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Primary Physiology > Physiology of Circulation > Flashcards

Physiology of Circulation Flashcards

1
Q

Layers of blood vessel wall

A

Adventitia - connective tissue and nerve fibres
Media - smooth muscle
Intima - Bm, endothelium, connective tissue

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2
Q

Characteristics of aortic wall
Characteristics of vena cava wall

A

Elastic and fibrous
Smooth muscle and fibrous

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3
Q

As well as delivery of blood what are the functions of the following blood vessels:
Aorta
Arteries
Arterioles
Capillaries
Venules
Veins

A

Aorta - storage of energy to maintain delivery in diastole and dampening of pulse pressure
Arteries - further dampening
Arterioles - control of pressure and distribution to capillary beds
Capillaries - exchange
Venules - collection
Veins - storage of blood, portal circulations

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4
Q

What is the function of wall thickness in blood vessels

A

Thick - Tensile strength to allow withstanding of pressure
Thin - exchange in capillaries

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5
Q

Function of elastic component in blood vessel walls

A

Smoothing of pulsetations and storage of energy to maintain flow in diastole

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6
Q

Function of smooth muscles in blood vessels

A

Control of vessel diameter

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7
Q

Difference between flow and flow velocity

A

Flow is volume of blood flowing per unit time (L/min)
Flow velocity is how fast fluid is moving at any given point (cm/s)

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8
Q

How does flow velocity vary over the diameter of a blood vessel in laminar flow

A

Faster in centre

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9
Q

What equation links flow and flow velocity

Implication to the differing stages of blood vessels (arteries, Arterioles capillaries etc)

A

Q=vA
Flow = velocity x area

As area enlarges and flow remains constant velocity falls

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10
Q

Flow velocity in aorta compared to capillaries, cross sectional area of both

A

Aorta 120cm/s. 4.5cm2
Capillaries 0-1cm/s. 4500cm2

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11
Q

Issue with turbulent flow and blood vessel constriction

A

High flow velocity and turbulent flow produce shear forces that can pull endothelium away from vessel wall and dislodge plaques causing thrombi and emboli

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12
Q

How can ohms law be analogous to cardiac function

A

V = I x R
MAP-CVP = CO x SVR

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13
Q

What are the sources of energy that drive blood flow?

A

Cardiac contraction
Elastic recoil of great vessels
Skeletal muscle contraction
Negative interthoracic pressure

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14
Q

Forces opposing blood flow through vessels

A

Friction (between fluid and vessel walls and between fluid layers), determined by vessel size and viscosity
Conversion of pump work into stored energy (eg into elasticity of deistended vessel walls or by gravity - depends of the pulsetyle nature of circulation

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15
Q

What law governs blood flow through a single vessel

A

Hagen poiseuille

Q = Pi(🔼P)r^4 / 8nL
Flow = Pi (pressure gradient) radius to power 4 / 8 viscosity length

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16
Q

Why does reality differ from Hagen poiseuille law

A

Blood vessels are not uniform in cross section
Blood vessel walls are elastic
Pressure gradients are not constant but pulsatilla
Blood behaves differently from Newtonian fluid because of the cellular component so viscosity is not the sole determinant of flow properties.

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17
Q

How does blood differ in viscosity from a Newtonian fluid

A

Cells - as haematocrit increases apparent viscosity increases more
Blood vessel diameter - as diameter falls apparent viscoicty of blood decreases as the cells stream in the centre of the vessel effectively reducing the hct
Flow velocity - apparent viscosity decreases at higher flow speeds due to less cell adherence to each other and vessel walls

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18
Q

Functions of the arterial system

A

Deliver blood to capillary beds
Convert high pressure pulsatilla blood flow into low pressure steady flow

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19
Q

What is the term for the effect of the arterial system on flow (converting from high pressure pulsetyle to low pressure constant

A

Hydraulic filtering or windkessel

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20
Q

Normal values for stroke volume and flow velocity
Peak velocity

A

Stroke volume 70-90ml
Flow velocity 70cm/s
Peak velocity 120cm/s

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21
Q

How do systolic pressures change through the arterial system
Why?

A

120 in aorta
increase in the initial arteries Distally (up to 40 higher in feet) but then decrease into the arteriolar to around 30 ready to enter capillaries

Initial increase due to propagation of pressure wave from reflection and resonance.

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22
Q

What is compliance of the arterial system

A

Change in arterial blood volume produced by unit change of arterial blood pressure

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23
Q

Do stiff arteries have high or low compliance

A

Low

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24
Q

How does arterial compliance change with age

A

Falls
Also compliance curve moves from linear relationship to curve (as pressure increases it has less effect on volume)

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25
Q

Factors that effect blood pressure

A

SVR
Blood volume
Stroke volume
Arterial compliance
Duration of systole

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26
Q

What determines diastolic pressure?

A

Systolic pressure
Arterial compliance
SVR
Duration

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27
Q

How does SVR effect SBP and DBP

A

Produces non linear pressure volume curve similar to ageing - ie higher pressures needed for same volume
Slows rate of diastolic blood pressure fall

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28
Q

Effect of arterial compliance on sbp and dbp

A

Much greater effect on sbp because of the curve of the pressure volume curve (linear relationship of pressure at lower volumes, then increasing pressures needed per unit volume at higher volumes)

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29
Q

Functions of the venous system

A

Collection and return of blood from capillary beds to heart
Reservoir of blood volume
Provision of preload

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30
Q

Rough venous pressures through the venous system

A

15-20 at end of capillary bed in venuoles
10-15 in small veins
5-6 in large extrathoracic veins

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31
Q

What are the characteristics of venous flow and influences

A

In small veins continuous
In great veins fluctuate with a c and v waves due to cardiac contraction and respiration

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32
Q

What mechanisms assist venous return to the heart

A

Gravity
Thoracic pump
Muscle pumps
Unidirectional valves

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33
Q

What is the major determinant of venous pressure

A

Gravity

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34
Q

Why is the venous pressure in the foot not around 115mmHg (0.77mmHg for every cm of height)
What is it in an erect individual? What about when walking

A

Presence of valves, venous obstruction etc.
usually around 80
Reduces to 30 when walking due to muscle pump

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35
Q

What is the physiology behind JVP

A

When erect pressure in the IJV is roughly atmospheric so it sits collapsed. The height of collapse is representative of RA pressures

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36
Q

What is venous pressure in the brain when erect
Clinical implications

A

Can be subatmospheric - around -20mmHg
Because skull is rigid container they don’t collapse but stay held open by surrounding tissues
Susceptible to air embolism if punctured or cannula open to air.

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37
Q

What volume of air in venous circulation would be problemous to cardiac output
What volume of air in arterial circulation would be problems to end organs esp brain

A

> 10ml
1-2ml

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38
Q

How does the thoracic pump work?
How is heart rate effected?

A

Inspiration interpleural pressure drops from -2 to -6mmHg
This transmits to central veins reducing CVP, increasing gradient with abdominal veins and thus augmenting venous return.
Increased gradient further still by flattening diaphragm increasing abdominal pressure
Blood then pools in pulmonary circulation resulting in small decrease in arterial pressure and thus increase in heart rate.

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39
Q

What can excentuate the changes of the thoracic pump?
Name?

A

Forced inspiration against closed glottis (muller manoeuvre)

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40
Q

Surface area of capillary network

A

6000m2

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41
Q

How is blood fed into capillary network

A

Arterioles to metarterioles which give rise to smooth muscle precapiliary sphincters gating the entry to capillaries

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42
Q

What is the innervation of arterioles, metarterioles and precapiliary sphincters

A

Arterioles - ANS
Metarterioles and precapiliary sphincters - ? Local/humoral agents

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43
Q

What is the state of most capillary beds at rest, how does blood flow?
What homeostatic function is this vital for?

A

Most are collapsed
Blood shunts past in anastomoses between arterioles and venules
Temp regulation

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44
Q

Size of capillaries?
Size of RBC
How much of the total blood volume do they hold

A

5micrometers widening to 9 micrometers at venous end
RBC 7micrometers
Hold 6% of circulating volume

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45
Q

What are the cells that support capillaries? What do they do

A

Pericytes
Release chemicals to control permeability
Secrete basement membrane

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46
Q

On which side of the capillary enothelial cells is the basement membrane

A

Outside

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47
Q

How do objects diffuse out of capillaries based on their properties

A

Small molecules <8nm can diffuse out of intracellular junctions/pores
Large molecules may cross cell cytoplasm in vesicles
Fat soluble molecules, oxygen, water and Co2 pass directly through cells

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48
Q

What adaptation do capillaries have in endocrine glands, renal glomeruli and intestinal villi that permits secretion filtration and absorption
Rough size

A

Fenestrations 20-100nm

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49
Q

What do liver and spleen capillary sinusoids contain that distinguishes them from other capillaries
Rough size
Implications

A

Discontinuous epithelium with gaps >1000nm
Albumin can diffuse out much more easily

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50
Q

Where does diffusion occur from capillaries

A

Endothelial defects including pores, intracellular junctions and fenestrations

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51
Q

What is filtration in capillaries

A

The movement of water and small solutes across the endothelium under influence of osmotic and hydrostatic gradients

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52
Q

How do large lipid insoluble molecules travel across the capillary wall

A

Pinocytosis (combined Endocytosis and exocytosis)

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53
Q

What is diffusion?

A

The movement of a substance down its concentration gradient

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54
Q

What determines rate of diffusion in or out of a capillary

A

Capillary permeability, capillary surface area, concentration gradient, capillary wall thickness

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55
Q

What factors contribute to capillary permeability for a specific substance

A

Substance related - size, charge, lipid solubility
Capillary related - number of gaps
Other - interactions between other solutes

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56
Q

What limits the diffusion of easily diffusible molecules such as gases across a capillary bed? Why?

A

Flow
Easy diffusion so reach equilibrium close to proximal end thus faster flow needed to remove more from distal end.

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57
Q

What is the term for the combination of forces moving fluid in and out of capillaries?
What does it compose and how does it change down the length of a capillary

A

Starling forces
Hydrostatic and colloid osmotic pressure
Proximal capillary higher hydrostatic pressure pushing fluid out into interstitium
Distal capillary lower hydrostatic pressure and fluid flows back in

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58
Q

What are proximal and distal capillary hydrostatic pressures
What is interstitial fluid hydrostatic pressure
What are capillary and interstitial fluid colloid oncotic pressures

A

33 to 15mmHg
1mmHg (-9 to 9)
25mmHg and 0

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59
Q

How much more fluid is filtered from capillary compared to reabsorbed?
Where does it go?

A

10%
Lymph

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60
Q

What is the typical volume of lymph drainage per 24 hrs
Other functions of lymph

A

2-4 litres
Return of leaked proteins
Absorption of particles proteins and high molecular weight molecules in inflamed tissues
Absorption of proteins and fat from metabolism and gastric absorption.

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61
Q

Where does lymph drain back to circulation

A

Junction of IJ and SC veins

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62
Q

What drives lymph flow

A

Nearby arterial pulsetation and skeletal muscle contraction with 1 way valves

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63
Q

Causes of tissue oedema

A

Increased capillary filtration (eg raised venous pressure in heart failure or venous obstruction)
Decreased capillary colloid osmotic pressure (eg hypoalbuminia)
Increased capillary permeability (inflammation)
Decreased lymph drainage (eg obstruction, filiariasis, lymphadenopathy)

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64
Q

Why is intrinsic control of circulation vital, especially in tissues such as heart and brain

A

Allows maintained blood flow independent of systemic disturbance.

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65
Q

What types of blood vessels are involved in the control of circulation

A

Resistance vessels - arterioles - changes in tone result in changes in perfusion pressure across vascular bed and effect flow through capillaries and alter vascular resistance
Capacitance vessels - venous system - changes in tone changes intravascular volume

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66
Q

How is muscle arranged in arterioles

A

Smooth muscle arranged circumferential in the tunica media

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67
Q

How are actin and myosin arranged in vascular smooth muscle

A

Not in striations

68
Q

What are the characteristics of a vascular smooth muscle contraction

A

Slow and long duration

69
Q

How are contractions triggered in vascular smooth muscle
What factors do so?

A

Calcium release in response to mediators NO action potential
Mediators such as catecholemines, ach and prostaglandins

70
Q

What nerve supply does most vascular smooth muscle have?

A

Sympathetic
Generally has a basal level of tone that varies up and down

71
Q

What vascular smooth muscle has a parasympathetic supply, what is the effect of stimulation

A

Small number of visceral vessels
Decrease in resistance when stimulated

72
Q

What are intrinsic methods of blood flow control through vessels (autoregulation)?

A

Metabolic regulation
Mechanical response
Endothelial regulation

73
Q

What is the basis of metabolic regulation of blood flow?
Examples

A

Hypoxia or injury causes release of metabolites increasing permeability and blood flow
Co2, acidosis, adenosine, ADP, AMP, K+, phosphate all cause dilation
Local mechanical damage causes serotonin release from platelets and constriction

74
Q

How does the mechanical response contribute to maintaining blood flow in autoregulation?

A

Vascular smooth muscle contracts in response to raised transmural pressure resulting in constant blood flow (and vica versa)

75
Q

What endothelial factors contribute to local control of blood flow?

A

Endothelial calls release various local factors effecting blood flow:
Prostacyclin, thromboxane A2, nitric oxide, endothelium’s

76
Q

What are the actions and relationship between prostacyclin and thromboxane A2

A

Prostacyclin is a vasodilator that inhibits platelet aggregation
Thromboxane A2 is a vasoconstrictor that promotes platelet aggregation

77
Q

How is nitric oxide synthesised
How is it inactivated

A

From arginine by NO synthase
Inactivated by haemoglobin

78
Q

What is the effect of endothelins on blood vessels

A

Vasoconstriction

79
Q

What key extrinsic humoral systems control blood flow?

A

Catecholamines
Vasopressin
Angiotensin
ANP
Kinins
Histamine

80
Q

Effect of adrenaline on blood vessel tone?

A

Dilates resistance vessels in skeletal muscle at low concentrations via beta effect
At high concentrations causes vasoconstriction by alpha adrenergic stimulation

81
Q

Where is noradrenaline generally released from?
General effect

A

Nerve endings
Vasoconstriction

82
Q

Other name for vasopressin
What is it?

A

ADH
9 amino acid peptide

83
Q

Primary effect of vasopressin?
Effect on blood vessels?
Other effects?

A

Free water retention in collecting duct
Systemic vasoconstriction in supranormal doses
Stimulates ACTH secretion from pituitary and promotes gluconeogenesis

84
Q

Overview of RAAS pathway

A

Renin synthesised and stored in juxtaglomerular apparatus in kidneys
Low renal perfusion triggers renin release
Renin causes angiotensinogen to cleave to angiotensin I
ACE in the lungs converts angiotensin I to II
Angiotensin II causes vasoconstriction, stimulates thirst and causes release of aldosterone from renal cortex
Aldosterone causes tubular reabsorption of sodium and thus osmotic reabsorption of water
Aldosterone also increases excitability of vascular smooth muscle potential in angiotensin II

85
Q

What is ANP
Released from atrial muscle cells proportional to stretch

A

17 amino acid peptide containing a ring formed by a disulphide bond between 2 cysteine residues

86
Q

Effects of ANP

A

Causes natriuretic
Lowers BP
Inhibits vasopressin secretion

87
Q

Types of kinins and origin
Effect on vascular tone
Metabolism

A

Bradykinin and Lysylbradykinin
Origin from kallikreins
Cause vasodilation
Metabolised by kininases eg ACE

88
Q

Origin of histidine
Where is it produced
What controls release
Effect

A

An amine formed from decarboxylation of histidine
Produced in cns, gastric mucosa and mast cells
Controlled by inhibitory H1+2+3 receptors
Potent vasodilator

89
Q

Which blood vessels contain no smooth muscle

A

Capiliaries, venuoles

90
Q

What nerve system supplies blood vessel smooth muscle
Where does it interact with the vessels?
How is tone decreased?

A

Sympathetic NS
Plexus in the adventitia then extend to the smooth muscle cells in the media
Fibres fire at background rate maintaining tone, decrease this rate causes relaxation

91
Q

What are the characteristics of the neurotransmitter and receptors in vascular smooth muscle SNS supply

A

Noradrenergic
Alpha 1 and 2 receptors causing vasoconstriction
Beta 2 receptors causing vasodilation

92
Q

What are the regions of the vasomotor centres? Where are they found?

A

Pressor region rostrally in ventrolateral medulla
Depressor region caudal in ventromedial medulla

93
Q

Inputs into the vasomotor centres?

A

Higher centres
Afferents from peripheral reflexes
Central chemoreceptors

94
Q

How does the pressor region of vasomotor centre respond to stimulation (with efferent pathway)

A

Stimulation of preganglionic neurones in the intermediolateral grey columns of the spinal cord. These fibres pass into the paravetebral sympathetic chain where they synapse and postganglionic fibres carry impulses to the heart, blood vessels and adrenal medulla
Stimulates vasoconstriction, increased heart rate and myocardial contractility and stimulates release at adrenal medulla

95
Q

How does stimulation of the depressor centre of the vasomotor centre result in a physiological effect

A

Inhibition of the pressor area and inhibition of sympathetic outflow at the spinal level.

96
Q

Where are baroreceptors located?
Where are chemoreceptors located?

A

B - Carotid sinuses, aortic arch, heart

C - Carotid bodies, aortic bodies

97
Q

What are the afferent pathways to the vasomotor centres from the peripheries?

A

Baroreceptors in carotid sinus and chemoreceptors in carotid bodies stimulate branch of glossopharyngeal nerve
Aortic arch baroreceptors and chemoreceptors in aortic bodies stimulate cardiac depressor nerves (branches of left and right vagus nerves)
Both the glossopharyngeal and vagal branches synapse at nucleus tractus solitaries in the dorsomedial medulla and send inhibitory connections from there to the vasomotor centres

98
Q

What higher centres influence the vasomotor centre?
In what way

A

Hypothalamus - anterior causes inhibition, posterior stimulates (also controls cutaneous dilation/constriction in response to body or external temp change)
Cerebral cortex - stimulation of motor or pre motor areas causes stimulation of vasomotor centre
Limbic system - emotional stimuli can cause depressor response with fainting and blushing

99
Q

What is the carotid sinus?
Where is it?

A

An enlargement of the internal carotid artery
Just above into origin

100
Q

What is a baroreceptor
What does it do

A

A coiled nerve ending in the walls of vessels/heart
Respond to degree of stretch thus to the transmural pressure of the vessel/heart. More stretch means faster nerve firing. Also responds to rate of change in pressure - fires faster in early systole compared to diastole - thus also responsive to pulse pressure and heart rate

101
Q

What effect do barorecepters have on the pressor areas of the brain?

A

Firing of baroreceptors due to high pressure causes inhibition of the pressor centre thus negative feedback

102
Q

What shape is the curve of MAP against baroreceptor output?
What happens in chronic hypertension

A

Sigmoidal but linear between 80-180mmHg
Plasticity of receptor - adapts to higher pressure and curve moves right (less firing at same MAP) - can also move back if treated.

103
Q

Which baroreceptors are most susceptible to blood pressure change
What else can trigger these receptors
Clinical correlation

A

Carotid sinus
External mechanical stimuli
CSM and slowing SVT/causing syncope

104
Q

What are the types of atrial baroreceptor?

A

Type a measures mainly systole
Type b measures mainly diastole

105
Q

What is the response of stimulation of atrial baroreceptors to increased filling?
Name and paradox? General clinical outcome to fluid bolus?

A

Bambridge reflex - high filling of atria triggers inhibition of pressor centre causing vasodilation and increases renal blood flow but also increases heart rate to clear the excess fluid. This is opposing the arterial stretch reflex which would lower heart rate. Generally if heart rate slow is sped up by fluid bolus, if fast slowed down by it.

106
Q

What is the effect of pulmonary stretch receptors on the vasomotor centre and the clinical effect?

A

Inhibitory
Inspiration results in vasodilation and decrease in BP

107
Q

What are the carotid and aortic bodies
Where are they located

A

Small masses of chromaffin tissue
Carotid - medial aspect of carotid sinuses
Aortic - anterior and posterior of aortic arch

108
Q

What triggers peripheral chemoreceptors

A

Reduction in arterial oxygen tension (PaO2)
Also respond to lower CO2 or raised H+

109
Q

Where do peripheral chemoreceptors responses activate?

A

Afferent impulses to both respiratory and circulatory centres

110
Q

Effect of peripheral chemoreceptors stimulation on pressor centre?

A

Hypoxia and hypercapnia result in increased blood pressure and transient bradycardia

111
Q

Where are central chemoreceptors
What triggers them

A

Vasomotor centre and other medullary centres
Triggered by changes in CO2 and pH

112
Q

Effect of central chemoreceptor stimulation on pressor centre

A

Increased pressor tone and bradycardia

113
Q

What is the overall effect of raised pCO2 on BP

A

Usually static - peripheral effect to vasodilate and chemoreceptor stimulation to vasoconstrict

114
Q

What is Cushing reflex?
Physiological cause

A

Vasomotor centre reflex in response to pressor cell ischaemia causing vasoconstriction and decreased heart rate
Increases blood pressure at cost of cardiac output maintaining cerebral perfusion pressure

115
Q

What is the effect of ischaemia on coronary artery chemoreceptors? Name and effect

A

Bezold jarish reflex - hypotension and bradycardia increasing coronary blood flow

116
Q

Afferent nerves involved in chemoreceptor reflexes

A

Glossopharyngeal - carotid
Vagus - aortic
Sympathetics - pulmonary and coronary

117
Q

Effect of pain on the vasomotor centres

A

Cutaneous pain stimulates pressor region causing hypertension
Visceral pain often results in depressor response due to stimulation of vagal or pelvic parasympathetic afferents (exception being large bowel which stimulates sympathetics)

118
Q

Blood volume in ml/kg
Adult Vs infant

A

70ml/kg in adult, 80ml/kg in infant

119
Q

Rough percentage volume of blood in veins and venules

A

66%

120
Q

Factors effecting cvp

A

Venous blood volume
Venous venomotor tone
Venous return to heart (cardiac demand)

121
Q

What percentage blood loss results in physiological change?
What are these changes?

A

5%
Decreased SBP and DBP
Decreased pulse pressure
Increased heart rate and contractility
Increased vaso and venoconstriction
Diversion of blood centrally from cutaneous, muscular and splanchnic circulations
Stimulation of adrenal medulla with release of catecholamines
Tachypnoea

122
Q

What reflexes lead to the changes seen in physiology following acute blood loss?

A

Baroreceptor reflex - selective vasoconstriction
Chemoreceptor reflex - especially important at SBP <60 when baroreceptor response blunted
Cerebral ischaemia response - MAP <40 directly stimulates adrenal medulla and augments above reflexes
Reabsorption of interstitial fluid - vasoconstriction reduces capillary hydrostatic pressure resulting in net absorption of fluid
Catecholamine release
Renal conservation of water and salt (RAAS, direct aldosterone release due to adrenal stimulation, vasopressin release)

123
Q

What is the valsalva manoeuvre? Pressure involved

A

Expiration against closed glottis
Generates thoracic pressure around 40mmHg

124
Q

Cardiovascular response to valsalva manoeuvre

A

Immediate increase in Bp as pressure transmitted into aorta and compression of pulmonary veins empties them into LA increasing LV output
Sustained High inter abdominal pressure reduces venous return
Blood pressure decreases
Low stimulation of baroreceptors causing tachycardia and increased SVR
Opening of glottis causes sudden fall in aortic pressure and blood pools in pulmonary vessels
Baroreceptors cause vasoconstriction
Cardiac output restored but ejects into contracted arterial system
Blood pressure overshoots
Baroreceptors stimulated causing vasodilation and bradycardia.

125
Q

What would b the effect of a valsalva manoeuvre in a patient with autonomic neuropathy?

A

High pressure causes fall in BP but no reflex tachycardia or overshoot hypertension.

126
Q

What reflexes are involved in cardiovascular response to exercise?

A

Cortical activation of sympathetic system in anticipation
Cardiovascular reflex due to stimulation of muscle mechanoreceptors
Local reflexes due to accumulation of metabolites
Baroreceptor reflexes

127
Q

Effects of reflexes in preparation for mild to moderate exercise

A

Increased cardiovascular performance
Redistribution of blood flow
Maintenance of cerebral blood flow
Increased oxygen consumption
Increased oxygen extraction

128
Q

Where is blood flow diverted away from in exercise

A

Skin (though increases as body temp rises)
Splanchnic regions
Kidneys
Inactive muscle

129
Q

Local changes in muscle mediated by metabolites produced in exercise

A

Arteriolar dilation with 20x blood flow vs resting
Large capillary recruitment
Net movement of fluid into interstitial compartment
Increased lymph flow due to increased muscle pump
Increased oxygen extraction and thus increased AV concentration gradient
Right shift in oxyhaemoglobin dissociation curve due to low pH, raised CO2 and raised temp

130
Q

What element of the hearts function changes to increase cardiac output in exercise

A

Heart rate - can increase up to around 180bpm
Stroke volume increases but by not such a great extent

131
Q

Why does stroke volume not increase dramatically in moderate exercise
Change in maximal exercise

A

Cardiac output increases due to heart rate acting to oppose the increased venous return caused by the increased muscle pump thus CVP remains much the same, thus no big change in preload - little shift in frank starlings curve.
In maximal exercise then frank starling effect contributes and SV increases

132
Q

Why does venous return increase in exercise?

A

Venomotor tone increase
Muscle pump increase
Redirection of blood
Enhanced thoracic pump due to increased resp rate and volume

133
Q

Why would haematocrit raise during strenous exercise

A

Increased capillary filtration
Loss of fluid from sweating and respiratory losses

134
Q

What happens to pulse pressure during exercise

A

Increases
SBP increases more then DBP

135
Q

What could occur during strenous exercise in autonomic neuropathy or beta blocker therapy

A

Hypotension/syncope as no sympathetic response to counteract local mediator diletation

136
Q

Where do the coronary arteries arise

A

Right - behind right cusp
Left - behind posterior cusp

137
Q

Which coronary artery has most flow in what distribution of people?

A

Right most in 50%
Left most in 20%
Equal in 30%

138
Q

What is the venous drainage of the heart
Physiological effect of venous drainage into left side of heart

A

66% drains via coronary sinus and anterior coronary veins into RA
Rest drains directly via small thebesian veins, arteriosinusoidal vessels and arterioluminal vessels.
Venous drainage into left side of heart produces a shunt (bypassing pulmonary circulation)

139
Q

What organs receive most cardiac output at rest?

A

Abdominal viscera 24%
Kidneys 20%
Skeletal muscle 20%
Brain 13%
Skin 9%
Heart 4%
Other 10%

140
Q

What is coronary blood flow volume at rest?

A

250ml

141
Q

What is average total blood flow at rest

A

5800ml/min

142
Q

How much oxygen does the heart need at rest?

A

10ml/min/100g
In adult around 30ml/min

143
Q

How is coronary artery blood flow determined

A

Driving force is arterial pressure determined by baroreceptor reflex
Flow is controlled by coronary vascular resistance controlled by:
- extravascular compression - diastole length
- metabolic demand - metabolites result in vasodilation
- autonomic system - SNS activation causes coronary vasodilation (though is countered by shorter diastole and increased demand)
- coronary perfusion pressure - difference between aortic and ventricular pressures driving blood through coronary circulation - autoregulates between 60 and 180mmHg

144
Q

What requires more oxygen demand on the heart - an increasing systolic pressure or an cardiac output

A

Increasing pressure puts more demand on heart

145
Q

What arteries supply cerebral circulation

A

Left and right internal carotid
Basilar formed from left and right vertebral

146
Q

Venous drainage of brain

A

Dural sinuses and cerebral veins into internal jugular veins

147
Q

What is the nervous supply to cerebral circulation

A

Sympathetic fibres from superior cervical ganglia enter skull around the carotid arteries through carotid canal
Cholinergic fibres from sphenopalatine ganglia and facial nerve
Sensory fibres from trigeminal ganglia

148
Q

Mean cerebral blood flow

A

55ml/min/100g

149
Q

What areas of the brain receive most blood flow

A

Grey matter, basal ganglia
Areas of the cortex are currently active

150
Q

How can cerebral blood flow be estimated?

A

Kety method - application of Ficks principle, done with nitrous oxide
Scintillography - using radioactive tracers
SPECT scanning - enhancing scintillography in MRI scanning
PET scanning
Doppler

151
Q

What is the main determinant of cerebral blood flow auto regulation

A

Local metabolic factors

152
Q

What does cerebral auto regulation achieve

A

A consistent blood flow of 55ml/min/100g over a range of MAPs from around 50-150mmHg even with varying pO2 and pCO2 by control of cerebrovascular resistance and cerebral perfusion pressure.

153
Q

What is cerebral perfusion pressure

A

CCP = MAP - (ICP+venous pressure)

154
Q

What is the effect of PaCO2 on cerebral blood flow

A

Low Co2 vasoconstriction and high vasodilates thus hyperventilation lowers cerebral blood volume but also cerebral blood flow

155
Q

Effect of PO2 on cerebral blood flow

A

Low pO2 vasodialates and high constricts

156
Q

Effect of ph on cerebral blood flow

A

Low ph vasodilates

157
Q

What metabolic factors influence local cerebral blood flow?

A

Adenosine and k

158
Q

What is the by volume contents of the skull cavity?

A

1400g brain tissue - 80%
75ml blood 10%
75ml CSF 10%

159
Q

What is the monro Kellie doctrine

A

Increase in any one brain component must result in a decrease in the others or an increase in ICP

160
Q

What is normal ICP

A

0-10 mmHg

161
Q

What would be a significantly raised ICP

A

> 15mmHg

162
Q

What is the blood brain barrier

A

An ultrafiltration barrier around the choroid plexuses and capillaries
Composed of epithelium, basement membrane, astrocyte feet

163
Q

What junctions form between cerebral capillary endothelial cells

A

Tight

164
Q

What crosses BBB freely

A

Water oxygen co2

165
Q

What crosses bbb in controlled manner

A

Glucose, ionised molecules

166
Q

What can only cross bbb when inflamed

A

Proteins

167
Q

Functions of bbb

A

Control ionic environment of brain
Protects brain from plasma changes of glucose
Protects brain from toxins
Prevent neurotransmitter release to systemic circulation.

Primary Physiology (15 decks)

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