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(SALMA) Physiology > CVS > Flashcards

CVS Flashcards

1
Q

what are the 3 steps of the cardiac cycle

A
  1. ventricular SYSTOLE (contraction)
  2. ventricular DIASTOLE (relaxation)
  3. atrial SYSTOLE (ventricular refilling)
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2
Q

what happens during ventricular contraction (4)

A
  1. ventricular pressure > atrial pressure
  2. AV valves close
  3. isovolumetric contraction - vP increases, no change to ventricular vol pre-ejection
  4. ventricular pressure > aortic pressure –> aortic valve opens and EJECTION BEGINS
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3
Q

what happens during ventricular relaxation (4)

A
  1. reduced ventricular ejection bc of ventricular relaxation
  2. aortic blood flow maintained by aortic distensibility (aortic volume decreases while aortic pressure remains constant)
  3. aortic pressure > ventricular pressure –> aortic valve closes
  4. isovolumetric relaxation - ventricular pressure decreases, no change to ventricular volume post-ejection
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4
Q

what is aortic blood flow maintained by

A

aortic distensibility (aortic vol decreases while aortic pressure remains constant)

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5
Q

what happens during ventricular refilling (3)

A
  1. atrial pressure > ventricular pressure –> AV valves open
  2. when atrial pressure = ventricular pressure, filling stops TEMPORARILY
  3. atrial booster (contraction) resumes filling
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6
Q

what is Starling’s law

A

stroke volume increases as end diastolic volume decreases

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7
Q

what is stroke volume

A

volume of blood pumped from the left ventricle per beat

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8
Q

what is the duration o systole

A

0.2-0.3 secs

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9
Q

what is the duration of diastole

A

0.5-0.6 secs

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10
Q

what is the ratio of time of systole:diastole

A

1/3 : 2/3

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11
Q

what is the effect of SNS on cardiac output

A

increases it by:

  • increasing heart rate
  • increases force of contraction
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12
Q

what is the effect of PNS on cardiac output

A

decreases it by:

  • decreasing heart rate
  • decreasing force of contraction
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13
Q

what are heart sounds: valves opening or closing

A

closing

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14
Q

what is excitation-contraction coupling?

A

the conversion of a chemical stimulus to a mechanical response

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15
Q

what are the 3 steps of excitation-contraction coupling

A
  1. motor neuron connects with muscle at NMJ
  2. ACh diffuses across synaptic cleft - depolarises sarcolemma
  3. depolarisation of sarcolemma causes calcium ions to be released, stimulating muscle contraction
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16
Q

what is a sarcolemma

A

cell membrane of muscle cell (separates sarcoplasm from extracellular surroundings)

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17
Q

what does the sarcomere run btwn

A

2 z lines

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18
Q

which band does the z line bisect

A

i

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19
Q

what does the a band have

A

myosin and actin

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20
Q

what is myosin made of

A

2 heavy chains (dual head)

4 light chains (made of alpha and beta myosin)

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21
Q

what is actin

A

double heli globular protein

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22
Q

where is f acts present

A

contractile proteins

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23
Q

what is tropomyosin

A

double peptide chain occupying groove btwn actin strands

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24
Q

what does tropomyosin do

A

regulate interaction of other 3 proteins

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25
Q

what are the 3 troponin’s

A

I, T, C

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26
Q

what is diff btwn troponin I, T, C

A

troponin I = inhibits myosin/actin interaction

troponin T = binds troponin complex to tropomyosin

troponin C = has high affinity to calcium and causes muscle contraction

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27
Q

what are the 7 steps of muscle contraction (sorry it’s so long)

A
  1. calcium ions released by excitation-contraction coupling
  2. calcium ions bind to troponin C, causing tropomyosin to move
  3. movement of tropomyosin causes myosin binding sites on actin filament to be exposed
  4. myosin heads bind to actin molecule, forming actin-myosin cross bridges
  5. ADP is released from myosin head, causing myosin head to nod forward/be pushed along (contraction)
  6. ATP attached to myosin head to detach it, causing cross bridges btwn myosin/actin to break down
  7. ATPase hydrolyses ATP –> ADP + Pi, causing myosin head to return to original position
  8. Continues until there is no more Calcium ions
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28
Q

what are myocytes connected by

A

gap junctions that form channels to allow ion flow btwn cells (to enable electrical coupling of neighbouring cells)

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29
Q

what does tropomyosin do when the muscle is relaxed

A

blocks the cross bridge binding sites on actin

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30
Q

what displaces tropomyosin

A

binding of calcium ions to troponin

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31
Q

where are calcium ions stored in a muscle

A

sarcoplasmic reticulum

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32
Q

what is a t tubule

A

extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells

they conduct impulses from sarcolemma down into the sarcoplasmic reticulum

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33
Q

what are the smallest branches of artery

A

terminal arterioles –> capillaries

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34
Q

what is the diameter of a capillary

A

3-40 micron

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35
Q

what is blood flow in capillaries regulated by

A

pre-capillary sphincters

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36
Q

wha are the 3 types of capillaries

A
  1. continuous (normal)
  2. fenestrated (kidneys, s intestine)
  3. discontinuous (liver sinusoids)
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37
Q

what is the structure of arteries/veins (internal to external, [5])

A
  1. tunica intima (endothelium and basement membrane)
  2. tunica media (vascular smooth muscle cells)
  3. internal elastic lamina
  4. tunica adventitia (fibroblasts)
  5. external elastic lamina
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38
Q

what are 3 differences btwn pulmonary vs systemic circulation

A
  • thin vs thick walls
  • minor vs substantial muscularisation
  • low vs high BP
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39
Q

equation for SV (Stroke vol)

A

EDV-ESV

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40
Q

what’s left ventricular filling pressure

A

diff btwn L atrial and L ventricular pressure

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41
Q

what is the precise equation for MAP

A

CO x TPR

= BP

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42
Q

what is the approximate equation for MAP

A

diastolic pressure + 1/3 (SP-DP)

remember: PP = SP - DP

so DP + 1/3 PP

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43
Q

what is pulse pressure

A

SP - DP

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44
Q

if resting BP is 120/80 mm Hg, what is the PP?

A

40 mmHg

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45
Q

what is the equation for cardiac output

A

SV x HR

remember SV = EDV - ESV

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46
Q

what is the equation for Ohm’s law (resistance)

A

flow = pressure gradient/resistance

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47
Q

what is the equation for Pouiselle’s law (resistance)

A

flow is proportional to radius^4

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48
Q

what is preload

A

EDV at the start of systole (how much sarcomeres are stretched)

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49
Q

what is afterload

A

ventricular pressure at thhe end of systole

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50
Q

define contracility

A

ability of the heart to contract more to incr BP

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51
Q

define elasticity

A

ability of the heart to return to normal shape post systolic stress

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52
Q

define compliance

A

ability for ventricles to expand to accommodate increasing blood volume

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53
Q

define resistance

A

opposition to the passage of a substance eg blood

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54
Q

why do we need peripheral circulation control (3)

A
  1. maintain blood flow n arterial pressure
  2. distribute blood flow
  3. homeostsis/autoregulation
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55
Q

what is the main site of resistance to vascular flow

A

arterioles

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56
Q

why are arterioles the main site of vascular resistance (googled)

A

cross-sectional area increase in the arterioles is not enough to make up for the increase in resistance going from aorta to arterioles.

This is different in capillaries since their total cross-sectional area is huge, and the change in resistance is smaller since the change in diameter going from arterioles to capillaries is smaller compared to going from aorta to arterioles.

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57
Q

what is myogenic autoregulation

A

smooth muscle contracts and relaxes in response to local BP change to ensure constant flow rate

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58
Q

what are 2 local vasoconstrictors

A
  • BP (myogenic auto regulation)
  • endothelin 1 (stimulated by angiotensin/ADH, released from endothelial cell –> binds to smooth muscle receptors and causes calcium release)
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59
Q

what is endothelin1 stimulated by

A

angiotensin and adh

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60
Q

how does endothelin 1 work

A
  • released from endothelial cell

- binds to smooth muscle receptors and causes calcium release

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61
Q

what are 3 local vasodilators

A
  • hypoxia
  • nitrous oxide
  • pH decrease (incr H+ and CO2)
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62
Q

what are neural factors in BP

A
  • BP deviates from norm
  • baroreceptors detect changes in BP
  • baroreceptors send impulse to brainstem
  • brainstem causes change to cardiac output and vessel diameter
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63
Q

name 3 hormonal vasoconstrictors

A

adrenaline (a1)
angiotensin I
adh

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64
Q

name 2 hormonal vasodilators

A

ANP

adrenaline (b2)

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65
Q

what is ANP

A

hormonal vasodilator

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66
Q

what does beta-2 receptor adrenaline do

A

vasodilates

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67
Q

what does alpha-1 receptor adrenaline do

A

vasoconstrict

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68
Q

which adrenaline receptors are found in the heart a lot

A

b2

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69
Q

what is hyperaemia

A

incr in blood flow

  • active when met activity is increased
  • reactive following an occlusion
  • compensate by myogenic auto regulation (good in coronary, poor in skin) with local vasdilators
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70
Q

what is diff btwn short and long term BP change

A

short - baroreceptors

long - volume change (ADH, renin angiotensin)

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71
Q

what do baroreceptors detect

A

changes in BP (sense pressure changes by responding to change in the tension of the arterial wall)

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72
Q

what are primary baroreceptors

A

arterial

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73
Q

what are secondary baroreceptors

A

cardiopulmonary

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74
Q

where are primary baroreceptors found

A
  • carotid sinus (more sensitive)

- aortic arch (less sensitive)

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75
Q

where is the carotid sinus

A

dilated area at base of the internal carotid just superior to bifurcation of intrernal/external carotid at level of superior border of thyroid cartilage

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76
Q

how do primary baroreceptors work

A
  • increase in BP
  • inhibition of SNS causes vasodilation
  • increased PNS to heart to - - decrease CO
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77
Q

how do secondary baroreceptors work

A
  • increase BP
  • inhibition of medullary vasoconstrictive area
  • BP falls
  • inhibit release of ADH, renin & angiotensin = lower bloodd vol
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78
Q

where are secondary baroreceptors found

A

systemic and pulmonary veins

atria

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79
Q

what is the afferent nerve supply to the heart

A

glossopharyngeal (IX)

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80
Q

what is the efferent nerve supply of the heart

A

vagus (X)

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81
Q

what are the components of central circulation

A

blood vessels (vasoconstriction/dilation)
heart (cardiac output)
kidneys (fluid control)

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82
Q

what are the effector vessels of the heart

A

arterioles

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83
Q

what is total peripheral resistance the same as

A

total arteriolar resistance

84
Q

what do central chemoreceptors detect (and here)

A
  • CO2 levels

- medulla

85
Q

what do peripheral chemoreceptors detect (and where)

A
  • O2 levels

- carotid/aortic body

86
Q

what is the frank-starling mechanism

A

EDV increase = SV increase (thus increased CO)

87
Q

what is the length-tension muscle relationship

A

muscle stretches for more volume - must contract more to push blood out

88
Q

what does increased EDV result in

A

increased contraction = increased SV = increased CO

89
Q

what does the p wave mean

A

atrial depolarisation

90
Q

how long is atrial depolarisation (p wave)

A

80-100ms

91
Q

what is the PR interval

A

slow conduction from AV node to His-Purkinje system

92
Q

how long is PR interval

A

120-200ms

93
Q

what is the QRS complex

A

ventricular depolarisation

94
Q

how long is QRS complex

A

60-100ms

95
Q

what is atrial depolarisation masked by

A

QRS

96
Q

what is ST interval

A

time btwn vent depolarisation and repolarisation

97
Q

what is the T wave

A

ventricular repolarisation

98
Q

what is the QT interval

A

ventricular depolarisation and depolarisaion

99
Q

how long is QT interval

A

200-400ms

100
Q

what timeframe does each ecg square rep

A

0.04s (or 40ms)

101
Q

*****what are the 5 steps of cardiac/myocyte action potential

A

is 2 de or re????
*****

0 Rapid depolarisation = Na+ inflow

1 Partial repolarisation = K+ outflow

2 Plateau = slow Ca2+ inflow (still K+ outflow)

3 Repolarisation = Ca2+ channels close, K+ outflow

4 Resting potential = still K+ outflow

102
Q

what are the 3 steps of pacemaker action potential

A
  1. Pacemaker potential [-60v]=
    - closed K+ channels
    - (T-type) Ca channels open [-40v]
    - Slow Ca2+ and Na+ influx
  2. Depolarisation =
    - AP begins when threshold released
    - More Ca2+ influx (L type)
  3. Repolarisation =
    - Ca channels close
    - K channels open –> EFFLUX
103
Q

what is the conduction pathway (from SA node to ventricular contraction)

A

SA node –> atrial contraction –> AV node –> bundle of His –> purkinje fibres (septum) –> l and r branches –> ventricular contraction

104
Q

do atrial impulses spread faster or ventricular

A

atrial

105
Q

how do AP spread from cell to cell

A

via gap junctions

106
Q

what is the cardiac axis

A

overall direction of electrical activity in heart (can be normal, left, or right deviated)

107
Q

what is blood composed of

A 
cellular component (45%)
fluid component (55%)
108
Q

what is in the cellular component of blood

A

RBC, WBC, platelets

109
Q

what are erythrocytes

A

RBC

110
Q

what are leukocytes

A

WBC

111
Q

how many leads in an ecg

A

12

112
Q

what are the diff ecg leads

A

3 bipolar leads (+ve to -ve)
6 chest leads (unipolar)
3 augmented leads

113
Q

which waves are positive for all leads apart from AVr

A

p and t

114
Q

is QRS positive on LHS or RHS leads

A

LHS

115
Q

what is plasma

A

serum liquid and proteins dissolved (eg globulins, albumin, fibrinogen)

116
Q

what is haematopoiesis

A

formation of blood cells n platelets which continues throughout life

117
Q

what do rbc and platelets share in common

A

both anucleate

118
Q

what is the lifespan of rbc

A

120d

119
Q

what is the lifespan of platelets

A

7-10d

120
Q

where does haematopoiesis (blood cell prod) occur in children and adults

A

children - all bone marrow

adults - only axial skeleton

121
Q

do rbc have mitochondria

A

no

122
Q

what is rbc prod stimulate by

A

EPO (erythropoietin) - released by kidneys

123
Q

where are rbc destroyed

A

liver n spleen

124
Q

what kind of env does o2 bind to iron in

A

aqueous

125
Q

what is anaemia

A

decrease in no. of rbc or Hb in blood

126
Q

what is acute anaemia

A

bleeding - less rbc in circulation

127
Q

what is pernicious anaemia

A

no b12/folate - rbc not prod quickly enough

128
Q

what are the 5 diff types of wbc

A
  1. neutrophils
  2. monocytes
  3. lymphocytes
  4. basophils
  5. eosinophils
129
Q

what s replication and differentiation (haemopoeisis) stimulate by

A

hormonal growth factors that stimulate precursor cells

RBC - epo
WBC - gm-csf
platelets - tpo

130
Q

what is a young rbc aka

A

reticulocyte

131
Q

which way does oxygen dissociation curve shift when pH is decreased

A

right

132
Q

what is a normal range of Hb

A

12.5-15.5 g/dL

133
Q

where is folate found

A

fruit/veg n food supplements

134
Q

where is b12 absorbed

A

terminal ileum

135
Q

what can cause b12 deficiency

A

lack of gastric parietal cells

lack of terminal ill function

136
Q

name some types of anaemia

A
  1. acute (injury) 2. chronic (inflammatory disorders) 3. iron deficiency (chronic blood loss eg bleeding)
137
Q

describe WBC

A
  • mature cells
  • circulate in blood
  • formed from immature precursor cells in bone marrow (which are derived from stem cells)
  • rate of prod is under hormonal control of G-CSF
138
Q

what is the most numerous type of wbc

A

neutrophils

139
Q

which WBC release chemotaxis/cytokines important in inflammatory responsee

A

neutrophils

140
Q

what are 2 types of monocytes

A

macrophages and dendritic cells

141
Q

what is diff btwn 2 types of monocytes?

A

macrophages: phagocytose bacteria n foreign material

dendritic cells: present antigens to immune system

142
Q

what do basophils do

A

migrate to tissues –> become mast cells

- mast cells fill w granules containing histamine and express IgE

143
Q

what are basophils important for

A

immune repsonse

144
Q

what do eoisonophils play an important role in

A

inflammation and allergic response

145
Q

what is the ratio of B:T lymphocytes

A

20:80

146
Q

where do b and t lymphocytes mature

A

B - Bone marrow

T - Thymys

147
Q

what do b lymphocytes do

A

generate antibodies when stimulated by foreign antigens

148
Q

what do t lymphocytes do

A

aid B cells - generate cellular immunity (helper cells)

149
Q

what are the 2 types of t lymphocytes

A

helper cells (CD4+) suppress/reg immune response

natural killer cells (CD8+) target damaged/infected cells

150
Q

which 2 WBC are involved in phagocytosing

A

neutrophils n monocytes

151
Q

which 2 wbc are involved in allergic response

A

basophils n eosinophils

152
Q

what are platelets

A

small cytoplasmic enucleate cells that block up holes in blood vessels

153
Q

how do platelets form a thrombus (3)

A

adhere
activate
degranulate

154
Q

list 4 proteins found in blood

A
  1. albumin
  2. imunoglobulins
  3. coagulation proteins
  4. carrier proteins
155
Q

what is the most numerous plasma protein

A

albumin

156
Q

which protein determines oncotic pressure of blood

A

albumin

157
Q

where is albumin produced

A

liver

158
Q

what are immunoglobulins produced by

A

b lymphocytes - generated when stimulated by foreign antigens

159
Q

when are IG produced

A

in response to non-self antigens

160
Q

what are coagulation proteins

A

series of enzymes that circulate in an inactive form

161
Q

vitamin k is essential for correct synthesis of WHICH coagulation factors

A

10
9
7
2

162
Q

which cells is tissue factor present on

A

every cell but endothelial cell

163
Q

what triggers the beginning of the coagulation cascade

A

bleeding

164
Q

what type of inheritance pattern is haemophilia

A

recessively x linked

165
Q

what type of inheritance pattern is von willebrand disease

A

autosomal dominant

166
Q

what is haemophilia

A

not enough clotting factors in blood

167
Q

what is VWF

A

lack of vwf

168
Q

where is vit k found

A

green veg

169
Q

is vit k fat or water soluble

A

fat

170
Q

what is vit k necessary for

A

functional activity of coagulation factors 2, 7, 9, 10

171
Q

where is the apex beat of the heart

A

5th intercostal space, mid-clavicular line

172
Q

what is the mediastinum

A

area btwn l and r pleura

173
Q

which plane divides superior and inferior mediastinum

A

sternal angle n t4/5

174
Q

how do papillary muscles attach to AV valves

A

chord tendinae

175
Q

which ventricle is systemic n why

A

left - thick walled n muscular

176
Q

where does coronary sinus drain blood from heart into

A

RA

177
Q

what separates smooth n trabeculated portions of RA

A

crista terminalis

178
Q

where do coronary arteries arise from

A

aortic root

179
Q

what does the left coronary artery divide into

A

left anterior descending / left anterior interventricular

circumflex

180
Q

where does LAD run

A

in anterior IV groove

181
Q

where does Cx artery run

A

left AV groove

182
Q

what dominant are most ppl

A

right

183
Q

what is gastrulation

A

mass movement n invagination of blastula to form 3 layers (outer –> inner)

  • ectoderm
  • mesoderm
  • endoderm
184
Q

what is a gastrula

A

trilaminar structure that the embryo blast develops into

185
Q

what does ectoderm develop

A

outside skin
nervous systems
neutral crest
pit/mamm/sweat glands

186
Q

what does mesoderm form

A

muscle
most systems
kidneys
blood

187
Q

what does endoderm form

A

GI tract

endocrine organs

188
Q

where is most of CVS formed from embryologically

A

mesoderm

189
Q

what are the 3 stages of cardiac formation

A
  1. formation of primitive heart tube
  2. cardiac loop
  3. cardiac septation
190
Q

when is heart formed in foetus

A

w3

191
Q

when does heart begin to beat

A

day 22

192
Q

in foetus, which side of heart is there more pressure?

A

right bc unfunctional lungs so incr vascular resistance in pulmonary circulation

193
Q

why is blood shunted from right to left atrium

A

down pressure gradient

194
Q

describe foetal circulation

A
  1. blood enters RA
  2. blood flows through foramen ovale
  3. blood pushes valve of foramen ovale to left
  4. blood enters LA
195
Q

what happens to pressure in RHS of heart at birth

A

drops - pressure greater in LHS (blood in LA pushes foramen ovale valve, closing atrial passageway)

196
Q

how does oxygenated blood from placenta enter foetus

A

umbilical vein

197
Q

what is myogenic tone

A

vascular smooth muscle is never relaxed

198
Q

what is the resp pump

A
  1. diaphragm descends, pushes abdominal cavity and increases intra-abdominal pressure, which is transmitted to abdominal veins
  2. simultaneously, pressure in the thorax decreases, decreasing RA pressure and intrathoracic veins (net effect of pressure changes btwn thorax n chest enhancing venous return)

this is the basis for the frank-starling mechanism

199
Q

how does anterior hypothalamus impact BP/HR

A

increases

200
Q

what is pacemaker potential

A

slow pos incr in voltage across membrane that occurs btwn end of 1 AP and beginning of next

201
Q

where is the AV node located

A

base of RA

202
Q

what is PS stim of heart controlled by

A

ACh - binds to muscarinic receptors

203
Q

What is S stim controlled by

A

Ad/NAd

204
Q

when does contraction of the hear muscle happen

A

with Ca entry to cells n and finishes before repolarisation

205
Q

what is resting membrane potential

A

-55 0 -60 mV

206
Q

release of what into sarcasm promotes sliding of actin n myosin

A

Ca2+

(SALMA) Physiology (12 decks)

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