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ESA 2 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

Give an example of a substance that moves through aqueous pores in the capillaries

A

Glucose
Amino acids
Lactate

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2
Q

Give an example of a substance that dissolves through the lipid bilayer of the endothelium

A

Carbon dioxide

Oxygen

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3
Q

What does the rate of diffusion depend on?

A

Area - generally large, depends on capillary density. More metabolically active means more capillaries.

Diffusion ‘resistance’ - Not a rate limiting factor. Depends on the nature of the molecule (small is best), nature of the barrier (pore size or number), path length (shorter is most active).

Concentration gradient - high concentration gradient increases rate of diffusion. The gradient must be maintained for exchange to continue.

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4
Q

Describe the nature of blood flow in the brain, heart muscle and kidneys.

A

Brain - high, constant flow

Heart muscle - high, increase during exercise

Kidneys - high, constant

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5
Q

What vasculature controls flow?

A

Arterioles and pre-capillary sphincters

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6
Q

Describe capacitance

A

Ability to store blood. Veins chanage distention to increase blood in them, providing a temporary store.

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7
Q

Describe the pacemaker of the heart

A

A small group of highly specialised cells which spontaneously generate action potentials that spread over the whole heart for coordinated contraction. One action potential at regular intervals.

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8
Q

Describe the spread of excitation in the heart.

A

Pacemaker in the SAN, located in the right atrium.
Spreads over the atria causing atrial systole
Reaches the AVN, delayed for ~120ms.
From the AVN, spreads down the septum.
Bundles of His are specialised to spread action potentials quickly down the apex. Spreads from the endocardial to the epicardial surface.
As the ventricle contracts it rotates slightly, pushing the blood towards the valves.

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9
Q

Describe isovolumetric relaxation

A

A rapid drop in pressure as the ventricles relax without blood moving out.

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10
Q

Describe isovolumetric contraction

A

Ventricular systole, all valves closed. No change in ventricular volume.

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11
Q

Describe diastasis

A

Filling of the ventricles stops as the atrial and ventricular pressure .

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12
Q

How to calculate cardiac output

A

Stroke volume x heart rate

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13
Q

Describe the changes to membrane proteins and ion movements in a ventricle during an action potential.

A

Voltage gated sodium channels open causing depolarisation.
Sodium channels become inactivated, transient outward K+ channels open. Slight hyperpolarisation.
Voltage-gated L-type calcium channel open, causing the platau. Some potassium channels are open.
Repolarisation as calcium channels inactivate (slowly). More potassium channels open.

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14
Q

Describe the changes to membrane proteins and ion movements in cardiac pacemaker cells during an action potential.

A

At -60mV, sodium channels are largely inactivated. There is no stable resting potential (pacemaker potential). A funny current if formed due to channel permeability to sodium and potassium, mainly allowing an influx of sodium. This activates on hyperpolarisation and is cyclic nucleotide gated (HCN channel).
Opening of L-type calcium channels causing an increased rate of depolarisation to +30mV.
Voltage-gated potassium channel repolarises to -60mV before depolarisation begins again.

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15
Q

Describe the HCN channel

A

Hyperpolarisation activated cyclic nucleotide gated channel
Can be activated by cAMP
Pacemaker channel
Allows sodium influx

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16
Q

Describe briefly the route a wave of excitation takes through the heart

A

Initiation by the SAN, spreads to the AVN where it is delayed. Then spreads down the bundles of His, then purkinje fibres down the interventricular septum, and up the walls of the ventricle.

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17
Q

What is the function of gap junctions in myocytes and what protein is found in them?

A

Excitation coupling

Connexon proteins

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18
Q

What is the function of desmosomes in myocytes and what protein is found in them?

A

Mechanical coupling

Cadherin

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19
Q

Describe how high intracellular calcium is triggered by the initiation of an action potential.

A

Depolarisation opens L-type calcium channels in the t-tubule system.
This causes a localised increase in calcium which opens CICR channels in the sarcoplasmic reticulum.

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20
Q

Describe the difference in initiation of calcium release in skeletal and cardiac muscle.

A

Skeletal - conformational change from depolarisation causes calcium release

Cardiac - calcium is required in the cell to cause release from the SR.

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21
Q

Describe how low calcium is resumed in cardiac myocytes after contraction.

A

SERCA in the sarcoplasmic reticulum brings calcium back in

NCX transports calcium out of the cell, with the assistance of Na/K ATPase.

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22
Q

Describe how high intracellular calcium in cardiac myocytes causes contraction.

A

Calcium binds to and activates TnC, causing a conformational change. This moves tropomyosin to reveal the myosin binding site on actin filaments.

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23
Q

What controls the tone of arteries, arterioles and veins?

A

Smooth muscle in the tunica media.

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24
Q

In smooth muscle of the tunica media, what is actin anchored to?

A

Dense bodies in the cytoplasm and dense bands on the membrane

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25
Q

Describe the pathway of events after activation of a GPCR with G-alpha(q)

A

DAG and IP3 release.

IP3 activates MLCK which enables phosphorylation of the light chain of myosin head, allowing it to bind.

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26
Q

Explain the role of protein kinase A in contraction of smooth muscle

A

PKA inhibits MLCK.

PKA regulated by cAMP

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27
Q

What reverses the action of MLCK?

A

MLCP

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28
Q

Describe the resistance and pressure in arteries.

A

Low resistance

High pressure

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29
Q

Describe the term total peripheral resistance.

A

Total resistance opposing blood flow in the peripheral circulation

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30
Q

Describe the importance of arteries having distensible walls.

A

If arteries were solid the pressure in systole would force the stroke volume into the arterioles, so in diastole the pressure would fall to zero.

Distensible walls allow the arteries to stretch in systole so more blood flows in than out (capacitance). As they recoil in diastole, flow continues into the arterioles, preventing such a rapid change in pressure.

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31
Q

What causes the notch in the pressure wave of an artery?

A

Opening of valves

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32
Q

Give the factors that affect systolic pressure.

A

Strength of the heart pumping
Total peripheral resistance
Compliance of arteries

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33
Q

What factors affect diastolic pressure?

A

Systolic pressure

Total peripheral resistance

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34
Q

Why is diastolic pressure a better measure of total peripheral resistance than systolic?

A

Its not diluted by compliance

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35
Q

Define pulse pressure

A

The difference between systolic and diastolic pressure (usually 40mmHg).

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36
Q

What is the effect of adrenaline on pulse pressure?

A

Increases because the heart works harder

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37
Q

State how you would calculate the average pressure in the systemic system.

A

Diastolic pressure + 1/3 pulse pressure

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38
Q

Why do arterioles have a high resistance?

A

They have a narrow lumen

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39
Q

What is the function of pre-capillary sphincters and where are they mainly found?

A

In skeletal muscle, control resistance. Can totally close off some capillaries.
Required there because there must be such significant changes in blood flow.

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40
Q

What is vasomotor tone, and describe what happens when it increases and decreases.

A

Tonic contraction of smooth muscle.

Increase - vasoconstriction. Increased resistance and contraction.

Decrease - vasodilatation. Decreased resistance and contraction (not dilation)

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41
Q

Give the factors affecting vascular smooth muscle contraction.

A

Majorly by vasomotor tone.
Antagonised by vasodilator factors
Actual resistance by a balance of the two

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42
Q

Describe reactive hyperaemia.

A

When circulation is cut off from an area, restoration causes an enormous increase for a short while.

This is because vasodilator metabolites are produced which relax vascular smooth muscle, and are not being removed as there is no blood flow. Eventually restores to normal.

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43
Q

Give some vasodilator metabolites.

A

H+ from anaerobic respiration
K+
Adenosine

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44
Q

Describe autoregulation

A

Supply pressure changes so blood flow to the tissue will change. This changes metabolite concentration and alters the resistance of arterioles so blood flow returns to appropriate levels for metabolism.

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45
Q

What effect does low TPR have on venous pressure and why?

A

Increases venous pressure. Its easier to leave the arterioles.

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46
Q

What is central venous pressure?

A

Pressure in the great veins which fill the heart in diastole.

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47
Q

What does central venous pressure depend on?

A

Return of blood from the body
Pumping of the heart
Gravity and muscle pumping

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48
Q

Why does gravity affect superficial veins more significantly than deep veins?

A

Deep veins are surrounded by interstitial fluid, so when gravity pulls the blood down it also does so to the fluid surrounding it, which helps to keep the pressure constant.

49
Q

What happens to total peripheral resistance as blood requirement increases?

A

It decreases

50
Q

Describe the difference between flow and velocity.

A

Flow - volume of fluid passing a given point per unit time

Velocity - rate of movement of fluid particles along a tube

51
Q

Describe the relationship between velocity and cross sectional area with a constant flow.

A

Velocity proportional to inverse of cross sectional area.

52
Q

Describe laminar flow.

A

Gradient of velocity from the middle to the edge of the vessel.
Highest in the centre, stationary at the edge.

53
Q

Describe turbulent flow

A

Velocity gradient broken down, flow resistance greatly increases.
Occurs when mean velocity increases past a threshold.

54
Q

What can you hear when there is laminar flow in an artery?

A

Nothing

55
Q

Describe what you would hear if there was turbulent flow in an artery.

A

Bruit

56
Q

Describe what is meant by viscosity.

A

The extent to which fluid layers resist sliding over each other.

57
Q

At a constant gradient of velocity, what is the relationship between mean velocity and cross sectional area?

A

Mean velocity is proportional to cross sectional area

58
Q

Describe the relationship between resistance and radius.

A

Resistance is proportional to 1/r^4

59
Q

Why is pressure in the arteries high?

A

Because of high resistance in the arterioles.

60
Q

If the heart increases cardiac output but resistance remains the same, what effect will this have on arterial pressure?

A

It will increase

61
Q

Describe what happens to veins and venules with distensible walls at low pressures.

A

In very low pressure the tube will collapse.
With an initial increase in pressure, nothing will happen.
There is a bigger increase in flow per increment of pressure.

62
Q

What is the difference between bronchial and pulmonary circulation?

A

Bronchial is part of systemic, meets metabolic requirements

Pulmonary is the blood supply to the alveoli for gas exchange.

63
Q

Why is the pulmonary circulation low pressure and low force?

A

Thin right ventricle
Arterioles have a small amount of smooth muscle
Many small, branching capillaries

64
Q

What is the pressure in the right ventricle?

A

15-30/0-8 mmHg

65
Q

What is the pressure in the left ventricle?

A

100-140/1-10 mmHg

66
Q

What is the pressure in the right atrium?

A

0-8 mmHg

67
Q

What is the pressure in the left atrium?

A

1-10 mmHg

68
Q

What is the pressure in the pulmonary artery?

A

15-30/4-12 mmHg

69
Q

What allows the pulmonary artery to maintain pressure during diastole?

A

Elastic recoil

70
Q

What is the special task that the pulmonary circulation is adapted for?

A

Sufficient gas exchange

71
Q

What is the optimum ventilation/perfusion ratio?

A

0.8

72
Q

Describe hypoxic pulmonary vasoconstriction.

A

In poorly ventilated alveoli, pO2 decreases and perfusion is decreased by vasoconstriction locally.

73
Q

How can emphysema cause right ventricular heart failure?

A

It causes chronic increased vascular resistance by hypoxic pulmonary vasoconstriction.
This increases afterload on the right ventricle, causing hypertrophy which can lead to heart failure.

74
Q

Where does pulmonary oedema tend to form and why?

A

It is caused by high hydrostatic pressure which is greatest in the base of the lungs due to the effect of gravity on the low pressure vessels.

75
Q

How is oxygen uptake by the lungs increased during exercise without increasing the rate of respiration?

A

There is an increase in cardiac output which is accepted by the lungs.
This causes an increase in arterial blood pressure so the apical capillaries open more, increasing oxygen uptake by the lungs.
Blood flow is increased so the capillary transit time is reduced.

76
Q

Describe the difference between oncotic pressure and hydrostatic pressure.

A

Oncotic - pressure exerted by large molecules which draws fluid into the capillaries

Hydrostatic - blood within the capillaries

77
Q

What features of the blood supply in the brain helps to keep a secure oxygen supply?

A

High capillary density
Small diffusion distance
High basal flow
High oxygen extraction

78
Q

What gives secondary oxygen supply to the brain?

A

Circle of Willis - anastamoses between the basilar and inferior carotid arteries

Myogenic autoregulation mechanisms maintain perfusion during hypetension

Metabolic factors regulate flow

Brain stem regulated other circulation

79
Q

Describe myogenic autoregulation of perfusion in the brain.

A

Originates in smooth muscle cells which respond to stretch by constricting.

80
Q

Describe metabolic regulation of perfusion in the brain.

A

Hypercapnia causes vasodilatation. Very sensitive to arterial pCO2

81
Q

How can panic hyperventilation cause dizziness and fainting?

A

Causes hypocapnia and cerebral vasoconstriction

82
Q

Describe regional action of metabolites in the brain that regulates perfusion.

A

Cause a local increase in blood flow, so high neuronal activity causes an increase in blood flow.
High pCO2, K+ concentration and adenosine and low pO2 causes vasodilatation.

83
Q

Describe Cushing’s reflex

A

Space occupying lesions increase the pressure in the brain, impairing blood flow.
This increases sympathetic vasomotor action which increases arterial blood pressure, maintaining blood flow.

84
Q

What allows the coronary arteries to fill with blood?

A

During diastole, backflow of blood into the aortic sinus

85
Q

What features of the coronary circulation allows consistent high perfusion of the heart muscle?

A

High capillar density
Small fibre diameter
Continual production of NO by coronary endothelium which increases vasodilatation
Metabolic hyperaemia (high adenosine/potassium concentration, low pH)

86
Q

Why are coronary arteries functional end arteries?

A

They have few anastamoses

87
Q

What are vasodilators in the skeletal muscle circulation?

A 
High [K+]
High inorganic phosphate
Adenosine
High [H+]
Adrenaline via beta-2 adrenoceptors
88
Q

What causes vasoconstriction in skeletal muscle circulation?

A

NA acting on alpha-1 adrenoceptors

89
Q

Describe how apical skin can cause increased heat loss.

A

Arterovenous anastamoses have rich sympathetic innervation which respond to changes in body temperature by neural control
Open to lose heat as it causes skin temperature to rise, increasing dissipation. Blood moves straight to the venous plexus

90
Q

Describe how non-apical skin can cause increased heat loss.

A

Sweating is increased,

Local mediators from the sweat glands vasodilate capillaries.

91
Q

What does oxygen demand of the heart depend on?

A

Heart rate
Wall tension (preload/afterload)
Contractility

92
Q

What does oxygen supply of the heart depend on?

A

Coronary blood flow (perfusion pressure/coronary artery resistance)
Carrying capacity of blood (haemoglobin/gas exchange)

93
Q

Give some pathologies which cause decreased oxygen supply to the myocardium.

A

Severe hypotension
Non-atheromatous narrowing
Severe anaemia

94
Q

Give some pathologies which can increase oxygen demand

A

Tachycardia
Thyrotoxicosis
Aortic stenosis

95
Q

How can thyrotoxicosis cause an increase in oxygen demand of the myocardium?

A

Increased heart rate and BMR

96
Q

How can aortic stenosis cause an increase in oxygen demand?

A

Increase afterload means the muscle has to work harder.

Low pressure at the bottom of the aorta can reduce filling of the coronary arteries so also decreases perfusion

97
Q

Give some modifiable risk factors for CAD

A 
Hyperlipidaemia
Cigarette smoking
Hypertension
Diabetes
Obesity and metabolic syndrome
98
Q

Give some non-modifiable risk factors for CAD

A

Age
Male
Family history

99
Q

What is the difference between a stable and vulnerable plaque?

A

Stable - small necrotic core, thick fibrous cap, less likely to fissure/rupture

Vulnerable - large necrotic core, thin fibrous cap, more likely to fissure/rupture

100
Q

How can a vulnerable plaque precipitate thrombosis?

A

Fibrous cap undergoes erosion or fissuring

Expose blood to thrombogenic material in the necrotic core

Platelet clot followed by fibrin thrombus

101
Q

What percentage of the lumen should be occluded before ischaemia?

A

70%

102
Q

How does a stable plaque clinically present?

A

No symptoms or stable angina

103
Q

How does an unstable plaque clinically present?

A

Acute coronary syndrome (a medical emergency)

104
Q

Describe the symptoms of angina.

A

Central and tightening pain
May radiate
Can be relieved within five minutes by rest or nitrates

105
Q

What clinical signs of angina risk factors may help to indicate it as a diagnosis?

A

Corneal arcus
High blood pressure
Left ventricular dysfunction
Intermittent claudication

106
Q

What characteristics can be seen on a stress ECG if a person has stable angina?

A

ST depression below or equal to 1mm

107
Q

What are the aims when treating stable angina?

A

Reduce oxygen demand (decrease preload/afterload, heart rate and contractility)
Increase blood flow
Stop progression, stabilise the plaque and inhibit thrombosis

108
Q

Give some drugs which can be used in the treatment of stable angina and their function

A

Beta blockers - decrease heart rate and contractility
Calcium channel blockers - decrease afterload as they cause peripheral vasodilatation
Nitrates - venodilator which decreases preload
Aspirin - decrease platelet aggregation which reduces thrombus formation if a plaque were to rupture or fissure
Statins - reduce LDL cholesterol by inhibiting HMG-CoA reductase. Decreases plaque progression.

109
Q

Describe percutaneous coronary intervention

A

Introduce a catheter through the femoral artery and progress to beyond the plaque. Inflate the balloon to open the artery and place the stent.

110
Q

Describe a CABG

A

Use an internal artery or vein to bypass a blockage

111
Q

What conditions cause a rise in cardiac biomarkers?

A

NSTEMI

STEMI

112
Q

What causes a STEMI?

A

Complete and persistent occlusion.
Large area of myocardium without circulation is affected.
Severe ischaemia with myocardial necrosis

113
Q

What causes an NSTEMI or unstable angina?

A

Non-occlusive thrombus which is brief.

Small area of myocardium is affected.

114
Q

Why is there ST elevation in STEMI but not NSTEMI?

A

Injury is transmural in a STEMI

115
Q

What are the symptoms of a myocardial infarction?

A

Extreme central crushing chest pain which persists at rest.
Anxiety, sweating, pallor, nausea, vomiting
Low blood pressure and breathlessness can cause fainting.
May have tachycardia and arrhythmia with signs of heart failure.

116
Q

Describe the different cardiac biomarkers which can be released during a myocardial infarction and when they can be detected.

A

cTnT and cTnI. Peak between 18 and 36 hours, decline over the next 2 weeks.

CK-MB only used if cardiac troponins are unavailable. Rise 3-4 hours after an attack, peak at 24 hours. Fall to zero after 48-72 hours.

117
Q

Describe the ECG changes during a STEMI and what causes them.

A

Wide and deep pathological Q waves due to necrosis
ST elevation due to injury
T wave inversion due to ischaemia
All seen in the leads facing the damage.

118
Q

Describe the long term treatments after an MI

A

Aspirin - decrease mortality and reinfarction
Beta blockers - decrease mortality and reinfarction
ACE inhibitors - improve survival
Statins - reduce mortality and reinfarction
Manage risk factors with lifestyle modification e.g. weight loss, exercise, diet, stop smoking and reduce alcohol intake.

119
Q

Give some complications of a myocardial infarction

A

Sudden cardiac death due to ventricular fibrillation or asystole.
Arrhythmia such as sinus tachycardia and sinus bradycardia
Heart block if AVN ischaemia. Second or third-degree heart block may require a temporary pacemaker.
Ventricular tachycardia/fibrillation due to ventricular ischaemia which causes re-entry circuits or an increase in automaticity
Heart failure due to loss of myocardium or decrease in myocardial contractility
Cardiogenic shock when over 40% myocardium is infarcted which severely decreases CO with inadequate perfusion of tissues.

ESA 2 (46 decks)

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