3. Cardio - Muscle/co

Front 1

What are cardiac myocyte sarcomeres similar to?

Back 1

Skeletal muscle sarcomeres

Front 2

So what is in cardiac sarcomere
-Thick filaments
-Thin filaments

Back 2

Thick = myosin
Thin = actin/troponin/tropomyosin

Front 3

What was in smooth muscle again?

Back 3

Ca/Calmodulin/MLCK to phosphorylate myosin.

Front 4

How does the source of calcium for myocyte contraction compare to that for smooth and skeletal myocytes?

Back 4

Cardiac depends on extracellular Calcium, which stimulates SR release of calcium too.
-Skeletal depends on intracell
-Smooth depends on extracell

Front 5

What are the 3 big differences in cardiac myocytes compared to other muscle cells?

Back 5

1. Automaticity in nodal cells
2. Plateau phase in in AP
3. Electrical CouPLING

Front 6

What are skeletal muscle cells coupled by?

Back 6

Intercalated disks

Front 7

Where are the intercalated disks?

Back 7

At the ENDS of cells

Front 8

What else is present at the intercalated disks?

Back 8

GAP JUNCTIONS

Front 9

What is the function of the gap junctions?

Back 9

Electrical coupling - flow of current from one cell to the next

Front 10

How does this mechanical and electrical coupling of cardiac muscle cells affect their contraction?

Back 10

The heart contracts as a syncytium!

Front 11

What has more mitochondria; skeletal or cardiac muscle?

Back 11

CARDIAC

Front 12

Where is there well vs poorly developed T-tubules in the heart muscle?

Back 12

Good T-tubules in Ventricles; poor in atria

Front 13

What determines the magnitude of tension that develops during the contraction of cardiac myocytes?

Back 13

The AMOUNT OF CALCIUM that enters the cell

Front 14

And what is the site of storage and release of this calcium? What triggers its release?

Back 14

SR calcium - triggered by calcium influx in response to membrane depolarization at the T-tubules

Front 15

How does cardiac muscle RELAX?

Back 15

By Ca-ATPase pumps that put the calcium back into the SR.

Front 16

So what determines the contractility of the heart muscle?

Back 16

The intracellular Calcium concentration

Front 17

How is contractility 'quantified'?

Back 17

With the EJECTION FRACTION

Front 18

What is the EF and what is its normal value?

Back 18

SV/EDV; the fraction of blood that filled the ventricles during diastole actually gets pumped out in systole - normally 55%

Front 19

so how do you calculate Ejection fraction?

Back 19

EDV - ESV
---------
EDV

Front 20

What do we call things that increase or decrease contractility?

Back 20

Pos or NEg INOTROPES

Front 21

What are 3 positive inotropes?

Back 21

1. Increased Heartrate
2. SNS
3. Cardiac glycosides (Digitalis)

Front 22

How is Increasing HEARTRATE a positive inotrope?

Back 22

It increases intracellular calcium by decreasing the time available to pump Ca back into the SR; so Ca accumulates in the cytosol

Front 23

What is a freakin funny name for this effect?

Back 23

The BOWDITCH STAIRCASE

Front 24

What is the Bowditch positive staircase?

Back 24

The stepwise increase in contractility with each heartbeat as Ca accumulates

Front 25

What are 2 ways that sympathetic stimulation increases contractility?

Back 25

1. Increases Ca influx during the plateau phase
2. Activates Ca ATPase on SR so that calcium increases in the SR

Front 26

How do the cardiac glycosides increase contractility?

Back 26

By inhibiting Na/K ATPase (compete for K binding) so that the gradient for Na/Ca exchanger is lost; Ca2+ can't be pumped OUT after contractions; so accumulates!

Front 27

What causes digitalis toxicity?

Back 27

Hypokalemia - less competition at the Na/K ATPase so Digitalis has a stronger effect than anticipated.

Front 28

Where can SNS stimulation increase contractility? By what receptors?

Back 28

-Both atria and ventricles
-B1 adrenergics

Front 29

Where can the PNS DECREASE contractility? By what receptors?

Back 29

-Only on the ATRIA
-muscarinic cholinergic receptors

Front 30

What is the Length-tension relationship in the ventricles similar to?

Back 30

The length-force relationship in skeletal muscle

Front 31

What is PRELOAD?

Back 31

EDV - the amount of blood that fills the ventricles at the end of diastole

Front 32

What is ESV?

Back 32

The amt of blood left in the ventricles after systole

Front 33

What is Stroke Volume?

Back 33

EDV - ESV

Front 34

What is ejection fraction again?

Back 34

EDV-ESV
------
EDV

Front 35

What is EDV equivalent to? Why?

Back 35

Right atrial pressure - Venous Return - whatever enters the heart must exit it

Front 36

What is Afterload?
-For the LEFT ventricle
-For the RIGHT ventricle

Back 36

LV = aortic pressure
RV = pulmonic pressure

Front 37

What increases afterload?

Back 37

Increases in pressure - how much the heart is pumping against

Front 38

What does the Frank Starling relationship say?

Back 38

Increasing EDV/RAP will increase SV/CO by increasing the force of contraction because the stretched muscle is at a more optimal length for contracting.

Front 39

So what does the increased contractility in response to increased VR/EDV result in?

Back 39

The heart pumps out whatever returns to it! CO=VR

Front 40

So on the Starling curve of SV/CO vs EDV/RAP, what will a positive inotrope do to the curve?

Back 40

Shift it up and to the left

Front 41

What will CHF do to the starling curve?

Back 41

Shift it way over to the right and down

Front 42

What will Digoxin do to the Starling curve of a CHF patient?

Back 42

Increase it and back a little to the left, but never all the way back to normal.