Cardiac Week 2

  1. In the basic terms what is excitation contraction coupling?
    Translating electrical excitation to mechanical contraction
  2. Describe what's going on in the heart during isovolumetric contraction.  What phase is this in the pressure loop diagram?
    Mitral and aortic valves closed.  Ventricle is contracting (increased pressure) but there is no change in volume.

    Phase II
  3. Describe what's going on in the heart during isovolumetric relaxation.  What phase is this in the pressure loop diagram?
    Mitral and aortic valves closed.  Ventricle is relaxing but there is no change in volume (no filling).

    Phase IV
  4. What is the normal EDV?
    120 ml
  5. What is the normal ESV?
    50 ml
  6. How do you calculate SV?  What is the normal value?
    EDV - ESV.  70 ml.
  7. What is SV?
    Amt blood ejected during each contraction.
  8. What is EF?
    Fraction of blood ejected during each contraction.
  9. How do you calculate EF?
    SV / EDV
  10. What is preload?  What measurement best defines it?
    Cardiac filling pressure, end diastolic pressure.  Volume that fills the ventricle before contraction.  

  11. What is afterload?
    • Tension that must develop in the ventricular muscle fibers to eject blood.  
    • Systemic arterial pressure.
    • Aortic pressure.
  12. What is cardiac work?
    Contraction or inotropy
  13. How does the body generate the energy required for contraction?
    From oxidation of fatty acids, lactate, and glucose
  14. What is usually on the x and y axis of a Starling curve?
    • X axis LVEDP (pressure)
    • Y axis SV (volume)

    Index of ventricular function against CO or SV
  15. What does the Starling Law state?
    With increased stretching of the heart during filling (increased preload), contractile force is increased.
  16. What is a limitation of the Starling Law?
    There is a point (like a rubber band), where if the heart is stretched too much it can no longer pump effectively.
  17. Stretching the RA with increased preload can increase HR by what percent?
  18. How is CO calculated?
    CO= HR x SV
  19. What are the 2 types of work performed by the heart?
    • 1) External work or pressure volume work
    • 2) Kinetic energy
  20. What does external work in the heart do?
    Moves blood from low pressure veins to high pressure arteries.
  21. What is the majority of work done in the heart?
    What represents this?
    • External work.
    • The pressure volume loop represents EW.
  22. What function does work done with kinetic energy serve in the heart?
    Ejects blood through pulmonic and aortic valves.  Acceleration work.
  23. What occurs during Phase I on the Pressure-Volume loop?
    Ventricle fills.  At start MV opens, ventricle fills, then MV closes.  Goes from ESV to EDV.
  24. What occurs during Phase II on the Pressure-Volume loop?
    Isovolumetric contraction.  MV and aortic valves both closed.
  25. What occurs during Phase III on the Pressure-Volume loop?
    Ejection.  Aortic valve opens, blood is ejected out of ventricle, aortic valve closes.
  26. What occurs during Phase IV on the Pressure-Volume loop?
    Isovolumetric relaxation.  MV and aortic valves are closed.
  27. If preload were to decrease independent of all other factors, how would this affect SV?  ESV?  EF?
    • Decreased SV.  
    • No change to ESV.  
    • Slight decrease EF.
  28. What does the line that goes thru point D in the pressure volume loop represent?
    Line starts at 0 and meets point D. Measures contractile strength.  Increased slope = increased contractility.
  29. If afterload were to decrease independent of all other factors, how would this affect SV?  ESV? EF?
    Increased SV.  Decreased ESV.  Increased EF.
  30. How can HTN lead to ventricular hypertrophy?
    There is a chronic increase in afterload, the ventricle needs to generate a higher LV pressure and wall tension to overcome aortic pressure and open the valve to eject the SV.  The wall of the ventricle gets thicker to adapt.
  31. What's the difference between concentric and eccentric ventricular hypertrophy?
    • Concentric- increased wall thickness
    • Eccentric- increased cavity size (dilation)
  32. Describe how increased afterload causes decreased SV.
    Increased afterload increases the length of Phase II (isovolumetric contraction), more pressure must be build up to open the aortic valve, this leaves less time for ejection as systole is a fixed amount of time.
  33. How would a decrease in inotropy (independent of other factors) affect SV, ESV, and EF?
    Decreased contractility leads to decreased SV, decreased EF, and increased ESV.
  34. In a real person, how does decreased preload affect ventricular function?
    Decreased preload (decreased EDV) causes decreased SV, decreased afterload.  The decrease in afterload leads to a slight decrease in ESV.
  35. In a real person, how does decreased afterload affect ventricular function?
    Decreased afterload leads to a slight increase in SV, decrease in ESV, and slight decrease in EDV (secondary to decreased ESV).
  36. In a real person, how does increased afterload affect ventricular function?
    Increased afterload decreases SV, increases ESV, this causes a slight increase in EDV (preload).  

    Increased preload partially offsets decreased SV caused by initial increased afterload.
  37. How does decreased inotropy affect ventricular function in a real person?
    Decreased contraction causes decreased SV, decreased EF, increased ESV, small increase in EDV
  38. What factors regulate CO (outside the heart)?
    ANS, lytes (K and Ca), Temp, arterial pressure
  39. What happens to the heart with hyperkalemia? Why?
    • -Increased K+ in the ECF (plasma) causes cardiac flaccidity and dilation.  HR and contractility decrease.  
    • -K+ maintains the RMP, increased K+ in the ECF leaves the cell hyperpolarized causing weak cardiac conduction.  
    • -Same effect with hypocalcemia
  40. What effect does hypercalcemia have on the heart?
    The heart becomes spastic due to direct effect of Ca++ on the contractile process.
  41. How does decreased temp affect the heart?
    HR decreases.
  42. How does hyperthermia affect the heart?
    Depends on duration.  At first, inotropy and HR increase (like with exercise).  But with prolonged hyperthermia contractility decreases as the metabolic stores become depleted.
  43. How does excitation of the SNS affect the heart?
    • Can increase HR by up to 200+ bpm
    • Can increase force of contraction
    • Between the 2, CO can increase by 2-3x!!
  44. How does inhibition of the SNS affect the heart?
    Decreases HR and contractility by up to 30%
  45. How does vagal (PNS) stimulation affect the heart?
    • Decreased HR and contractility.
    • Contractility can decrease by 50% or more.
  46. Does the PNS affect HR or contraction more?
    Affects HR more as the vagal fibers go to the atria.
  47. What causes S1?
    • AV valve closure at start of systole
    • Soft sound
  48. What causes S2?
    Semiluminar valve closure immediately after end of systole.
  49. What causes S3, when is it normal?  Abnormal?
    Rapid inflow of blood into the ventricle.  Occurs 1/3 of way through diastole.  S/t heard in normal kids, common in HF patients.
  50. What are similarities and differences between a murmur and a bruit?
    • Both are used to describe turbulent flow.
    • Murmur is reserved for the heart, can be heard due to narrowed or regurg valve, septal defects.

    Bruit usually describes blood vessels.
  51. Describe the path of the conducting system in the heart.
    SA node-internodal pathways-AV node-AV bundle- L and R bundle branches.
  52. Where is the SA node located?
    In the RA on the posterior lateral wall, below and lateral to the SVC entrance.
  53. What part of the heart is responsible for self excitation?
    The SA node
  54. How does the RMP of the PM cells compare to the ordinary cardiac myocyte?
    It is less negative, -55mv vs -90 mv

    This is because the cell membrane is leaky to Na+ and Ca++ ions which go from ECF to ICF
  55. How does the depolarization of the PM cells compare to the ordinary cardiac myocyte?
    Depolarization is more gradual in PM cells.  In the PM cells the fast Na+ channels are inactivated (inner inactivation gate is closed), so the slow Ca++ (Ca-Na) is activated and causes the AP.
  56. What factors cause self excitation?
    • High ECF Na+
    • Open Na+ channels causes Na+ to leak inside which increases the RMP, at -40 mV Na-Ca channels become activated and cause the AP
  57. What 2 factors prevent permanent depolarization of the SA node?
    • 1) Na+Ca++ (slow) channels become inactivated and close
    • 2) K+ channels open, K+ moves out to restore RMP
  58. Where is the AV node located?
    Posterior wall of the RA, behind the tricuspid valve.
  59. Why is there a conduction delay between atria and ventricles?  Is this a bad thing?
    • -Conduction delay occurs due to resistance to conduction secondary to fewer gap junctions (AV node and AV bundle fibers)
    • -The delay is good because it allows atria to empty and ventricles to fill prior to contraction.
  60. What makes up the Purkinje system?  What does it do?
    AV node, AV bundle, transmits AP to ventricles
  61. What fibers have the fastest speed of transmission? Why?
    Purkinje fibers due to highly permeable gap junctions at intercalated discs (ions flow in easily)
  62. SNS involves what NT?  What effect does it have?
    Norepi, beta 1 stimulation causes increased permeability to Na+ and Ca++ ions, they move in and cause a more positive RMP (closer to threshold), this accelerates self excitation and increases HR
  63. What part of the heart does the SNS innervate?
    All parts of the heart.
  64. What part of the heart does the PNS innervate?
    SA and AV nodes mostly by vagi
  65. What NT is involved at the end organ in the PNS?  How does it affect the heart?
    Ach.  When it's released there is increased permeability of the cardiac muscle fiber to K+, this causes K+ to leak outside, leaving the cell hyper polarized (takes stronger stimuli to reach threshold), this slows the HR
  66. What does the P wave on the EKG represent?
    atrial depolarization, remember, depolarization occurs before contraction
  67. What does the QRS wave represent?
    Spread of AP through ventricles.
  68. What does the T wave represent?
    ventricular repolarizaton.
  69. Where is atrial repolarization seen on the EKG?
    It's not as it gets buried in the QRS.
  70. Where are the 3 limb leads located?
    LA, RA, and LL
  71. What does lead I look at?
    Travel of current from RA (-) to LA (+), current travels R to L, QRS is (+)
  72. What does lead II look at?
    Travel of current from RA (-) to LL (+), current travels R to L (towards +), QRS is (+)
  73. What does lead III look at?
    Travel of current from LA (-) to LL (+), current travels (-) to (+), QRS is (+)
  74. What are the precordial leads?
    The chest leads, V1 - V6
  75. What are the augmented unipolar limb leads?
    • aVR (+) terminal on RA
    • aVL (+) terminal on LA
    • aVF (+) terminal on LL
  76. In which precordial leads is the QRS negative?
    V1 and V2
  77. In which precordial leads is the QRS positive?
    V4, V5, V6
  78. Is the QRS (+) or (-) in V3?
    It's a transition lead so neither.
  79. T or F, monitoring 1 lead is sufficient intraoperatively?
    F, we should monitor 1 limb lead and 1 precordial lead.
Card Set
Cardiac Week 2
Cardiac Week 2