4.3 Circulation Flashcards
Single Circulatory System
Closed Circulatory System
2 chambered heart
Blood is oxygenated at gills
Blood is deoxygenated as it travels around the body
Double Circulatory System
Pulmonary- Takes blood to the lungs
Systemic- Takes blood around the rest of the body
Advantages of Double Circulatory System
1) Blood pressure to the body tissues is higher
2) Blood pressure to the lungs is lower
This avoids damage to capillaries
Increases time for gas exchange
3) Organisms can develop larger bodies
Plasma
Transports digested food products
Transfers heat round the body
Erythrocytes (Red blood cells)
Transports O2 + some CO2
Have a biconcave shape + no nucleus
Leukocytes (White blood cells)
Granulocytes
Agranulocytes
Granulocytes
Neutrophils (phagocytosis)
Basophils (histamines)
Eosinophils (response to parasites)
Agranulocytes
Monocytes
Lymphocytes
Platelets
Fragments of megakaryocytes
Involved in blood clotting
Haemoglobin
Has 4 polypeptide chains
Globular- each haem can pick up 4 molecules of O2
Partial Pressure
As ppO2 increases it becomes easier for O2 to load onto haemoglobin
When ppO2 is high, O2 loads onto haemoglobin
When ppO2 is low, O2 dissociates from the Hb
High affinity Hb- Curve to the left
Loads O2 easily
Releases it less easily
Organism has a low metabolic rate
Slow release of O2 into tissues
Low affinity Hb- Curve to the right
Takes up O2 less readily
Releases it more easily
Organisms have a high metabolic rate
Rapid release of O2 to tissues
More important to have a Hb that releases O2 more rapidly than take it up
Anaerobic Conditions
Hb can become saturated with O2 at very low ppO2
Has high affinity for O2 + loads with O2
When O2 is used up + respiration produces CO2
which changes Hb’s shape making it unload
Foetal Hb
Different quaternary structure to adult Hb
Has higher affinity for O2 than adult at same ppO2
Loads at a ppO2 at which adult Hb dissociates
Myoglobin
Higher affinity for O2 than adult + foetal Hb
Stores O2 in muscle - extends aerobic respiration
Only unloads when the ppO2 is very low
Veins
Carries blood from tissues to heart
Thin walls- Low pressure
Large lumen to reduce resistance to flow
Many valves to prevent back flow
Blood at low pressure
Capillaries
Allows exchange of materials between blood + tissues
Permeable walls - Only 1 cell thick
Very small lumen
No valves
Blood pressure falls
Blood changes form oxygenated to deoxygenated
Arteries
Carry blood from heart to tissues
Thick walls with smooth elastic layers- resists high pressure
Small lumen
No valves
Blood at high pressure
Blood usually oxygenated
Heart
Myogenic
Capable of contracting without nervous impulse
Vena Cava
Deoxygenated blood from body to heart
Pulmonary Artery
Deoxygenated blood form from heart to lungs
Pulmonary Vein
Oxygenated blood from the lungs to heart
Aorta
Oxygenated blood from the heart to body
Diastole (Relaxation)
Blood enters the atria from the vena cava and the pulmonary vein
Increased atrial pressure opens atrioventricular valves
Blood flows into ventricles
Walls of both atria and ventricles are relaxed
Ventricle relaxation reduces the pressure inside the ventricle
Pressure is lower in the ventricle than in the aorta and pulmonary artery
Semi lunar valves close
Atrial Systole
Walls of atria contract
Blood pushed into ventricles
Ventricle walls are relaxed to receive the blood
Ventricular Systole
Pause to allow ventricles to fill
Increase in BP in ventricles closes AV valves to prevent back flow into atria
AV valves close
Pressure rises which opens semi lunar valves
Blood leaves through the aorta and pulmonary artery
Heartbeat control
Depolarisation starts at SAN
Depolarisation spreads across atria - causing atrial systole
Stimulates AVN
Passes stimulation down the bundle of His
Stimulation passes to purkinje fibres
Stimulation passes up the heart
Ventricles contract
Atherosclerosis Chemistry
Damaged Tissues release platelets
Platelets release thromboplastin
Thromboplastin combines with prothrombin + calcium to make thombin
Thrombin combines with fibrinogen to make fibrin
Fibrin makes a clot
Atherosclerosis
The hardening of arteries caused by the build up of atheroma
Atherosclerosis steps
1) Endothelium is damaged
This increases the risk of blood clotting
2) This leads to an inflammatory response
3) White blood cells move to the site of damage
4) Over time WBC build up + harden
Leads to atheroma formation
5) Build up of atheroma leads to narrowing of the artery
This restricts blood flow
Increases the blood pressure
Damages the endothelial lining + process is repeated
non-modifiable factors of atherosclerosis
Male Sex
Age
Male Sex
Testosterone increases the amount of LDL’s in the blood which carries large amounts of cholesterol
Age
As you get older, your blood vessels begin to lose their elasticity + narrow slightly
More likely to suffer from atherosclerosis
Modifiable factors of atherosclerosis
Smoking
Weight
Smoking
Chemicals in tobacco damage the arterial linings
Build up of plaque is more likely
Arteries narrow
Weight
High BP
Damage to blood vessel linings
Type 2 Diabetes
damage to blood vessel linings
Hydrostatic Pressure
Pressure of the blood from heart contractions
Oncotic Pressure
The tendency of water to move back into the capillaries by osmosis
Tissue Fluid Artery End
Hydrostatic pressure inside the capillaries is higher than oncotic pressure forcing water in
Tissue fluid is forced out the capillaries by hydrostatic pressure
Tissue Fluid Venous End
Hydrostatic pressure inside is less than the oncotic pressure outside
Tissue fluid is forced back into the capillary by the higher pressure outside
Loss of hydrostatic pressure is due to
Loss of blood volume
No pulse pressure
Excess tissue fluid
Tissue fluid drains into lymphatic system
They merge to form larger vessels
Vessels drain the TF back into the bloodstream via the subclavian valves
Role of Lymph Glands
1) Have lymphocytes which produce antibodies
2) Antibodies are released back into the bloodstream
3) Helps remove pathogens
Lymph Vessels
Have valves to prevent back flow
Fluid is moved through vessels via skeletal muscle contractions
Aortic Pressure
1) Aortic pressure rises when blood leaves ventricles
2) Elasticity causes recoil action
causes a rise in pressure before relaxation phase
Atrial Pressure
Pressure is always low due to thin walls
1) Pressure peaks when atria contract
2) Drops when AV valve closes + walls relax
3) Gradual increase in pressure when atria fill
4) Pressure drops when AV valves open + blood moves into ventricles
Ventricular Pressure
1) Starts low but slowly increases as blood enters the atria
AV valves close
Pressure higher than in aorta so blood forced through SL valves
2) large pressure increase when ventricle walls contract
3) Pressure walls when ventricles relax
Ventricular Volume
1) Rises when atria contract + ventricles fill
2) Drops when blood is forced out through SL valves
3) Volume increases again as ventricles fill with blood
