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My1 Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

what is autorhythmicity

A

Ability for heart to beat without external stimuli

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2
Q

Where do you find Pacemaker cells

A

SA node of heart, upper right atrium near super vena cava

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3
Q

A heart controlled by SA node is said to have what

A

Sinus rhythm

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4
Q

Do pacemaker cells have a resting membrane potential?

A

No

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5
Q

What do pacemakers have instead and why?

A

They have pacemaker potential, constantly moving towards threshold for AP. Continuous spontaneous pacemaker potentials.

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6
Q

What is stage 4 of pacemaker AP

A

decreased efflux of K, transient influx of Ca and funny current (influx of Na)

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7
Q

What are the phases of the AP in pacemaker cells

A

Stage 4: spontaneous depolarisation, stage 0: upstroke, stage 3, depolarisation

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8
Q

What is stage 0 of pacemaker AP

A

Upstroke due to Ltype Ca channels opening - influx

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9
Q

What happens in stage 3 of pacemaker AP

A

repolarisation as K channels re-open and inactivation of . ltype Ca

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10
Q

Myocardial cells pass the impulse from the __ node to the __ node via ___.

A

SA, AV, gap junctions (cell-to-cell current flow)

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11
Q

why is conduction delayed in AV node

A

so atria can fully contract

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12
Q

what are the structures that pass AP to ventricles (bundle + fibres)

A

His, left and right bundles, purkinje

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13
Q

what are the phases of cardiac cells (different from pacemakers)

A

phase 4: resting potential Phase 0: upstroke phase 1: early repolarisation, phase 2: plateau, phase 3: repolarisation

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14
Q

explain phase 0 of cardiac cells:

A

fast depolarisation by na influx

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15
Q

explain phase 1 of cardiac cells

A

closure of Na channels and transient K efflux

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16
Q

explain phase 2 of cardiac cells

A

l type calcium channels open and ca influx

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17
Q

explain phase 3 of cardiac cells

A

closure of l type ca channels and activation of k channels for an efflux

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18
Q

explain phase 4 of cardiac cells

A

resting membrane potential

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19
Q

what effect does sympathetic chain have on heart

A

speeds it up

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20
Q

what effect does parasympathetic chain have on heart

A

slows it down

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21
Q

what nerve has a constant effect on the SA and AV? lowering its HR from 100bpm to 70

A

vagus nerve exhibiting vagal tone

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22
Q

what is bradycardia and tachycardia

A

bradycardia is 60 bpm, tachycardia is 100bpm

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23
Q

what does the vagal nerve do

A

slows heartrate and increases AV node delay, slope of pacemaker potential decreases,

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24
Q

what is the neurotransmitter and receptor of the parasympathetic chain in the heart

A

M2 receptor, acetly choline (ACh)

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25
Q

what drug is a competitive inhibitor of acetylcholine and is used in bradycardia

A

atropine

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26
Q

what is a negative chronotropic effect

A

slows heart rate

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27
Q

which nerve branch supplies the AV, SA and myocardium of the heart

A

sympathetic

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28
Q

what effect does sympathetic have on heart

A

increases HR, decreases AV nodal delay, increases force of contraction (positive chronotropic effect)

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29
Q

what is the neurotransmitter and receptor of sympathetic in the heart

A

noradrenaline of B1 adrenoreceptors

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30
Q

describe cardiac myocytes structure

A

striated with central nucleusand regular arrangement of contractile proteins

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31
Q

what are myocytes electrically coupled with

A

gap junctions

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32
Q

what are gap junctions

A

protein channels that ensure excitation reaches all cardiac cells

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33
Q

what do desmosomes do

A

within intercalated discs provide adhesion

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34
Q

what do muscle fibres contain for contracting

A

myofibrils

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35
Q

what do myofibrils contain

A

thick and thin filaments, myosin and actin

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36
Q

describe myosin

A

thick and appears dark

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37
Q

describe actin

A

thin and appears light

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38
Q

within each myofibril, what are actin and myosin arranged into

A

sarcomeres

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39
Q

What is essential for myosin and actin contraction

A

ATP and calcium

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40
Q

what does calcium do in myosin actin activation

A

binds to troponin C on myosin head allowing crossbridge to form

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41
Q

where is calcium released from

A

SR

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42
Q

what is calcium induced calcium releases

A

an influx of calcium will cause calcium to be released from SR causing contraction

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43
Q

what is the refractory period

A

a short length of time following an AP where it is not possible to produce another AP

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44
Q

Why is the refractory period necessary

A

to prevent continuous (tetanic) contractions of the heart

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45
Q

in the plateau stage the closure of Na channels means cell cant be depolarised, and in descending phase k channels are open do cell cant be depolarised, what effect is this

A

refractory period

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46
Q

what is the stroke volume

A

the volume of blood ejected by the ventricles per beat

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47
Q

the end diastolic volume (EDV) - the end systolic volume (ESV) is equal to?

A

stroke volume

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48
Q

EDV dictates the cardiac afterload true/false

A

false it’s the preload.

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49
Q

What is EDV determined by

A

venous return

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50
Q

what is the frank-starling curve

A

the relationship between EDV, SV and venous return

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51
Q

what does the frank-stirling curve mean

A

the greater the EDV, the greater the SV and therefore venous return

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52
Q

what is the optimal length for energy in cardiac muscle

A

stretching (for increases EDV)

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53
Q

what and when is afterload?

A

resistance the heart pumps into? after heart contracts

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54
Q

how does sympathetic control of the heart have a positive inotropic effect

A

greater activation of ca channels in SR, reduces duration of systole and diastole

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55
Q

does the parasympathetic nerves cause a inotropic (contractility effect)

A

no

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56
Q

where are adrenaline and noradrenaline released from to have a inotropic and chronotropic effect

A

adrenal medulla

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57
Q

what is cardiac output and equation

A

volume of blood pumped by ventricles per min CO = SV x HR

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58
Q

what is the cardiac cycle

A

the events occurring from the beginning of one heartbeat to the next

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59
Q

what is diastole

A

ventricles relax and fill with blood from atria

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60
Q

what is systole

A

ventricles contract and pump blood to aorta and pulmonary artery

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61
Q

what is the order of events in cardiac cycle

A

passive filling, atrial contraction, isovolumetric ventricle contraction, ventricular ejection, isovolumetric ventricular relaxation

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62
Q

what are the steps in passive filling (valves, pressures, % full)

A

AV valves open, pressure in atria and ventricles close to 0, aortic valves close and aortic pressure is around 80, ventricles become 80% full

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63
Q

what are the steps in atrial contraction (ECG)

A

P wave in ECG shows atrial depolarisation, contraction occurs between p and QRS. when atria finish contraction = EDV

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64
Q

steps of isovolumetric ventricular contraction (ECG, pressure, valves, heart sounds)

A

contraction is after QRS, the ventricular pressure rises, when it exceeds atrial pressure AV valves shut producing first heart sound, pressure rises around closed space

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65
Q

steps of ventricular ejection? pressure, valves, SV, ECG, heart soundsSS

A

when pressure exceeds aortic/ pulmonary, the valves open, SV is ejected leaving ESV, T wave shows repolarisation, pressure falls, when below aortic/ pulmonary valves close to produce 2nd heart sound, vibration is dichroitic nothc

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66
Q

isovolumetric ventricular relaxation (sound, pressure, valves)

A

2nd heart sound signals start, the pressure falls, when below atrial pressure the AV valves open again

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67
Q

when do the heart sounds occur

A

during ventricular contraction, mitral valve (S1), and at the start of ventricular relaxation, aortic valve (S2)

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68
Q

why does the pressure of the heart and aorta never return to 0

A

due to elastic properties of arteries, would have too much pressure exerted on them and collapse and recoil

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69
Q

what is the JVP and what can it be used to identify

A

indirect measure of central venous pressure, shows right sided heart failure.

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70
Q

what is BP

A

the outwards hydrostatic pressure exerted by the blood on vessel walls

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71
Q

what is systolic BP (and normal range)

A

pressure exerted on aorta when heart contracts >120

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72
Q

what is diastolic BP (and normal range)

A

pressure on aorta when heart relaxes >80

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73
Q

what are the values for hypertension

A

140/90

74
Q

what is pulse pressure? normal ranges

A

difference between diastolic and systolic 30-50mmHg.

75
Q

in what fashion does blood flow in the arteries

A

laminar

76
Q

what pressures do BP cuffs exert and how do they work

A

external exceeds internal so no sound, if external between systolic and diastolic can here turbulent flow.

77
Q

peak systolic pressure reveals what sound

A

1st korotkoff (first sound heard when checking BP)

78
Q

what is heard in the 2nd and 3rd korotkoff sounds

A

intermittent sounds due to turbulent flow

79
Q

when is diastolic ‘heard’?

A

When the sounds dissapears, 5th korotkoff sound.

80
Q

the pressure gradient between the ___ and the ___ ___, drives ____ circulation

A

aorta, right atrium, systemic

81
Q

pressure gradient = ___ - ____

A

MAP - central venous pressure (right atrium) which is close to 0.

82
Q

what is the mean arterial blood pressure?

A

average arterial BP during single cardiac cycle

83
Q

how long is diastole compared to systole

A

twice as long

84
Q

what are the 2 equations for MABP

A

MABP = [(2 x diastolic) + systolic]/3 MABP = DBP + 1/3 pulse pressure

85
Q

what re the ranges of normal for MABP

A

70-105

86
Q

what MABP is needed to perfuse major organs

A

at least 60

87
Q

what happens if MABP too high

A

damage blood vessels and extra strain on heart

88
Q

what is the relationship between MABP, CO and SVR

A

MABP = CO x SVR (CO = HR x SV)

89
Q

what do baroreceptors detect

A

changes in BP

90
Q

where do baroreceptors send signals too

A

medulla

91
Q

what are the effectors of baroreceptor

A

heart and blood vessels

92
Q

in what loop do baroreceptors work

A

negative feedback

93
Q

where do you have baroreceptors

A

carotid and aortic

94
Q

what happens if baroreceptors detect too low BP

A

carotid baroreceptors decrease firing, vagal activity decreases, sympathetic increases, vasoconstriction

95
Q

what happens if baroreceptors detect too high BP

A

carotid baroreceptors increases firing, vagal activity increases, sympathetic decreases, vasoconstriction decreases

96
Q

what is postural hypotension

A

when someone stands from lying quickly and BP rapidly drops

97
Q

how is postural hypotension corrected in a healthy person

A

venous return rapidly drops, MAP decreases so baroreceptors decrease rapidly

98
Q

in a person with diagnosed postural hypotension what does there body do? (baroreceptors)

A

baroreceptors fail to respond to gravitational shifts

99
Q

what are risk factors for postural hypotension

A

age, meds, disease, reduced blood volume, prolonged bed rest

100
Q

what is a positive test for postural hypotension

A

drop within 3 mins of lying to standing: systolic at least 20, diastolic at least 10

101
Q

symptoms of postural hypotension

A

light headedness, dizziness, blurred vision, faints and falls

102
Q

baroreceptors can detect chronic hypertension? true/false

A

false, they can only detect acute changes

103
Q

the total body fluid is made of ICF and ECF in what ratios

A

2/3 ICF, 1/3 ECF

104
Q

what is ECF composed of

A

plasma volume and interstitial fluid volume

105
Q

what happens if plasma volume falls

A

fluid is moved from interstitial compartment

106
Q

___ is controlled if ECFV is controlled

A

MABP

107
Q

hormones that regulate ECFV generally regular what 2 substances

A

salt and water

108
Q

what 3 hormones mainly control ECFV

A

renin-angiotensin-aldosterone system (RAAS), natriuretic peptides NP, antidiuretic hormone (ADH)

109
Q

if there is low BP in the kidney (low Na in renal tubular fluid), what is released

A

renin

110
Q

renin converts ___ produced in the ___ to ____

A

angiotensinogen produced in liver to angiotensin I

111
Q

what is angiotensin I converted too

A

angiotensin II

112
Q

what enzyme converts angiotensin I to angiotensin II and where is it produced

A

ACE in the lungs

113
Q

angiotensin II stimulates the adrenal cortex to release what

A

aldosterone

114
Q

what does aldosterone do

A

retain water and sodium from kidneys

115
Q

apart from stimulate the release of aldosterone, what else does angiotensin II do?

A

causes vasoconstriction and increases the release of ADH

116
Q

what do natriuretic peptides do?

A

cause excretion of salt and water in kidneys and decreases renin release. (decrease BP).

117
Q

what are the 2 types of NP

A

atrial NP and brain-type NP

118
Q

where is ANP stored and when is it released

A

atrial myocytes, in response to atrial distension

119
Q

where is BNP synthesised and what is it cleaved to?

A

synthesised in brain, ventricles and other, pre-BNP –> postBNP –> BNP.

120
Q

where is the precursor of ADH stored and where is it synthesised

A

posterior pituitary and hypothalamus

121
Q

what stimulates the release of ADH

A

it increases BP, low ECFV and high plasma osmolality

122
Q

what are the main resistance vessels

A

arterioles

123
Q

what type of vessels hold the most blood at rest

A

veins

124
Q

what is the stroke volume influenced by

A

Preload, afterload and contractility

125
Q

what is the relationship for MAP

A

MAP = CO (HR x SV) x SVR

126
Q

resistance is directly proportional to what 2 things, and inversely to what 1 thing

A

vessel length and viscosity, and radius (mainly controls it)

127
Q

what type of nerve supply acts on arterial smooth muscle

A

sympathetic

128
Q

artery smooth muscles are partially constricted at rest by sympathetic nerves, what is this called?

A

vasomotor tone

129
Q

where is adrenaline produced

A

adrenal medulla

130
Q

where are alpha receptors found

A

skin, gut kidney

131
Q

where are beta receptors found

A

cardiac and skeletal

132
Q

can intrinsic controls override extrinsic ones?

A

yes, to match their perfusion needs

133
Q

name some metabolites that cause relaxation and hyperaemia (6) - opposites cause constriction

A

decreased PO2, increased CO2, decreased pH (acid), increases EC K, increases osmolality, adenosine

134
Q

name some local humoral agents that are dilators, often released in injury

A

histamine, bradykinin, NO

135
Q

where is NO produced, what is it’s precursor and enzyme

A

vascular endothelium, amino acid l-argine –> NO by NOS

136
Q

how is NO production stimulated

A

stress on endothelium causes it’s release for vasodilation.

137
Q

what can cause damage to endothelium

A

high BP, high cholesterol, diabetes, smoking

138
Q

what humoral agents causes constriction

A

serotonin, thromboxane, leukotrienes, endothelin

139
Q

what physical intrinsic controls apply

A

temp and myogenic response

140
Q

what 4 factors affect venous return

A

venomotor tone, blood volume, resp pump and skeletal pump

141
Q

what nerves supply venous smooth muscle

A

sympathetic

142
Q

where are large veins situated and what type of valves are in place

A

in-between skeletal muscle, one way valves

143
Q

during exercise sympathetic nerve activity increases to cause increases HR and SV, this causes reduced flow to what areas

A

kidney and gut

144
Q

during exercise, what type of muscles metabolic needs override vasomotor drive

A

skeletal and cardiac, ie increased blood flow

145
Q

what is ‘shock’

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion

146
Q

what are the 4 types of shock

A

hypovolaemic, cardiogenic, obstructive and disruptive

147
Q

what is hypovolaemic shock and what can cause it

A

loss of blood volume, haemorrhage, vomiting and diarrhoea

148
Q

what is cardiogenic shock and what can cause it

A

heart muscle has decreased contractility, MI can cause it

149
Q

what is disruptive shock and what can cause it

A

loss of sympathetic tone to blood vessels, can be from neurogenic shock (trauma) and sepsis

150
Q

what is obstructive shock and what can cause it

A

increases pressure in thoracic cavity which decreases venous return, can be caused by pneumothorax, cardiac tamponade

151
Q

how do you treat shock (generally)

A

ABCDE, O2, volume replacement (except cardiogenic)

152
Q

how does vasoactive shock arise

A

release of vasoactive mediators causes vasodilation

153
Q

in hypovolaemic shock there are compensatory mechanisms until what % of blood loss

A

30%.

154
Q

where do the right and left coronaries arise from

A

base of the aorta

155
Q

where does most of the coronary venous blood drain too

A

coronary sinus right atrium

156
Q

what is the only way to increase o2 in the heart? (what doesn’t work)

A

increase flow, O2 extraction is not possible

157
Q

what effects does low PO2 have on coronary arterioles

A

vasodilation

158
Q

what effect does sympathetic nerves have on coronary arteries

A

dilate it to increase SV and HR

159
Q

when does peak coronary flow occur

A

diastole

160
Q

which arteries supply cerebral circulation

A

internal carotids and vertebral

161
Q

what arteries anastomose to form the circle of willis, what arises from this

A

basilar and carotid, major cerebral arteries

162
Q

if one artery is obstructed can cerebral perfusion be maintained? what if a smaller branch is blocked?

A

Yes perfusion can be maintained, deprive small region of the brain = stroke

163
Q

how does the brain respond to decreases PCO2

A

vasoconstriction, why hyperventilating leads to fainting

164
Q

how does autoregulation in cerebral circulation work?

A

increased MAP causes constriction, decreased MAP causes dilation. only works between 60-160 mmHg

165
Q

how does increases intracranial pressure affect blood flow? what can cause this?

A

increased cranial pressure decreases flow so as not to damage brain, can happen in trauma (swelling) and tumours

166
Q

in the pulmonary circulation, why do the absorption forces exceed filtration

A

to prevent oedema

167
Q

why does hypoxia in lungs cause vasoconstriction

A

to prevent blood from going to poorly ventilated areas of the lungs

168
Q

in exercise, what overcomes the sympathetic vasoconstrictor tone in skeletal muscle

A

local hyperaemia and adrenaline

169
Q

what is interstitial fluid

A

extracellular fluid, the space between cells and blood

170
Q

how does gas, exchangeable proteins, soluble substances and plasma proteins cross capillary walls

A

diffusion, vesicular transport, pores and they don’t

171
Q

how is capillary fluid driven

A

pressure gradients

172
Q

what is the NET filtration pressure

A

forces favouring filtration - forces favouring reabsorption

173
Q

where do forces favouring filtration occur

A

capillaries

174
Q

where do forces favouring reabsorption occur

A

venules

175
Q

where does excess fluid drain

A

lymphatic system

176
Q

what factors affect filtration in capillaries

A

capillary hydrostatic pressure and interstitial fluid osmotic pressure

177
Q

what factors affect reabsorption in venules

A

capillary osmotic pressure and interstitial hydrostatic pressure

178
Q

what is oedema?

A

an accumulation of fluid in the interstitial space, can compromised gas exchange in lungs

179
Q

what can raised capillary hydrostatic pressure (reduced filtration) that can cause pulmonary oedema

A

raised venous pressure, LV failure, prolonged standing

180
Q

how does left ventricular failure cause pulmonary oedema

A

raised pressure in LA which increases pulmonary pressure and capillary pressure.

My1 Cardiology (16 decks)

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