The aorta and elastic arteries Flashcards

1
Q

How is the heart an intermittent pump?

A

There are parts of the cycle where the heart is resting.
However the tissues need continued perfusion from the heart, so there are elastic arteries to allow this.

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2
Q

What do elastic arteries do?

A

Elastic arteries convert the intermittent pumping of the heart into continuous flow.
In the capillaries the flow is continuous because there’s no pressure variations.

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3
Q

What is elasticity?

A

The ability to resume its normal shape spontaneously after being stretched or compressed.

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4
Q

What is compliance?

A

How easily a structure stretches.
Compliance is inversely proportional to elasticity

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5
Q

What is elastin?

A

Highly elastic protein present in connective tissue.
Critical for tissues and structures which require elasticity - lung, skin, bladder, blood vessels.

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6
Q

What is the half-life of elastin?

A

Very long half-life, it is not turned over quickly.
It is highly cross-linked so is very stable and not susceptible to enzymatic breakdown.
There are not many mechanisms to repair it.

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7
Q

What are the components of elastic arteries?

A

Different blood vessels have the same components of endothelium, elastin, smooth muscle and collagen, but different balances.
Elastic arteries have lots of elastin and collagen.

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8
Q

What is the Windkessel effect?

A

The high blood pressure stretches the elastin, and elastic energy is stored in the elastin at the end of systole.
In diastole, the elastin recoils and the energy is transferred to the blood to force it forwards - elastic recoil.
The elastin then returns to its original shape.

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9
Q

How are pressure oscillations changed?

A

Pressure oscillations are fully dampened when the blood reaches the capillaries.
The vessels are smaller, so there is resistance to flow.
There is also friction as the blood moves in the vessels.
The pulse pressure width decreases.

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10
Q

What is arterial blood pressure?

A

The driving force for flow, determined by the elastic arteries.
Mean ABP = (SP-DP)/3 + DP
It is divided by three to account for the increased time spent in systole.

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11
Q

How does pressure change with gravity?

A

Further down in the body, blood pressure increases.
Further up, blood pressure decreases.

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12
Q

What is hydrostatic pressure in blood?

A

The pressure exerted by the blood on the walls of the blood vessels due to the force of gravity.

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13
Q

What is the equation for hydrostatic pressure?

A

P = pgh
p = density of blood
g = acceleration due to gravity
h = height of fluid column

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14
Q

How does the height of the fluid column affect pressure?

A

At the heart the pressure is 120mmHg.
1 meter down it would be 120 + 78mmHg.

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15
Q

What are the postural effects on arterial pressure?

A

When lying down, there is very little difference between arterial and venous pressure.
When standing, pressure changes, but the venous and arterial system are similarly effected by gravity so the difference is the same.

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16
Q

What factors influence systolic and diastolic pressure?

A

Elastin content of the elastic arterial wall.
Cardiac output
Total peripheral resistance (by the body)
Volume of circulating blood
Viscosity of blood
Therefore affects mean arterial pressure.

17
Q

What are the main contributors to systolic pressure?

A

Stroke volume
Aortic / arterial distensibility
Ejection velocity
Diastolic pressure of previous beat

18
Q

How does ejection velocity affect systolic pressure?

A

Blood enters the arterial system must faster than it can be cleared, increases systolic pressure.

19
Q

How does aortic/ arterial distensibility affect systolic pressure?

A

The ability of the vessels to stretch and recoil can change.
e.g. with age - arteriosclerosis.

20
Q

How does the diastolic pressure of the previous beat affect systolic pressure?

A

Diastolic pressure is the starting point for developing systolic pressure.
Increased diastolic pressure can lead to increased systolic pressure.

21
Q

How does stroke volume affect systolic pressure?

A

Anything that increases venous return, will affect systolic pressure.
Anything that increases or decreases contractility.
Anything that increases or decreases vascular resistance (to expansion).

22
Q

What are the main contributors to diastolic pressure?

A

Arteriolar resistance
Aortic/ arterial distensibility
Heart rate

23
Q

How does arteriolar resistance affect diastolic pressure?

A

Vasoconstriction increases total peripheral resistance, increases diastolic pressure. Because the blood cannot go into vessels, so generates pressure before it.
Vasodilation decreases TPR, decreases diastolic pressure.

24
Q

When does TPR increase naturally?

A

e.g. during exercise, because of vasoconstriction to non-skeletal muscles such as the gut, increases TPR.

25
Q

How does aortic/arterial distensibility affect diastolic pressure?

A

Reduced elastic recoil lowers diastolic pressure.
Because the vessels can’t expand, and DP is not maintained.

26
Q

How does heart rate affect diastolic pressure?

A

A very high heart rate means a reduced time for the peripheral run off before the next heartbeat.
Starting diastolic pressure will be higher.

27
Q

How does pulse pressure change with changes in DP and SP?

A

Pulse pressure widens because systolic pressure increases and diastolic pressure increases.

28
Q

What is arteriosclerosis?

A

Elastic arteries become less elastic with age.
Increased collagen alters the elastin: collagen ratio so it is less elastic - increases systolic pressure (decreased compliance), decreased diastolic pressure (decreased elastic recoil).
Increased risk of atherosclerosis with age.

29
Q

Why is there an increased risk of atherosclerosis?

A

With age, systolic pressure is increased and there is decreased compliance.
Decreased or increased diastolic pressure depending on the stage.

30
Q

How does arteriosclerosis occur?

A

Macrophages enter the vessel wall through a lesion and become foam cells which are inflammatory, and then develops into a fatty streak.
Lipids accumulate in the blood vessel, then grows into an atheroma.
Plaques form, with a very inflammatory necrotic core of dead cells.
Complex lesions can rupture and then the necrotic core exits, the platelets accumulate and clot elsewhere, and it is very inflammatory and thrombogenic.