Lecture 3 Cardiac Mechanics

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Contents

Slide 23

  • started here on 01/21/11 at 9AM.


  • Handed out corrected last page of heart cycle.
    • The notes are wrong, the new page is correct.


Slide 24

  • Missed some stuff.
  • Do you have enough ATP to keep all this going?
    • When you increase contractility, you also increase your ATP demand.
    • For actin / myosin cross bridges more often per unit time.
  • Oxygen is also needed to make sure we can make the ATP.
    • So heart failure is a lack of oxygen that cuases a lack of ATP.

  • SL = sarcolemma
  • TnI is troponin ihibitor unit.
  • Norepinephrine can interact with beta recetpors.
    • This turns on adeneylel cyclase to make cAMP.
  • Then PKA increases ca opening on membrane and SR.
  • This gets troponin c activated; it moves out of the way.
  • The faster it gets out of the way the more m-a interaction / unit time.
    • This means stronger heart.
  • More ca means a faster, stronger reaction.
  • Phospholaminin inhibits ... something to slow contraction.
  • cAMP activates TnI to inhibit the a-m interaction.
    • This is slightly delayed.
    • In heart failure, this relaxation doesn't work well b/c ca is sticking around.

  • Rate and contractility are highly coordinated.
  • AS rate and contraction go up, it doesn't effect relaxation.

Contractility

Pressure-volume curve

  • This is just a conceptual idea, not something used clinically.
  • Cardiac output can be measured, though.
  • We can also get an end-diastolic pressure of the left ventricle via pulmonary wedge.
  • Increased contractility can move much more blood.
  • Increased contractility means we move more blood given an end diastolic pressure.

Practical applications

  • You can do a stress test with a catheter in the lungs! Whoa.
  • Pt starts at 1, proceeds to 2, then nervous system notices the drop in arterole blood pressure so she moves to 3 (atria increase contractility, arteriels constrict, etc.).
  • What's going on at "4"?
    • Chest pain, weakening, can't keep walking or exercising.
    • Her contractility has decreased and she cannot perfuse her tissue.
    • Her end-diastolic volume would be high.
    • Cardiac output is down, though.

28 yo m

  • Mitral valve is stenosed, so blood doesn't get through well so there is too little. So sympathetics to ventricle increase to make sure that what blood is there gets pumped hard. Sympathetic stim increases left vent mass.
  • Elevated atrial pressure activates a reflex that makes the pt feel like they aren't getting enough air.
    • This happens with MI pts, too.
  • Pt is tired because as left ventricle generates a higher systolic pressure, the right vent has to push through the lungs and against the increased venous pressure.
  • A is the correct answer.

65 yo m

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