Cardiac muscle

Question 1

What appearance properties does a cardiac myocyte share with skeletal muscle?

Answer 1

• Multinucleated cells

- Sarcomeres with A and I bands and a Z line

Question 2

How does a cardiac myocyte differ in appearance from a skeletal muscle cell?

Answer 2

• Myocytes are branched
• Intercalated discs separate adjacent myocytes (with gap junctions and desmosomes)
• T-tubules only invaginate at the Z-line

Question 3

The cardiac action potential has a ______ phase, creating a ______ absolute refractory period. It is also _____-dependent.

Answer 3

Plateau; long; Calcium

Question 4

Why do cardiac myocytes have gap junctions? Described what happens here

Answer 4

To allow action potentials to propagate quickly and to contract as two organized syncytia. If a neighboring cardiac myocyte was stimulated to produce an action potential, some positive charge can move into a cell and depolarize its membrane, opening voltage gated Na+ channels and starting an action potential there.

Question 5

How do calcium levels rise in a cardiac myocyte?

Answer 5

Some calcium enters the sarcoplasm via L-type calcium channels. This calcium binds to high affinity sites on Ryanodine receptors on the SR, causing massive release of Ca2+ (most impt mech). The NCX exchanger may also work in reverse to bring Ca2+ into a cell.

Question 6

How does a cardiac myocyte clear Ca2+ from its sarcoplasm?

Answer 6

SERCA pumps ATP back into the SR (most impt mech). Also PMCA pumps Ca2+ outside of the cell and the NCX uses the Na+ gradient to push 1 Ca2+ out of the cell while letting 3 Na+ in.

Question 7

What happens when Ca2+ binds the high affinity site on the Ryanodine receptor? The low affinity site?

Answer 7

High affinity- Ryanodine receptor releases Ca2+ from the SR (Calcium-induced Ca2+ release) which propagates down along the SR
Low affinity- Ryanodine closes and stops releasing Ca2+

Question 8

How does Ca2+ regulate contraction? Is this more similar to skeletal muscle or smooth muscle regulation?

Answer 8

It binds to Troponin C which moves tropomyosin off of actin.

Skeletal muscle

Question 9

Does the heart contract by twitch? Tetanus/summation? Does recruitment occur?

Answer 9

The heart can only contract by twitch. The long absolute refractory period prevents summation and tetanus. It does not recruit other motor units.

Question 10

What does the Frank-Starling law of the heart say?

Answer 10

The ventricle will pump whatever amount of blood you put into it. An increase in EDV (and thus in length and tension) corresponds to an increase in SV

Question 11

What happens to Po (maximum load) if a cardiac myocyte is stretched? What about shortening (change in length)? Work? Power?

Answer 11

Increased length increases maximum load and distance of shortening. Thus it also increases work and power

Question 12

Why does tension increase in heart muscle cells with increasing length even when thick and thin filaments have maximal overlap?

Answer 12

The increased stretch increases the sensitivity of the muscle. Troponin C is better able to bind Ca2+ when it’s more stretched out thus it is more likely to move off of actin and allow contraction.

Question 13

How does norepinephrine increase tension in a cardiac myocyte?

Answer 13

Norepi binds B1 adrenergic receptor, stimulating an increase in cAMP, activating PKA and increasing calcium release. This increases tension in the cell (and is an increase in contractility)

Question 14

What effect does norepi administration have on the duration of a twitch? Why?

Answer 14

It decreases duration. It inactivates phospholamban which acts as a brake on SERCA. Thus, Ca2+ can be cleared more effectively.

Question 15

How long does it take for an AP to change after norepi administration? For an increase in tension?

Answer 15

AP- immediately

Tension- about 8 heartbeats

Question 16

On a Ca2+- tension curve, what effect does increased sensitivity have? What effect does increased contractility have?

Answer 16

Increased sensitivity shifts the curve up b/c more tension is created at the same Ca2+ level. Increased contractility shifts the curve up along the curve b/c more Ca2+ is released

Question 17

On a length-tension curve, what effect does increased contractility have?

Answer 17

It shifts the curve up. At any length, the muscle can produce more tension b/c it has greater Ca2+ levels in its sarcoplasm

Question 18

What happens to Po (maximum load) if a cardiac myocyte experiences an increase in contractility? What about shortening (change in length)? Work? Power?

Answer 18

Po and shortening increase b/c the length-tension curve is shifted up. Thus, work and power also increase

Question 19

In skeletal muscle, work = _______ x __________. In cardiac muscle, work= ________ x __________. Thus, ______ is analogous to _______ and ______ is analogous to _______.

Answer 19

Skeletal muscle: W= force (tension) x change in length
Cardiac muscle W= pressure x change in volume
Force is analogous to pressure; length is analogous to volume

Question 20

When (in terms of pressure) will the LV fill? When will it empty?

Answer 20

It will fill when P(atrium) > P(ventricle)

It will empty when P(ventricle) > P(aorta)

Question 21

What occurs when the mitral valve is open? When it is closed and the aortic valve is closed? What happens when the aortic valve is open? What about when it and the mitral valve are both closed

Answer 21

Mitral valve open- ventricle fills
-> isovolumic contraction
Aortic valve open- ventricle empties
-> isovolumic relaxation

Question 22

What can you say about P (atrium) and P (ventricle) when the mitral valve closes? How about P (aorta) and P (ventricle) when the aortic valve closes?

Answer 22

Mitral valve close: P(atrium) = P(ventricle)

Aortic valve close: P(ventricle)= P aorta

Question 23

What does the end-systolic pressure volume relationship (ESPVR) curve tell us about the the cardiac cycle? Can this curve change? If so, how?

Answer 23

It defines the maximal pressure that can be generated by the LV at any given volume.
It can shift. Norepi administration shifts the curve to the L, allowing the ventricle to fill with more blood, increasing contractility.

Question 24

What is compliance- both mathematically and in words?

Answer 24

How easy something is to fill. C= change in volume/ change in pressure

Question 25

What is elastance? How is it related to compliance?

Answer 25

Elastance is the inverse of compliance. E = change in P/ change in V

Question 26

What does the ESPVR tell us about the heart? What about the end-diastolic pressure volume relationship (EDPVR)? How does increased compliance change these curves?

Answer 26

ESPVR- index of myocardial contractility/ systolic function
EDPVR- passive properties of the myocardium
Both are plotted on vol v. pressure graphs so compliance = 1/slope
Increased compliance moves both curves closer to the X-axis (makes them flatter, allows for more filling (V) at a given P)

Question 27

How can one define preload and afterload for the LV pressure-volume loop? How does this change our calculation of work?

Answer 27

Preload= EDV, how much blood fills the LV
Afterload= P(ventricle) at end of systole. This is equal to P(aorta) and is the pressure against which the heart has to move blood.
W= Preload x Afterload

Question 28

Define: stroke volume. How do you calculate it?

Answer 28

The volume of blood ejected by the ventricle in 1 contraction. SV= EDV-ESV

Question 29

Define: ejection fraction. How do you calculate it? What is a normal value for a healthy ventricle?

Answer 29

The fraction of EDV that is ejected out of the LV in 1 contraction. EF= SV/EDV
Healthy individuals have EF >.55

Question 30

How does sensitization (and the Frank-Starling law) change the LV pressure-volume loop?

Answer 30

Increased EDV means the heart does more work (and SV increases). The muscle also shortens more because of the increased preload.

Question 31

How does increased contractility change the pressure-volume loop?

Answer 31

The muscle can shorten more thus more tension is created and the heart does more work, creating a greater stroke volume

Question 32

How does an acute increase in afterload (P(aorta)) affect the pressure-volume loop?

Answer 32

Increased afterload means increased pressure which corresponds to less shortening (and a lower stroke volume) and an increase in tension so a larger total load for the muscle

Question 33

How does increased parasympathetic input affect the heart? Increased sympathetic input?

Answer 33

Para- negative chronotropic effect- slows HR at the SA node
Symp- Positive chronotropic effect- increase HR at the SA node- and positive inotropic effect- increases contractility (and thus SV). These combine to increase cardiac output

Question 34

How does increased arterial pressure (after load) affect the heart? Increased preload (EDV)?

Answer 34

Increased afterload decreases stroke volume and thus CO as well. Increased preload increases SV (Starling law) and also increases CO.

Question 35

How would insufficient (regurgitant) valves change the pressure-volume loop?

Answer 35

Isovolumic contractions would distort (become round instead of straight vertical lines). EDV may also increase

Question 36

How would an aortic or mitral valve stenosis change the pressure-volume loop?

Answer 36

It would increase pressure for blood to move through that valve

Question 37

How would dilated cardiomyopathy change the pressure-volume loop?

Answer 37

EDV would increase but the heart would not eject as much blood. PV loop shifts to the R and may compress