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HOM > Heart > Flashcards

Heart Flashcards

1
Q

Potential energy = ?

A

mass x gravity x height

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2
Q

Why must blood flow change with O2 not glucose usage?

A

O2 runs out before glucose does

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3
Q

Why must skeletal muscle perfusion be controlled?

A

Maximal perfusion is impossible

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4
Q

What is the epicardium?

A

Thin connective tissue covering heart

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5
Q

What is the SA node innervated by?

A

Vagus nerve

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6
Q

What cells are platelets fragments of?

A

Megakaryocytes (bone marrow cell which produces platelets)

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7
Q

What are the three plasma proteins?

A

Fibrinogen, albumin, globin

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8
Q

What electrically divides the atria and ventricles?

A

Collagen proteins within the rings

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9
Q

Equation relating power and flow?

A

Power = flow x gravity x height

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10
Q

What is the critical closing pressure?

A

As pressure increases flow increases, but some elastic arteries snap shut and need minimum pressure

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11
Q

What is the P wave?

A

atrial depolarisation

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12
Q

What is the PQ delay from?

A

AV delay

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13
Q

What is the QRS phase?

A

Ventricular depolarisation

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14
Q

What is the QR interval?

A

Spreading down septum

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15
Q

What is the RS interval?

A

Spreading up sides of ventricules

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16
Q

What is the ST phase?

A

Plateau phase (ventricular contraction)

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17
Q

What is the T wave?

A

Repolarisation of ventricles

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18
Q

Which valve closes between ventricular filling and isovolumetric contraction?

A

Mitral valve closes

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19
Q

Which valve closes between ventricular ejection and isovolumetric relaxation?

A

Aortic valve closes

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20
Q

Does aortic or ventricular pressure get higher?

A

Aortic

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21
Q

What are the aortic and ventricular pressures like when flow into aorta is at maximum?

A

Equal

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22
Q

What kind of blood flow does aortic stenosis cause?

A

Turbulent blood flow

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23
Q

How does heart rate affect the ratio of systole:diastole?

A

Lowers the ratio

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24
Q

Why is right ventricular pressure lower than left?

A

Lung resistance to blood flow is less

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25
Q

When does most coronary blood flow occur?

A

Diastole - usually squeezed shut by pressure

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26
Q

What is angina?

A

Temporary insufficiency of blood flow to heart causing acidosis and pain

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27
Q

What is the value of central venous pressure?

A

Very close to zero

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28
Q

What is the usual value of total peripheral resistance?

A

1

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29
Q

What is Fick’s principle in the heart?

A

Blood flow is proportional to the difference between O2 concentration as blood goes in compared to when it comes out

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30
Q

How do you measure cardiac output using O2?

A

rate of O2 from air / (arterial conc O2 - venous conc O2)

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31
Q

What is the dicrotic notch?

A

Sudden drop in pressure after systolic contraction - caused by backflow of arterial blood while valve is still closing, coincides with aortic valve closure

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32
Q

Velocity = ?

A

Flow / cross-sectional area

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33
Q

How does stenosis of the aortic valve affect velocity and pressure?

A

Increases velocity, decreases pressure

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34
Q

Blood pressure in foot is higher so how does blood flow up pressure gradient?

A

Trade gravitational energy for pressure

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35
Q

What is Darcy’s law?

A

Q is proportional to (P1 - P2) so Q = (P1-P2)/R so CO = (Pa - CVP)/TRP

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36
Q

Two types of fluid flow?

A

Turbulent or laminar

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37
Q

How does laminar flow affect blood cells and endothelial lining?

A

Blood cells not colliding, little damage to endothelial lining

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38
Q

What is a cell deficient marginal layer?

A

Red blood cells in centre during laminar flow

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39
Q

Where does turbulent flow occur?

A

Ventricle and aorta (large diameter, high velocity)

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40
Q

What is Reynolds number?

A

Ratio of inertial forces (disordering) and viscous forces (ordering)

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41
Q

Equation of Reynolds number?

A

(velocity x diameter x density)/viscosity

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42
Q

Above what value of Reynolds number is turbulent flow?

A

2000

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43
Q

Definition of viscosity?

A

Force required to move fluid at a certain rate

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44
Q

Force and velocity are shear ?

A

Force = shear stress, velocity = shear rate

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45
Q

Viscosity = ?

A

shear stress / shear rate

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46
Q

Why are high and low viscosity bad?

A

High is bad because heart must work harder, low is bad because need more blood pumped for the same pressure

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47
Q

What determines resistance during laminar flow?

A

Internal friction within fluid

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48
Q

Resistance is proportional to?

A

Tube length, viscosity and 1/radius^4

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49
Q

Flow = ?

A

[(P1-P2) x pir^4] / 8nL

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50
Q

Wall tension = ?

A

Transmural pressure x radius

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51
Q

Why does smooth muscle have wall tension? What about larger blood vessels and capillaries?

A

To resist transmural pressure - larger blood vessels need more, endothelial wall is enough in capillaries

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52
Q

What is preload?

A

End diastolic pressure OR volume of left ventricle OR stretch on myocytes of left ventricle

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53
Q

How does VR affect preload?

A

Raised VR = raised preload because higher venous pressure = more blood back to heart

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54
Q

Stretch = wall tension SO what is preload proportional to?

A

End diastolic pressure x cubedroot of volume

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55
Q

What is Starling’s preparation?

A

Aorta ligated (brain not functioning, blood still goes through coronary circulation), external circuit to change and measure venous pressure, arterial pressure, resistance and compliance, aorta connected to pressure gauge, rubber tubes can be squeezed

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56
Q

What represents the elastic aorta in Starling’s preparation?

A

Air chamber

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57
Q

Which ventricle is Starling’s law for?

A

Both

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58
Q

What is the ANREP effect?

A

10 minutes after stretch a rise in force ocurs

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59
Q

Why does Starling’s law require extrinsic controls?

A

Could cause arterial pressure to rise too high

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60
Q

Ratio of pre:postganglionic fibres in sympathetic neurones?

A

1:10

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61
Q

Ratio of pre:postganglionic fibres in parasympathetic neurones?

A

1:3

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62
Q

Which neurotransmitter can be released further away and diffuse?

A

NA

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63
Q

Which neurotransmitters do parasympathetic neurones use?

A

ACh - nicotinic then muscarinic

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64
Q

Which neurotransmitters do parasympathetic neurones use?

A

ACh (nicotinic) then NA

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65
Q

Where are Beta1 receptors found?

A

Heart and interstitial smooth muscle

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66
Q

Where are Beta2 receptors found?

A

Bronchi and vascular smooth muscle (relax)

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67
Q

What are alpha 2 receptors?

A

Presynaptic receptors

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68
Q

What are alpha 1 receptors?

A

Traditional receptors (vasoconstriction)

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69
Q

Are pre and postganglionic myelinated or unmyelinated?

A

Pre is myelinated, post is unmyelinated

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70
Q

How do catecholaines affect metabolic rate?

A

Stimulate it (maintains effects of neuronal sympathetic activity)

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71
Q

Which cells need catecholamines?

A

Ones with no sympathetic innervation

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72
Q

What proportion of their maximum diameter does tone keep arterioles at?

A

1/2

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73
Q

Is there more or less tone in the parasympathetic nervous system? What’s the exception and why?

A

Less tone apart from vagus (to keep heart rate depressed)

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74
Q

What takes up noradrenaline which has leaked?

A

Sympathetic neurones and smooth muscle

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75
Q

Where do preganglionic fibres in adrenal medulla terminate? What is released?

A

Modified nerve cells, release 80% adrenaline and 20% noradrenaline

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76
Q

What kind of incompetence does heart transplant cause? Why?

A

Chronotropic incompetence - higher resting heart rate and slower rise due to no vagus nerve

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77
Q

What does dromotrophy mean?

A

Conduction

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78
Q

Why is length-tension curve a straight line that carries on increasing in cardiac muscle?

A

Better overlap and more sensitive to Ca2+

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79
Q

What is mean systemic pressure “zero point” value?

A

7mmHg

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80
Q

What happens to venous pressure with every heartbeat?

A

Goes down a little bit

81
Q

In arteries CO=?

A

ABP-MSP / TPR

82
Q

In veins VR = ?

A

MSP-RAP / RVR

83
Q

What happens in transmural pressure gets too low?

A

Vessels will collapse

84
Q

What value is central venous pressure normally at?

A

Close to zero

85
Q

What happens to stroke volume if heart rate goes up?

A

Decreases

86
Q

What happens to pressure and CO if circulation is constricted?

A

Both increase`

87
Q

What happens to MSFP, CO and RAP is stressed volume is doubled?

A

MSFP and CO double, RAP still zero

88
Q

WHat connects myosin to Z line?

A

Titin

89
Q

WHy does heart have increased Ca2+ sensitivity?

A

Decreased lattice spacing

90
Q

Three causes of shock?

A

Hypovolaemic, cardiogenic, distributive

91
Q

Two effects of sympathetic stimulation?

A

Venoconstriction causing increased MSFP and heart rate

92
Q

Cause of heart failure?

A

Heart doesn’t know body is unable to increase cardiac output

93
Q

Effects of heart failure?

A

MSFP and RAP still increase, but if RAP increases so must capillary pressure so get oedema

94
Q

How do Guyton’s curves work?

A

A graph for CO and VR, when they are equal you know the actual values since CO and VR must be equal

95
Q

Components of septicaemic shock?

A

Distributive and cardiogenic components

96
Q

Pulse pressure = ?

A

P systolic - P diastolic

97
Q

What increases pulse pressure?

A

Excercise, age, aortic valve leakage

98
Q

Where are the stretch receptors?

A

Carotid sinus and aortic arch

99
Q

Which nerves do stretch receptors connect to?

A

Carotis sinus nerve to nerve IX and vagus

100
Q

Which valve closes at the start of systole?

A

Mitral

101
Q

Which valve closes at the start of diastole?

A

Aortic

102
Q

What happens to mean ABP if baroreceptors are denervated?

A

MEAN ABP stays the same but has less of a tight range

103
Q

WHat in brain area that baroreceptors and chemoreceptors feed into?

A

NTS in medulla (nucelus tractus solitarius)

104
Q

What does NTS stimulate?

A

Cardioinhibitory area, vasomotor area

105
Q

What does cardioinhibitory area increase?

A

Vagal tone

106
Q

What does vasomotor area increase?

A

Sympathetic tone

107
Q

WHich pathway do cardioinhibitory and vaso-motor areas use?

A

Bulbospinal pathway to preganglionic sympathetics

108
Q

Why can CO be measured using O2 consumption?

A

Oxygen consumption is proportional to CO

109
Q

Which adrenoceptors are for NA and which for adrenaline?

A

NA = alpha1 and beta1, A = beta2

110
Q

Where is alpha1 adrenoceptor and what does it do?

A

Vascular smooth muscle esp skin, for vasoconstriction

111
Q

Where is beta1 adrenoceptor and what does it do?

A

Cardiac, increased HR and contractility

112
Q

Where is beta2 adrenoceptor and what does it do?

A

Vascular smooth muscle esp skeletal, vasodilation

113
Q

Why are arterioles a good place to regulate flow?

A

Big drop in pressure here and muscular walls

114
Q

What regulates arteriole diameter?

A

Availability of actin to myosin, activity of myosin head

115
Q

What happens to arterioles in low O2?

A

Dilate

116
Q

What’s involve in local control of arteriole diameter?

A

Metabolites, myogenic (stretch), paracrine (from endothelium/inflammatory)

117
Q

What does caldesmon do to muscle?

A

Actin and myosin can’t bind

118
Q

What removes caldesmon from actin?

A

Calmodulin or phosphorylation

119
Q

What is the myogenic effect?

A

Tension in walls is proportional to radius, if you try and stretch it tension will go up so it shrinks

120
Q

What do NA and ACh cause endothelium to do in normal blood vessels?

A

NA causes constriction, ACh causes relaxation

121
Q

What does damage done by obesity, smoking and diabetes to endothelial lining cause?

A

Less vasodilatory signalling pathways, so vasoconstriction

122
Q

What is shear-stress induced release of NO?

A

Signalling upstream, metabolites all washed downstream and make endothelium produce NO, turbulence where the is big diameter change, NO diffuses upstream - so waste products determine blood flow

123
Q

What does NO synthase inhibitor do?

A

Acts as paracrine regulator, diffuses into smooth muscle, hyperpolarises it, reduces Ca2+, inhibits MLCK, turned off by phosphodiesterases

124
Q

How does NA cause SR Ca2+ release?

A

NA > alpha1 receptor > G-protein (Galphaq) > PLC > IP3 > SR Ca2+ release

125
Q

How does adrenaline cause decreased MLCK activity?

A

adrenaline > beta2 receptor > G-protein (Galphas) > adenyl cyclase > cAMP > PKA > decreased MLCK activity

126
Q

Which metabolite reduces Ca2+?

A

NO

127
Q

What increases Ca2+?

A

NA, depolarisation, stretch

128
Q

What inhibits MLCK?

A

adrenaline (via beta2) and NO

129
Q

What activated MLCK?

A

Ca2+ - CaM

130
Q

How does aspirin work?

A

Inhibits cyclo-oxygenase 1 irreversibly, inhibits thromboxane which causes platelet aggregation (also inhibits PGI2 which does the opposite but inhibits this less)

131
Q

What is the carotid sinus composed of?

A

Modified smooth muscle

132
Q

What are the carotid bodies?

A

Chemoreceptors

133
Q

How does positive ionotropic effect work?

A

NA > beta1 > AC > cAMP > PKA. Then, the PKA sensitizes troponin to Ca2+, phosphorylates DHP to increase Ca2+ conc, inhibits phospholamban so inhibition of SERCA removed so Ca2+ stored inside SR for next time

134
Q

Flow of X equals?

A

capillary area x permeability of X x change in conc

135
Q

Volume flow =

A

hydraulic permeability x (change in hydrostatic pressure - change in colloid osmotic pressure)

136
Q

How is autotransfusion caused?

A

Low venous pressure and sympathetic arteriolar constriction causes fluid to move back to blood

137
Q

What does lymphoedema cause in skin?

A

Moves it away from capillaries

138
Q

What is congestive heart failure?

A

Raised atrial pressure with lower arterial pressure than the body wants

139
Q

What changes are there during the fast phase of exercise hyperaemia?

A

Increased extracellular K+ from act pots, decreased O2, decreased pH, increased lactic acid, increased extracellular ATP and ADP, increased CO2 and temperature

140
Q

How can you measure blood flow during exercise hyperaemia?

A

Venous occlusion plethysmography, invasive flow monitoring, or IR spectroscopy

141
Q

Is circulation or breathing at fault for muscle limit?

A

Circulation (muscles could do more if given more blood)

142
Q

What is the secondary chemoreceptor response?

A

Response to response to hypoxia

143
Q

What are the two causes of hypoxia?

A

Inability to breathe, reduced O2 concentration

144
Q

What are the two ideal responses to hypoxia?

A

Conservation of O2, increased blood to tissues

145
Q

How do inwardly rectifying channels work?

A

Increased in extracellular K+ should cause depolarisation but does opposite in smooth muscle (hyperpolarises, closes Ca2+ channels, muscle relaxes) because ions coming in makes it easier for ions to get back out

146
Q

What do inwardly rectifying channels cause?

A

K+-induced vasodilation from local vasodilatory stimuli

147
Q

What is central venous pressure in a healthy heart?

A

0

148
Q

What do low pressure baroreceptors detect?

A

RAP (if elevated it suggest circulation is overfilled so can’t maintain venous pressures like in heart failure

149
Q

What happens if low presure baroreceptors are denervated?

A

Rise in mean ABP

150
Q

What do low pressure baroreceptors detect?

A

SHort term changes in ABP

151
Q

What do low pressure baroreceptors do with increased pressure?

A

Firing rate increases, goes to NTS via vagus, then to hypothalamus, decreases fluid and sodium retention

152
Q

What is functional hyperaemia?

A

Increased local blood flow e.g. following inflated cuff experiment

153
Q

What changes are there in arterioles following increased metabolism or reduced blood flow?

A

Reduced PO2, increased PCO2, decreased pH, increased adenosine, increased extracellular K+

154
Q

What local changes stimulate vasodilation?

A

Decreased pH and increased lactic acid

155
Q

When can acetylcholine not dilate arteries?

A

When endothelium is not intact

156
Q

Which tissues have more beta2 than alpha1 receptors?

A

Coronary blood vessels and skeletal muscle

157
Q

What do beta2 receptors trigger?

A

Vasodilation

158
Q

What does NA from sympathetic nerves do?

A

Acts on alpha1 receptors allowing skeletal muscle blood flow to be restricted if necessary

159
Q

What do ACh and NA do to arteries?

A

ACh dilates them, NA constricts them

160
Q

How does endothelium removal affect NA action on capillary artery constriction?

A

It doesn’t

161
Q

What is the signal from the endothelium to vascular smooth muscle?

A

NO

162
Q

How is NO production stimulated?

A

ACh and bradykinin stimulate production by the action of NO synthase on L-arginine in the endothelium

163
Q

What is bradykinin?

A

A vasodilator peptide

164
Q

How does NO inhibit MLCK?

A

Lipophilic, diffuses quickly, stimulates soluble guanylyl cyclase in vascular smooth muscle, a cGMP dependent protein kinase then phosphorylates MLCK

165
Q

How does viagra work as a vasodilator?

A

Reduces cGMP breakdown and inhibits cGMP-specific phophodiesterase type 5

166
Q

What things does the endothelium release?

A

Pro-coagulants, anti-coagulants, fibrinolytics, antibacterials, growth factors

167
Q

What are eicosanoids?

A

Arachidonic acid derivatives involved in clotting and inflammatory responses

168
Q

What synthesizes eicosanoids?

A

Cyclo-oxygenase

169
Q

WHat is the vasoconstrictory prostaglandin?

A

PG-F

170
Q

What is the vasodilatory prostaglandins?

A

PGs I, D E

171
Q

What produces thromboxane A2?

A

Platelets

172
Q

What does thromboxane A2 do?

A

Vasoconstrictor, also causes platelet aggregation

173
Q

WHat opposes thromboxane A2 action?

A

Prostacyclin

174
Q

What produces prostacyclin?

A

Produced by endothelium

175
Q

Why can endothelium damage lead to reduced blood flow and clotting?

A

Alters balance between prostacyclin and thromboxane A2 in favour of thromboxane A2

176
Q

What is interstitial oedema?

A

If rate of fluid movement out of capillaries is greater than removal by lymphatics

177
Q

What can localised oedema result from?

A

Lymphatic blockage, increased capillary leakiness to proteins in inflammation, ischaemia reperfusion injury and in the brain following head injury

178
Q

How much must interstitial fluid volume increase before general oedema is noticable?

A

30%

179
Q

What is ischaemia?

A

Restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism

180
Q

Why can you get heart failure and hypertension at the same time?

A

Get heart failure when ABP is lower than the set point and can’t be raised, body responds to this as it does to haemorrhage (venoconstriction, arteriolar vasoconstriction, and fluid retention) which raises TPR and MSFP

181
Q

Why can TPR influence CO in a failing heart?

A

Maintianing CO with increased TPR needs increased cardiac work

182
Q

What do the symptoms of heart failure result from?

A

Inability to increase CO, increased atrial pressure

183
Q

WHich drugs can inhibit response to low blood pressure?

A

ACE inhibitors, diuretics, beta adrenergic blockers, by lowering MSFP and TPR

184
Q

What does rise in interstitial K+ do during exercise hyperaemia?

A

Hyperpolarises arteriolar smooth muscle which closes VG Ca2+ channels and therefore relaxes the muscle - should cause depolarisation however may do opposite because of enhanced NaKATPase and enhanced inward rectifying channels

185
Q

What blocks inwardly rectifying K+ channels?

A

Barium

186
Q

How does muscle pump cause functional hyperaemia?

A

Contraction accelerate VR which enhances CO but may also reduce venous pressures to enhance pressure gradient through capillaries

187
Q

In cats, what do sympathetic cholinergic nerves do to blood flow at the start of exercise?

A

Increase it

188
Q

What do increased oxygen offloading cause in RBCs?

A

ATP and NO release

189
Q

What do ectonucleotideases do?

A

Produce vasodilatory adenosine by ATP

190
Q

WHat enhances ectonucleotidease activity?

A

Low O2

191
Q

How is some ATP released by active muscle?

A

Partly by GFTR channels in response to reduced intracellular pH linking pH changes to vasodilation

192
Q

How does adenosine cause vasodilation?

A

Acts on A2A receptors to increase cAMP levels in smooth muscle which activates PKA which in turn opens K ATP channels, hyperpolarises cell

193
Q

Why is venoconstriction and increased sympathetic stimulation needed is exercise?

A

Because exercise causes TPR drop which needs CO increase to maintain ABP

194
Q

What happens during blood loss?

A

Lowered MSFP, low VR and CO, lowered blood pressure, baroreceptors detect changes, reduce inhibition of medullary vasomotor areas, symp nerves increase arteriolar and venous tone and HR, vagal tone to heart decreases, catecholamines, ATII and ADH released

195
Q

What happens if blood is still being oxygenated during hypoxia?

A

Ideal response is to increase CO to compensate

196
Q

What is reflex response to reduced amount of O2 as in diving?

A

Detected by carotid and aortic bodies, chemorecptors and then integrated in the medulla, causes slowed heart rate and systemic vasoconstriction mediated by vagal reflex and sympathetic nervous system - DIVE REFLEX

197
Q

What does the dive reflex cause?

A

Keeps cardiac work to a minimum and the sympathetic drive overwhelms the metabolic vasodilation to divert available blood to tissues with little sympathetic vasoconstrictor innervation (brain and heart)

198
Q

What is response to reduced PO2 from altitude?

A

Secondary chemoreceptor response - reduced PO2 causes increased rate and depth of breathing but then pulmonary stretch receptors send afferent impulses via vagus nerve to medulla and stimulate vasomotor centre, causes venoconstriction, inhibits cardio-inhibitory centre and causes pattern of vasodilation/constriction favouring vital tissues causing net CO rise

HOM (7 decks)

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