Cardio - Physio

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honotay
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63266
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Cardio - Physio
Updated:
2011-02-03 20:55:35
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cardio formulas
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Cardio info and formulas for medical physiology
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  1. Stroke Volume
    Volume of blood ejected by each ventricle in 1 beat.

    SV = EDV - ESV ml/beat
  2. Ejection Fraction
    Fraction of EDV ejected in 1 beat.

    EF = SV/EDV
  3. Cardiac Output
    Volume of blood ejected by each ventricle per minute.

    CO = SV * HR ml/min
  4. 1st Heart Sound
    due to closure of both AV valves
  5. 2nd Heart Sound
    due to closure of both semilunar valves (mitral and tricuspid)
  6. Mitral Stenosis
    narrowing/obstruction @ opening of mitral valve

    diastolic murmur appears
  7. Mitral Insufficiency
    leaky mitral valve, regurgitation from LV to LA during vent. systole

    systolic murmur appears
  8. Aortic Stenosis
    narrowing around aortic valve, increased afterload, LV hypertrophy

    systolic murmur appears
  9. Aortic Insufficiency
    leaky aortic valve, regurgitation from aorta to LV

    diastolic murmur appears
  10. Isovolumetric Contraction
    ventricles full (EDV), QRS, pressure closes AVV = 1st heart sound
  11. Rapid Ejection
    SLV open, max P, V decreases
  12. Reduced Ejection
    P falling, ejection @ lower rate, ESV remains in ventricles @ the end
  13. Isovolumetric Relaxation
    P falls, SLV's close, 2nd heart sound, V remains same as ESV
  14. Rapid Filling
    P falls below that of atria, AV valves open, max filling, V increases, P low as ventricles are relaxing
  15. Reduced Filling
    filling continues, blood flow less, P gradient is low, LONGEST phase (can do w/o)
  16. Atrial Systole
    end of ventricular diastole, P wave - atria contract, small amt of blood into ventricles - EDV - ventricles ready for next systole
  17. Fick's Principle
    cardiac output = (O2 taken up by lungs per minute) / (O2 content of pulm vein - O2 content of pulm artery)
  18. Frank-Starling Relationship
    SV is inversely proportional to EDV
  19. Frank-Starling Curve
    (Cardiac Function Curve)
  20. Mech of Starling's Relationship
    • 1. increase in venous return
    • 2. increase in ventricular filling + EDV
    • 3. stretching of ventricular muscle fibers
    • 4. increase in initial length of muscle fibers
    • 5. more crossbridges during contraction
    • 6. increase mycardial tension
    • 7. increase in SV and CO
  21. Effect of contractility:
    Increase?
    Decrease?
  22. Effect of preload on SV?
    • increase = increase
    • decrease = decrease
  23. Effect of afterload on SV?
    • increase = decrease
    • decrease = increase
  24. Effect of myocardial contractility on SV?
    • positive inotropic agents (digoxin) = increase
    • negative inotropic agents = decrease
  25. Effect of loss of myocardial tissue (MI) on SV?
    decrease
  26. Normal mean circulatory filling P
    about 7
  27. Effect of changing total blood vol on vascular function curve?
  28. What changes the cardiac function curve?
    change in myocardial contractility
  29. What changes the vascular function curve?
    change in blood volume
  30. Effect of increasing contractility on combined curves?
  31. Effect of changing TBV on combined curves?
  32. Effect of changing TPR on combined curve?
  33. Progressive changes in heart failure? (combined curves)
  34. Mean arterial pressure formula?
    MAP = CO * TPR
  35. Short term control of BP changes?
    baroreceptors in carotid sinus/aortic arch
  36. Long term control of BP changes?
    • low BP sensed in kidney - renin secreted - converts angiotensinogen to angiotensin I in plasma - ACE converts angiotensin I to angiotensin II in lungs -
    • in kidney stimulates aldosterone secretion - increased Na+ reabsorption
    • in hypothalamus stimulates secretion of ADH - increased H2O reabsorption in kidney
    • salt + water retention = increased arterial BP
  37. Starling equation
    Jv = Kf [(Pc - Pi) - (πc - πi)]

    • Jv = net pressure
    • P = hydrostatic
    • π = oncotic (protein)
    • c = capillary
    • i = interstitial
  38. + Starling P vs - Starling P
    favors filtration vs favors reabsorption
  39. Kf
    • permeability of capillary wall
    • assumed to be 1 unless given
  40. Movement of fluid @ arterial end of capillary vs at venous end
    • @ arterial end - favors filtration
    • @ venous end - favors reabsorption
  41. Why does capillary hydrostatic pressure decrease along the length of the capillary?
    • not all fluid is reabsorbed at venous end (about 85%)
    • proteins do not move so oncotic pressures remain stable
    • lower pressure at venous end
  42. P wave
    atrial depolarization
  43. QRS complex
    ventricular depolarizatioin
  44. T wave
    ventricular repolarization
  45. segments vs intervals
    • segments are events
    • intervals are time periods
  46. PR segment
    AV delay
  47. PR interval
    SA firing to AV firing
  48. QT interval
    ventricular depolarization to repolarization
  49. ST segment
    amount of Ca2+ influx
  50. HR and R-R interval
    • HR = 60 (seconds) / R-R interval
    • R-R interval = 1 cardiac cycle length
  51. Sinus tachycardia
    >100 bpm and regular
  52. Sinus bradycardia
    <60 bpm and regular
  53. 1st degree heart block
    • prolonged PR interval
    • slow conduction through AV node
  54. 2nd degree heart block
    progressive lengthening of PR interval ending in 1 dropped beat
  55. 3rd degree heart block
    • no impulses conducted
    • atria and ventricles beat independently
    • freq of P waves > QRS complexes
  56. ECG in angina
    • ST segment depression
    • T wave inversion
  57. ECG in MI
    • elevated ST segment
    • pathologic Q wave
    • inverted T wave
  58. ECG in hyperkalemia
    • tall t waves
    • long PR interval
  59. SA node
    pacemaker
  60. AV node
    AV delay - allows time for ventricular filling
  61. Atrial internodal pathways
    conduct from SAN to AVN
  62. Bundle of His
    from atria to ventricles
  63. Bundle branches
    run in R and L ventricles
  64. Purkinje fibers
    run in ventricluar muscles, fastest conducting component of all
  65. Fast response type action potential


    • phase 0 - rapid depolarization, vg Na+
    • phase 1 - initial brief repolarization, vg Na+ close, outward K+ due to high electrochemical gradient
    • phase 2 - plateau, vg Ca2+
    • phase 3 - rapid repolarization, vg K+
    • phase 4 - resting phase
  66. What is the role of Ca2+ in the fast response AP?
    enters during plateau phase via vg channels and causes release of additional Ca2+ from sarcoplasmic reticulum to generate contraction
  67. Slow response type AP


    • phase 4 - unstable resting phase, gradual depolarization due to:
    • 1- inward Na+ channels
    • 2- decreased K+ conductance
    • phase 0 - vg Ca2+ channels
    • phase 3 - vg K+ channels
  68. Positive chronotropic effect
    • sympathetic effect on SA node
    • NE binds with beta-1 receptors in - increased HR
  69. Positive dromotropic effect
    • sympathetic effect on AV node
    • increased conduction in AV node, decreased AV delay
  70. Negative chronotropic effect
    • parasympathetic effect on SA node
    • ACh binds w/M2 receptors - decreased HR
  71. Negative dromotropic effect
    • parasympathetic effect on AV node
    • decreased velocity of conduction - longer AV delay

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