

66
Q

rPA agent

A

reteplace (ratavase)

2 bolus

67
Q

TNK-tPA agent

A

tenecteplase (TNKase)

1 bolus

68
Q

fibrinolytics are only

A

fibrin-specific & should be combined with ASA(162-325 once in ER), clopidogrel(300mg loading dose) & and anticoag(heparin, enoxaparin or fondaparinux)

69
Q

before fibrinolytic use

A

patients should ALWAYS be screened for contraindications!!

70
Q

absolute CIs to fibrinolytics

A 
active internal bleeding
intracranial bleed (ever)
intracranial tumor or aneurym or AV malformation
aortic dissection
head/facial trauma (3mo)
prior ischemic stroke (3mo)
71
Q

relative CI to fibrinolytics

A 
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
Q

fibrinolytics are only used in people with

A

STEMI

73
Q

secondary preventio of ACS: includes control of

A
  • hypertension/prevention of HF
  • dyslipidemia
    diabetes
    lifestyle
74
Q

life style modification for secondary prevention of ACS

A
  • obesity/diet/alcohol
  • exercise at least 30-60 min of mod-intensity at least 5/wk
  • medical rehab recommended after ACS
75
Q

secondary ACS prevention: beta blockers

A
  • 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
Q

secondary ACS prevention: ACEI/ARB

A
  • prefer to initiated w/in 24 hours but do not initiate early IV ACEI due to risk of hypotension
77
Q

secondary ACS prevention: aldosterone antagonists

A
  • eplerenone or spironolactone

- for those with LVEF 5mEq/dL

78
Q

secondary ACS prevention: dyslipidemia

A
  • high dose statin in ALL ACS pts regardless of baseline LDL
  • recommended w/in 24 hours
  • plaque stabilizing effect-> decreased mortality
79
Q

stents placed during PCI are

A

“platelet-philic” and require some duration of dual antiplt therapy for minimum of 1 year

80
Q

antithrombotic therapy for those in medical management or fibrinolysis

A
  • significantly benefit from 2-4 wks of dual antiplt therapy & probably from 12 months of DAPT
81
Q

prevention of GI bleeding in those with increased risk of GI bleeding

A
  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
Q

triple antithrombotic therapy

A

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 (12 decks)

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