Contractility and CO

Question 1

CO

depends on cardiac factors and coupling factors. What are they?

Answer 1

Cardiac factors= HR and contractility

Coupled factors = preload and afterload

Question 2

What is contractility proportional to?

Answer 2

Contractility is proportional to the amount of Ca2+ that is availble to bind to troponin located on actin.

Question 3

Length tension curve in cardiac muscle

Answer 3

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.

Question 4

In the heart, as pressure increses (filling of the ventricles increases), what happens to tension

Answer 4

increases

Question 5

What limb does the heart operate on?

Answer 5

Ascending limb

Question 6

Our heart is operating at what force? What happens when we contract?

Answer 6

Our heart is operating at a force below optimum. When we contract, we reach an optimal length.

Question 7

What is another name for preload?

Answer 7

End diastolic volume.

Preload is the amount of blood that we can eject from the LV (thus, the volume at the end of diastole)

Question 8

How do we get the most accurate reading of our prelad?

Answer 8

The amount of tension in the RV/LV just before it contracts.

Question 9

Draw the EDV and ventricular pressure curve.

Indicate where preload is at and what this graph means

Question 10

What is afterload?

Answer 10

Afterload is the pressure needed to eject the blood frmo our LV (thus, our aortic pressure).

It will usually be between 70-80 mmHg.

Question 11

What happens to the velocity of contraction if we increase afterload?

Answer 11

Increase afterload= decrease velocity.

Question 12

When is velocity of contraction the greatest, compared to afterload?

Answer 12

Afterload= 0= greatest velocity.

Question 13

Draw the velocity of contraction vs. afterload graph

Question 14

Where is our preload and afterload on the cardiac cycle graph?

Answer 14

Afterload- pressure the semilunar valve opens

Preload= the amount of blood in the ventricle right before we eject it.

Question 15

How do we calculate SV?

Answer 15

EDV-ESV

usually about 70mL

Question 16

How do we calculate the ejection fraction (the percentage of blood ejected)?

Answer 16

EDV-ESV (SV/ EDV

Question 17

What does our ejection fraction tell us?

Answer 17

The measure of efficiency and contractility

Question 18

Normal CO

Answer 18

Usually about 5

Question 19

What is the Frank Starling Relationship

Answer 19

The volume of blood that we eject from the ventricle

will depend on the amount of blood present at the end of diastole.

Question 20

The volume of blood at our EDV relates to what?

Answer 20

Venous return, which should be near CO.

Question 21

An increase in chronotropy will increase our HR.

How will this effect ionotropy?

Answer 21

Should increase; increase force of contraction because less Ca2+ is leaving the cell, producing a stronger force of contraction

Question 22

How will in a + ionotropy effect/-ionotropy effect alter our CO (SV) vs EDV graph?

Draw

Question 23

Ventricular pressure loop

Draw and label

1. Phases of cardiac cycle
2. EDV
3. Preload
4. Max pressure during ejection
5. End of systole
6. AV valve closure
7. Afterload
8. Opening and closing of semilunar valves.

Question 24

Increasing preload will do what do the presure volume loop?

What effects will we see?

Draw

Answer 24

Increase preload= increase EDV (SV) = increase VR= increase BV=

= afterload and contractility will remain the same.

Number one will shift to the right

Question 25

Increasing afterload will do what to the P/V loop? decrease in afterload? Draw.

Answer 25

**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.

Question 26

When do we see an increased afterload?

Answer 26

Aortic stenosis and HTN.

Question 27

How does an increase in contractility alter our PV loop? draw

Answer 27

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.

Question 28

Sympathetic activation via B1 receptors on our ventricular myocytes will increase force of contraction (ionotropy). How does this occur?

Answer 28

1. **Sarcolemma Ca2+ channels** will be phosphorylated 2. **Phospholambam** will be phosphorylated- helping SERCA resequester Ca2+= increase force of contraction. 3. Phosphorylate **troponin I**, which will inhibit it. Allowing Ca2+ to bind to troponin C.

Question 29

Parasymphthatic activation will produce a _____ ionotropic effect where? What happens?

Answer 29

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.

Question 30

What happens to contractility as HR increases?

Answer 30

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).

Question 31

What is the result of increased contractility d/t increased HR?

Answer 31

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.

Question 32

**Cardiac glycosides** causes a **positive ionotropic effect** and is used to tx heart failure. How?

Answer 32

1. Inhibits K+ from binding to Na/K ATPase, thus, inhibiting channel. 2. Causes an increase in Na+ concentration 3. Activates the NCX. 4. 3 Na+ leave, 1 Ca+ enters 5. Ca2+ intracellular increases **6. + ionotropic effect**

Question 33

Minute work

Answer 33

CO (also called volume work)\* aortic pressure (aka pressure work) CO \* aortic pressure

Question 34

**Stroke work** **is performed by the LV.** ## Footnote How do we calculate? What does this represent?

Answer 34

**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

Question 35

What requires more oxygen: Pressure work (aortic pressure) volume work (cardiac output)?

Answer 35

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.

Question 36

CO= [in relation to O2]

Answer 36

**O2 consumption/ [O2 in the pulmonary vein- O2 in the pulmonary artery]**

Question 37

How are CO and VR related?

Answer 37

An increase in VR= increase CO= increase right atrial pressure= increase EDV--\> increase fiber length of diastolic fiber.

Question 38

In a steady state, The volume of blood as CO ejected by the LV will be what?

Answer 38

Equal to VR.

Question 39

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

Answer 39

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.

Question 40

What elevate or depresses our cardiac function curve? \*\*\*CF curve stays bound to the left corner. Draw

Answer 40

**Increase**: increase inotropy, HR, decrease in afterload **Depress**: decrease in inotropy, HR and increase afterload

Question 41

**How do we increase our mean systemic pressure?**

Answer 41

Increase in blood volume or by a decrease in venous capacitance (where blood is shifted from the veins to the arteries). ## Footnote **A shift of the vascular function--\> Right**

Question 42

What determines the slope of the venous return curve?

Answer 42

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

Question 43

What causes a shift in the vascular function curve (venous return curve)

Answer 43

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

Question 44

Positive ionotropic effects on the curve

Answer 44

+ 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)

Question 45

Negative ionotropic effects on the curve

Answer 45

decreased contractility= decrease CO Cardiac function curve stays anchored, REMEMBER

Question 46

Increase blood volume to curve

Answer 46

Increase blood volume--\> increase mean systemic pressure, shifting the venous curve to the R. ---CO and right atrial pressure increase----

Question 47

Decrease in blood volume **(hemmorhage)**

Answer 47

decrease mean systemic pressure= shift venous return curve to the L CO and right atrial pressure decreases

Question 48

What changes both the CO and venous return curve at the same time? Draw an increased \_\_\_\_

Answer 48

**TPR, SVR or afterload.** ## Footnote 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-----

Question 49

What happens during cardiac failure

Answer 49

decreased **ionotropy and vascular compliance** increased **BV and SVR**