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88 Cards in this Set
- Front
- Back
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What are risk factors for NStemi?
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Age
Men ≥45 years; Women ≥55 years or premature menopause ± ERT Family history of premature CHD MI or sudden death ≤55 years (male) or ≤65 (female) Cigarette smoking (other tobacco too) Hypertension ≥140/90 mmHg or treated HDL <40 mg/dL High LDL (level depends on other risk factors) |
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What is the pathophys of Nstemi? If cholesterol increases what does it lead to?
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Narrowing of coronary arteries
increase in cholesterol = plaque formation |
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How is a thrombus treated? What does a thrombus formation lead too?
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Plaque rupture triggers coagulation cascade = thrombus
Thrombus formation = ischemia = myocardial damage |
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What does an incomplete thrombus formation lead too?
What does a complete occlusion lead too? |
Incomplete thrombus formation = Unstable Angina or Non ST-segment Myocardial Infarction
Complete occlusion = ST-segment Myocardial Infarction |
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Where does intrinsic and extrinsic pathway meet?
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factor 10 is the common pathway
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Progressive narrowing of artery leads to what diagnosis?
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chronic stabel angina?
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Plaque Rupture = ____ ___ = Partial occlusion = ___/____
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Plaque Rupture = Thrombus formation = Partial occlusion = UA/NSTEMI
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Plaque Rupture = Thrombus formation = Complete occlusion = ____
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Plaque Rupture = Thrombus formation = Complete occlusion = STEMI
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Signs and symptoms of ACS? What symptom may diabetics not have?
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Chest Pain
± radiation Diabetes may not have this because there is peripheral neuropathy Diaphoresis Weakness Syncope Nausea/vomiting Dyspnea Fever +/- BP elevation +/- HR elevation Increased WOB +/- enzyme elevation |
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What does T wave, st segment and st interval mean?
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T wave- ventricular repolarization
ST segment: close together it is the faster your heart is working St interval: is elevated meaning that it requires more force electricity because of more resistance due to dead muscle tissue |
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What happens in a STEMI EKG?
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ST elevation is seen, looks like tomb stone
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what is the difference in symptoms between stemi and nstemi?
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EKG changes
Nstemi does not have EKG changes |
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When diagnosing Nstemi why do you look at the chemistry?
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Chemistry: +/- sodium, def want to know Scr. Scr is an indicator of break down of muscle, want to see if patient has renal failure. Because of ventricular remodeling and drug clearance. All the drugs we are going to use are going to go though the kidney, that why scr is so important
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When diagnosing Nstemi why do look at the CBC?
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CBC: hemoglobin--> know if there anemic. Platelet count -->see if they have inflammation,
Major drug to use for non stemi--> Heparin-->want to know baseline platelets for this, make sure they aren't developing HIT |
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When diagnosin Nstemi--> when do you look at lipids in a patient with an MI?
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check in first 24 hours because TC and HDL will rapidly goes down after 24 hours.
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When diagnosing Nstemi when do you look at AST and ALT?
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Blood flow not traveling to liver, can get liver failure
Liver is effected by statins so be anywhere |
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When there are elavated cardiac enzymes will it be stemi or non stemi?
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nstemi
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What are goals of therapy for ACS?
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Restoration of blood flow
Prevention of death or other ischemic complications Liver failure, kidney failure, heart failure needs to be prevented Relief of ischemic symptoms |
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What does MONA stand for?
What do you start MONA |
morphine
oxygen niroglycerin aspirin Ideally started within the first 30 minutes of presentation |
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What is Morpines MOA?
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Restores Arterial and venous vasodilation
Pain relief Hits the mu kappa |
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How is morphine dosed?
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2 – 5 mg IV every 15 – 30 minutes
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What SE of Morphine?
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Hypotension
Respiratory depression Nausea/vomiting/constipation Pain relief |
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What is MOA of oxygen?
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Increase O2 supply
Mismatch of supply and demand that’s why we give them O2 |
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What is the progression of O2 delivery?
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Nasal cannula High flow mask (lot more oxygen) Non-rebreather CPAP/BIPAP (Continuous positive airway pressure) Dogs love CPAP Intubation
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What is MOA of nitroglycerin?
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Acts as a NO donor which promotes venodilation
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how is nitroglycerin dosed sublingual, IV, Paste, PO and Patch?
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Sublingual: 0.4mg SL x 1, then call 911 for suspected ACS
IV: 5-10 mcg/min then increase every 5-10 minutes to effect Paste: 1-2” q6h PO: 10 mg q6h Patch: 0.2 – 0.8 mg/hr |
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What are SE of Nitroglycerin?
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Hypotension
Tachycardia Headache Tolerance – need nitrate-free interval |
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What is aspirin MOA?
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Inhibits the formation of TXA2 = inhibits platelet aggregation
Irreversible |
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How is aspirin dosed?
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325mg chewed x 1
Don’t use Enteric coded |
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What are SE of aspirin?
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GI upset
Bleeding Nasal pollups, anaphylaxis |
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What are the 7 components of the TIMI Risk score?
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Age ≥ 65
> 3 coronary risk factors (FHx, HTN, HLD, DM, active smoker) Prior coronary stenosis ≥ 50% ST-segment depression ≥0.5 mm ≥ 2 angina events in previous 24 hours ASA use w/in 7 days Elevated cardiac biomarkers |
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What is the point scale for the TIMI risk score?
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Low Risk = 0-2 points
Med Risk = 3-4 points High Risk = 5-7 points |
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What is MOA of UFH?
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Binds to antithrombin III and accelerates its action inhibiting thrombin formation and ultimately the conversion of fibrinogen to fibrin
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What are the recommendations for UFH in Nstemi?
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Class I with antiplatelet therapy for early invasive or conservative
Class I with PCI |
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How do you dose UFH in Nstemi? (bolus and infusion) duration?
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Bolus: 60units/kg
Infusion: 12-15units/kg/hr (Target aPTT 1.5-2.0x control) Continue for 48 hours or until end of PCI |
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what are contraindications of UFH in nstemi?
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Active bleeding
HIT/HITT Severe bleeding risk or recent stroke |
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What is MOA of LMWH?
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MOA:
Inhibits factor Xa and some thrombin |
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What are recommendations of LMWH in nstemi?
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Class I with aspirin for conservative or invasive approach
Class IIa as alternative to UFH for PCI |
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What is the dosing for enoxaprin in nstemi?
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Enoxaparin (Lovenox®): 1 mg/kg SC Q12hrs (CrCL ≥30 mL/min); 1mg/kg SC q24h (CrCL 15-29 mL/min)
Give supplemental dose of 0.3 mg/kg IV at time of PCI (if last dose 8-12 hours prior) |
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What are contraindications of LMWH in nstemi?
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Active bleeding
HIT/HITT Severe bleeding risk or recent stroke Avoid if CABG planned/required |
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What is MOA of Bivalirudin?
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Direct, reversible binding to thrombin
Direct thrombin inhibitor |
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When is Bivalirudin given in nstemi?
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Only given if early invasive strategy planned (Class I)
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What is bolus/infusion dose of bivalurdin?
Dosing bivalurdin while using PCI? |
Early therapy:
Bolus – 0.1 mg/kg Infusion – 0.25 mg/kg/hr PCI: Bolus - 0.5 mg/kg Infusion - 1.75 mg/kg/hr |
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contraindication of bivalirudin?
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Active bleeding
Severe bleeding risk |
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What is MOA of fondaparinux?
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Binds directly to factor Xa
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What is recommendation for fondaparinux in Nstemi?
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Class I recommendation for invasive or conservative approach
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How do you dose fondaparinux in Nstemi?
If PCI is being used what is the dose? |
Dose: 2.5 mg daily
If PCI, give with 50-60 units/kg bolus (not well studied) Continue to hospital discharge |
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What are contraindication of fondaparinux?
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Active bleeding
Severe renal disease (SCr ≥3.0 mg/dL or CrCL <30 mL/min) |
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What patients with Nstemi should ASpirin be used in?
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Should be used in all patients! (Class I)
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What is aspirin MOA?
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Inhibits thromboxane A2 and prevents platelet activation/aggregation
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How do you dose aspirin by itself?
How do you dose aspirin with a stent in? |
160-325 mg once on Day 1
75-162 mg daily for patients not receiving stent (continue indefinitely) 162-325 mg daily for patients receiving stent (see STEMI for duration) |
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What is MOA of clopidogrel?
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Irreversible binding to ADP receptor
Prevention of further platelet activation and release of aggregation/adhesion factors |
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What is bolus and continuous dose of plavix?
What is dose with Bare metal Stent What is dose with drug-eluting stent? |
300 mg bolus dose (I), 600 mg bolus dose (IIb)
75mg daily for 1 year Bare Metal Stent (BMS): 75 mg for min 1 month (1 year ideally) Drug-Eluting Stent (DES): 75 mg for 12-15 months |
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What is MOA of Prasugrel?
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Irreversible binding to ADP receptor
Prevention of further platelet activation and release of aggregation/adhesion factors |
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What patients should prasugrel only be started in?
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Should only be initiated in patients with known anatomy
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Why do you need to know the anatomy of the patient when dosing prasugrel?
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Know where the blockage already is
You want to know this anatomy because you cant reverse presugrel, 5 o 7 days for drug to get out of your system CABG bleeding was much high on prasugrel |
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What is the prasugrel loading dose in all patients? What is the dose after?
What is the duration? |
60 mg load (all patients)
10 mg daily (≥60 kg), 5 mg daily (<60 kg) Continue for at least 12 months (Class I) or up to 15 months (Class IIb) if stent placed |
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What are contraindication of PRasugrel? (3)
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Age ≥75 years unless with DM or prior MI
Active bleeding Prior Stroke/TIA |
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What s the MOA of Glycoprotein IIb/IIIa Inhibitors
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Bind to GP IIb/IIIa receptor and prevent fibrin cross-linking of platelets
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What are 3 recommendations for Glycoprotein IIb/IIIa Inhibitors?
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Class IIa for tirofiban or eptifibatide in high-risk patients
Class I if undergoing PCI Class IIb if not undergoing PCI |
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What are 3 contraindications with Glycoprotein IIb/IIIa Inhibitors?
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Active bleeding
Thrombocytopenia Dialysis (eptifibatide) |
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What is PCI dose of Eptifibatide
(Integrilin®) What is the non PCI dose? |
PCI
Bolus: 180 mcg/kg x 2 Infusion: 2 mcg/kg/min x 18-24 hrs (1 mcg/kg/min if CrCL <50) non pci Bolus: 180 mcg/kg x 1 Infusion: 2 mcg/kg/min x 12-72 hrs (1 mcg/kg/min if CrCl <50) |
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what is the PCI dose ofAbciximab (ReoPro®)
What is the non PCI dose? |
PCI
Bolus: 0.25 mg/kg Infusion: 0.125 mg/kg/hr x 12 hrs nonpci dose Not recommended |
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What is the PCI dose for Tirofiban
(Aggrastat®)? Nonpci dose? |
PCI
Bolus: 25 mcg/kg Infusion: 0.15 mcg/kg/min x 18 hrs nonPCI Bolus: 0.4 mg/kg over 30 min Infusion: 0.1 mcg/kg/min x 18-72 hrs |
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What are 6 additional drug classes therapies used for NStemi?
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Beta-blockers
HMG-CoA Reductase inhibitors (Statins) Angiotensin Converting Enzyme Inhibitors (ACEIs) Angiotensin Receptor Blockers (ARBs) Aldosterone Antagonists Calcium Channel Blockers |
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What are recommendations for B-Blockers in Nstemi?
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Class I for oral agents without contraindication
Everyone get a BB |
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What is the Pharmacologic Actions:
of B-Blockers? |
Reduces post-MI mortality – primarily through arrhythmia prevention
Improves contractility of the myocardium |
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What are contraindications of B-Blockers
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Acute heart failure
Reduced EF Shock PR interval >0.24s or 2nd/3rd degree block HR <60bpm or SBP <90 mmHg Severe, uncontrolled reactive airway disease |
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What BB dosage form is preferred in NSTEMI? When should it be started?
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Oral agents are preferred and should be started within 24 hours unless contraindicated
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What BB agents are used in ACS? What are there dosing?
What should they all be titrated too? |
Metoprolol tartrate 25-50 mg Q6h (can consolidate to BID at discharge)
Propranolol 40-80 mg Q6-8h Atenolol 50-100 mg daily Titrate all to HR of 50-60 bpm |
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Why do ACEI have mortality benefit post-MI?
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Decrease in stroke, MI, and death from CV causes
Prevent ventricular remodeling following MI |
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What are recommendations of ACEI?
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Should be started on all patients unless contraindicated
Class IIa in patients who are low-risk |
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What are contraindications of ACEI?
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Hyperkalemia (K >5.5 mEq/L)
AKI Bilateral renal artery stenosis History of ACEI intolerance SBP <100 mmHg Pregnancy |
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What 4 ACEI are used in Nstemi?
What are there initial dosing and target doses? |
Captopril: intial 6.25-12.5 mg BID-TID, target 50 mg BID-TID
Enalapril: initial 2.5-5 mg BID, target 10 mg BID lisinopril: initial2.5-5 mg daily target 10-20mg daily Ramipril: intial 1.25-2.5 mg daily, target dose: 5mg bid or 10 mg daily |
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What do ARBs prevent?
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prevent ventricular remodeling and progression of HF
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What are recommendations for ARB?
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Class I for all patients intolerant to ACEI
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What ARB agents are used in NSTEMI?
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Candesartan 4-8 mg daily (titrate to 32 mg daily)
Valsartan 40 mg BID (titrate to 160 mg daily) Continue therapy indefinitely if tolerated |
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What are contraindication of ARBS in NSTEMI?
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SBP <100 mmHg
Bilateral renal artery stenosis Hyperkalemia (K >5.5 mEq/L) AKI Pregnancy |
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HMG-CoA Reductase Inhibitors have proven secondary prevention of what?
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post mi
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When using statins in ACS, when do you obtain a lipid profile?
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Obtain lipid profile within 24 hours post MI (Class
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When should Lipid lowering therapy should be started?
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during the hospitalization, if not directly following event
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When using statins in ACS, what should agents be titrated too?
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Agents should be titrated to achieve LDL <100 mg/dL
Optional goal of <70 mg/dL |
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What is recommendation of aldosterone antagonists?
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Class I to start in all post-MI patients with:
EF < 40% SCr < 2.5 mg/dL Serum K+ < 5.0 mEq/L Already on ACEI |
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what does aldosterone antagonist provide inhibiton of?
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Provides inhibition of aldosterone-mediated ventricular remodeling and progression of HF
Provides additional morbidity and mortality benefit when added to standard therapy |
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What aldosterone antagonist agents are used? Dosing? what should be titrated too?
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Eplerenone 25 mg daily (titrate to 50 mg daily)
Spironolactone 12.5 mg daily (titrate to 25-50 mg daily) Pick this because more evidence, big SE, not great for male patients, painful swelling of man boobs |
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What are recommendations for calcium channel blockers?
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Class I for patients with continued angina on appropriate doses of nitrates/β-blocker
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What CCB agents can be used? What are there doses? Duration?
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Diltiazem 120-360 mg SR daily
Verapamil 180-240 mg SR daily Nifedipine 30-90 mg SR daily Amlodipine 5-10 mg daily Continue agent indefinitely |
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What are contraindications of CCB?
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Contraindications:
Pulmonary edema Evidence of LV dysfunction SBP <100 mmHg PR interval >0.24s or 2nd/3rd degree block |
