Cardiology 2

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Cardiology 2
2011-07-18 16:19:37
DPAP2012 Cardiology

Cardiology flashcards made by previous students.
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  1. Single largest killer of US men & women
  2. CHD causes what % of US deaths?
    1 in 5
  3. ___ % of pts experiencing an MI will die from it
  4. Number US deaths/year from CHF
  5. Pts with CHF: prognosis
    70% women & 80% of men under 65 will die within 8 years
  6. Increase in heart failure deaths in past decade
  7. CHF effect on risk of sudden heart failure death:
    increases risk x8
  8. lifetime risk devt of A-fib
    1 in 4
  9. Inferior MI: EKG correlation
    (II, III, aVF); RCA; left circumflex if left dominant
  10. Anterior MI: EKG correlation
    (V2-V5); LAD
  11. Lateral MI: EKG correlation
    (I, aVL, V5-V6); Left circumflex
  12. Inferolateral MI: EKG correlation
    (II, III, aVF, I, aVL); Large RCA, or Left dominant Left circumflex
  13. Anterolateral MI: EKG correlation
    (V4-V6, I, aVL); Left circumflex
  14. NYHA Class I:
    No limitations or symptoms with normal activity
  15. NYHA Class II:
    Slight limitations; normal activity (moderate exertion) results in symptoms.
  16. NYHA Class III:
    Marked limitation; minimal activity/ exertion/ ADLs results in symptoms (none at rest)
  17. NYHA Class IV:
    Symptoms present with minimal activity and at rest/nocturnally.
  18. Most common causes of heart failure:
    Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy (diastolic non-compliant CHF more common in hypertension than Systolic (end stage hypertensive dz))
  19. Structural causes of heart dz
    myocardial dz; pericardial dz
  20. Types of myocardial dz
    Cardiomyopathy; myocarditis
  21. 3 functional categories of cardiomyopathy
    dilated; hypertrophic; restrictive
  22. 3 types of myocarditis
    infectious; toxic; idiopathic
  23. 3 types of pericardial dz
    Pericarditis; Pericardial effusion / tamponade; Pericardial constriction
  24. ACC/AHA CHF Guidelines: Stage A
    At risk without known disease
  25. ACC/AHA CHF Guidelines: Stage B
    Heart disease-asymptomatic
  26. ACC/AHA CHF Guidelines: Stage C
    Prior or current symptoms
  27. ACC/AHA CHF Guidelines: Stage D
    Advanced or refractory
  28. CHF risk factors
    Age; Hypertension; Tobacco abuse; Diabetes mellitus; Obesity; ETOH/Substance abuse
  29. CHF precipitators
    Coronary artery dz/MI; Valvular or congenital heart dz; Hypertension….diastolic dysfn; ETOH/substance abuse; Viral Infxns; PG; Idiopathic
  30. MI pathophysiology (4 steps)
    1 plaque rupture; 2 plt activation aggregation; 3 fibrin generation; 4 thrombus formation
  31. 2 pathways for ischemic heart dz progression
    Progressive intraluminal narrowing; Sudden disruption/fissuring of plaques
  32. Progressive intraluminal narrowing tend to:
    to produce collateral blood supply & more likely to cause worsening stable/unstable angina (>75%)
  33. Sudden disruption/fissuring of plaques likely to:
    to rupture, causing ACS (Acute Coronary Syndrome) or Acute MI (25-75%)
  34. Tobacco: CAD risks
    2x risk for 1/2 to 1 pack/day; 3x risk for > 1 pack/day; risk declines 50% after one year of tobacco cessation
  35. Most common causes of heart failure:
    Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy
  36. Which type of non-compliant CHF is more common in HTN?
    Diastolic more than Systolic (end stage hypertensive dz)
  37. What precipitates conduction system problems?
    Coronary artery dz/MI (ischemia induced); congenital; anything that causes CHF
  38. CAD signs/symptoms
    Chest pain/pressure/tightness; Jaw/ neck/ throat/scapular/ arm pain; SOB/ Dyspnea on exertion; N&V; Diaphoresis; Fatigue
  39. Deoxygenated blood draining from the heart itself enters the right atrium via:
    the coronary sinus & thebesian veins
  40. Second most common cause of sudden death in young adults
    Anomalous coronary arteries (4-15% of young people with sudden cardiac death); 1-2% of population
  41. Which valves do/do not have chordae/papillary mx?
    AV valves do; semilunar valves do not
  42. period of ventricular contraction
  43. period of ventricular relaxation
  44. the load that stretches the cardiac muscle prior to contraction
  45. the resistance against which the left ventricle must contract
  46. ability of cardiac muscle to shorten, when given a load
    myocardial contractility
  47. myocardial contractility is increased by:
    sympathetic stimulation/action
  48. myocardial contractility is decreased by:
    myocardial injury
  49. afterload comprises:
    blood volume/viscosity; resistance in aorta & other peripheral vessels
  50. Preload is increased by:
    inspiration or increasing venous return to right heart)
  51. Amount of blood remaining after ejection:
    end systolic volume
  52. In diastole, _____% of ventricular filling occurs before atrial contraction
  53. SV=
    EDV (end diastolic volume) – ESV (end systolic volume)
  54. CO =
    HR x SV (normal about 5 L/min)
  55. Adult normal cardiac blood volumes:
    SV=70ml, EDV=135ml, ESV=65ml, CO=5L total blood
  56. volume of blood ejected from each ventricle during one minute
    Cardiac output
  57. volume of blood ejected with each heartbeat
    Stroke volume
  58. Starling’s Law:
    SV increases as the EDV increases
  59. Ejection Fraction formula:
    EF% = SV/EDV
  60. A quantitative measure of contractility
    Ejection Fraction
  61. Normal EF
    67% (at DUMC: >55%)
  62. Annulus:
    fibrous ring surrounding each of the 4 cardiac valves; fn: to provide structural support to the heart
  63. narrowing or obstruction to forward flow while valve is open
  64. backward leakage during time when valve is closed
    Regurgitation / Insufficiency
  65. S1 = _____ valve closing
    Mitral (Systole)
  66. S2 = _____ valve closing
    Aortic valve closing (diastole)
  67. S3 may indicate:
    CHF (sounds like: Ken-Tuc-Key)
  68. S4 may indicate:
    HTN or CAD (sounds like: Tenn-es-see)
  69. Which heart sound is always pathological?
  70. Left & right coronary arteries arise from what part of the aortic root?
    Sinuses of Valsalva
  71. Branches off the left main coronary artery
    LAD; Left circumflex
  72. Right Dominant: Septum supplied by:
    Distal branches from RCA (supply the septum 70%)
  73. Left Dominant: Septum supplied by:
    Distal branches from LCx (supply the septum 20%)
  74. SA Node is supplied by:
    RCA 60% of the time & by LCX 40% of the time
  75. AV node supplied by:
    dominant artery (RCA or LCx)
  76. small vascular channels that interconnect the normal coronary arteries
    Collateral Vessels
  77. Function of collateral vessels in normal myocardium
    Nonfunctional because no pressure gradient is present
  78. S/S of conduction problems
    palpitations; dizziness; presyncope/ syncope
  79. Myocardial dz categories
    Cardiomyopathy; Myocarditis
  80. MI Pathophysiology steps
    1. Plaque rupture; 2. Plt activation/aggregation; 3. Fibrin generation; 4. Thrombus formation
  81. Cardiac ischemia risk factors
    Age; Gender ? FH; Sedentary Lifestyle; Tobacco; HTN; DM/insulin resistance; Hyperlipidemia
  82. DM increases risk/incidence of:
    Diffuse dz; small vessel dz; CHF & death rates post MI; death or MI post CABG & PCI
  83. Recommended for sedentary lifestyle
    Devoted exercise 30 min/day, 5 d/wk; initially under med supervision
  84. Causes of coronary ischemia leading to chest pain
    Atherosclerosis; Vasospastic disorders; stenosis or HCM; Coronary thrombosis/ embolization; Acute aortic dissection
  85. Causes of noncardiac CP
    Pericarditis; myocarditis; MVP; chostocondritis; C- or T-spine dz/thoracic outlet; GI/gall bladder; PE; pneumonia; pneumothorax
  86. JNC7: Normal
    SBP <120; DBP <80
  87. JNC7: Pre-HTN
    SBP 120-139; DBP 80-89
  88. JNC7: HTN, Stage I
    SBP 140-159; DBP 90-99
  89. JNC7: HTN, Stage II
    SBP >160; DBP >100
  90. ATP III: High total Chol =
    >200 mg/dl
  91. ATP III: Hypertriglyceridemia
    >150 mg/dl
  92. ATP III: Low HDL Cholesterol
    < 40 mg/dl
  93. ATP III: High LDL (& known CAD)
    > 100 mg/dl
  94. ATP III: High LDL (> 2 Risk Factors)
    > 130 mg/dl
  95. ATP III: High LDL (< 2 Risk Factors)
    > 160 mg/dl
  96. Before a dx of CAD, diabetics risk of MI =
    risk of non-diabetic with prior MI
  97. Almost all MI’s result from:
    coronary atherosclerosis & superimposed coronary thrombosis
  98. Antithrombotics include:
    Fibrinolytics, anticoagulants, antiplatelet drugs
  99. Use of fibrinolytics
    STEMI only
  100. Anticoagulants: acute & chronic
    Acute: UFH, LMWH, DTIs; chronic: warfarin
  101. UFH vs LMWH re: inactivating thrombin
    UFH > LMWH
  102. Beta blockers AEs
    Hypotension; Decrease HR, heart block; May worsen HF symptoms; CNS (fatigue, malaise, depression); Bronchospasm (use ß1 selective agents)
  103. Irreversibly binds to ADP receptor on platelets; Full reversal requires removal of plts
  104. Fibrinolytics: absolute CI
    Prior hemorrhagic CVA; any cerebrovascular events < 1 year; active internal bleeding; Known intracranial neoplasm; suspected aortic dissection
  105. Fibrinolytics: relative CI
    BP > 180/110; Use of anticoags w/ INR > 2; Noncompressible vascular punctures; Prolonged CPR (> 10 minutes); PG or Menstruation; Trauma < 2-4 weeks prior; Major surgery < 3 weeks prior
  106. UFH: main risk =
  107. UFH: used for:
    Both STEMI and NSTEMI
  108. ATPIII/heparin has greatest effect on:
    Factor II (thrombin)
  109. Can use to monitor LMWH
    Factor Xa
  110. UFH/LMWH AEs
    Bleeding, HIT, osteoporosis
  111. UFH vs LMWH: which inhibited by PF4 (thus limited effect vs ACS)?
  112. UFH vs LMWH: req dose adjustment for renal:
  113. Catheter thrombosis during PCI
  114. Bivalirudin used in STEMI in place of:
    UFH / LMWH
  115. Add warfarin for:
    pts w/ USA or NSTEMI w/anticoag indication (to maintain INR 2.0-3.0)
  116. Clopidogrel dosing
    usu loading & maint doses
  117. Clopidogrel AEs
    Bleeding; Thrombocytopenia; Leukopenia; TTP
  118. Clopidogrel: who gets:
    All STEMI/NSTEMI (2-4 wks to 1 yr)
  119. GP IIb/IIIa inhibs: who gets:
    STEMI pts going for PCI
  120. GP IIb/IIIa inhibs: not recommended if:
    PCI is not planned
  121. Fredrickson phenotype I
    Serum conc of chylomicrons elevated; trigs are elevated to >99th percentile
  122. Fredrickson phenotype IIa
    Serum LDL chol elevated; the total chol is >90th percentile. Triglyceride and/or apolipoprotein B may also be ≥ 90th percentile
  123. Fredrickson phenotype IIb
    Serum LDL & VLDL elevated; TC and/or trigs may be ≥ 90th percentile and apolipoprotein B ≥ 90th percentile
  124. Increased Apo A-I prodn has what effect in animals?
    Anti-atherogenic (reduced atherosclerosis progression; regression of existing dz)
  125. Rationales for screening:
    High chol & CHD are common; rel btw TC & LDL & risk of CHD & coronary mortality; lowering LDL in mod/hi risk pt => few CV events; dyslipidemia (not LDL) common in early onset CHD; screen tests commonly avail
  126. Mechanisms by which oxidized LDL causes atherogenesis
    Endothelial damage; changes in vasc tone; Monocyte/ macrophage recruitment; increased LDL uptake by macrophages (foam cell formation); Induction of GF; Increased plt aggregation; Formation of auto-Abs to oxidized LDL
  127. HDL antiatherogenic properties include:
    Reverse chol transport; antioxidation; protection vs thrombosis; maintenance of endothelial fn; maintenance of low blood viscosity thru permissive action on red cell deformability
  128. Process whereby excess cholesterol in cells and in atherosclerotic plaques is removed
    Reverse cholesterol transport
  129. Mgmt of Low HDL-C
    Wt reduction & inc physical activity; LDL-C is primary target of tx; Non-HDL-C is secondary target of tx (if trigs ³200 mg/dL); consider nicotinic acid or fibrates
  130. Fredrickson phenotype III
    Serum VLDL remnants & chylomicrons elevated; TC & trigs >90th percentile
  131. Fredrickson phenotype IV
    Serum VLDL elevated; TC may be >90th percentile & may also see trigs >90th percentile or low HDL
  132. Fredrickson phenotype V
    Elevated serum chylomicrons & VLDL; triglycerides >99th percentile
  133. Hypertriglyceridemia & CHD: Assoc disorders
    Accumul of chylomicron remnants & VLDL remnants; generation of small, dense LDL-C; assoc w/ low HDL-C; increased coagulability (inc plasminogen activator inhibitor (PAI-1); inc factor VIIc; activation of prothrombin to thrombin
  134. ATPIII chol screening for pt w/o CHD:
    LDL < 160 & 0-01 risk factor; or LDL <130 & >1 risk factor: rescreen in 5 yrs
  135. ATPIII risk determination Step 1
    1. Fasting lipid level
  136. ATPIII risk determination Step 2
    2. determine CHD equivalents
  137. ATPIII risk determination Step 3
    3. Major CHD factors other than LDL
  138. ATPIII risk determination Step 4
    4. If >1 non-LDL CHD factor (in pt w/o CHD or equivalent): use modified Framingham criteria
  139. ATPIII risk determination Step 5
    5. Detn risk category to establish LDL goal, when to initiate tx lifestyle changes, & when to consider drug tx
  140. ATP III criteria: Metabolic syndrome
    3 of 5: abd obesity (waist men >40 in & women >35 in; trigs ≥150 or tx for hi trigs; HDL <40 (M) & <50 (F) or tx for low HDL; BP ≥130/85 or tx for hi BP; FPG ≥100 or tx
  141. IDF metab syndrome defn
    Inc waist girth plus any 2: 1. Trigs >150 or tx; HDL <40 (M) & <50 (F) or tx; SBP >130, DBP >85, or HTN tx; FPG >100 or prior dx type 2 DM
  142. Summary: CV risk factors in DM pts
    Type I: hi trigs & HTN; Type 2: dyslipid, HTN, ins resistance, obesity, FH atherosclerosis; SMK NOT risk factor for I or 2
  143. 3 levels of prevention
    Primary: remove risk factors; secondary: early detection & tx; tertiary: reduce complications
  144. (A) fat contribute to CV dz; (B) fat may be cardioprotective
    A. Saturated & trans fat; B. monounsaturated & polyunsaturated fat
  145. Lipids carried by LPs for:
    energy utilization; lipid deposition; steroid hormone prodn; bile acid formation
  146. Lipoprotein consists of:
    esterified & unesterified chol, trigs, phospholipids, & protein
  147. Protein components of the lipoprotein =
    apolipoproteins or apoproteins.
  148. Apolipoproteins =
    cofactors for enzymes and ligands for receptors
  149. Defects in apolipoprotein metabolism lead to:
    abnormalities in lipid handling
  150. Very large particles that carry dietary lipid =
  151. Chylomicrons are assoc with:
    Apolipoproteins (including A-I, A-II, A-IV, B-48, C-I, C-II, C-III, and E)
  152. LDL carries:
    cholesterol esters
  153. LDL assoc with:
    apolipoprotein B-100.
  154. HDL carries:
    cholesterol esters
  155. HDL is associated with:
    apolipoproteins A-I, A-II, C-I, C-II, C-III, D, and E
  156. One mechm by which LDL promotes atherosclerosis
    oxidative modification
  157. VLDL carries:
    endogenous trigs (& to a lesser degree chol)
  158. Major apolipoproteins assoc with VLDL:
    B-100, C-I, C-II, C-III, and E
  159. Intermediate density lipoprotein (IDL) carries:
    chol esters & triglycerides
  160. IDLs are assoc with:
    apolipoproteins B-100, C-III, and E
  161. Fn of CETP
    transfers oxidized lipids from LDL to HDL
  162. The oxidized lipids in HDL are reduced by:
    HDL apolipoproteins
  163. The liver wrt reduced lipids
    Liver takes up reduced lipids from HDL more rapidly than from LDL
  164. Hypoalphalipoproteinemia =
    Low serum HDL; assoc w/ increased risk of overt CHD
  165. Framingham: MI risk
    MI risk increases by 25 percent for every 5 mg/dL decrement in HDL below median values
  166. Low HDL: risk factors
    SMK; sedentary;obese; insulin resistant/ DM; hypertriglyceridemia; chronic inflammatory dz
  167. Cardioprotective HDL =
    >60 mg/dL (>75 assoc w/ longevity syndrome)
  168. Strategies for HDL metab as tx target
    Increase apo A-I prodn; promote reverse chol transport; delay HDL catabolism
  169. Effect of ETOH (wine, beer) on HDL-C
  170. Theoretical effect of CTEP inhibitors
    Lower LDL; increase HDL
  171. Familial Dyslipidemias
    Fredrickson phenotypes III, IV, & V
  172. high levels of trigs may directly promote:
  173. high levels of trigs assoc w/ increases in:
    fibrinogen, clotting factors VII & X, & blood viscosity
  174. ATP III: normal trigs
  175. ATP III: borderline high trigs
  176. ATP III: high (trigs)
  177. ATP III: very high (trigs)
    =/> 500
  178. Primary concern w/ ATPIII borderline high:
    Metabolic syndrome
  179. Primary concern w/ ATPIII High category
  180. Primary concern w/ ATPIII Very High category
  181. ATP III recommends Chol screening how often?
    at least every 5 yrs for pts 20 or older
  182. Pts w/ borderline-high chol & <2 risk factors should be rescreened:
    within 1-2 yrs
  183. Framingham risk factors
    Age, TC, HDL, BP, & SMK
  184. Framingham focuses on which lipid:
    TC (but LDL is primary tx target)
  185. Framingham 10-yr CHD risk categories
    r >20%, 10-20%, and <10%
  186. Low HDL-C is an Independent Predictor of CHD Risk even when:
    LDL-C is Low
  187. Metab syndrome/girth increases genetic susceptibility to:
    dyslipidemia, hypertension, type 2 DM