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HOM > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

How long does it take a particle to move a distance x

A

t α x^2

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2
Q

What does Eisenstein’s equation mean for diffusion

What does this mean for the heart

A

It is extremely slow over long distances but very fast over short distances (especially if x<1)

It is hopelessly and catastrophically slow as the heart wall is ~1cm

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3
Q

How is an infarction characterised

A

The formation of a dense wedge shaped block of dead tissue on the heart following interrupted blood flow

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4
Q

What is ischaemia

A

Lack of oxygenated blood supply to tissue

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5
Q

How many litres of blood will the heart pump in an average human life time

A

~200,000,000

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6
Q

Why does breathing rock the heart

A

Its base is attached to the diaphragm

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7
Q

Are the two atrioventricular valves the same

A

No: Right Side is Tricuspid (R-S-T)

Left is mitral valve (bicuspid)

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8
Q

Where are the semi lunar valves?

What connective tendons do they have

A

Separate ventricles and arteries
(Both have 3 cups)

They don’t have any due to their shape

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9
Q

What are the 3 layers In blood vessels

A

Tunica initima (made of endothelium and elastic connective tissue)

tunica media, (dense population of smooth muscle arranged concentrically with fibres it elastin)

tunica adventitia (contains collagenous extracellular matrix )

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10
Q

Which tunica varies most in thickness between vessels

A

Media

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11
Q

What is the tunica media like in large arteries

A

Thick so they can expand and recoil to smooth pressure changes

These vessels can temporarily store energy

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12
Q

Nearly all body cells are within ___ of a capillary

A

10μm

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13
Q

How much of the blood is in the veins

A

2/3

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14
Q

Can veins constrict

A

Some can

Venoconstriction aids venous return to help maintain cardiac output

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15
Q

Where does oxygenated blood come from in the fetus

A

The placenta

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16
Q

How is the foetus well adapted to

Having limited oxygen

A

Foetal haemoglobin binds greater concentrations of oxygen and releases it at lower oxygen tensions

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17
Q

What is P50

A

Partial pressure of oxygen at which 50% of haemoglobin is saturated with oxygen

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18
Q

How does the foetal haemoglobin curve for P50 compare with maternal haemoglobin

A

Foetal is shifted higher and to the left

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19
Q

What are the 3 foetal shunts

A

Ductus venosus
Foramen ovale
Ductus arteriosus

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20
Q

What does the ductus venosus do

A

Shunts oxygenated blood from the placenta to the heart, bypassing the liver

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21
Q

How does oxygenated blood travel from the placenta

A

Through umbilical cord to the right atrium, bypassing the lungs

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22
Q

What does the foramen ovale do

A

Shunts blood from the right atrium to the left atrium

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23
Q

What does the ductus arteriosus do

A

Shunts blood from the pulmonary artery to the descending aorta

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24
Q

What does the cardiac cycle represent

A

All the events associated with blood flow through the heart during one complete heartbeat

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25
Q

What is the cardiac cycle

A

Blood is pumped through the 4 chambers. After systole there is a period of relaxation during which the ventricles refill. The atria then contract together to fill the ventricles. The ventricles then contract synchronously without any delay

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26
Q

What is contraction and relaxation

A 
Contraction= systole 
Relaxation= diastole
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27
Q

Give the 5 stages of the cardiac cycle

A 
Atrial systole 
Isovolumetric contraction 
Ventricular ejection 
Isovolumetric relaxation
Late diastole
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28
Q

What is the proportion of blood that enters the ventricles

A

80% when atria are relaxed

20% when atria contract

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29
Q

What is the additional flow of blood from the atria into the ventricles during exercise

A

The atrial boost

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30
Q

Why does some blood go back into the venae cavae

A

There are no one way valves so a small amount is forced back when the atria contract

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31
Q

Where can the retrograde movement of blood to the vena cava during atrial systole be seen

A

In the jugular when someone has their head and chest elevated about 30%

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32
Q

What does it mean if an observable jugular pulse is higher on a sitting person

A

Right atrial pressure is higher than normal

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33
Q

Describe isovolumetric contraction

A

This is ventricular contraction without any change in ventricular volume

Ventricular systole begins as the spiral muscle bands contract and squeeze blood upwards
Blood pushing on AV valves forces them closed
With these valves and semilunar valves closed the blood has nowhere to go so pressure quickly builds

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34
Q

Describe ventricular ejection

A

As the ventricles contract, they generate enough pressure to open the semi-lunar valves and blood is ejected into the arteries.
High pressure blood forces out the low pressure blood, pushing it further into the vasculature
Ventricular blood enters the aorta faster than old blood can leave the aortic tree hence arterial pressure rises and large elastic arteries expand

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35
Q

Describe isovolumetric relaxation

A

After ejection, the ventricles relax and pressure falls rapidly
As pressure falls below aortic pressure, a small amount flows backwards and closes the aortic valve
The final 1/3 of ventricular blood flows away from the heart against a pressure gradient

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36
Q

What is the diacrotic notch

A

A brief rise in arterial pressure when blood flows backwards after ejection

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37
Q

What is late diastole

A

When both sets of chambers are relaxed and ventricles begin to fill with blood passively before atrial systole

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38
Q

What is the simplest direct assessment of heart function

A

Auscultation

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39
Q

What do lub and dub represent

A

Lub- closure of AV valves

Dub- closure of semilunar valves

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40
Q

What does a whooshing sound mean in auscultation

A

Valvular incompetence

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41
Q

What are the 3 main parts of a normal ECG and what do they reflect

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

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42
Q

Why is atrial repolarisation not shown on an ECG

A

It is masked by the QRS

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43
Q

What is the RR interval used to measure

A

Heart rate on an ECG

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44
Q

What can channelopathies affecting myocardial Na and K channels result in

A

Long Q-T syndrome

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45
Q

What was the trouble with the drug Seldane

A

It caused long Q-T syndrome

It was a non sedating antihistamine that binds to K repolarisation channels

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46
Q

What is point A ot the pressure volume loop

A

Ventricle has completed contraction and contains minimum amount of blood. It is relaxed so pressure is at a minimum
Once pressure in the left atrium exceeds that of left ventricle, the mitral valve opens, increasing volume in left ventricle.
Relaxing ventricle expands so volume increases with no change in pressure

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47
Q

What is point B of cardiac pressure loops

A

Ventricle after atrial systole

It now contains maximum volume

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48
Q

What is end diastolic volume

A

When the ventricle is maximally full after relaxation

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49
Q

What happens after point B in loop

A

When ventricular contraction begins, mitral valve closes. As both valves are closed, pressure increases dramatically with no change in volume

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50
Q

What is point C on loop

A

Isovolumetric contraction

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51
Q

How is point D reached

A

Aortic valve opens so volume falls rapidly

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52
Q

What is end systolic volume

A

The blood left at the end of ventricular contraction

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53
Q

What does the width of the heart pressure volume loop represent

What about the area

A

Difference between EDV and ESV (ie the stroke volume)

Ventricular stroke work

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54
Q

How is point A returned to?

A

Isovolumetric relaxation

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55
Q

What is aortic stenosis

A

When left ventricular emptying is impaired due to high outflow resistance caused by reduction of valve orifice area when it opens
This increases the pressure gradient across aortic valve such that systolic pressure within ventricle is increased
It also increases the force opposing ventricular emptying, increasing end systolic volume

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56
Q

What does heart contractility depend on

A

How much the myocytes are stretched

Stretch α force of contraction

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57
Q

Describe the experiment about increased preload and the Starling Law

A 
Peripheral resistance (afterload) and heart rate are constant, preload is increased. This increases cardiac output and must be solely due to increased stroke volume. 
Ventricular and Aortic pressure is increased as more blood is ejected. This causes ventricular walls to stretch, increasing the EDV and stimulating the Frank- Starling Mechanism
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58
Q

Describe the experiment involving increased afterlaod

A

Heart rate and filling pressures are maintained and peripheral resistance is increased
Heart finds it harder to force blood round the system so there is increases aortic and left ventricular pressure
As it is pumping against greater resistance, stroke volume falls. Also due to having a higher ESV
However EDV will also increase so walls will stretch and will stimulate the Frank Starling mechanism

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59
Q

Increasing the after load has a bi-phasic effect. What does this mean

A

There is an initial fall in cardiac output followed by a recovery of cardiac output

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60
Q

What is the Anrep effect

A

Sustained myocardial stretch activates stretch-dependent Na+/H+ exchangers, bringing Na+ into the sarcolemma and reducing the Na gradient brought about by the NCX.
NCX stops working properly and Ca builds up in the sarcolemma so is taken up by SERCA pumps
This increases Ca induced Ca release and therefore increases force of contraction

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61
Q

Where do both parasympathetic and sympathetic branches to the heart come from

A

The cardiovascular centre in the medulla oblongata

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62
Q

What do impulses from the cardiac accelerator nerves do

A

Releases noradrenaline which binds to β1 receptors on cardiac muscle fibres
At the SAN this increases frequency of contraction
At contractile fibres in the ventricles, noradrenaline increases contractility

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63
Q

What is the positive chrono-tropic effect

A

Increased frequency of contraction

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64
Q

What does it mean to have a positive inotropic effect

A

Increased contractility

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65
Q

How do parasympathetic nerves reach the heart

What do they release

What does it do

A

Vague nerves

Acetylcholine which acts on muscarinic receptors in the nodes

Reduces heart rate but no effect on contractility

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66
Q

What are the endocrine influences on the heart

A

Adrenaline (released from the medulla) acts on β1 receptors to increase frequency and contractility

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67
Q

What is the initial membrane potential of the SAN

…

A

-60 mV

It can depolarise spontaneously

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68
Q

What is the pacemaker potential

What is changed to affect heart rage

A

The SAN’s slowly increasing potential

The slope to get to threshold (~-40 mV)

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69
Q

What is Darcy’s Law

A

Q= ΔP/R

It is the hydraulic equivalent of Ohm’s law

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70
Q

What is perfusion pressure

A

ΔP or Pa-Pv

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71
Q

What is blood flow equivalent to

A

Perfusion pressure
—————————-
Vascular resistance

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72
Q

What is cardiac output equivalent to

A

Blood pressure
————————
Vascular resistance

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73
Q

What is arterial pressure determined by

A

Cardiac output and vascular resistance

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74
Q

What does cardiac output =

A

Stroke volume x heart rate

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75
Q

Why does blood lose energy as it flows

A

Friction from the walls

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76
Q

Describe laminar flow

A

The flow of a liquid through a tube can be thought of as parallel streams, with the stream closer to the wall being the slowest because there is the greatest friction and the subsequent layers slide past at increasing velocities.

In a Newtonian fluid this forms a parabola

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77
Q

How is the parabola of laminar flow different in blood from water

A

Is is blunter in blood

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78
Q

In addition to friction, what 3 factors affect resistance to laminar flow

A 
Tube radius (r)
Tube length (L)
Viscosity (η)
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79
Q

Give Poiseuille’s Law

A

R ~ Lη/r^4

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80
Q

What does Poiseuille’s law mean? (3)

A

1- The resistance to fluid flow offered by a tube increases as the length of the tube increases

2- resistance increases as viscosity increases

3- resistance decreases as radius increases

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81
Q

Capillaries are v small so have a small radius. How do they decrease resistance despite this?

A

They are short (<1mm usually)

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82
Q

Why may capillaries not want to have low resistance

How is this achieved

A

Gives more time for diffusion

Connected in parallel so Have a huge cross sectional area

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83
Q

What is blood viscosity determined by

How is it calculated

A

The ratio of red blood cells to plasma

Haematocrit

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84
Q

Normally viscosity is constant. Why would it change

A

Increases in haematocrit occur with residence at high altitudes

Decreases can occur due to anaemia

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85
Q

What is the Fahræus-Lindqvist effect

A

A decrease in viscosity as the tube’s diameter decreases

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86
Q

Why does the Fahræus-Lindqvist effect occur

A

Erythrocytes move towards the centre of the vessel. This leaves a plasma cell-free layer adjacent to the wall.
As it has fewer red blood cells it’s effective viscosity is lower so reduces resistance to blood flow

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87
Q

How are resistance and radius related

A

R is inversely proportional to r^4

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88
Q

Where does the greatest reduction in pressure occur

A

As blood flows into the arterioles

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89
Q

What characterises the SNS

Consider ganglia and NTs

A

Short pre-ganglion is fibres
Pre-ganglionic NT is ACh
Post-ganglionic NT is noradrenaline

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90
Q

What is the peripheral vascular resistance controlled by

A

Sympathetic nervous system

Contains mostly vasoconstriction nerves

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91
Q

How does noradrenaline affect blood vessels

A

Causes vasoconstriction

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92
Q

What are arterioles and venules innervated by

A

Sympathetic vasoconstrictor nerves

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93
Q

What does constriction of
a) arterioles
b) venules
Mean?

A

a) increased arterial blood pressure due to increased total peripheral vascular resistance
b) increased venous return

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94
Q

What is the most efficient way to dial ye blood vessels

A

Inhibit sympathetic tones

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95
Q

How does adrenaline affect blood vessels

Why is it different

A

Vasoconstriction in peripheral circulation to maintain MAP
However it causes vasodilation in skeletal muscle

Allows us to redistribute oxygen and nutrients to where they are most needed

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96
Q

Can the vasodilator arterial response to ACh change

Why

A

It can become a vasoconstrictor response if the endothelial lining is rubbed away

ACh acts indirectly: ACh stimulates the endothelium to secrete nitric oxide (NO) which causes vasodilation

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97
Q

Is NO stored in the endothelial layer

A

No

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98
Q

How is NO formed in the endothelial layer

A

Arginine is cleaved by NO synthase which is regulated by the intracellular Ca-calmodulin complex.
This means that agents which promote extracellular Ca2+ entry increase the rate of NO synthesis

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99
Q

What is a blood pressure monitor called

A

Syphgmomanometer

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100
Q

How does a syphgmomanometer work

A

Cuff is inflated beyond arterial pressure so blood flow is cut off. Then pressure is released
When pressure falls below systolic arterial pressure, blood flows again. As blood flows through the compressed artery a thumping noise is heard. When it is first heard this is the systolic pressure, and when it disappears is the diastolic pressure.

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101
Q

What is the sound heard on a syphgmomanometer

A

The Korotkoff sound

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102
Q

What does MAP=?

A

D+ (1/3)(S-D)

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103
Q

What is arterial stiffness

A

A measure of the rigidity of blood vessels

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104
Q

Why may arterial stiffness increase

A

With age and disease, vessels deposit calcium and collagen

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105
Q

How can an increase in pulsatility be calculated

A

An increase in the systolic: diastolic pulse (SD ratio)
Or
An increase in Pulsatility Index (S-D/mean)

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106
Q

What does increases PI signify

A

Increases vascular resistance

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107
Q

What does the simplest reflex arc include

A

A sensor which sends information to the brainstem (integrator) via afferent pathways. The integrator sends commands to effector organs via efferent pathways

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108
Q

What are arterial mechanoreceptors usually referred to as

Where are they

A

Arterial baroreceptors

Carotid sinus and aortic sinus

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109
Q

What happens when the carotid baroreceptors are stimulated

A

Send afferent info to the medulla via carotid sinus nerves, which join onto the glossopharyngeal nerve

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110
Q

What happens when the aortic baroreceptors are stimulated

A

Send info to brainstem via the aortic nerve which joins into the vagus nerve

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111
Q

What kind of fibres does the vagus nerve contain

A

Both efferent and afferent

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112
Q

What do baroreflexes do

A

Restore arterial blood pressure to normal

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113
Q

Give consequences of

a) hypotension
b) hypertension

A

a) reduces perfusion of oxygenated blood to tissues

b) damages fragile circulations such as in the brain

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114
Q

What is the reason for the location of each baroreceptor

A

Carotid- maintains blood pressure for the cerebral circulation
Aortic- governs systematic arterial blood pressure homeostasis

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115
Q

Are the baroreceptors finically active?

What does this mean

What stimulates them

A

Yes

They send continuous bursts of APs to the brainstem via their respective afferent pathways

Stretch of the baroreceptor fibres. This increases the frequency of APs triggered

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116
Q

What happens when frequency of APs from baroreceptors increases

A

Stimulation of cardiac inhibitory centre which increases efferent parasympathetic discharge and inhibition of cardiac acceleratory centre

This decreases heart rate and force of contraction so decrease cardiac output

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117
Q

What else does increased AP frequency from baroreceptors cause other than in heart

A

Signals sent to vasomotor centre to reduce sympathetic discharge which leads to a fall in arteriolar and venomotor tone

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118
Q

How can the sensitivity of arterial baroreflex be assessed

A

Measuring heart rate responses to controlled changes such as injecting a vasoconstrictor drug (eg phenylephrine)

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119
Q

What is phenylephrine

A

A synthetic form of noradrenaline which causes peripheral vasoconstriction, thus increasing arterial blood pressure

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120
Q

What is sodium nitroprusside

A

A vasodilator which will cause a fall in blood pressure

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121
Q

When testing baroreceptor sensitivity what can be set up

What should it look like

How can sensitivity be calculated

A

A stimulus response curve, with heart rate on y and blood pressure in x

Sigmoidal

At the maximum slope, Sensitivity = ΔHR/ΔP

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122
Q

What is central re-setting

A

Occurs during defence reaction

A rise in ABP is not accompanied by a fall in heart rate as the baroreflex is reset centrally to operate at a higher pressure

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123
Q

What is peripheral resetting

A

When pressure is raised in a sustained manner, the curve shifts right so the set point changes

This allows greater resting pressure without a sustained increase in AP frequency from baroreceptors but may lead to hypertension

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124
Q

Give an example of peripheral resetting

A

At birth
Foetal ABP is ~40mmHg but a newborn’s is double that
Peripheral resetting shifts from foetal set point to post natal set point

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125
Q

What did Blanco and colleagues discover in 1988

A

Baroreceptor sensitivity decreases with age since the slope diminished from foetal to post natal life

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126
Q

Where are the arterial chemoreceptors

A

Aorta and carotid bodies

They have the same innervation as the baroreceptors

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127
Q

What is peripheral chemoreceptor tissue made of

A

Glomus cells which act as O2 sensors and are stimulated by a fall in PO2 in arterial blood

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128
Q

What do glomus cells contain

A

Lots of mitochondria and dark vesicles, which contain peptides needed for chemotransduction

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129
Q

What is hypoxaemia

A

Environmental hypoxia which results in A fall in arterial PO2 (PaO2)

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130
Q

Does hypoxaemia cause an increase or decrease in AP frequency

A

Increase

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131
Q

What are the axes of the chemoreflex function curve

How is sensitivity found

Where is the set point

A

discharge (y)
PaO2 (x)

Gradient of slope

The end of the curve where it becomes a straight line

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132
Q

What is peripheral chemoreceptor resetting

Give an example

A

Shift of chemoreceptor discharge curve towards a different PO2

Birth

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133
Q

What is the PO2 of adult blood and foetal blood

What does this mean for foetal chemoreceptors

A

Adult: 90-100 mmHg
Foetal: 25-40 mmHg

They have a lower set point and must reset at birth

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134
Q

What happens if the arterial chemoreceptors do not shift their set point at birth

A

They are silenced by the oxygen rich extra uterine environment which may lead to cot death (SIDS)

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135
Q

What are the cardiovascular responses to hypoxia

A

Increased heart rate and blood flow, especially to brain, heart and adrenal glands
Promoted vasodilation in peripheral circulation

136
Q

Describe the experiments of Daly and Scott

A

They induced hypoxia in dogs that were either allowed to breathe spontaneously or mechanically.
In spontaneously breathing dogs, hypoxia elicited an increase in respiratory rate and decrease in femoral vascular resistance
Dogs with controlled ventilation, who were not allowed to hyperventilate, hypoxia produced reduced heart rate and increased femoral vascular resistance

137
Q

What did Daly and Scott conclude

A

Hypoxia elicits Primary chemoreflex cardiovascular responses which became modified by hyperventilation to the secondary response

138
Q

What is the primary chemoreflex cardiovascular response

A

A fall in heart rate and increases resistance

139
Q

How does the body know to do first or second response to hypoxia

A

During hyperventilation, stretch receptors in the lung increase their afferent discharge to the brainstem. The is inhibits Vagal discharge to the heart and sympathetic outflow to peripheral circulation

140
Q

What response is given when an adult mammal dives under water

A

Primary

141
Q

Why does a foetus make breathing movements

A

To develop intercostal muscles and alveoli

142
Q

Why may foetal hypoxia occur

What action does the foetus take to tackle hypoxia

A

Compression of umbilical cord

Ceases to make breathing movements as movement takes up energy

143
Q

During foetal hypoxia, which response is taken

A

Primary (like a diving adult)

There is reduced heart rate and increased femoral resistance

144
Q

Current =

A

g x ΔV

Conductance x voltage difference

145
Q

When are cells more polarised than Ek

A

Almost never

Perhaps in skeletal muscle post fatigue which can hyperpolarise beyond Ek due to Na pump activatity

146
Q

Why do inward rectifiers never conduct inwards

A

K+ currents are always outwards

147
Q

The conductance of an inward rectifier increases as…

A

The electro-chemical gradient becomes less outwards

148
Q

Simply, how do inward rectifiers work

A

Like a swing door that only opens inwards- small amounts of extracellular K can get in but if lots of intracellular K is present the door slams shut

149
Q

When do inward rectifiers conduct well and poorly in the cardiac cycle

A

Conduct well at resting potential as this is close to Ek

But conduct a lot less well in plateau phase when Vm&raquo_space; Ek

150
Q

Why do inward rectifiers have low conductance in the plateau phase

A

Prevents too much K+ being lost

151
Q

Why is the current of K+ small when Ek is close to Vm

A

Ik= gk(Vm-Ek) so Ik is small here

152
Q

Why is Ik small at plateau phase

A

gk is small

153
Q

Describe Guyton’s experiments

WhAt did he find

A

He replaced dog’s hearts with high output pumps

Reducing pumping capacity below normal reduced CO
Increasing pumping capacity did not increase CO

154
Q

What concepts did Guyton’s experiments show

A

The heart is necessary to maintain CO but it does not normally limit CO

155
Q

Flow=?

A

Pressure gradient
—————————
Resistance

156
Q

What happens if Pv (venous pressure) becomes negative relative to atmospheric pressure

A

Tubing will collapse

157
Q

Why does increasing heart rate or contractility in isolation not increase cardiac output

A

The heart can not increase increase arteriovenous pressure gradient beyond the point where Pv becomes negative as this would collapse veins and limit venous return and hence cardiac output

158
Q

What is the main determinant of cardiac output

A

Mean systemic filling pressure

159
Q

What must you do to increase arterial pressure?

Why can you not do this?

What, then, is the solution?

A

To increase Pa you must decrease Pv

Pv=0 usually so would become negative If decreased

Increase mean systemic pressure

160
Q

How do you increase mean systemic pressure

A

Filling circulation or venoconstriction

161
Q

What volume of blood is the stressed volume

A

~20%

162
Q

Are veins compliant

What happens if they get too stretched

A

Yes very

They become stiff

163
Q

As blood is pumped from the veins to the arteries, is the venous fall in pressure greater than the arterial increase in pressure

A

No as veins are much more compliant than arteries (almost 10-fold)

164
Q

How to calculate compliance

A

ΔV/ΔP

165
Q

What is maximum arteriovenous pressure gradient set by

What does this imply? (2)

A

Mean filling pressure

1) The heart cannot change the mean pressure
2) Mean pressure determines maximum cardiac output

166
Q

Cardiac output=?

A

(ABP- RAP)
——————
TPR

167
Q

How is ABP-RAP created and limited

A

Created by the heart and limited by MSFP

168
Q

What is TPR

A

Total Peripheral Resistance: treats all vascular pathway resistance as one resistance but is primarily determined by arteriolar resistances

169
Q

Why is RAP often excluded from CO equation

A

It is v small

170
Q

How is CO measured by the body

A

It is not directly measured

It is instead regulated to maintain ABP

171
Q

Why would an increase in MSFP increase RAP, if CO was constant?

A

Pressure would increase throughout the system so greatest % increase would be in the right atrium where P was initially lowest

172
Q

In reality what happens if RAP increases

A

Stroke volume would increase (Frank-Starling) and so CO would increase. This would ensure RAP stays close to 0

173
Q

Why does increased TPR not decrease CO

A

Increased TPR=increased afterload which results in ventricular stretch (Frank Starling) so SV and CO remain constant

174
Q

What happens if heart rate increases in isolation

A

SV drops and CO barely changes as the heart cannot pull blood from the venous circulation

175
Q

How can you double MSFP

A

Increase blood volume by 20% (this doubles the stressed volume)

176
Q

What happens if you increases blood volume by 20%

A

Doubles MSFP

Doubles CO

177
Q

What happens if 20% of blood is lost

What stops this happening

A

MSFP is reduced to zero

As 60% of blood is in the venules and small veins, venoconstriction means MSFP can be maintained until about 40% of circulating volume is lost. Venoconstriction can triple MSFP

178
Q

Why does venoconstriction not really affect TPR

A

TPR is primarily determined by arterioles

179
Q

Why does arteriolar constriction not affect MSFP

A

<1% of blood is there

180
Q

Why is venous return reduced by increased RAP

When is VR=0

A

VR = (MSFP-RAP)/RvR

When MSFP=RAP

181
Q

How does a decrease in RAP affect VR

A

VR increases

182
Q

Are VR and CO equal

Why

A

Yes they must be

The heart cannot create or store blood

183
Q

What is RvR

Can it change

A

Resistance to venous return

It can, especially in exercise, but isn’t specifically regulated

184
Q

Why does it appear as if venous return drops as RAP increases

A

Difference between MSFP and RAP gets smaller

185
Q

How would raising MSFP affect the RAP vs VR graph

What would happen if you reduced RvR

A

It would shift upwards

Increase the slope without changing MSFP (ie root of the function wouldn’t change)

186
Q

Why does increasing RAP increase CO

A

Frank Starling

187
Q

What to remember about CO and VR vs RAP curves

A

MSFP only shifts VR curve

TPR only shifts CO curve

188
Q

What is shock

A

When cardiac output is inadequate to supply sufficient metabolic substrates for aerobic respiration

189
Q

What is hypovolaemic shock

A

Severe loss of circulating volume

190
Q

What is cardiogenic shock

What’s distributive shock

A

Shock caused by cardiac pathology

Shock due to a severe fall in vascular tone

191
Q

How to find MSFP on VR vs RAP graph
Or
CO vs RAP graph

A

X intercept

192
Q

Describe the process of systolic blood pressure to diastolic BP

A

The heart rapidly ejects blood into the aorta, causing pressure to rise to a peak (systolic BP) and creating a pressure gradient so blood flows away from the aorta and pressure drops to a trough (diastolic BP)

193
Q

What are the usual values of systolic and diastolic blood pressure

A

120-80mmHg

194
Q

How to calculate mean blood pressure from pressure wave

A

Diastolic pressure + 1/3 of pulse pressure

195
Q

How to calculate pulse pressure

A

Systolic - diastolic BP

196
Q

How does mean BP change with age and between genders

A

Increases with age

Higher in men

197
Q

Why does pulse pressure increase in exercise

How does this affect mean pressure

A

Blood flows away faster in diastole when TPR drops

Mean pressure stays constant as systolic pressure increases as diastolic pressure decreases

198
Q

ABP=?

A

CO x TPR

199
Q

What are the 3 mechanisms for monitoring blood pressure

A

High pressure baroreceptors
Arterial chemoreceptors
Low pressure baroreceptors

200
Q

Where are elastic lamellae found

A

Intermeshed with stretch sensitive nerve endings in regions with little collagen and smooth muscle in baroreceptors

201
Q

Do the baroreceptors all deal with the same pressure changes

A

No
Carotid sinus is more sensitive than aortic
Between them they cover 50-200 mmHg

202
Q

Describe Heymans’ Nobel Prize winning experiment

A

Carotid sinus of Dog B was connected to circulation of Dog A. A was given noradrenaline, increasing its BP and this triggered an immediate reflex fall in BP in B

203
Q

What happens to ABP if arterial baroreceptors and chemoreceptors are denervated

Why

Why is this important

A

ABP becomes much more more variable but mean ABP remains constant

Variability is due physiological changes such as changes in posture
Constancy of mean suggests it is also controlled by other mechanisms

Demonstrates importance of high pressure baroreceptors and chemoreceptors in the short term control of ABP

204
Q

When do arterial chemoreceptors affect ABP

A

ONLY When BP is very low or when PO2 is massively reduced

205
Q

How do medullary chemoreceptors detect high arterial CO2

A

Reduction in brain pH

206
Q

Where else to stretch detectors exist

What are these areas called

A

Low pressure areas
Eg junction of atria and corresponding veins

Cardiopulmonary baroreceptors

207
Q

What do cardiopulmonary baroreceptors detect

What happens if they are denervated along with aortic/ carotid denervation

A

RAP

if RAP is raised, it suggests the circulation is over filled such that the heart can not maintain low venous pressure

Mean ABP rises as well as increases variability

208
Q

What does low RAP suggest

A

CO is working maximally for the current MSFP

209
Q

What happens when cardiopulmonary baroreceptors are triggered

A

As pressure increases, Firing rate increases Along vagus to nucleus tractus solitarius (NTS) in the medulla and then onto hypothalamus.
Fluid and Na are retained, raising circulating volume and MSFP

210
Q

How can a drop in ABP before exercise be avoided

A

Inputs to the medulla from the cortex (where the decision to exercise is taken), from the cerebellum (as part of the coordinated motor programme) and from muscle and joint receptors

211
Q

Describe sympathetic efferents controlling ABP

A

Bulbospinal pathways activate glutamatergic synapses between T1 and L3.
These pre-ganglionic neurons have nicotinic synapses with nerves of prevertebral and paravertebral ganglia.
Post ganglionic nerves run with large blood vessels to muscular arteries, arterioles and veins
Sympathetic activity generally causes vasoconstriction through noradrenaline on α1 adrenoreceptors

212
Q

a) What does arteriolar vasoconstriction increase

b) What about venoconstriction

A

a) increases TPR

b) increased MSFP

213
Q

What is the resting potential frequency of sympathetic vasoconstrictor nerves

Why is resting frequency not 0

A

1-4 Hz but can raise to 10Hz to reduce flow to almost 0

So sympathetic inhibition can reduce ABP
Also means that damage to a nerve will reduce BP there

214
Q

What do chromaffin cells do

A

Release adrenaline which acts similarly to sympathetic innervation (by acting on α1 receptors)

215
Q

Does adrenaline affect all organs equally

A 
No 
Some tissues (notably coronary blood vessels and skeletal tissue) have more β2 than α1 so vasodilation occurs here
216
Q

How do we know Vagal stimulation to the heart shows tonic activity in slowing heart rate

A

Inhibition of the vagus at rest using atropine produces accelerated heart rate

217
Q

TPR can fall by upto 6 times during exercise. How is ABP maintained

A

CO must be increased, requiring venoconstriction to increase MSFP, as well as reduced Vagal and increased sympathetic heart stimulation

218
Q

What is hypertension

Why is it a problem a

A

ABP>140/90mmHg

Leads to overwork of the heart and vessel damage

219
Q

What is atherosclerosis

A

A build up if inflammatory lipid deposits beneath vessel endothelium

220
Q

How does atherosclerosis cause problems

A

Narrowing of blood vessels, restricting flow

Endothelial damage (prompting thrombosis): local and distant blockage

Weakening of vessel walls, leading to aneurysm

221
Q

What is the difference between the cardiac hyper trophy caused by exercise vs hypertension

A

Exercise causes eccentric hypertrophy where ventricular volume increases with muscle mass

Hypertension causes concentric hypertrophy where the heart expands inwards, reducing ventricular volume

222
Q

Give the 3 main problems of concentric hypertrophy

A

Increased myocardial demand

Diastolic disfunction (cardiac filling and stroke volume is impaired)

Increased risk of arrhythmia

223
Q

What is systolic dysfunction

A

When the heart is unable to fully empty

224
Q

Why can flow only be regulated by resistance

A

Flow=pressure gradient/ resistance

As pressure gradient is constant, flow can be determined by regulating upstream arteriolar resistance

225
Q

What are the 3 principles mechanisms for regulation of arteriolar resistance

A

Nerves
Hormones
Local tissue metabolism

226
Q

Why is CO usually proportional to VO2 (volume of oxygen used per minute)?

How can this knowledge be used?

A

Cardiac output ~ VO2

VO2 can be used as a proxy for CO in Studies of atheletes

227
Q

Flow is always a function of ____ and ____

A

Pressure gradient and resistance

228
Q

Give the equation for flow through a capillary bed downstream from a single arteriole: Q=…

A

Pa-Pv
———————
R(pre) +R(cap) +R(post)

229
Q

What can flow through a capillary bed downstream of a single artery be simplified to

Why

A

Q~ 1/Ra

Arteriolar resistance makes up 70% of total series resistance and is the only directly regulated resistance and the pressure gradient is constant

230
Q

What is Ra

How does this differ from central, autonomic control of arteriolar resistance

A

Ra = local control of arteriolar resistance

Ra matches local blood flow to local metabolic demand whilst central control deals with TPR to maintain Constant mean ABP

231
Q

What forms does local Vaso-control take

What forms does central control take

A

Local: metabolic, myogenic, or from vasoactive compounds released by capillary endothelium

Central: neurogenic or endocrine

232
Q

How is arteriolar smooth muscle arranged

A

Circumferentially

233
Q

What is tension in vascular smooth muscle a function of

A

Ca2+ concentration as well as modulation via phosphorylation of Myosin Light Chain Kinase

234
Q

What are the 2 broad intracellular control systems that all control pathways for vascular smooth muscle converge on?

A

Regulation of myosin binding site of actin by caldesmon and regulation of myosin light chain kinase by phosphorylation

235
Q

What is functional hyperaemia simply

A

A profound increase in blood flow after circulation has been cut off for some time

236
Q

Which changes of the blood typically accompany increases metabolism

What do these factors promote

A 
Reduced PO2
Increased PCO2
Decreased pH
Increased adenosine
Increased extracellular K+

Vasodilation of systemic arterioles

237
Q

Do reduced PO2 and increased PCO2 affect all circulations equally

A

No
It promotes vasodilation of arterioles in skeletal muscle
But
Promotes vasoconstriction in pulmonary circulation where such changes reflect poor ventilation

238
Q

Which changes accompany aerobic metabolism

What do these stimulate? What is this a direct effect of?

A

Decreases pH
Increased lactic acid concentration

Vasodilation

Intracellular pH on smooth muscle

239
Q

Does phosphorylation of MLC promote or inhibit binding to actin

What happens if it is phosphorylated when bound to actin

A

Promotes

Latch bridge formation can occur

240
Q

When can MLC be phosphorylated

A

When MLCK is activated by Ca-calmodulin (uses ATP)

241
Q

What happens if pressure changes in cerebral vascular beds

What does this mean

Why may this lead to problems

Which other vascular beds act like this

A

Vascular diameter changes to reduce flow change

Increases pressure leads to increased resistance and flow increases much less than expected

It may cause poor lymphatic drainage

In the heart and kidneys

242
Q

Where is the optimal place to detect local changes in metabolism

A

Capillary endothelium

243
Q

What was nitroglycerin

What are the side effects

A

Angina drug

Causes severe headaches

244
Q

Adrenaline acts on α1 receptors. What else does it act on, causing vasodilation, and what are these linked to?

A

β2 receptors which are linked to the G protein Gαs, which activates adenylate cyclase, raising cAMP levels and activating PKA

245
Q

What does PKA do

A

Phosphorylates myosin light chain kinase, reducing its activity and so reducing phosphorylation of MLC

246
Q

What are eicoanoids

A

Arachnidonic acid derivatives, mostly involved in clotting and inhibitory responses

247
Q

How are eicosanoids synthesised

What is the clinical significance of this enzyme

A

By cyclo-oxygenase

It is inhibited by aspirin

248
Q

2 forms of prostaglandins

A

Vasoconstrictory

Vasodilatory

249
Q

What is thromboxane A2

What opposes it

A

An eicosanoid produced by platelets and a very potent vasoconstrictor

Prostacyclin (produced by the endothelium)

250
Q

What is the rationale behind using aspirin to prevent MI

A

It irreversibly blocks COX-1, which is required to produce thromboxane A2 and prostacyclin.
However, endothelial cells have nuclei but platelets don’t. Therefore, endothelium can produce more prostacyclin (which opposes clotting) but thromboxane A2 is significantly diminished so the chance of thrombosis is decreases

251
Q

As exchange between tissue and capillaries occurs, it exchange rate falls. How is this opposed?

A

Blood flows to deliver fresh plasma restoring the concentration gradient

252
Q

How many capillaries perfuse at rest

A

20-24%

253
Q

How do ions and water get through capillary walls

A

Water can pass through cells via aquaporins (AQP1) and between cells

Crystalloids ONLY diffuse between cells

254
Q

How do colloids diffuse through capillary walls

What if this goes wrong

A

They don’t (capillaries are normally impermeable to colloids such as plasma proteins)

Protein permeability can increase inflammation

255
Q

How are capillaries classified

A

According to their “leakiness”

256
Q

Name the 3 types of capillary

A

Continuous

Fenestrated

Sinusoidal

257
Q

Discuss continuous capillaries

A

Most common variety with interendothelial junctions about 10-15nm wide, allowing relatively easy passage of water and ions

258
Q

Where are continuous capillaries different

A

Brain and testes where interendothelial junctions are very tight

259
Q

Where are fenestrated capillaries found

How are they specialised

A

Epithelia such as small intestine

They have fenestrae (“windows”) through the cells to allow ion diffusion through as well as around

260
Q

Discuss sinusoidal capillaries

A

Found in liver

Large gaps between cells as well as fenestrae to allow trans-endothelial passage of proteins

261
Q

What is Fick’s Law

What is each term

A

Q=AP([X]c - [X]if)

Q= flow
A= capillary surface area
P= permeability
[X]if= concentration of X in intestinal fluid
[X]c= concentration of X in capillary
262
Q

How to increase capillary surface area

A

Increase number of capillaries that are perfusing in a tissue

263
Q

Can capillary permeability change

A

Yes

Endothelial cells can change shape such as increases leakiness in response to histamine as part of inflammatory response

264
Q

What does capillary concentration of X depend on

A

Rate of delivery into capillary (capillary blood flow x arterial concentration)
Rate of extraction from capillary (Q)

265
Q

How to calculate rate of delivery to capillary

A

capillary blood flow x arterial concentration

266
Q

What does [X]if depend on

A

Rate at which X is used

Rate of extraction from capillary

267
Q

Is water movement across capillary walls diffusive

A

No it is convective

The driving force is hydrostatic pressure difference (ΔP) and Δπ (effective osmotic pressure difference)

268
Q

How does capillary hydrostatic pressure change along a capillary

A

It drops due to resistance and water movement

269
Q

Can Pif be negative

A

Yes In non encapsulated organs

270
Q

What exerts osmotic pressure

A

Only solute that cannot easily cross the capillary wall ie the colloid

271
Q

What does “colloid” include

What is their total concentration

A

Albumin
Globulins
Fibrinogen

1.5 mM

272
Q

What was Starling’s equation (for capillaries!)

What does each term mean

A

Jv = K((Pc-Pif)-σ(πc-πif))

Jv= volume flow
K= hydraulic permeability
σ= colloid reflection coefficient
The rest is just net filtration pressure (ΔP-Δπ)

273
Q

What is σ

A

A factor between 0 and 1 to account for capillary leakiness

274
Q

What does a σ of 1 mean

A

Total impermeability to protein so full osmotic pressure is exerted

275
Q

What happens to pressure at the venous end of capillaries in feet when standing

A

Increases

276
Q

How does capillary pressure relate to venous and arterial pressure

Why

A

Closely follows venous but not arterial

Pc must always be greater than venous pressure however high resistance arterioles between arteries and capillaries, high ABP is not associated with increases capillary blood flow or increased Pc

277
Q

Does reduced ABP lead to reduced Pc

Why

A

Yes

Directly (resistance in arterioles) and sympathetic drive for arteriolar resistance/ vasoconstriction

278
Q

What is autotransfusion

A

When tissue fluid helps buffer blood volume after a drop in Pc

279
Q

Why does haematocrit drop after blood loss

A

Tissue fluid dilutes blood to maintain blood volume

280
Q

Usually there is a net outward movement of water from capillaries. Why do we not all swell up

A

Lymphatic system drains the tissues

281
Q

Where do fluids return from the lymphatic system to the venous

A

Via the thoracic duct at the subclavian veins

282
Q

How do initial lymphatics prevent water escaping

A

They have many interendothelial junctions behaving as microvalves allowing fluid in but not out. These empty into larger lymphatics which have valves and some smooth muscle

283
Q

What is lymphoedema

A

When lymph drainage is blocked

284
Q

What is interstitial oedema

A

When rate of filtration of fluid out of capillaries exceeds its removal of lymphatics And fluid collects in the interstitium

285
Q

Why is oedema bad

A

Increases distance of capillaries to tissues interfering with solute exchange

286
Q

What happens in severe end stage. Heart failure

A

Failure to adequately perfuse organs resulting in organ failure

287
Q

What is the heart’s job on the most basic level?

What does “heart failure” imply?

A

To pump blood from veins to arteries

Atrial pressure is too high and arterial pressure is too low

288
Q

What should RAP be and why

A

Close to 0 otherwise it impedes venous return

289
Q

Why is it possible to find hypertension and heart failure in the same patient if “heart failure” involves a ABP that is “too low”?

A

Heart failure occurs and ABP is lower than the set point and it cannot be raised

290
Q

What happens when ABP is lower than the set point and cannot be raised

A

The body responds as it does to a haemorrhage
It increases sympathetic drive causing venoconstriction, vasoconstriction, and retention of fluids.
This raises TPR and MSFP.

291
Q

What happens when TPR is raised in heart failure?

MSFP?

A

Increased TPR means increasing cardiac workload

CO is normally limited by MSFP but in heart failure CO is limited by the heart so increasing MSFP makes v little difference. Instead atrial pressure will rise

292
Q

What do the symptoms of heart failure result from

A

1) inability to adequately raise CO

2) increases atrial pressure

293
Q

What is the problem with increases atrial pressure

A

It implies raised venous pressure and therefore raised capillary pressure which leads to oedema

294
Q

Difference between pulmonary and peripheral oedema

A

Pulmonary is left side heart failure

Peripheral is right side heart failure

295
Q

How can heart failure be treated if the valves are fine

A

Drugs that inhibit responses to low BP such as ACE inhibitors, diuretics and beta adrenergic blockers

These lower MSFP and TPR thus reducing oedema and cardiac oxygen demand

296
Q

What is functional hyperaemia

A

Increased blood flow to muscles to meet increased metabolic demand

297
Q

What are the distinct phases of functional hyperaemia

A

Phase I~ very rapid increase in blood flow from 2-20 seconds after initiation of contractions

Phase II~ from about 20s about contractions during which there is a slow increase in blood flow to sustained high levels

298
Q

How do we know that increased extracellular K+ is a factor of Phase one in hyperaemia

A

Muscle APs produce immediate increases in extracellular [K+]

299
Q

What is the effect of interstitial [K+] increase in Phase I of hyperaemia

A

It hyperpolarises arteriolar smooth muscle, closing VG Ca2+ channels , thus relaxing the muscle

300
Q

What is the expected result of raised extracellular [K+]

What actually happens in Phase I and why

A

Depolarisation

Hyperpolarisation occurs
Raised [K+] enhances Na/K ATPase activity
And enhances activation of inward rectifying K+ channels
(Therefore intracellular K+ and K+ permeability both increase)

301
Q

How do we know that increased extracellular K+ is a factor of Phase one in hyperaemia

A

Muscle APs produce immediate increases in extracellular [K+]

302
Q

What is the effect of interstitial [K+] increase in Phase I of hyperaemia

A

It hyperpolarises arteriolar smooth muscle, closing VG Ca2+ channels , thus relaxing the muscle

303
Q

What is the expected result of raised extracellular [K+]

What actually happens in Phase I and why

A

Depolarisation

Hyperpolarisation occurs
Raised [K+] enhances Na/K ATPase activity
And enhances activation of inward rectifying K+ channels
(Therefore intracellular K+ and K+ permeability both increase)

304
Q

How can vasodilation in phase I of hyperaemia be reduced and by how much?

A

Blockade of Na/K ATPase (by ouabain) or of inward rectifiers (using barium)

Upto 60%

305
Q

What are the 2 fast causes of functional hyperaemia

A

Increased extracellular K+

Muscle pump

306
Q

What is muscle pump

A

Contractions accelerate venous return

This enhances CO but may reduce local venous pressure which enhances pressure gradient through capillaries

307
Q

In some animals but not in humans (🙄) what else plays a role in phase I?

What happens in the cat?

A

Neurogenic vasodilation

Sympathetic cholinergic nerves cause a direct increase in blood flow

308
Q

How does adrenaline affect phase I

A

Causes vasodilation: it may not be fast enough to contribute to phase I but could be an anticipatory response

309
Q

Is Phase II controlled by one main factor

How do we know

A

No

Multiple redundancies exist, meaning inhibition of one factor changes magnitude of hyperaemia slightly but other factors compensate for it

310
Q

How does increased extracellular K+ affect phase II

A

It is important?

311
Q

How likely is a direct effect of reduced PO2 on muscle arterioles during hyperaemia and why?

A

Although PO2 falls in capillaries during exercise, it does not fall in the vicinity of arterioles

312
Q

What does increases offloading of O2 from haemoglobin during hyperaemia lead to? (2)

A

Release of ATP and NO from red blood cells

Low O2 enhances ectonucleotidease activity that produce vasodilatory adenosine from ATP

313
Q

What does adenosine do in hyperaemia

A

Accumulates around active muscle fibres

It is a strong vasodilator, acting on A2A receptors, increasing cAMP levels in smooth muscle

314
Q

How is pH linked to vasodilation

A

ATP is released partly via CFTR channels in response to reduced intracellular pH

315
Q

What happens when cAMP levels rise in smooth muscle

A

PKA is activated which opens K(ATP) channels which hyperpolarises the cell, acting synergistically with increased K+

316
Q

What is the effect of lactic acid on hyperaemia

A

No direct effect that is distinct from it effect on pH

317
Q

What happens to TPR during exercise

What does this necessitate? How is this achieved?

A

Drops to ~20% of its resting value

An increase in CO to maintain ABP
Sympathetic venoconstriction, reduced cardiac Vagal stimulation and increased myocardial sympathetic stimulation

318
Q

How is resistance to venous return reduced in exercise

A

The muscle pump

319
Q

How much do MSFP, VR, and CO change in exercise

How does the muscle pump affect RvR

How do all the above factors affect ABP

A

MSFP: increases 3x
VR and CO: increase 6x

RvR is halved

ABP actually increases in exercise

320
Q

How can you separate central command to exercise from actual occurrence

What does this indicate

A

Using curare to block the NMJ

Heart rate increases without actually exercising

321
Q

What is the role of baroreceptors in exercise

A

Maintain stability of BP around a raised set point

322
Q

How would you test to see if O2 uptake is the limiting factor in exercise

What is the result

A

Measure performance at normal and raised levels of PO2

Raising inhales PO2 does not significantly improve performance

323
Q

How would you test to see if The ability for muscles to perform is the limiting factor in exercise

What is the result

A

Compare power output when pedalling an exercise bike with 1 leg vs with 2 legs

With 2 legs it is less than double with 1
This suggests during 2 legged muscles are not able to reach maximum output

324
Q

What is the ultimate limitation on whole body power output in exercise

A

Circulation

325
Q

The response to haemorrhage usually comprises of which 2 stimuli

A

Reduced blood volume

Pain

326
Q

Uncompensated blood loss causes, sequentially…

A

Reduction in blood volume, MSFP, venous return/ CO, and blood pressure

327
Q

How does the body respond to blood loss

A

Arterial and low pressure baroreceptors detect these changes, reducing inhibition of medullary vasomotor areas

328
Q

Other than baroreceptors, how else may medullary vasomotor areas be stimulated?

A

Cortex and hypothalamus May stimulate the medulla as a response to pain/ fear

329
Q

What is the response once medullary vasomotor centres are stimulated in haemorrhage

What is the overall effect

A

Sympathetic nerves increase arteriolar and venous tone and heart rate (Vagal Tone to heart falls)
Catecholamines, angiotensin II and ADH are released

Vasoconstriction

330
Q

What are the micro vascular changes after haemorrhage

A

1) reverse stress relaxation (when smooth muscle contracts when stretch is reduced)
2) mobilisation of tissue fluid as reduced Pc shifts the balance of Starling forces towards reabsorbtion of fluid

331
Q

What happens long term and then even longer term after haemorrhage

A

10 minutes: renal conservation of water and salt. Thirst and sodium appetite act to restore circulating volume

24-48 hours: plasma proteins are replaced by synthesis in the liver

5-7 days: increases RBC production replaces those lost

332
Q

How is increased red blood cell production stimulated

A

By a release of erythropoietin from kidneys in response to reduced O2 delivery

333
Q

What was the triggering event for public awareness for cardiovascular disease

A

Death of Franklin D Roosevelt whose blood pressure had soared to 300/190 in 1945

The Framingham Heart Study (1948) resulted from this

334
Q

Who realised the cardiovascular system is a closed circulatory system

A

William Harvey

335
Q

Name an adaptation of the heart that compensates for the high oxygen demand

A

Cardiac myocytes contain more myoglobin than skeletal muscle cells

HOM (11 decks)

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