Cardiac Dynamics Flashcards
When does the L type Voltage gated channel open?
When the membrane potential reaches btw -10 to +10 mV, due to the depolarization of the cell by Na+.
Ryanadine Receptors -
They bind Ca2+ and these receptors are located on the Sarcoplasmic Reticulum
What is the most common Type of Ca2+ channel?
L Type Ca2+ channel (long lasting)
What is the most important method by which Ca2+ ions are removed from the Cardiac muscle cell?
Via ATP Dependent Ca2+ pumps on the SR
What are the 2 ways that a cardiac muscle cell can remove Ca2+?
- ATP dependent Ca2+ pump
2. Na+/Ca2+ Exchange pump (3 Na+ for 1 Ca2+)
What are the sources of Activating Ca2+ in Skeletal and Cardiac muscles?
Skeletal: SR
Cardiac: SR and extracellular space
Is there Spontaneous Electrical Activity in the Skeletal and Cardiac muscles?
Skeletal: No
Cardiac: Yes
Are there gap junctions within Skeletal and Cardiac muscle?
Skeletal: no
Cardiac: Yes there are many
Is there conduction of electrical activity btw cells in Skeletal and Cardiac muscle?
Skeletal: No
Cardiac: Yes
Does stretching of Skeletal and Cardiac muscle increase muscle activity?
Skeletal: NO
Cardiac: Some
Is there a lot of innervation (nerves) within Skeletal and cardiac muscle?
Skeletal: Every cell is innervated
Cardiac: There is variable innervation
What type of nerve stimulation do Skeletal and Cardiac muscle receive?
Skeletal: Excitation stimulation
Cardiac: Excitation and Inhibition stimulation
Do hormones have an effect on contraction in Skeletal and Cardiac muscle?
Skeletal: Some effect
Cardiac: LARGE effect
What are the 3 ways to Reduce Ca2+ in the Cytosol?
- Na+/Ca2+ pump: 1 Na+/3 Ca2+
- ATP dependent Ca2+ pump in Sarcolemma (membrane)
- ATP dependent Ca2+ pump in Sarcoplasmic Reticulum
How does the SR cause Cardiac Contraction?
- 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
How does the SR causes Cardiac Relaxation?
- 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
In detail, describe Beta adrenergic Signaling (i.e.NE).
- NE binds B1 receptors
- Gs-protein Activates Adenylate Cyclase
- Adenylate Cyclase forms cAMP
- Cyclic AMP activates PK
- PK Phosphorylates: Slow Ca2+ channels and Phospholamban.
- Ca2+ channels cause contraction and Phospholamban facilitates Relaxation
In detail, describe Cholinergic Signaling (ACh).
- ACh binds muscarinic REceptors
- This activates G1-proteins
- G1-protein reduces ADenylate Cyclase activity and cAMP production
- This antagonizes contraction and relaxation
What are the 3 ways in which Ca2+ can be released from the SR?
- Ca2+ induced Ca2+ release
- Charged mov’t coupled Ca2+ release using a spanning protein
- Inositol Triphosphate (IP3) induced Ca2+ release
What happens when Ca2+ gets released from the SR? (Hypothesis)
- Activation of neighboring Ca2+ channels on SR
- Cytosolic Ca2+ uptake in SR
- Efflux of Ca2+ by Na+/Ca2+ exchanger
- Ca2+ is buffered by intracellular binding proteins.
What are the 2 Hypothesis of the Graded Contractile Response Mechanism?
- Small Ca2+ influx: Not enough Ca2+ to open up neighboring Ca2+ channels, cuz exchangers and pumps get rid of Ca2+ quickly
- Large Ca2+ influx: exchangers and pumps can’t Efflux Ca2+ fast enough, allowing activation of neighboring Ca2+ channels, and channels on SR
In vitro preload -
Varies with the RESTING LENGTH
In vivo Preload -
determined by the VENOUS PRESSURE and EDV
In vitro Afterload -
Determined by the APPLIED LOAD
In vivo Afterload -
Determined by the ARTERIAL PRESSURE
LV: Systemic Arterial Pressure
RV: Pulmonary Arterial Pressure
What is the range of the optimal length of the cardiac muscle?
1.95 - 2.25 microns
Is the cardiac muscle usually set at its optimal length? Why or why not?
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.
How do you increase SV?
You increase contractility and or Preload
How do you decrease SV?
Increase Afterload
What happens to End Diastolic Volume during Positive Inotropy? Negative Inotropy?
The EDV stays the same.
However, the CO and SV increases during + Inotropy and decreases during - Inotropy
What measurement is DEPENDENT on changes in length?
What measurement is INDEPENDENT on changes in length?
Frank Starling Mechanism (Preload) = Length dependent changes
Contractility (dP/ft) = Length Independent changes
What is a positive Inotrope and give an example?
A + Inotrope increases contractility: NE and Epinephrine
What is a negative Inotrope and give an example.
A negative Inotropy decreases contractility (ACh)
How do you increase CO w/o increasing EDV?
You increase contractility by increasing Ca2+ via Catecholamines!
What physiological causes an increase in Contractility?
When:
1) myocardial fiber length stays the same
2) but there is an increase in pressure development and
3) and faster muscle shortening
