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41 Cards in this Set
- Front
- Back
Angina pectoris
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-deep, poorly localized chest or arm discomfort
-assoc with physical exertion or emotional stress -relieved promptly with rest and/or use of sublingual nitroglycerin |
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Drugs used for stable angina
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-Nitrates
-Betat antagonists -Ca channel blockers -goals: prevent MI and death, alleviate symptoms, freq of attacks and improve QOL |
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Nitrates
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-MOA: vasodilation --> dec O2 demand; dilation of coronary arteries
-for acute attacks and prevention of attacks in conjunction with bblockers -IV, SL, buccal, spray-rapid acting -Isosorbide dinitrate (acute attack and prophlaxis) -Isosorbide mononitrate** -most commonly used long acting (prophylaxis) |
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Nitrates AE
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1. flushing
2. HA 3. postural hypotension 4. Tolerance** -store in tightly closed glass container in cool place away from light -6mo shelf life for tablets -DI: Viagra, Levitra, Cialis --> can lead to hypotension -CI: hypertropic cardiomyopathy |
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Bblockers and chronic angina
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-MOA: reduce O2 demand by reducing contractility, HR and BP
-often preferred for chronic prophylaxis -start in pts with ACS, MI and left vent dysfunction -AE: bradycardia, heart failure, bronchospasm, peripheral vasoconstriction |
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Ca channel blockers
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-MOA: vasodilation of systemic arterioles and coronary arteries in myocardial contractility, dec in conduction velocity of SA and AV
-Verapamil and diltiazem --> less peripheral vasodilation, greater cardiac effects including reduced heat rate -Dihydropyridines- peripheral vasodilation |
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role of Ca channel blockers
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-Variant or Prinzmetals angina
-good for pts with CI, intolerance of B-blockers -effect for chronic prophylaxis |
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Ca channel blockers AE/CI
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1. Diltiazem and verapamil not in severe heart failure or heart blocks
2. constipation 3. HR elevation with nifedipine and dihydropyridines 4. DO NOT USE short acting nifedipine as it may precipitate MI |
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Ranolazine
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-new dug for chronic angina
-MOA: modulator of metabolic pathways in myocardial tissues -AE: dizzy, HA, N, watch EKG (inc QT interval) |
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Unstable angina
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-new onset angina
-more frequent and longer lasting -may respond less to rest and nitroglycerin -rest angina (severe) -tx similar to NSTEMI |
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NSTEMI
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-ECG does not show ST segment elevation but elevated cardiac markers necessary for dx
-therapy is same as AMI except no thrombolysis |
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Cause of ACS
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-rupture of atherosclerotic plaque --> plt activation --> clotting cascade --> arterial thrombus
-pharmacotherapy: 1. antiplts- aspirin, plavix, glycoproteins IIBIIIAs 2. anticoagulants 3. fibrinolytics for STEMI 4. traditional therapies |
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unstable angina/NSTEMI
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M- morphine sulfate (used for pts whose sx not relieved after 3 serial sublingual NTG tablets)
O- oxygen N- nitrates- reduces myocardial O2 demand and improves supply A- aspirin |
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Morphine sulfate
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-analgesic of choice after 3 SL nitro tabs fails to alleviate ischemic pain
-reduces sympathetic effects on heart -venodilation, arterial dilation, reduce work of breathing and good for pulmonary edema -AE: hypotension and respiratory depression |
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Nitrates
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-SL then IV and increase for pain relief
-reduce preload and after load, reduce O2 demand, dilate coronary arteries -AE: hypotension so do not give to pts with SBP <90 |
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Beta-blockers for UA/NSTEMI
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-competitively block the effects of catecholamines on cell membrane beta-receptors
-should be started ASAP in the absence of CI |
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ACE inhibitors for UA/NSTEMI
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-shown to reduce mortality rates in pts
-HTN or LV dysfunction persists after nitrates and BB -should be administered orally within the first 24h to UA/NSTEMI pts with pulmonary congestions or LV ejection fraction < or - to .40 |
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CI and precautions with B-blockers
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-pts with marked first-degree AV blocks
-any form of second or third degree AV block in the absence of functioning pacemaker -hx of asthma -severe LV dysfunction with CHF |
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Antiplatelet therapy
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-Aspirin
-in pts with UA/NSTEMI -chewable preferred (gets into blood stream quicker) -reduction in mortality -continue indefinitely -CI: allergy, active bleeding, hemophilia, untx HTN, active peptic ulcer |
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PLavix (clopidogrel)
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-rapid onset of action
-MOA: antiplt -add to ASA since both inhibit plts in different ways in pts with planned percutaneous coronary intervantion -plavix continued for at least 1 month with metal stents and several months with drug implanted stents |
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Glycoprotein II/IIIA inhibitors
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-antiplt
-Abciximab (reopro), tirofiban (aggrestat) -block aggregation -used with ASA and heparin for pts with UZ/NSTEMI and AMI -monitor blood heme and plt counts, surveillance of bleeding -CI: renal failure |
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Anticoagulants
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1. Unfractionated heparin - for UA/NSTEMI IV use; target aPTT is 1.5-2.4 times normal control
-cant use it that long 2. Low molecular wt heparins- Enoxaparin- SQ 3. Bivalirudin (direct thrombin inhibitor) 4. Fondaparinux (factor Xa inhibitor) |
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Acute MI- ST elevation MI
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-chest pain most common complaint
-heartburn, anxiety, SOB -Q waves, St elevation, ST depression, T wave inversions |
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Therapy of AMI
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-MONA
-B-blocker -reperfusion ASAP!- PCI, fibrinolysis (tPA)re -unfractionated heparin -ACEI |
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reperfusion therapy for STEMI
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-hospital
-PCI capable --> treat with PCI within 90 min -Non PCI capable --> evaluate/tx with fibrinolysis within 30 min of presentation |
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Fibrinolytic therapy
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-up to 50% reduction in mortality
-indications: STEMI presentation w/in 24hrs of CP onset; ases for C/I and start within 30 min of hospital arrival -types: tPA, reteplase, tenecteplase (IV) -given with UFI, enoxaprin or fondaparinux -if given within first 2 hrs may abort MI |
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Fibrinolysis
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-eligibility: ST elevation, present w/in 12 hrs of pain; consider in those presenting early to a facility without expert PCI; asses CI ASAP (door to needle <30 min)
-complications: major bleeding, ICH -watch for changes in MS, focal neuro deficits, HA, papilledema!! |
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fibrinolytics absolute CI
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1. previous hemorrhagic stroke, other strokes or CVAs within 1 yr
2. known intracranial neoplasm 3. active internal bleeding 4. suspected aortic dissection |
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fibronolytic therapy- evaluation of outcome
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-ECG --> ST elevation should normalize
-relief of chest pain 90min-2hrs -onset of ventricular arrhythmias (IV lidocaine or cardioversion if necessary) |
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PCI
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-preferred over finbrinolysis
-can undergo within 12 hrs of sx onset -give with ASA, parenteral anticoag and GP IIB, IIIA inhibito -lower short term mortality -less nonfatal reinfarction and recurrent ischemia -less hemorrhagic strokes |
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GP IIB/ IIIa inhibitors role in STEMI
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-give abciximab IV ASAP before PCI with our without stenting
-lower mortality, higher patency, better LVEF -monitor for bleeding |
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treatment of complicated MI- the basics
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1. hypotension-IV fluids, vasopressors such as DA
2. cardiogenic shock 3. low output state- order echo, start dobutamine 4. pulmonary edema: O2, morphine, ACEI, nitrates, loop diuretics 5. Arrhythmias |
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Cardiogenic shock
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-pump failure usually due to extensive LV infarct: hypotension, sings of poor perfusion, pulmonary edema
-need immediate revascularization usually with CABG -medical stabilization |
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treatment of complicated MI- the basics
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1. hypotension-IV fluids, vasopressors such as DA
2. cardiogenic shock 3. low output state- order echo, start dobutamine 4. pulmonary edema: O2, morphine, ACEI, nitrates, loop diuretics 5. Arrhythmias |
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Vasopressors
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-sed to INCREASE PVR and BP
-Dopamine (IV): acts at low doses to dilate renal and coronary arteries; higher doses stimulate alpha1 receptors causing vasoconstriction AND beta 1 receptors causing inc contractility -NE: potent vasoconstrictor for severe hypotension |
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Cardiogenic shock
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-pump failure usually due to extensive LV infarct: hypotension, sings of poor perfusion, pulmonary edema
-need immediate revascularization usually with CABG -medical stabilization |
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Inotropics
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-stimulate the heart to pump
-Dobutamine: B1 agonist used a IV infusion to inc CO -onset is rapid with short half life requiring infusion |
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Vasopressors
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-sed to INCREASE PVR and BP
-Dopamine (IV): acts at low doses to dilate renal and coronary arteries; higher doses stimulate alpha1 receptors causing vasoconstriction AND beta 1 receptors causing inc contractility -NE: potent vasoconstrictor for severe hypotension |
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major cause of MI-related mortality
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-arrhythmia
-VF and pulseless VT --> cardiovert--> amniodarone -sustained polymorphic V-tach -sustained monomorphic VT w/symptoms -sustained VT without sx --> amniodarone |
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Inotropics
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-stimulate the heart to pump
-Dobutamine: B1 agonist used a IV infusion to inc CO -onset is rapid with short half life requiring infusion |
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major cause of MI-related mortality
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-arrhythmia
-VF and pulseless VT --> cardiovert--> amniodarone -sustained polymorphic V-tach -sustained monomorphic VT w/symptoms -sustained VT without sx --> amniodarone |