Angina And Acs

Front 1

Angina pectoris

Back 1

-deep, poorly localized chest or arm discomfort
-assoc with physical exertion or emotional stress
-relieved promptly with rest and/or use of sublingual nitroglycerin

Front 2

Drugs used for stable angina

Back 2

-Nitrates
-Betat antagonists
-Ca channel blockers
-goals: prevent MI and death, alleviate symptoms, freq of attacks and improve QOL

Front 3

Nitrates

Back 3

-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)

Front 4

Nitrates AE

Back 4

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

Front 5

Bblockers and chronic angina

Back 5

-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

Front 6

Ca channel blockers

Back 6

-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

Front 7

role of Ca channel blockers

Back 7

-Variant or Prinzmetals angina
-good for pts with CI, intolerance of B-blockers
-effect for chronic prophylaxis

Front 8

Ca channel blockers AE/CI

Back 8

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

Front 9

Ranolazine

Back 9

-new dug for chronic angina
-MOA: modulator of metabolic pathways in myocardial tissues
-AE: dizzy, HA, N, watch EKG (inc QT interval)

Front 10

Unstable angina

Back 10

-new onset angina
-more frequent and longer lasting
-may respond less to rest and nitroglycerin
-rest angina (severe)
-tx similar to NSTEMI

Front 11

NSTEMI

Back 11

-ECG does not show ST segment elevation but elevated cardiac markers necessary for dx
-therapy is same as AMI except no thrombolysis

Front 12

Cause of ACS

Back 12

-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

Front 13

unstable angina/NSTEMI

Back 13

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

Front 14

Morphine sulfate

Back 14

-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

Front 15

Nitrates

Back 15

-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

Front 16

Beta-blockers for UA/NSTEMI

Back 16

-competitively block the effects of catecholamines on cell membrane beta-receptors
-should be started ASAP in the absence of CI

Front 17

ACE inhibitors for UA/NSTEMI

Back 17

-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

Front 18

CI and precautions with B-blockers

Back 18

-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

Front 19

Antiplatelet therapy

Back 19

-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

Front 20

PLavix (clopidogrel)

Back 20

-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

Front 21

Glycoprotein II/IIIA inhibitors

Back 21

-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

Front 22

Anticoagulants

Back 22

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)

Front 23

Acute MI- ST elevation MI

Back 23

-chest pain most common complaint
-heartburn, anxiety, SOB
-Q waves, St elevation, ST depression, T wave inversions

Front 24

Therapy of AMI

Back 24

-MONA
-B-blocker
-reperfusion ASAP!- PCI, fibrinolysis (tPA)re
-unfractionated heparin
-ACEI

Front 25

reperfusion therapy for STEMI

Back 25

-hospital
-PCI capable --> treat with PCI within 90 min
-Non PCI capable --> evaluate/tx with fibrinolysis within 30 min of presentation

Front 26

Fibrinolytic therapy

Back 26

-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

Front 27

Fibrinolysis

Back 27

-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!!

Front 28

fibrinolytics absolute CI

Back 28

1. previous hemorrhagic stroke, other strokes or CVAs within 1 yr
2. known intracranial neoplasm
3. active internal bleeding
4. suspected aortic dissection

Front 29

fibronolytic therapy- evaluation of outcome

Back 29

-ECG --> ST elevation should normalize
-relief of chest pain 90min-2hrs
-onset of ventricular arrhythmias (IV lidocaine or cardioversion if necessary)

Front 30

PCI

Back 30

-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

Front 31

GP IIB/ IIIa inhibitors role in STEMI

Back 31

-give abciximab IV ASAP before PCI with our without stenting
-lower mortality, higher patency, better LVEF
-monitor for bleeding

Front 32

treatment of complicated MI- the basics

Back 32

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

Front 33

Cardiogenic shock

Back 33

-pump failure usually due to extensive LV infarct: hypotension, sings of poor perfusion, pulmonary edema
-need immediate revascularization usually with CABG
-medical stabilization

Front 34

treatment of complicated MI- the basics

Back 34

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

Front 35

Vasopressors

Back 35

-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

Front 36

Cardiogenic shock

Back 36

-pump failure usually due to extensive LV infarct: hypotension, sings of poor perfusion, pulmonary edema
-need immediate revascularization usually with CABG
-medical stabilization

Front 37

Inotropics

Back 37

-stimulate the heart to pump
-Dobutamine: B1 agonist used a IV infusion to inc CO
-onset is rapid with short half life requiring infusion

Front 38

Vasopressors

Back 38

-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

Front 39

major cause of MI-related mortality

Back 39

-arrhythmia
-VF and pulseless VT --> cardiovert--> amniodarone
-sustained polymorphic V-tach
-sustained monomorphic VT w/symptoms
-sustained VT without sx --> amniodarone

Front 40

Inotropics

Back 40

-stimulate the heart to pump
-Dobutamine: B1 agonist used a IV infusion to inc CO
-onset is rapid with short half life requiring infusion

Front 41

major cause of MI-related mortality

Back 41

-arrhythmia
-VF and pulseless VT --> cardiovert--> amniodarone
-sustained polymorphic V-tach
-sustained monomorphic VT w/symptoms
-sustained VT without sx --> amniodarone