Cardiac Dynamics

Question 1

When does the L type Voltage gated channel open?

Answer 1

When the membrane potential reaches btw -10 to +10 mV, due to the depolarization of the cell by Na+.

Question 2

Ryanadine Receptors -

Answer 2

They bind Ca2+ and these receptors are located on the Sarcoplasmic Reticulum

Question 3

What is the most common Type of Ca2+ channel?

Answer 3

L Type Ca2+ channel (long lasting)

Question 4

What is the most important method by which Ca2+ ions are removed from the Cardiac muscle cell?

Answer 4

Via ATP Dependent Ca2+ pumps on the SR

Question 5

What are the 2 ways that a cardiac muscle cell can remove Ca2+?

Answer 5

1. ATP dependent Ca2+ pump

2. Na+/Ca2+ Exchange pump (3 Na+ for 1 Ca2+)

Question 6

What are the sources of Activating Ca2+ in Skeletal and Cardiac muscles?

Answer 6

Skeletal: SR
Cardiac: SR and extracellular space

Question 7

Is there Spontaneous Electrical Activity in the Skeletal and Cardiac muscles?

Answer 7

Skeletal: No
Cardiac: Yes

Question 8

Are there gap junctions within Skeletal and Cardiac muscle?

Answer 8

Skeletal: no
Cardiac: Yes there are many

Question 9

Is there conduction of electrical activity btw cells in Skeletal and Cardiac muscle?

Answer 9

Skeletal: No
Cardiac: Yes

Question 10

Does stretching of Skeletal and Cardiac muscle increase muscle activity?

Answer 10

Skeletal: NO
Cardiac: Some

Question 11

Is there a lot of innervation (nerves) within Skeletal and cardiac muscle?

Answer 11

Skeletal: Every cell is innervated
Cardiac: There is variable innervation

Question 12

What type of nerve stimulation do Skeletal and Cardiac muscle receive?

Answer 12

Skeletal: Excitation stimulation
Cardiac: Excitation and Inhibition stimulation

Question 13

Do hormones have an effect on contraction in Skeletal and Cardiac muscle?

Answer 13

Skeletal: Some effect
Cardiac: LARGE effect

Question 14

What are the 3 ways to Reduce Ca2+ in the Cytosol?

Answer 14

1. Na+/Ca2+ pump: 1 Na+/3 Ca2+
2. ATP dependent Ca2+ pump in Sarcolemma (membrane)
3. ATP dependent Ca2+ pump in Sarcoplasmic Reticulum

Question 15

How does the SR cause Cardiac Contraction?

Answer 15

• During Depolarization, Ca2+ influxes and binds Ryanadine Receptors.
• Upon binding to Ryanadine, the stored masses of Ca2+ is released, binds to Trop C and contraction occurs

Question 16

How does the SR causes Cardiac Relaxation?

Answer 16

• Protein Kinases Phosphorylated Phospholamban, causing Phospholamban to lose its ability to block Ca2+ uptake.
• Therefore, Ca2+ channels are unblocked and open and the SR can uptake Ca2+ form the Cytosol for storage

Question 17

In detail, describe Beta adrenergic Signaling (i.e.NE).

Answer 17

1. NE binds B1 receptors
2. Gs-protein Activates Adenylate Cyclase
3. Adenylate Cyclase forms cAMP
4. Cyclic AMP activates PK
5. PK Phosphorylates: Slow Ca2+ channels and Phospholamban.
6. Ca2+ channels cause contraction and Phospholamban facilitates Relaxation

Question 18

In detail, describe Cholinergic Signaling (ACh).

Answer 18

1. ACh binds muscarinic REceptors
2. This activates G1-proteins
3. G1-protein reduces ADenylate Cyclase activity and cAMP production
4. This antagonizes contraction and relaxation

Question 19

What are the 3 ways in which Ca2+ can be released from the SR?

Answer 19

1. Ca2+ induced Ca2+ release
2. Charged mov’t coupled Ca2+ release using a spanning protein
3. Inositol Triphosphate (IP3) induced Ca2+ release

Question 20

What happens when Ca2+ gets released from the SR? (Hypothesis)

Answer 20

1. Activation of neighboring Ca2+ channels on SR
2. Cytosolic Ca2+ uptake in SR
3. Efflux of Ca2+ by Na+/Ca2+ exchanger
4. Ca2+ is buffered by intracellular binding proteins.

Question 21

What are the 2 Hypothesis of the Graded Contractile Response Mechanism?

Answer 21

1. Small Ca2+ influx: Not enough Ca2+ to open up neighboring Ca2+ channels, cuz exchangers and pumps get rid of Ca2+ quickly
2. Large Ca2+ influx: exchangers and pumps can’t Efflux Ca2+ fast enough, allowing activation of neighboring Ca2+ channels, and channels on SR

Question 22

In vitro preload -

Answer 22

Varies with the RESTING LENGTH

Question 23

In vivo Preload -

Answer 23

determined by the VENOUS PRESSURE and EDV

Question 24

In vitro Afterload -

Answer 24

Determined by the APPLIED LOAD

Question 25

In vivo Afterload -

Answer 25

Determined by the ARTERIAL PRESSURE LV: Systemic Arterial Pressure RV: Pulmonary Arterial Pressure

Question 26

What is the range of the optimal length of the cardiac muscle?

Answer 26

1.95 - 2.25 microns

Question 27

Is the cardiac muscle usually set at its optimal length? Why or why not?

Answer 27

No it is not set at its optimal length. It is set below its optimal length. This is to allow for the compensation for any extra volume (via the Frank Starling mechanism). If it operated at Optimal length at all times, it wouldn't be able to compensate for extra volume efficiently.

Question 28

How do you increase SV?

Answer 28

You increase contractility and or Preload

Question 29

How do you decrease SV?

Answer 29

Increase Afterload

Question 30

What happens to End Diastolic Volume during Positive Inotropy? Negative Inotropy?

Answer 30

The EDV stays the same. | However, the CO and SV increases during + Inotropy and decreases during - Inotropy

Question 31

What measurement is DEPENDENT on changes in length? | What measurement is INDEPENDENT on changes in length?

Answer 31

Frank Starling Mechanism (Preload) = Length dependent changes Contractility (dP/ft) = Length Independent changes

Question 32

What is a positive Inotrope and give an example?

Answer 32

A + Inotrope increases contractility: NE and Epinephrine

Question 33

What is a negative Inotrope and give an example.

Answer 33

A negative Inotropy decreases contractility (ACh)

Question 34

How do you increase CO w/o increasing EDV?

Answer 34

You increase contractility by increasing Ca2+ via Catecholamines!

Question 35

What physiological causes an increase in Contractility?

Answer 35

When: 1) myocardial fiber length stays the same 2) but there is an increase in pressure development and 3) and faster muscle shortening