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115 Cards in this Set
- Front
- Back
What is the definition of coronary artery disease?
|
-myocardial ischemia secondary to increased myocardial work and/or decreased myocardial oxygen supply
-reversible myocardial ischemia the produces disturbances in myocardial function w/o causing myocardial necrosis |
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Name the 5 clinical syndromes of reversible ischemia. Which 3 are acute coronary syndromes?
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-stable angina pectoris
-variant or Prinzmetal's angina -Silent myocardial ischemia -Syndrome X -Unstable angina ACS= unstable angina, non-STEMI and STEMI |
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What is the pathophysiology of stable angina pectoris?
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large single- to multi- vessel atherosclerotic CAD, coronary artery vasospasm or both
->75% atherosclerotic reduction causes sx |
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What factors affect myocardial oxygen demand?
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-basal O2 requirements
-ventricular wall stress -HR -contractility O2 demand=HR x SBP |
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What factors affect myocardial oxygen supply?
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Coronary blood flow
-Vascular resistance (metabolic control, compressive forces, autoregulation, neural factors, humoral factors) -diastolic phase duration O2 carrying capacity |
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What is the definition of stable angina pectoris?
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discomfort in the chest or adjacent areas caused by myocardial ischemia
-anginal episodes quality, frequency, severity, duration of sx, time of day, etc have not changed over the past 2 months |
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How is stable angina subclassified?
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-Fixed threshold
-Variable threshold -Mixed angina |
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What is the clinical presentation of stable angina? (PQRST)
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P: precipitating factors and palliative measures
-exercise, weather changes, large meal, stress/ fear/anger, coitus -pain relieved with nitroglycerin Q: quality of pain -heavy weight on chest, SOB w/ feeling of constriction, burning/tightness/crushing feeling, gradual inc in intensity then gradual dec R: region and radiation -over sternum between epigastrium and pharynx, lower jaw, lower cervical or upper thoracic spine, L interscapular or suprascapular area -radiates to L arm and shoulder, jaw, right arm (maybe) S: severity of pain T:timing and temporal pattern -duration 0.5-30 min |
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Explain the New York Heart Association's Functional Classification of angina pectoris
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-Class I: sx occur w/ unusual activity; minimal to no functional impairment
-Class II: sx occur w/ prolonged or slightly more than usual activity; mild functional impairment -Class III: sx occur with usual ADL; moderate functional impairment -Class IV: sx occur at rest; severe functional impairment |
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What is the definition of Variant (Prinzmetal's) angina?
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syndrome of cardiac pain that occurs exclusively at rest
shows ECG ST-segment elevation |
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What causes variant (Prinzmetal's) angina?
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-coronary artery spasm
-reduction in myocardial oxygen supply (inc HR, BP) |
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What are the clinical characteristics of variant (Prinzmetal's) angina?
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-similar to stable angina, but pain occurs at rest and is more intense
-occurs more in early morning hours |
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What is the definition of silent myocardial ischemia?
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-objective documentation of MI through exercise ECG testing that happens w/o angina
|
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How is silent myocardial ischemia classified?
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-Class I: pts w/ ischemia that is totally asymptomatic
-Class II: pts who have both symptomatic and unsymptomatic episodes |
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What causes silent MI and what it the lack of pain due to?
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-Unknown: possibly secondary to dec myocardial oxygen supply or inc. myocardial oxygen demand or both
-lack of pain: defects in pain perception, altered physiologic response to ischemia, or less ischemia than symptomatic episodes |
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What is the definition of syndrome X?
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-microvascular angina
-occurence of effort angina and exercise-induced ECG changes despite no coronary artery stenosis or coronary artery spasm -angina with ST-segment depression |
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How is ischemic heart disease diagnosed?
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-ECG: ST segment depression, T wave inversion, ST segment elevation in Prinzmetal's
-Exercise tolerance testing:BP and HR response -Exercise Electrocardiography: determine risk stratification and assess need for surgical/medical treatment; determine LVEF -Cardiac imaging: stress testing w/ thallium 201 myocardial perfusion screening; radionuclide angiocardiography (Technetium-99m), electron beam computerized tomography) -Cardiac catheterization and coronary angiography: only definitive dx |
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What are the goals of therapy for stable angina?
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-minimize the frequency and severity of angina and increase functional capacity
-reduce cardiovascular morbidity and mortality |
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What are the guidelines for management of stable angina (ABCDE)?
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A: aspirin and antianginals
B: Beta Blocker and Blood Pressure C: Cholesterol and Cigarettes D: Diet and Diabetes E: Education and Exercise |
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What effect do nitrates, BB, nifedipine, verapamil, and diltiazem have on HR, contractility, SBP, and LV volume?
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HR
-inc.: nitrates, nifedipine -dec: BB, verapamil, diltiazem (to lesser extent) contractility -dec: BB, verapamil, nifedipine/diltiazem (to lesser extent) SBP -dec: all LV volume: -inc: BB -Dec: nitrates, CCB (to lesser extent) |
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What is the mechanism of action of nitrates?
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-vasodilation
-enhance collateral blood flow -reverse coronary artery spasm -antiplatelet activity? |
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Explain nitrate tolerance.
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-dec response in presence of continuously or frequently admin nitrates
-due to depletion of sulfhydryl donors impairing the intracellular formation of nitric oxide and S-nitrosothiols, resulting in dec. formation of cGMP -Require nitrate free period of at least 10-12 hours |
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What are the adverse effects of nitrates?
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-HA (throbbing or pulsating)- take OTC analgesics
-hypotension, dizziness, lightheadedness, facial flushing (not w/ SL) -reflex tachycardia |
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When is nitrate therapy contraindicated?
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-When phosphodiesterase inhibitors have been used 24 hours (viagra) and 36-48 hours (cialis) prior
-Causes fatal hypertensive events (significant BP dec) |
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What are the monitoring parameters of nitrates?
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-BP
-HR -# chest pain episodes -# SL tablets needed |
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What is the mechanism of action of beta blockers?
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-competitively inhibit binding of catecholamines to B adrenergic receptor
-dec HR -enhance diastolic filling -dec. contractility: (-) iontrope -dec. AV nodal conductance: (-) dronotrope |
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What factors do you look at to determine which beta blocker to use?
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-cardioselectivity: atenolol and metoprolol
-intrinsic sympathomimetic activity: do not use in post-MI pt -lipophilicity: high-propanolol low-atenolol Know carvedilol, metoprolol, metoprolol XL, and atenolol |
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What are the adverse effects of beta blockers?
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-cardiac: sinus bradycardia, sinus arrest, AV block, reduced LVEF
-bronchoconstriction -fatigue, depression -nightmares -sexual dysfunction -intensification of insulin-induced hypoglycemia and peripheral vascular complications -Withdrawal syndrome: dec. dose gradually over 1-2 week period |
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What are the monitoring parameters of beta blockers?
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-BP
-HR goal 50-60bpm (<100bpm for exercise) |
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What is the mechanism of action of CCBs?
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-block the transmembrane flux of calcium into cardiac and vascular smooth muscle-> reduces the excitation-contraction-coupling mechanism responsible for myocardial and smooth muscle contraction
-DHPs: similar effects to nitrates (primarily vascular effects) -non-DHPs: similar effects to beta blockers and some vasodilator effects |
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What are the adverse effects of CCBs?
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DHPs: hypotension, HA, ankle edema
-nifedipine, nicardipine, isradipine: reflex tachycardia, flushing, dizziness non-DHPs: bradycardia, AV nodal conduction disturbances, HF, hypotension, HA, dizziness, edema -verapamil: constipation |
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What are the monitoring parameters of CCBs?
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-HR <60bpm at rest + <100bpm exercise
-BP <140/<90 -ankle edema in DHPs |
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What is the mechanism of action, indication, ADR, and drug interactions of ranolazine (Ranexa)?
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MOA: unknown; inh. late inward Na+ channel
Indication: chronic angina w/ inadequate response to other antianginals ADR: QT prolongation, constipation, HA, dizziness, nausea DI: substrate of CYP 3A4, 2D6, and p-gp |
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What are the therapeutic goals and treatment strategies for CV risk reduction?
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Dyslipidemia: LDL<70-100mg/dl
-statins, plant sterols/stanols, Omega 3 FA Hypertension: <140/<90 or DM <130/<80 -BB and ACEIs Diabetes Mellitus: HgB A1C < 7% Smoking cessation Diet: <7% saturated fat, <200mg/dl cholesterol Physical activity: 30-60 min 3-4 days/week |
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When should ACEI therapy be added to management of chronic stable angina pectoris?
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Consider in pts w/ LVEF<40%, HTN, DM, or CKD
-reduces CV events in high risk CAD pts Ramipril 10mg/day studied |
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When should anti-platelet therapy be used in pts with stable angina?
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Reduces CV events by inh. plt aggregation
Primary prevention -ASA if pts >50yo with additional risk factor (HTN, DM, FH, etc) Secondary prevention -absence of coronary artery stents: ASA 75-162 mg/day or clopidogrel 75mg/day if CI to ASA indefinitely -presence of drug eluding stent: ASA 75-162mg/day + clopidogrel (min 15 months) -presence of bare metal stent: ASA 75-162mg/day + clopidogrel (min 12-15 months) |
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What are the adverse effects of antiplatelet therapy?
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-ASA: bleeding
-ticlopidine, clopidogrel, prasugrel: N/D, dyspepsia, anorexia, rash, pruritus, uticaria, ecchymoses, bleeding, NEUTROPENIA, aplastic anemia, thrombocytopenia, cholestasis, hepatitis |
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What are the monitoring parameters of antiplatelet therapy?
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-CBC
-s/sx of bleeding: bruising, occult blood |
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How should stable angina be treated acutely?
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SL nitroglycerin tablets (0.15-0.6mg) or spray (0.4mg/spray)
|
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Which chronic therapy is best for treating stable angina?
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-BB reduce CV events- use if no CI (vasospastic angina, conduction disturbances; monitor in pts w/ lung disease, DM, peripheral vascular disease, and depression)
-CCB useful in pts w/ lung disease, DM, peripheral vascular disease |
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What combinations of antianginals should be used to treat stable angina?
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-nitrates and BB
-non-DHPs and nitrates -DHPs and BB -triple therapy for severe angina/CAD that doesn't allow for surgical correction |
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What antianginals are used to treat variant (Prinzmetal's) angina?
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-nitrates
-CCBs -combo nitrate + CCBs NO BBs! |
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How should one take SL nitroglycerin tablets?
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-Sit down (dec. BP- don't want to faint)
-Tablet under tongue -in 5 min, if pain not gone, call 911 -take 2nd tablet -in 5 min if pain not gone, take 3rd tablet |
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What is the definition of unstable angina?
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-Worsening angina or angina lasting >20min
-not relieved or only partially relieved by SL nitroglycerin |
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What is the definition of acute myocardial infarction?
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necrosis of cardiac muscle caused by prolonged dec. in oxygen delivery to the affected muscle
-thrombus formed at site of plaque- totally occludes the artery |
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What causes acute coronary syndromes? (pathophysiology)
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-atherosclerotic CAD- 85%
-severe coronary vasospasm- 15% (drug-induced: cocaine, triptans, TZDs, amphetamines, oral contraceptives, estrogen-containing products) cocaine causes vasospasm and atherosclerosis with long-term use -Tissue death moves like a wave: in 30min goes through the ventricular wall (transmural MI) -ventricular wall remodeling: aldosterone promotes growth of scar: use BB, ACEI/ARBs, aldosterone inh. |
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What determines short and long term morbidity and mortality?
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-LV function
-age>70 -HTN -Afib -infarct size, anterior location -previous MI -female sex -infarct artery patency, cardiac marker conc. |
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What is the clinical presentation of acute coronary syndromes?
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-prolonged (>30min for MI; <30min for unstable angina) substernal chest discomfort
-radiates to neck, throat, jaw, shoulders, arms -N/V, diaphoresis, SOB, sense of impending doom |
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What type of patient do silent MIs typically happen to?
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-women
-older men -diabetics |
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What will a physical examination show on a pt with acute coronary syndrome?
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-s/sx of LV or RV dysfunction
-variable HR, low grade fever, inc. RR, SBP 90-100 -abnormal heart sounds: S3 and S4 (LV dysfunction) -leukocytosis -signs of severe hyperlipidemia: corneal arcus, xanthelasma, tendon xanthomas |
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What changes will you see in a 12-lead ECG of a pt with acute coronary syndrome?
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-ST depression
-ST elevation: STEMI -Q wave changes -T wave changes |
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What biochemical cardiac markers will you look at for a pt dx with acute coronary syndrome?
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-cardiac troponin I (cTnI)/ cardiac troponin (cTnT): elevated (>0.4ng/ml)- higher the conc., worse the MI
-creatinine kinase (CK-MB): elevated -takes 24 hours to get lab results back |
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What is the initial treatment of all ACS in the ER department?
|
OMAN
-Oxygenation: mask or nasal cannula (goal O2 sat>90%) -Morphine sulfate: MS 2-4mg IV every 5-20min in increments of 2-8 mg for pain relief and pt comfort -Aspirin 162-325mg chewed and swallowed (3 baby or 1 normal) -Nitrates: SL nitroglycerin every 5 min; evaluate for IV nitrates (do not use if pt took PDE inh 24-36 hrs prior) |
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What are the goals of therapy for acute coronary syndromes?
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-rapid and complete coronary artery reperfusion and minimize infarct size: thrombolytics
-relief of ischemic chest discomfort: nitrates -prevention of reinfarction:BB, ACEI -prevention of ventricular remodeling (and reduced systolic dysfunction and LVEF): BB, ACEI/ARBs, aldosterone inh. -identification and tx of hemodynamically significant dysarhythmias: lidocaine, amiodarone, cardiofibrillator |
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What medications will be given within the first 24 hours?
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Nitrates: IV NTG 5-10mcg/min titrated to 75-100 (max 200) until sx relief or limiting SE
-CI: SBP <90mmHg or >30mmHg from baseline, severe bradycardia (<50bpm) or tachycardia (>100bpm) or suspected RV infarction Analgesia: MS 2-4 mg IV every 5-30 min in increments of 2-8mg or meperidine -D/C NSAIDs before STEMI and during hospitalization Anxiolytics Stool softeners: 100 mg docusate sodium daily ASA: 162-325 mg chewed and swallowed; 75-162mg daily if no stent;162-325 mg daily x 30days if bare metal stent, 3-6months for drug eluding stent, then 75-162 mg daily indefinitely Clopidogrel/ Prasugrel: Plavix 300mg loading (600 if PCI) then 75mg/day for 14days-1 yr (12-15 months if PCI) -do not give loading dose in pts >75yo -D/C 5 days prior to CABG -Use indef. if ASA allergy Prasugrel 60mg load followed by 10mg (5mg if wt<60kg) x 12-15 months if primary PCI -D/C 7 days prior to CABG |
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Explain the interaction between PPIs and plavix. Does this happen with PPIs and prasugrel?
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-Clopidogrel req. conversion to active metabolite mediated by CYP2C19
-Prasugrel has multiple pathways -Pts taking PPIs or if poor CYP2C19 metabolizers will have reduced formation of the active metabolite and will have higher CV events |
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What is the key treatment for patients with ACS?
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Open artery through reperfusion
-PCI (more effective) -fibrinolysis |
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What is the door to procedure time for PCI and fibrinolysis?
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-Primary PCI door to balloon time: 90min
-Fibrinolytic door to needle time: 30min |
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What criteria is used to determine if reperfusion therapy is necessary?
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-chest discomfort consistent with MI
-ST-segment elevation |
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What are the direct fibrinolytic medications? What are the indirect fibrinolytic medications
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Direct
-rt-PA -rscu-PA -UK Indirect -Streptokinase -APSAC |
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What is the difference between a hemostatic plug and thrombus?
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Composition
-Hemostatic plug has red cells in it as well as plts and fibrin Both affected by fibrinolytics |
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What is the dosing of streptokinase in ACS?
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1.5million units in 50ml NS or D5W over 60 min
|
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What is the dosing of t-PA, rt-PA (alteplase, Activase)
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-15mg bolus
-0.75mg/kg (max 50mg) over 30 min -0.5mg/kg (max 35mg) over 60 min |
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What is the dosing of Reteplase (Retavase)
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10units IV, repeat dose in 30 min
|
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What are the ADR of streptokinase?
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-antigenicity and allergic reactions
-hypotension -hemostatic defect -intracerebral bleeds |
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What is the dosing of Tenecteplase (TNKase) in ACS?
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< or = 60kg: 30mgIV
60-69.9kg: 35mg IV 70-79.9kg: 40mg IV 80-89.9kg: 45mg IV > or = 90kg: 50mg IV |
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What are the ADR of direct fibrinolytics?
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-hemostatic defect
-intracerebral bleeds |
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What are absolute CI of fibrinolytic therapy in ACS?
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-prior Intracranial hemorrhage
-known structural cerebral vascular lesion or malignant intracranial neoplasm -ischemic stroke within 3 months -suspected aortic dissection -severe active bleeding -significant closed head or facial trauma within 3 months prior |
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What are some relative CI of fibrinolytic therapy in ACS?
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-poorly controlled HTN (SBP>180mmHg; DBP>110mmHg)
-traumatic or prolonged (10+min) CPR or major surgery in last 3 weeks -internal bleeding in last 2-4 weeks -pregnancy -active peptic ulcer -current use of anticoagulants |
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What are the monitoring parameters of thrombolytic use?
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-prompt relief of chest pain
-prompt resolution of ECG findings -reperfusion arrhythmias -early CK peak -maintenance or restoration of hemodynamic instability -s/sx of bleeding: bloody stools, bruising -baseline CBC, plt count, INR/aPTT, daily CBC -mental status changes |
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What is rescue PCI?
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-treat in catheter lab, because no changes; already given full thrombolytic
-inc. bleeding risk |
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What is facilitated PCI?
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-give 1/2 dose of thrombolytic agent, then 1 hour later taken to cath lab
-done at academic medical centers -dissolve some of the clot before going to cath lab |
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What is the rationale for using BB in ACS?
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-limit myocardial damage and/or mortality (dec. myocardial demand)
-reduce risk of reinfarction and/or mortality (reduce Vfib threshold) -Use within first 12-24 hours |
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What doses of BB are used in ACS?
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-Oral dosing is preferred
Oral (early: lower doses more often) -Metoprolol: 25-50mg every 6 hours -Propanolol: 40-80mg every 6-8 hours -Atenolol: 50-100mg daily -Carvedilol: 25-50mg BID |
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What are the monitoring parameters of BB for pts with ACS? How often should these be monitored for oral admin? for IV admin?
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-BP, HR, 12 lead ECG, s/sx of heart failure
-Oral: every shift during hospitalization -IV: every 5 minutes |
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How long should ACS pts be on anticoagulation?
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-48 hrs to 8 days or end of hospitalization
-May or may not stop if PCI -This is used to prevent extention of clot |
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What doses of anticoagulants should be used in ACS pts taking fibrinolytics?
|
-Take simultaneously with fibrinolytics
Heparin -60units IV/kg bolus (max 4000units) -12 units/kg/hr (max 1000) infusion UFH: use infusion if SK (3 hours past) LMWH: -enoxaparin 30mg IV bolus + 1mg/kg/hr SC Q12h until discharge |
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What anticoagulants should be used in pts not receiving thrombolytics or primary PCI?
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-prophylaxis therapy
-enoxaparin |
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What are the three GP IIb/IIIa inhibitors? What are their dosages?
|
-Abciximab, eptifibitide, tirofiban
-ONLY for PCI -Abciximab: 0.25mg/kg bolus + 0.125mg/kg/min (max 10mg) up til 12 hours post-PCI -eptifibitide: 180mcg/kg IV bolus + 2mcg/kg/min infusion; repeat 180mcg/kg bolus 10 min later; continue infusion 12-18hrs post-PCI -tirofiban:25mcg/kg IV bolus + 0.1mcg/kg/min infusion continued until 18 hrs post-PCI |
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When should an ACEi be given to a patient with ACS?
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-within the first 24 hrs, but after PCI, fibrinolytics, etc
-Use in pts w/ LVEF<0.4, DM, or CKD |
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When should an aldosterone antagonist be given to a pt with ACS?
|
-in addition to ACEi or ARB in pts with LVEF<40% with HF sx or DM
-use eplerenone 25mg initial, then 50mg daily -spironolactone 12.5mg initial, then 25-50mg daily |
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When should magnesium be given to a pt with ACS?
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-ONLY when LOW magnesium
|
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When should CCBs be used in pts with ACS?
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-pts with ischemia who cannot tolerate BB
-only use verapamil or diltiazem |
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What are the goals of therapy for unstable angina/ non-ST segment elevation MI?
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-prevent MI and death by inh. extension of thrombus
-reverse ischemia and relieve chest pain by inc. myocardial O2 supply, dec. myocardial O2 demand or both -differentiate between UA from non-STEMI |
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If you don't use PCI in a pt with UA or NSTEMI, how is clopidogrel used
|
-same dose as STEMI, but continue clopidogrel for at least 9 months
|
|
What are the CI of GP IIb/IIIa therapy?
|
-active internal bleeding
-hx of hemorrhagic stroke -intracranial neoplasm -acute pericarditis -uncontrolled HTN -THROMBOCYTOPENIA |
|
What are the monitoring parameters of GPIIa/IIIb therapy?
|
-s/sx of bleeding
-baseline: CBC, plt count, SCr -daily: CBC, plt count 2-4 hrs post initiation and daily |
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What are the MP for anticoagulant therapy in UA/NSTEMI?
|
-Hgb/ Hct daily for 3 days
-plts daily -s/sx of bleeding |
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What is the difference in dosing of enoxaparin for STEMI vs. NSTEMI
|
-give supplemental dose of enoxaparin 0.3mg/kg IV bolus in UA/NSTEMI pts that undergo PCI
|
|
How are thrombolytics used in UA/NSTEMI?
How are ACEi/ARBs/ aldosterone antag used in these pts? |
-not used!
-ACEi/ ARBs are used the same -aldosterone antag are not used |
|
Describe the anatomical structure and function of the cardiac conduction system.
|
•Sinus Node= pacemaker of heart (60-100bpm); found in the high right atrium
•Atrioventricular (AV) node (40-60bpm); found in lower right atrium •Ventricular tissue (30-40bpm) oBundles: left divides because left ventricle is larger than the right ventricle (arterial pressure> venous pressure) •Functions to electrically depolarize cells in waves to generate contractions |
|
Explain PQRST.
|
•P=atrial depolarization
•PR interval= time for impulse to travel through AV node •Q=phase 0 •QRS= depolarization time o Na+ blocker will inc QRS •T= phase 3 repolarization •QT= overall ventricular repolarization o Use this calculation to determine if the relative refractory period is prolonged |
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Explain what is happening in the different phases of the cardiac action potential. (include ions)
|
•Phase 0: Depolarization- mediated by movement of Na+ ions into myocytes through fast Na+ channels
•Phase 1: Repolarization-mediated by movement of K+ ions out of myocytes through K+ channels •Phase 2: Repolarization (plateau)- a balance of movement of K+ ions out of myocytes through K+ channels and movement of Na+ and Ca2+ ions into myocytes through slow Na+ and slow Ca2+ channels •Phase 3: Repolarization-movement of K+ ions out of myocytes greatly exceeds movement of Na+ and Ca2+ ions into myocytes |
|
Explain the relationship between the cardiac action potential and the electrocardiogram (ECG).
|
•Q= phase 0
•S=phase 2 (start of plateau) •T hump=extent of phase 3 |
|
What drugs slow the PR interval?
What does this mean? |
-non DHP CCBs
-amiodarone -digoxin -BB PR>0.2 sec = primary AV block |
|
What drugs slow the QRS?
|
-flecainide
-propafenone -Na+ channel blockers |
|
What drugs slow the QT interval?
What does this mean? |
-K+ channel blockers
-QT>0.5 sec = Torsades de Pointe |
|
What is the calculation of a QTc?
|
QTc= QT / (RR)^1/2
|
|
What are the normals values of : PR interval, QRS duration, QT interval, and QTc interval?
|
PR interval: 0.12-0.2 sec
QRS duration: 0.08-0.12 sec QT interval: 0.38-0.46 sec QTc interval: 0.36-0.44 sec |
|
What are the three mechanisms of cardiac arrhythmias?
|
Abnormal impulse formation
-spontaneous impulse generation in normally latent pacemaker tissue (SA node, AV node, His/Purkinje system, specialized atrial fibers) -influenced by cholinergic and sympathetic stimulation Abnormal impulse conduction-Reentry -two pathways for impulse conduction with an area of unidirectional block; one pathway has slowed impulse conduction Both changes in automaticity rate with depolarizations happening where they should not be and reentry |
|
What are the 4 classes of the Vaughan Williams classification system?
|
Some Block Potassium Channels
Class I: Sodium channel blockers Class II: Beta Blockers Class III: Potassium channel blockers Class IV: Calcium channel blockers |
|
Which drugs change automaticity? Which drugs change repolarization? Which drugs change conduction velocity?
|
Automaticity slowing
-Class I drugs: Procainamide, Lidocaine, Flecainide, Propafenone Repolarization/ inc. refractory period -Class III drugs: amiodarone, dofetilide, dronedarone, ibutilide, sotalol -Class IA: procainamide Conduction velocity dec. -Class I drugs: (Flecainide, propafenone>procainamide>lidocaine) |
|
What are examples of supraventricular arrhythmias?
|
-sinus bradycardia
-AV nodal block -sinus tachycardia -atrial fibrillation -paroxysmal supraventricular tachycardia |
|
What are examples of ventricular arrythmias?
|
-ventricular premature depolarizations
-ventricular tachycardia -ventricular fibrillation |
|
Explain sinus bradycardia (features, mechanism, etiologies/ risk factors, sx, and treatment)
|
Features: HR < 60
Mechanism: Decreased automaticity of SA node Etiology: -MI/ischemia -Abnormal sympathetic/parasympathetic tone -Hyperkalemia, hypermagnesemia -Drugs: digoxin, B-blockers, diltiazem, verapamil, amiodarone, dronedarone Symptoms: Hypotension, dizziness, fainting Treatment: -Atropine (AE: tachycardia, urinary retention, blurred vision, dry mouth, mydriasis) -Pacemaker |
|
Explain atrial fibrillation (features, mechanism, etiologies/ risk factors, sx, and treatment)
|
Features:no full atrial contractions
HR 120-180 with irregularly irregular rhythm and absent P waves Mechanism: Abnormal atrial automaticity (via pulmonary vein), re-entry via multiple simultaneous circuits Mortality: Stroke and development of HF Etiology: Hypertension, CAD, HF Valvular heart disease, rheumatic heart disease, hyperthyroidism, post-surgery -Idiopathic -Drugs: sympathomimetics, theophylline, alcohol Symptoms: Palpitations, dizziness, lightheadedness, SOB, angina, hypotension, exacerbations of HF Treatment: -based on type of Afib -goal: HR < 100bpm or reduction by 20% with sx relief -if hemodynamically unstable (SBP<90, HR>150bpm, loss of consciousness)-> DCC immediately |
|
What is the treatment plan for pts with 1st detected episode or persistent Afib?
|
Ventricular rate control
-no HF: CCB or BB -with HF: digoxin or amiodarone Stroke prevention -1st episode: heparin -persistent: warfarin and/or aspirin Conversion to sinus rhythm -<48 hrs, DCC ->48hrs, warfarin x 3 weeks then DCC or heparin IV and TEE to r/o atrial clot, then DCC if DCC unsucessful -no HF: flecainide, propafenone, ibutilide -with HF: amiodarone, dofetilide, ibutilide |
|
What is the treatment plan for pts with paroxysmal or permanent Afib?
|
ventricular rate control
-no HF: CCB or BB, then add digoxin, then only amiodarone -with HF: BB, BB + digoxin, then only amiodarone stroke prevention -warfarin or aspirin maintenance of sinus rhythm -treat disease-induced -with CAD and/or HF: amiodarone, dofetilide, sotalol -no CAD, no HF: propafenone or flecainide, dofetilide, dronedarone, sotalol |
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What is the CHADS2 score?
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shows risk of bleeding
Chronic heart failure 1 pt Hypertension 1 pt Age> or = 75 1 pt Diabetes mellitus 1 pt Stroke or TIA hx 2 pts |
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Explain paroxysmal supraventricular tachycardia (PSVT).
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•Features: HR 120-250
-Regular rhythm -Narrow QRS complex -Spontaneous initiation and termination •Mechanism: Re-entry within AV node (single re-entrant circuit) Other minor mechanisms •Etiology: -Heart disease -Fever, infection -Electrolyte abnormalities -Idiopathic •Symptoms:Palpitations, dizziness, weakness, syncope, angina exacerbation, HF exacerbation Treatment oTerminate PSVT, restore sinus rhythm -Vagal maneuvers (non-PCOL): carotid sinus massage, coughing, Valsalva maneuver -Adenosine -Verapamil -Diltiazem -Digoxin -Esmelol -Propranolol -Metoprolol -Amiodarone oPrevent recurrence -AV nodal radiofrequency catheter ablation (non-PCOL) |
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What is the algorithm for termination of hemodynamically stable PSVT?
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1) vagal maneuvers
2) adenosine (6,12,12) no-HF -diltiazem or verapamil, then BB, digoxin with HF -digoxin, then amiodarone |
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Explain ventricular premature depolarizations (VPD)/ ventricular premature contractions (VPC).
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•Features: Ectopic beats from ventricular muscle fibers
-Wide QRS complexes -Variable frequency (that increases with age) •Types oSimple: Single beats oComplex: Pairs/couplets -Every second beat/ bigeminy -Every third beat/ trigeminy -Every fourth beat/ quadrigeminy •Mechanism: increased automaticity of ventricular muscle fibers •Etiology: CAD, MI -Can occur in normal individuals -Drugs: sympathomimetics, antiarrhythmics, TCAs -Anemia -Hypoxia -Cardiac surgery •Symptoms: Often asymptomatic Palpitations, syncope •Treatment:Asymptomatic VPDs SHOULD NOT BE TREATED -Symptomatic VPDs: PO B-blockers, PO amiodarone (2nd line) |
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Explain ventricular tachycardia.
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•Features: HR 100-250
-Regular rhythm -Wide QRS complexes -Series of consecutive VPDs •Types oNon-sustained: 3 or more consecutive VPDs, lasting < 30 seconds, terminating spontaneously o Sustained: VT lasting longer than 30 seconds •Mechanism: Increased automaticity in ventricular tissue Re-entry within ventricles •Etiology: CAD, MI, HF (major), Hypokalemia, hypomagnesemia •Symptoms: May be asymptomatic (non-sustained) Hypotension, palpitations, syncope •Implication: May progress to ventricular fibrillation and then death; sudden cardiac death Treatment oTerminate VT/restore sinus rhythm -Lidocaine -Procainamide -Amiodarone oPrevent recurrence of VT -ICD -Amiodarone -Sotalol oReduce risk of sudden cardiac death: ICD |
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What is the algorithm for termination of hemodynamically stable VT?
What is used for prevention of recurrence and sudden cardiac death? |
With MI
-lidocaine -then procainamide -then amiodarone No MI -procainamide -then amiodarone Prevention: -ICD -amiodarone -sotalol |
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Explain ventricular fibrillation.
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•Features: Irregular, disorganized ventricular rhythm
-No recognizable QRS complexes •Etiology: MI, HF, cardiomyopathy, CAD •Symptoms:Syndrome of sudden cardiac death (patient collapses, no HR, no BP) •Treatment: Defibrillation! -Drugs to facilitate:epinephrine or Vasopressin, then Amiodarone, then Lidocaine then sodium bicarb |