Cardiovascular Physiology Flashcards

1
Q

What is the role of the cardiovascular system?

A

Blow flow to tissues
Homeostasis
Transport of hormones

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2
Q

What are 2 circulations arranged in?

A

Systemic + pulmonary

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3
Q

What is systemic?

A

Left side of the heart pumping blood to the rest of the body

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4
Q

What is the pulmonary?

A

Deoxygenated to the lungs

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5
Q

Which part does blood pressure measure?

A

Systemic

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6
Q

Describe veins

A

Thin layers of muscle
=low pressure

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7
Q

Describe arteries

A

Thick, muscular walls
= high pressure

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8
Q

What is the biggest artery?

A

Aorta

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9
Q

Describe arterioles

A

Smaller arteries
Thick, muscular walls
= modest pressures

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10
Q

Describe capillaries

A

Thickness of single endothelial cell
= low pressure

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11
Q

Describe venules

A

NO thick muscular walls
= low pressure

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12
Q

Where is arteriole B.P generated?

A

In the left ventricle

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13
Q

Describe ventricular muscle relaxation

A

Diastole
Ventricular filling

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14
Q

Describe ventricular muscle contraction

A

Systole
Ejection of blood into arteries

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15
Q

Why is measuring ejection of blood important?

A

Measure of cardiac output
Called ejection factor

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16
Q

Describe the pressure gradient that is proportional to blood flow

A

Tube exerts resistance to flow
As it moves = friction = loses energy to surroundings (arteriole walls)
= pressure decreases = creation of pressure gradient

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17
Q

What is stroke volume?

A

Vol of blood pumped by one ventricle

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18
Q

What is cardiac output?

A

Vol pumped per ventricle per minute

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19
Q

What is venous return?

A

Vol of blood returning to the heart

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20
Q

What should VR be equal to?

A

CO

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21
Q

What is infarction?

A

Death of muscle

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22
Q

Describe cardiac muscle contraction

A

Similar to smooth muscle
BUT troponin

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23
Q

What are increases levels of troponin in the blood a sign of?

A

Cardiac infarction

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24
Q

Describe AP trigger ventricular contraction

A

AP enters cell
Ca2+ gates open
Entry of Ca2+
Triggers more Ca2+
Binds to troponin

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25
Q

Describe relaxation of ventricular contraction

A

Occurs when Ca2+ unbinds
Ca2+ pumped back into SR
Ca2+ exchanged with Na+
Na+ gradient maintained by NaK pump

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26
Q

What are the specialisations of cardiac muscle?

A

Intercalated discs
= packed full of proteins = gap junctions
= connect muscles together

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27
Q

Describe the cells of the SAN

A

Groups of cells that can spontaneously fire APs
= do NOT need external stimuli

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28
Q

What do gap junctions allow?

A

Adjacent cardiomyocytes to communicate chemically + electrically

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29
Q

Briefly describe the spread of electrical activity

A

Originates in SAN
Spreads via gap junctions
Waves of electrical activity lead to mechanical activity

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30
Q

What does an ECG do?

A

Record what happens in the whole of the heart electrically

31
Q

What is the annulus fibrosis?

A

Fibrous tissue that sits between atrial + ventricular muscle
Non-conducting

32
Q

What is the annulus fibrosis?

A

Fibrous tissue that sits between atrial + ventricular muscle
Non-conducting

33
Q

What are the different parts of the ECG?

A

P wave
P-R interval
QRS complex
Q-T interval
S-T segment
T wave

34
Q

What is a P wave?

A

Atrial depolarisation

35
Q

What is a P-R interval?

A

Interval between beginning of excitability of atria + ventricles

36
Q

What is the QRS complex?

A

Ventricular depolarisation

37
Q

What is the Q-T interval?

A

Contraction
BUT also ventricular repolarisation

38
Q

What S-T segment?

A

All ventricular tissue depolarised

39
Q

What is T wave?

A

Ventricular repolarisation
= SWITCHING OFF

40
Q

What determines the no. of times the heart will beat?

A

No. of times SAN fires

41
Q

How can HR be modified?

A

Increase sympathetic, decrease parasympathetic

42
Q

What happens if there is a more forceful contraction?

A

= more blood forced out
= influences SV

43
Q

What is contractility?

A

Amount of Ca2+ in cystolic muscle

44
Q

Describe Starling’s Law

A

Stretch LV = more forceful contraction = increased blood

45
Q

How do you calculate CO?

A

HR X SV

46
Q

What do transmitters do?

A

Bind to receptors on cardiac cell membrane which lead to opening/closing of channels

47
Q

What is the sympathetic transmitter?

A

Noradrenaline (adrenaline)

48
Q

What is the parasympathetic transmitter?

A

Acetylcholine

49
Q

What does activation of sympathetic nerves do?

A

Cause release of noradrenaline
Increase opening of HCN channels
Open Ca2+ channels
HR increases

50
Q

What does noradrenaline do?

A

Bind to beta1 adrenoreceptors on cardiac pacemaker + myocyte cells

51
Q

What does sympathetic stimulation do to the SAN pacemaker activity?

A

Changes rate of firing
= fires more quickly + reaches threshold quicker

52
Q

What does opening of Ca2+ channels do?

A

Depolarises quicker

53
Q

What does activation of parasympathetic do?

A

Cause release of Ach
Decreases opening of HCN channels
Slows opening of Ca2+ channels
Opens K+ channels
HR decreases

54
Q

What does parasympathetic stimulation do to SAN pacemaker activity?

A

Slows down = makes it harder to reach threshold
= fires less frequently

55
Q

What does Ach bind to?

A

Muscarinic cholinergic receptors

56
Q

Why is parasympathetic constantly on?

A

Normal intrinsic rate is too high
= on SAN to decrease HR

57
Q

Decsribe the sequence of mechanical events

A

Ventricular filling
Atrial contraction
Isovolumetric ventricular contraction
Ventricular ejection
Isovolumetric ventricular relaxation

58
Q

What is isovolumetric ventricular contraction?

A

NO difference in blood vol
= has to overcome aortic BP
= then ventricular ejection
ONLY BRIEF

59
Q

What does the AVN delay allow?

A

Atrial systole to be complete

60
Q

What is atrial systole?

A

Stretch ventricle
= doesn’t pump blood out

61
Q

What is preload?

A

The amount of pressure/stress that is put on the heart (LV) when blood returns to the heart

62
Q

What is End Diastolic Vol (EDV)?

A

Vol of blood in LV at end of diastole

63
Q

What is the difference between LV EDV + LV ESV equal to?

A

SV

64
Q

Describe heterometric (intrinsic) cardiac workload

A

Starling’s Law
= cardiac muscle stretched
= more forceful contraction

65
Q

Describe heart failure

A

Actin + myosin are physically separated
= SV decreased
= blood going in BUT not enough being pumped out
= LV becomes overstretched
= less forceful contractions

66
Q

What are the effects of sympathetic nerve stimulation on cardiac workload?

A

Increase in SV without change in initial fibre length
Increase in contractility
= positive inotropic effect

67
Q

What is an example of a positive inotropic drug?

A

Norepinephrine

68
Q

Describe homeometric (extrinsic) mechanisms

A

Effects of catecholamines
Produce more forceful BUT shorter contraction

69
Q

Describe norepinephrine + epinephrine results

A

Bind to beta1 on myocardial cell
Activates cAMP 2nd messenger
= phosphorylation
= EITHER open Ca2+ channels or phospholamban
Which BOTH = more forceful contractions + shorter duration

70
Q

What controls mean arterial BP (MAP)?

A

LV generates it
Arteries/arterioles cause resistance

71
Q

What are the main factors that determine MAP?

A

CO
Total peripheral resistance

72
Q

So how do you calculate MAP?

A

CO X TPR

73
Q

What do carotid + aortic baroreceptors do?

A

Keep BP within limits
Change their rate of firing based on pressure changes
Blood vessels vasoconstrict/dilate