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Physiology > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

function of the heart

A

to pump oxygen and glucose around the body

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2
Q

properties of an effective heart

A
  • Regular contractions at an appropriate rate for metabolism
  • Guaranteed time for ventricular filling after atrial and ventricular contractions
  • Contraction duration long enough for physical movement of fluid
  • Contractile strength sufficient to generate appropriate pressures
  • Ventricular pressure directed towards exit valves
  • Co-ordination of left and right, and atrial and ventricular contractions
  • Matched volumes of emptying anf filling
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3
Q

where is the heart located

A
  • The heart is located centrally in the thoracic cavity above the diaphragm
  • Contained within mediastinum
  • 2/3 offset to the left of the midline of the sternum
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4
Q

1

A

superior vena cava

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5
Q

2

r

A

right pulmonary artery

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6
Q

3

A

right pulmonary veins

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7
Q

4

A

pulmonary semilunar valve

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8
Q

5

A

right atrium

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9
Q

6

A

tricuspid valve

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10
Q

7

A

right ventricle

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11
Q

8

A

inferior vena cava

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12
Q

9

A

aorta

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13
Q

10

A

left pulmonary artery

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14
Q

11

A

pulmonary trunk

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15
Q

12

A

left pulmonary veins

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16
Q

13

A

left atrium

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17
Q

14

A

aortic semilunar valve

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18
Q

15

A

bicuspid valve

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19
Q

16

A

chorda tendinae

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20
Q

17

A

interventricular septum

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21
Q

18

A

papillary muscle

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22
Q

19

A

left ventricle

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23
Q

20

A

apex of heart

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24
Q

21

A

descending aorta

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25
Q

where does the superior vena cava come from

A

upper body

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26
Q

what kind of blood is in superior vena cava

A

deoxygenated

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27
Q

where does the right pulmonary artery go to

A

right lung

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28
Q

what kind of blood is in the right pulmonary artery

A

deoxygenated

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29
Q

where do the right pulmonary veins come from

A

right lung

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30
Q

what kind of blood is in the right pulmonary veins

A

oxygenated

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31
Q

where does the inferior vena cava come from

A

lower body

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32
Q

what kind of blood is in the inferior vena cava

A

deoxygenated

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33
Q

where does the aorta go

A

systemic organs

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34
Q

what kind of blood is in the aorta

A

oxygenated

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35
Q

where does the left pulmonary artery go

A

to the left lung

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36
Q

what kind of blood is in the left pulmonary artery

A

deoxygenated

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37
Q

where do the left pulmonary veins come from

A

left lung

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38
Q

what kind of blood is in the left pulmonary veins

A

oxygenated

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39
Q

wheredoes the descending aorta go

A

lower body

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40
Q

what kind of blood is in the descending aorta

A

oxygenated

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41
Q

what seperates the atria from the ventricles

A

septum

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42
Q

septum function

A

prevents blood mixing across the hear

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43
Q

approximately how much does the heart weigh

A

250-350 grams

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44
Q

why is ventricular muscel thicker than atrial muscle

A

ventricles pump blood further than the atria, so they work harder

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45
Q

why is the left ventricular muscle thicker than the right

A

enables left ventricle to develop greater pressure as it pumps blood to all the organs not just the lungs like the right

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46
Q

what is the pericardium

A

tough double-layered membranous sac which attaches heart to surrounding tissues

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47
Q

two layers of pericardium

A
  • 1 visceral layer - attached to heart surface
  • 1 parietal layer - outer pericardial layer
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48
Q

what is pericardial fluid and what is its function

A

Lubricating fluid between layers reduces friction during movement of the heart’s surface with contraction

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49
Q

what is pericarditis

A

Inflammation of the pericardium which causes pain due to friction as the heart beats

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50
Q

when do pericardiac seizures occur

A
  • when there is too much fluid in the pericardium
    • Causes: covid, cancer, circulation issues, TB
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51
Q

1

A

myocardium

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52
Q

2

A

endocardium

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53
Q

3

A

parietal pericardium

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54
Q

4

A

visceral pericardium

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55
Q

5

A

pericardial cavity

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56
Q

three layers of the heart’s wall

A
  • Epicardium: - outer layer of connective tissue
  • Myocardium - middle layer of cardiac muscle
  • Endothelium - inner layer of epithelial cells
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57
Q

describe cardiac muscle

A
  • Striated appearance
  • Ordered sarcomere arrangement
  • Irregular shaped cells
  • Single centralised nuclei
  • Intercalated disks:
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58
Q

intercalated discs

A

gap junctionsthat link adjacent cardiac muscles so that electrical impulses can travel between cells and causes to contract almost simultaneously

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59
Q

why does the myocardium not require external neural input

A

myocardial cells can self-generate eclectrical activity

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60
Q

name the two pacemaker areas

A
  • Sinoatrial node (SA node)
  • Atrioventricular node (AV node)
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61
Q

what is activity of the myocardium controlled by

A

the autonomic nervous system

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62
Q

what is hypertrophy of the heart

A

changes to the heart’s structure

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63
Q

two physiological causes of heart hypertrophy and their outcomes

A

pregnancy & exercise
- eccentric muscular remodelling
- enhanced function
- improved metabolism

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64
Q

three pathological causes of hypertrophy

A
  • hypertension
  • infarction
  • diabetes
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65
Q

effects of hypertention

heart hypertrophy

A
  • concentric remodelling
  • fibrotic lesions
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66
Q

effects of infarction

heart hypertrophy

A
  • eccentric dilation
  • fibrotic lesions
  • impaired EF
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67
Q

effects of diabetes

heart hypertrophy

A
  • fatty and fibrotic lesions
  • increased ventricular mass
  • diastolic dysfunction
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68
Q

fibrous skeleton

A

layer of fibrous connective tissue separating the atrial myocardium from the ventricular myocardium

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69
Q

how are valves adhered to the myocardium

A

by papillary muscles and chorda tendineae

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70
Q

valves function

A

to prevent blood from flowing backwards

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71
Q

when do the AV valves open

A

when atrial pressure is higher than ventricular pressure

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72
Q

when do AV valves close

A

when ventricular pressure is higher than atrial pressure

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73
Q

another name for the bicuspid valve

A

mitral valve

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74
Q

what is valve prolapse

A
  • Occurs when ventricular pressure is so great one or more valve cusps is pushed into the atria
  • The edges of the cusps can no longer meet properly when the valve closes, and the valve cannot seal completely
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75
Q

where is the aortic valve found

A

between the left ventricle and the aorta

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76
Q

where is the pulmonary valve located

A

between the right ventricle and the pulmonary trunk

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77
Q

when do the semilunar valves open

A

hen ventricular pressure is greater than arterial pressure (when the ventricles contract)

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78
Q

when do the semilunar valves close

A

When the ventricles relax and ventricular pressure becomes lower than arterial pressure

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79
Q

1

A

right AV valve (tricuspid)

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80
Q

2

A

aortic valve

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81
Q

3

A

left AV valve (bicuspid)

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82
Q

4

A

pulmonary semilunary valve

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83
Q

what word describes the contractile activity of the heart

A

myogenic

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84
Q

what does myogenic mean

A

contractions are triggered by signals originating from within the muscle, not the CNS

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85
Q

Autorhythmicity

A

the ability of the heart to generate signals that trigger its contractions on a periodic basis ie to generate its own rhythm

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86
Q

two types of autorhythmic cells

A
  • pacemaker cells
  • conduction fibres
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87
Q

pacemaker cells function

A

initiate action potentials and establish the heart rhythm

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88
Q

conduction fibres function

A

transmit action potentials through the heart

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89
Q

what are contractile cells

A

cells that generate the contractile force

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90
Q

what is the SA node

A

Cardiac pacemaker

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91
Q

where is the SA node located

A

within right atrial wall at junction with superior vena cava

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92
Q

intrinsic rate of SA node

A

80-100 A.P. per min

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93
Q

conduction speed of SA node

A

0.05m/sec

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94
Q

where is the AV node located

A

above cardiac septum at the junction of atria and ventricles

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95
Q

intrinsic rate of AV node

A

40-60 A.P. per min

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96
Q

conduction speed of AV node

A

0.05m/sec

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97
Q

where is the bundle of his located

A

left and right Branches run down ventricular septum to apex of the heart

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98
Q

instrinsic rate of bundle of his

A

20-40 A.P. per min

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99
Q

conduction speed od bundle of his

A

1m/sec

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100
Q

where are purkinje fibres located

A

throughout ventricular myocardium from apex to base

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101
Q

intrinsic rate of purkinje fibres

A

15-40 A.P. per min

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102
Q

conduction speed of purkinje fibres

A

4m/sec

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103
Q

electrical pathway of heart (simple)

A

SA node → atria and AV node → bundle of His → purkinje fibres → ventricles

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104
Q

1

A

interatrial pathway

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105
Q

2

A

SA node

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106
Q

3

A

right atrium

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107
Q

4

A

internodal pathway

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108
Q

5

A

right ventricle

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109
Q

6

A

right branch of bundle of his

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110
Q

7

A

AV node

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111
Q

8

A

left atrium

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112
Q

9

A

left branch of bundle of his

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113
Q

10

A

left ventricle

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114
Q

11

A

purkinje fibres

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115
Q

why is the SA node the pacemaker of the heart

A

Pacemaker cells in the SA node have a faster inherent rate of spontaneous depolarization and the SA node and AV node are connected by conduction fibers the SA node drives the depolarization of the cells in the AV node and throughout the heart

116
Q

how does excitation spread through the heart

A
  • action potential initiated in pacemaker cells → wave of excitation moves through the atria → atria depolarise → atria contract → wave of excitation moves through ventricles → ventricles depolarise → ventricles contract
  • Rapid transmission of action potentials is possible because all cardiac muscle cells are connected by gap junctions, which permit electrical current to pass in the form of ions from one cell to another.
117
Q

electrical activity during heartbeat (detailed)

A
  1. Action potential initiated in the SA node and travels to the AV node by internodal pathways, and to atrial muscle by interatrial pathways
  2. The AV node transmits action potentials slower than other cells of the conduction system (called the AV nodal delay) to stop the atria and ventricles contracting simultaneously
  3. From the AV node, the impulse travels through the bundle of His. The AV node and bundle of His are the only electrical connection between the atria and the ventricles.
  4. The signal splits into left and right bundle branches; which conduct impulses to the left and right ventricles
  5. From the bundle branches, impulses travel through Purkinje fibers which spread through the ventricular myocardium from the apex upward toward the valves. From these fibers, impulses travel through the rest of the myocardial cells
118
Q

cardiac action potential explanation

A
  • A cardiac contractile cell fires an action potential when it is depolarized to threshold by a stimulus
  • Normally, this stimulus is a circulating electrical current originating in neighboring cells
  • This current enters the cell through gap junctions that connect it with its neighbors.
  • The current then exits the cell by passing through the plasma membrane, and in doing so it triggers depolarization.
119
Q

pacemaker (SA node) action potential

A

Slow depolarisation after action potential → causes potassium channels to open → potassium leaves the cell → cell becomes hyperpolarised → funny channels open → sodium enters cell → cell depolarised → funny channels close → T-type calcium channel opens temporarily → causes more depolarisation to fire the action potential → L-type calcium channel opens → lots of calcium enters cell → L-type calcium channels close → postassium channels open → reset membrane potential

120
Q

ventricular action potential

A

resting membrane potential → action potential arrives from Bundle of His → initiates ventricular action potential → increase in Ca2+ entry to cell → depolarisation occurs → fast sodium channels open → Na+ ions enter and cause rapid depolarisation → L-type Ca2+ channels open → Ca2+ enters cell → contraction is initiated → Ca2+ and Na+ channels close → K+ channels open → K+ hyperpolarises cell → membrane potential returns to resting level

121
Q

what occurs during P wave of ECG

A

atrial depolarisation

122
Q

how long does P wave of ECG last

A

80-100ms

123
Q

what occurs during QRS complex of ECG

A

ventricular depolarisation and atrial repolarisation

124
Q

how long does QRS complex of ECG last

A

80-100ms

125
Q

what occurs during ST segment of ECG

A

time during which ventricles are contracting and emptying

126
Q

how long does ST segment of ECG last

A

70-80ms

127
Q

what occurs during T wave of ECG

A

ventricular repolarisation

128
Q

how long does T wave ECG last

A

200ms

129
Q

what occurs during the TP interval of an ECG

A

ventricles are relaxing and filling

130
Q

functions of an ECG

A
  • Assessment of orientation of the heart
  • Localisation of areas that do not conduct electrical activity normally
  • Assessment of myocardial hypertrophy or atrophy
  • Accurate measurement of heart rate
131
Q

systole

A

period of cardiac contraction

132
Q

diastole

A

period of cardiac relaxation

133
Q

5 mechanical phases of the cardiac cycle

A
  1. late diastole
  2. atrial systole
  3. isovolumic ventricular contraction
  4. ventricular ejection
  5. isovolumic ventricular relaxation
134
Q

what occurs during the late diastole phase of the cardiac cycle

A

both sets of chambers are relaxed and ventricles fill passively

135
Q

what occurs during the atrial systole phase of the cardiac cycle

A

atrial contraction forces a small amount of additional blood into the ventricles

136
Q

what occurs during the isovolumic ventricular contraction phase of the cardiac cycle

A

first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves

137
Q

what occurs during the ventricular ejection phase of the cardiac cycle

A

as ventricular pressure rises and exceeds arterial pressure, the semilunar valves open and blood is ejected

138
Q

what occurs during the isovolumic ventricular relaxation phase of the cardiac cycle

A

as ventricles relax, pressure in ventricles falls, blood flows back onto the cusps of the semilunar valves, closing them

139
Q

what does one pressure volume loop represent

A

one cardiac cycle

140
Q

when does diastole begin

PV loop

A

at the end of isovolumic relaxation

141
Q

what happens to LV volume during diastole

PV loop

A

it increases

142
Q

what happens to LV volume at end-diastole

A

it is maximal

143
Q

what happens when end-diastole is reached

PV loop

A

isovolumic contraction begins

144
Q

what happens at the peak of isovolumic contraction and what is it called

A

LV pressure exceeds aortic pressure and blood begins to eject from the LV into the aorta - this is the systolic ejection phase

145
Q

what does ESVP stand for

pressure volume loop

A

end-systolic pressure-volume point

146
Q

what happens during systolic ejection phase and what is it called

A

LV volume decreases until aortic pressure exceeds LV pressure and the aortic valve closes, which the ESPV

147
Q

what is stroke volume represented as

pressure volume loop

A

by the width of the PV loop as the volume difference between end-systolic and end-diastolic volumes

148
Q

what does the area within the loop represent

pressure volume loop

A

stroke work

149
Q

what is load-independent LV contractility also known as

A

Emax

150
Q

what is load-independent LV contractility or Emax

A

the maximal slope of the ESPV point under various loading conditions, known as the ESPV relationship

151
Q

what does ESPVR stand for

A

ESPV relationship

152
Q

what is effective arterial elastance (Ea)

A

a component of LV afterload and is defined as the ratio of end-systolic pressure and stroke volume

153
Q

what is the ratio of Ea:Emax at under steady conditions (at optimal LV pump efficiency)

pressure volume loop

A

it is approaching 1

154
Q

what does the loop of a cardiac cycle in acute myocardial infarction (heart attack) look like

A
  • LV contractility (Emax) is reduced
  • LV pressure, SV, and LV stroke work may be unchanged or reduced
  • LVEDP is increased
155
Q

what does a loop representing a cardiac cycle in cadiogenic shock (acute heart failure) look like

pressure volume loop

A
  • Emax is severely reduced
  • LVEDV and LVEDP are increased
  • SV is reduced
156
Q

cardiac output

A

volume of blood ejected by each ventricle each minute

157
Q

do systemic and pulmonary systems recieve similar amounts of blood from the heart

A

yes

158
Q

venous return

A

volume of blood returning to atrium each minute, it must be equivalent to cardiac output

159
Q

three factos that influence cardiac outout

A
  • metabolism
  • age
  • body size (body surface area BSA)
160
Q

explain how BSA influences cardaiac input

A
  • Cardiac output increases approximately in proportion to BSA
  • Gives rise to the Cardiac Index (cardiac output per square metre of BSA)
161
Q

two components which control cardiac output

A
  • heart rate
  • stroke volume
162
Q

what is the autonomic nervous system

A
  • Involuntary branch of PNS
  • Sympathetic and parasaympathetic branches (often have opposing effects)
163
Q

central output of the autonomic nervous system

A
  • Parasympathetic nervous system (vagus) via nucleus ambiguous
  • Sympathetic nervous system via rostral ventrolateral medulla
  • Sympathetic chain
164
Q

what does EDV stand for

A

end diastolic volume

165
Q

what is end diastolic volume (EDV)

A

volume of blood in ventricle at end of diastole

166
Q

what does ESV stand for

A

end systolic volume

167
Q

what is end systolic volume (ESV)

A

volume of blood in ventricle at end of systole

168
Q

what is ejection fraction

stroke volume

A

% EDV ejected with each stroke (ranges 50-75%) A good index of ventricular function

169
Q

what is the approximate SV at rest

A

70ml (EDV = 40ml; ESV = 70ml)

170
Q

three factors controlling stroke volume

A
  • preload
  • contractility
  • afterload
171
Q

what is starling’s law

A

The more the heart chambers fill, the stronger the ventricular contraction and therefore the greater the stroke volume

  • Frank-Starling Law is the relationship between EDV, contraction strength, and SV
172
Q

what is the frank starling mechanism

A
  • The Frank-Starling Mechanism is a Length Tension Relationship due to the varying degree of stretching of the myocardium by the EDV
  • As EDV increases the myocardium is increasingly
    stretched and contracts more forcefully
  • Therefore increased preload (EDV), increases contractility,
    which then increases stroke volume
173
Q

is preload intrinsic or extrinsic

A

intrinsic mechanism

174
Q

explain preload

A
  • Preload is the wall stress S (force applied to unit cross-sectional area) in resting myocardium
  • The preload (diastolic wall stress) depends on the end diastolic pressure P, chamber radius r and wall thickness (w)
    • Laplace’s Law: S=Pr/2w
175
Q

what is laplace’s law

A
  • States that for a hollow sphere, the internal pressure (P) is proportional to the wall tension (T) and inversely proportional to the internal radius (r)
  • Tension is a force euqal to wall stress (S) times wall thickness (W)
  • Increasing the radius reduces the curvature, and therefore the inward component of the wall stress so pressure falls
176
Q

how to find internal pressure with wall tension

laplace’s law

A
177
Q

how to find internal pressure with wall stress and wall thickness

A
178
Q

what is contractility

A

the force of contraction achieved from a given initial fibre length

179
Q

is contractility an intrinsic or extrinsic mechanism

A

has both intrinsic and extrinsic influences

180
Q

how can contractility force be measured

A

either by increased contractility and/or by increasing the resting fibre length through end-diastolic stretch (Frank-Starling Mechanism)

181
Q

what are psitive inotropic agents

A

factors that increase
contractility

182
Q

name some positive inotropic agents

A

sympathetic neurotransmitters noradrenaline, circulating adrenaline, Beta agonists, digoxin and reduced beat interval

183
Q

what are negative inotropic agents

A

factors which reduce contractility

184
Q

name some negative inotropic agents

A

ischemia, acidosis, heart failure, anaesthetics, parasympathetic fibre activity, Beta anatagonists and calcium channel blockers

185
Q

what is afterload

A

he force per unit cross-sectional area (stress) that opposes the shortening of an isotonically contracting muscle.

186
Q

is afterload an intrinsic or extrinsic mechanism

A

extrinsic

187
Q

what does afterload depend on

A

arterial pressure, chamber radius and wall thickness

188
Q

percentage of people under 65 with heart failure

A

1%

189
Q

percentage of people between 25 and 84 who have heart failure

A

7%

190
Q

percentage of people over 85 with heart failure

A

15%

191
Q

what happens to stroke volume in systolic heart failure

A

a smaller than normal SV is ejected (the heart’s contractility is weakened)

192
Q

what can help in early stages of systolic heart failure

A

sympathetic stimulation helps to compensate (augmented by expanded blood
volume, controlled by kidneys)

193
Q

is the circulatory system open or closed

A

closed

194
Q

what is pressure

circulatory system

A

the force exerted by blood against vessel walls

195
Q

how does flow occur

circulatory system

A

Flow occurs from high pressure to low pressure

196
Q

what does the heart do

flow

A

creates a pressure gradient for the bulk flow of blood

197
Q

flow equation

A
198
Q

how is blood flow calculated

A

as flow per unit time
Flow = Volume/Time (volume flow rate)

199
Q

what is flow dictated by

A
  • pressure gradients in the vasculature
  • resistance in the vasculature
200
Q

what is the pressure gradient across the pulmonary circuit

A

he pressure in pulmonary arteries take away the pressure in pulmonary veins
- Pulmonary arterial pressure is 15 mm Hg
- Pulmonary venous pressure is 0 mm Hg
- Pressure gradient = 15 - 0 = 15 mm Hg

201
Q

what is the pressure gradient across the systematic system

A

the pressure in the aorta minus teh pressure in the vena cave just before it empties into the right atrium

202
Q

what is the pressure in the aorta

A

he mean arterieal pressure (MAP) = 85mm Hg

203
Q

what is the pressure in the vena cava

A

the central venous pressure = 0mm Hg

204
Q

pressure gradient equation

systemic circuit

A

Pressure gradient = MAP - CVP = 85 - 0 = 0 mm Hg

205
Q

pulse pressure equation

A

Pulse pressure = systolic - diastolic = 110 - 70 = 40

206
Q

MAP equation

A
  • MAP = diastolic + 1/3 pulse = 70 + (40/3) = 70 = 13.3 = 83.3 mm Hg
  • MAP = 2/3 diastolic + 1/3 systolic
207
Q

poiseuille’s law

A
208
Q

factors affecting resistance to flow

A
  • Length of vessel
  • Viscosity of fluid
  • Radius of the vessel
209
Q

which of the factors affecting resistance to flow is most important

A

Radius of the vessel

210
Q

example of how vessel radius is critical in pathological conditions

A

atherosclerosis - the deposition of fats into the arterial wall

211
Q

how does vasoconstriction affect arteriole radius

A

Decrease radius by contracting smooth muscle → increase resistance → decrease blood flow

212
Q

how does vasodilation affect arteriole radius

A

Increase radius by relaxing smooth muscle → decrease resistance → increase blood flow

213
Q

what is arteriole radius dependent on

A

the contraction state of smooth muscle in arteriole wall

214
Q

what is the state of smooth muscle contraction in an arteriole wall while at rest

A

arteriolar tone (partially contracted) - this maintains some resistance and pressure becuase if there is no pressure at all upstream haemodynamics are impacted causing a vicious cycle

215
Q

what are extrinsic factors

A

factors which are neuronal and hormonal

216
Q

two examples of extrinsic factors influencing vasodilation and vasoconstriction

A
  • Autonomic nervous system (sympathetic nervous system causes constriction)
  • Hormones - eg. adrenaline causes constriction
217
Q

what are intrinsic factors

A

those which are conrolled locally

218
Q

examples of intrinsic factors influencing vasoconstriction and vasodilation

A
  • metabolism
  • changes in blood flow
  • stretch of arteriolar smooth muscle
  • locally secreted chemical messengers
219
Q

explain how metabolism influences vasoconstriction and vasodilation

A

increases in metabolism decreases O2, and causes vasodilation (active hyperemia)

220
Q

explain how changes in blood flow influence vasoconstriction and vasodilation

A

reduction in blood flow causes vasodilation: (reactive hyperemia)

221
Q

explain how stretch of arteriolar smooth muscle influences vasoconstriction and vasodilation

A

when perfusion pressure is high it causes vasoconstriction: (myogenic response) the purpose of this is to keep blood flow constant (autoregulate)

222
Q

name fur vasodilators

A

nitric oxide, prostacyclin, adenosine, bradykinin

223
Q

name a vasoconstrictor

A

endothelin-1

224
Q

what does TPR stand for

A

total peripheral resistance

225
Q

what is total peripheral resistance or TPR

A

the amount of force exerted on circulating blood by the vasculature of the body

226
Q

two factors which influence TPR

A
  • arteriolar radius
  • blood viscosity
227
Q

name intrinsic factors which influence arteriolar radius

A
  • response to stress - compensates for changes in longitudinal force of floq
  • myogenic responses to stretch - minor role in acve and reactive hyperemia
  • heat and cold
  • histamine release - involved in injuries and allergic responses
  • local metaboli changes in O2 and other metabolites - important in matching blood flow with metabolic needs
228
Q

extrinsic factors influencing arteriolar radius

A
  • vasopressin - hormone important for fluid balance - vasoconstrictor effect
  • angiotensin II - hormone important for fluid balance - vasoconstrictor effect
  • epinephrine and norepinephrine - hormones which reinforce sympathetic nervous system
  • sympathetic activity - exterts generallised vasoconstrictor effect
229
Q

what does blood viscosity depend on

A

number of red blood cells

230
Q

what does CVP stand for

A

central venous pressure

231
Q

what is CVP

A
  • the pressure in the large veins of the thoracic cavity that lead into the heart
  • Pressure gradient between central veins and atria drives blood back into the heart
  • Venous pressure – atrial pressure = 5 - 10 mm Hg
232
Q

what does a decrease in venous pressure cause for venous return

A

A decrease in venous pressure decreases driving force for venous return

233
Q

what effect does a decrease in venous return have on blood flow to an organ

A

Decrease in venous return → decreases end-diastolic volume → decreases stroke volume → decreases cardiac output → decreases blood flow to organ

234
Q

factors affecting CVP and venous return

A
  • skeletal muscle pump
  • respiratory pump
  • Blood volume: decreased blood volume decreases CVP (bleeding, dehydration…)
  • Venomotor tone (sympathetic nerves constrict veins) favors venous return
235
Q

how does inspiration increase blood flow to heart

A

thoracic pressure decreases → abdominal pressure raises → increases blood flow to the heart

236
Q

how does expiration increase blood flow to the heart

A

thoracic pressure increases → abdominal
pressure falls, valves prevent backward flow, so, blood driven towards the heart

237
Q

three determinants of mean arterial pressure

A
  • Heart rate
  • Stroke volume
  • Total peripheral resistance - combined resistance of all blood vessels
238
Q

Effects of Cardiac Output on Mean Arterial Pressure

A

increase of MAP when TPR stays the same

239
Q

Effects of Total Peripheral Resistance on Mean Arterial Pressure

A

increase of MAP when CO remains the same

240
Q

what happens when MAP is less than normal

A
  • Hypotension
  • Inadequate blood flow to tissues
241
Q

what happens when MAP is greater than normal

A
  • Hypertension
  • Stress on heart and walls of blood vessels
242
Q

normal blood pressure

A

less than 120 systolic and less than 80 diastolic

243
Q

elevated blood pressure

A

120-129 systolic and less than 80 diastolic

244
Q

hypertension stage 1

A

130-139 systolic or 80-89 diastolic

245
Q

hypertension stage 2

A

greater than 139 systolic or greater than 90 diastolic

246
Q

when does systolic pressure occur

A

with ventricular contraction

247
Q

when does diastolic pressure occur

A

with ventricular refilling

248
Q

what is pulse pressure at rest

A

40 mm Hg

249
Q

what can high pulse pressures at rest indicate

A

vascular disease

250
Q

how is blood pressure measured (auscultation)

A
  • Recorded at heart level via brachial artery
  • Korotkoff sounds via turbulent flow, upon cuff pressure release
  • Inflate cuff above expected systolic pressure.
  • Slowly deflate cuff: blood flows when blood pressure is greater than cuff pressure
  • Clear tapping audible via stethoscope indicates Systolic Pressure
  • Diastolic pressure indicated at disappearance of muffled sound
251
Q

what does short term refer to in regulation of MAP

A

seconds to minutes

252
Q

what is short term regulation of MAP

A

regulation of cardiac output and total peripheral resistance

253
Q

what structures does short term regulation of MAP involve

A

heart and blood vessels

254
Q

what type of control is short term regulation of MAP

A

Primarily neural control

255
Q

what does long term refer to in regulation of MAP

A

minutes to days

256
Q

what is long term regulation of MAP

A

regulation of blood volume

257
Q

what structures are involved in long-term regulation of MAP

A

kidneys

258
Q

what type of control is used in long term regulation of MAP

A

primarily hormonal control

259
Q

explain the renin-angiotensin-aldosterone system

A
  • Decreased NaCl/decreased ECF volume/decreased arterial blood pressure → increased production of renin by kidney → combines with already circulating angiotensinogen (produced by liver) → forms angiotensin I → combines with angiotensin-converting enzyme produced by lungs → forms angiotenstin II
    • stimulates adrenal cortex to produce aldosterone → travels to kidney → makes kidney increase Na+ reabsorption by kidney tubules (increased Cl- reabsorption follows passively → Na+ (and Cl- conserved) → Na+ (and Cl-) osmotically hold more H2O in ECF → H2O is conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
    • increases vasopressin → increases H2O reabsorption by kidney tubules → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
    • increases thirst → increases fluid intake → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
    • increases arteriolar vasoconstriction → more H2O conserved → corrects decreased NaCl/decreased ECF volume/decreased arterial blood pressure
260
Q

neural control of MAP

A
  • Negative feedback loops
  • The detectors are called baroreceptors
  • The integration centre are the cardiovascular centres in the brainstem
  • The controllers are the autonomic nervous system
  • The effectors are the heart and blood vessels
261
Q

what are baroreceptors

A
  • Baroreceptors are stretch receptors - specialised nerve endings that respond to stretch of vessel wall
  • They have an indirect response to changes in blood pressure
262
Q

what are arterial baroreceptors

A
  • high pressure baroreceptors
  • sinoaortic baroreceptors
263
Q

where are arterial baroreceptors found

A

in the carotid sinus and the aortic arch

264
Q

explain type A baroreceptors

A
  • Myelinated
  • Low pressure (30-90 mmHg)
  • Important at rest
265
Q

explain type A baroreceptors

A
  • Myelinated
  • Low pressure (30-90 mmHg)
  • Important at rest
266
Q

explain type C baroreceptors

A
  • Unmyelinated
  • High pressure (70-140 mmHg)
  • Increasingly active at higher pressures
267
Q

where are cardiac and venous baroreceptors found

A

in walls of large systemic veins and walls of the atria

268
Q

what are cardiac and venous baroreceptors

A

Low pressure baroreceptors and are volume receptors

269
Q

explain the parasympathetic input to the cardiovascular system

A

input to:
- SA node (which decreases heart rate)
- AV node

270
Q

explain sympathetic input to cardiovascular system

A

input to:
- SA node (increase heart rate)
- AV node
- Ventricular myocardium (increase contractions)
- Arterioles (increase resistance)
- Veins (increase venomotor tone)

271
Q

explain the baroreceptor reflex with an example

A
  • A person who had been lying down stands up quickly
  • Gravity causes venous pooling in the legs → causes a decrease in VR → a decrease in CO → a decrease in blood pressure
  • Baroreceptors sense the decrease and the reflex occurs
  • The reflex causes increased sympathetic and decreased parasympathetic activity
  • CO and TPR are increased
  • Blood pressure is increased back to normal.
272
Q

explain the bainbrdge reflex

A
  • Vena cava stretch receptors → neural mediated increase in heart rate
  • Avoids venous congestion
273
Q

explan how artrial stretch receptors are an input to the cardiovascular system

A
  • Myelinated vagal afferents sensitive to blood volume
  • Located at junction of great veins and atria
  • Influence endocrine regulation of blood volume via:
    • Hypothalamic ADH → renal water retention
    • Renin-Angiotensin-aldosterone system (RAS) → renal salt & water retention
    • Atrial Natriuretic Peptide → renal salt & water excretion
274
Q

where in the brain receives input from baroreceptors

A

nuceleus tractus solidaruis in medulla

275
Q

where does the NTS send outputs to

A
  • Parasympathetic NS (vagus)
    • via nucleus ambiguus
    • cardiac control (limits heart rate)
  • Sympathetic NS
    • via rostral ventrolateral medulla
    • cardiac and blood vessel control (increased contractile strength/tone)
  • Hypothalamus & amygdala
    • Allows these areas to override the baroreceptor reflex during stress
    • Allows a stress-associated increase in BP to occur
276
Q

what does parasympathetic stimulation to the heart cause

A

decreased heart rate → decreased cardiac output → decreased blood presssure

277
Q

what does sympathetic simulation to the heart cause

A
  • → contractile strength of heart → increase stroke volume → cardiac input → increase blood pressure
278
Q

what does sympathetic stimulation to the arterioles cause

A

increase vasoconstriction → increase in total peripheral resistance → increase in blood pressure

279
Q

what does sympathetic stimulation to the veins cause

A

increase in vasoconstriction → increase in venous return → increase in stroke volume → increase in cardiac output → increase in blood pressure

280
Q

what does haemorrhage cause

A
  • Baroreceptor reflex
  • Increase in sympathetic activity
  • Decrease in parasympathetic activity
281
Q

how does haemorrhage effect the GI tract

A
  • Increased resistance
  • Decreased blood flow
282
Q

how does haemorrhage effect the brain

A
  • Vasculature not subject of extrinsic control
  • No change in resistance
  • Blood diverted from GI tract to brain
283
Q

three hormones that control MAP

A
  • epinephrine
  • vasopressin
  • angiotensin II
284
Q

how does epinephrine control MAP

A
  • Released by adrenal medulla in response to sympathetic activity
  • Increases mean arterial pressure
  • Acts on heart
    • Increases heart rate
    • Increases stroke volume
  • Acts on smooth muscle of arterioles
    • Increases TPR
  • Acts on smooth muscle of veins
    • Increases venomotor tone
285
Q

how does epinephrine control MAP

A
  • Released by adrenal medulla in response to sympathetic activity
  • Increases mean arterial pressure
  • Acts on heart
    • Increases heart rate
    • Increases stroke volume
  • Acts on smooth muscle of arterioles
    • Increases TPR
  • Acts on smooth muscle of veins
    • Increases venomotor tone
286
Q

how do vasopressin and angiotensin II control MAP

A
  • Vasoconstrictors
  • Increase TPR
  • Increase MAP

Physiology (6 decks)

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