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76 Cards in this Set

  • Front
  • Back

Two groups of IHD

Chronic CAD (stable angina: increased demand)
ACS: decreased supply
Stable angina
Chest pain reproducible
Relieved by rest/NG
Of typical duration/quality
Associated with exertion
UA
Ischemic discomfort of new onset, occurs at rest, severe and in crescendo pattern (more severe, prolonged, frequent)
NSTEMI
UA criteria + evidence of myocardial necrosis
White thrombi
Platelet rich
Red thrombi
Fibrin/cell rich
Anti-ischemic therapy options
Nitrates, morphine, BB, CCB
Nitrates MOA
No released from endothelium
Venous (Arterial at higher doses)
Venous: lowers preload/MVO2
Arterial: lowers BP/AL/relieves coronary artery vasospasm (improves O2 flow)
Nitrates dosing
SL: 0.4mg Q5min X 3 doses
IV: 5mcg/min --> increase by 5mcg/min Q3-5 mins up to 20mcg/min then increase by 10mcg/min up to 200mcg/min (400 max)
Nitro tolerance
Develops in 24-48 hours: make sure to have nitrate-free interval (10-12 hours/day)
Titrate down to avoid withdrawal
Nitrate benefit groups
HF, persistent ischemia, no C/I, uncontrolled high BP
AE Nitro
headache, flushing, hypotension, tachycardia
When to D/C Nitro
post PCI/CABG
Beta blockers MOA
Block B1 (reducing HR, contractility, and O2 demand: improve filling time)
BB Benefits
Reduce re-infarction, infarct size, arrhythmias
BB benefit groups
HD stable + no signs ADHF
AE BB
hypotension, bradycardia, acute HF, AV block
CCB MOA
Inhibit influx of Ca in myocardial/vascualr SM cells: vasodilation
When to use CCB
Only if C/I to BB --> start BB is CCB is being used for HTN
(data shows little benefit other than for Sx control)
AE CCB
Acute HF, LVSD
C/I: WPW, SBP <90, Systolic HF
Benefit groups: CCB
Coronary vasopasm/cocaine-induced (Printzmetal): can also use NTG
BB will worsen through unnopposed B2
Aspirin dose
Initial: 325mg/maintain 81mg/<100mg with ticagrelor
OASIS-7 Tiral
High vs. low dose ASA
Platelet 3 Step
1. Adhere: via GP1b and vWF
2. Activation: release ADP, 5HT, TXA2 and expression GP2a/3b receptor
3. Adhere: fibringoen/VWF to GP2a/3b receptors
ASA dosing CABG
Continue through CABG
CREDO trial
long-term use clopidogrel had lower risk of death, MI, stroke vs. placebo
Prasurgerl benefits over plavix
Faster onset, stronger action, less DDI
Trition-timi 38: lower MI, stroke, death but more bleeding
Prasurgerl c/I
stroke, >75y/o, <60kg
Ticagrelor benefits over plavix
Not a prodrug, reversible, PLATO: lower MI, stroke, death but more bleeding
Benefits of G2b/3a inhibitors
reduce risk of re-infarction and need for repeat PCI when added to therapy
High risk patients who benefit from G2b/3a
DM, elevated troponin, ST seg elevation (meta-analysis showed lower death/MI)
Two uses of G2b/3a
1. High risk patients undergoing PCI
2. Low risk patients with unremitting ischemia who will eventually undergo PCI/angiography
Primary PCI G2b/3a
In combo with UHF + ASA
A E or T is fine
Recurrent ischemia G2b/3a
Despite ASA, clopidogrel, ACoag
E or T (A only for PCI)
Anticoag choices early invasive
UFH, LMWH, FX, Bivali
Anticoag for CABG
UFH (shorter duration of action)
Preference for fondaparinux
High bleeding risk
OASIS-5: non-inferior to enoxaparin with less bleeding
Must be given with UFH due to lack of 2 blocking
ACUITY trial
Bivali superior to heparin/G2b + less bleeding
Warfarin for ACS patients (4 patient groups)
Triple therapy INR: 2-2.5
Patients with LV thrombus, extensive ventricular wall motion abnoramities, history of TE disease/A-fib
Eptifibatide (integrilin) Indication
1. ACS (UA/NSTEMI): medically managed + PCI
2. PCI support (STEMI)
Dose Eptifibatide ACS
ACS: Bolus 180mcg/kg (max 22.6mg) over 1-2 mins  CI 2mcg/kg/min (max: 15mg/hr) until discharge or CABG (hold 4 hours prior) up to 72 hours
*PCI w/in 72hrs: CI at time of PCI up to 18-24 hours or discharge (</96 hours total)
WITH UFH + ASA
Eptifibatide dosing PCI
PCI: Bolus 180mcg/kg (max 22.6mg) over 1-2 mins right before PCI  CI 2mcg/kg/min (max: 15mg/hr)  2nd bolus 10 mins after 1st  CI 18-24 hours or discharge
*D/C heparin post PCI
Renal/hepatic Eptifibatide
ACS: <50: 180mcg/kg bolus (max 22.6mg)  1mcg/kg/min (max: 7.5mg/hr)

PCI: <50: 180mcg/kg bolus (max: 22.6mg) right before PCI then CI of 1mcg/kg/min (max: 7.5mg/hr) + 2nd bolus 180mcg/kg (max 22.6mg) 10 mins after 1st
No liver
Eptifibatide DDI
Antiplatelets, anticoagulants, NSAIDs, etc.
Eptifibatide MOA
*Glycoprotein 2a/3b inhibitor (blocks binding of VWF and fibrinogen)
*Reversibly blocks platelet aggregation + prevents thrombosis
*Effects persist over infused and are reversed when infusion ends
Eptifibatide PK
Onset: 1 hour
½ life (E): 2.5 hours
Duration: platelet function restored in 4 hours
E: Urine
Eptifibatide AE
Bleeding, hypotension, thrombocytopenia, injection site reaction
Eptifibatide monitoring
Renal function, PT, aPPT
Abciximab Indication
1 ACS (UA/NSTEMI) not responsive to med therapy with planned PCI <24 hours
2 PCI
3 STEMI undergoing PCI

*With ASA and UFH (min)
Abciximab dose PCI
PCI: 0.25mg/kg bolus 10-60 mins prior to PCI  CI 0.125mcg/kg/min (max 10mcg/min) for 12 hours
Abciximab dose ACS unresponsive to med therapy
0.25mg/kg bolus then 18-24 hour CI of 10mcg/min (stop 1 hour post PCI)
Abciximab STEMI
0.25mg/kg bolus at time of PCI  CI 0.125mcg/kg/min (max: 10mcg/min) up to 12 hours
Abciximab renal/hepatic
None: metabolized by proteases
Abciximab interactions
Dextran, antiplatelets, NSAIDs, etc
Abciximab MOA
*Fab antibody fragment
*Glycoprotein 2a/3b inhibitor (inhibits platelet aggregation)
Abciximab PK
Onset: rapid
½ life (E): 30 mins (platelet function may remain abnormal for up to 7 days post infusion)
M: proteases
TTP: 30 mins to platelet inhibition
Abciximab AE/monitoring
Bleeding, hypotension, chest pain, nausea
thrombo, AB development

Monitor: aPPT, H/H
Tirofiban Indications
1 ACS (UA/NSTEMI)
2 PCI (unlabeled)

*With heparin
Tirofiban dosing ACS
ACS: 0.4mcg/kg/min for 30 mins then 0.1mcg/kg/min: continue through and post angiography (12-24 hours)
Tirofiban dosing PCI
PCI: 25mcg/kg over 3 mins at time of PCI  CI 0.15mcg/kg/min up to 18-24 hours
Tirofiban renal/hepatic
<30: reduce by 50%
No hepatic
Tirofiban MOA
*Reversible antagonist of fibrinogen binding to GP 2b/3a receptor
Tirofiban PK
1/2: 2 hours
E: urine
Tirofiban AE/monitoring
Bleeding, bradycardia, nausea

Monitor: CBC, aPTT (heparin)
Bivalirudin Indications
1 PCI +/- HIT/HITTS*
2 UA/NSTEMI early invasive (UL)
3 STEMI primary PCI (UL)
4 HIT (UL)

*With ASA and provisional GP 2b/3a
Bivalirudin dosing PCI +/- HIT
PCI +/- HIT: 0.75mg/kg bolus right before PCI  1.75mg/kg/hr CI (up to 4 hours post)  CI of 0.2mg/kg/hr up to 20 hours if needed after
Bivalirudin dosing UA/NSTEMI
0.1mg/kg bolus  0.25mg/kg hour CI  bolus 0.5mg/kg at time of PCI + CI 1.75mg/kg/hr up to 4 hours post PCI
*CABG: D/C 3 hours prior and dose with UFH
*Med management: 0.25mg/kg/hr up to 72hrs
Bivalirudin renal/hepatic
PCI: 10-29: 1mg/kg/hr; dialysis (0.25mg/kg/hr)
Cardiac surgery/HIT: no adjustment per manufacturer
Bivalirduin MOA
Specific and reversible DTI: binds both circulating and clot-bound thrombin
*Prevents fibrinogen to fibrin, activation of V, VIII, XIII
Bivalirudin PK
Onset: immediate
Duration: baseline coagulation times 1 hr post-DC
½ life (E): 25 mins (1 hr <30)
Bivalirudin AE

Bleeding, hypotension, pain, headache, nausea, back pain

ARA indications post-MI

Already on ACE and BB


LVEF <40, and either Sx HF or DM unless CI!

Anticoag initial conservative

LMWH/fonda > UFH 2a recommendation

STEMI lytic therapy: anticoag

After fibrinolysis for at least 48 hours with IV UFH or SC LWMH (preferred) or FX for up to 8 days

In high risk patients, cardic ath is looking for what?

1. whether occluded or partially occluded epicardial arteries exist


2. which ones cna be intevened on


3. whether to make an intervention, stent or PTCA

UFH vs. enxoparain with tenecteplase

Clearance of UFH is not as altered (preferred choice)



Tenec also has shorter 1/2 life than alteplase