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Anatomy > Structure and function of the heart > Flashcards

Structure and function of the heart Flashcards

1
Q

what is the ratio of muscle in left to right of heart

A

4-6 times more pressure in left side

3:1 ratio in muscle mass between Left and right

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2
Q

what happens to blood pressure throughout the body?

A

drops once blood leaves the heart

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3
Q

what is capillary mean pressure?

A 
systemic = 17mmHg
Pulmonary = 7mmHg
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4
Q

Conduction of cardiac AP?

A 
intercalated disces
interconnected cardiac muscle cells
secured by desmosomes
linked by gap junctions
propagate action potentials
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5
Q

how are action potentials conducted in cardiac muscle?

A

local changes in currents cause passive depolarisation of adjacent muscle cells through gap junctions

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6
Q

excitation-contraction coupling

A

T tubule transfers action potential into cell
high concentration of calcium in T tubule
calcium moves intracellularly through L type calcium channels and increases intracellular concentration or once calcium has moved from extracellular to intracellular it
binds to ryanodine receptors on sarcoplasmic reticulum which causes release of calcium –> calcium induced calcium release

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7
Q

altering calcium release

A

anything that alters calcium release or storage alters contractility and relaxation

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8
Q

what impacts calcium release or storage?

A

calcium ion channel blockers - non-dihydropyridines
beta blockers - blocks effect of adrenaline and noradrenaline
caffeine

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9
Q

What are the basic mechanics of cardiac contraction?

A 
preload
afterload
contractility
heart rate 
PACE
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10
Q

How to calculate stroke volume?

A

SV = end diastolic volume - end systolic volume

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11
Q

what is end diastolic volume?

A

volume of blood in heart just before contraction

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12
Q

what is end systolic volume?

A

volume of blood after contraction - left over

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13
Q

what is isovolumetric contraction?

A

pressure is changing - contracting but volume is same

valves are closed

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14
Q

preload

A

increases in end diastolic volume leads to increases in myocardial performance/ contractility

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15
Q

why does an increase in EDV cause increased myocardial performance?

A

physical and activating factors

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16
Q

physical factors that increase myocardial performance

A

more optimum myofilament overlapping
decrease lattice spacing - decreased distance between myofilaments so increased probability of interaction between contractile components

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17
Q

activating factors that increase myocardial performance

A

increase in calcium ion sensitivity by multiple mechanisms
increased calcium release
increase calcium sensitivity

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18
Q

what happens if you increase end diastolic volume?

A

increases contractility and increases stroke volume as the volume in the heart increases due to increase in venous return

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19
Q

what is afterload?

A

what the heart has to pump against

higher the pressure in systemic/ pulmonary circulation = more force/ work required by the heart

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20
Q

what happens when there is an increase in end systolic volume?

A

needs to increase pressure in ventricle to meet that in aorta and so increases volume so thre is less opportunity for the muscle to shorten
shifts the pressure-volume loop to the right
stroke volume decreases

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21
Q

when is there an increase in end systolic volume?

A

chronic hypertension

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22
Q

when is there a fall in contractility?

A

MI
heart failure
weak, floppy ventricle

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23
Q

what impact does decreased contractility have?

A

reduced stroke volume

reduction in cardiac output

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24
Q

what happens when there is a fall in compliance?

A

stiff, fibrotic ventricle
more difficult to contract and recoil
decrease in stroke volume

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25
Q

when is there a fall in compliance?

A

ageing

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26
Q

contractility

A

noradrenaline/ adrenaline binds to beta 1 adrenoreceptor on GPCR
causes adenyl cyclase to be activated, converting ATP to cAMP which ultimately causes an increase in calcium and increase contractility

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27
Q

what does dual innervation mean?

A

both sympathetic and parasympathetic innervations

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28
Q

SAN and AVN

A

are dual innervated

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29
Q

Innervation of atria

A

sympathetic and small amount of parasympathetic innervation

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30
Q

innervation of ventricles

A

only really have sympathetic innervation

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31
Q

what does caffeine do?

A

increases calcium

increases contractility

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32
Q

control of contractility

A

sympathetic drive to ventricular muscle fibres - noradrenaline at beta 1 receptors in cardiac muscle cells
hormonal control by circulating adrenaline and noradrenaline

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33
Q

how to calculate the ejection fraction?

A

stroke volume/ end diastolic volume

expressed as a %

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34
Q

what is ejection fraction?

A

quantification of contractility

measure of the ability of the ventricle to contract

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35
Q

Ranges of ejection fraction

A

> 75% could indicate hypertrophic cardiomyopathy
55-70% normal or heart failure with preserved ejection fraction
40-55% abnormal - maybe clinically insignificant
<40% = heart failure, can be very low

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36
Q

importance of contractility

A

most important factor in mortality

37
Q

heart rate regulation

A

neuronal and endocrine

38
Q

positive ionotropic

A

increase in heart contractility

39
Q

chronotropic

A

affect on heart rate
positive = increase HR
negative = decrease HR

40
Q

which hormones affect HR?

A

adrenaline and noradrenaline = increase

acetylcholine = decrease

41
Q

what happens to the heart at rest?

A

increase parasympathetic activity

42
Q

bowditch effect

A

aka staircase phenomenon

increased heart rate causes increase contractility strength

43
Q

atrial reflex

A

aka bainbridge reflex
stretch receptors in right atrium tirgger increase in heart rate through sympathetic activity due to venous return increase

44
Q

sympathetic activity

A

increases permeability of membrane to sodium ions
increase so sodium moves into cell spontaneous depolarisation
reduces time to initiate depolarisation

45
Q

Parasympathetic activity

A

decreases permeability of the membrane to sodium and increases potassium leaving the cell
decreases spontaneous depolarisation
increases time to initiate depolarisation - causes hyperpolarisation

46
Q

what does a selective beta 1 antagonist affect?

A

reduced contractility
reduced heart rate
reduced renin release

47
Q

how does a beta 1 antagonist affect renin release?

A

reduced renin secretion via selective beta 1 inhibition at juxtaglomerular cells

48
Q

what determines how blood travels through blood vessels?

A

flow
pressure
resistance

49
Q

flow

A

volumber per unit of time

blood flow is determined by pressure change and resistance to flow

50
Q

pressure

A

driving force behind blood flow, generated by heart. Blood flows from high to low pressure regions

51
Q

resistance

A

an impediment to flow, high resistance means a higher pressure gradient is needed to achieve the same flow

52
Q

what affects resistance to blood flow

A

blood viscosity
vessel length
vessel radius

53
Q

blood viscosity

A

thicker the blood the higher the resistance to flow. Increase in RBC count, LDL, smoking etc.

54
Q

vessel length

A

the longer the vessel, the higher the resistance to flow. Unlikely to change by much in an adult

55
Q

vessel radius

A

the narrower a vessel is the higher the resistance to flow.

56
Q

what is the most important variable affecting resistance to blood flow?

A

vessel radius

57
Q

resistance to blood flow formula

A

8nL/Pi x r^4
n = blood viscosity
L = vessel length
r = vessel radius

58
Q

flow equation

A 
Q = change in pressure/R
Q = flow
59
Q

what are the functions of the CVS?

A

delivery of oxygen and nutrients to tissues and removal of waste products
distributes hormones, fluids and electrolytes
immune function
thermoregulation

60
Q

what are the 2 circulations?

A

pulmonary and systemic circuits

61
Q

pulmonary circuit

A

is a specialised circulation that is relatively short, simple and operates at a lower pressure than the systemic circulation

62
Q

specialised circulations

A

circulation is specialised within specific organs
most tissues receive enough blood to meet metabolic needs, whilst other tissues receive more blood than they need - reconditioning organs

63
Q

reconditioning organs

A

tissues that receive more blood than they need metabolically

64
Q

cardiac output in pulmonary and systemic circulation

A

equal in both

65
Q

resistance to flow in pulmonary and systemic circulation

A

low in pulmonary as short and simple and high in systemic as long and complex

66
Q

pressure in pulmonary and systemic circulation

A

low in pulmonary - 25/10mmHg

high in systemic - 120/80mmHg

67
Q

mean arterial pressure/ pulse pressure

A

approximates to diastolic pressure plus 1/3 of the difference between systolic and diastolic pressure because more time is spent in diastole

68
Q

BP

A

refers to mean arterial blood pressure

69
Q

what is the dicrotic notch?

A

when the aortic valve shuts causing a small dip in pressure

70
Q

pressure changes in circulation

A

decreases from LV, aorta/ arteries, arterioles, capillaries and veins

71
Q

pressure changes in LV

A

ranges from 120-0 mmHg

72
Q

pressure changes in aorta and arteries

A

smaller pressure changes- pressure is maintained

73
Q

when is the biggest pressure drop?

A

arterioles because of their small radius and so high resistance
blood rubs against walls and loses energy

74
Q

exchange vessels

A

capillaries - main interface with tissues

75
Q

veins

A

hold the largest share of blood in the whole circulation = capacitance vessels

76
Q

what determines mean arterial blood pressure?

A

cardiac output
total peripheral resistance
blood volume

77
Q

what is total peripheral resistance?

A

can be controlled by constricting or dilating of muscular arteries and arterioles

78
Q

another phrase for total peripheral resistance

A

systemic vascular resistance

79
Q

what is the most important factor in BP?

A

total peripheral resistance

80
Q

what regulates BP?

A

autonomic NS

humoral

81
Q

autonomic NS regulation of BP

A

short-term

influences cardiac output and vascular resistance

82
Q

humoral control of BP

A 
aldosterone
adrenaline
ADH
atrial natriuretic peptide
angiotensin II 
short and long-term regulation
influences vascular resistance and blood volume
83
Q

what are arterial baroreceptors?

A

stretch receptors/ mechanoreceptors
in aortic arch and carotid sinus
continuously monitor BP by monitoring stretch of vessel walls

84
Q

where are chemoreceptors found?

A

carotid body

85
Q

baroreceptor neural pathway

A

input to the cardiovascular centre in medulla oblongata
via glossopharyngeal nerve from carotid sinus or via vagus nerve from aortic arch
causes an autonomic nervous system response

86
Q

what do baroreceptors do?

A

responsible for rapid, short-term control of BP

87
Q

firing rate for BP

A

increases firing rate when BP increases

decreases firing rate when BP decreases

88
Q

Controlling high BP

A

increased firing to brain via glossopharyngeal and vagus nerves to medulla
increased firing down vagus to reduce HR, acts on SAN and decreased down sympathetic innervation to SAN and muscles of heart via Beta 1
decreased sympathetic activity to arterioles and veins via alpha 1 causing vasodilation and decreased systemic vascular resistance so BP falls

89
Q

controlling low BP

A

parasympathetic activity is decreased to the heart and sympathetic activity increases to heart and vascular smooth muscle

Anatomy (16 decks)

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