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76 Cards in this Set
- Front
- Back
Two groups of IHD |
Chronic CAD (stable angina: increased demand)
ACS: decreased supply |
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Stable angina
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Chest pain reproducible
Relieved by rest/NG Of typical duration/quality Associated with exertion |
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UA
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Ischemic discomfort of new onset, occurs at rest, severe and in crescendo pattern (more severe, prolonged, frequent)
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NSTEMI
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UA criteria + evidence of myocardial necrosis
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White thrombi
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Platelet rich
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Red thrombi
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Fibrin/cell rich
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Anti-ischemic therapy options
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Nitrates, morphine, BB, CCB
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Nitrates MOA
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No released from endothelium
Venous (Arterial at higher doses) Venous: lowers preload/MVO2 Arterial: lowers BP/AL/relieves coronary artery vasospasm (improves O2 flow) |
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Nitrates dosing
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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) |
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Nitro tolerance
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Develops in 24-48 hours: make sure to have nitrate-free interval (10-12 hours/day)
Titrate down to avoid withdrawal |
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Nitrate benefit groups
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HF, persistent ischemia, no C/I, uncontrolled high BP
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AE Nitro
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headache, flushing, hypotension, tachycardia
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When to D/C Nitro
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post PCI/CABG
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Beta blockers MOA
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Block B1 (reducing HR, contractility, and O2 demand: improve filling time)
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BB Benefits
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Reduce re-infarction, infarct size, arrhythmias
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BB benefit groups
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HD stable + no signs ADHF
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AE BB
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hypotension, bradycardia, acute HF, AV block
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CCB MOA
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Inhibit influx of Ca in myocardial/vascualr SM cells: vasodilation
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When to use CCB
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Only if C/I to BB --> start BB is CCB is being used for HTN
(data shows little benefit other than for Sx control) |
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AE CCB
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Acute HF, LVSD
C/I: WPW, SBP <90, Systolic HF |
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Benefit groups: CCB
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Coronary vasopasm/cocaine-induced (Printzmetal): can also use NTG
BB will worsen through unnopposed B2 |
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Aspirin dose
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Initial: 325mg/maintain 81mg/<100mg with ticagrelor
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OASIS-7 Tiral
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High vs. low dose ASA
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Platelet 3 Step
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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 |
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ASA dosing CABG
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Continue through CABG
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CREDO trial
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long-term use clopidogrel had lower risk of death, MI, stroke vs. placebo
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Prasurgerl benefits over plavix
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Faster onset, stronger action, less DDI
Trition-timi 38: lower MI, stroke, death but more bleeding |
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Prasurgerl c/I
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stroke, >75y/o, <60kg
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Ticagrelor benefits over plavix
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Not a prodrug, reversible, PLATO: lower MI, stroke, death but more bleeding
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Benefits of G2b/3a inhibitors
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reduce risk of re-infarction and need for repeat PCI when added to therapy
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High risk patients who benefit from G2b/3a
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DM, elevated troponin, ST seg elevation (meta-analysis showed lower death/MI)
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Two uses of G2b/3a
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1. High risk patients undergoing PCI
2. Low risk patients with unremitting ischemia who will eventually undergo PCI/angiography |
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Primary PCI G2b/3a
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In combo with UHF + ASA
A E or T is fine |
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Recurrent ischemia G2b/3a
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Despite ASA, clopidogrel, ACoag
E or T (A only for PCI) |
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Anticoag choices early invasive
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UFH, LMWH, FX, Bivali
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Anticoag for CABG
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UFH (shorter duration of action)
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Preference for fondaparinux
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High bleeding risk
OASIS-5: non-inferior to enoxaparin with less bleeding Must be given with UFH due to lack of 2 blocking |
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ACUITY trial
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Bivali superior to heparin/G2b + less bleeding
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Warfarin for ACS patients (4 patient groups)
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Triple therapy INR: 2-2.5
Patients with LV thrombus, extensive ventricular wall motion abnoramities, history of TE disease/A-fib |
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Eptifibatide (integrilin) Indication
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1. ACS (UA/NSTEMI): medically managed + PCI
2. PCI support (STEMI) |
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Dose Eptifibatide ACS
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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 |
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Eptifibatide dosing PCI
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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 |
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Renal/hepatic Eptifibatide
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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 |
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Eptifibatide DDI
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Antiplatelets, anticoagulants, NSAIDs, etc.
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Eptifibatide MOA
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*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 |
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Eptifibatide PK
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Onset: 1 hour
½ life (E): 2.5 hours Duration: platelet function restored in 4 hours E: Urine |
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Eptifibatide AE
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Bleeding, hypotension, thrombocytopenia, injection site reaction
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Eptifibatide monitoring
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Renal function, PT, aPPT
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Abciximab Indication
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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) |
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Abciximab dose PCI
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PCI: 0.25mg/kg bolus 10-60 mins prior to PCI CI 0.125mcg/kg/min (max 10mcg/min) for 12 hours
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Abciximab dose ACS unresponsive to med therapy
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0.25mg/kg bolus then 18-24 hour CI of 10mcg/min (stop 1 hour post PCI)
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Abciximab STEMI
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0.25mg/kg bolus at time of PCI CI 0.125mcg/kg/min (max: 10mcg/min) up to 12 hours
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Abciximab renal/hepatic
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None: metabolized by proteases
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Abciximab interactions
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Dextran, antiplatelets, NSAIDs, etc
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Abciximab MOA
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*Fab antibody fragment
*Glycoprotein 2a/3b inhibitor (inhibits platelet aggregation) |
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Abciximab PK
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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 |
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Abciximab AE/monitoring
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Bleeding, hypotension, chest pain, nausea
thrombo, AB development Monitor: aPPT, H/H |
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Tirofiban Indications
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1 ACS (UA/NSTEMI)
2 PCI (unlabeled) *With heparin |
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Tirofiban dosing ACS
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ACS: 0.4mcg/kg/min for 30 mins then 0.1mcg/kg/min: continue through and post angiography (12-24 hours)
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Tirofiban dosing PCI
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PCI: 25mcg/kg over 3 mins at time of PCI CI 0.15mcg/kg/min up to 18-24 hours
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Tirofiban renal/hepatic
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<30: reduce by 50%
No hepatic |
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Tirofiban MOA
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*Reversible antagonist of fibrinogen binding to GP 2b/3a receptor
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Tirofiban PK
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1/2: 2 hours
E: urine |
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Tirofiban AE/monitoring
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Bleeding, bradycardia, nausea
Monitor: CBC, aPTT (heparin) |
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Bivalirudin Indications
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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 |
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Bivalirudin dosing PCI +/- HIT
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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
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Bivalirudin dosing UA/NSTEMI
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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 |
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Bivalirudin renal/hepatic
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PCI: 10-29: 1mg/kg/hr; dialysis (0.25mg/kg/hr)
Cardiac surgery/HIT: no adjustment per manufacturer |
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Bivalirduin MOA
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Specific and reversible DTI: binds both circulating and clot-bound thrombin
*Prevents fibrinogen to fibrin, activation of V, VIII, XIII |
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Bivalirudin PK
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Onset: immediate
Duration: baseline coagulation times 1 hr post-DC ½ life (E): 25 mins (1 hr <30) |
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Bivalirudin AE
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Bleeding, hypotension, pain, headache, nausea, back pain |
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ARA indications post-MI |
Already on ACE and BB LVEF <40, and either Sx HF or DM unless CI! |
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Anticoag initial conservative |
LMWH/fonda > UFH 2a recommendation |
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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 |
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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 |
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UFH vs. enxoparain with tenecteplase |
Clearance of UFH is not as altered (preferred choice)
Tenec also has shorter 1/2 life than alteplase |