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int med exam 0828 > cardiology 2: CAD/Angina > Flashcards

cardiology 2: CAD/Angina Flashcards

1
Q

what are the 3 steps in evaluation of patient with chest pain?

A
  1. determine the probability of CAD
  2. noninvasive testing for diagnosis and risk stratification
  3. additional workup based on estimated risk
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2
Q

what determines to need to go through to further CAD risk stratification

A
  • medium to high pretest probability
  • low probability does not need to be tested
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3
Q

for which patient with chronic stable angina do you do an echocardiogram?

A

assess LV systolic dysfunction only in patients with:

  • prior MI
  • pathological Q waves
  • heart failure
  • arrhythmias
  • heart murmur
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4
Q

In working up a patient with chronic stable angina, what do you do for low/intermediate/high risk patient?

A
  • Low risk - medical management
  • intermediate-risk - stress imaging/further tests
  • high risk - coronary angiogram
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5
Q

what is the treatment for chronic stable angina to prevent MI and death?

A
  • antiplatelet therapy: aspirin/plavix
  • high dose statin
  • beta blockers (if LVEF<40%)
  • Ace inhibitors (if LVEF<40%, DM, HTN, CKD)
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6
Q

what is the medical therapy treatment for symptoms relief for chronic stable angina?

A
  • beta-blocker as initial therapy
  • CCB
  • Ranexa
  • Nitrates
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7
Q

what are the guidelines for aspirin in women for cardiovascular disease prevention?

A

do not use aspirin in healthy women<65 for primary prevention of MI.

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8
Q

what population is more at risk for MI without chest pain or atypical chest pain?

A
  • age>75
  • diabetics
  • women
  • those with prior CAD
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9
Q

what are inferior MIs associated with?

A
  • mitral regurgitation due to papillary muscle dysfunction
  • VSD (anterior and inferior)
  • stable arrhythmias: junctional escape/mobitz 1
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10
Q

when do troponins first elevate and peak? Is it sensitive or specific?

A
  • elevate first at 4 hours
  • peak at 44 hours
  • elevated 10-14 days
  • It is sensitive, not specific
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11
Q

Troponins can be elevated in which conditions?

A
  • chronic renal failure
  • myopericarditis
  • HF
  • PE
  • sepsis
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12
Q

when does CKMB first elevate, peak, and return to normal? sensitive or specific?

A
  • initial elevation: 3-12 hour
  • Peak in 24 hours
  • Return to normal in 2-3 days
  • specific test
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13
Q

what are the prehospital guidelines for chest pain?

A
  • ASA
  • nitroglycerin provided no PDE
  • ECG
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14
Q

what are the high risk features of ACS?

A
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15
Q

what are the 3 groups after evaluation for ACS?

A
  • noncardiac chest pain
  • possible ACS
  • definitive ACS
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16
Q

what do you do for possible ACS?

A
  • observe at least 12 hours from symptoms onset
  • 2 sets of cardiac markers/ekg
  • stress study/LV function
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17
Q

what are the general anti-ischemic measures for all patients with ACS?

A
  • continuous ECG
  • aspirin
  • NTG
  • morphine
  • oral beta-blocker
  • ACE/ARB
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18
Q

which parenteral anticoagulants is preferred if CABG?

A

unfractioned heparin if CABG

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19
Q

when do you give fibrinolytic therapy for ACS? when do you not give?

A
  • Do not give for UA/NSTEMI because it increases mortality
  • Give fibrinolytic therapy for ACS patient with STEMI or new LBB if immediate PCI is not available.
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20
Q

what is the general acute ischemia pathway for UA/NSTEMI?

A
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21
Q

what is the possible ACS algorithim?

A
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22
Q

what is the definitieve ACS algorithim?

A
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23
Q

when do patients chosen for early conservative therapy need immediate angiography?

A
  • if they have recurrent symptoms, ischemia, heart failure, serious arrhythmia .
  • EF<40%
  • stress test reveals not low risk
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24
Q

what is early conservative treatment for UA/NSTEMI?

A
  • anticoagulant for 48 hours
  • dual antiplatelet therapy (ASA +cllopridogrel, ticagrelor)
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25
Q

what is long term antiplatelet therapy after UA/NSTEMI WITHOUT stent?

A

ASA + plavix/ticagrelor x 1 month to 1 year

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26
Q

what is long term antiplatelet therapy after UA/NSTEMI with BMS?

A
  • ASA 162-325mg/dl x 1 month then 75-162mg/d for life
  • clopridogrel, prasugrel, or ticagrelor x 1 month to 1 year
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27
Q

what is long term antiplatelet therapy after UA/NSTEMI with a DES?

A
  • ASA 162-325mg/d for 3-6 months, then 75-162 for life
  • clopridogrel, prasugrel or ticagelor for at least 1 year.
  • Consider continuing for longer than 1 year.
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28
Q

what agents do you use for patients with cocaine and methamphetamine users with ST elevation?

A
  • give nitro, CCB, and benzodiazepines
  • DO NOT give beta blocker
  • If ST-segments elevated, and no immediate improvement with treatment, proceed with angiogram/fibrinolytics
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29
Q

what do you give for STEMI or new LBBB MI?

A
  • aspirin, beta blocker, nitrate prn
  • UFH, enoxaparin, or bivalirudin
  • give clopridogrel, prasugrel, or tiacgelor
  • abciximab (GP2b/3a) only if immediate PCI
  • PCI/fibrinolytic therapy
  • PCI should be done within 12 hours of chest pain onset and within 90 min of arrival to ED.
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30
Q

what the reperfusion therapies you consider for those with STEMI/new LBBB?

A
  • PCI or fibrinolytic therapy
  • PCI preferred for patients with high bleeding risk, inability to comply with DAPT or anticipated invasive/surgical procedures within the year.
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31
Q

what are the absolute contraindications to fibrinolytic therapy?

A
  • previous hemorrhaigc stroke or CVA within 1 year
  • intracranial neoplasm
  • active internal bleeding
  • suspected aortic dissection
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32
Q

what are the relative contraindications for fibrinolytic therapy?

A
  • persistent BP>180/110
  • remote non-hemorrhagic stroke>1 year
  • concurrent use of anticoagulants with INR 2-3; bleeding diathesis
  • recent 2-4 weeks surgery
  • previous exposure to fibrinolytic
  • pregnancy
  • active peptic ulcer
  • noncompressible vascular puncture
  • advanced age
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33
Q

If urgent CABG planned, what should be held/started?

A
  • aspirin held
  • Statin continued
  • short acting (eptifabitide)GP2b/3A discontinued at least 2-4 hours
  • abciximab discontinued at least 12 hours before CABG
  • start oral beta blocker within 24 hours if no signs of HF, AV blocks, asthma
34
Q

what is the primary cause of in-hospital death from STMEI?

A

LV dysfunction post MI

35
Q

what frequently accompanies right ventricular infarction?

A
  • accompanies inferior MI
  • occlusion of proximal right coronary artery
    *
36
Q

what clinical triad to you see in inferior MI with RVI?

A
  • triad of hypotension, clear lung fields, elevated JVP
  • kussmaul sign frequently present (paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration.)
37
Q

what do you see on EKG and right heart cath for RVI?

A
  • ST elevation in V1 and ST elevation in lead 3 > lead 2.
  • STEMI in V3R-V7R
  • Elevated RAP pressure of >10 with decreased PCWP and CO
38
Q

how does the management of RVI compare to LVI?

A
  • avoid nitrates and preload reducing agents
  • FLuid support is essential
  • inotropic support typically with dobutamine
39
Q

what is the treatment of Afib with hemodynamic instability?

A

emergent treatment with DC synchronized cardioversion.

40
Q

what is the treatment for sustained VT with a pulse accompanied by hemodynamic instability?

A

DC synchronized cardioversion

41
Q

what ist eh treatment VF and pulseless VT?

A

defibrillation (DC unsynchronized cardioversion)

42
Q

what is the treatment of sustained VT not associated with hemodynamic instability?

A
  • amiodarone
  • correct any potassium or magnesium deficiencies
  • routine prophylatic use of lidocaine to prevent VT is no longer recommended.
43
Q

which patients with VT after MI get DC cardioversion?

A

VF, pulseless VT, VT with pulse and hemodynamic instability

44
Q

what are the indications for temporary pacing?

A
  • symptomatic bradyarrhythmias unresponsive to medical treatment
  • asystole or sinus arrest
  • Mobitz type 2/3rd degree AV block
45
Q

why is bradycardia and AV block more common with inferior MIs than anterior MIs?

A
  • increased vagal tone and AV nodal ischemia with inferior MIs.
  • AV block with anterior MI implies large amount of destruction of IV septum and frequently requires permanent pacing.
46
Q

who requires ICD?

A
  • those with develop sustained VT/VF >48 hours post - STEMI with LVEF is typically re-evaluated 40 days following revascularization
  • ICD indicated if there are baseline episodes of VT.
47
Q

what increases HDL?

A
  • exercise
  • estrogens
  • niacin
  • EtoH
48
Q

what decreases HDL?

A
  • smoking
  • androgens
49
Q

what are the 4 statin benefit groups?

A
  1. clinical ASCVD
  2. LDL>190
  3. age 40-75, with LDL 70-189
  4. age 40-75 with LDL 70-189 with an estimated 10-year ASCVD risk>7.5%
50
Q

what groups does CABG improve symptoms and survival?

A
  • left-main
  • left-main equivalent (2 vessel disease with 1 vessel being proximal LAD)
  • 3 major CAD
  • multivessel CAD or proximal LAD with LV dysfunction
  • complex 3 vessel CAD
  • multivessel CAD with DM
51
Q

what groups benefit with CABG for survival?

A
  1. 3 vessel disease with significant LV dysfunction
  2. left-main or left main equivalent disease
  3. diabetes
52
Q

with saphenous vein bypass, what percentage of veins occluded in 10 years? how about internal mammary grats?

A
  • Vein has 5 words, 50% chance open in 10 years
  • LIM-artery has 9 words, 90% open in 10 years
  • diabetics do better with mammary grafts
53
Q

name 3 drugs used with drug eluding stents (the drug in the stent)?

A

sirolimus, paclitaxel and everolimus

54
Q

how do you calculate LDL?

A

LDL = TC - HDL - 1/5 of TGL

55
Q

who should receive a high-intensity statin regardless of levels?

A

all patients with CAD regardless of lipid levels

56
Q

how do you define a high-intensity vs medium intensity statin?

A
  • high-intensity statin lower LDL cholesterol at least 50% on average
  • medium intensity statin lower LDL cholesterol by at least 30-50% on average
57
Q

what are the two major causes of PAD?

A

diabetes (5x) and smoking (2x)

58
Q

what is buerger’s disease?

A

atherosclerosis in typically smoking males<30 years old involving medium and small arteries.

59
Q

how would you differentiate vascular claudication from lumbar spinal stenosis?

A
  • lumbar spinal stenosis is caused by pseudoclaudication, relieved by sitting down and flexing the spine but not by standing still. Exacerbated by anything that extends the spine.
  • Vascular claudication is relieved by sitting down or standing still.
60
Q

what antiplatelet therapy is recommended in PAD?

A

aspirin or plavix.

61
Q

what do you need to watch out for when prescribiling cilostazol? MOA?

A
  • phosphodiesterase inhibitor that increase cAMP in platelets resulting in reversible inhibition of platelet aggregation.
  • use only if LV function normal as patients with class 3/4 have increased mortality with any phosphodiesterase inhibitor.
62
Q

what is primary raynaud’s phenomenon? tx?

A

constriction of small arteries and arterioles when cold leading to acryocyanosis.

Associated with livedo reticularis

tx with CCB

biofeedback/nitro if CCB not effective

63
Q

where does atherosclerosis most commonly occur in the neck?

A

within the common carotid bifurcation and proximal internal carotid artery

64
Q

people with atherosclerosis carotid artery disease are at the highest risk of having?

A

MI than TIA/CVA

65
Q

when is carotid endarterectomy indicated?

A

patients who experience nondisabling ischemic stroke or symptomatic TIA symptoms within 6 months should undergo endarterectomy if:

  • the diameter of the lumen of ipsilateral internal carotid artery is reduced by >70% by noninvasive imaging or >50% by angiography
  • anticipated rate of perioperative stroke/mortality>6%
66
Q

when should you suspect internal carotid artery dissection? what should you see on physical exam?

A
  • patient with the unilateral headache associated with either TIAs or a dilated pupil.
  • look for cholesterol emboli on the funduscopic exam.
67
Q

what is the medical treatment for TIA secondary to atherosclerosis?

A
  • ASA alone
  • ASA + dipyridamole
  • clopidogrel alone
68
Q

what are the causes of cerebral embolic events of cardiac origin?

A
  • Afib
  • MI
  • ventricular aneurysm
  • valvular
69
Q

when or at what size is surgery indicated for thoracic aortic aneurysms?

A
  • 5cm if Marfans
  • 5.5cm in the ascending aorta
  • 6cm in the descending aorta
  • greater than 1cm per year
  • compression of surrounding structures
  • symptomatic
70
Q

what type of aneurysms dissect vs rupture?

A

thoracic dissect and rupture

abdominal tend to rupture rather than dissect

71
Q

at what size is surgery indicated for AAA?

A
  • AAA>5.5cm
  • expand >0.5cm in 6 months
  • symptomatic (abdominal/back pain, + pulsatile mass + hypotension)
72
Q

screening for asymptomatic AAA?

A
  • 4- until 5.4cm monitored with US or CT every 6-12 months
  • place on beta-blockers during the observation period
73
Q

what conditions require infective endocarditis antibiotic prophylaxis

A

High-risk patients that have:

  • all dental procedures involving gingival tissue or periapical region of teeth or perforation of the mucosa
  • respiratory tract procedures
  • skin or musculoskeletal infection
  • not indicated for any GI/GU procedures
74
Q

what is a high risk group of patients that would need antibiotic prophylaxis?

A
  • prosthetic valves
  • a previous episode of endocarditis
  • Congenital heart disease (unrepaired cyanotic CHD, repaired CHD within 6 months of the procedure, repaired CHD with residual defects)
  • cardiac transplant patients with valve lesions
75
Q

what is the preferred regimen for IE oral prophylaxis for dental procedures?

A

amoxicillin 2g orally 30-60 minutes before procedure

76
Q

what is the preferred regimen for IE prophylaxis for dental procedures unable to take oral medications?

A

ampicillin or cefazolin or ceftriaxone 30-60 minutes before the procedure

77
Q

what is the preferred regimen for IE oral prophylaxis for dental procedures if they are allergic to penicillin?

A

clindamycin or cephalexin or azithromycin

78
Q

following acute rheumatic fever, how long does it take for valvular dysfunction to occur?

A

20 years

79
Q

how do you distinguish the joint affliction of rheumatic fever vs rheumatoid arthritis?

A

rheumatic fever does not have the joint deformities and has a negative RF factor

80
Q

what key associations for rheumatic fever? (mnemonic + dx)

A
  • JONES CAFE PAL
  • Major: Joint involvement, O - heart , nodules (subcutaneous), Erythema marginatum, Sydenham chorea
  • Minor: CRP increased, arthralgia, Fever, ESR elevation, Prolonged PR, anamensis of rheumatism, leukocytosis
  • 2 major + group A strep infection/ASO titer
  • 1 major + 2 minor + group A strep infection/ASO titer
  • MCC mitral stenosis and tricuspid stenosis
81
Q
A
82
Q
A

int med exam 0828 (24 decks)

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