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Cardio MT2 > MT2_9_Chronic Stable Angina > Flashcards

MT2_9_Chronic Stable Angina Flashcards

1
Q

What is significant CAD defined as?

A
  • CAD greater than or equal to 70% diameter stenosis of one major epicardial artery
  • greater or equal to 50% diameter stenosis from left main coronary artery
  • vasospasm, uncontrolled HTN, valvular heart disease, hypertrophic cardiomyopathy
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2
Q

Define stable angina

A
  • predictable, not changing in frequency, intensity, or duration
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3
Q

Define unstable angina

A
  • presents as rest
  • new onset (less than 2 months)
  • severe pain that is more frequent, longer duration, lower threshold
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4
Q

What are the considerations for high risk unstable angina?

A
  • more than 20 min
  • pulmonary edema
  • hypotension
  • angina at rest w ST elevation
  • worsening MR murmur
  • s3, new worsening rales
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5
Q

Lifestyle modifications for CAD?

A
  • reduce cholesterol
  • reduce saturated fat
  • increase unsaturated fat
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6
Q

PE requirement
Lipid Management
Diabetes management

A
  • moderate intensity 30-60min 5d/week, or vigorous for 20min, 3d/week
  • lipid management goal LDL less than 70, or high intensity statin
  • diabetes: HbA1C less than 7
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7
Q

Explain how NSAIDs and Aspirin work

A
  • at low doses, aspirin inhibits cox-1, inhibiting clots from forming and sparing PG anti-thrombotic properties. The higher the dose, the more thrombotic patient will get.
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8
Q

Safest COX2 inhibitor?

Pain management strategy in CVD?

A
  • avoid, but naproxen is ok

- apap, ASA, opioids, then non COX2 selective NSAIDs

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9
Q

What is the general approach to treating CSA?

A
    1. balance O2 supply and demand (increase supply, decrease demand)
    1. slow progression of the disease
    1. provide prophylaxis against thrombus formation

therefore, use

  1. an antiplatelet
  2. abtianginal/antiischemic
  3. disease modifying therapy
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10
Q

Common anti platelets used?

A
  • aspirin
  • clopidogrel
  • prasugrel
  • ticlopidine
  • ticagrelor, cangrelor, voraxapar
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11
Q

What to monitor for when patient is on aspirin?

A
  • CBC
  • Platelets
  • Bleeding (GI)
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12
Q

When is clopidogrel most effective regarding use?

A
  • additive benefit when used in combo with aspirin for UA/NSTEMI or post-PCI
  • only used as an alternative to ASA for monotherapy in patients with CAD
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13
Q

Monitoring for clopidogrel?

A
  • CBC
  • Bleeding
  • DDI
  • DC 5 days prior surgery
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14
Q

So what is the recommendation for clopidogrel use?

A
  • when ASA is absolutely CI (75mg daily)
  • combo with aspirin post PCI, refractory anginal issues despite revascularization attempts
  • anginal issues, not a candidate for revasc.
  • ACS
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15
Q

Prasugrel efficacy/use?

Monitor

Dose

CI

DC

BBW

A
  • ONLY inpatients with ACS + PCI.
  • more effective than clopidogrel, but higher risk of bleeding
  • monitor: bleeding, CBC, plt
  • dose 60mg loading, then 10mgQD
  • CI: pts with a hx of stroke/TIA
  • DC 7-10 days before surgery
  • BBW: bleeding
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16
Q

Why is ticlopidine no longer used?

A
  • agranulocytosis ,plt, bleeding risk
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17
Q

Is ticagrelor a prodrug?

What does it do? reduces the rate of ____events and vascular death in ____ vs. clopidogrel, with more ____

A

no

  • thrombotic CV events
  • ACS
  • higher major bleeding
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18
Q 
For ticagrelor, avoid aspirin
DC
ADR
DDI
AVOID
Pregnancy 
Dose
A
  • doses higher than 100
  • 5 days before surgery
  • bleeding/dyspnea
  • DDI w 3A4/5 substrate
  • avoid in severe hepatic impairment
  • category C
  • 180mg PO load, 90 PO BID
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19
Q

Cangrelor monitoring and ADRs

Dose

A
  • monitor for bleeding, do not give with clopidogrel or prasugrel
  • preg C

NOT FOR CSA

30mcg/kg IV bolus, then 4

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20
Q 
Vorapaxar
MOA
Indication
CI
DDI
A
  • par1 receptor antagoinst
  • oral, competitive reversible binding
  • reduce the risk of heart attacks, stroke, death, in patients with PREVIOUS MI or PAD
  • CI in CVA or TIA
  • DDI: 3A4 inhibitors and inducers
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21
Q

What are the main drugs NOT recommended in CSA? (3)

A
  • ASA + clopidogrel + warfarin (only for CAD), or in patients who had a PCI with a need for warfarin
  • dipyridamole (increases induced ischemia)

ticolpidine

22
Q

CSA anti platelet recommendations?

A
  • Aspirin
  • Clopidogrel, only when ASA is CI
  • clopidogrel + ASA in refractory ischemia or post PCI
  • ticagrelor (only if started on when pt had ACS)
  • vorapaxar for refractory patients
23
Q

What is the main role of antianginals? Name them

A

Increasing supply

- BB, CCB, Nitrates, Ranolazine

24
Q

Non cardioselective BBs

A
  • ptns (propanolol, timolol nadolol, sotalol)
25
Q

Cardioselctive BBs

A

maa

metoprolol, atenolol, acebutolol

26
Q

ISA BBs

A

acebutolol, pindolol, oxyprenolol

27
Q

Lipophilicity of BBs

A

propanolol>metoprolol>atenolol

28
Q

How do BBs work?

A
  • decrease demand by decreasing HR and contractility
  • increase supply by increasing diastolic time and decreasing after load
  • blocks sympathetic effects
29
Q

What to monitor when pt is on a BB?

A
  • CP
  • HR (goal is 55-60) to lower the MVO2
  • BP due to rebound HTN
  • EKG
  • Bronchospasm (if pt is on a steroid and a LABA) no BB! not even a cardioselevtive one!
  • cocaine alpha 1 is vasoconstriction, avoid BB because it inhibits only beta, leaving alpha
30
Q

Should CAD patients get a BB?

Depression

Renal issues

When is a BB CI?

A
  • yes, w/wo prior hx of MI
  • all patients w IHD should get a BB
  • no propanolol
  • no atenolol
  • acute ischemia caused by cocaine/stimulant OD
31
Q

For CCBs, what do we monitor for?

A
  • HR
  • BP
  • DDI (d and v)
  • peripheral edema
  • constipation
  • HA, flushing, dizziness
32
Q

For nonDHP CCB, what to look out for? CI?

A
  • bradycardia
  • heart block
  • do not use if LVEF is less than 40%
  • CI in heart failure and severe AV block
33
Q

For DHP CCB, look out for…

A
  • reflex tachycardia

- peripheral edema

34
Q

Sp, when are CCB indicated?

A
  • substitute for BB or add w BB if tx is unsuccessful with a BB, no difference if DHP or NDHP
  • avoid short acting DHP (nifedipine)
35
Q

What is the DOC for ischemia secondary to vasospasm. (prinzmetal) or due to cocaine/stimulant use?

A

CCBs!

36
Q

What is the MOA of nitroglycerin?

A
  • decrease in demand by decreasing preload and/or after load, decreasing wall stress
  • coronary artery vasodilatation, increase supply
37
Q

Compared to BB and CCB, do nitrates affect long term outcomes?

A
  • reduce in anginal frequency, and increase in exercise tolerance
  • no effect on long term patient outcomes though
38
Q

What to monitor for nitro?

A
  • BP
  • HR
  • Headache
  • nitrate free interval
39
Q

What is the recommendation for immediate relief of angina? regarding nTG

A
  • spray
  • substitute for BB or add on
  • SL Nitro 0.4mg q5min once, then ER if doesn’t work
40
Q

How does ranolazone work?

A
  • inhibits late sodium from going into the cell, to decreses contractility, HR, decreasing demand.
  • is preferred bc it has no effects on HR and BP, so pt with a low BP may use it
41
Q

What to monitor for ranolazine?

Cyps

PGP

A
  • ADR: constpiation, NV, headache, QTc prolongation
  • caution in cyp3A4 inhibitors with will increase ranolazine levels (dilt,verap, azaleas, macrolides)
  • pgp substrates like digox will increase ranolazine levels
  • avoid use with other meds that cause QTc prolongation (antiarrhythmics)
42
Q

When to recommend ranolazine? Dose?

A
  • adjunct therapy for STABLE patients with REFRACTORY angina OR as monotherapy
  • dose initially 500mg PO2x, then 1000mg 2x
43
Q

What meds are used to modify the artherosclerotic process?

A

ACE, ARBs, lipid lowering therapy

44
Q

What is the MOA of ACE inhibitors?

A
  • counteracts effects of vasoconstriction, fluid retention, cardiac remodeling, inhibiting ACEI or blocking the AT1 receptor
  • increases bradykinin (vasodilatory)
45
Q

What have ACEI been shown to improve?

A
  • long term outcomes post MI
46
Q

When should patients recieve an ACE?

A
  • stable CAD + DM and/or LV dysfunction

including those w HTN,DM, CKD

47
Q

What to monitor for in ACE/ARB?

A
  • BP
  • Renal fx
  • serum K
  • angioedema
    cough, dysguesia
48
Q

When should an ACE be initiated?

A
  • all patents post MI, continued indefinitely

- early in stable high risk patient

49
Q

When is an ACE inhibited?

A
  • AKI (significant increasing SCr trend)

- severe chronic kidney disease (SCr greater than 3.0)

50
Q

What are the lipid goals in patient with CAD?

A
  • LDL less than70 (high risk)
  • TG less than 150
    HDL greater than 40(m), 50(w)
  • TC less than 200e
  • high-intensity statin is recommended in ALL CAD PATIETNS regardless of LDL
51
Q

What to monitor for a statin?

A
  • LFT
  • Myopathy
  • CK
  • DDI

Cardio MT2 (12 decks)

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