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Y1 Summary > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

define autorhythmicity

A

the heart generates its own electrical impulse in the absence of external stimuli

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2
Q

define sinus rhythm

A

heart whose pace its controlled by the sa node

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3
Q

which cells exhibit spontaneous pacemaker potential

A

sa node cells

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4
Q

function of gap junctions

A

cell to cell current flow for spread of depolarisation from sa to av node

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5
Q

what takes the membrane to the ap threshold

A

pacemaker potential

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6
Q

what ion movement happens in the pacemaker potential

A

decreased k+ efflux, slow na+ influx

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7
Q

what ion movement represents the repolarisation phase of the sa node action potential

A

k+ efflux

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8
Q

what ion movement represents the depolarisation phase of the sa node action potential

A

ca influx though L type ca channels

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9
Q

in the ventricular action potential what does phase 4 represent

A

the resting membrane potential

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10
Q

in the ventricular action potential what does phase 3 represent

A

K+ efflux, repolarisation

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11
Q

in the ventricular action potential what does phase 0 represent

A

depolarisation, fast na+ influx

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12
Q

in the ventricular action potential what does phase 1 represent

A

slow k+ influx

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13
Q

in the ventricular action potential what does phase 2 represent

A

ca+ influx through L type ca channels

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14
Q

in the ventricular action potential what does the plateau phase represent

A

phase 2, ca+ influx through L type ca channels

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15
Q

from the sa node where does excitation next spread

A

av node

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16
Q

from the av node where does excitation next spread

A

bundle of his

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17
Q

from the bundle of his where does excitation next spread

A

L & R branches

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18
Q

from the L & R branches where does excitation next spread

A

purkinje fibres

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19
Q

what allows rapid spread of excitation through the ventricles

A

the bundle of his & the purkinje fibres

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20
Q

what is vagal tone

A

parasympathetic stimulation (<hr>

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21
Q

what does vagal tone bring the intrinsic HR down from? and to what?

A

100bpm to 70bpm on average

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22
Q

how does the vagus nerve supply the heart

A

parasympathetic to AV & SA node, increases AV node delay

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23
Q

what is the parasympathetic supply to the heart

A

cn x

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24
Q

through what receptor does the parasympathetic system supply the heart

A

m2

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25
Q

through what neurotransmitter does the parasympathetic system supply the heart

A

acetylcholine

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26
Q

mechanism of atropine

A

inhibits aceytlcholine

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27
Q

what is a -ve chronotropic effect

A

decreases hr

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28
Q

where is the sympathetic supply to the heart

A

sa node, av node, myocardium

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29
Q

effect of sympathetic supply to the heart

A

positive inotropic & positive chronotropic

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30
Q

through what receptor does the sympathetic system supply the heart

A

beta 1

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31
Q

contractile unit of the heart

A

myofibril

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32
Q

resistance in gap junctions

A

low

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33
Q

actin

A

thin, light filament

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34
Q

myosin

A

thick, dark filament

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35
Q

in the sliding filament theory where is the atp binding site

A

on myosin heads

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36
Q

what ion is required for the sliding filament theory

A

ca++

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37
Q

does the sliding filament theory require energy

A

yes

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38
Q

what is excitation contraction coupling

A

the action potential switching on ventricular systole

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39
Q

what effect does extracellular ca++ have in the excitation contraction coupling

A

stimulate release from intracellular ca++ from sarcoplasmic reticulum

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40
Q

in excitation contraction coupling when does the action potential stop

A

when ca++ influx stopsq

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41
Q

in excitation contraction coupling how is ca++ transported back to the sarcoplasmic reticulum

A

ca+ATPase

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42
Q

what happens during ca++ influx in the plateau phase

A

diastole

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43
Q

what happens in systole (excitation contraction coupling)

A

ca++ binds to troponin, pulling troponin tropomysin complex to expose cross bridge binding sites

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44
Q

clinical benefit of the refractory period

A

prevents tetanic contractions of the heart

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45
Q

stroke volume definition

A

volume of blood ejected by each ventricle per heart beat

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46
Q

what is preload

A

end diastolic volume

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47
Q

frank-starling curve:

A

increased end diastolic volume, increased stroke volume

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48
Q

in cardiac muscle optimal length when stretching/relaxed

A

stretching

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49
Q

what law matches SV in RV & LV

A

starling’s (intrinsic control)

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50
Q

afterload definition

A

force against the lv contracting to eject blood into the systemic circulation

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51
Q

what effect does increased afterload have on edv

A

increased

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52
Q

cause of continuous increased afterload

A

hypertension

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53
Q

compensation for hypertension increased afterload

A

lvh

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54
Q

effect of sympathetic system on frank-starling curve

A

shifts left

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55
Q

what effect do b-blockers have on the frank-starling curve

A

shift right

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56
Q

what effect does heart failure have on the frank-starling curve

A

shifts right

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57
Q

what volume of blood is pumped out by each ventricle per minute

A

5 litres

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58
Q

cardiac output definition

A

blood volume pumped by each ventricle per minute

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59
Q

cardiac output formula

A

co = sv X hr

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60
Q

cardiac cycle definition

A

events occuring from beginning of one heart beat to the beginning of next

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61
Q

ventricle 80% full by what

A

passive filling

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62
Q

what causes the av valves to shut

A

ventricular pressure > atrial pressure

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63
Q

what causes the ap valves to open

A

ventricular pressure > aortic/pulmonary pressure

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64
Q

what causes the ap valves to shut

A

ventricular pressure < aortic/pulmonary pressure

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65
Q

causes of third heart sound

A

lv systolic dysfunction, e.g. LVF, CHF, or mitral regurg or constrictive pericarditis

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66
Q

causes of fourth heart sound

A

hypertension, aortic stenosis, LVH, myocardial ischaemia, HOCM

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67
Q

components of jvp

A

a, c, v

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68
Q

what is a in the jvp

A

atrial contraction

69
Q

what is c in the jvp

A

tricuspid bulging into the atrium during systole

70
Q

what is v in the jvp

A

atrial filling

71
Q

what vein is the jvp

A

external jugular vein

72
Q

what is an ecg

A

vector graph of voltage V time

73
Q

ecg dipole; what does magnitude represent

A

mass of cardiac muscle involved

74
Q

ecg dipole; what does direction represent

A

electrical activity at any instant

75
Q

ecg; what is a lead

A

measures potential difference between 2 parts of the body

76
Q

ecg; when is maximum deflection

A

when lead axis parallel to dipole

77
Q

ecg; when is minimum deflection

A

when lead axis perpendicular to dipole

78
Q

ecg; upward deflection

A

towards +ve recording electrode

79
Q

ecg; downward deflection

A

away from +ve recording electrode

80
Q

what plane are the chest leads in

A

horizontal

81
Q

what plane are the augmented limb leads in

A

frontal

82
Q

what plane are the standard limb leads in

A

frontal

83
Q

where is V1 in the standard limb leads

A

right sternal edge, 4th intercostal

84
Q

where is V2 in the standard limb leads

A

left sternal edge, 4th intercostal

85
Q

where is V3 in the standard limb leads

A

halfway between v2 & v4

86
Q

where is V4 in the standard limb leads

A

5th interocostal, mid-clavicular line

87
Q

where is V5 in the standard limb leads

A

anterior axillary line, 5th intercostal

88
Q

where is V6 in the standard limb leads

A

midaxillary line, 5th intercostal

89
Q

which leads detects rhythm distrubances

A

lead ii

90
Q

where is standard limb lead 1

A

right arm to left arm

91
Q

where is standard limb lead 2

A

right arm to left leg

92
Q

where is standard limb lead 3

A

left arm to left leg

93
Q

what does the p wave represent & duration

A

atrial depolarisation, 0.08-0.1

94
Q

what does the q wave represent

A

interventricular septum depolarisation

95
Q

what does the pr interval represent & duration

A

av node delay, 0.12 - 0.2

96
Q

what does the qrs complex represent & duration

A

ventricular depolarisation, <0.1 seconds

97
Q

what does the s wave represent

A

ventricular bases depolarisation

98
Q

what does the t wave represent

A

ventricular repolarisation

99
Q

at which points on an ecg are the atria/ventricles completely depolarised

A

isoelectric

100
Q

how to count hr from ecg

A

300/big squares between QRSs

101
Q

how to count irregular hr from ech

A

number of QRSs in 30 big squares x 10

102
Q

why are there 12 ecg leads

A

determine the axis of the heart in the thorax, voltage criteria changes, to see st segment or t wave changes in specific regions of the heart (ischaemia)

103
Q

blood pressure definition

A

outwards hydrostatic pressure exerted by blood on blood vessel walls

104
Q

what kind of blood flow can’t be auscultated

A

laminar

105
Q

map definition

A

average arterial bp during 1 cycle

106
Q

map formula (both of them)

A

2x diastolic + systolic / 3

and diastolic + 1/3(systolic-diastolic)

107
Q

where is central venous pressure measured

A

ra / svc

108
Q

tpr definition

A

sum of resistance of peripheral vasculature in systemic circulation

109
Q

main resistance vessels

A

arterioles

110
Q

where are the baroreceptors

A

aortic arch & carotid sinus

111
Q

through what nerves do the baroreceptors send signals to the brain

A

cn ix & cn x

112
Q

where is the control centre for regulating map

A

medulla

113
Q

short term regulation of map

A

baroreceptor reflex (decreases vagal tone)

114
Q

what causes postural hypotension

A

failure of baroreceptor reflex

115
Q

how much body fluid does icf make up

A

2/3

116
Q

what makes up ecf

A

pv + interstitial fluid volume

117
Q

decreased plasma volume causes

A

fluid shift from interstitial compartment to plasma compartment

118
Q

where is renin released from

A

kidneys

119
Q

what is the rate limiting strep in raas

A

renin secretion

120
Q

where is aldosterone released from

A

adrenal cortex

121
Q

effect of aldosterone

A

increases h2o & na retention to increased plasma volume, and cause thirst

122
Q

when is anp released

A

hypovolaemic state

123
Q

effect of anp

A

induces h2o & na excretion

124
Q

adh aka

A

vassopressin

125
Q

where is adh synthesed

A

hypothalamus

126
Q

where is adh stored

A

pituitary

127
Q

when is adh secretion stimulated

A

decreased extracellular fluid volume & increased extracellular fluid osmolarity

128
Q

effect of adh

A

increases h2o reabsorption, increased plasma volume, concentrates urine

129
Q

which ‘system’ is activated when you haven’t drank enough

A

adh

130
Q

tpr regulated by changing what

A

radius of arterioles

131
Q

during rest where is most blood volume

A

veins

132
Q

blow flow resistance is inversely proportional to what

A

blood vessel radius to the power of 4

133
Q

blood flow resistance proportional to what

A

blood viscosity & blood vessel length

134
Q

true/false: no parasympathetic innervation of arterial smooth muscle

A

false, only penis & clitoris

135
Q

extrinsic tpr control (nerves)

A

sympathetic discharge

136
Q

increased vasomotor tone causes

A

vasoconstriction

137
Q

where are alpha receptors located

A

skin, gut, kidneys, arterioles

138
Q

what does alpha receptor activation cause

A

vasoconstriction

139
Q

where are beta 2 receptors

A

cardiac & skeletal muscle arterioles

140
Q

what does beta 2 receptor activation cause

A

vasodilation

141
Q

extrinsic tpr control; hormones

A

adrenaline, antiduiretic hormones & angiotensin 2

142
Q

____ control can over ride _____ control of tpr to match blood flow in tissues to metabolic needs

A

intrinsic, extrinsic

143
Q

which local metabolites cause vasodilation & metabolic hyperaemia

A

decreased local PO2, increased local PCO2, decreased H+, increased K+

144
Q

which local humoral agents cause vasodilation

A

histamine, bradykinin, nitric oxide

145
Q

when are local humoral agents released

A

injury/inflammation

146
Q

function of nitric oxide

A

regulates blood flow

147
Q

how is nitric oxide produced

A

by artery’s/arterioles endothelium by nitric oxide synthase

148
Q

what activates nitric oxide

A

increased blood flow

149
Q

which local humoral agents cause vasoconstriction

A

serotonin, thromboxane AS, leukotrienes, endothelin

150
Q

name causes of endothelial damage

A

increased BP or cholesterol, diabetes

151
Q

what does shear stress cause

A

vasodilation

152
Q

effect of increased temp on blood vessels

A

vasodilation

153
Q

effect of increased map on blood vessels

A

vasoconstriction

154
Q

define venomotor tone

A

veins partially constricted at rest due to sympathetic stimulation

155
Q

effect of increased venomotor tone

A

increased map, increased venous return

156
Q

acute response to exercise

A

increased HR, SV & CO, decreased blood flow to gut/kidneys, vasodilation to skeletal/cardiac muscle, increased systolic and decreased diastolic blood pressure, decreased tpr

157
Q

chronic response to exercise

A

decreased blood pressure, increased parasympathetic tone, decreased renin release, vasodilation

158
Q

what kind of metabolism occurs during shock

A

anaerobic

159
Q

what effect stroke volume

A

preload, afterload and contractility

160
Q

effect of cardiogenic shock on frank-starling curve

A

down a lot

161
Q

example of cardiogenic shock

A

mi

162
Q

examples of obstructive shock

A

cardiac tamponafe, tension pneumothorax, pe, severe aortic stenosis, increased intrathoracic pressure

163
Q

examples of distributive neurogenic shock

A

spinal cord, decreased sympathetic drive

164
Q

types of distribute shock

A

neurogenic and vasoactive

165
Q

examples of vasoactive shock

A

sepsis, anaphylaxis (increased capillary permeability)

166
Q

management of cardiogenic shock

A

inotrope

167
Q

management of septic shock

A

vassopressors (vasoconstrict)

168
Q

haemorrhagic shock presentation

A

small volume pulse, cool peripheries

Y1 Summary (6 decks)

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