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Cardiovascular Health > Unit 1: Cardiovascular System > Flashcards

Unit 1: Cardiovascular System Flashcards

1
Q

Describe the pericardium

A

Its a fibrous sac of connective tissue. Its compose of 2 layers;

  1. Fibrous pericardium - outermost layer
  2. Serous pericardium - lies deep to the fibrous pericardium
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2
Q

Describe the serous pericardium. State its function

A

Has parietal and visceral layers.
Outer layer of serous pericardium = parietal layer
Inner layer of serous pericardium= visceral
Function=acts as mechanical protection for the heart and big vessels, and a lubrication to reduce friction between the heart and the surrounding structures. It secretes fluid which lubricates the heart

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3
Q

What exists between the parietal and visceral layers of the serous pericardium?

A

Pericardial cavity which contains pericardial fluid

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4
Q

Outline how inflammation can affect pericardial function (Pericarditis)

A

Pericarditis is the inflammation of the pericardium, a thin, two-layered sac that surrounds the heart. The layers have a small amount of fluid between them to prevent friction when the heart beats. When the layers are inflamed, it can result in chest pain. Recurrent inflammation leads to scarring of the space between the 2 layers of the pericardial sac

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5
Q

What’s another name of the visceral layer of the serous pericardium?
What lies deep to the epicardium? Describe it.

A

Epicardium

Myocardium - cardiac muscle. It is the thickest section of heart wall. Contains cardiomyocytes

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6
Q

What is the septum of the heart?

What is atrial septal defect (ASD), VSD and AVSD?

A

Septae separates left and right sides of the heart
ASD - abnormal connection between left and right atria as the septae are not fully formed at birth
VSD - abnormal connection between left and right ventricles as the septae are not fully formed at birth
AVSD - large hole in the atrial & ventricular portion of the septum

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7
Q

Name the atrioventricular valve located between the RA and right ventricle (RV

A

Tricuspid valve

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8
Q

State the function of the right atria and whether the blood is oxygenated or deoxygenated.
State the fucntion of the coronary sinus

A

The RA receives venous return (VR) from the systemic circulation via the “Great Veins” (Superior vena cava (upper body), inferior vena cava (lower body and also from the coronary sinus. The coronary sinus also delivers deoxygenated blood from the myocardium

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9
Q

State the function of the right ventricle

A

Delivers deoxygenated blood to the lungs via pulmonary arteries

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10
Q

Function of the left atria?

A

Receives oxygenated blood from the lungs via the pulmonary veins

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11
Q

Function of the left ventricle?

Name the valve in this chamber

A

On contraction of the heart (SYSTOLE) the LV ejects blood into the systemic circulation via the aorta and pulmonary trunk
Aortic valve

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12
Q

How are the structures of the chorda tendinae and papillary muscles related to their function?

A

There are 5 papillary muscles in the heart originating from the ventricular walls. These muscles attach to the tricuspid and mitral valve leaflets via the chordae tendineae and functionally prevent regurgitation of ventricular blood via tensile strength by preventing prolapse or inversion of the valves during systole

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13
Q

Describe the funciton of the coronary arteries

A

The coronary arteries supply essential nutrients
and oxygen to the highly aerobic cardiac muscle fibres. The heart muscle must receive blood directly via its
own specific blood supply – i.e. the coronary circulation. Healthy coronary arteries are essential
to normal cardiac muscle functioning

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14
Q

Describe the left coronary artery

A

runs towards the left side of the heart where it divides into its 2 main branches:
⇒ The anterior descending branch (anterior interventricular artery) – supplying the interventricular septum and the anterior walls of both ventricles.
⇒ The more minor circumflex artery – which supplies the left atrium and posterior aspect of the left ventricle

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15
Q

Describe the right coronary artery

A

Supplies blood to the wall of the RV and part of the posterior LV.
Also supplies the SAN, AVN, Bundle of His

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16
Q

Describe the impact of few anastomoses (interconnecting vessels) between coronary arteries

A

There are very few of them. This means that if there is a sudden occlusion of a coronary artery all
the myocardial fibres distal to the occlusion and dependent on the blocked vessel may potentially
die (myocardial Infarction)

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17
Q

What anatomical location of the heart are the coronary arteries located?

A

The coronary arteries lie in the epicardium of the heart, but give off smaller branches that perpendicularly penetrate the myocardial muscle mass travelling towards the endocardium.

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18
Q

Describe the coronary artery blood flow

A

Blood flow is intermittent. During the
contractile phase of the ventricles – (systole), intra-muscular pressure compresses the coronary
arteries stopping blood flow. As a consequence significant coronary artery blood flow and therefore
myocardial perfusion only occurs during diastole (relaxation phase of the cardiac cycle). The
myocardium makes up for this intermittent pattern of coronary artery perfusion by being extremely
efficient at extracting O2 from the coronary blood supply. This efficiency can be demonstrated by
examining the resting a-vO2 difference of coronary blood and comparing it to the a-vO2 difference
of skeletal muscle blood

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19
Q

What is a-vO2?

A

Difference in O2 content in arterial compared to venous blood. When the arterial O2 content supplying a tissue is recorded directly and compared to the O2 content of venous blood leaving the tissue, the difference corresponds entirely to the amount of O2 extracted and utilised by that tissue

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20
Q

What is the a-vO2 of skeletal muscle and of cardiac muscle?

A

The a-vO2 difference in blood from skeletal muscle at rest is 25% - venous blood is therefore still very oxygenated (~75%). Coronary artery blood: a-vO2 difference is 65 – 70 % at rest.

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21
Q

Why does the myocardium need more O2 upon exercise?

A

This is because the heart;

  • beats faster (which requires more energy use – i.e. ATP production which in turn requires a greater supply of O2)
  • It contracts more forcefully (which requires more energy use – i.e. ATP production which in turn requires a greater supply of O2)
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22
Q

How does the myocardium get more O2 during exercise?

A

the coronary arteries just vasodilate. The smooth muscle in the wall structure relaxes which increases the size of the arterial lumen. Increasing the dimensions of the coronary artery lumens increases the volume of blood, which can pass through the arteries and therefore be delivered to the myocardium

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23
Q

What is the trigger for coronary artery vasodilation?

A

O2 deficiency and CO2 excess

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24
Q

What is the function of the cardiac fibrous skeleton?

A
  1. Reinforces vessel exit points (at the aorta and pulmonary trunk)
  2. Reinforces valves which are anchored into the fibrous skeleton
  3. Forms a non-excitable zone between atria and ventricles to prevent spontaneous electrical/mechanical activity of the 2 hemispheres of the heart
  4. Acts as a tendon and orientates muscle fibres
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25
Q

What 3 types of cells exist in the myocardium?

A
  1. myocardial / myocytes cells
  2. pace-maker cells
  3. cells of the intrinsic cardiac conducting system (ICS)
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26
Q

WHat are excitable cells?

A

Are polarised when at rest/inactive, can become depolarised and they produce action potentials

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27
Q

Define the function of pacemaker cells?

A

They produce action potentials

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28
Q

What are intercalated discs?

A

They are located between muscle fibres

They contain desmosomes and gap junctions/nexi

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29
Q

What are desmosomes?

A
  1. They provide cell to cell cohesions (rivets) which prevents the heart muscle fibres from rupturing neighbouring muscle cells when it contracts
  2. They optimise force transmission along the long axis of the heart
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30
Q

What are gap junctions (nexi)?

A

They propagate action potentials across the whole of the myocardium of the atria and the ventricles through their low resistance, high conductance channels

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31
Q

Where do action potentials arise from in the heart?

A

Pacemaker cells

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32
Q

What is the mitochondrial composition of skeletal and cardiac muscle?

A

Type 2 skeletal muscle (fast twitch can be aerobic or anaerobic)- 2%
Type 1 skeletal muscle (slow twitch type 1 are purely aerobic) - 12-15%
Cardiac muscle - 25-35%

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33
Q

Describe the function of the sarcoplasmic reticulum (SR)

A

SR is a system of membranous tubules that lie around the myofibrils and lie underneath the sarcolemma (cell membrane).
Functions of the SR:
1. Stores Ca2+
2. Releases Ca2+ (so that it can bind to troponin to facilitate cross bridge formation)
3. It takes up Ca at the end of a contraction so it can re-store it so that the next time an AP arrives the Ca2+ is ready for another cardiac contraction. Average resting HR= 72 bpm (beats per minute)

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34
Q

Main difference between the SR of the skeletal and cardiac muscle?

A

In skeletal muscle (m.) the SR releases enough Ca2+ for the skeletal m to contraction. In cardiac m the SR only releases 80% of necessary Ca2+. There needs to be another way that Ca is supplied to troponin - this is called calcium-induced- calcium release CICR

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35
Q

Describe the journey of the action potential as it travels along the skeletal muscle fibre

A

An AP travels along the sarcolemma of the muscle fibre, it passes along each t-tubule which causes the terminal cisternae of the SR to release Ca2+ into the muscle cytoplasm. This Ca2+ binds to troponin C
The sarcoplasmic reticulum is located in the terminal cisternae and Ca2+ is stored here

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36
Q

Describe the journey of the action potential as it travels along the cardiac muscle fibre.
What is the name of the process described?

A

In cardiac muscle the AP travels across the sarcolemma and depolarises it which causes opening of voltage-gated Ca2+ channels (in the sarcolemma).

  • A small amount of Ca from the interstitial fluid moves down its concentration gradient, enters the muscle fibre via the voltage gated Ca channels and then enters the SR of the cardiac muscle fibre (mf)
  • This small amount of Ca2+ entering from the ECF causes the SR to release larger amounts of Ca2+ which causes more release of Ca2+ from the SR. Ca2+ binds to troponin and contraction occurs

-This is called calcium induced calcium release (CICR)

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37
Q

What occurs in the cardiomyotes when the sympathetic nervous system is activated?

A

More Ca2+ channels open than usual as there are receptors on the sarcolemma of myocardial fibres that are sensitive to circulating hormone epinephrine/adrenaline and to the neurotransmitter norepinephrine/noradrenaline

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38
Q

What are the net effects in the heart of up/down-regulating sympathetic activity?

A

Allows the opening/closing of more or less Ca2+ channels

It allows manipulation of force production and volume of blood ejected

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39
Q

Define inotropy

When would inotropy occur?

A

An increased force of contraction caused by a sympathetically increased Ca2+ influx
Also called increased contractility

During exercise/severe haemorrhage

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40
Q

What do beta blocker drugs do?

A

Reduce contractility/amount of Ca2+ coming into the cells across the sarcolemma. They block the SNS receptors on the myocardial sarcolemma which limits the opening of Ca2+ channels, Ca2+ influx, CICR, Ca2+ availability to troponin and force production

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41
Q

Name a beta-blocker drug

When is it used?

A

Propanolol

When myocardial blood supply is limited e.g. in people who have atheromias

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42
Q

Describe how inotropes (drugs) work?

A

Inotropes cause the opening of more Ca2+ channles in the sarcolemma than is normal which increases the Ca2+ influx into the cardiac muscle cell. This means there is more Ca2+ acting on the SR which escalates the amount of Ca2+ available to troponin, increasing amount of cross bridge formation and increases force generation of the heart. The drugs mimic the effects of the sympathetic nervous system and enhance CICR to produce more forceful contractions.

Its used in acute heart failure, speticaemia

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43
Q

Define auto-rhythmicity

A

inherent ability to spontaneously depolarise and create APscontraction

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44
Q

Define neurogenic and myogenic

A

Skeletal mm = neurogenic. Contraction occurs in response to an AP which is generated from within the neurological system. If you dont activate your nerves you dont activate your muscles
Cardiac mm = myogenic- the inherent ability of cardiac cells to spontaneously depolarise and generate action potentials (they can do this without the need for input from the neurological system). Also called auto-rhythmicity

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45
Q

What are pacemaker cells?

A

Specialised collections of cells – modified myocytes with unstable RMPs (can spontaneously depolarise)
- Are capable of producing APs without external
input.
- Once generated APs will be conducted through-out the heart at a rate set by the rate of production of APs at the SAN.

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46
Q

How is the sino-atrial node (SAN) modulate?

A

The inherent rate of the SAN is modulated by either of the 2 arms of the autonomic nervous system - ANS. The ANS has two opposing arms i.e. the sympathetic and parasympathetic n.s. Both arms innervate the SAN and the AVN. Sympathetic speeds up heart rate (HR). Parasympathetic slows down HR

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47
Q

What hormones are released when the sympathetic nervous system?

A

SNS is a mixture of sympathetic nerves and hormones i.e. catecholamines (epinephrine and norepinephrine or adrenaline and noradrenaline). They make contact with the pacemaker cells

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48
Q

What are the 2 cardiac centres of the brain? Where are they located?

A

Cardio-acceleratory
Cardio-inhibitory
Both in medulla oblongata in the brainstem

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49
Q

What does the cardio-inhibitory centre do?

A

The neurons of the cardioinhinitory centre give rise to the parasympathetic/vagus nerve which innervates the SAN and the AVN. This causes heart rate to decrease - become less than 100 beats per minute i.e. this is the state the heart is at rest

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50
Q

What does the cardio-acceleratory centre do?

A

When sympathetic n.s is activated it sends APs down to the SAN and AV node which increase heart rate and it also sends APs to the kidney to each of the adrenal glands.
In adrenal medualla (in kidneys) the catecholmines are stored. When the adrenal glands are stimulated (by sympathetic n.s.) it releases catecholamines into the blood stream which when they reach the heart influence the SAN, AVN and ventricular muscles mass
This causes heart rate to become greater than 100 beats per minute (e.g. during physical or emotional stress)

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51
Q

Describe the function of the intrinsic conduction system of the heart.

A

It is a number of structural parts of the heart which generate and conduct APs across the myocardium of the heart as quickly and as orderly as possibly

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52
Q

What does the intrinsic conduction system (ICS) of the heart consist of? Briefly outline each

A
  1. Sino-atrial node (SAN)
  2. Gap junctions
  3. Inter-atrial pathway
  4. Inter-nodal pathway - ensures prompt delivery of the AP to the AVN
  5. Atrio-ventricular node (AVN) - connects atria and ventricle
  6. Atrio-ventricular tract / bundle / bundle of His - are high speed conducting pathways
  7. Bundle branches
  8. Purkinje fibres - make contact with cardiac ventricular muscle fibres
53
Q

Why can the action potential only pass from atria to ventricle at one point?

A

AP can only exit the atria at the AVN as the AVN sits at the level of the fibrous skeleton (which physically and electrically separates the 2 hemispheres) so there is no leakage of APs between atria and ventricles. There is no gap junctions between atria and ventricles for the same reason. And also because each compartment have different functions

54
Q

Define and outline the action potential hierarchy of the heart.
Why can all components of the ICS spontaneously depolarise and produce APs?

A

It is the order in which tissues can most efficiently produce APs

  1. SAN – 100 APs per min
  2. AVN – 40 - 60 APs per min
  3. Bundle branch ~ 40 APs per min
  4. Purkinje fibres ~ 20+ APs per min
  5. Muscle fibres can also produce APs

If there is a failure at one level the next most efficient system will take over

55
Q

Outline the main electrical events of the ECG

A

P-Q interval - Atrial depolarisation
Q-T interval - includes ventricular depolarisation and ventricular re-polarisation
R- Ventricular depolarisation
T - Ventricular re-polarisation

56
Q

Outline the 6 steps in the ECG

A
  1. Atrial depolarisation, initiated by the SA node causes P wave
  2. With atrial depolarisation complete the impulse is delayed for 0.1 seconds at the AV node
  3. Ventricular depolarisation begins at apex causing QRS complex. Atrial re-polarsation occurs
  4. Ventricular depolarisation is complete
  5. Ventricular re-polarisation begins at apex causing T wave
  6. Ventricular polarisation is complete
57
Q

Describe the 2 ways ventricles fills

A

Active filling - as the atria fill with blood, it contracts and pushes blood over the open AV valve into the ventricle
Passive filling - 70-80% of ventricular filling occurs passively which occurs during diastolic phase (when atria and ventricles are relaxed (for 0.4 seconds)

58
Q

How does the aortic value open?

A

left ventricle pressure is greater than aortic pressure

59
Q

Outline how blood moves from atria to ventricles before depolarisation of the atria occur

A

Blood moves from left side of heart into systemic circulation under high pressure. The blood moves all over the body from high to low pressure gradient
ONCE blood gets back to right atria it remains there until blood is there to increase pressure to a point of opening the right AV valve. This allows blood to move (actively) into the ventricles.
The same occurs in the left side of the heart where the blood returns to the left atrium from the pulmonary circulation

60
Q

Describe atrial kick.

A

After atria depolarise a bit more blood is squeezed into the ventricles due to contraction of the atria. This ensures the ventricles are optimally filled before they contract

61
Q

What would happen if atrial kick did not occur?

A

Ventricles would have to rely entirely on passive filling.
Only level low levels of physical activity would be able to be performed (3 METS).
Cardiac output would be too low to adequately perfuse skeletal muscle so you would not be able to exercise.
Heart failure - myocardium cannot produce adequate force and atria kick would have a huge impact

62
Q

How does the aorta allow the rapid ejection of blood from the left ventricle?

A

There is a high composition of elastic fibres in the aorta in the left ventricle. This makes this artery easily stretched - this is needed as the ventricles deposits a high volume of blood into this early aorta

63
Q

What is arterial sclerosis?

A

Calcification within the artery wall which prevent the artery from being fully distensible
During systole the pressures within the aorta is already high. In order to successfully eject blood the left ventricle needs to generate high pressure than is in the exit vessel. So in arterial sclerosis the ventricle has to generate greater pressure than normal meaning the heart has a greater metabolic demand and needs more coronary artery perfusion. Overtime the heart may fail
In the short term the sclerosis causes raised systolic blood pressure (hypertension)

64
Q

At rest is the same amount of time spent in systole as in diastole?
Why is ventricular systole longer than atrial systole?

A
  1. 3 second in ventricular systole (needs longer than atrial as the muscle mass in ventricles is larger than atrial muscle mass.)
  2. 1 second in atrial systole
  3. 4 second in atrial and ventricular diastole
65
Q

Finish the equation: Cardiac output (CO) = __ x ___

A

CO = Stroke volume (SV) x Heart Rate (HR)

66
Q

What is the function of the SAN?

A

The heart intrinsic pacemaker setting the heart beat at 100 beats per minute which would be inefficient so the SAN receives dual innervation from the 2 arms of the autonomic n.s. - only one arm is active at a time i.e. SNS and PNS (parasympathetic )

67
Q

When SNS is activated where are catecholamines released from?

A

Adrenal medulla of the kidneys

68
Q

What impacts positive chronotropes?

A 
Increase heart rate due to stimulation of sympathetic n.s.
Epinephrine
Thyroxine
Heat
Infection 
Hypercalcaemia
69
Q

What impacts negative chronotropes?

A

Parasympathetic n.s
Myocardial ischaemia/hypoxia - causes heart rate (HR) to slow
hyperkalaemia - too much K+ in blood stream which reduces HR
Hypothermia - all metabolic rate slow down

70
Q

What 3 factors impact stroke volume?

What would an increase in these 3 factors do to SV?

A

Contractility
Pre-load (filling)
After-load (emptying)

Increased contractility, pre-load and after-load all cause an increased SV

71
Q

Define cardiac output (CO).

Define stroke volumes (SV).

A

Volume ejected per ventricle per minute

Volume ejected per ventricle per contraction

72
Q

What is amount of blood ejected from each ventricle at rest from a healthy heart?

A

70mL per ventricle

73
Q

Describe the equation that represents how SV is linked to ventricle blood volume

A

SV = End diastolic volume (EDV) - End systolic volume (ESV)

Volume of blood in the ventricle at the end of diastole
ESV - volume of blood in the ventricles at the end of systole

74
Q

Do the ventricles eject 100% of the blood during each cardiac cycle?

A

60% of blood volume is ejected from the ventricle. This means that every time the heart beats there is a residual volume of blood (40%) left in the ventricles i.e. incomplete emptying

75
Q

What is cardiac reserve?

A

COmax - COrest

76
Q

How will the HR, SV and CO differ from an unfit vs fit person?

A

The fitter person will eject a larger SV when at rest, their resting HR will be lower

77
Q

How can you get more blood out of the heart?

A 
Increase venous return (VR)
Lengthen diastole (to increase the filling time to allow more blood in as blood enters the heart during diastole)
Increase the force of contraction (which will increase SV and CO)
78
Q

How does the heart increase pre-load?

A
  1. Increase time available for filling i.e. HR. Increasing HR means a shorter diastole and less filling time. This means optimal filling and emptying may not be achieved
  2. Volume of venous return - filling is due to venous return. Increasing venous return increases filling which increases stroke volume.
79
Q

What determines the degree of filling and emptying - SV?

A

∆ degree of filling determined by:

  1. Filling time (i.e HR) - pre-load
  2. Volume of venous return - pre-load

∆ degree of emptying determined by:

  1. Force of contraction - contractility
  2. Arterial blood pressure
80
Q

What factors increase VR (venous return)?

A

Increased skeletal muscle pump activity
Increased respiratory pump activity
Venoconstriction (SNS switched on constricts veins) (the contraction/relaxation of veins)

81
Q

What is the impact of stretch on myocytes?

A

Increased stretch on myocyte increases force of contraction which increases stroke volume and CO

82
Q

How does stretching muscle fibres affect SV?

A

Stretching muscle fibres optimises actin/myosin overlap which optimises cross bridge opportunities which means more force production. More force means larger stroke volume (volume of blood ejected per contraction)

83
Q

What is the Frank-Sterling Law of the heart?

A

The heart has the intrinsic ability to adjust it’s force production and therefore its SV in proportion to myocardial fibre length.

84
Q

How does contractility affect SV?

What causes contractility?

A

Increased contractility causes increased force independent of fibre length
Sympathetic nervous system (SNS) (and the release of catecholamines, which are a mixture of adrenaline and noradrenaline) hormones, drugs

85
Q

How does the Frank-Sterling Law of the heart relate to contractility?

A

Increase in length i.e. filling. causes a proportional increase in force production

86
Q

How do catecholamines affect contractility?

A

Catecholamines released from adrenal medulla bind to receptors on the ventricular muscle mass
This means more Ca2+ channels open on the sarcolemma of the muscle fibres of the heart which increases CICR
This increases contractility/inotropy

87
Q
  1. What are positive inotropes?

2. What are negative inotropes?

A
  1. sympathetic n.s. + catecholamines
    - digoxin, dobutamine, dopamine - used in acute onset heart failure (short-term) (not used long term)
  2. Altered metabolic states - force generation decreases e.g. myocardial ischaemia, acidosis
    - beta-blockers, propanolol, Ca2+ channel blockers (e.g. verapamil - all of these drugs reduce contractility
88
Q

What is after-load?

A

The pressure that the heart has to eject blood against normally 80mmHg in the aorta i.e diastolic BP

89
Q

What happens to after-load if blood pressure increases?

What happens to SV?

A

After-load increases if pulmonary (right ventricle after load increases) or systemic blood pressure increases
(if diastolic blood pressure increases the after-load on left ventricle increases)

  • The higher the blood pressure the lower the stroke volume. As the ventricles have to overcome diastolic blood pressure so it needs to contract more forcefully which is not sustainable
90
Q

What does the 120/80 represent in blood pressure?

A

120 mmHg its is normal blood pressure/homeostasis
It reflects the peak pressure obtained in systole – the pressure that the left ventricle must produce in order to eject blood into the aorta.
80 mmHg represents the lowest pressure obtained in diastole – and is therefore the normal resting pressure in the aorta.

91
Q

What factors determine blood pressure?

A

Cardiac output x total peripheral resistance (TPR)

Total peripheral resistance is determined by:

  1. Blood viscosity
  2. Vessel length
  3. Radius of the blood vessel

TPR is the resistance encountered by the blood as it passes through a vessel

92
Q

What is Poiseuilles Law?

A

R = L8n/ pie r4

R = resistance
L = length of vessel
n= viscosity
8 = constant
pie = constant
r4 = 4th power of vessel radius

Resistance is proportional to length and viscosity and is inversely proportional to the 4th power of the radius

93
Q

Define viscosity in relation to TPR

A

Viscosity is an internal resistance to flow, as components of the fluid interact or pass by each other causing friction. The viscosity of blood and is primarily determined by haematocrit - i.e. the percentage of blood volume composed of erythrocytes.

94
Q

What factors increase/decrease haematocrit?

What is the average haematocrit?

A

Increase: severe dehydration, polycythaemia (altitude response or COPD)

Decrease: Malnutrition (inadequate proteins for RBC synthesis), severe anaemia

An average haematocrit is ~ = 40% (males = 42%, females = 38%)

95
Q

Define vessel length in relation to TPR

A

The longer the length of a vessel the greater is the resistance to flow. There is a correlation between body size / build / height of subject and BP. The tall / obese person will have significantly longer vessels compared to the average person – which increases resistance to flow, impacts on TPR and is reflected in a higher BP

96
Q

Define vessel diameter in relation to TPR

A

Since resistance is inversely related to the 4th power of the radius, small changes in vessel calibre have significant impact on resistance and flow
Arterioles have the largest impact on TPR

97
Q

Outline the structure of blood vessels

A
  1. Outer - tunica externa/adventita - made of densely packed collagen fibres to provide strength and has elastin which allows distension
  2. Middle - tunica media - made of smooth muscle
  3. Inner - tunica intima - made of endothelial cells

(capillaries do not have these 3 layers, instead they have 1 layer which is called the endothelial layer)
- these 3 layers are present in arteries and in veins

98
Q

Do blood vessels have receptors?

A

There are receptors on the blood vessels which are responsive to the autonomic n.s. (only the sympathetic n.s. - the parasympathetic n.s. has no impact on them)

99
Q

What does vasodilation and vasoconstriction do to blood pressure

A

Vasodilation -> reduces resistance ->reducesBP

Vasoconstriction -> increases resistance-> increases BP

100
Q

What is the vasomotor centre (VMC)?

A

A collection of neurones in the medulla oblongata which is responsible for vasodilation and vasoconstriction of veins and arterioles. It controls this via sympathetic activity
It controls the baroreceptor reflex in the heart

101
Q

Define vasomotor tone and how the VMC controls vasoconstriction and vasodilation

A

Is a continuous low level of APs from the VMC (via sympathetic nervous system) which travel to arterioles and veins causing vasoconstriction or vasodilation

An increased firing of APs cause blood vessel constriction (due to contraction of smooth muscle). A decreased firing of APs cause blood vessel dilation (due to relaxation of smooth muscle)

102
Q

Do sympathetic innervation of veins affect venous return, total peripheral resistance or blood pressure?

A

Sympathetic innervation only affects venous return

103
Q

How does exercise affect blood pressure (systolic and diastolic BP) figures?

A

Systolic will be higher than at rest.

Diastolic will be the same

104
Q

Name 3 reasons why maintaining normal blood pressure is important?

A
  1. Adequate organ perfusion
  2. Normal organ function - too low BP can cause ischaemia/necrosis. Too high BP can damage fragile tissues like endothelium or kidneys (which are fragile)
  3. Health
105
Q

What mechanisms affect TPR via VMC activity?

A

Baroreceptors - free nerve endings that detect stretch.
Chemoreceptors
Higher brain centres

106
Q

Where are baroreceptors located?

A

In the aortic arch

In the carotid sinus of the carotid artery

107
Q

How do baroreceptors influence blood pressure?

A

Baroreceptors are stimulated by high pressure which cause APs to fire to VMC which causes vasodilation of smooth muscle in blood vessels which reduces TPR and returns BP back to normal range.

When blood pressure is normal it inhibits the VMC input

108
Q

How do baroreceptors affect CO of the heart?

A

Cardiac output is reduced when blood pressure is high
VMC and cardio-inhibitory centre cross-talk which causes AP to fire from cardio-inhibitory centre via the parasympathetic n.s. to the pacemaker cells in the conducting system slowing down the generation of AP and slowing down heart rate

109
Q

How do chemoreceptors affect TPR of arterioles via VMC?

A

Activation of chemoreceptors will:

  1. Increase VMC activity -> causes vasoconstriction of arterioles (increase in sympathetic discharge form VMC) -> increases TPR and BP
  2. Increase cardio-excitatory centre activity -> increases CO

Chemoreceptors detect a drop in arterial O2 and a rise in arterial C02 and H+ concentration

110
Q

How is blood pressure brought back to normal homeostasis?

A

High bp activates baroreceptors via VD, HR and inotropy

Low bp activates chemoreceptors via VC, HR and inotropy

111
Q

What is the role of higher brain centres on blood pressure?

A

Cortex, hypothalamus, limbic system can all affect cardiac and vascular function by interacting with the VMC to increase blood pressure, increasing HR, driving up CO and TPR

112
Q

What are the 2 factors that affect TPR directly i.e. do not interact with the VMC?

A
  1. Hormones:
    • Catecholamines (nor-epinephrine) - part of the SNS so every time the SNS is activated catecholamines are released
    • Vasopressin / Anti-diuretic hormone (ADH)
    • Angiotensin II
    • Atrial natriuretic factor
  2. Chemical factors:
    • Metabolic factors i.edecreased O2 and nutrients, K+,H+, lactic acid, adenosine causes localised vasodilation (VD)
    • Inflammatory mediators e.g. histamines, kinins & prostaglandins -> usually local VD
    • Nitric oxide (NO)
    • Endothelins
113
Q

What are catecholamines?
What are the 2 components of catecholamines?
What do they act on?

A

Catecholamines act as both a neurotransmitter and a hormone

Epinephrine (80%)
• acts on heart↑SV&↑HR

Nor-epinephrine (20%) acts on vessels
• Acts on arterioles and veins

114
Q

What is vasopressin?

A

Anti-diuretic hormone (ADH)
Diuresis=urine formation. ADH regulates urine formation so the body isnt depleted of total water and of blood volume

Action of ADH is to …
1. Conserve blood volume
• ADH is released when blood pressure is low in order to raise blood pressure back to normal e.g. during volume/pressure crises e.g haemorrhage

2.profound vasoconstriction of smooth muscle

115
Q

What is the hormone released during a hypotensive situation?

A

Angiotensin 2

Renin is released from kidneys, cascade of chemical interactions occur in which angiotension 2 is made in order to raise BP

116
Q

Describe how angiotensin 2 is made

A

When systemic blood pressure is low the kidney is hypoperfused and mades renin which acts on a pro-hormone made in the liver called angiotensiogen

  • Renin converts it to angiotensin 1
  • Lung release ACE (angiotensin converting enzyme) which converts angiotensin 1 to angiotensin 2
117
Q

Once made, what is the function of angiotensin 2?

A
  1. Switches on sympathetic activity
  2. Increases aldosterone secretion from the adrenal gland (kidneys)
  3. Causes arteriolar vasoconstriction and increases blood pressure
118
Q

What is atrial natriuretic hormone and what is its function?

A

Atrial natriuretic hormone/atrial natriuretic factor/peptide

  • Released when BP is high
  • It acts on arterioles causing vasodilation in order to decrease TPR to normalise BP
  • Is stored in cardiomyocytes (right atrium)
119
Q

What hormone is affected by an increase in BP (blood volume)?

A

Atrial natriuretic hormone

120
Q

What is the primary function of the chemical factors that directly affect TPR?

A

Metabolic factors- ensure O2 and nutrients are still being supplied to the exercised area
Inflammatory mediators allow the healing/inflammatory response to occur
Nitric oxide - a powerful vasodilator
Endothelin - released by endothelial cells. A powerful vasoconstrictor

121
Q

What 3 factors affect blood pressure?

A

Its regulated by the interplay of;
cardiac output (CO=HRxSV)
total peripheral resistance
blood volume

122
Q

What is the average adult blood volume?

A

5 litres

123
Q

How do the kidneys maintain normal blood volume?

A

When you drink more fluids blood volume also increases which increases blood pressure
The raised BP means that blood perfusing the kidneys is under higher pressure than normal which means more fluid is sent to the bladder for excretion. This normalises BP

When blood volume is low, blood pressure is low, renal filtration pressures are low and less water is lost via urine. This normalises BP

124
Q

Describe the capillary shift mechanism

A

A way of regulating blood volume. It involves shifting water/fluid across the capillary walls from the capillary blood to the interstitial spaces (or visa versa)

125
Q

Where should blood pressure (BP) be measured on a person?

A

As BP is the pressure in the major arteries it needs to be measured as close to the heart as possible i.e. the brachial artery (the further away you go the BP will decrease and it will not be a true representation of the aortic BP)

126
Q

Define hydrostatic pressure

A

The pressure within the capillaries. It is essentially a filtrating pressure forcing fluid out of the capillary into the interstitial spaces

127
Q

Define osmotic pressure

A

The attraction of water to the plasma proteins (albumin, fibrogen, globulins, prothrombin) within the capillary

128
Q

What is Starling Law of the heart?

A

The two opposing forces within the capillary: the hydrostatic pressure which seeks to expel water and the osmotic pressure which seeks to retain water

Cardiovascular Health (9 decks)

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