Lecture x2 - CVS (Bevin Cardiac Electrical Activity - APs) ANNNNND Jones Anatomy of Heart #2

Question 1

SA node APs - pacemarker potential:

1. What is lower in nodal tissue than myocardial cells and what about the RMP (compare with eg nervous tissue)?
2. What are the cells in the SA node called?
3. So these SA nodal (Pacemaker) cells; are they stable or unstable? What does this mean?

Answer 1

3. That they’ll just generate APs spontaneously

Question 2

Okay, the SA node action potential has 3 phases - what are they?

What about the time lenght of the AP? What’s that like?

Answer 2

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Question 3

Phase 4: Pre-potental or pacemaker potential

1. What is the initial potentual of an SA node cells is about what?
2. So the intial potential of an SA node cells declines spontaneously - what does this mean?
3. What is this slowly declining potential called?
4. SO in your own words, explain what ‘pacemaker potential’ refers to

Answer 3

2. It’s referring to it becoming less negative if it ‘declines’
3. It refers to the spontaneous positive increase in voltage (decline in mem potential) across the cell’s membrane that occurs between the end of one AP and the beginning of the next AP

Question 4

Phase 4 continued: Pre-potential or pacemaker potential

1. The decay of the pacemaker potential over time, is firstly caused by what?
2. SO how do ‘funny Na channels’ differ from the nervous tissue’s voltage-gated Na channels? How are they the same?
3. i(f) vs i(b) - how are they different?
4. What’s the second factor that will contribute to the decaying of the pacemaker potential (i.e. contributes to it becoming less negative initially)?
   - what does Gk stand for?
   - what does i(k) stand for
5. “As a result, the outward current ______ falls progressively allowing the inward ______ current to dominate increasingly and depolarisation continues
6. Buuuuuut these two don’t do the whole job. At about -50mV to -40mV, what beings to open? A small inward current of _____ contributes to the final _____ of the pacemaker potential and triggers the _____ ______

Answer 4

2. Diff bc opened by polarisation (negative environment) but same bc still will move the potential up the page
3. I think i(f) is the funny inward Na+ current caused by the opening of the funny Na channels (since the enviornemt was negative) but the i(b) is the inward backgorund current of any ion? I thinkkkk
4. Gradually falling mem permeability to K+ (Gk) with depolarisation of the membrane - so the positivty makes the K+ permeability fall. i(k) refers to the outward current of K (not the permeability of K)
5. Oh right because K+ leaving means you have negativity inside cell so you bring the AP down (increase K+ permeability = move the AP down the page). So reduced i(k) (declining K conductance)

Question 5

Phase 0: Upstroke

1. Okay so you get the upshoot but is it fast or slow? Compare it with voltage-gated Na channels. What channels are being used here?
2. What is the 0 phase of the AP due primarily to?
3. What is the progressive depolarisation opposed by? What is the phase called?
4. What does it mean when it says ‘one AP turns on the next one’?
5. Why is it good if there are no pauses in the AP cycle?

Answer 5

1. Still gonna get upshoot but SA nodes dont have the v-gated Na channels - need to have somehing else
   - diff channels called Ca lazy channels and once you get to threshold, those will open and Ca will cause depolarisation
   - these channels are gonna cause a slow rising in the upstroke of the AP because the cells of SA node (and AV node) lack the functional fast sodium channels
2. Slow inward current of the Ca ions (iCa) - increased G(Ca)
3. The outward K+ current, i(k) - the downstroke is called Late Repolarisation (phase 3)
4. Threshold then open the L type and you get to the positives and open K channels to push it back down. If you push it back down, you’ll get rral negative so the funny Na channesl will open again. As soon as you repolarise, you create environemnt to create next AP. Funny Na open by -ve voltages - then you come back down and you turn them on again so no pause.
5. Good bc if there was a pause, then would need somethig to start it but bc it just flows, you get this continuous beating. Buuuuut we want to be able to vary the rate that it happens at

Question 6

Autonomic control of the heart rate:

1. What is HR controlled by?
   - how many discharges/min?
2. What input (autonomic or somatic) ontrols the rate of SA node discharge?
3. The SA node is innervated by both parasym and symp nerve fibres - what is the nerve called for each thing? Which increases and which one recuded the HR?
4. But in essence how does the symp speed it up?

Answer 6

1. Change HR by changing the frequency of the SA pacemaker APs
   - normally 100 discharges/min
2. Autonomic
3. Parasym = vagus nerve (reduce HR) and symp = cardiac nerve (increase HR)
4. By making the steep of the pacemaker pre-pot steeper

Question 7

Symapthetic stimulaiton:

1. Following symp stimulation, the _____ of the pacemaker potential is increased - draw mentally what that looks like for APs in sucession
2. The increased heart rate is a reuslt of the rate of something being increased - what is it?
3. So what neurotransmitter is released by the sym nerve endings?
4. What does this neurotransmitter bind to?
5. What happens to sodium and calcium conductances? What about calcium and sodium currents?
   - what are these: G(Na), G(Ca), i(Ca) and i(f)
6. In essense, what happens to the slope?
7. The intracellular signalling - tell me what happens using the terms: NA, receptor, cAMP, i(f), protein, Ca
8. Protein kinase A also phosphorylates the K channels involved in repolaisation - what’s the effect of this? What would happen without this effect?

Answer 7

1. So the beat interval is closer bc the pacemaker potentual is steeper and that means you get to threshold faster and to do this, you manipulate the Ca channels with SNS stimulation
2. The spontaneous rate of SA node deopolarisation being increased

Question 8

Parasym nerve stimulation decreases heart rate:

1. What two things does the parasym stimulation of the SA node so? So you take longer to get to ______ hence the HR slows
2. Reduced slope of pacemaker pot by the intracellular signalling that you are going to explain in terms of: neurotransmitter, receptor, cAMP, symp stimulation, i(f) and i(ca), slope
3. Hyperpolaristion by intracellular signalling that you are going to explain in terms of: neurotransmitter, channels, GK, RMP

Question 9

Parasym versus symp:

1. What’s natural HR?
2. What domiantes at rest?
3. What does parasym get the rate down to?
4. What’s this called? “Vagal….”
5. If you decrease parasmy or increase sym - what cardia is it?
6. What’s good about having book accelerator and break?

Answer 9

6. Fine control

Question 10

1. So SA node dominates AN node and conducting system - why?
2. What sort of pacemaker is AV?
3. How many bpm for AV and purkinje?
4. What’s the advantage and disadvantge to these low order pacemakers?
5. What to use if heart doesnt beat?

Answer 10

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Question 11

Excitation-conduction system: this coordinated contraction is due to the existence of the excitation-conduction system

1. What 1-e things does the exication conduction system consist of?
2. Why pause at the AV node?
3. AP has to pass through what to get to ventricles?

Answer 11

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Question 12

What does a cardiac cell look like in terms of

• comparison to skeletal
• comparison to smooth
• nucleus
• shape
• special feature - what’s in the special features? (3)

Answer 12

Cardiac cells have both elements of skeletal muscles and smooth muscles. They have the length-tension relationship - skeletal muscles have this. They are also striated like skeletal muscle but not as regularly as skeletal, I think? But like smooth muscle, they are mononucleated. The shape of cardiac is staggered/branched so that if one cell dies, the conduction can still pass.

At the end of the myofibres, there are intercalated discs and these discs contain 3 things:

1. Fascia aderens - tight adhesion belts in the vertical component of the intercalated disc that links the actin with the actin of the other cell - like a physical connection so if one cell contracts, there is a physical propagation
2. Desomosomes - also in the vertical component and these connect the cytokeratin from one cell to the cytokeratin in the other cell. It keeps the cells held together
3. Gap junctions - these are in the horizontal component because they would probably break if they were in the plane of the contraction. They’re openings in the cell membrane of both cells that allows the passage of ions etc through like Ca. This is the electrochemical propagation of contraction

Question 13

Myocardium

1. What’re the cells called?
2. The cells in the myocardium are ______, may branch at either end are joined at their boundaries by structures called intercalated disks which contain gap-junctions. 􀀁
3. What do gap junctions permit? What is syncytium?
4. “The only thing that can make the ventricles contract is the a stimulus only arriving at one specific point from SA node” - true or flase?

Answer 13

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Question 14

1. The SA node generates APs at about what rate per minute? What is the rate modulated by? So what do you get as the rate after the modulation?
2. What’s the speed of the AP through the atria muscles?
3. What the speed of the AP conductance through the AV node? What does this provide?
4. AP conducted rapidly through what three things after AP passes the AV node?
5. Is the spread equally fast as #4 above or slower when it goes through the ventricular myocardium?
6. WHat does all of the above allow in terms of depolarisation and contraction?
7. The rapidly conduction system comprises modified myocardial cells called what?
8. So what are the conduction velociities through:
   - atria
   - AV node
   - Bundle of His, bundle branches
   - Purkinje fibres
   - Ventricles

Answer 14

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Question 15

Ventricular muscle cell action potential

1. What’re the fiive phases of cardiac action potential?
2. What’s the time length of this AP?
3. What are the ionic currents that each phase? What causes this plateu phase?
4. What is the.K condunctance (outward current of K???? idk) like in the resting membrane potential of ventricles? SO what’s the potential?

Answer 15

3. Ca competes with K and we end up with unchanging mem pot until K backgorund current dominating and bringing us back down

Question 16

Phase 0: Upstroke

1. Okay so the adjacent cell draws _____ from the RMP and AP reaches threshold at ____mV, then the membrane’s ____ _____ changes; the cell rapidly _____ - overshoots to a positive potential of ______
2. What is the depolarisation aka the rapid increase in permeability of what?
3. So after the threshold potential has been reached by the increased in permability to Na ions, what opens? So you can increase in ____ _____ about 100 times. These channels are self-inactivating - what does that mean?
4. This will lead to i(Na) - what does that stand for?
5. Why doesn’t membrane potential reach the equilibrium potentual of Na?

Answer 16

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Question 17

Phase 1: Early repolarisation

1. Why is the overshoot (phase 0) so brief? What does G(Na) have to do with this?
2. Within a couple of ms, the membrane voltage ____ a few mV, owing to what?

Question 18

Phase 2: Plateau phase

1. Caridac muscle cells display a unique feature called the plateau. What is it? Is it a repolarisation or what?
2. It is a small but sustainted inward current of ____ down their _____ gradient - due to the opening of what?
3. Calcium channels - are they voltage operated? So when do they begin to activate? During rapid ____
4. What is the inward Ca++ current almost sufficient to counterbalance?
5. What does i(Ca) almost stabalise the potential at?
6. In the later part of the plateau phase, the calcium channels are beginning to inactivate so the inward current during this part of the stage is due partly to what ions passing through the what? So this will perpetuate the plateau phase

Answer 18

1. Sustainted depolarisation

Question 19

Phase 3: Late repolarisation

1. Towards the end of plateau phase, what starts to increase as the Ca channels inactivate?
2. Potassium leaves the cell generating the what?
3. This produces….
4. What’s the differnece between i(to) and i(k)?

Question 20

Phase 4: RMP

1. Maintained by what 2 things?

Question 21

1. If you have a look at the graph that overaps the mechanical and electrical activity - what can you say about the duration of the AP and then cardiac contraction?
2. SO as a result, the contractile force cannot what?

Question 22

Absolute and relative refractory period

1. During what period are the cardiac myocytes inexcitable?
2. What is this called and how long does it last? How long is the AP?
3. In summary, why are the cardaic cells inexcitable during ARP?
4. How long does relative refractory period last? When is it?
5. Can you trigger an AP in the ARP/RRP? What can trigger an AP then? This is called a ‘curtailed’ AP - what are its features?
6. So we dont want tetany in the cardiac muscle - why? What 2 things are protecting us from that?

Answer 22

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Question 23

Types of arteries

1. What are the two types of arteries? Which of the two would you find closer to the heart vs away from the heart?
2. Explain the different functions of the elastic vs muscular artery
3. Explain the histology of the basic layers of arteries and veins and then the differences that you find between
   - Muscular artery
   - Elastic artery
   - Vein
4. In a vein, which layers acts to alow it to be a capcitance vessel as well as stop it from overdistending

Answer 23

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Question 24

Epicardium!

1. What things run through here? (3)
2. What’s the white open space?
3. What attaches to the top of the epicardium?
4. What innerbates the heart at the SA, AV and muscle - wht about jsut Sa and AV?
5. What does an athrosclerotic coronary artery look like? Describe in terms of: intima, lipid, IEL, proliferation, macrophages, medial thickness, yeah
6. What should the intima look like in a healthy person?

Answer 24

6. Healthy should be one cell thin so shouldnt even see it

Question 25

Venous valves

1. What’s the purpose of venous valves?
2. So when skeletal muscles around the deep veins contracts, what happens to the blood?
   - in fact, how to differentiate deep vs superifical vein
3. Explain varicose veins then

Answer 25

2. Flow up since cant flow down since valves stop flow down. Superificual veins shouldnt have skeletal muscles surrounding them

Question 26

How to differentitat lymph vs vein - three things (in the white box on slide 39). What’s te pale blue thing in the middle of lymphs?

What happens to plasma post-mortem aka what you see on slides

Answer 26

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Question 27

Capillaries

1. What do they look like on a transverse section of cardiac muscle?
2. So the heart contrains continuos caps - what do tey look like? What about thier diameter? Can you see a nucleus on everyone of them? Why/why not?
3. Where are the tight junctions in the caps?
4. Why is it good to not have much space between interstitium and lumen?
5. What does a fenestrated cap look like? What about sinusoidal?
6. So wat are the 4 ways of transport across caps? (slide 43)

Answer 27

2. Nucleus only on the ones where the nucleus has been transected
3. Diffuse faster and more efficent

Question 28

1. What’s a coronary angiogram?
2. What does a normal artery vs an artery that has a plaque look like? What happens to:
   - media
   - lumen
   - lipid
3. What’s an intravascular ultrasound?
4. What’s a percutaneous coronary intervention?

Answer 28

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Question 29

For this percutaneous coronary intervention - what arteries can be used?

What’s the deal with femoral artery bleeding after needle prick?

What do we use to access the right side of the heart? What’s the danger of using these vessels? So what’s used now?

Answer 29

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Question 30

1. Trace the path of the great saph vein - what is its draining point?
2. Do the same with the small saph vein
3. Two reasons for why SFJ is imp - what are they?
4. If we were to harvest this for a bypass graft - does that mean distal grat saph is cut off from drainage option? Like if you took a piece out from thigh - how does calf drain?
5. Why are perforating branches important?

Answer 30

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