Lecture 3 Cardiac Mechanics

From Iusmphysiology

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(Created page with ' ===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 som…')
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*continued here from [[Lecture 2 Heart Cycle]] on 01/20/11 at about 11:05AM.
 +
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==Cardiac mechanics==
 +
*This is one of the more difficult parts of the course.
 +
**This will take up to two days.
 +
*these are the rules that get us from actin and myosin to a beating heart.
 +
 +
===Objectives===
 +
*These objectives are a bit complicated.
 +
**may have to have multiple thought processes and graphs and charts in mind.
 +
**Be actively involved.
 +
 +
===The left and right ventricles: the high and low pressure pumps===
 +
*The two sides are very diff:
 +
**left is massive, strong, heavy muscular wall
 +
**Left has high diastolic, left atrium has to work at higher pressure both passively and actively.
 +
**right is relatively weak with thin musculature, works at low pressures
 +
**The right atrium has lower pressures because it is easy to fill the right ventricle.
 +
 +
 +
*PCW: pulmonary capillary wedge pressure.
 +
**Very few collaterals in microvessels of the lung
 +
**Running a catheter through the femoral vein, the right atrium, the right ventricle, the pulmonary valve, the pulmonary artery, until it plugs, you can measure the downstream pulmonary vein pressure pressure.
 +
**This pressure approximates the left atrial pressure without getting into the arterial system.
 +
**This is pretty easy.
 +
 +
 +
*Both vents have to pump the same volume.
 +
**if off by 0.5%, you'll die in about a half hour
 +
**blood would fill veins or lungs or whatever.
 +
 +
 +
*Cardiac work:
 +
**Ideally: systolic pressyre * stroke volume
 +
**However, some energy goes into distending arteries.
 +
***Mean arterial pressure * stroke volume is a better measure of work
 +
**Work describes the strength of the heart.
 +
 +
 +
*Diastolic filling pressures:
 +
**left:
 +
***works at very high pressures,
 +
***requires more atrial pressure to fill it because of the thick muscle wall
 +
**right:
 +
***rarely above 30 mmHg, 0-8 or even negative diastolic pressures because the wall is so thin
 +
**Recall that thoracic pressure is constantly varying: -3 mmHg
 +
**This affects mostly the right ventricle which is thinner.
 +
*running hard and fast generates more negative and more positive pressures when breathing
 +
**this turns out to be beneficial for the right ventricle
 +
**Helps expand the right ventricle to make pumping less work on the right ventricle muscle tissue.
 +
 +
====Muscle mass and shape of ventricular chambers====
 +
*There is a thick left wall.
 +
*The septum is really part of the thick left wall.
 +
*The right ventricle looks like a bellows connected on the side.
 +
*The right ventrcle, the way it hangs off as a bellows is good for increasing volume of the ventricle, but is bad for generating lots of pressure (because the SA is so large).
 +
**the right ventricle fails more rapidly than the left once it starts to have problems getting blood to and through the pulmonary system.
 +
*The cone-shaped left ventrcile is just about ideal for generating high pressures.
 +
**heavy walled, conical, lots of force with little surface area.
 +
 +
===Translation of contraction and shortening of ventricular muscle into cardiac pumping===
 +
*How do we get from sarcomeres to ejection of blood from a ventricle?
 +
*Muscles can do two things to change forces:
 +
**Change tension
 +
**Change length
 +
*They are built to pull on things to which they are connected.
 +
*Recall that tension = force / length
 +
*We also know, via the laplace relationship (Tension = pressure * radius) that:
 +
**pressure = force / surface area
 +
**Laplace describes the relationship between length and radius and force and pressure.
 +
*So, since the radius is determined by the length of the muscle (the more it shortens, the more the radius goes down), we can say that:
 +
**pressure (inside the heart) = tension (on muscle cells) / radius (of the chamber)
 +
*This deduction does not work for the right ventrcle because it is shaped like a bellows, but it works nicely for the left ventricle.
 +
*So we graph tension and pressure together (y axis) because they are proportional.
 +
*and we graph cell length and radius together (x axis) because they are proportional.
 +
*The bottom curve is the passive curve, with no muscular action potentials causing contraction.
 +
**This shows the resistance (or tension) on a muscle simply as it is stretched without APs firing.
 +
*The top curve is the total tension curve.
 +
I don't understand what this shows.
 +
*The active tension curve
 +
**this describes the heart cycle
 +
**Starts partially empty; has pumped out a bunch of the blood in the last ventricular systole.
 +
***bottom left corner of parallelogram
 +
**Fill passively by venous and atrial pressure.
 +
***Radius increases while tension increases only passively--that is, in a manner similar to the passive tension curve.
 +
***Bottom line
 +
**Then the ventricle undergoes isovolumetric contraction
 +
***Now the muscle is squeezing down on the blood in the ventricle to build up pressure, but it has not yet pushed any blood out, so the volume remains the same.
 +
***The right verticle line of the parallelogram.
 +
**Then the left ventricle ejects blood into the aorta
 +
***The ventricle muscle fibers get shorter and the tension decreases.
 +
***Top line of parallelogram.
 +
**Ventricle stops contracting
 +
***The tension decreases but the volume remains the same.
 +
***The left verticle line of the parallelogram.
 +
 +
====Sarcomere length====
 +
*Why do we worry about the volume and length parameter?
 +
*Heart muscle lives at an interesting sarcomere length.
 +
*They can move from 1.3 to 3.x.
 +
*In the low 2 microns they generate their best tension.
 +
*Longer or shorter they generate less tension.
 +
*Mammalian hearts peak tension at about 2.2 microns; but they live at about 70% of that: 1.6 or 1.7 microns.
 +
**That's where the heart beats from at rest.
 +
*when we stretch the heart a bit, there will be increased length, getting closer to the ideal of 2.2 and thus tension can go up.
 +
*We don't ever get to the point that we overstretch the cardiac sarcomeres.
 +
**Dosn't happen in normal people.
 +
***two reasons:
 +
****Hard to stretch heart inside pericardium.
 +
****Heart resists being stretched.
 +
**Can happen in sick people.
 +
 +
 +
*Why does tension change at the extremes of length?
 +
**Too short: actin and myosin overlap so much that they can't move along one another very far and therefore can't shorten much and therefore can't generate much tension
 +
**Too long: actin and myosin aren't overlapped enough to generate many cross bridges
 +
 +
===Starling principle===
 +
*Starling:
 +
**discovered first hormone
 +
**dying of heart failure (1920s, 1930s), described heart failure
 +
 +
 +
*Living at just below our ideal tension length means that we can use an increase in blood volume
 +
**that is, the amount of blood put into the ventricle can change the length of the sarcomeres--more blood, longer sarcomere--such that increased blood volume can move the sarcomeres to better tension generating lengths (say from 1.4 microns to 2.1 microns
 +
 +
====Starling principle====
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===Slide 23===
===Slide 23===

Revision as of 16:51, 27 January 2011

Contents

Cardiac mechanics

  • This is one of the more difficult parts of the course.
    • This will take up to two days.
  • these are the rules that get us from actin and myosin to a beating heart.

Objectives

  • These objectives are a bit complicated.
    • may have to have multiple thought processes and graphs and charts in mind.
    • Be actively involved.

The left and right ventricles: the high and low pressure pumps

  • The two sides are very diff:
    • left is massive, strong, heavy muscular wall
    • Left has high diastolic, left atrium has to work at higher pressure both passively and actively.
    • right is relatively weak with thin musculature, works at low pressures
    • The right atrium has lower pressures because it is easy to fill the right ventricle.


  • PCW: pulmonary capillary wedge pressure.
    • Very few collaterals in microvessels of the lung
    • Running a catheter through the femoral vein, the right atrium, the right ventricle, the pulmonary valve, the pulmonary artery, until it plugs, you can measure the downstream pulmonary vein pressure pressure.
    • This pressure approximates the left atrial pressure without getting into the arterial system.
    • This is pretty easy.


  • Both vents have to pump the same volume.
    • if off by 0.5%, you'll die in about a half hour
    • blood would fill veins or lungs or whatever.


  • Cardiac work:
    • Ideally: systolic pressyre * stroke volume
    • However, some energy goes into distending arteries.
      • Mean arterial pressure * stroke volume is a better measure of work
    • Work describes the strength of the heart.


  • Diastolic filling pressures:
    • left:
      • works at very high pressures,
      • requires more atrial pressure to fill it because of the thick muscle wall
    • right:
      • rarely above 30 mmHg, 0-8 or even negative diastolic pressures because the wall is so thin
    • Recall that thoracic pressure is constantly varying: -3 mmHg
    • This affects mostly the right ventricle which is thinner.
  • running hard and fast generates more negative and more positive pressures when breathing
    • this turns out to be beneficial for the right ventricle
    • Helps expand the right ventricle to make pumping less work on the right ventricle muscle tissue.

Muscle mass and shape of ventricular chambers

  • There is a thick left wall.
  • The septum is really part of the thick left wall.
  • The right ventricle looks like a bellows connected on the side.
  • The right ventrcle, the way it hangs off as a bellows is good for increasing volume of the ventricle, but is bad for generating lots of pressure (because the SA is so large).
    • the right ventricle fails more rapidly than the left once it starts to have problems getting blood to and through the pulmonary system.
  • The cone-shaped left ventrcile is just about ideal for generating high pressures.
    • heavy walled, conical, lots of force with little surface area.

Translation of contraction and shortening of ventricular muscle into cardiac pumping

  • How do we get from sarcomeres to ejection of blood from a ventricle?
  • Muscles can do two things to change forces:
    • Change tension
    • Change length
  • They are built to pull on things to which they are connected.
  • Recall that tension = force / length
  • We also know, via the laplace relationship (Tension = pressure * radius) that:
    • pressure = force / surface area
    • Laplace describes the relationship between length and radius and force and pressure.
  • So, since the radius is determined by the length of the muscle (the more it shortens, the more the radius goes down), we can say that:
    • pressure (inside the heart) = tension (on muscle cells) / radius (of the chamber)
  • This deduction does not work for the right ventrcle because it is shaped like a bellows, but it works nicely for the left ventricle.
  • So we graph tension and pressure together (y axis) because they are proportional.
  • and we graph cell length and radius together (x axis) because they are proportional.
  • The bottom curve is the passive curve, with no muscular action potentials causing contraction.
    • This shows the resistance (or tension) on a muscle simply as it is stretched without APs firing.
  • The top curve is the total tension curve. 
I don't understand what this shows.
  • The active tension curve
    • this describes the heart cycle
    • Starts partially empty; has pumped out a bunch of the blood in the last ventricular systole.
      • bottom left corner of parallelogram
    • Fill passively by venous and atrial pressure.
      • Radius increases while tension increases only passively--that is, in a manner similar to the passive tension curve.
      • Bottom line
    • Then the ventricle undergoes isovolumetric contraction
      • Now the muscle is squeezing down on the blood in the ventricle to build up pressure, but it has not yet pushed any blood out, so the volume remains the same.
      • The right verticle line of the parallelogram.
    • Then the left ventricle ejects blood into the aorta
      • The ventricle muscle fibers get shorter and the tension decreases.
      • Top line of parallelogram.
    • Ventricle stops contracting
      • The tension decreases but the volume remains the same.
      • The left verticle line of the parallelogram.

Sarcomere length

  • Why do we worry about the volume and length parameter?
  • Heart muscle lives at an interesting sarcomere length.
  • They can move from 1.3 to 3.x.
  • In the low 2 microns they generate their best tension.
  • Longer or shorter they generate less tension.
  • Mammalian hearts peak tension at about 2.2 microns; but they live at about 70% of that: 1.6 or 1.7 microns.
    • That's where the heart beats from at rest.
  • when we stretch the heart a bit, there will be increased length, getting closer to the ideal of 2.2 and thus tension can go up.
  • We don't ever get to the point that we overstretch the cardiac sarcomeres.
    • Dosn't happen in normal people.
      • two reasons:
        • Hard to stretch heart inside pericardium.
        • Heart resists being stretched.
    • Can happen in sick people.


  • Why does tension change at the extremes of length?
    • Too short: actin and myosin overlap so much that they can't move along one another very far and therefore can't shorten much and therefore can't generate much tension
    • Too long: actin and myosin aren't overlapped enough to generate many cross bridges

Starling principle

  • Starling:
    • discovered first hormone
    • dying of heart failure (1920s, 1930s), described heart failure


  • Living at just below our ideal tension length means that we can use an increase in blood volume
    • that is, the amount of blood put into the ventricle can change the length of the sarcomeres--more blood, longer sarcomere--such that increased blood volume can move the sarcomeres to better tension generating lengths (say from 1.4 microns to 2.1 microns

Starling principle

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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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