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Semester Three > CVS L01-L14 > Flashcards

CVS L01-L14 Flashcards

1
Q

What is the value for normal pulse pressure? L02

A

40mmHg

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2
Q

Define cardiac output L02

A

Volume of blood pumped per min

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3
Q

What happens if Right CO > Left CO? L02

A

Pulmonary oedema

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4
Q

Define stroke volume L02

A

Volume ejected per contraction

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5
Q

What happens if Left CO > Right CO? L02

A

Peripheral oedema

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6
Q

What arrangement are vascular beds in? L02

A

Parallel

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7
Q

What arrangement are the right and left sides of the heart? L02

A

In series with each other

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8
Q

Define systole L02

A

Phase of ventricular contraction and ejection

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9
Q

What is the equation for cardiac output? L02

A

CO = SV x HR

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10
Q

Define diastole L02

A

Phase of ventricular relaxation and filling

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11
Q

What do you feel when you take someone’s pulse? L02

A

Pulse pressure

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12
Q

What determines blood pressure? L02

A
  1. Resistance to blood flow

2. Blood volume

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13
Q

What are the three different cardiac action potentials? L04

A

Sino-atrial node, atrio-ventricular node, and non-nodal potentials

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14
Q

What is the primary pacemaker of the heart? L04

A

The sino-atrial node

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15
Q

What is the resting membrane potential of SAN cells? L04

A

They do not have a true resting membrane potential

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16
Q

Why do SAN cells not have a true resting membrane potential? L04

A

So they can generate regular, spontaneous action potentials

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17
Q

Do SAN cells contains fast Na+ channels? L04

A

No, there are no fast Na+ channels in either the SAN or AVN

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18
Q

What 3 things happen in phase 4 of an SAN cell action potential? (the pacemaker potential) L04

A
  1. Na+ influx through slow Na+ channels causing depolarisation
  2. Then Ca2+ influx by T-type calcium channels at around -50mv
  3. Then Ca2+ influx by L-type calcium channels at around -40mV
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19
Q

What is the rough value of the membrane potential of SAN cells? L04

A

-60mV

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20
Q

What type of calcium channels predominate depolarisation in phase 0 of an SAN cell action potential? L04

A

L-type; they increase Ca2+ conductance causing further depolarisation. The rate of depolarisation is slower than phase 4 because the number of open T-type calcium channels close.

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21
Q

What channels open in phase 3 (repolarisation) of an SAN cell action potential? L04

A

K+ channels

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22
Q

What happens to the L-type calcium channels in phase 3 of an SAN cell action potential? L04

A

They become inactivated and close, decreasing gCa2+

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23
Q

How are SAN cell action potentials similar to AVN action potentials? L04

A

Neither use fast sodium channels

Both are determined by slow Ca2+ influx and K+ efflux

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24
Q

What is the intrinsic firing rate for the SA node? L04

A

100 bpm

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25
Q

What predominates in determining HR? L04

A

Vagal tone

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26
Q

What receptor do the catecholamines act upon in heart muscle? L04

A

Beta1 receptors

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27
Q

What neurotransmitter and its receptor does the parasympathetic nervous system stimulate in heart muscle? L04

A

Acetylcholine (Ach) on M2 receptors

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28
Q

What effect does sympathetic stimulation have on the heart rate? L04

A

Positive chronotropic effect (increases HR). It does this by increasing the slope of the pacemaker potential.

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29
Q

What effect does parasympathetic stimulation have on the heart rate? L04

A

Negative chronotropic effect (decreases HR). It does this by hyperpolarisation (opens K+ channels) thus decreasing the slope of the pacemaker potential.

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30
Q

What junctions are present in the heart for conducting action potentials between myocytes and what is the name of this mechanism? L04

A

Gap junctions; Excitation-Contraction Coupling (ECC)

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31
Q

What is the speed for SA node action potential conduction? L04

A

0.5m/sec

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32
Q

What is the speed for AV node action potential conduction? L04

A

0.05m/sec

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33
Q

Why is the AVN conduction rate slower than the SAN conduction rate? L04

A

AV delay; to ensure complete atrial depolarisation and contraction (systole)

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34
Q

What is the speed for the Bundles of His action potential conduction? L04

A

2m/sec

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35
Q

What is the speed for Purkinje fibre action potential conduction and what is the reason for this? L04

A

4m/sec; for rapid ventricular depolarisation

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36
Q

Which interval will decrease on an ECG if you increase AVN contraction due to sympathetic stimulation? L04

A

The P-R interval

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37
Q

What is the resting membrane potential of non-nodal cells in the heart? L04

A

-90mV

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38
Q

Why is the resting membrane potential of non-nodal cells very stable and negative? L04

A

So you do not have spontaneous contraction; you do not want it contracting until necessary so it is therefore far away from threshold level

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39
Q

What is the absolute refractory period for a non-nodal cell action potential? L04

A

200ms

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40
Q

What is the relative refractory period for a non-nodal cell action potential? L04

A

50ms

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41
Q

Why is there long refractory periods in cardiac muscle compared to skeletal muscle? L04

A

As you do not want temporal summation in cardiac muscle

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42
Q

Atrial and ventricular myocytes and Purkinje fibres conduct what type of action potential? L04

A

Non-pacemaker action potentials; they are fast response with a true resting membrane potential

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43
Q

What is happening in phase 4 of a non-pacemaker action potential? L04

A

K+ channels are open meaning a negative membrane potential

Both Na+ and L-type calcium channels are closed

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44
Q

What causes the initial depolarisation in phase 0 of a non-pacemaker action potential? L04

A

Na+ channels open causing Na+ influx and K+ channels close

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45
Q

What causes the initial repolarisation in phase 1 of a non-pacemaker action potential? L04

A

Transient K+ channel opening causing K+ efflux

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46
Q

Why is there a plateau in phase 2 of a non-pacemaker action potential? L04

A

Large increase in slow Ca2+ influx through L-type Ca2+ channels means repolarisation is delayed

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47
Q

What happens in phase 3 of a non-pacemaker action potential? L04

A

Inactivation of Ca2+ channels

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48
Q

What are 5 things that can change the rate of SAN firing? L04

A
  1. Changes in autonomic activity
  2. Circulating hormones
  3. Serum ion concentrations e.g. hyperkalaemia causes bradycardia
  4. Cellular hypoxia
  5. Drugs e.g. CCBs cause bradycardia by inhibiting slow Ca2+ channels
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49
Q

When does systole begin and end? L06

A

Begins with contraction of the ventricles and ends when ejection ceases

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50
Q

When does diastole begin? L06

A

Begins when ejection ceases, filling starts after sufficient relaxation

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51
Q

If the pressure in the atrium is less than in the ventricle is the AV valve open or closed? L06

A

Closed

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52
Q

If the pressure in the aorta is more than in the left ventricle is the aortic valve open or closed? L06

A

Closed

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53
Q

Which valves are open in atrial systole? L06

A

AV valves only

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54
Q

What does the P wave on an ECG represent? L05/6

A

Atrial depolarisation

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55
Q

Why does blood not flow back into the vena cava? L06

A

Inertial effects of venous return

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56
Q

When does EDV occur? L06

A

At the end of atrial systole

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57
Q

What is the typical left ventricular EDV? L06

A

120ml; represents ventricular pre-load

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58
Q

What does the QRS complex on an ECG represent? L05/6

A

Ventricular depolarisation

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59
Q

What causes the first heart sound (S1)? L05/6

A

Closure of the atrio-ventricular valves when ventricular P > atrial P

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60
Q

Which valves are open during rapid ejection of the ventricles? L06

A

Semilunar valves only

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61
Q

What does the T-wave represent? L05/6

A

Ventricular repolarisation

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62
Q

Why does outward flow of blood still occur when atrial pressure exceeds ventricular pressure at the end of systole? L06

A

Kinetic/inertial energy of the blood; blood continues to eject due to momentum

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63
Q

What causes the second heart sound (S2)? L05/6

A

The semilunar valves closing

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64
Q

What is the typical left ventricular ESV? L06

A

50ml

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65
Q

What is the equation for stroke volume? L06

A

SV = EDV - ESV

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66
Q

What is a typical value for normal stroke volume? L06

A

120ml - 50ml = 70ml

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67
Q

What is the equation for ejection fraction and what percentage should it be above for healthy heart function? L06

A

Ejection fraction = stroke volume/EDV

It should be above 55%

68
Q

Why is the right side of the heart less muscular? L06

A

It only has to overcome the pressure of the pulmonary arteries, which is a low resistance pressure system

69
Q

Why do the ventricles never fully empty? L06

A

The blood is pushing against TPR, and it allows the SV to increase or decrease

70
Q

What happens to EDV in an

a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07

A

a) Increases
b) No change
c) No change

71
Q

What happens to ESV in an

a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07

A

a) No change
b) Increases
c) Decreases

72
Q

What happens to SV in an

a) increase in pre-load
b) increase in after-load
c) increase in contractility? L07

A

a) Increases
b) Decreases
c) Increases

73
Q

The intrinsic regulation of the energy of cardiac contraction is due to the effects of what, and what is the name of this law? L08

A

Stretch; Starling’s law

74
Q

What are the two factors affecting the muscle-length tension relationship? L08

A

Number of crossbridges formed and sarcomere length

75
Q

When does peak tension of cardiac muscle occur? L08

A

At optimum sarcomere length there is maximum overlap leading to maximum number of cross bridges; so there is peak tension

76
Q

What is pre-load? L08

A

Initial stretching of the cardiac myocytes prior to contraction

77
Q

If you increase pre-load, what effect does this have on SV? L08

A

Increases SV

78
Q

Name some factors that will increase pre-load. L08

A

Increase in CVP
decrease in venous compliance
increase in thoracic blood volume
Decrease in HR
Increase in atrial contractility (from symp. or filling)
Increase in ventricular compliance
Increase in aortic pressure

79
Q

Name some factors that will increase CVP. L08

A 
Moving from standing to lying down (decreased pooling) 
Increase in skeletal muscle pump
Increase in venous constriction
Increase in respiratory muscle pump 
Increased total circulating volume
80
Q

What is the main function of Starling’s law? L08

A

To balance the SV for the two ventricles

81
Q

How does a high HR affect EDV? L08

A

Decreases EDV because passive filling time is reduced (P-P interval shortens)

82
Q

What is the Frank-Sterling mechanism? L08

A

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return

83
Q

What is contractility/inotropy? L08

A

Change in force of contraction at any given EDV; due to altering intracellular Ca2+ level (NOT due to stretch)

84
Q

What determines the level of intracellular Ca2+? L08

A

Sympathetic nerves and circulating agents

85
Q

What effect does increasing levels of intracellular Ca2+ have on contractility? L08

A

Increases it/ Positive inotropic effect

86
Q

What is negative inotropy? L08

A

A decrease in cardiac contractility

87
Q

What can decrease contractility? L08

A

Hypoxia, ischaemia, heart failure

88
Q

How do you increase SV by Starling’s law? L08

A

Increase pre-load

89
Q

How do you increase SV by inotropy? L08

A

Increase intracellular Ca2+ levels

90
Q

If there is an increase in force due to increased filling pressure- is this Starling’s law or increased contractility? L08

A

Starling’s law

91
Q

Why does high afterload cause hypertrophy? L08

A

A larger ventricle is needed to overcome the higher afterload; needed with high ABP

92
Q

What do class I anti-arrhythmics do and what effect do they have? L09

A

V-gated Na+ channel blockers

They slow depolarisation

93
Q

What is an example of a class I anti-arrhythmic? L09

A

Lidocaine

94
Q

What do class II anti-arrhythmics do and what effect do they have? L09

A

Beta-blockers

Takes longer time to reach threshold

95
Q

What is an example of a class II anti-arrhythmic? L09

A

Propanolol

96
Q

What do class III anti-arrhythmics do and what effect do they have? L09

A

K+ channel blockers

They prolong repolarisation

97
Q

What is an example of a class III anti-arrhythmic? L09

A

Amiodarone

98
Q

What do class IV anti-arrhythmics do and what effect do they have? L09

A

Slow Ca2+ channel blockers

Slow action potential

99
Q

What is an example of a class IV anti-arrhythmic? L09

A

Verapamil

100
Q

What class of drug is Digoxin and what is its mechanism? L09

A

Cardiac glycoside

Partial inhibition of Na+/K+ ATPase means slow Na+ accumulation and less Ca2+ efflux

101
Q

What is the mechanism for Adenosine? L09

A

Opens K+ channels and causes hyperpolarisation

102
Q

What is an example of a Phosphodiesterase inhibitor (PDE)? L09

A

Milirinone, Enoximone

103
Q

How do PDEs work? L09

A

Increased cAMP leads to increased Ca2+ entry so an increase in contractility

104
Q

What happens in the aorta during systole? L10

A

It distends to accomodate SV and energy is stored

105
Q

What happens in the aorta during diastole? L10

A

The aortic walls recoil to propel blood forward

106
Q

What are the features of laminar flow? L10

A

Normal pattern, highly efficient, follows Poiseuille’s law, cannot hear

107
Q

What are the features of turbulent flow? L10

A

Where flow velocity is high, inefficient, not Poiseuille’s law, can hear (murmurs and Korotkoff sounds)

108
Q

What determines systolic pressure? L10

A

Stroke volume

109
Q

What factors will increase systolic pressure? L10

A

Increased preload, increased afterload, and increased contractility

110
Q

What determines diastolic pressure? L10

A

Arteriolar resistance and HR

111
Q

What factors will increase diastolic pressure? L10

A

Increased vasoconstriction, atherosclerosis and very high HR

112
Q

What happens to pulse pressure with age? L10

A

It increases as arterial compliance decreases

113
Q

How do endothelial factors affect vasoconstriction/dilation of blood vessels? L10

A

Nitric oxide, EDHF, and prostacyclin cause vasodilation

ET-1 causes vasoconstriction

114
Q

How do local factors affect vasoconstriction/dilation of blood vessels? L10

A

Metabolic: Increased metabolism due to active/functional hyperaemia increases blood flow from dilation

Myogenic: Reflex vasoconstriction in response to higher intravascular pressure e.g. in kidney

115
Q

What is the cerebral autoregulatory range? L10

A

Mean arterial pressure between 60-170mmHg

116
Q

How do central neural mechanisms affect vasoconstriction/dilation of blood vessels? L10

A

SNS activity:
Norad on alpha-1 receptors on blood vessels causes vasoconstriction
Norad on beta-2 receptors on skeletal muscle causes vasodilation (fight/flight)

117
Q

How do hormonal mechanisms affect vasoconstriction/dilation of blood vessels? L10

A

Adren on alpha-1 receptors causes vasoconstriction
Adren on beta-2 receptors causes vasodilation
ADH and AGII cause vasoconstriction

118
Q

What is the thickness of a capillary wall? L11

A

Single endothelial cell; 0.5µm

119
Q

What is the velocity in a capillary? L11

A

1mm/sec

120
Q

What are the three exchange mechanisms in a capillary? L11

A

Diffusion, vesicular transport and bulk flow

121
Q

What is diffusion in a capillary used for? L11

A

Lipid-soluble substances

122
Q

What is the equation for Fick’s Law? L11

A

Rate of diffusion = Permeability coefficient x conc. grad. x area

123
Q

What is vesicular transport in a capillary used for? L11

A

Lipid-insoluble substances e.g. proteins, antibodies

Use other methods e.g. pinocytosis

124
Q

What is bulk flow in a capillary used for? L11

A

Water, electrolytes, small molecules

125
Q

What are the size of the fenestrations in fenestrated capillaries? L11

A

60nm

126
Q

What are the forces that counteract filtration in a capillary? L11

A

Starling forces

127
Q

At what hydrostatic pressure (Pc) does blood enter the arteriolar end of a capillary? L11

A

35mmHg

128
Q

What is capillary osmotic pressure (πc)? L11

A

25mmHg

129
Q

At what hydrostatic pressure (Pc) does blood leave the venous end of a capillary? L11

A

15mmHg

130
Q

If Pc > πc in a capillary, what happens? L11

A

Filtration out the capillary

131
Q

If Pc < πc in a capillary, what happens? L11

A

Reabsorption into the capillary

132
Q

What percentage of blood does the venous system hold? L11

A

60-80%

133
Q

What is the equation for compliance? L11

A

change in volume/ change in pressure

134
Q

What effect does a fall in venous capacitance have on venous return? L11

A

Increased venous return

135
Q

Which receptors are responsible for vasoconstriction on blood vessels? L12

A

Alpha-1 and alpha-2 adrenoceptors

136
Q

Which receptors are responsible for renin release? L12

A

Beta-1 adrenoceptors

137
Q

Antagonist for alpha receptors? L12

A

Phentolamine

Doxazosin

138
Q

What effects on the heart will beta-receptor activation have? L12

A

Positive chronotropic effect (increased HR)
Positive inotropic effect (increased contractility rate)
Increased automaticity

139
Q

How does a beta-agonist e.g. adrenaline affect the heart? L12

A

Increased Ca2+ channel opening

Increased K+ conductance for faster repolarisation

140
Q

What is adrenaline used to treat? L12

A

Asystole
Ventricular fibrillation
Anaphylaxis

141
Q

What is dobutamine (beta-1 agonist) used to treat? L12

A

Cardiogenic shock

142
Q

What is phenylephrine (alpha-1 agonist) used to treat? L12

A

Nasal congestion

143
Q

What is doxazosin (alpha-1 antagonist) used to treat? L12

A

Hypertension

Raynaud’s syndrome

144
Q

What are beta-blockers used for? L12

A

Angina
Heart failure
Arrhythmias
Hypertension

145
Q

How do beta-blockers lower blood pressure? L12

A

Decrease CO
Block renin release (beta-1 receptors in kidney)
Inhibit catecholamine effects

146
Q

What is the effect on the cardiovascular system of parasympathetic stimulation? L12

A

Negative chronotropic effect on SAN
Slow AVN conduction
(Limited vasodilation due to limited innervation)

147
Q

Which receptors does atropine block? L12

A

Cardiac M2 receptors

148
Q

Blood flow to coronary muscle is _____ L13

A

Intermittent

149
Q

When is 85% of the blood flow to the left side of heart? L13

A

During diastole

150
Q

What happens during systole in the left side of the heart’s coronary vessels? L13

A

They are compressed by the high pressure in the ventricle = extra vascular compression

151
Q

What determines the left side coronary flow during diastole? L13

A

Aortic pressure

152
Q

When is right side coronary flow highest? L13

A

During systole

153
Q

Name some examples of local factors that increase blood flow. L13

A

Adenosine
Prostaglandins
Nitric Oxide
Potassium

154
Q

Name the dense capillary network of the brain. L13

A

Circle of Willis

155
Q

Functional adaptations of cerebral flow? L13

A

High basal flow (15% of CO)

Peripheral vasoconstriction to protect cerebral circulation

Autoregulation between 60-170mmHg

Very responsive to CO2 levels

Neuronal activity-evoked functional hyperaemia e.g. local factors to increase blood flow

156
Q

What is CPP? L13

A

Cerebral Perfusion Pressure

157
Q

What exists in cutaneous circulation to allow blood to go quickly through ateriolar network? L13

A

AV anastomoses

158
Q

What is bradykinin? L13

A

Local vasodilator

159
Q

Describe Raynaud’s syndrome. L13

A

“Overreactive” skin vessels
Cold or emotional stimuli causes extreme vasoconstriction
Numbness, pain and burning sensation in hands and feet

160
Q

What do indirect vasodilators do? L14

A

Block vasoconstriction

161
Q

What do direct vasodilators do? L14

A

Affect calcium channels

162
Q

Drugs used in angina pectoris? L14

A 
Beta-blockers
Ivabradine 
GTN 
Isosorbide mononitrate 
Ca2+ channel blockers e.g. verapamil
163
Q

How does GTN work? L14

A

Increased cGMP levels to cause relaxtion in systemic vessles

164
Q

Side effects of GTN? L14

A

Hypotension; syncope, headaches

165
Q

5 uses of vasodilators? L14

A 
Hypertension
Angina pectoris
Peripheral vascular disease e.g. Raynaud's
Impotence
Hair loss

Semester Three (12 decks)

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