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Yr 1 CVS > Physiology of CVS > Flashcards

Physiology of CVS Flashcards

1
Q

pumps are in ____

meaning output to all organs is ____

A

series

equal

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2
Q

most vascular beds are in ____

meaning:

A

parallel

all tissues get oxygenated blood
and
allows regional redirection

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3
Q

exception to parallel vascular beds

A

liver and gut circulation- in series

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4
Q

pressure difference =

A

mean arterial pressure

  • central venous pressure
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5
Q

what controls the resistance and flow in each vascular bed

A

arterioles

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6
Q

what controls capacitance and fractional distribution of blood

A

veins and venules

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7
Q

1/2 the diameter will reduce blood flow by

A

16 fold

radius to the power of 4

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8
Q

aorta is a ___ artery

structure + function

A

elastic

wide lumen and elastic wall- dampens pressure variations

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9
Q

other arteries are ___

structure + function

A

muscular

wide non elastic lumen
low resistance conduit

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10
Q

resistance vessels are ___

structure + function

A

arterioles

narrow lumen, thick wall to control resistance and flow

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11
Q

exchange vessels are ___

structure + function

A

capillaries

narrow lumen THIN wall- for passage

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12
Q

capacitance vessels are ___ ___

structure + function

A

venules and veins

wide lumen and distensible wall

low resistance conduit and reservoir
allows distribution of blood between veins and rest of circulation

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13
Q

where are mitral valves (left AV valve)

A

between left atrium and left ventricle

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14
Q

where are tricuspid valves (right AV valve)

A

between right atrium and right ventricle

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15
Q

all valves are

A

passive

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16
Q

purpose of chordae tendinae

A

stops valves inverting

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17
Q

purpose of papillary muscle

A

lets tendons move so it doesn’t stop valves

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18
Q

pulmonary and aortic valves are also known as

A

semilunar

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19
Q

cardiac muscles vs skeletal muscles with tetanus

A

skeletal muscles can hold contractions- exhibit tetanus

cardiac muscles can’t hold contractions- no tetanus

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20
Q

cardiac muscles forms a functional syncytium, what does that mean?

A

cells work together to make 1 big muscle

electrically connected by: gap junctions
physically connected by: desmosomes
which form intercalated discs

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21
Q

why can’t cardiac muscles have tetanus contractions

A

long refractory period

long action potential

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22
Q

ionic basis of non pacemaker action potentials in cardiac cells

A

resting membrane- leaky K+ so -90mV

initial depolarisation- increase in NA+

plateau (unique to cardiac)- increase in Ca2+ L type and decrease in K+

repolorisation- decrease in Ca2+ and increase in K+

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23
Q

ionic basis of pacemaker action potentials in cardiac cells

A

they have a prepotential:
decrease in K+, increase in Ca2+ T type and Na+

action potential is by increase in Ca2+ L type

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24
Q

purpose of SA node

A

fastest/main pacemaker

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25
Q

purpose of annulus fibrosus

A

non conducting- blocks signals

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26
Q

purpose of AV node

A

delay box- so ventricles don’t constrict before atria

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27
Q

purpose of bundle of His and purkinje fibres

A

rapid conduction system- ensures all parts of the ventricle conducts at the same time

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28
Q

ECG: what is the P wave

A

atrial depolarisation

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29
Q

ECG: what is the QRS wave and how long should it be

A

ventricular depolarisation

0.08s

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30
Q

ECG: what is the T wave

A

ventricular repolorisation

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31
Q

ECG: large square is ___ seconds

A

0.2

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32
Q

ECG: gap between P and QRS should be

A

0.18s

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33
Q

ECG: what is the PR interval and normal time

A

time from atrial depolorisation to ventricular depolorisation
(from start of P to start of Q)

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34
Q

what’s the QT interval and how long should it be

A

time spent while ventricles are depolarised

0.42s at 60bpm (changes with HR)

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35
Q

how to measure HR from and ECG

A

count how many R waves in 30 large squares

and times by 10

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36
Q

bradycardia range

A

below 60bpm

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37
Q

tachycardia range

A

above 100bpm

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38
Q

ECG: what is STEMI

A

elevation of the S-T segment, indication of something wrong

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39
Q

whats worse STEMI or NSTEMI heart attack

A

NSTEMI is worse

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40
Q

peak aortic pressure happens in ______

and value

A

systole

120

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41
Q

pulse pressure

A

40

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42
Q

minimum aortic pressure happens at ____

and value

A

diastole

80

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43
Q

average end diastolic volume

A

140

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44
Q

average end systolic volume

A

60

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45
Q

how to calc stroke volume

A

EDV-ESV

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46
Q

average stroke volume

A

80

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47
Q

how to calculate ejection fraction

and value

A

SV/EDV

2/3

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48
Q

A
C
V
waves on cardiac cycle chart

A 
A = contraction of Aorta
C = ventricle contraction and mitral valve bulging into aorta
V = blood flowing from lungs into aorta
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49
Q

phases of cardiac cycle order

A

IRS IRS with Contraction first as it starts with a C

Isometric contraction
Rapid ejection
Slower ejection
Isometric relaxation
Rapid filling
Slower filling
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50
Q

what causes first heart sound (lub)

A

closure of AV mitral and tricuspid valves

in systole

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51
Q

what causes second heart sound (dubb)

A

closure of semi-lunar (aortic and pulmonary) valves in systole

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52
Q

causes of third heart sound

A

rapid passive filling phase

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53
Q

causes of 4th heart sound

A

active filling phase

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54
Q

causes of systolic murmur

A

stenosis of aortic/pulmonary semilunar valves

or regurgitation or mitral and tricuspid valves

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55
Q

causes of diastolic murmur

A

stenosis of mitral/tricuspid valves

regurgitation through aortic/ pulmonary valves

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56
Q

cause of continuous murmur

A

septal defect

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57
Q

how does the sympathetic nervous system effect the heart

A

releases noradrenalin and adrenalin

acting on beta 1 receptors on SA node

increases slope of the pacemaker potential

increasing heart rate

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58
Q

how does parasympathetic nervous system effect the heart

A

vagus releases ACh

acts on muscarinic receptors

hyperpolarises cells aaand decreases slope of pacemaker potential

decreases heart rate

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59
Q

starlings law

A

energy of a contraction is proportional to the initial length of cardiac muscle fibre - preload

60
Q

3 ways to control SV

A
  1. alter preload
  2. alter afterload
  3. change contractility using neural regulation
61
Q

in vivo preload is affected by

A

how full the ventricle is - EDV

62
Q

Control of stroke volume through preload: INCREASED venous return effects on stroke volume

A

increases EDV

so INCREASES SV

63
Q

Control of stroke volume through preload: DECREASED venous return effects on stroke volume

A

decreases EDV

so INCREASES Stroke Volume

64
Q

Control of stroke volume through preload: what does regulation of preload (EDV) ensure

A

self regulation- SV between L and R ventricles are the same

65
Q

what is afterload

A

the load the muscle must push against to contract

66
Q

Control of stroke volume through afterload: how does TPR effect stroke volume

A 
TPR INCREASES
aortic pressure increases
ventricle needs to work harder to push open aortic valve
less energy is left to eject the blood
SV DECREASES
67
Q

Control of stroke volume through neural regulation: sympathetic

A

sympathetic activation INCREASES CONTRACTILITY- ionotropic effect

gives strong short contraction

INCREASES SV

68
Q

Control of stroke volume through nuera;: parasympathetic

A

no effect

69
Q

why does parasympathetic NS have no effect on SV

A

does not innervate ventricular muscle

70
Q

measuring arterial blood pressure

A

uses korotkoff sounds

first tapping sounds- systolic reading

end of sounds- diastolic reading

71
Q

pressure wave in arteries is affected by

A

SV
velocity of ejection
elasticity of arteries
TPR

72
Q

order of locations of highest pressure to lowest

A 
LV- 120
arteries- 90-95
arterioles- 95- 40
capillaries- 40-20
venules and veins- 20-5
RA
73
Q

pressure in arteries

A

90

74
Q

pressure in arterioles

A

40

75
Q

pressure in cappiliaries

A

20

76
Q

pressure in veins

A

5

77
Q

pressure in pulmonary circulation is

A

1/5th of systemic

78
Q

velocity is related to

A

total cross section

fastest is aorta an vena cava

slowest is capillaries

79
Q

things that effect venous return 1: how does gravity effect blood flow

A

DOES NOT affect driving pressure from arteries to veins

DOES cause venous distension legs- deceases: EDV, preload, SV, CO and MAO
and orthostatic hypotension

DOES cause venous collapse in neck- can estimate central venous pressure

80
Q

things that effect venous return 2: skeletal muscle pump

A

rhythmic contraction increase venous return and EDV

prevents loss in preload

81
Q

things that effect venous return 3: respiratory pump

A

increased resp rate and depth increases venous return and EDV

82
Q

things that effect venous return 4: venomotor control

A

contraction of smooth muscle surrounding venules and veins

mobolises capacitance and increases EDV and preload

83
Q

things that effect venous return 4: venomotor control

A

contraction of smooth muscle surrounding venules and veins

mobolises capacitance and increases EDV and preload

84
Q

things that effect venous return 5: systemic filling pressure

A

pressure created in ventricles and transmitted through CVS

85
Q

why is it important to control venous return

A

it effects EDV

so it effects proload

which effects pumping ability of the heart

86
Q

2 main parts of a clot

A

platelet plug

fibrin clot

87
Q

how is fibrin made

A

fribrinogen is converted to fibrin by thrombin

88
Q

anti clotting mechanisms in endothelium

A

Stops blood contacting collagen
-no platelet aggregation

Produces prostacyclin and NO
-both inhibit platelet aggregation

Produces tissue factor pathway inhibitor (TFPI)
-stops thrombin production

Expresses thrombomodulin
-binds thrombin & inactivates it

Expresses heparin
also inactivates thrombin

Secretes tissue plasminogen activator (t-PA)
plasminogen converts to plasmin & digests clot

89
Q

continuous capillaries: where are clefted and non clefted found

A

just clefts: most capillaries inc muscle

non clefts or pores: brain- creates the blood brain barrier and stops K crossing

90
Q

what are fenestrated capillaries

and where are they found

A

capillaries with clefts AND pores

needed for specialised fluid exchange- intestine and kidney

91
Q

non polar substances pass using

A

diffusion across phospholipid membrane

92
Q

polar substances use

A

clefts and pore to pass through membrane and still use diffusion

93
Q

example of carrier mediated transport

A

glucose transported in the brain

94
Q

simple way to remember diffusion

A

more O2 is needed

the more it gets diffused

95
Q

how do starling forces effect water

A

hydrostatic pressure causes about 20l to leave vessels

while osmotic pressure causes 17l to return

remaining 3l goes to lymphatics which eventually drains to vena cava

96
Q

causes of oedema

A

lymphatic obstruction from filariasis or surgery

raised CVP in ventricular failure

hypoproteinemia (proteins cause osmotic pressure so nor proteins mean less goes back into blood)

increased capillary permeability in inflammation

97
Q

why is MAP important

A

main driving force pushing blood through circulation

98
Q

MAP = ? X ?

A

CO X TPR

99
Q

MAP too low can cause

A

syncope

100
Q

MAP too high causes

A

hypertension

101
Q

the 2 levels of control that insure blood flow is sufficient and MAP is sufficient

A

local/intrinsic mechanisms- for each individual tissue

central/ extrinsic mechanisms- ensure TPR and thus MAP stays in righ balance

102
Q

Local control of blood flow: active metabolic hyperaemia

trigger

A

increased metabolic activity

103
Q

Local control of blood flow: active metabolic hyperaemia

leads to

A

release of paracrine signal- EDRF or NO
causing arteriolar dilation
washing out metabolites

104
Q

Local control of blood flow: active metabolic hyperaemia

why does it happen

A

to ensure blood supply is matched to the metabolic needs of a tissue

105
Q

Local control of blood flow: pressure (flow) autoregulation

trigger

A

decrease in perfusion pressure

106
Q

Local control of blood flow: pressure (flow) autoregulation

leads to

A

decrease in MAP and therefore decrease in flow

metabolites accumulate

releases paracrine signal

dilating arterioles and returning flow to normal

107
Q

Local control of blood flow: pressure (flow) autoregulation

why does it happen

A

ensures that a tissue maintains blood supply despite changes in MAP

108
Q

Local control of blood flow: Reactive hyperaemia

trigger

A

occlusion of blood supply

109
Q

Central control of blood flow: hormonal

A

adrenalin from adrenal medulla
binds to alpha 1
constriction
decrease flow and increase TPR

BUT in some tissues- skeletal and cardiac muscle
it also activates beta 2
causing DILATION
increasing flow and decreasing TPR
significant in exercise
110
Q

Local control of blood flow: Reactive hyperaemia

leads to

A

increase in blood flow

an extreme version of pressure autoregulation

111
Q

Local control of blood flow: Reactive hyperaemia

real life example

A

arm goes red after getting BP taken

112
Q

Local control of blood flow: injury response

causes activation / release of

A

c-fibre- pain

substance P

mast cell

histamines

113
Q

Local control of blood flow: injury response

leads to

A

arteriolar dilation

so increases blood flow and permeability

114
Q

Local control of blood flow: injury response

why it happens

A

aids in delivery of blood born leucocytes to the injured area

115
Q

Central control of blood flow: neural

sympathetic and parasympathetic actions

A

sympathetic:
arteriolar constriction

decrease flow and increase TPR

Parasympathetic:
no effect usually
except in genitalia and salivary glands

116
Q

control of blood flow: special area- coronary circulation

A

blood supply gets interrupted during systole

so shows active hyperaemia- high sensitivity to metabolites
and has a lot of beta 2 receptors

swamping any possible constriction

117
Q

control of blood flow: special area- cerebral circulation

A

needs to be kept stable whatever

so shows excellent pressure auto regulation

118
Q

control of blood flow: special area- pulmonary circulation

A

decreases in O2 causes arteriolar constriction- opposite most tissues

ensures blood is directed to a better ventilated part of lungs

119
Q

control of blood flow: special area- renal circulation

A

shows excellent pressure autoregulation

as it needs to rely on MAP to filter properly

120
Q

2 SENSORY components of arterial baroreflex

A

aortic arch baroceptor

carotid sinus baroceptor

121
Q

how doe constriting veins increase BP

A

increases preload strength and volume

increasing CO

122
Q

how does constricing arterys increase bp

A

increasing TPR

123
Q

INTERGRATER component of arterial baroreflex

A

medullary cardiovascular centre

124
Q

EFFECTOR component of arterial baroreflex: parasympathetic

A

vagus activation

SA nodes releases acetylcholine

hypopolorising pacemaker cells slowing them

125
Q

EFFECTOR component of arterial baroreflex: sympathetic activation

A

SA node releases noradrenalin

works on beta 1

pacemaker cells depolarise faster
and increases Ca+ in ventricle
and constricts blood vessels

126
Q

aortic arch nerve supply

A

vagus nerve

127
Q

other inputs to the medullary cardiovascular centres

A

cardiopulmonary baroreceptors
blood volume

central chemoreceptors
pCO2 pO2

chemoreceptors in muscle
metabilite conc

joint receptors
join movement

higher centres
hypothalamus and cerebral cortex

128
Q

how does Valsalva manoeuvre effect heart

A

increases thoracic pressure in aorta

reduces venous filling pressure
decreasing VR EDV SV CO and MAP

reduced MAP is detected by baroreceptors initiating a reflex in CO and TPR

BASICALLY it stops venous return reducing preload and CO

129
Q

how does Valsalva manoeuvre effect heart

A

increases thoracic pressure in aorta

reduces venous filling pressure
decreasing VR EDV SV CO and MAP

reduced MAP is detected by baroreceptors initiating a reflex in CO and TPR

BASICALLY it stops venous return reducing preload and CO

130
Q

how do changes in posture effect the CVS

A

standing causes blood to pool in legs

reducing: EDV, preload, SV, CO and MAP

131
Q

how does the body correct the cvs after standing

A

baroreceptors detect loss in MAP
The information is sent to, and integrated in, the medullary cardiovascular centres.

and will cause
A parasympathetic - dis-inhibition of HR causing an increase in CO

And sympathetic:
increase in HR causing an increase in CO

increase in contractility causing an increase in SV and CO

venoconstriction causing an increase in preload, stroke volume and CO

arteriolar constriction causing an increase in TPR

132
Q

main organ that controls long term BP

A

kidneys- controlling plasma volume an therefore MAP

133
Q

how does the kidney control plasma volume

A

by controlling how much water is passed out or reabsorbed:

using Na+ transport to change osmotic gradient

it can make the collecting duct very permeable to water, increasing reabsorption, little urine and higher plasma volume- therefore increasing BP

or make the collecting duct less permeable, decreasing absorption increasing urine and reducing plasma volume- therefore reducing BP

134
Q

what hormones regulate kidney absorption

A

RAAS system

ADH and vasopressin

atrial natriuretic peptide and brain natriuretic peptide

135
Q

RAAS system: where is renin produced?

A

juxtaglomerular (granule cells) in the kidney

136
Q

RAAS system: what triggers renin production

A

Activation of sympathetic nerves to the juxtaglomerular apparatus

Decreased distension of afferent arterioles (the “renal baroreflex”)

Decreased delivery of Na+/Cl- through the tubule

ALL ARE SIGNS OF LOW MAP

137
Q

what does renin do

A

Converts inactive angiotensinogen to angiotensin I

Which is in turn converted by angiotensin converting enzyme to angiotensin II

138
Q

what does angiotensin II do

A

Stimulates release of aldosterone from the adrenal cortex

  • Increases Na+ reabsorption in the loop of Henle
  • Therefore reduces diuresis and increases plasma volume

Increases release of ADH from the pituitary

  • Increases water permeability of the collecting duct
  • Therefore reduces diuresis and increases plasma volume
  • And increases sense of thirst

and vasoconstricts- increasing TPR

ALL INCREASE MAP

139
Q

what part of the pituitary releases ADH

A

poosterior

140
Q

what trigger release of ADH

A

signs of low plasma volume of MAP:

A decrease in blood volume (as sensed by cardiopulmonary baroreceptors and relayed via medullary cardiovascular centres)

An increase in osmolarity of interstitial fluid (as sensed by osmoreceptors in the hypothalamus)

Circulating angiotensin II (triggered by the renin-angiotensin-aldosterone system)

141
Q

what does ADH do

A

Increases the permeability of the collecting duct to H2O, therefore REDUCES diuresis and increases plasma volume

Causes vasoconstriction (hence its alternative name, vasopressin), therefore INCREASING MAP

142
Q

where are Atrial natriuretic peptide and brain natriuretic peptide (ANP BNP) produced

A

myocardial cells in the atria & (despite the name)

and the ventricles

143
Q

what triggers ANP and BNP

A

increased distension of atria and ventricles- sign of increased MAP

144
Q

what does ANP and BNP do

A

increase excretion of Na+

inhibit secretion of renin

act on medullary CV centres to decrease MAP

145
Q

all systems in long term control of blood pressure a

A

negative feedback loops

Yr 1 CVS (3 decks)

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