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cell bio physiology > CV (cardiovascular physiology) > Flashcards

CV (cardiovascular physiology) Flashcards

1
Q

What is the advantages with multicellularity?

A

Specialization - can make organs and tissues and they can be specific to do certain things (e.g can move if u have a muscle)

Can form an internal environment (which can be controlled to some degree). - not dependent on what’s happening on the outside - allows survival in cold and hot climates

Allows growth

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2
Q

What are the disadvantages with multicellularity?

A
  1. Energy costs - specialisation means more complexity so risk of integration (e.g if brain and muscle are talking together properly)
  2. Competition for limited resources in same organism. (e.g Tumour, they get to certain stage where they outgrow their blood supply and then they die)
  3. Need to be coordinated intracellular signals
  4. Diffusion is slow - bulk flow of nutrients and metabolites via pressure gradient is needed.
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3
Q

What is the equation for the length of time for diffusion over a certain length?

A

T = x^2 / 2D

where x = distance

D = diffusion constant

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4
Q

What are the differences between bulk flow and diffusion

A

They are methods by which molecules move from one place to another place

Bulk flow is the movement of a fluid down a pressure gradient.

Diffusion is the movement of molecules down a concentration gradient.

  1. Bulk flow is pressure gradient dependent whereas Diffusion is concentration gradient dependent.
  2. In bulk flow, the whole solution moves whereas in Diffusion the movement is dependent in solute concentration differences through the solvent
  3. Bulk flow is RAPID whereas diffusion is SLOW.
  4. Bulk flow needs energy to produce pressure differences whereas Diffusion doesn’t need energy
  5. Bulk flow is modified by pressure changes whereas Diffusion is altered by temperature, area of interaction (the larger the surface area the more effect), particle size (the bigger then the slower it will be), concentration gradient (the greater it is the more movement will be seen)
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5
Q

Why do we need to have low blood pressure in the lungs?

A

If not then we’d bleed into the lungs and have to thicken vessels (don’t want to thicken the vessels)

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6
Q

The development of the heart: internal and external

A

OUTSIDE
1. Endocardial tubes fused to make a single primitive heart region.

  1. Ventricle grows, it pushes down and pushes up the atrium to the top.

DIAGRAM IN ON

INSIDE

  1. pinching of the central region (separates the artial and ventricle region)
  2. partial septa grows between left and right artria , allowing things to go through
  3. A full septum grows between left and right ventricle not allowing anything to go thorugh
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7
Q

The flow of blood through the heart

A

Inferior/superior vena cava > right atrium > tricuspid valve > right ventricle > pulmonary semilunar valve > pulmonary arteries > oxidated blood to pulmonary veins > left atrium > bicuspid valve > left ventricle > aortic semilunar valve > aorta to other tissues/organs

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8
Q

Similarities in a skeletal myocyte and cardio myocyte

A

Have a sarcomere
Sliding filament contraction

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9
Q

4 Differences in skeletal myocyte and cardio myocyte

A

Skeletal:
Large multinucleate cells
Peripherally placed nulcei
Long unbranched cells
Only contract on synaptic signal

Cardio:
Small binucleate cells
Centrally placed nuclei
Branching cells
Automatic contraction

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10
Q

What does a short latent period mean?

A

If get multiple signals, u can increase the strength of the contraction

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11
Q

Why is actio potential in the cardiac muscle longer than in skeletal and motor?

A

From opening of voltage gated calcium ion channels which are important in the action potentials in the heart (so a wide plateau).

  1. resting potential
  2. Na+ channels opens
  3. na+ channels close, fast k+ channels open
  4. Ca2+ channels open, fast K+ channels close
  5. Ca2+ close, slow K+ channels open
  6. resting potential
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12
Q

what are L-type voltage gated calcium channels

A

On membrane there are L-type voltage gated calcium channels and also in T-tubules. When theyre activated (by the voltage change by sodium ions) they open and calcium is released into the cytoplasm of the cell.

DIAGRAM IN ON

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13
Q

Are the extracellular concentration of Na+ greater than the intracellular concentration? What about potassium and chlorine?

A

Na greater in extracellular
K greater in intracellular
Cl greater in extracellular

Allows for gradient

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14
Q

What is RyR?

A

On the sarcoplasmic rectiular, there’s another calcium channel (RyR), at low concentrations it causes something to remain open (not good). BUT If high doses then keeps it closed so never get enough calcium into the cell

Under normal circumstances, Ca+ binds to RyR and causes Ca+ to be released from the sarcoplasmic/endoplasmic reticulum. This Ca+ will activate the myofilaments.

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15
Q

Explain how the sliding filament model happens in cardiomyocytes

A
  1. calcium enters sarcoplasm (through voltage gated Ca channels and RyR)
  2. binds to cardiac troponin-C
  3. moves tropomyosin away from myosin binding site on actin, exposing binding site to initiate cross-bridge binding
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16
Q

What are the three subunits of troponin and explain them

A

Troponin T (TnT) - ties troponin complex to actin and tropomyosin molecules

Troponin I (TnI) - inhibits ATPase in actin-myosin interaction

Troponin C (TnC) - Binds calcium ions that regulate contractile process-pulling tropomyosin away from myosin binding site on actin.

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17
Q

Myosin molecule

A

2 heavy chains, head region (actin binding site, atp-binding site

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18
Q

How does calcium initiate the cross-bridge thing

A
  1. Calcium binds troponin-C causes conformational change by pulling of troponin-T and tropomyosin.
  2. exposes the myosin binding site on actin and inhibiting of troponin-I (atp-ase inhibitor)
  3. Release of bound ADP and inorganic phosphate from the myosin head induces the power stroke
  4. Myosin head pivots and bends at neck, pulling on the actin causing muscle contraction.
  5. Exposes ATP binding site, new ATP molecule binds to myosin head causing it to detach from the actin.
  6. ATP hydrolysed into ADP and inorganic phosphate
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19
Q

What are refractory periods?

A

Refractoriness is a state after a response to a stimuli when a similar stimuli fails to induce a response (a period of recovery).

So if there’s a second stimulus during this period then there won’t be a response

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20
Q

In which channels are refractoriness seen?

A

In cardiac muscle, voltage gated Na and Ca channels show refractory periods and won’t immediately reopen when stimulated again.

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21
Q

What effect do opening and closing Na+, Ca++, and K+ channels have on the refractory period? DIAGRAM IN ON

A

Opening fast Na+ channels initiates depolarization

Opening Ca++ channels whilst closing K+ channels sustains depolarization and contributes to sustaining the refractory period

Opening K+ channels whilst closing Na+ and Ca++ restores the resting state

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22
Q

Why in cardiac muscle, there is a period of relaxation after the first contraction? 3 reasons!

A
  1. Pump has to refill heart
  2. When heart beats, the capillaries are forced to close so need period of time to open them to bring blood and nutrients to heart
  3. Allows heart muscle to rebuild its ATP concentration, to allow the next beat to occur.
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23
Q

What is the frank starling law?

A

The greater the initial length of the sarcomere, the greater the force of contraction will be up to 2micrometers because bringing more points where the myosin head group can interact with actin

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24
Q

Because of the latent period and gap junction the beating becomes…

A

Coordinated with an action potential spreading from the initial cell.

because the heart muscle is myogenic (muscle tissue)

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25
Q

If beating isn’t coordinated over the heart as a whole it will fail as a pump, what will happen then?

A

Fibrillation - irregular unsynchronized contraction of muscle fibers

not good

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26
Q

What is the myocardium and what is the advantage of how it’s arranged?

A

Consists of interlacing bundles of cardiac muscle fibers arranged spirally around the circumference of the heart.
When cardiac muscle contracts & shortens, a wringing effect is produced, pushing blood upwards from the apex towards the exit of the major arteries of the heart

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27
Q

How is regulation of the heart achieved?

A
  1. muscle in the atrial side and ventricle can be viewed as functional syncytia (due to gap junctions) but there is physical separation of them.
  2. specialised neuromyocardial cells which initiate and conduct the cardiac impulse: pacemaker, conducting
  3. Pacemaker cells setting the frequency of the heart beat (can be modified by endocrine or nervous system)
  4. Conducting cells that conduct from the pacemaker unit to the rest of the heart in a defined matter (give a coordinated beat so lower part of heart beats before upper)
  5. Strength of beat is controlled by degree of filling (frank starling), resistance of peripheral vasculature, endocrine/autonomic nervous system control)
28
Q

What are the benefits of the fibrous heart skeleton between the atria and ventricles?

A
  1. Formed from dense irregular connective tissue so provides framework for the attachment of the cardiac muscle tissue.
  2. Anchors heart valves by forming supportive rings at their attachment points (all 4 valves)
  3. Separates atria and ventricles physically and electrically. So, insulates atria and ventricles so impulses don’t spread randomly throughout the heart
29
Q

Difference in how artia and venticles work

A

Ventricle - contraction of heart

Atrium - wider functions (e.g endocrine control pathway and immunity and defence)

30
Q

What are chordae tendinae? What happens if these get damaged?

A

Strands of connective tissue binding parts of valve to the wall of the heart.

Damage to these leads to failure of the false

31
Q

What are purkinje fibres?

A

Transfer the action potential in a defined way so the apex of the heart will beat first and then the wall.

Coordinated transfer

They’re under the endocardium (under the lining epithelial inner surface of the heart). Large.

32
Q

Describe the conduction system

A

Initiated by pacemaker in the SA node.
Conduction spreads along the muscle fibres of atria and the internodal tracts and bachmanns bundle (modified cardiac muscle fibres)

Then, the impulse is carried to the venricles across the ffibrous skeleton only at the atrioventricular (AV) node (where it’s slowed down slightly) and passes the interventricular wall (the wall between the two ventricles) by AV bundle. This divides into smaller branches containing purkinje fibres.

33
Q

What happens if the SA node fails (e.g because of insufficient blood supply)?

A

Area with the next fastest intrinsic rate of firing (AV node) will drive the heart contraction.

Not ideal because that means the ventricle beats first and the atrium wont beat in time with it.

34
Q

Different cells of the heart

A

Muscle cells (atrial and ventricular)
Pacemaker and conducting cells
Endothelial cells in coronary vessels
Fibroblasts (important if there’s scarring in the heart)
Axons (nervous supply)
Lining epithelial cells - endocardium (inside of heart), epicardium (outside of heart)

35
Q

What is the epicardium?

A

Site of coronary vessels. Consists of loose connective tissue with both autonomic nerves and adipose cells.

36
Q

SA and AV nodes have similar action potentials, what does this mean.

A

The resting membrane potential is much higher, closer to 0.

Closer to threshold.

It’s not stable either

This is because of sodium leaking. so they called these the “funny currents”

These nodes contain a channel called HCN channels, (hyperpolarization and cyclic nucleotide channels), these modify how the “funny current” runs and are modified by adrenaline.

37
Q

What is an ECG?

A

Measures the change of action potential over the cell membrane.

The summated effect of the action potentials, the changes observed are caused by current changes at the skin caused by heart muscles APs

(btw current runs positive to negative)

38
Q

What does the reading of a signal depend on?

A
  1. Size of the potential difference
  2. the plane the lead is in (line between the electrodes)
  3. the vectoral summation of the current
  4. The direction of charge in relation to the electrodes
39
Q

Describe ECG contraction (long) diagram in ON.

A
  1. excitation at SA node, wave of depolarisation (negative to positive) - gives P wave (atrial depolarisation)
  2. Atria contracts, at the same time, wave reaches AV node (slows down here), atria contracts
  3. The atria polarises, causes T polarisation wave of the atria. Occurs at the same time as depolarisation of ventricular walls. T wave is usually lost because it’s a lot weaker (unless there’s some issue).
    The summation of the wave going down the ventricular wall causes the Q wave.

3b. The inner walls of ventricles depolarise, producing R wave.

3c. The outer ventricle walls contract producing S wave (due to summation of mass of ventricle contracting) (main body and outer wall depolarising)

  1. ventricle contracts
  2. repolarisation of ventricles (T wave) - in the same direction as P wave because summation of all the waves
  3. there’s also a U wave - purkinje fibres (long action potential but rarely see this wave)
40
Q

What are the equations for eindovens law

A

Lead 1 = vLA-vRA
Lead 2 = vLL-vRA
Lead 3 = vLL-vLA

Lead 1 + Lead3 = Lead 2

41
Q
A

P wave - atria contract, push 15% blood into ventricle

Q wave - wall of ventricle depolarises, ventricle contracts,

T wave - relaxation of heart, repolarisation

Once pressure is lower in ventricle than in aorta, the AV valve closes

42
Q

What is sinus tachycardia? in ON

A

Increasing heart rate, driven by anxiety, shock, or a fever.
Causes SA node to work a bit faster

43
Q

What is sinus bradycardia? in ON

A

Caused by less signalling in SA node.
Shows fitness, common in young people

Can be caused by carotid sinus syndrome (pressure on carotid sinus on the neck causes people to collapse)

Can occur in hypothyroidism (low levels of thyroid activity), hypothermia.

44
Q

What is sinus arrhythmia?

A

Changes in heart rate occurs over a cycle.
Caused by altered vagal tone at the SA node.

Occurs in fit people as they breath. Changing pressure in the chest, there’s burrow receptors in chest that feed back to the brain to the SA node which gives slowing of the heart as u breathe in and then it speeds up again.

45
Q

What is left sided deviation of the heart caused by? give 3 examples.

A

Deep breathing (expiration)
Obesity
Left side hypertrophy (e.g if something causes left side of the heart muscle to get thicker)

46
Q

What is right sided deviation of the heart caused by? give 3 examples.

A

Deep breathing (Inspiration)
Pulmonary hypertension (induce the right side to get thicker)
defects in pulmonary valves.

47
Q

The blood vessel walls are organized into 3 concentric layers, what are they?

A

Intima (endothelium), media (layer of smooth muscle cells), adventitia (connective tissue)

48
Q

How is the tunica adventitia arranged in the arteries?

A

Longitudinally and it’s THIN (it’s thick in the veins)

49
Q

5 roles of the endothelium

A
  1. Acts asa selective permeability barrier (stuff like O2 and Co2 can pass through easily but other things have to pass by paracellularor trans pathway).
  2. A nonthrombogenic barrier between blood platelets (produce PGI2/prostocyclin that block clot forming)
  3. modulation of blood flow and vascular resistance (produce vasoconstricting/dilating agents
  4. Regulates immune response: done by controlling interaction of neutrophils, monocytes, lymphocytes with the endothelial surface
  5. Hormonal synthesis/growth factors
50
Q

Structure of the blood vessels

A

Elastic artery - large vessel (e.g aorta)
Muscular arter (smaller)
Arteriole (point of major pressure drop)
Capillary (no muscle, just endothelial layer),
Venule,
Vein,
Large vein (e.g vena cava)

51
Q

What do thick walls and elastic walls do in arteries?

A

Thick - resist high blood pressure
Elastic - allow expansion and retain BP at diasole

52
Q

What do thin walls and muscle in veins do?

A

Thin walls - allow distention (dilation)

Muscle in veins - allow increase in venous return when needed

53
Q

Why is there a pressure drop at the capillaries?

A

Mainly related to fluid leaving the capillary bed

54
Q

What is the aortic and capillaries velocity of the blood flow at rest? don’t really remember numbers, just which is slower/faster

A

In aorta, 330mm/sec
Capillaries 0.3mm/sec so significantly slower

55
Q

How long is blood in capillaries for?

A

1 to 3 seconds which is sufficient time for equilibrium with gas that’s been carried in

56
Q

Why does diastolic blood pressure need to be around 60mmHg?

A

if it went down, none of the blood would go to the heart. It maintains pressure.

57
Q

What is collateral flow?

A

If one of the vessels broke down, there would still be blood coming in from somewhere else. However, our arteries and veins aren’t good at this.

58
Q

How does blood return to the heart via veins?

A

When contracts, blood pushes through valve and then fall back on it, then moves up the next contraction.

59
Q

Venous return of the blood to the heart requires….

A

Muscular activity (movement) and valves in veins. So, if a person stands perfectly still then the venous pump fails and the venous pressures in the lower legs increases to the gravitational value (90mmHg).

Pressures in capillaries increase causing fluid to leak into the tissue space and legs swell.

Failure in valves = varicose veins

60
Q

What to do if fluid leakage occurs at capillaries? Do we have a second return system?

A

Yes, Lymphatics.
Lymphatics return fluid from tissues to bloodstream.

They are “blind-ended” tubes - one end but the other end it just stops. Highly permeable

Tissues around lymphatics can put pressure on them to move the stuff inside forward.

These lymphatic capillaries will drain into lymphatic vessels which have complete endothelium. These fuse together to become larger: right lymphatic trunk and thoracic duct.

These empty into the jugular and subclavian veins (just above the heart). They also have valves to prevent backflow.

61
Q

Lymphatics carry lipids from the guy into the circulation, bypassing the liver, what does this do?

A

It can give nutrients to the rest of the body instead of the liver.

62
Q

Why does the CVS need to be regulated?

A

Because it takes a lot of energy
Needs to give nutrients to places that require them.

63
Q

How is the CVS controlled globally (whole body controls)?

A

Autonomic nervous system - this regulates the amount of blood going to certain areas when stressed!

Circulatory responses at the heart - can make heart beat stronger

64
Q

How is the CVS controlled locally (different regions have different needs)?

A

e.g through tissue pH and nitric oxide

65
Q

Cardiac output is the sum of….it depends on….

A

Local blood flows to tissues. It depends on venous return (the heart can only pump what it receives)

66
Q

What are the main local regulators of blood flow?

A

Vasodilators acting on pre-capillary sphincter (diagram of this in ON): e.g Adenosine produced and leaking.

Also CO2 and Lactic acid (pH will drop)

So hyperaemia = increased blood flow to these regions.

67
Q

What is nitric oxide signalling?

A

Lots of receptors on the surface of surface of endothelial cells which respond to histamine, adenosine, endothelin.

They bind to receptors and activates a nitric oxide enzyme thing to covert arginine to citruline (releases NO). This NO moves over to smooth muscle cells where it causes guanylate cyclase to function. This takes GTP to convert it cyclic GMP.

Cyclic GMP causes activation of protein kinase G. This phosphorylates and activates myosin light chain kinase, causing the smooth muscles to relax.

cell bio physiology (10 decks)

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