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Physiology Flashcards

1
Q

Function of the CVS

A

BULK FLOW SYSTEM:

  • O2 and CO2
  • Nutrients
  • Metabolites,
  • Hormones
  • Heat
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2
Q

Equation for “flow”

A

Flow = change in pressure/ resistance

change in pressure = mean arterial pressure - central venous pressure

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3
Q

Resistance in blood vessels

A

Resistance = Radius ^4

controlled by arterioles which act like taps and control flow to each vascular bed

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4
Q

Capacitance

A

The ability of a body to store blood

veins and venules = capitance vessels
store lots of blood

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5
Q

“in series” arrangement + examples

A

Blood flows through both, one after the other - output must be equal or blood backs up.

E.G.
right heart –> lungs –> left heart
hypothalamus –> anterior pituitary
gut –> liver

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6
Q

Reasons for vascular beds in parallel

A

All tissues get oxygenated blood,

Allows regional redirection of blood

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7
Q

Elastic arteries + function

A

Pulmonary arteries and aorta.

Maintains a relatively constant (and high) pressure

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8
Q

Function of muscular arteries

A

Low resistance

Delivers blood from elastic arteries to resistance vessels

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9
Q

Resistance vessels + function

A

Arterioles.
Control resistance and therefore flow,
Allow regional redirection of blood

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10
Q

Capacitance vessels + function

A

Veins and venules.
Low resistance,
Reservoir of blood (to be distributed to rest of circulation when needed - fracitonal distribution of blood)

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11
Q

The functional syncytium

A

Cardiac muscle cells act as one big cell.
They are joined…
Electrically by gap junctions,
Physically be desmosomes.

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12
Q

Intercalated discs

A

alternating desmosomes and gap junctions

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13
Q

Permeability of ion channels in different phases of non-pacemaker action potentials

A

RESTING MEMBRANE POTENTIAL:
-High PK+

INITIAL DEPOLARISATION:
-Increase PNa+

PLATEAU:

  • Increase PCa2+ (L-type)
  • Decrease PK+

REPOLARISATION:

  • Decrease PCa2+
  • Increase PK+
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14
Q

P-wave corresponds to…

A

Atrial depolarisation

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15
Q

QRS Complex corresponds to…

A

Ventricular depolarisation

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16
Q

T wave corresponds to…

A

Ventricular repolarisation

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17
Q

The PR interval corresponds to…

A

Time from atrial depolarisation to ventricular depolarisation

(mainly due to transmission through the AV node)

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18
Q

Normal range of the PR interval

A

0.12 - 0.2 seconds

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19
Q

Duration of the QRS complex corresponds to…

A

Time for the whole ventricle to depolarise

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20
Q

Normal time for duration of the QRS complex

A

0.08 seconds

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21
Q

The QT interval corresponds to…

A

Time spent while the ventricles are depolarised

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22
Q

Normal time of QT interval

A

~0.42 seconds at 60bpm

varies with heart rate

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23
Q

Measuring heart rate from an ECG

A

*Measured from the rhythm strip

Count the R waves in 30 large squares (6 seconds) and multiply by 10

OR count number of small squares between each QRS complex and divide into 300.
e.g 300/5 boxes = 60bpm

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24
Q

STEMI

A

ST Elevated Myocardial Infarction.

Elevation of the ST section on an ECG indicates a more severe heart attack (severe muscle damage)

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25
Q

Non-STEMI

A

Non-ST Elevated Myocardial Infarction

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26
Q

Normal Sinus Rhythm

A

Normal rhythm of the heart set by the sinoatrial node

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27
Q

Sinus Tachycardia

A

Fast heart rate because of rapid firing of the sinoatrial node.
>100 bpm

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28
Q

Sinus Bradycardia

A

Slow heart rate because of slow firing of the sinoatrial node.
<60 bpm

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29
Q

Exchange vessels

A

Capillaries

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30
Q

Mean arterial pressure (MAP)

A

The average blood pressure in the arterial circulation over the whole cardiac cycle

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31
Q

Central Venous Pressure (CVP)

A

The blood pressure in the right atrium, measured in the superior vena cava

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32
Q

Cardiac Output

A

The volume of blood pumped through the circulatory system in a minute (L/min)

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33
Q

Sinoatrial node

A

A mass of cardiac muscle cells that act as the pacemakers

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34
Q

Function of the atrioventricular node

A

Receives APs from the sinoatrial node and conducts it to the ventricles.
Delays AP until blood moves from atria to the bundle of His.

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35
Q

Function of the Bundle of His

A

Conducts APs from the AV node to the ventricles

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36
Q

Purkinje fibres

A

Receive APs from the branches of the bundle of His and distribute it to the myocardium of the ventricles, causing them to contract.

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37
Q

1st heart sound caused by…

A

Mitral and tricuspid valves closing

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38
Q

2nd heart sound caused by…

A

Aortic and pulmonary valves closing

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39
Q

Valves during Systole

A

Aortic and pulmonary open

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40
Q

Valves during diastole

A

Mitral and tricuspid open

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41
Q

Stroke volume =

A

End diastolic volume - end systolic volume

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42
Q

Ejection fraction =

A

Stroke volume ÷ end diastolic volume

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43
Q

Estimated mean arterial pressure =

A

Diastolic pressure + (pulse pressure÷3)

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44
Q

Pulse pressure =

A

Systolic pressure - diastolic pressure

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45
Q

Systolic pressure (+ normal value)

A

Maximum pressure in arteries during systole

120mmHg

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46
Q

Diastolic pressure

+Normal value

A

Minimum arterial pressure at the end of diastole

80mmHg

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47
Q

Normal mean arterial pressure

A

~93mmHg

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48
Q

Normal pulse pressure

A

~40mmHg

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49
Q

End diastolic volume (+normal value)

A

Volume in ventricle at end of diastole

~130ml

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50
Q

End systolic volume (+ normal value)

A

Volume in ventricle at end of systole

~60ml

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51
Q

a-wave

A

Slight increase in atrial pressure due to atrial contraction

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52
Q

c-wave

A

Increase in atrial pressure due to ventricle contraction (mitral valve closing).
The mitral valve pushed into the atrium, decreasing volume in atrium.

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53
Q

v-wave

A

Slow increase in atrial pressure throughout systole due to venous return from lungs

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54
Q

Isometric contraction period

A

Period at the start of systole, between mitral valve closing and aortic valve opening.

Ventricular contraction increases pressure but volume remains constant

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55
Q

Isometric relaxation period

A

Period at start of diastole, between aortic valve closing and mitral valve opening.

Ventricular pressure decreases because of ventricle relaxation but volume remains the same.

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56
Q

Ejection phases

A

Once the aortic valve opens during systole, blood is ejected into the aorta.

Start= rapid ejection phase

Then = slower ejection phase

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57
Q

Ventricular filling phases

A

Once the mitral valve opens during diastole, blood flows into the ventricles from the atria.

Start = rapid ventricular filling

Then = slower ventricular filling

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58
Q

Formation of the aorticopulmonary septum

A

Ingrowth of the bulbar ridges in the walls of the truncus arteriosus and bulbus cordosis

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59
Q

Early pacemakers

A

1st - primordial atrium
then - sinus venosus

SA node develops during 5th week

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60
Q

Lymphatic system development

A

6 primary lymph sacs develop around main veins at end of embryonic period (become groups of lymph nodes in early foetal life)

lymphatic vessels connect the sacs layer

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61
Q

dextrocardia

A

Heart tube loops to the left instead of the right so faces right.

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62
Q

Atrial Septal Defect (ASD) types

A
  1. foramen secundum defect (enlarged foramen ovale)
  2. endocardial cushion defect with foramen primum defect
  3. sinus venosus defect (drainage of pulmonary veins into right atrium)
  4. common atrium (failure of septal development)
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63
Q

Ventricular Septal defect (VSD)

A

Most common in the membranous septum.

Many close spontaneously

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64
Q

Patent Ductus Arteriosus

A

The ductus arteriosus fails to close after birth, causes shunt.
Associated with maternal rubella infection.

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65
Q

Transposition of great arteries/vessels

A

Aorta and pulmonary trunk are switched due to:

  1. failure of aorticopulmonary septum to spiral
  2. defective migration of neural crest cells (menchymal cells) to form aorticopulmonary septum
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66
Q

Tetralogy of Fallot

A

Made up of 4 cardiac defects:

  1. Pulmonary valve stenosis
  2. VSD
  3. Dextroposition of aorta
  4. Right ventricular hypertrophy (wall thickening)

CAUSE: Anterior displacement of aorticopulmonary septum = pulmonary stenosis + aorta takes blood from right.

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67
Q

Coarctation of the Aorta

A

Constriction of aorta, usually opposite ductus arteriosus.

Possible cause: muscle tissue of DA incorporated into aorta. when DA contracts after birth, so does aorta.

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68
Q

Aberrant subclavian artery

A

The right subclavian artery has an abnormal origin on the left and must cross behind the trachea and oesophagus and may constrict them.

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69
Q

Double aortic arch

A

A right aortic arch develops in addition to the left one. Forms a vascular ring around the trachea and oesophagus which usually causes dificulty breathing and swallowing.

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70
Q

Vitelline Veins

A

Carry blood from the yolk sac to the sinus venosus

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71
Q

Umbilical veins

A

Carry oxygenated blood from the placenta to the embryo

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72
Q

Cardinal veins

A

Drain the body of the embryo

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73
Q

The circulatory system is formed from the…

A

Lateral plate splanchnic mesoderm

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74
Q

The pericardium if formed from the…

A

intra-embryonic coelom

75
Q

The lateral plate somatic mesoderm forms the…

A

Parietal serous pericardium and fibrous pericardium

76
Q

The outflow tracts (aorta and pulmonary trunk) are formed by the…

A

Truncus arteriosus and Bulbus cordis

77
Q

The bulbus cordis forms…

A

parts of the outflow tracts and the right ventricle

78
Q

The primitive ventricle forms…

A

the left ventricle

79
Q

The primitive atrium forms

A

parts of the left and right atria

80
Q

The sinus venosus forms

A

The right atrium,
SVC,
AV node,
bundle of His

81
Q

The AV node and Bundle of His are formed from…

A

The sinus venosus and cells of the AV canal

82
Q

Fate of aortic arch 1

A

Forms maxillary arteries

83
Q

Fate of aortic arch 2

A

Disappears early

84
Q

Fate of aortic arch 3

A

Forms:
Common carotid arteries,
1st part of internal carotid arteries

85
Q

Fate of left aortic arch 4

A

Distal aortic arch

86
Q

Fate of right aortic arch 4

A

Proximal right subclavian artery

87
Q

Fate of aortic arch 5

A

Regresses (if it forms at all)

88
Q

Fate of right aortic arch 6

A

Proximal right pulmonary artery

89
Q

Fate of left aortic arch 6

A

Left pulmonary artery + ductus arteriosus

90
Q

Proximal umbilical arteries form…

A

Internal iliac arteries,

Superior vesicle branches (to bladder)

91
Q

Distal umbilical arteries form…

A

Medial umbilical ligaments

92
Q

Fate of right umbilical vein

A

Degenerates completely

93
Q

Fate of left umbilical vein

A

forms Ligamentes teres

94
Q

Cardinal veins form

A

SVC and IVC

95
Q

Ductus venosus becomes…

A

The ligamentum venosum of the liver

96
Q

The oval foramen becomes…

A

the oval fossa

97
Q

The ductus arteriosus becomes…

A

The ligamentum arteriosum

98
Q

Function of the ductus venosus

A

Allows a portion of blood from the umbilical vein to bypass the liver

99
Q

Foramen ovale (definition and function)

A

An opening between the atria (in the foramen secundum) which allows blood to bypass the lungs.

opened due to increased pressure in the right side of the heart due to hypoxic pulmonary vasoconstriction.

100
Q

Ductus arteriosus

A

Connects the pulmonary artery to the aorta, allowing blood to bypass the lungs.

101
Q

Formation of the bulboventricular loop

A

The bulbus cordis and ventricle grow faster than the rest of the primitive heart tube, causing it to loop to the right.

102
Q

Formation of the aortic sac and arches

A

When the heart tube fuses, the 2 ventral aortae partially fuse to form an aortic sac.

6 aortic branches/arches arise from the sac (not at the same time)

103
Q

Function of the endocardial cushions

A

Separate the left and right atrioventricular canals,

Form the cardiac valves

104
Q

Foramen primum

A

a gap between the septum primum and endocardial cushion

105
Q

Foramen secundum

A

A gap in the septum primum

106
Q

Sources of tissue for the formation of the membranous interventricular septum

A

Aorticopulmonary septum
Bulbar ridges
Endocardial cushions

107
Q

Sections of fused primitive heart tube (superior to inferior)

A 
Truncus arteriosus,
Bulbus cordis,
Ventricle,
Atrium,
Sinus venosis
108
Q

Gradual depolarisation of pacemaker cells in caused by…

A

Gradual decrease PK+,
Early increase PNa+,
Late increase PCa2+ (T-type)

109
Q

Rapid depolarisation of pacemaker cells caused by…

A

Increase PCa2+ (L-type)

110
Q

Excitation-contraction in cardiac muscle

A

Ca2+ is released from the sarcoplasmic reticulum AND outside the cell.
Regulation of Ca2+ release can be used to vary strength of contraction

Ca2+ binds to troponin = contraction

111
Q

Length of cardiac muscle AP (+ consequences)

A

Long: 250msec (2msec in skeletal)

Because L type Ca2+ ions maintain contraction

= long refractory period
= no tetanus

112
Q

Area of the pressure volume loop

A

Increases as the heart’s work increases.

e.g. due to exercise/ hypertension

113
Q

Ejection fraction

114
Q

Dicrotic notch

A

Increase in aortic pressure when aortic valve shuts

115
Q

Sympathetic effect on heart rate

A 
Releases noradrenaline. 
(+ circulating adrenaline)
Acts on B1 receptors on sinoatrial node.
Increases slope of pacemaker potential.
= tachycardia
116
Q

Parasympathetic effect on heart rate

A

Vagus nerve releases ACh.
Acts on muscarinic receptors on SA node.
Hyperpolarises cells AND decreases slope of pacemaker potential.
= bradycardia

117
Q

Sympathetic effect on stroke volume

A 
Releases noradrenaline.
(+ circulating adrenaline)
Acts on B1 receptors on myocytes.
Increases contractility
= shorter, stronger contraction
118
Q

Parasympathetic effect on stroke volume

A

Little/ no effect.

Vagus nerve does not innervate ventricular muscle

119
Q

Preload (+ factors it depends on)

A

The initial (resting) length of muscle fibres.

Controlled by end diastolic volume (EDV), which is controlled by venous return

120
Q

Starling’s law

A

The energy of the contraction is proportional to the initial length of the cardiac muscle fibre.

*Due to the length-tension relationship

121
Q

Effect of preload on stroke volume

A

Increased preload = increased stroke volume

↑venous return = ↑EDV = ↑SV.

122
Q

Afterload (+ factors it depends on)

A

The load against which the muscle tries to contract

Controlled by the arterial pressure against which the blood is expelled, which depends on total peripheral resistance (TPR).

123
Q

Effect of afterload on stroke volume

A

Increased afterload = decreased stroke volume

↑TPR = ↑Arterial pressure = more energy used opening aortic valve = low SV

124
Q

Cardiac output =

A

Heart rate x Stroke volume

125
Q

significance of shorter contraction with increased contractility

A

Shortens systolic phase,
More time for ventricular filling
Maintains EDV and therefore preload + SV

126
Q

Korotkoff sounds

A

Heard with a stethoscope on the brachial artery.

CP   >  SBP = silence
CP   <  SBP = tapping
CP <<  SBP = thumping
CP <<< SBP = muffled
CP   <  DBP = silence

*CP = cuff pressure

127
Q

Relationship between blood velocity and total cross-sectional area of vessels

A

Total flow through all vessels must be equal so vessels with low velocity of blood flow have high total cross-sectional area and vice versa.

flow is fastest in aorta and vena cava, slowest in capillaries

128
Q

Factors affecting pressure and flow in veins

A 
Gravity,
Skeletal muscle pump,
Respiratory pump,
Venomotor tone,
Systemic filling pressure
129
Q

Effect of gravity on venous pressure

A

Venous distension (pooling of blood) in legs = less blood in heart = low EDV = low preload = low SV = low MAP/ venous pressure

= decreased baroreceptor firing rate

130
Q

Skeletal muscle pump

A

Muscle activity from rhythmic exercise promotes venous return

131
Q

Respiratory pump

A

Inhalation decreases thoracic pressure and draws blood back to the heart

132
Q

Venomotor tone

A

State of contraction of smooth muscle around veins.

contracts to increase venous return when more blood is needed - mobilises capacitance

133
Q

Processes of transport between capillaries and tissues

A 
Diffusion (across membrane/through channels),
Carrier-mediated transport
Bulk flow (Starling's forces)
134
Q

Capillaries in the brain

A

Completely continuous; no clefts or channels.

This only exists in the brain and is the basis of the blood-brain barrier

135
Q

Blood clotting process

A
  1. formation of a platelet plug

2. formation of a fibrin clot
thrombin converts fibrinogen to fibrin

136
Q

Anti-clotting mechanisms of the endothelium

A

Stops blood contacting collagen (no platelet aggregation).

Produces prostacyclin and NO (inhibit platelet aggregation).

Produces Tissue Factor Pathway Inhibitor (TFPI) (stops thrombin production).

Expresses thrombomodulin and heparin (inactivate thrombin).

Secretes tissue plasminogen activator (t-PA) (activates plasminogen to form plasmin which digests clots)

137
Q

Active (metabolic) hyperaemia

A 
INCREASED METABOLIC ACTIVITY:
metabolites accumulate,
Triggers the release of EDRF (NO),
Causes arteriolar dilation,
increases flow.

*This matches blood supply to the metabolic needs of that tissue.

138
Q

Pressure (flow) autoregulation

A 
DECREASED MAP CAUSES DECREASED FLOW:
metabolites accumulate,
Triggers release of EDRF (NO),
Causes arteriolar dilation,
increases flow.

*Ensures a tissue maintains its blood supply despite changes in MAP

139
Q

Reactive hyperaemia

A 
OCCLUSION OF BLOOD SUPPLY:
metabolites accumulate,
Triggers release of EDRF (NO),
Causes arteriolar dilation,
increases flow.

*occlusion of blood supply causes subsequent increase in blood flow.

140
Q

Injury response

A

INJURY:
triggers mast cell to release histamine
causes arteriolar dilatation
increased blood flow + permeability

*aids delivery of leukocytes to injured area

141
Q

Sympathetic effect on arteriolar tone

A

Releases norepinephrine,

Binds to a1 receptors on some smooth muscle (e.g. arterioles supplying skin, kidney),
Causes arteriolar constriction

Binds to b2 receptors on other smooth muscle (e.g. arterioles supplying heart, brain)
Causes arteriolar dilation

142
Q

Parasympathetic effect on arteriolar tone

A

Usually no effect

143
Q

Hormonal effect of epinephrine on arteriolar tone

A

SMOOTH MUSCLE:
binds to a1 receptors,
causes arteriolar constriction,
decreases flow

SKELETAL and CARDIAC MUSCLE:
activates b2 receptors,
causes arteriolar dilatation,
increases flow through that tissue

144
Q

Local (intrinsic) controls of arteriolar tone

A

Active hyperaemia,
Pressure autoregulation,
Reactive hyperaemia,
Injury response.

145
Q

Factors controlling blood flow in coronary circulation

A

Blood flow interrupted during systole but…

Shows excellent active hyperaemia,
Expresses many b2 receptors (swamp any sympathetic arteriolar constriction)

146
Q

Factors controlling blood flow in cerebral circulation

A

Shows excellent pressure autoregulation

147
Q

Factors controlling blood flow in pulmonary circulation

A

Decreased O2 causes arteriolar constriction (opposite to most tissues),
Ensures blood is diverted to the best ventilated parts

148
Q

Factors controlling blood flow in renal circulation

A

Filtration depends on pressure so shows excellent pressure autoregulation
(pressure independent from MAP)

149
Q

Poiseuille’s law meaning

A

Radius is used to control blood flow

150
Q

Importance of Mean Arterial Pressure (MAP)

A

MAP is the driving force pushing blood through the circulation

Too low = syncope
Too high = hypertension

151
Q 
Arterial Baroreceptors 
(location and function)
A

Located in the aortic arch and carotid sinuses

Stretch receptors: fire more APs when artery walls are more stretched by high BP.

152
Q

Sensory fibres of the arterial baroreceptor reflex

A

Aortic arch –> Medullary cardiovascular centres:
Vagus nerve

Carotid sinus –> Medullary cardiovascular centres:
Glossopharyngeal nerve

153
Q

Parasympathetic arterial baroreflex response

A

Hyperpolarises SA node (decreases slope of pacemaker potential).
Impulse travels in vagus nerve

154
Q

Sympathetic arterial baroreflex response

A

Noradrenaline acts on b1 receptors to Increase slope of pacemaker potential in SA node,

Noradrenaline acts on b1 receptors on myocytes in the ventricles to increase contractility

Stimulates adrenal medulla to release adrenaline,

Acts on a1 receptors in smooth muscle causing arteriolar constriction and venoconstriction

155
Q

The arterial baroreceptor input

A

APs travel from arterial baroreceptors to the medullary cardiovascular centres.

More APs = higher BP = parasympathetic response

Less APs = lower BP = sympathetic response

156
Q

Other inputs to cardiovascular medullary centres

other than arterial baroreceptor input

A 
Cardiopulmonary baroreceptors,
Central chemoreceptors,
Chemoreceptors in muscle +
Joint receptors (more blood to exercising areas),
Higher centres
157
Q

Cardiopulmonary baroreceptors (low pressure baroreceptors)

A

Located in large systemic veins and pulmonary vessels.

Respond to blood volume - important in the long-term regulation of blood pressure.

Send sympathetic signals to juxtaglomerular cells when blood volume (=pressure) is low

158
Q

MAP =

159
Q

Effect on CVS of standing and reflex response

A

Standing = pooling of blood in veins/ venules of lower limbs
= ↓VR = ↓EDV = ↓preload = ↓SV = ↓CO = ↓MAP
= ↓baroreceptor firing rate

RESPONSE:
↓Vagal tone
↑ sympathetic tone
= ↑MAP

160
Q

High contractility

A

Shorter, sharper contractions.

Caused by (nor)adrenaline acting on b1 receptors on myocytes

161
Q

Effect of the Valsalva manoeuvre

A
  1. increased thoracic pressure (TP) initially increases MAP
  2. Increased TP decreases; VR, EDV, SV, CO, MAP
  3. Baroreceptors initiate reflex = increased CO + TPR and therefore MAP
162
Q

Effect of releasing the Valsalva manoeuvre

A
  1. Decreased TP initially decreases MAP
  2. VR is restored, increases EDV, SV and therefore MAP
  3. MAP decreases to normal
163
Q

Clinical use of the Valsalva manoeuvre

A

Used to measure strength of baroreceptor reflex

164
Q

Kidney regulation of plasma volume

A

Modulating Na+ transport out of the collecting duct determines how big the osmotic gradient out of the collecting duct is.
Modulating collecting duct permeability to water determines if water follows it:

Increasing collecting duct permeability = lots of water reabsorption - conserves plasma volume, little urine.

Decreasing collecting duct permeability = little water reabsorption - reduction in plasma volume, lots of urine.

*These processes are modulated by hormone systems.

165
Q

Triggers of renin production

A

Sympathetic activation to juxtaglomerular cells. (caused by decreased plasma volume sensed by CP baroreceptors, relayed via medullary CV centres)

Decreased distension of afferent arterioles

Decreased delivery of Na+/ Cl- through distal convoluted tubule. detected by Macula densa cells.
(Low Na+ = low filtration pressure/MAP)

166
Q

Juxtaglomerular (granular) cells

A

Specialised cells around the efferent and afferent arterioles.
Releases renin in response to triggers.

167
Q

Activity of renin

A

Converts inactive angiotensinogen into angiotensin I

168
Q

Creation of angiotensin II

A

Angiotensin I in converted to angiotensin II by angiotensin converting enzyme

169
Q

Actions of Angiotensin II

A

Increases release of ADH from the posterior pituitary gland

Stimulates release of aldosterone from the adrenal cortex

Causes vasoconstriction

170
Q

Triggers of ADH release

A

Decreased blood volume (sensed by CP baroreceptors, relayed via medullary CV centres)

Increased osmolarity of ISF (sensed by osmoreceptors in the hypothalamus)

Circulating angiotensin II (from the renin-angiotensin-aldosterone system)

171
Q

Effects of ADH

A

Increases permeability of the collecting duct (decreases diuresis, increases plasma volume)

Increases sense of thirst

Causes vasoconstriction

172
Q

Effects of aldosterone

A

Increases Na+ reabsorption in the loop of Henle:

  • decreses diuresis
  • increases plasma volume
173
Q

Diuresis

A

Urine production

174
Q

Triggers of Atrial Natriuretic Peptide production

A

Increased MAP

  • > distension of atria
  • > production of ANP by myocardial cells in atria
175
Q

Triggers of Brain Natriuretic Peptide production

A

Increased MAP

  • > distension of ventricles
  • > production of BNP by myocardial cells in ventricles
176
Q

Effects of ANP/BNP

A

Increased excretion of Na+ (natriuresis)

Inhibits release of renin

Acts of medullary CV centres to reduce MAP

177
Q

Pacemaker action potential

A
  1. Pacemaker potential (pre-potential)
    - spontaneous gradual depolarisation
  2. Action potential - once threshold is reached
    - rapid depolarisation
178
Q

Reason for rapid conduction through bundles of His and purkinje fibres

A

ventricular cells contract together giving a short, sharp contraction to expel lots of blood

179
Q

Pressure-volume loop x-axis

A

Left ventricular volume (ml)

180
Q

Pressure-volume loop y-axis

A

Left ventricular pressure (mmHg)

181
Q

Pressure throughout the vascular tree

A

Elastic arteries damp down pressure variations from the ventricles
Pressure falls throughout the vascular tree, driving blood forward

182
Q

Systemic filling pressure

A

The small pressure difference that pushes blood through the veins

183
Q

Function of the blood-brain barrier

A

Protects the brain from circulating pathogens

x1 - Cardiovascular (8 decks)

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