6.2 The blood system

William harvey

English physician, modern understanding of circulatory system

beliefs before harveys findings: Galens view

• Arteries and veins were separate blood networks (except where they connected via invisible pores)

• Veins were thought to pump natural blood (which was believed to be produced by the liver)

• Arteries were thought to pump heat (produced by the heart) via the lungs (for cooling – like bellows)

harveys proposal

• Arteries and veins were part of a single connected blood network (he did not predict the existence of capillaries however)

• Arteries pumped blood from the heart (to the lungs and body tissues)

• Veins returned blood to the heart (from the lungs and body tissues)

systemic circulation

The left side of the heart pumps oxygenated blood around the body

pulmonary circulation

the right side of the heart pumps de-oxygenated blood to the lungs

the heart has what type of circulatory system

a double

arteries

transport blood at high pressure from the from the ventircles to body tissues and the lungs(deoxygenated here, usually oxygenated)

arteries specialised structure

• They have a narrow lumen (relative to wall thickness) to maintain a high blood pressure (~ 80 – 120 mmHg)

• They have a thick wall containing an outer layer of collagen to prevent the artery from rupturing under the high pressure

• The arterial wall also contains an inner layer of muscle and elastic fibres to help maintain pulse flow (it can contract and stretch)

labelled a diagram of the artery

how does the blood flow through the arteries

in repeated surges called pulse

muscle fibre function

form a rigid arterial wall that is capable of withstanding the high blood pressure without rupturing

• Muscle fibres can also contract to narrow the lumen, which increases the pressure between pumps and helps to maintain blood pressure throughout the cardiac cycle

elastic fibre function

allow arterial wall to stretch and expand upon the flow of a pulse through the lumen

capillaries

exchange materials between cells in tissues and blood travelling at a low pressure, has permeable walls

capillary adaptations

one cell thick/wide

-1 wall layer: Tunica Intima

aorta>

arteries>arterioles > capillaries decreasing arterial pressure as total vessel volume is increased

3 types of capillary structure

continous

fenestrated

sinusoid

continuos capillary structure

continuos with endothelial cells held together by tight junctions to limit permeability of large molecules

fenestrated capillary structure

contain pores, aids absorbtion eg. in the kidney

sinusoid capillary structure

open spaces between cells + permeable to large molecules eg.liver

how does blood flow through the capillaries

very slowly and at a very low pressure in order to allow for maximal material exchange

• high blood pressure is dissipated by extensive branching of vessels and narrowing of the lumen eg.o2

where are high and low hydrostatic pressure found at a capillary

high at arteriole end forcing materials into tissue

low at venuos end allowing materials from tiisue to enter bloodstream eg.co2

veins

transports bloodt at low pressure to the atria of the heart

veins specialised structure

• They have a very wide lumen (relative to wall thickness) to maximise blood flow for more effective return

• They have a thin wall containing less muscle and elastic fibres as blood is flowing at a very low pressure (~ 5 – 10 mmHg)

• Because the pressure is low, veins possess valves to prevent backflow and stop the blood from pooling at the lowest extremities

label the structure of a vein

how does muscle contraction affect veins

when they contract the squeeze the vein + cause blood to flow from the site of compression increasing the rate of return of deoxygenated blood

the wall layers in arteries and veins

Tunica Adventitia

Tunica Media

Tunica Intima

identification of blood vessels

• They have a very wide lumen (relative to wall thickness) to maximise blood flow for more effective return

• They have a thin wall containing less muscle and elastic fibres as blood is flowing at a very low pressure (~ 5 – 10 mmHg)

• Because the pressure is low, veins possess valves to prevent backflow and stop the blood from pooling at the lowest extremities

flow of blood through the heart

vena cava>right atrium>tricuspid valve>right ventricle> pulmonary valve>pulmonary artery>lungs>pulmonary vein>Left atrium> bicuspid valve>left ventricle> aortic valve> aorta

what is the heart contraction

myogenic(the signal for cardiac compression arises within the heart tissue itself)

where is the heart beat initiated

the SA node, the ‘pace maker’

what happens if the SA node fails

the AV node can maintain cardiac contractions but slower

• if both fail, a final tertiary pacemaker (Bundle of His) may coordinate contractions at a constant rate of roughly 30 – 40 bpm

what happens if there is no pacemaker

cardiac cells act independently, irregular and uncordianted beats which requires defibrillation

conduction of a heart beat

an impulse is initiated in the Sa node which triggers a depolarisation that spreads across the atria causing it to contract.

it reaches the AV node where the impulse is delayed for 12s to allow filling of the ventricle.

the AV budnles carries the impluse down through the septum where they meet the purkinje fibres which carry the impulse up the wall of the ventricles causing them too contract

external signals which increase HR

nerve signals from the brain(rapid changes)

endocrine signals(more sustained changes)

blood pH or changes to blood pressure

how nerve signals affects hr

involuntary from the medulla oblongata

• The sympathetic nerve releases the neurotransmitter noradrenaline to increase heart rate

• The parasympathetic nerve releases the neurotransmitter acetylcholine to decrease heart rate

how hormones affect the heart

• The hormone adrenaline (a.k.a. epinephrine) is released from the adrenal glands (located above the kidneys)

• Adrenaline increases heart rate by activating the same chemical pathways as the neurotransmitter noradrenaline

systole

the contraction of the heart

diastole

the relaxation of the heart

atrial systole

the period when the atria are contracting

• The atrioventricular valves are open as the pressure in the atria exceeds the pressure in the ventricles

• The semilunar valves are closed as the pressure in the ventricles is less than the pressure in the aorta and pulmonary artery

Atrial systole happens around 0.13 seconds after ventricular systole

Atrial systole forces blood from the atria into the ventricles

ventricular systole

the period where the ventricles are contracting

• The atrioventricular valves are closed as the pressure in the ventricles exceeds the pressure in the atria

• The semilunar valves are open as the pressure in the ventricles exceeds the pressure in the aorta and pulmonary artery

diastole

both chamblers are relaxed

blood flows into av valves open, semilunar closed

coronary arteries

blood vessels that surround the heart and nourish the cardiac tissue to keep the heart working

• if blocked will cause a heart attack

coronary occlusion(Atherosclerosis)

hardening and narrowing of the arteries due to the deposition of cholesterol

• occurs when fatty deposists devlop in the artery significantly reducing the diameter of the lumen

• consequently this increases pressure + damage on the arterial wall

• damaged is repared with fiberous tissue(sig less elastic)

• As the smooth lining of the artery is progressively degraded, lesions form called atherosclerotic plaques

• If the plaque ruptures, blood clotting is triggered, forming a thrombus that restricts blood flow

• If the thrombus is dislodged it becomes an embolus and can cause a blockage in a smaller arteriole

consequences of coronary occlusion

heart attack

blod clots

coronary heart disease

-treated by bipass surgery or creating a stent

risk factors for coronary occlusion

• Age – Blood vessels become less flexible with advancing age

• Genetics – Having hypertension predispose individuals to developing CHD 

• Obesity – Being overweight places an additional strain on the heart

• Diseases – Certain diseases increase the risk of CHD (e.g. diabetes)

• Diet – Diets rich in saturated fats, salts and alcohol increases the risk

• Exercise – Sedentary lifestyles increase the risk of developing CHD

• Sex – Males are at a greater risk due to lower oestrogen levels

• Smoking – Nicotine causes vasoconstriction, raising blood pressure