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year 1 > CARDIO PHYSIOLOGY > Flashcards

CARDIO PHYSIOLOGY Flashcards

1
Q

what kind of membrane potential do pace maker cells in the heart exhibit

A

spontaneous pacemaker potential

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2
Q

what gives rise to the pacemaker potential in a pacemaker cell

A

decrease in K+ efflux
slow Na+ and K+ influx
transient Ca2+ influx

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3
Q

what kind of calcium channels allow the transient Ca2+ influx in the PMP

A

T-type Ca2+ channels

T for transient

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4
Q

what gives rise to the rising phase of the pace maker action potential and what are the channels involved
(depolarisation)

A

opening of Ca2+ channels - Ca++ influx

L-type Ca2+ channels

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5
Q

what gives rise to the falling phase of pacemaker action potential (repolarisation)

A

opening of K+ channels - K+ efflux

inactivation of L-type calcium channels

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6
Q

what is the funny current

A

Na and K influx

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7
Q

why is there AV nodal delay

A

cells are small and slow to conduct

allows time for atrial systole to precede ventricular systole

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8
Q

what is the other name for phase 0 of ventricular contractile cells action potential

A

depolarisation / rising phase

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9
Q

what is responsible for phase 0 of ventricular contractile cells action potential

A

fast Na+ influx

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10
Q

what occurs in phase 0 of ventricular contractile cells action potential

A

reversal of resting membrane potential from -90 to +20

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11
Q

what occurs in phase 1 of ventricular contractile cells action potential

A

closure of Na+ channels and transient K+ efflux

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12
Q

there is some repolarisation in phase 1 of ventricular contractile cells action potential
true/false

A

true

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13
Q

what is the other name for phase 2 of ventricular contractile cells action potential

A

plateau phase

unique to contractile cardiac muscle cell

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14
Q

what occurs in phase 2/plateau phase of ventricular contractile cells action potential

A

Ca++ influx

K+ efflux in background causes it to balance

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15
Q

can an AP be generated in phase 2?

A

no

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16
Q

what channels are responsible for phase 2

A

L-type Ca++ voltage gated channels

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17
Q

what state are the sodium channels in in phase 2

A

closed

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18
Q

what is the other name for phase 3 of ventricular contractile cells action potential

A

falling phase / repolarisation

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19
Q

what causes phase 3 of ventricular contractile cells action potential

A

inactivation (closure) of ca++ channels

opening of K+ channels - K+ efflux

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20
Q

can an AP be generated during phase 3

A

no

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21
Q

what is the resting membrane potential of a ventricular cardiac muscle cell

A

-90

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22
Q

what charge is ventricular contractile cells action potential depolarised to

A

+20

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23
Q

what occurs at phase 4 of ventricular contractile cells action potential

A

membrane rests are membrane potential

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24
Q

how does vagal stimulation have a negative chronotropic effect on the heart

A

cell hyperpolarises - takes longer to reach threshold
slope of PMP decreases
frequency of PMP decreases
negative chronotropic effect

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25
Q

how does sympathetic stimulation have a positive chronotropic effect on the heart

A

slope of PMP increases
reaches threshold quicker
frequency of AP increases
positive chronotropic effect

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26
Q

what does sympathetic stimulation supply

A

SA node
AV node
myocardium

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27
Q

what does parasympathetic stimulation supply

A

SA and AV nodes

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28
Q

what neurotransmitter and receptor are working in the heart with parasympathetic stimulation

A

ACh on M2 receptors

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29
Q

what neurotransmitter and receptor are working in the heart with sympathetic stimulation

A

NA on B1 receptors

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30
Q

sympathetic stimulation decreases AV nodal delay

true/false

A

true

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31
Q

parasympathetic stimulation increases AV nodal delay

true/false

A

true

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32
Q

what does SS do to the pacemaker cell K+ efflux

A

decrease

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33
Q

what does SS do to the pacemaker cell Na+ and Ca++ influx

A

increase

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34
Q

what does PSS do to the pacemaker cell K+ efflux

A

increase

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35
Q

what does PSS do to the pacemaker cell Na+ and Ca++ influx

A

decreases

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36
Q

what is atropine

A

competitive inhibitor of ACh

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37
Q

what do hypoxia and hypercapnia do to the PMP slope

A

increase

–> positive chronotropic effect

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38
Q

what does hypokalaemia do to the PMP slope

A

increases

–> positive chronotropic effect

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39
Q

what does hyperkalaemia do to the PMP slope

A

decreases

–> negative chronotropic effect

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40
Q

what cells “provide mechanical adhesion between adjacent cardiac cells to ensure tension is developed and transmitted to the next cell”

A

desmosomes

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41
Q

where are desmosomes found

A

within intercalated discs

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42
Q

do cardiac muscle cells have neuromuscular junctions

A

no

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43
Q

is actin or myosin thick and dark

A

myosin (bigger word)

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44
Q

how do cardiac muscle cells contract

A

actin slides over myosin to produce muscle tension

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45
Q

for what 2 reasons does ATP bind to myosin heads

A

energise it

or breakdown cross bridge between myofibrils

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46
Q

if calcium is present what happens to the energised myosin

A

calcium switches on cross bridge formation
binds to troponin complex on myosin, causes conformational change which exposes actin binding site and cross bridge forms

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47
Q

what happens to the energised myosin head if no calcium is present

A

goes into resting state - cross bridge binding sites are covered by troponin-tropomyosin complex

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48
Q

what happens once myosin binds to actin

A

bending - myosin and actin overlap)

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49
Q

after bending, what happens if ATP is present

A

ATP breaks down the cross bridge and cycle starts again

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50
Q

after bending what happens if ATP isn’t present

A

rigor complex formed

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51
Q

what is calcium usually stored

A

in the sarcoplasmic reticulum in lateral sacs

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52
Q

what is the release of calcium from SR dependent on

A

presence of extracellular Ca++

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53
Q

explain calcium induced calcium release

A

Ca++ influx during plateau phase of AP causes Ca++ to be released from SR to cause contraction

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54
Q

how is relaxation achieved in cardiac muscle cell

A

removal of ca++ back into SR or out of cell

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55
Q

what is the optimal fibre length of cardiac muscle cells

A

stretching

as opposed to skeletal which is the resting muscle length

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56
Q

what does the refractory period prevent happening

A

tetanic contractions (continuous)

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57
Q

what is the EDV

A

end diastolic volume

volume of blood remaining in each ventricle following diastole

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58
Q

what is the determining factor of EDV

A

VR

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59
Q

what is the equation for SV

A

EDV - ESV

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60
Q

what is SV

A

volume of blood ejected by each ventricle per heart beat

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61
Q

what is the preload

A

volume of blood in each ventricle before contraction

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62
Q

what is the afterload

A

resistance against which the heart has to pump after contraction

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63
Q

what does an increased EDV do to the force of contraction and why

A

increased EDV increases force of contraction

stretch increases troponin affinity for calcium

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64
Q

how does VR affect SV

A

VR increases
EDV increases
stretch increases
SV increases

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65
Q

what is the frank starling law

A

the greater the EDV the greater the SV during systole

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66
Q

how does FS compensate for increased afterload

A 
increased after load
decreased SV
increased EDV
increased stretch
increased contractile force
SV returns to normal
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67
Q

what way does sympathetic stimulation shift the FS curve

A

to the left - increased SV
Frank Starling’s Law states that the more the ventricles are filled with blood/ the greater the EDV - the greater the systolic contractions. Sympathetic simulation increases systolic contraction and shifts the curve to the left.

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68
Q

what way does shock shift the FS curve

A

to the right

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69
Q

what way does exercise shift the FS curve

A

to the left

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70
Q

what is the equation and definition of CO

A

CO = SV x HR

volume of blood pumped out by each ventricle per minute

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71
Q

what is the average CO in a resting adult

A

5L

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72
Q

with a HR of 75 what would diastole equal and what would systole equal

A

D - 0.5s

S - 0.3s

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73
Q

what is the pulse pressure and what is it normally

A

systolic - diastolic BP

30-50

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74
Q

what are the 5 stages of the cardiac cycle

A 
passing filling
atrial contraction
isovolumetric ventricular contraction
ventricular ejection
isovolumetric ventricular relaxation
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75
Q

what occurs during passive filling

A

AV valves open
blood flows into ventricles
pressures in atria and ventricles close to 0

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76
Q

what happens during atrial contraction

A

remaining atrial volume fills ventricles by atrial systole completing EDV

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77
Q

what on the ECG represents atrial depolarisation

and what represents atrial contraction

A

atrial depolarisation - p wave

atrial contraction - P - QRS

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78
Q

what occurs during isovolumetric ventricular contraction

A

AV valves shut as Pa < Pv

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79
Q

what happens during ventricular ejection

A 
aortic/pulmonary valves open and Pv > Parteries
SV ejected
ESV left
ventricular pressure falls 
aortic and pulmonary valves shut 
S2
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80
Q

what does dicrotic notch represent

A

aortic valve closing

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81
Q

what does s2 signal

A

the start of isovolumetric ventricular relaxation (diastole)
ventricle again a closed box
when ventricular pressure falls below Pa AV valves open
- Pa increasing as it fills with blood (VR)
- Pv decreasing due to relaxation

82
Q

when is S1 in cardiac cycle

A

isovolumetric ventricular contraction

83
Q

when do the aortic and pulmonary valves open

A

ventricular ejection

84
Q

what does the QRS complex represent

A

ventricular depolarisation

85
Q

what is blood pressure

A

outward force exerted by blood on blood vessel walls

86
Q

when is turbulent blood flow heard through a stethoscope

A

when external pressure is between S and D pressure

87
Q

what is the 1st Korotkoff sound

A

peak systolic pressure

88
Q

what is the 5th korotkoff sound

A

no sound - diastolic pressure

measurement taken after last sound

89
Q

what is MAP

A

average arterial BP during a single cycle

90
Q

what is the nucleus tractus solitarius

A

1st synapse of all CVS afferents in medulla

91
Q

give 5 different equations for MAP

A

DP + 1/3 (SP - DP)

[(2 x DP) + SP]/2

DP + [SP - DP]/3

CO x TPR

SV x HR x TPR

92
Q

diastolic portion is twice as long as systolic portion

true/false

A

true

93
Q

what is the main way of controlling resistance to blood flow

A

changes to blood vessel radius

94
Q

resistance to blood flow is directly proportional to what

A

thickness and length of vessel

95
Q

how is resistance linked to radius

A

directly proportional to 1/radius^4

96
Q

how is NO produced

A

by vascular endothelium
from AA L-arginine
through enzymatic action of NO synthase (NOS)

97
Q

what is flow dependent nitric oxide formation

A

sheer stress on vascular endothelium due to increased blood flow causes release of calcium in endothelial cells and subsequent activation of NOS

98
Q

what is receptor stimulated nitric oxide formation

A

vasoactive substances act as chemical stimuli to induce NO formation

99
Q

what does NO do when released from vascular endothelium

A

diffuses into adjacent SMCs where it activated cGMP which stimulates smooth muscle relaxation

100
Q

what are baroreceptors

A

mechanoreceptors sensitive to stretch

101
Q

what happens when there is higher BP re baroreceptor

A

higher BP

greater the firing of baroreceptors in afferent neurones

102
Q

where are carotid baroreceptors found and what nerve do they fire through

A 
carotid sinus
CN IX (glossopharyngeal)
103
Q

where are aortic baroreceptors found and what nerve do they fire through

A 
aortic arch
CN X (vagus nerve)
104
Q

what happens in high BP is sustained

A

firing decreases and is reset to a higher steady level

105
Q

where is CV control centre in brain

A

medulla

106
Q

how does decreased firing of baroreceptors increase BP

A 
decreased firing
decreased parasympathetic activity
increased sympathetic activity
increased vasoconstriction
increased SVR and tone in veins increases VR and SV
increased BP
107
Q

what is postural hypotension

A

failure of BRR to adjust to gravitational shifts in blood

108
Q

how do proteins move across vascular bed into interstitial fluid

A

vesicular transport

109
Q

where is renin released from

A

juxtapulmonary apparatus in kidney

110
Q

where is angiotensinogen produced

A

liver

111
Q

where is ACE produced

A

pulmonary vascular endothelium

112
Q

where is aldosterone released from

A

adrenal cortex

113
Q

what does aldosterone do

A

increases thirst and acts on kidneys to increase ADH - Na+ and water retention
systemic vasoconstriction - endothelia produced - increases SVR

114
Q

what cells release secrete renal tubular fluid

A

macula densa - specialised cells of kidney tubules

115
Q

where is ANP synthesised and stored

A

atrial myocytes

116
Q

what does ANP do and how

A

decreases BP
causes excretion of Na+ and water
decreases renin release, vasodilates

117
Q

what is ANP released in response to

A

atrial distension - hypervolaemic state

or neurohormonal stimuli

118
Q

is there is high serum BNP and N-terminal piece of pro-BNP what should you suspect

A

heart failure

119
Q

what is ADH release monitored by

A

osmoreceptors in brain close to hypothalamus

120
Q

where does ADH act

A

kidney tubules

121
Q

ADH causes a small degree of vasoconstriction due to endothelin production
true/false

A

true

122
Q

what is the vasomotor tone

A

vascular smooth muscle is partially constricted at rest due to tonic discharge of sympathetic system

123
Q

what is the neurotransmitter and receptor in vasomotor tone

A

NA

alpha-1 adrenoreceptors

124
Q

where is adrenaline released from

A

adrenal medulla

125
Q

what does adrenaline on alpha receptors cause

A

vasoconstriction

126
Q

what does adrenaline on beta receptors cause

A

vasodilation

127
Q

where are beta receptors mainly found

A

skeletal and cardiac muscle arterioles

128
Q

what does vasomotor tone do to the SVR and MAP

A

increases

129
Q

what is the venomotor tone

A

stimulation of sympathetic nerve fibres in venous smooth muscle causing venous constriction

130
Q

what does venomotor tone do to the VR, MAP and SV

A

increases

131
Q

local metabolic conditions can override extrinsic control of vascular smooth muscle
true/false

A

true

132
Q

does decreased local PO2 cause systemic vasodilation?

A

yes

133
Q

does increased local PCO2 cause systemic vasodilation?

A

yes

134
Q

does decreased osmolarity of ECF cause systemic vasodilation?

A

no

increased osmolarity of of ECF causes vasodilation

135
Q

does adenosine release cause systemic vasodilation?

A

yes

136
Q

does increased local H+ cause systemic vasodilation?

A

yes

137
Q

does decreased local K+ cause systemic vasodilation?

A

no

increased local K+ causes systemic vasodilation

138
Q

what happens to resistance vessels in the brain and kidney when MAP falls

A

resistance vessels dilate to increase flow

139
Q

how does muscle activity increase VR to heart

A

large veins lie in limbs between skeletal muscle

contraction of muscle aids VR

140
Q

prothrombotic, pro-inflammatory and pro-oxidant agents are all endothelial produced vasoconstrictors or vasodilators

A

vasoconstrictors

141
Q

which cause vasoconstriction and which cause vasodilation -

endothelin
histamine
serotonin
bradykinin
prostaglandins
thromboxane A2
leukotrienes
nitric oxide
A 
vasodilators -
histamine
bradykinin
prostaglandins
nitric oxide
vasoconstrictors - 
serotonin
thromboxane A2 
leukotrienes
endothelin
142
Q

during exercise what happens to blood flow to kidneys and gut

A

decreases due to vasomotor tone causing vasoconstriction in this areas

143
Q

during exercise what happens to blood flow to skeletal and cardiac muscle

A

increases - vasodilation in these areas due to metabolic hyperaemia which overrides sympathetic effects

144
Q

when does physiological splitting of S2 occur

where is this heard

A 
INspiration (INnocent)
pulmonary area (left 2nd ICS at sternal border)
145
Q

what is shock

A

abnormality in the circulatory system resulting in inadequate tissue perfusion and oxygenation –> anaerobic metabolism –> accumulation of waste –> cellular failure

146
Q

what kind of pulse is seen in hypovolaemic shock

A

fast pulse

147
Q

what are 3 causes of non-hemorrhagic hypovolaemic shock

A

vomiting
diarrhoea
excessive sweating

148
Q

what is the 3 end stages common to all shock

A

DECREASED SV
DECREASED CO AND BP
LOW PERFUSION AND OXYGENATION

149
Q

what is hypovolaemic shock

A

loss of blood volume

150
Q

what is cardiogenic shock

A

sustained hypotension due to decreased cardiac contractility

151
Q

what is an example of obstructive shock

A

tension pneumothorax

152
Q

what happens in obstructive shock

A 
increased intrathoracic pressure
decreased VR (reduced gradient)
reduced EDV
153
Q

what is neurogenic shock

A

loss of sympathetic tone (vasomotor) so increased vasodilation

154
Q

what kind of pulse is seen in septic shock

A

bounding

155
Q

what is an example of vasoactive shock

A

anaphylaxis

156
Q

what is an example of disruptive shock

A

septic shock

157
Q

what happens in vasoactive/disruptive shock

A

release of vasoactive mediators/abnormal distribution of BF in smallest BVs
increased vasodilation and increased capillary permeability

158
Q

until what point can compensatory mechanisms (baroreceptors/chemoreceptors) work with BV loss

A

up until 30% is lost

159
Q

what is the treatment for shock

A

ABCDE

1) high flow oxygen
2) volume replacement
3) shock specific treatment

160
Q

what is given for obstructive shock

A

immediate chest drain for tension pneumothorax

161
Q

what is given for septic shock

A

vasopressors

162
Q

what is given for cardiogenic shock

A

inotropes

163
Q

how does heart increase oxygenation

A

increase coronary flow

already has 75% oxygen extraction so this can’t be increased - organ of highest O2 demand

164
Q

when is the peak coronary flow

A

diastole

165
Q

what 2 arteries supply the brain

A

internal carotid arteries

vertebral arteries

166
Q

is grey or white matter more sensitive to hypoxia in the brain

A

grey

167
Q

what artery is formed from the joining of the 2 vertebra arteries

A

basilar artery

168
Q

how is the circle of willis formed

A

basilar artery anastomoses with internal carotids

169
Q

where do cerebral arteries arise from

A

circle of willis

170
Q

when does auto regulation of cerebral flood flow fail

A

MAP <60 or >100

171
Q

what does decreased PCO2 cause in the brain

A

cerebral vasoconstriction

172
Q

why does hyperventilation lead to fainting

A

decreased PCO2 causes cerebral vasoconstriction

173
Q

what is the equation for CPP

A

MAP - ICP

174
Q

which end are the forces for filtration greater than forces for absorption and vice versa

A

forces for filtration - greater at arterial end

forces for absorption - greater at venule end

175
Q

capillary hydrostatic pressure and interstitial fluid osmotic pressure are forces for

A

filtration

176
Q

capillary osmotic pressure and interstitial fluid hydrostatic pressure are forces for

A

absorption

177
Q

what is NET filtration

A

forces for filtration - forces for absorption

178
Q

why does reduced capillary osmotic pressure cause oedema

A

reduced driving force driving blood back into capillary

179
Q

what is the JVP a wave

A

Atrial contraction

180
Q

what is the JVP c wave

A

bulging of tricuspid valve into atrium during ventricular Contraction

181
Q

what is the JVP v wave

A

rise of atrial pressure during atrial filling

182
Q

true / false

JVP waves occur before RA pressure waves

A

false

JVP waves occur after RA pressure waves

183
Q

what does exercise do to the SBP / DBP / PP

A

SBP increases
DBP decreases
Pulse pressure increases

184
Q

what is ischaemic stroke

A

obstruction due to emboli or atherothrombosis causing interrupted blood supply to brain

185
Q

what is haemorrhage stroke

A

rupture of damaged artery causing interrupted blood supply to brain

186
Q

what are varicose veins

do they cause a reduction in CO

A

pooling of blood in lower limbs due to incompetent valve

no - due to chronic compensatory mechanism of increasing BV

187
Q

LDL is taken up from blood into where

A

intimate of artery

188
Q

what is LDL oxidised to

A

atherogenic OXLDL

189
Q

what role do monocytes play in atherosclerosis disease progression

A

migrate across endothelium into intima where they become macrophages and take up OXLDL

190
Q

what are macrophages converted to when they take up OXLDL and what does this form

A

foam cells –> fatty streak

191
Q

what does the release of inflammatory substances cause

A

division and proliferation of SMCs into the intima

192
Q

what does an atheromatous plaque consist of

A

lipid core (dead foam cells) and fibrous cap (SMCs and connective tissue)

193
Q

what % of total body fluid is made up by ECF

A

1/3

194
Q 
which one of the following does not stimulate endothelin production
ADH
Angiotensin II
mechanical shearing force
prostacyclin
A

prostacyclin

195
Q

what germ layer is the heart derived from

A

mesoderm

196
Q

what is involved in primary haemostasis

A

the formation of a soft clot - platelets bind to fibrinogen to form a soft clot

197
Q

what is involved in coagulation

A

formation of a solid clot by the end process or propagation when thrombin cleaves fibrinogen to form fibrin.

198
Q

how many branches of the aorta are there during embryological development

A

6

199
Q

what is the function of the vitelline veins

A

drain the yolk sac

200
Q

Which layer of a blood vessel contains endothelial cells, basal lamina and connective tissue?

A

tunica intima

201
Q

umbilical veins carry…

A

oxygenated blood

year 1 (45 decks)

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