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Cardiovascular II Final Exam > Coronary Artery Disease: Angina--Stable/Unstable (Johnston) > Flashcards

Coronary Artery Disease: Angina--Stable/Unstable (Johnston) Flashcards

1
Q

Atherosclerotic coronary arteries from plaques can undergo

A
  • Fissuring or Erosion
  • Triggers THROMBUS formation to cause ischemia to myocardium
  • cytokines enhance inflammation and attract platelets and aggregate forming thrombus
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2
Q

Things involved in platelet aggregation

A
  • LDL and oxidation of LDL takes place in macrophages (FOAM cells) which induces cholestrol efflux/elaboration
  • Macrophages also elaborate cytokines, eicosanoids, radicals and proteinases to induce INFLAMMATION
  • When plaques rupture, platelets adhere, build up prodcucing an obstructive flow (causing hemodynamic compromise)
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3
Q

Risk factors for atherosclerosis

A
  • Hyperlipidemia–high LDL, low HDL, high TG, High lipoprotein(a)
  • Smoking
  • Diabetes Mellitus–AHA/MAJOR risk factor
  • Hypertension
  • Family history of coronary heart disease, ischemic stroke or peripheral vascular disease (PVD)
  • Obesity
  • Physical inactivity (need 10-60 min med. intensity 4-7 days/wk)
  • Psychosocial stress
  • Sleep disturbances
  • Age & gender (male>55 y/o female >65 y/o)
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4
Q

Characteristics of Metabolic syndrome

A
  • Insulin resistant
  • HTN
  • High TG, Low HDL
  • Hyperuricemia
  • Hypercoagulable (hyperviscosity)
  • Obese: BMI>30
  • Desirable: BMI 21-24
  • BMI= weightx705/Height
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5
Q

Angina Pectoris

A
  • Chest discomfort (chest pain)

- Most frequent expression of myocardial ischemia

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6
Q

Chronic stable angina

A

consequence of imbalance between oxygen supply-demand

-Low risk of plaque rupture (small lipid core and thick fibrous cap)

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7
Q

Supply angina

A
  • Decreased oxygen delivery to tissue leads to ischemia

- Ex: coronary vasoconstriction, stenosis, platelets release serotonin and thromboxane A2

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8
Q

Demand angina

A
  • Increase myocardial oxygen requirements and workload can lead to ischemia
  • Ex: excercise, stress, emotion, fear, thyrotoxicosis
  • LVH due to AS
  • Anemia (low oxygen carrying capacity)
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9
Q

Effects of ischemia (disturbances)

A
  • Mechanical consequences
  • Biochemical consequences
  • Electrical consequences (vtach, vfib)
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10
Q

Mechanical consquences of ischemia

A
  • Heart failure (LVF or RVF or both)
  • Angina, if ischemia is prolonged or dvelop coronary occlusion, may lead to myocardial necrosis
  • Segmental akinesis, bulging (dyskinesis) (decreased perfusion and not beating as effectively)
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11
Q

Biochemical consequences of ischemia

A
  • Fatty acids cant be oxidized
  • Increased LACTATE production
  • Reduced pH with metabolic acidosis
  • Higher the lactic acid the higher the mortality!!
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12
Q

Electrical consequences of ischemia

A
  • V tach and V fib
  • Inversion of T wave
  • Transient displacement of ST segment:
  • ST depression=subendocardial
  • ST elevation=subepicardial
  • Electrical instability–VT, VF
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13
Q

Localization of LAD infarction/ischemia

A
  • ANTERIOR wall infarction

- Leads V1-V6

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14
Q

Localization of RCA infarct/ischemia

A
  • Inferior wall infarction (RV infarction)
  • II, III, AVF
  • V3R-V6R
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15
Q

Localization of Circumflex artery infarct/ischemia

A
  • LATERAL wall
  • Leads I, AVL
  • V5-V6
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16
Q

Localization of Posterior descending artery

A
  • POSTERIOR wall infarction

- V1-V3 (see RECIPROCAL CHANGES)

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17
Q

Differential diagnosis for MI on ECG (things that can look somewhat similar)

A
  • MI
  • Pericarditis
  • Diffuse ischemia
  • ECG changes related to hypokalemia (would see U waves and FLATTENED T waves)
  • Borderline normal
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18
Q

Significance of an S3 gallop

A
  • Impending LV dysfunction leading to heart failure (in adults)
  • In children/adolescence it is normal
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19
Q

Sysolic murmur over apex with radiation into left axilla indicates what kind of valvular disorder?

A

-Mitral valve regurgitation likely from PAPILLARY muscle insufficiency (hypoperfusion of papillary muscle)

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20
Q

What are CV and Non cardiac causes of chest pain

A
  • CV: Angina, MI, pericarditis, aortic dissection
  • Pulmonary: Pneumonia, pneumothorax, pleurisy
  • Other Non-CV: Anemia, sickle cell, HYPERthyroidism
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21
Q

Non-chest pain symptoms of chronic ischemic heart disease

A
  • Dyspnea
  • Non chest locations of discomfort (exertional or rest)
  • Mid-epigastric or abdominal
  • Diaphoresis
  • Excessive fatigue and weakness
  • Dizziness & syncope
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22
Q

Angina symptoms THreshold vary among patients; certain levels of activity may provoke anginal attack: why??

A
  • Differences in anatomy (narrow vs fixed)

- Fixed CA stenosis/fixed O2 supply; produces ischemia because of increased O2 demand

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23
Q

Typical history of ischemic heart disease

A
  • Men 50-60 yo
  • Women 60-70 yo
  • Chest discomfort brought on by exertion/emotion/excitement; relief by rest usually predictable, stable, not occurring more often, not lasting longer
  • may take nitro prophylactically if they know they will get it because of stressful situation is coming, etc
  • if attack comes on, have patient take nitroglycerin and if it doesn’t go away have them take another one and if it still doesnt go away take one more and have them call ER
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24
Q

Discomfort associated with Coronary artery disease

A
  • description varies but common ones are:
  • Heavy, pressure, sqeezing, tightness, smothering, choking, dullness, ache, sharp, heart burn, indigestion, gas
  • Substernal, clinched first–Levine’s sign
  • Crescendo/decrescendo pattern, lasts 15-20 min
  • May radiate into L shoulder, down ulnar surface of forearm/hand; both arms
  • May radiate or arise in neck, jaw, teeth, epigastric, or back
  • May be precipitated by heavy meal, cold exposure
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25
Q

Anginal equivilant is

A
  • Due to ischemia but NOT classic chest pain but rather:

- Dyspnea, fatigue, faintess and gastric eructations (belching)

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26
Q

Pathogenesis of anginal equivalent

A

-ischemia causing an elevated LV filling pressure that leads to pulmonary edema–diabetic, elderly, women

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27
Q

PE findings of angina patient

A
  • often normal but some other ones include:
  • xanthelasma (soft, yellowish spots on eyelids)
  • xanthomas
  • diabetic skin lesions
  • nicotine stains
  • pale
  • absent peripheral pulses
  • FH of premature IHD
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28
Q

Include what tests in PE for angina?

A
  • Cardiac impulse–will be abnormal (LV dyskinetic)
  • Bruits–carotid, abdominal aorta, femorals
  • Gallop–S3, S4 or both
  • Systolic murmur of MR if papillary muscle is dysfunctional; associated with inferior or inferior-posterior ischemia due to right coronary artery disease (RCA)
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29
Q

Things that mimic Angina in absence of CAD

A
  • AS
  • AI
  • Pulmonary HTN
  • Hypertrophic Cardiomyopathy
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30
Q

Acute Coronary Syndrome (ACS) includes

A
  • Unstable angina

- Non-ST elevation myocardial infarction (NSTEMI)

31
Q

Unstable angina

A
  • New or worsening chest pain
  • Tempo has changed, more severe, prolonged, more frequent; may occur at rest, awaken from sleep
  • Pain lasting MORE than 20 min
  • Using more medication for relief
  • Less effort to provoke symptoms
  • No evidence of myocyte necrosis (no elevation of troponin I or Ck-MB)
32
Q

Chest pain WITH elevation of cardiac enzymes (troponin I or CK-MB) and WITHOUT ST elvation is said to have a

A

-non-ST elevation myocardial infarction (NSTEMI)

33
Q

ST depression is

A
  • Usually always abnormal (anything more than 0.5mm depression (half of one square))
  • ST elevation can be normal (depending on race, amount of elevation, etc)
34
Q

Both unstable angina and NSTEMI are called?

A

-Non-ST segment elevation ACS or NSTE ACS

35
Q

Pathology of ACS

A

-have an atherosclerotic plaque rupture or erosion; platelet aggregation and thrombus leading to partial occlusion of artery

36
Q

Stable angina ECG

A
  • Normal in 50% of patients (resting)
  • During anginal attack may have displaced ST segment; most common change is ST depression (subendocardial injury-ischemia
  • May show old MI
37
Q

Unstable Angina/NSTE ACS ECG:

A
  • Magnitude of ST segment depression correlates with prognosis
  • If ST segment depressed 1 mm or greater in 2 or more leads–almost 4x as likely to die within 1 year
  • if 2 mm or greater ST segment depression–almost 6x likely to die within a year
  • If ST depression is 2mm or greater in more than one region of ECG, mortality is 10 fold
38
Q

Differential diagnosis of NSTE ACS

A
  • Pulmonary Embolism
  • Aortic Dissection–no associated EKG changes
  • VHD (AS, AI, hypertrophic cardiomyopathy)
  • Myocarditis–pericarditis
  • Stress cardiomyopathy–takotsubo syndrome (broken heart)–associated with high emotional stress–often transient, increased catecholamines–deeply inverted T waves–looks very much like MI!!
39
Q

Pulmonary embolism ECG changes

A

-Sinus tachycardia
-RBBB
-A fib
S1q3T3
–NONSPECIFIC

40
Q

AS and AI ECG changes

A

-LVH associated changes

41
Q

Hypertrophic cardiomyopathy ECG

A

-HUGE QRS voltage complexes

42
Q

Myocarditis-Pericarditis ECG changes

A
  • ST segment elevation

- T wave inversion

43
Q

Typical Lab findings of CAD/MI

A
  • Cardiac enzymes: Troponin I; detected in 2-4 hours in NSTEMI
  • Increased CK-MB (after 3-6 hours)
  • Brain Natriuretic Peptide–increase BNP associated with increase mortality in NSTE ACS–indicates ventricle stretching/dilation
  • CRP–inflammatory biomarker (non-specific)
  • CMP: BUN, creatinine, liver panel electrolytes, CBC,
  • FLP (fasting lipid profile, TSH)
44
Q

Prognosis–signs of high risk for coronary event

A
  • Positive stress test at low work load
  • ST depression greater than 5 minutes after completion of test
  • Decrease in BP–systolic fall > 10 mmHg during excercise
  • V T during excercise
  • Reduced EF during exercise (stress echo)
45
Q

Stress testing–done when? sensitivity and specificity?

A
  • exercise electrocardiography (preferred if patient is suspected to have angina)
  • Safe–only 1 death or MI per 2500 tests
  • 70% sensitive, 75% specific
46
Q

Contraindications to stress testing

A
  • Recent MI or acute MI
  • Unstable arrhythmias
  • acute PE
  • aortic dissection
  • unstable angina
  • severe AS
  • decompensated HF
  • Endocarditis
  • DVT
47
Q

Put patient on pharmocalogical stress test IF? What pharmacologic agents are used for this kind of stress test?

A
  • Patient unable to exercise
  • Use Adenosine/ regadenosine
  • Vasodilators–increase HR
  • Dobutamine–increase HR
48
Q

Nuclear Myocardial perfusion imaging–use what test? useful in?

A
  • SPECT (Single photon emission computer tomography)

- LBBB, LVH, digitalis effect

49
Q

Stress echocardiogram used with?

A

Excercise or dobutamine

50
Q

Stress echocardiogram detects?

A

-Wall motion abonormality and ejection fraction (EF)

51
Q

Stress echocardiogram prototype? Detects? Specificity?

A
  • Cardiac Computer Tomographic Angiography (CCTA)
  • Detects coronary calcification
  • Specificity only 50% identifying patients with obstructive CAD
52
Q

Chest X ray in CAD

A
  • usually not very helpful
  • usually normal unless history of MI, HF or VHD
  • Cardiomegalia in HTN, VHD, cardiomyopathy, pericardial effusion
53
Q

Coronary Angiography is synonymous with?

-Used for?

A
  • synonymous with cardiac catheterization
  • Gold standard for anatomic definition of CAD
  • Used for patient being considered by revascularization (CABG–coronary artery bypass graft or PCI–percutaneous coronary intervention)
  • PCI–90% success; stent insertion
54
Q

CABG used mainly for

A

-for L main disease or 3 vessel disease

55
Q

Treatments of patients with stable angina–general measures

A
  • Rule out and control aggrevating conditions: associated noncardiac diseases, associated cardiac disease, use of drugs aggrevating angina
  • Smoking cessation
  • Dietary counseling for body weight and lipid control
  • Excercise prescription
  • Treat to target: HTN, blood lipids, dibetes
56
Q

Pharmacologic therpay to prevent MI/Death/Reduce symptoms:

A

Following are evidence based:

  • Aspirin
  • Beta blocker
  • ACEI
  • Statins
  • Nitro/Nitrates
  • CCB
57
Q

Aggrevating conditions associated with CAD and what to do

A
  • Obesity–weight loss if obese; consult dietitian
  • HTN–Treat to goal
  • Hyperthyroid–Meds, RAI
  • Anemia–Find cause and treat
  • Smoking–Cease
  • Hyperlipidemia–Statins
  • Diabetes–ADA diet, oral agents, insulin
58
Q

Aspirin MOA

A
  • Cyclooxygenase inhibitor of platelet activation
  • Inhibit TxA2 production
  • Clopidogrel-blockers in ADP induced platelet aggregaion
59
Q

Beta blocker MOA

A
  • Block binding of catecholamines to beta receptor
  • Decreases HR, workload, contractility, O2 demand, ischemia and symptoms
  • Decreases CV mortality
  • Prior MI
60
Q

Contraindications to Beta blockers

A
  • Decompensated HF, hypotension, advanced AV block

- can exacerbate HF

61
Q

ACEI MOA

A
  • Blocks conversion of A1 to Aqq
  • Decreases CV mortality
  • Useful in diabetics (renal protection) and patients with LV systolic dysfunction
62
Q

Nitrates MOA

A
  • Vasodilator of vascular smooth muscle; metabolized to nitric oxide to relax smooth muscle and coronaries
  • Relieves ischemia and angina due to vasoconstriction
  • decreases preload (venodilation)
  • Nitrate intolerance; need 8-12 hours nitrate free interval
  • Don’t take with PDE inhibitor!!
63
Q

CCB–facts and MOA

A
  • NOT shown to decrease mortality
  • Vasodilate
  • decrease workload, O2 demand, vasospasm (non-DHPs–verapamil)
  • Decrease HR because Verapamil has negative ionotropic effect
  • Use verapamil WITH CAUTION in patients with IMPAIRED LV function!!
64
Q

Ranolazine

A
  • Inhibits inward Na current and decreases intracellular calcium
  • Johnston has it under CCBs
65
Q

Myocardial revascularization–when to use CABG vs PCI

A
  • CABG for L main or 3 vessel CAD multivessel with LVEF less than 50%
  • PCI–1 to 2 vessel disease
66
Q

Variant angina or prinzmetal angina

A
  • Transient ST segment elevation during chest pain in absence of severe CAD
  • Spasm of coronary
  • Chest pain predominantly at rest; awaken from sleep
  • Relieved by nitro
67
Q

Tx of variant (prinzmetal angina)

A

-DHP CCB (amlodipine)

68
Q

Management strategies for LOW risk patient–what antianginal, antiplatelet, antigcoagulant and cath procedures/meds to use?

A
  • Antianginal: BB, Nitro, CCB, statin
  • Antiplatelet: ASA/clopidogrel
  • Anticoagulant: UF heparin
  • Cath: revascularization if appropriate
69
Q

Management strategies for HIGH risk patient–what antianginal, antiplatelet, antigcoagulant and cath procedures/meds to use?

A
  • Antianginal: BB, Nitro, CCB
  • Statin–plaque stabilization, restore endothelial function
  • Antiplatelet: ASA/clopidogrel or Prasigreel or Ticagrelor Glycoprotein inhibitor IIb/IIIa at time of catheter or PCI (blocks platelet inhibitors that impaires fibrinogen binding and inhibits platelet aggregation)
  • Anticoagulant: UFH or Enoxaparin
  • Cath: Revascularization if appropriate
70
Q

Hyperlipidemia adult treatment NCEP guideline III

A
  • For all patients with prior events, a CHD risk equivalent, or a 10 year risk of 20% or greater goal is:
  • LDL-C less than 70 mg/dl
  • HDL-C goal greater than 60 mg/dl (35 old value) < 40 do lipid analysis
  • TG high is 150 mg/dl (200 was old limit)
  • Total chol less than 200 mg/dl
71
Q

A 1% decrease in total cholestrol yields a

A

-3% decrease in risk of CAD

72
Q

Treatment of CAD/Angina drugs

A
  • Statins for hyperlipidemia
  • Aspirin
  • Nitrates
  • B blocker
  • ACEI
  • Ranexa (Ranolizine)–inhibits late phase of inward N current during repolarization
73
Q

Lifestyle modifications for CAD/ Angina

A
  • Diet–reduce calories with goal of ideal BMI:
  • low saturated fat <7%
  • Low cholestrol <200
  • High fiber 25-30g/day
  • fish oil or fish 1-2x/wk
  • antioxidants–vit C
  • excercise regularly
74
Q

protective against atherosclerosis

A
  • 2g Na (reduce Na consumption)

- reduce alcohol

Cardiovascular II Final Exam (13 decks)

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