cardiac 2

  1. systole and diastole basic defs
    systole - period during wich contraction of heart occurs

    diastole - period during which the heart is relaxed and filling with blood, and the period when the coronary arteries are filling
  2. prolonged PR interval indicates...?
    block at AV node
  3. ST elevation indicates...?
    full thickness infarct
  4. 1st degree, 2nd degree, and complete heart block
    • 1st - if there's a minor disease in the AV node
    • 2nd - more severe disease
    • complete - SA and AV nodes aren't communicating
  5. P wave
    atrial depol
  6. QRS complex
    vent. depol
  7. T wave
    vent repol
  8. Q (can have a dot on top of it too) means what?
    what influences it?
    • Q = cardiac output = HR x SV
    • influencing factors - HR, SV, contractility, preload, afterload, a-vO2 diff (amount of O2 used)
  9. cardiac output (Q) normal range
    5-20L/min (20 at max exercise)
  10. Oxygen uptake (VO2) formula and values
    • VO2 =  HR x SV x a-vO2 diff
    • <14 ml/kg -- get on transplant list
    • 15 ml/kg -- min for functional activity
    • 35-38 ml/kg -- ok for middle aged folk
    • 102 ml/kg -- total bad ass
  11. myocardial oygenation (MVO2) is highly correlated w what? 
    • HR and RPP
    • HR x SBP = RPP (rate pressure product)
  12. amount of O2 body uses at rest, amount heart uses
    • body - 20-30% of available oxygen
    • heart - ~70% (much smaller reserve, so it's easier to infarct)
  13. pulse pressure def
    SBP minus DBP
  14. chronotropic effects
    • effects that change the heart rate.
    • Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
    • Positive chronotropes increase heart rate; negative chronotropes decrease heart rate.
  15. inotropic effects
    • alters the force or energy of muscular contractions.
    • Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents increase the strength of muscular contraction.
  16. preload basic def, why it's helpful
    • amount of tension on a muscle before it contracts
    • this maximizes the blood pushed out by maximizing cross bridges (so more blood in --> more blood out)
  17. Why would beta blockers be given to cardiac pts?
    They decrease HR and contractility. This lowers the O2 demand and metabolic demands, so there's less risk of ischemia.
  18. Frank Starling Mechanism
     stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume)
  19. afterload
    • the force against which the heart must contract in order to move the blood
    • this is diff for L ventand R vent bc they're pusing blood to diff places that have diff pressures
  20. if there's not enough O2, muscles can't...?
    release calcium, so they can't fully relax or fully contract
  21. atherosclerosis def
    • a disease of muscular arteries in which the inner layer becomes thickened by fatty deposits and fibrous tissue
    • frequently involves coronary + cerebral vessels
  22. fatty streaks in atherosclerosis
    • subednothelial accumulations of large "foam cells" that are mostly derived from macrophages
    • fatty streadks cause signals in endothelium to become disrupted
  23. fibrous plaques in atherosclerosis
    • more advanced lesions than fatty streaks
    • the source of clinical manifestations of the disease
    • most changees occur in the intimal layer
    • looks gray and waxy, and elevates into the lumen causing some occlusion
    • create a fibrous cap
  24. role of fibrous cap in fibrous plaques
    seperates a necrotic core of cell debris, degenerated foam cells, cholesterol crystals, etc from the arterial lumen
  25. 5 types of complicated lesions seen in atherosclerosis
    • calcification
    • plaques rupture
    • hemorrhage
    • fragmentation
    • weakening of vessel wall
  26. details on calcification in atherosclerosis
    usually of fibrous plaque --> pipelike rigidity of vessel wall --> increased fragility
  27. more about "plaques rupture" in atherosclerosis
    this exposes thrombogenic material to circulating blood --> platelets build up --> thrombosis (clot)
  28. thrombus
    a stationary blood clot along the wall of a blood vessel, frequently causing vascular obstruction. Some authorities differentiate thrombus formation from simple coagulation or clot formation.
  29. more about hemorrhaging in atherosclerosis
    hemorrhaging into fibrous cap form rupture of the cap or blood vessels that vascularize the plaque --> hematoma
  30. more about weakening of vessel wall in atherosclerosis
    • embolization of fragments of disrupted atheroma to distal sites --> stroke
    • weakenting of vessel wall --> aneruism --> rupture --> tamponade + MI
  31. atheroma
    A deposit or degenerative accumulation of lipid-containing plaques on the innermost layer of the wall of an artery.
  32. signaling (which becomes disrupted in endothelium as a result of fatty streaks)
    • plaque builidup and swelling limits the signaling, and healthy signaling (hormone release and other communication?) results in  vessels relaxing, blood passing w/o adhering, prevents smooth muscle migration, etc.
    • endothelial cells scred vasoactive substances that directly modulate the contraction of the smooth muscle cells in the medial layer - so if they're in trouble, smooth muscle contraction is too
  33. Heather, just want to remind you that simply studying these cards isn't enough
    In your notes you keep telling yourselve to visit her slides. You should probably do that before any exams.
  34.  When endothelial cells become injured or dysfunctional, atherosclerosis may occur. Stuff you'll see when you have injured endothelial cells:
    • permiability of endoltheilial layer may increase
    • may lose their antithrombitic properties
    • reduced secretion of vasokilaters, impairing the smooth muscle relaxation in the media layer
    • secrete increased amounts of mitogenic substances (platelet derived growth factors) that recruit smooth muscle cells into the intima
    • secrete chemotactic factors that attrace other key cells toward intima
  35. 4 major modifiable risk factors for heart disease
    • tobaco smoking
    • hypertension
    • dyslipidemias
    • diabetes mellitus
  36. about tobacco being a modifiable CRF
    • relative to nosmokers, smokers are 1.35-2.4 times more likely to get heart disease (1.43-3.5x more likely for heavy smokers)
    • tobacco smoking decreases circulating HDL
    • gives inappropriate stim of symp nervous system
  37. hypertension as a modifiable CRF
    BP norm, high norm
    Cholesterol healthy total
    Desired LDL if no known heart disease, if heart disease
    HDL norm
    • see slides! I can't get them at the lib.
    • Norm: (120-129)/(80-84)
    • Hi Norm (130-139)/(85-89)
    • healthy total <200mg/dl
    • LDL < 130 if no known heart disiease
    • LDL < 100 if known heart disease
    • HDL > 35 or 40 (exercise will raise it)
  38. dyslipidemias (a modifiable CRF)
    • abnormal circulating libid levels
    • countries w low saturated fat intake and low serum cholesterol levels have low incidence of heart idsease
    • < 10% of diet should be saturated fat
  39. diabetes as a modifiable CRF
    the risk is related to what?
    • risk is relative to glycosylation of lipoproteins or increased platelet adhesiveness
    • risk is ~1.3x norm if there's good glucose control
  40. desired trigliceride level (i'm not sure if this is for folks with DM or everyone)
  41. esp w DM pts, look at pre and post exercise glucose
    what are you looking for?
    • if <100 before exercise, give a cracker
    • if pre-exercise >260 check for urinary ketones
    • if >300 ask pysician about exercise
  42. exercise's impact on blood glucose
    Usually exercise loweres blood glucose, but if it's already very high, exercise will raise it.
  43. 3 minor modifiable CRFs
    • obesity
    • sedentary lifestyle
    • stress
  44. obesity as a minor modifiable CRF
    • 20% above ideal wt will increase risk of heart disease, esp if it's around belly
    • obesity is associated w HTN, DM, sedentary lifestyle
  45. sedentary lifestyle is a minor modifiable CRF
    recommended exercise time
    expected positive results of exercise
    • it's recommended you exercise 30 minutes at mod intensity 5-7 days/week 
    • exercise raises HDL, lowers BP, helps normalized blood glucose, increases fibrinolysis, decreases plately aggregability (so yr less likely to have a clot)
  46. reasons stress is a minor modifiable CRF
    • stress raises plately activation bc of increased leveles of chatecholemines
    • platelet secreted proteins are noted in persons undergoing emotional stress
    • depression is also a CRF
  47. 3 major non-modifiable CRFs
    • advanced age
    • male gender
    • family history of heart disease
  48. caveat about old age being a major non-modifiable CRF
    old folks respond to risk factor modification just like young'uns
  49. most common manifestaion of ischemic heart disease
    angina "strangling in the chest"
  50. stable angina
    • comes on w exertion, stress, emotions, or a big meal
    • subsides w rest
  51. variant angina
    happens when? result of what?
    • usually happens when at rest,
    • result of coronary artery vasospasm rather than an increase in myocardial demand
  52. unstable angina comes on when?
    • comes after slight exertion or when at rest
    • high freq of progression to MI
  53. 3 factors contributing to myocardial oxygen supply
    • diastolic perfusion pressure
    • coronary vascular resistance (from external compression or intrinsic regulation from local metabolites, endothelial factors, neural innervation)
    • oxygent carrying capacity - enoug hemogobin around to carry the O2
  54. 3 major factors in myocardial oxygen demand
    • wall tension - more wall tension + pressure in chamber stresses cross bridges --> increased O2 demand
    • HR - the higher the HR the more the heart needs O2
    • contractility - the harder it has to contract to move blood, the greater the O2 demand
  55. when vessel is stenosed _% it needs to be fully dilated to get blood thru
    _% stenosed and the blood flow can't meet basal req.
    • 70%
    • 90%
  56. endolthelial cell dysfunction leads to what 2 things?
    • inappropriate vasoconstriction of coronary arteries
    • loss of normal anithrombotic properties

    i wrote to see slides...
  57. endothelial cell dysfunction leads to imbalance of O2 suppy/demand how? 3 ways
    • decreased aortic perfusion pressure
    • severe decrease in blood oxygen carrying capacity
    • profound increase in myocardial O2 demand (such as in marked increase in wall stress)
  58. silent ischemia def, how it's id'd, common in who?
    • episodes of ischiemia in absense of symptoms (ie anginga)
    • seen in EKG changes
    • common in diabetics - they have neuropathies so might not feel angina, may only have the "short of breath" symptom
  59. syndrome X
    • patients with typical symptoms of angina pectoris who have no evidence of significant atherosclerotic coronary stenosis
    • may be due to inadequate vasodialator reserve

    pt has typical symptoms of angina but no CAD, but shows evidence of CAD on ETT (exercise tolerance test)

    it's thought that vessels may not be dilating properly during periods of increased myocardial O2 demand
  60. basic myocardial infarct def
    condition of irreversible necrosis of heart muscle that results from prolonged ischemia
  61. 2 other names for a subendocardial MI
    subendocardial = non ST elev = non Q wave
  62. 2 other names for a transmural MI
    transmural = ST elev = Q wave
  63. transmural aka ST elev aka Q wave MI
    • spans thickness of myocardium
    • results from prolonged total occlusion of an epicardial coronary arter
    • causes a change in contractility
  64. subendcardial aka non ST elev aka non Q wave MI
    exclusively involve the innermost layers of the myocardium (that area is at greatest risk for ischemia as wall tension increases bc blood supply to here must travel furthest
  65. why is a subendocardial MI a non-ST wave MI?
    bc the signal can still travel in a relatively normal way thru the outer layers of the heart
  66. what's happening with the EKG in a "Q-wave MI?"
    • the QRS complex is widened
    • this doesn't reverse w time
  67. Q wave vs non-Q wave MI comparing mortality and risk of another infarct
    Q wave MI: higher risk of mortality, lower risk of another infarct (bc pt's dead?)

    non Q wave MI: lower risk if immediate death, higher risk of another MI (that's bc it's usually a smaller infarct and multi vessel)
  68. EKG change after an MI
    acute: ST segment elevation
  69. EKG change after an MI
    hours later
    • ST segment elevation
    • decreased R waves
    • Q waves begin

    (this is in a pic in the slides)
  70. EKG change after an MI
    day 1-2
    • T waave inversion
    • Q wave deeper
  71. EKG change after an MI
    days 3+
    • ST normalizes
    • T wave inverted
  72. EKG change after an MI
    weeks later
    • ST and T normalize
    • Q wave persists
Card Set
cardiac 2
cardiac 2