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TZ Cardiac Surgery 2016 > Coronary > Flashcards

Coronary Flashcards

1
Q

facilitated PCI

A

full or 1/2 dose fibrinolysis, with or without Glycoprotein IIb/IIIa receptor antagonist, with immediate transfer for planned PCI within 90-120min

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2
Q

rescue PCI

A

failed reperfusion with fibrinolysis –> transfer for PCI

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3
Q

pharmacoinvasive strategy

A

fibrinoytic rx either prehospital or at a non-PCI-capable hospital, followed by immediate transfer to a PCI-capable hospital for early coronary angiography and PCI

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4
Q

which STEMI pt is best suited for immediate interhospital transfer without fibrinolysis?

A
  1. shock or other high risk features
  2. high bleeding risk
  3. late presentation (>3 -4 hour post sx onset)
  4. short transfer times
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5
Q

Which STEMI pt is best suited for pharmatoinvasive strategy?

A
  1. low bleeding risk

2. very early presentation (

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6
Q

CAPTIM Trial

A

(Comparaison de l’Angioplastie Primaire et dela thrombolyse)

fibrinolysis (prehospital) within 2 hours of sx onset has a significantly lower 5-year mortality rate vs. Primary PCI

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7
Q

Which trials suggest prehospital fibrinolysis may be superior to PCI

A

CAPTIM
WEST
USIC Registry
Swedish Registry of cardiac Intensive care

#

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8
Q

survival to hospital discharge post resuscitation for Sudden cardiac death; if initial recorded rhythm is

  1. any rhythm
  2. VF
  3. VF, followed by emergency PCI
A
  1. 7.9%
  2. 22%
  3. 60%

#

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9
Q

Class 1 Indication for cooling in STEMI and out of hospital cardiac arrest (B)

A

Therapeutic hypothermia (32-34 degrees) as soon as possible (ie before cath) for 12-24 hours shown to improve neurological outcome

#

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10
Q

What % of STEMI pts who survive to reach hospital will have a cardiac arrest during hospitalization

A

5%

#

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11
Q

causes of “no-reflow” phenomenon

A

restoration of epicardial flow in the infarct artery, but suboptimal myocardial perfusion

  1. Inflammation
  2. endothelial injury
  3. edema
  4. atheroembolization
  5. vasospasm
  6. myocyte reperfusion injury
*assoc'd w lower survival rate
#
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12
Q

Management of “no-reflow” phenomenon

A
  1. GP IIb/IIIa antagonist (abciximab)
  2. vasodilators (nitroprusside, verapamil, adenosine)
  3. metabolic pathway inhibitors (nicorandil, pexelizumab)
  4. manual thrombus aspiration
    #
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13
Q

abciximab facts

A
  • aka ReoPro
  • glycoprotein IIb/IIIa receptor antagonist
  • made from the Fab fragments of an immunoglobulin that targets the glycoprotein IIb/IIIa receptor on the platelet membrane. Inhibits plt aggregation
  • plasma T1/2 10min, second phase T1/230 minutes. can occupy plt receptor for up to 48 hours after the infusion has been terminated, low level activity up to 15 days.
  • no renal dose adjustment.

#

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14
Q

Which stent has the lowest rates of in stent thrombosis

A 
cobalt-chromium everolimus-eluting stents
#
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15
Q

GP IIB/IIIa receptor antagonists

A
  1. abciximab (ReoPro)
  2. tirofiban
  3. eptifibatide (integrelin)
    #
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16
Q

P2Y12 receptor inhibitors

A
  1. clopidogrel
  2. prasugrel
  3. ticagrelor
    #
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17
Q

Which P2Y12 should NOT be given if Hx of stroke or TIA

A

prasugrel

  • also not beneficial in pts older than 75 yo or low CrCl

#

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18
Q

Which PPI interferes with clopidogrel metabolism

A 
omeprazole
- BUT does not translate into worse clinic outcome
#
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19
Q

antiplatelet response to clopidogrel may vary due to:

A
  1. patient phenotye (obesity, DM)
  2. enteric ABCB 1 polymorphism
  3. hepatic CYP450 enzyme polymorphisms (esp CYP 2C19*2) - VERY IMP

#

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20
Q

WHat did TRITON-TIMI 38 show re. clopidogrel

A

Carriers of the reduced function CYP2C19*2 allele had
1. sign reduce level of active metabolite of clopidogrel
2. diminished platelet inihibition
3. increased rates of MACE and stent thrombosis
#

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21
Q

what is clopidogrel

A
  • thienopyridine
  • IRreversible antagonist of platelet ADP P2Y12 receptor

#

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22
Q

prasugrel facts

A
  • thienopyridine P2Y12 R antagonists; IRreversible
    -more powerful & more rapidly active than clopidogrel
    #
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23
Q

ticagrelor facts

A
  • reversible, nonthienopyridine ADP P2Y12 receptor antagonist
  • no metabolic conversion needed
    #
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24
Q

tirofiban facts

A

1

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25
Q

eptifibatide facts

A

1

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26
Q

what is UFH

A
  • highly sulfated glycosaminoglycan - the most negatively charged biological molecule
  • normally stored basophils and in mast cells and released at site of vascular injury

#

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27
Q

Bivalirudin fact

A
  • direct thrombin inhibitor (reversible); IV only
  • short, synthetic peptide
  • inhibits both circulating and clot-bound thrombin & inhibits thrombin-mediated platelet activation and aggregation.
  • does not require a binding cofactor
  • T1/2: = 25 minutes
    T1/2 in Severe renal dysfunction (≤ 29 mL/min) = 57 minutes
    T1/2 in Dialysis-dependent = 3.5 hours
    #
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28
Q

Fondaparinux facts

A
  • synthetic pentasaccharide with similar molecular structure as ATIII binding site of heparin
  • not to be used as sole anticoagulant in PCI; contraindicate in low CrCl

#

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29
Q

fibrinolytic agents

A 
Fibrin specific:
1. tenecteplase (TNK-tPA)
2. reteplase (rPA)
3. Alteplase (tPA)
non-fibrin specific
1. streptokinase

#

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30
Q

how long before pre elective CABG to d/c

  1. clopidogrrel
  2. ticagrelor
  3. prasugrel
  4. abciximab
  5. eptifibatide or tirofiban
A 
clopidogrel - 5 days
ticagrelor - 5 days
prasugrel - 7 days
abciximab - 12 hours
tirofiban or eptifibatide - 2-4 hours
2014 AHA guidelines
#
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31
Q

in STEMI pts, rate of TIMI 2-3 flow 90 min post

1. TNK-tPA 2. rPA 3. tPA 4. treptokinase

A
  1. 85% 2. 84% 3. 73-84% 4. 60-68%
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32
Q

absolute contraindications to fibrinolysis

A
  • any ICH
  • known structural vascular lesions
  • known intracranial neoplasm
  • ischaemic stroke 4.5 hours - 3 months
  • suspected aortic dissection
  • active bleeding/bleeding diathesis
  • significant closed head/facial trauma within 3 mo
  • intracranial/intraspinal surgery within 2 mo
  • severe uncontrolled hypertension
  • streptokinase, prior rx within 6 mo

#

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33
Q

relative contraindications to fibrinolysis

A
  • hx of poorly ct’d HTN
  • SBP >180mmHg or DBP >110
  • hx of ischaemic stroke >3mo
  • dementia
  • traumatic or prolonged CPR (>10min)
  • major sx
    #
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34
Q

class I indication for antiplatelet rx post fibrinolysis in STEMI pts

A 
ASA 162-325mg loading; continue indefinitely (can use 81mg)
clopidogrel loading  300mg 75 yo; continue 14days - 1 year
#
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35
Q

class I indication for anticoagulant rx post fibrinolysis in STEMI pt

A 
UFH (aPTT 1.5-2x control); enoxaparin; Fondaparinux
#
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36
Q

STEMI pt, post fibriniolysis, develops HIT; what to use

A 
Bivalirudin
#
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37
Q

what should prompt Rescue PCI

A 
60-90min post fibrinolysis lack of resolution of ST elevation by 50% in the worst lead (and absence of reperfusion arrhythmias @ 2 hours) = TIMI flow less than 3
#
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38
Q

contraindication to Betablockade

A
  1. signs of HF
  2. low output state
  3. increased risk of cardiogenic shock
  4. prolonged 1st degree (>0.24sec) or high grade AV block
  5. reactive airway disease

#

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39
Q

contraindications to ACE/ARB

A
  1. hypotension
  2. shock
  3. renal failure
  4. bilateral renal artery stenosis
  5. hyperkalemia
  6. allergy

#

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40
Q

Which group of patients benefit most from ACE inhibitors

A

-anterior MI
-HF or EF less than 40%
#

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41
Q

which CCB to avoid in STEMI pts

A

immediate-release nifedipine (causes reflex sympathetic activation with tachycardia)

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42
Q

oxygen use in STEMI

A
  • only if O2Sat less than 90%
  • increases coronary arterial resistance

#

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43
Q

why are NSAIDs and COX2 inihibitors contraindicated in STEMI pts

A 
increase risk of death, reinfarction, cardiac rupture, hypertension, renal insufficiency and HF
#
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44
Q

use of IABP in cardiogenic shock patients post STEMI

A

class IIa

45
Q

use of LVAD in refractory cardiogenic shock pts post STEMI

A

class IIb

46
Q

Cardiogenic shock in pts with STEMI is caused by

A
  1. extensive LV infarction (pump failure)
  2. mechanical complications (pap m. rupture, Ventricular septal rupture, free-wall rupture wih tamponade, RV infaction)
    #
47
Q

timeline for developement of cardiogenic shock

A
  1. pump failure: 15% at time of presentation; 85% during hospitalization
  2. mechanical complications: bimodal; most within 24 hrs, remainder within the first week
    #
48
Q

RV infarction triad

A 
1. hypotension 2. clear lung fields 3. elevated JVP
#
49
Q

most sensitive ECG marker for RV infarct

A 
1-mm ST elev in V1 and V4R
#
50
Q

which drugs to avoid in RV failure

A 
nitrates and diuretics
#
51
Q

which papillary m. more likely to rupture

A 
posteromedial, due to single blood supply
#
52
Q

survival after emerency MVR for acute severe MR due to pap m. rupture

A

20% operative mortality
5 year survival 60-70%
#

53
Q

when does ventricular septal rupture post STEMI pts occur

A

within first 24 hours
*ALWAYS EMERGENCY SURGICAL REPAIR EVEN IF HEMODYNAMICALLY STABLE
#

54
Q

surgical mortality in ventricular septal rupture patients

A

mortality: 20-87%
-higher with inferior-basal defects than anterior-apical
#

55
Q

RFs for LV free-wall rupture post MI

A

-first MI
-anterior infarction
-elderly
-women
other RFs
-HTN during acute phase of STEMI, lack of antecedent angina, absence of collateral blood flow, Q waves on ECG, use of Corticosteroids or NSAIDS, fibrinolytics >14hours after sx onset
#

56
Q

LV free-wall rupture operative mortality post repair

A 
60%
#
57
Q

LV aneurysm after STEMI

A 
occur in less than 5% of pt
#
58
Q

how frequently does recurrent ischemic events occur within first 30days afteer ACS

A 
15-20%
#
59
Q

how soon after stopping ASA does plt aggregation return to normal

A

50% of pts within 3 days
80% of pts within 4 days
#

60
Q

discontinuation of clopidogrel may result in

A 
rebound increase in plt activity and increase of ischaemic events
#
61
Q

RFs for bleeding and transfusion in CABG pts

A

-older
-low preop red blood volume (anemia or small body size)
-antiplt or antithrombotic drugs
- congenital clotting disorders
-undergoing reoperation
-complex or emergency procedures
-non-cardiac comorbidities
#

62
Q

transfusion related complications

A 
a-fib, renal failure, prolonged ventilatory support, serious infection, cardiac complications, neurological events, and prolonged ICU stay and hospital stay, later reduction of quality of life, reduced early and late survival after surgery
#
63
Q

what are high risk features in ACS pts

A
  1. recurrent refractory ischemia dna ssoc’t ECG ST changes despite max med rx
  2. very high-risk coronary artery anatomy (LM+RCA)
    #
64
Q

epsilon aminocaproic acid facts

A

1

65
Q

tranexamic acid facts

A

1

66
Q

who should have early CABG without discontinuing clopidogrel

A 
pts high risk for early, potentially fatal ischemic event 
#
67
Q

pts with high bleeding risk, but also high ischemic risk, what to do?

A

d/c clopidogrel 3-5 days before OR and bridge with UFH and reversible IV GP IIbIIIa inhibitor, stop 4 hours pre-op

68
Q

recent ACS at low risk for recuent ischemia, meds?

A

d/c clopidogrel 5 days before CABG; continue ASA & heparin until OR

69
Q

how to mitigate transfusion risk in clopidogrel pts undergoing CABG

A
  • alert transfusion medicine
  • meticulous hemostasis
  • OPCAB
  • transfuse plt
  • antifibrinolytics (epsilon aminocaproic acid or tranexamic acid)
  • topical hemostatic agents
70
Q

What are the goals of revascularization

A

improve prognosis, enhance quality of life or both

71
Q

name two second generation DES

A

everolimus eluting stent

zotarolimus eluting stent

72
Q

name a first generation DES

A

paclitaxel-eluting stent (TAXUS)

73
Q

Limitations to scoring systems

A

fail to take into account commonly encountered non-cardiac vulnerabilities, such as failty and disability (which are independent predictors of adverse outcomes after cv surgery)

74
Q

side effects of heparin (non-HIT/HITT)

A
  1. elevated serum aminotransferase levels (80%)
  2. hyperkalemia due to heparin-induced aldosterone suppression (5-10%)
  3. alopecia and osteoporosis with chronic use
75
Q

Heparin activity

A

binds and activates AT3 by conformational change

  • antithrombin 3 inactivates Xa directly (any size heparin works)
  • thrombin is inactivated by binding heparin and activated AT3 (ternary complex) (needs big molecure UFH)
  • monitor by aPTT
76
Q

fondaparinux facts

A

synthetic pentasaccharide (almost identical to AT3 binding pentasaccharide sequence of Heparin)

77
Q

where do we get heparin from

A

beef lung & porcine intestinal mucosa

78
Q

1 IU of heparin

A

1 IU of heparin = 0.002mg of pure heparin = amount needed to keep 1ml of cat blood fluid @ 0degrees for 24hours

79
Q

whats the T1/2 of UFH & LMWH

A

UFH = 1 hour; LMWH = 4-5hours

80
Q

what proportion of Inferior STEMI pts have RV infaction;

A

1/3

81
Q

Rx of RV infarction

A

maintain RV pre-load, reduce RV afterload, inotropic support, immediate reperfusion.
Avoid nitrates and diuretics!
restore AV synchrony or cardiovert from Afib may b needed

82
Q

LV free-wall rupture Sx

A 
recurrent CP & ST-T wave changes, and rapid progression to hmodynamic collapse, PEA and death
#
83
Q

mech of arrhythmias post STEMI

A 
- ongoing ischemia, hemodynamic and electrolyte abn, reentry, enhanced automaticity 
#
84
Q

compared to STEMI pts without VT/VF:

Early VT/VF (before completion of PCI) and late VT/VF 90day MR

A 
early: 2x higher; late 5x higher
#
85
Q

associated factors for VT/VF

A 
HF, Hypotension tachycardia, shock and TIMI flow grade
#
86
Q

treatment of VT/VF

A
  1. immediate defibrillation/cardioversion
  2. antiarrythmic drugs according to ACLS

prevention of VT/VF:
1. early (within 24hour) betablock
2. correcction of electrolyte and acid/base abnormalities
3. optimize myocardial perfusion
4. irradication of ongoing ischemia
5. rx assoc’d complications ie HF or Shock
*do not give prophylacic lidocaine
*PVCs, stable, non-sustained VT, accelerated idioventricular rhythms due to reperfusion DO NOT REQUIRE RX AS THEY ARE NOT INDICATIVE OF SCD RISK.
#

87
Q

Late (>48 hour) in-hospital sustained VT/VF ?ICD

A 
Class I indication for ICD placement for secondary prevention of SCD
#
88
Q

STEMI with reduced LVEF, ?ICD

A 
reassess ICD need for primary prevention of SCD >/= 40 days after discharge to allow for recovery from myocardial stunning (use TTE to assess LVEF)
#
89
Q

Cause of superventricular arrythmias (Afib/flutter 8-22% of STEMI pts)

A
  1. excesive sympathetic stimulation
  2. atrial stretch due to LV or RV volume/pressure overload
  3. atrial infarction
  4. pericarditis
  5. electrolyte abnormalities
  6. hypoxia
  7. underlying lung disease
    #
90
Q

RFs for supraventricular arrythmias post STEMI

A
  1. Older pts
  2. HF
  3. HTN
    #
91
Q

Incidence of Afib in STEMI

  1. during hospitalization
  2. 2 years
A
  1. 6.3% (assoc’d w shock, HF, stroke and 90day mortality)

2. 30% (if EF

92
Q

sinus bradycardia in STEMI

A 
common early after STEMI
- esp inferior MI
- usually self limiting
-give atropine
- temporary pacing if atropine not sufficient
#
93
Q

incidence of AV block and intraventricular conduction delay post STEMI

A

complete HB:
3.7% inferior/osterior MI (usually transient; rx conservatively)
1% anterior//lateral MI (worse prognosis)
Varying degree of AVblock = 7%
BBB = 5%
#

94
Q

acute pericarditis post STEMI

A

Class I: ASA 650mg QID
Class IIb: acetaminophen, colchicine, narcotic if ASA not effective
III steroids & antiinflammatories baaaad
#

95
Q

What is dressler’s syndrome

A 
acute pericarditis pain >1 week + malase + fever + incrreased inflammatory biomarkers
#
96
Q

sx of acute pericarditis

A 
chest pain (pleuritic or positional, radiates to trapezius ridge) and associated with friction rub
recurrent or worsening ST elevation without early T-wave inversion
#
97
Q

management if see pericardial effusion > 1cm or enlarging post STEMI

A 
STOP ANTICOAGULATION; R/O FREEWALL RUPTURE, HEMORRHAGIC CONVERSION OR AORTIC DISSECTION
#
98
Q

incidence of HIT

A

1-5% of patients receiving heparin
25-50% of the above will get HITT
#

99
Q

in STEMI pt w HIT who require stenting, which anticoagulant to use?

A 
bivalirudin
#
100
Q

in CABG pt with HIT, which anticoagulant to use?

A 
?
#
101
Q

STEMI Pt who has a bleeding complication, has increased risk of :

A 
recurrrent MI, stroke, death, longer hospital stay and increased cosst
#
102
Q

all bleeding risk compared to asa alone:

  1. ASA + plavix
  2. ASA + VKA
  3. Plavix + VKA
  4. triple rx
A
  1. asa+plavix 1.7x
  2. asa+vka 2x
  3. plavix+vka 2.5-4x
  4. triple rx 3-4x

#

103
Q

RFs for bleeding in patients with ACS:

A
  1. older than 75
  2. female
  3. HF or shock
  4. DM
  5. body size
  6. hx of GIB
  7. STEMI or NSTEMI (vs. UA)
  8. severe renal dysfunction (CrCl less than 30ml/min)
  9. elevated WBC
  10. Anemia
  11. fibrinolysis
  12. invasive strategy
  13. inappropriate dosing of antithrombotic meds
  14. chronic oral anticoagulant rx

#

104
Q

signs of retroperitoneal bleeding w PCI

A
  1. intraprocedural or post procedural hypotension and bradycardia/tachycardia
  2. high vascular puncture site
  3. unexplained decrease in hemoglobin

#

105
Q

strongest of predictor of death after STEMI

A

HF or significant LV systolic dysfunction

106
Q

secondary prevention of CAD

A
  1. cardiac rehab
  2. ASA
  3. lipid-lowering Rx
  4. Beta blockers
  5. ACE-I
  6. smoking cessation
    #
107
Q

strongest predictor of SCD after STEMI

A 
timing and character of ventricular arrhythmias and residual LV systolic function
#
108
Q

indication of ICD post STEMI

A
  1. if LVEF less than or equal to 0.35 AND NYHA class II or III
  2. if LVEF less than 0.3, regardless of sx
109
Q

indications for CRT post STEMI

A
  1. residual LV function
  2. NYHA class
  3. QRS duration
  4. LBBB morphology

TZ Cardiac Surgery 2016 (15 decks)

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