Contractility and CO Flashcards
CO
depends on cardiac factors and coupling factors. What are they?
Cardiac factors= HR and contractility
Coupled factors = preload and afterload
What is contractility proportional to?
Contractility is proportional to the amount of Ca2+ that is availble to bind to troponin located on actin.
Length tension curve in cardiac muscle
Similar to skeletal muscle.
Cardiac muscle depends on the degree of myofilament overlap.
It generates the most tension at a certain length. Once that length is supassed, tension decreases.
In the heart, as pressure increses (filling of the ventricles increases), what happens to tension
increases
What limb does the heart operate on?
Ascending limb
Our heart is operating at what force? What happens when we contract?
Our heart is operating at a force below optimum. When we contract, we reach an optimal length.
What is another name for preload?
End diastolic volume.
Preload is the amount of blood that we can eject from the LV (thus, the volume at the end of diastole)
How do we get the most accurate reading of our prelad?
The amount of tension in the RV/LV just before it contracts.
Draw the EDV and ventricular pressure curve.
Indicate where preload is at and what this graph means
What is afterload?
Afterload is the pressure needed to eject the blood frmo our LV (thus, our aortic pressure).
It will usually be between 70-80 mmHg.
What happens to the velocity of contraction if we increase afterload?
Increase afterload= decrease velocity.
When is velocity of contraction the greatest, compared to afterload?
Afterload= 0= greatest velocity.
Draw the velocity of contraction vs. afterload graph
Where is our preload and afterload on the cardiac cycle graph?
Afterload- pressure the semilunar valve opens
Preload= the amount of blood in the ventricle right before we eject it.
How do we calculate SV?
EDV-ESV
usually about 70mL
How do we calculate the ejection fraction (the percentage of blood ejected)?
EDV-ESV (SV/ EDV
What does our ejection fraction tell us?
The measure of efficiency and contractility
Normal CO
Usually about 5
What is the Frank Starling Relationship
The volume of blood that we eject from the ventricle
will depend on the amount of blood present at the end of diastole.
The volume of blood at our EDV relates to what?
Venous return, which should be near CO.
An increase in chronotropy will increase our HR.
How will this effect ionotropy?
Should increase; increase force of contraction because less Ca2+ is leaving the cell, producing a stronger force of contraction
How will in a + ionotropy effect/-ionotropy effect alter our CO (SV) vs EDV graph?
Draw
Ventricular pressure loop
Draw and label
- Phases of cardiac cycle
- EDV
- Preload
- Max pressure during ejection
- End of systole
- AV valve closure
- Afterload
- Opening and closing of semilunar valves.
Increasing preload will do what do the presure volume loop?
What effects will we see?
Draw
Increase preload= increase EDV (SV) = increase VR= increase BV=
= afterload and contractility will remain the same.
Number one will shift to the right
Increasing afterload will do what to the P/V loop?
decrease in afterload?
Draw.
Increased afterload= greater pressure needed= reduced SV = reduced ECF
Increase pressure during isvolumetric ventricular contraction because we need more pressure to drive out the blood= increase in point 2.
When do we see an increased afterload?
Aortic stenosis and HTN.
How does an increase in contractility alter our PV loop?
draw
Increase in contractility= increase SV= increase in EF%= less blood is left in the heart
shift the curve to the left because are increasing the amount of blood we pump out.
Sympathetic activation via B1 receptors on our ventricular myocytes will increase force of contraction (ionotropy).
How does this occur?
- Sarcolemma Ca2+ channels will be phosphorylated
- Phospholambam will be phosphorylated- helping SERCA resequester Ca2+= increase force of contraction.
- Phosphorylate troponin I, which will inhibit it. Allowing Ca2+ to bind to troponin C.
Parasymphthatic activation will produce a _____ ionotropic effect where?
What happens?
PNS activation will produce a NEGATIVE ionotropic effect in the atria only.
Decreases inward Ca2+ influx during the plateau.
ACh increases K+ efflux via the K+ ACh channel.
What happens to contractility as HR increases?
We will see the positive staircase effect.
Increase HR (+chronotropic effect) will cause less Ca2+ to leave the cell and enter SR.
As a result, this will increase contractility (+ ionotropic effect).
What is the result of increased contractility d/t increased HR?
Postextrasystolic potentiation–> Extra beat occurs too quickly, leaving more Ca2+ in the cell. Next AP will produce a stronger FOC.
After, HR returns to normal.
Cardiac glycosides causes a positive ionotropic effect and is used to tx heart failure.
How?
- Inhibits K+ from binding to Na/K ATPase, thus, inhibiting channel.
- Causes an increase in Na+ concentration
- Activates the NCX.
- 3 Na+ leave, 1 Ca+ enters
- Ca2+ intracellular increases
6. + ionotropic effect
Minute work
CO (also called volume work)* aortic pressure (aka pressure work)
CO * aortic pressure
Stroke work is performed by the LV.
How do we calculate?
What does this represent?
SV * aortic pressure.
This represents the area inside the pressure volume loop. Increase stress work= work harder to beat.
To tell if it is increase= look to see if the loop is bigger or smaller
What requires more oxygen:
Pressure work (aortic pressure) volume work (cardiac output)?
Pressure work (aortic pressure).
The LV works harder than the RV even though CO is the same because systemic pressure is greater than pulmonary. You can see this more in aortic stenosis or systemic HTN.
CO= [in relation to O2]
O2 consumption/ [O2 in the pulmonary vein- O2 in the pulmonary artery]
How are CO and VR related?
An increase in VR= increase CO= increase right atrial pressure= increase EDV–> increase fiber length of diastolic fiber.
In a steady state,
The volume of blood as CO ejected by the LV will be what?
Equal to VR.
Describe the cardiac function (CO) and vascular fx (VR) curve.
This tells us that CO can be altered by changing the cardiac function curve or the vascular fx curve.
draw
At equillibrium, CO= VR at a specific preload.
Mean system pressure is the RAP when there is no flow in the cardiovascular syste,
Cardiac function curve= frank sterling relationship. it shows that CO is a function of EDV.
What elevate or depresses our cardiac function curve?
***CF curve stays bound to the left corner.
Draw
Increase: increase inotropy, HR, decrease in afterload
Depress: decrease in inotropy, HR and increase afterload
How do we increase our mean systemic pressure?
Increase in blood volume or by a decrease in venous capacitance (where blood is shifted from the veins to the arteries).
A shift of the vascular function–> Right
What determines the slope of the venous return curve?
Resistance to arterioles
Clockwise rotation= decrease in TPR–> increase in VR–> increase CO
Counterclockwise roation= increase in TPR–> decrease VR–> decrease CO.
This will not change the Pmc, because the changes required are so small unless both arteries and veins are constricted
What causes a shift in the vascular function curve (venous return curve)
Shift up–> increase in blood volume or decrease in venous compliance= increase CO
Shift down–> decrease in blood volume or increase in venous compliance= reduce CO
Positive ionotropic effects on the curve
+ ionotropic effects= increase contractility and CO.
intersection shifts higher to a higher CO and lower atrial pressure (because increase in SV, more blood is ejected from the heart at each beat)
Negative ionotropic effects on the curve
decreased contractility= decrease CO
Cardiac function curve stays anchored, REMEMBER
Increase blood volume to curve
Increase blood volume–> increase mean systemic pressure, shifting the venous curve to the R.
—CO and right atrial pressure increase—-
Decrease in blood volume (hemmorhage)
decrease mean systemic pressure= shift venous return curve to the L
CO and right atrial pressure decreases
What changes both the CO and venous return curve at the same time?
Draw an increased ____
TPR, SVR or afterload.
Increase TPR= decrease in CO and VR
=Venous return curve shifts counterclockwise (d/t decrease VR)
=CO curve shifts down (d/t increased aortic pressure)
—–right atrial pressure does not change—–
What happens during cardiac failure
decreased ionotropy and vascular compliance
increased BV and SVR
