Phys lecture 1: Cardiac excitation contraction

Question 1

Describe the parasympathetic and sympathetic innervation of the heart.

Answer 1

parasympathetic fibers originate in the cardioinhibitory center of the medulla oblongata, travel along the vagus N to innervate the SA node (left vagus N) and the AV node (right vagus)

sympathetic fibers arise in the cardioacceleratory center of the medulla oblongata, travel along the sympathetic trunk–> cardiac Ns to terminate on the SA and AV nodes and ventricles

Question 2

Describe the conduction system of the heart.

Answer 2

1. SA node spontaneously depolarizes
   2a. AP travels rapidly thru internodal pathways to the AV node
   2b. depolarization travels (more slowly) thru atrial myocytes and they contract
2. AV node slows conduction signal
3. AP moves to bundle of His and purkinje fibers to the apex of the heart
4. depolarization wave spreads upward from the apex (thru myocytes –> contraction)

Question 3

Why does the AV node need to slow doen the depolarization?

Answer 3

to allow time for the ventricles to fill before contracting

Question 4

T or F: In health, the ventricles do not spontaneously depolarize

Answer 4

T (want the contraction to be in synchrony)

Question 5

Describe the phases of the ventricular action potential (AP)

describe polarization and channels for each phase

Answer 5

phase 4 = resting potential (-85mV)
- I-K1 potassium channel active

phase 0 = rapid depolarization (to +50mV)
- from opening/activating of Na channels when cells reach threshold of -60 mV

phase 1 = small and transient repolarization
- I-TO K+ channels open and allow some K+ to exit)

phase 2 = stable depolarized state
-balance of Ca-in and K-out channel activity

phase 3 = repolarization
-activation of K+ channels (IK1, IKATP, IKAch) and inactivation of Ca channels

4 = resting potential

Question 6

T or F: all the cells in the heart have the same electrical profile

Answer 6

F: they all are different

Question 7

Describe the electrical profile (AP) of the SA node

Answer 7

1. the SA node is hyper/re-polarized at -60 mV
2. this hyperpolarized state activates I-f channels
3. Na enters cell and depolarizes it
4. at -40 mV, I-f (Na) channels inactivate and Ca channels activate and moves into cells
5. at peak of depolarization Ca channels close and K+ channels open
6. repolarization of cell

Question 8

What is the minimum potential of ventricular cells? SA node?

Answer 8

• 85 mV

- 60 mV

Question 9

Rank the parts of the conduction system from fastest to slowest.

Answer 9

Bundle of HIis and Purkinje cells > ventricular muscle > atrial muscle > SA and AV nodes

Question 10

What part of the cardiac conduction system has the highest rate of spontaneous discharge? Why is this important?

Answer 10

SA node = it sets the pace of AP firing (pacemaker cells)

Question 11

Does atrial and/or ventricular muscle have spontaneous discharge activity?

Answer 11

No, but they will if damaged

Question 12

Does the AV node, bundle of His, and Purjunke cells have spontaneous discharge activity?

Answer 12

Yes, BUT it is at a slower rate than the SA node, therefore the SA node sets the pace of AP firing

These cells can take over if the SA node is not operating or cannot transmit signals!!!!!!

Question 13

What is the intrinsic rate of the SA node (parasympathetic and sympathetic activity absent)?

Answer 13

100-120 bpm

**SA node is the pacemaker

Question 14

If the SA node is damaged, who will take over?

Answer 14

V node, bundle of His, and Purjunke cells BUT it will be a slower pace than the SA node

Question 15

What are 3 effects that parasympathetic activity has on the heart?

Answer 15

1. dec HR
2. decreases conduction velocity (esp at AV node)
3. dec excitability of LATENT pacemakers (BOH, PJF)

Question 16

What are 3 effects that sympathetic activity has on the heart?

Answer 16

1. inc HR
2. inc conduction velocity (esp at AV node)
3. increases excitability of LATENT pacemakers
4. decreases (makes more negative) the threshold for Ca channel activation (=inc depolarization at SA node)

Question 17

What effect does Ach have on the time to conduct an AP thru the AV node?
Norepi?

Answer 17

ACh: inc time = slower (parasympathetic)

Norepi: dec time = faster (sympathetic)

Question 18

What effect does Ach have on the time to conduct an AP thru the bundle of his?
Norepi?

Answer 18

no effect = symp and para symp act on the AV node to control conduction velocity… once the signal is fired in the AV node and reaches the BOH it will travel v quickly

Question 19

How is our resting HR different than the spontaneous rate of the SA node? Why is the important?

Answer 19

At rest, parasympathetic activity prevails (over sympathetic) to keep our HR ar ~60 bmp which is less than the spontaneous SA rate of 100 bmp

Question 20

T or F: At rest, parasymp NS is at work and not the symp NS

How has this been proven?

Answer 20

F: both are firing at rest, but parasympathetic prevails

**giving alpha and beta blockers experimentally (blocks both para and symp activity) shows that resting HR is lower than spontaneous SA rate (= parasymp prevails at rest!)

Question 21

How do we go from an AP to a contraction?

Answer 21

depolarization of cells (from an AP) causes Ca channels to open and Ca to enter the cell –> this inc in intracell Ca triggers Ca release from SR (Ca induced Ca release)

Question 22

What 2 things regulates the strength of muscle contraction?

Answer 22

1. intracell Ca levels

2. initial length of cardiac fibers (determines sensitivity of myofilaments to Ca)

Question 23

How is muscle contraction reversed? (normal process, i.e. we dont want the muscle to always be contracted)

Answer 23

Ca uptake by SR

Question 24

Why must the Ca that enters the cell eventually be efflux-ed?

Answer 24

if not, the cell will become calcified

Question 25

How is Ca efflux-ed? What are the transporters?

Answer 25

Ca-ATPase

NaCa antiporter that is driven by NaK-ATPase created Na gradient

Question 26

How is Ca taken into the cells? (Transporters)

Answer 26

Ca channels 
NaCa antiporter (ATP driven)

Question 27

Describe the mechanism of chatecholamine-induced cardiac cell sympathetic activation

Answer 27

Epi/Nor epi binds B-AR ->
activation of GPCR ->
Adenylate cyclase active ->
cAMP increases ->
PKA active and phosphorylate/activate ramadine receptor and Ca channels
Ca released from SR
= increase intracell Ca = inc contractility

Question 28

Describe the mechanism of chatecholamine-induced cardiac cell parasympathetic activation

Answer 28

Ach binds M2R
inhibits AC
dec cAMP
PKA inactive 
Ca stays in SR and power stoke is blocked (troponin not released)

Question 29

Why would sympathetic activity accelerate both cardiac contractility and relaxation

Answer 29

relaxation accelerated do that you can have contraction occur sooner

Question 30

What is lusitrophy?

Answer 30

cardiac relaxation

Question 31

What is inotrophy?

Answer 31

cardiac contraction

Question 32

What do chatecholamines accelerate the rate of?

Answer 32

cardiac contraction and relaxation

intracell Ca decline

Question 33

EDV - ESV =

Answer 33

SV

Question 34

What determines preload?

Answer 34

EDV

Question 35

What determines SV?

Answer 35

EDV

Question 36

How muscle muscle cell stretch cause an inc on contractility

Answer 36

stretch …

1. stretch activated Ca channels open (slow response)
2. increases Ca sensitivity/less Ca needed to generate tension (fast response)

Question 37

T or F: increasing the length of the sarcromere increases the cardiac force generated

Answer 37

T