Lecture 3 Cardiac Mechanics

From Iusmphysiology

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*continued here from [[Lecture 2 Heart Cycle]] on 01/20/11 at about 11:05AM.
*continued here from [[Lecture 2 Heart Cycle]] on 01/20/11 at about 11:05AM.
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==Cardiac mechanics==
==Cardiac mechanics==
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====Starling principle====
====Starling principle====
 +
*So let's look at a heart cycle and how volume can affect it.
 +
*Start with the relaxed ventricle.
 +
*The volume increases passively and the pressure increases--following the passive tension curve.
 +
Shouldn't the bottom line curve upward more rapidly at the end to represent active filling--the volume and pressure would both increase more rapidly (steaper slope) when the atrium is contracting.
 +
**Atrium systole, at resting heart rates, only contributes a small portion of the ventricular volume.
 +
**At high exercise, the atrial systole becomes important.
 +
*Heart is filled, AV node fires, ventricular pressure increases but there is no change in pressure.
 +
*Then ventricular pressure exceeds diastolic arterial pressure such that the aortic valve opens and the ventricle explosively ejects blood.
 +
**The line is curved as it runs negatively.
 +
**The curved part of the line is because of the rapid ejection phase: when the volume is decreasing (blood is exiting the ventricle) but the pressure is still rising (because the blood isn't leaving as fast as the ventricle is still contracting to increase pressure).
 +
**Note that the pressure doesn't get to the total tension line because there is blood leaving the system so the pressure doesn't build up to the pressures the heart could put on a volume of blood.
 +
***We call this contractility: the best the heart can do given a pressure and volume curve.
 +
*We can measure contractility by measuring the ventricular volume throughout heart cycles (to generate the box on this graph) as we vary the total blood volume.
 +
**This will generate a straight line along the top left point (where the ventricle undergoes isovolumetric relaxation) when you put all the cycles on one graph.
 +
**The red line is the contractility.
 +
====Cardiac work====
 +
*We can use contractility to look at cardiac work.
 +
*The work inside the graph cicrle is calculated as mean arterial pressure * stroke volume
 +
**That is: cardiac work = mean arterial pressure * stroke volume
 +
*We care about this because we can use drugs and hormones to change the stroke volume.
 +
**These change the EDV and the ESV
 +
**Recall that SV = EDV (volume of blood in ventricle just before it starts to undergo isovolumentric contraction) - ESV (volume of blood in the ventricle just as it starts to undergo isovolumetric relaxation)
-
======
+
====Vigor of contractility====
 +
*Starling described how changes in EDV could change contractility.
 +
**We also call it heterometric regulation.
 +
**it all means, stretch it more, it works better.
 +
*If we increase the pt's blood volume, we get the dotted box.
 +
**We can do this with infusion or with venous contraction, ''et cetera''.
 +
*8Note that the area is bigger so there is more work.
-
======
+
====Preload effect====
 +
*Preload is a term that describes the pressure that effectively stretches the ventricle when filling it with blood.
 +
*Increased preload can be caused by:
 +
**increased venous pressure
 +
**increased atrial contraction
 +
**increased ventricular stretch resistance
 +
*Venous pressure is generally the culprit in the case of increased preload.
-
======
 
-
======
+
*Causes of preload increase:
 +
**Venous contraction
 +
***cold weather causes sympathetic response to decrease blood flow at periphery, this increases the venous pressure, and thus the preload increases
 +
**Blood volume expansion
 +
***Drinking lots of liquid will expand the blood volume and increase EDV.
-
======
 
-
======
+
*Effects of preload increase:
 +
**We usually assume that the EDV goes up when the preload goes up; and this is usually a safe assumption unless the pt is sick.
 +
**The stroke volume will go up when EDV goes up.
 +
**The arterial pressure will go up.
 +
**The ejection fraction will go up, too.
 +
***Healthy = 65-70%
 +
***50% is not too good
 +
***<50% is pretty bad
-
======
 
-
======
+
====Decreased preload====
 +
*Preload decreases when the venous pressure decreases or the atrial contraction pressure decreases.
-
======
 
-
======
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*Causes of preload decrease:
 +
**Dilation of veins
 +
**Loss of blood volume
-
======
 
-
======
+
*Effects of preload decrease:
 +
**Decreased EDV
 +
**Decreased SV
 +
**Decreases arterial pressure
-
======
+
====Changes in arterial pressure====
 +
*Now we'll talk about changes in the pressure against which the ventricles are pumping.
 +
*The pressure against which the ventricles must force blood is called '''after load'''.
 +
*The after load is a function of:
 +
**Arterial pressure
 +
**Distensibility of larger arteries
 +
***As we age they become less distension, so after load goes up.
-
======
+
=====Afterload increase=====
 +
*Results of afterload increase:
 +
**Heart fills normally
 +
**Work is used to develop pressure, not shortening
 +
**Stroke volume decreases (because we can't spend work on shortening)
 +
**Heart ends up bigger (higher volume) at the end of systole than in the previous cycle
-
======
+
*Causes of afterload increase
 +
**Atherosclerotic buildup
-
======
+
=====Afterload decrease=====
 +
*Results of afterload decrease:
 +
**pump just fine, don't have to
 +
**heart gets smaller at the end of systole than in the previous cycle
-
======
+
*Cause of afterload decrease:
 +
**vascular resistance went down, bp followed
 +
**Cardiac work also improves
 +
***Heart uses work to push a bigger volume at a lower pressure
 +
**Ejection fraction increases
 +
**Higher cardiac output
 +
**Less arterial pressure
-
======
+
===Cardiac contractility===
 +
*Hypertension would generate subnormal cardiac output so the body has to adjust the wya the heart works.
 +
**so SV will be OK but it could be better
 +
*Fixing blood pressure will decrease afterload and increase SV and make the heart more efficient.
-
======
+
====Consequences of altered contractility====
 +
*If we couldn't change contractility, we'd be in bad shape because resting contractility wouldn't even get us up a flight of stairs.
 +
*How fast can contractility change?  two beats of the heart.
 +
**Less in very healthy people.
 +
**5 seconds to ramp it up
 +
**Norepi and epi
 +
*What's different in elevated contracility?
 +
**For a given volume, we can have higher pressure, more work done, and more blood ejected.
 +
**Thishappens all the time.
 +
*What's different in reduced contractility?
 +
**Less work, less pressure, less pressure
 +
**Sympathetics go to sleep when we sleep.
 +
**Think headrush upon standing quickly from relaxed position.
-
======
+
====Increasing contractility====
 +
*We could do this with an unexpected loud noise.
 +
*Sympathetics drop epi and norepi
 +
*More pressure, more volume for a given EDV.
 +
*We always want to look at the EDV when asked about contractility changes.
 +
**If EDV hasn't changed much and the heart is then the contractility went up.
 +
*Typical results:
 +
**Heart gets filled and generates very high pressures.
 +
**Increases stroke volume.
 +
**Higher ejection fraction
 +
**Smaller ESV
 +
*Causes:
 +
**Sympathetic nervous system
 +
***Adjusts contractility moment to moment
-
======
+
====Decreased contractility====
 +
*The heart is bigger with decreased contractility but isn't pumping well:
 +
**Low pressures
 +
**Less stroke volume
 +
*If you don't pump the blood into the arteries, it stays in the venous system.
 +
*If the venous system gets filled with blood from the periphery, the venous system goes up.
 +
**This causes distended neck veins.
 +
**This also inflates the heart, too, such that it stretches a bit more (increased venous pressure, increased preload).
 +
*Effects:
 +
**Low SV
 +
**Decreased ejection fraction
 +
**Increased EDV
 +
**Low pressures
 +
*Causes:
 +
**Decreased sympathetic activity
 +
**Inadequate coronary blood flow / cardiac tissue damage
 +
***MI, no seatbelt / airbag thus jostled heart,
-
======
+
====Actual contractility recordings====
 +
*Pressure goes up, heart increases contractility, then
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*Beta adrenergic signaling
 +
**Faster formation of pressure, more pressure, faster relaxation (faster Ca removal from the muscle)
 +
**All the phases of the cardiac cycle go faster
 +
**Note that vent may start smaller because the atria didn't fill the ventricle.
-
======
 
-
======
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*We can think about contractility as a function of the left ventricular pressure
 +
**We do this because the LVP can be measured via cath.
 +
**We can use a cath to measure pressure in isovolumetric contraction
 +
**This is only done when the patient is really sick, though.
 +
**The contractility is the first derivative of pressure: dp / dt
 +
**The steeper the slope (when changes in pressure during isovolumetric contraction is plotted over time), the better the contractility.
-
======
 
-
======
+
*We can also think about the left ventricular volume
 +
**There is a faster ejection and larger ejection of the left ventricle volume
 +
**There is also a larger SV.
 +
**Higher arterial pressure
 +
**May not have a larger EDV; might pump blood out so well that venous passive pressure couldn't keep up and thus there is less blood dropped into the ventricle such that it may get smaller.
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*stopped here on 01/20/11 at 12:00PM
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*started here on 01/21/11 at 9AM
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===Slide 23===
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*started here on 01/21/11 at 9AM.
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===Slide 24===
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===Contractility issues===
-
*Missed some stuff.
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*The heart not only contracts faster but also relaxes faster when contractility is increased via sympathetics.
 +
*The bottom line of contractility is how much Ca is available to the actin and myosin control systems.
 +
**When heart is activated, most Ca comes from SR via cdcr via ryanidine.
 +
*Removal of this Ca determines relaxation.
 +
**Cardiac muscle is not always revved up with tons of Ca-removing machinery.
 +
**But when we increase contractility, we also increase the cells' ability to remove Ca from the cytoplasm, thus making relaxation faster.
*Do you have enough ATP to keep all this going?
*Do you have enough ATP to keep all this going?
-
**When you increase contractility, you also increase your ATP demand.
+
**When you increase contractility, you also increase your ATP demand because we need lots of ATP to pump the Ca out.
**For actin / myosin cross bridges more often per unit time.
**For actin / myosin cross bridges more often per unit time.
*Oxygen is also needed to make sure we can make the ATP.
*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.
**So heart failure is a lack of oxygen that cuases a lack of ATP.
-
=== ===
+
===Biochemical regulation of contractility by Beta Adrenergic Stimulation:===
*SL = sarcolemma
*SL = sarcolemma
*TnI is troponin ihibitor unit.
*TnI is troponin ihibitor unit.
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**In heart failure, this relaxation doesn't work well b/c ca is sticking around.
**In heart failure, this relaxation doesn't work well b/c ca is sticking around.
-
=== ===
+
===Effect of Heart Rate on Contractility===
*Rate and contractility are highly coordinated.
*Rate and contractility are highly coordinated.
*AS rate and contraction go up, it doesn't effect relaxation.
*AS rate and contraction go up, it doesn't effect relaxation.
===Contractility===
===Contractility===
-
*
 
===Pressure-volume curve===
===Pressure-volume curve===
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===65 yo m===
===65 yo m===
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*Moved on to [[Lecture 4 Arterial Blood Pressure]] on 01/21/11 at 9:32AM.
*Moved on to [[Lecture 4 Arterial Blood Pressure]] on 01/21/11 at 9:32AM.

Current revision as of 22:12, 27 January 2011


Contents

[edit] 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.

[edit] Objectives

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

[edit] 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.

[edit] 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.

[edit] 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.

[edit] 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

[edit] 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

[edit] Starling principle

  • So let's look at a heart cycle and how volume can affect it.
  • Start with the relaxed ventricle.
  • The volume increases passively and the pressure increases--following the passive tension curve. 
Shouldn't the bottom line curve upward more rapidly at the end to represent active filling--the volume and pressure would both increase more rapidly (steaper slope) when the atrium is contracting.
**Atrium systole, at resting heart rates, only contributes a small portion of the ventricular volume.
**At high exercise, the atrial systole becomes important.
  • Heart is filled, AV node fires, ventricular pressure increases but there is no change in pressure.
  • Then ventricular pressure exceeds diastolic arterial pressure such that the aortic valve opens and the ventricle explosively ejects blood.
    • The line is curved as it runs negatively.
    • The curved part of the line is because of the rapid ejection phase: when the volume is decreasing (blood is exiting the ventricle) but the pressure is still rising (because the blood isn't leaving as fast as the ventricle is still contracting to increase pressure).
    • Note that the pressure doesn't get to the total tension line because there is blood leaving the system so the pressure doesn't build up to the pressures the heart could put on a volume of blood.
      • We call this contractility: the best the heart can do given a pressure and volume curve.
  • We can measure contractility by measuring the ventricular volume throughout heart cycles (to generate the box on this graph) as we vary the total blood volume.
    • This will generate a straight line along the top left point (where the ventricle undergoes isovolumetric relaxation) when you put all the cycles on one graph.
    • The red line is the contractility.

[edit] Cardiac work

  • We can use contractility to look at cardiac work.
  • The work inside the graph cicrle is calculated as mean arterial pressure * stroke volume
    • That is: cardiac work = mean arterial pressure * stroke volume
  • We care about this because we can use drugs and hormones to change the stroke volume.
    • These change the EDV and the ESV
    • Recall that SV = EDV (volume of blood in ventricle just before it starts to undergo isovolumentric contraction) - ESV (volume of blood in the ventricle just as it starts to undergo isovolumetric relaxation)

[edit] Vigor of contractility

  • Starling described how changes in EDV could change contractility.
    • We also call it heterometric regulation.
    • it all means, stretch it more, it works better.
  • If we increase the pt's blood volume, we get the dotted box.
    • We can do this with infusion or with venous contraction, et cetera.
  • 8Note that the area is bigger so there is more work.

[edit] Preload effect

  • Preload is a term that describes the pressure that effectively stretches the ventricle when filling it with blood.
  • Increased preload can be caused by:
    • increased venous pressure
    • increased atrial contraction
    • increased ventricular stretch resistance
  • Venous pressure is generally the culprit in the case of increased preload.


  • Causes of preload increase:
    • Venous contraction
      • cold weather causes sympathetic response to decrease blood flow at periphery, this increases the venous pressure, and thus the preload increases
    • Blood volume expansion
      • Drinking lots of liquid will expand the blood volume and increase EDV.


  • Effects of preload increase:
    • We usually assume that the EDV goes up when the preload goes up; and this is usually a safe assumption unless the pt is sick.
    • The stroke volume will go up when EDV goes up.
    • The arterial pressure will go up.
    • The ejection fraction will go up, too.
      • Healthy = 65-70%
      • 50% is not too good
      • <50% is pretty bad


[edit] Decreased preload

  • Preload decreases when the venous pressure decreases or the atrial contraction pressure decreases.


  • Causes of preload decrease:
    • Dilation of veins
    • Loss of blood volume


  • Effects of preload decrease:
    • Decreased EDV
    • Decreased SV
    • Decreases arterial pressure

[edit] Changes in arterial pressure

  • Now we'll talk about changes in the pressure against which the ventricles are pumping.
  • The pressure against which the ventricles must force blood is called after load.
  • The after load is a function of:
    • Arterial pressure
    • Distensibility of larger arteries
      • As we age they become less distension, so after load goes up.
[edit] Afterload increase
  • Results of afterload increase:
    • Heart fills normally
    • Work is used to develop pressure, not shortening
    • Stroke volume decreases (because we can't spend work on shortening)
    • Heart ends up bigger (higher volume) at the end of systole than in the previous cycle
  • Causes of afterload increase
    • Atherosclerotic buildup
[edit] Afterload decrease
  • Results of afterload decrease:
    • pump just fine, don't have to
    • heart gets smaller at the end of systole than in the previous cycle
  • Cause of afterload decrease:
    • vascular resistance went down, bp followed
    • Cardiac work also improves
      • Heart uses work to push a bigger volume at a lower pressure
    • Ejection fraction increases
    • Higher cardiac output
    • Less arterial pressure

[edit] Cardiac contractility

  • Hypertension would generate subnormal cardiac output so the body has to adjust the wya the heart works.
    • so SV will be OK but it could be better
  • Fixing blood pressure will decrease afterload and increase SV and make the heart more efficient.

[edit] Consequences of altered contractility

  • If we couldn't change contractility, we'd be in bad shape because resting contractility wouldn't even get us up a flight of stairs.
  • How fast can contractility change? two beats of the heart.
    • Less in very healthy people.
    • 5 seconds to ramp it up
    • Norepi and epi
  • What's different in elevated contracility?
    • For a given volume, we can have higher pressure, more work done, and more blood ejected.
    • Thishappens all the time.
  • What's different in reduced contractility?
    • Less work, less pressure, less pressure
    • Sympathetics go to sleep when we sleep.
    • Think headrush upon standing quickly from relaxed position.

[edit] Increasing contractility

  • We could do this with an unexpected loud noise.
  • Sympathetics drop epi and norepi
  • More pressure, more volume for a given EDV.
  • We always want to look at the EDV when asked about contractility changes.
    • If EDV hasn't changed much and the heart is then the contractility went up.
  • Typical results:
    • Heart gets filled and generates very high pressures.
    • Increases stroke volume.
    • Higher ejection fraction
    • Smaller ESV
  • Causes:
    • Sympathetic nervous system
      • Adjusts contractility moment to moment

[edit] Decreased contractility

  • The heart is bigger with decreased contractility but isn't pumping well:
    • Low pressures
    • Less stroke volume
  • If you don't pump the blood into the arteries, it stays in the venous system.
  • If the venous system gets filled with blood from the periphery, the venous system goes up.
    • This causes distended neck veins.
    • This also inflates the heart, too, such that it stretches a bit more (increased venous pressure, increased preload).
  • Effects:
    • Low SV
    • Decreased ejection fraction
    • Increased EDV
    • Low pressures
  • Causes:
    • Decreased sympathetic activity
    • Inadequate coronary blood flow / cardiac tissue damage
      • MI, no seatbelt / airbag thus jostled heart,

[edit] Actual contractility recordings

  • Pressure goes up, heart increases contractility, then
  • Beta adrenergic signaling
    • Faster formation of pressure, more pressure, faster relaxation (faster Ca removal from the muscle)
    • All the phases of the cardiac cycle go faster
    • Note that vent may start smaller because the atria didn't fill the ventricle.


  • We can think about contractility as a function of the left ventricular pressure
    • We do this because the LVP can be measured via cath.
    • We can use a cath to measure pressure in isovolumetric contraction
    • This is only done when the patient is really sick, though.
    • The contractility is the first derivative of pressure: dp / dt
    • The steeper the slope (when changes in pressure during isovolumetric contraction is plotted over time), the better the contractility.


  • We can also think about the left ventricular volume
    • There is a faster ejection and larger ejection of the left ventricle volume
    • There is also a larger SV.
    • Higher arterial pressure
    • May not have a larger EDV; might pump blood out so well that venous passive pressure couldn't keep up and thus there is less blood dropped into the ventricle such that it may get smaller.


  • stopped here on 01/20/11 at 12:00PM
  • 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.


[edit] Contractility issues

  • The heart not only contracts faster but also relaxes faster when contractility is increased via sympathetics.
  • The bottom line of contractility is how much Ca is available to the actin and myosin control systems.
    • When heart is activated, most Ca comes from SR via cdcr via ryanidine.
  • Removal of this Ca determines relaxation.
    • Cardiac muscle is not always revved up with tons of Ca-removing machinery.
    • But when we increase contractility, we also increase the cells' ability to remove Ca from the cytoplasm, thus making relaxation faster.
  • Do you have enough ATP to keep all this going?
    • When you increase contractility, you also increase your ATP demand because we need lots of ATP to pump the Ca out.
    • 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.

[edit] Biochemical regulation of contractility by Beta Adrenergic Stimulation:

  • 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.

[edit] Effect of Heart Rate on Contractility

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

[edit] Contractility

[edit] 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.

[edit] 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.

[edit] 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.

[edit] 65 yo m

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