WHY HAVE A HEART AND CIRCULATION?
The purpose of the heart and circulation is to move substances around the body.
In small creatures such as unicellular creatures- substances such as oxygen, carbon dioxide and digestive products are moved around the organism by diffusion.
Diffusion- is the movement of molecules or ions from a region of their high concentration to a region of their low concentration by relatively slow random movement of molecules.
More complex organisms are too large to move their substances around their bodies quickly enough they have a heart to pump it instead of relying on diffusion
TABLE: TYPE OF CIRCULATORY SYSTEM
CARDIAC CYCLE
PHASE 1: ATRIAL SYSTOLE
• Blood under low pressure flows into left and right atria from pulmonary veins and vena cava.
• Atria fill> pressure of blood against atrioventricular valves pushes them open>blood begins to leak into ventricles> atria walls contract>forcing blood into ventricles.
PHASE 2: VENTRICULAR SYSTOLE
• Ventricles contract from base of heart and upwards> increasing pressure in ventricles> blood pushed up and out through arteries> atrioventricular valves close due to pressure > this prevents blood from flowing back into atria.
PHASE 3: DIASTOLE
• Atria and ventricles relax in this phase.
• Elastic recoil of heart wall= lowers pressure in atria and ventricles> closes the semi-lunar valves= prevents back-flow.
• Coronary arteries fill> low pressure in atria= helps draw blood into heart<from veins.
SUMMARY
• In atrial systole the atria contract, forcing blood into the ventricles.
• In ventricular systole the ventricles contract, pushing blood up and into arteries.
• In diastole, elastic recoil as the heart relaxes= causing low pressure in the heart.
o This helps refill the chambers with blood<from veins.
TABLE: BLOOD VESSELS
HOW DOES BLOOD MOVE THROUGH THE VESSELS?
BLOOD CLOTTING
1. Blood vessel wall is damaged or blood flows very slowly= a blood clot is more likely to form.
2. Platelets stick to damaged wall of blood vessel.
3. Thromboplastin is released from damaged tissue and from platelets.
4. Ca2+ and vitamin K in plasma.
5. Platelets stick to damaged wall and to each other forming a platelet plug.
6. Fibrin mesh traps blood cells, forming a clot.
7. Prothrombin→ thrombin is an enzyme that catalyzes the conversion of soluble fibrinogen→ to insoluble fibrin.
• Only arteries get atherosclerosis because blood is under high pressure= high chance of it
happening to walls
o Low pressure in veins means there is less of a risk of damage to the walls
• Blood clotting can lead to atherosclerosis (which then leads to CVD)
o Because atherosclerosis increases the chance of blocking an artery with fatty deposits
or just directly blocking the artery
ATHROMA FORMATION
1. Endothelium is damaged, possibly due to high blood pressure or toxins from cigarette smoke.
2. There is an inflammatory response. WBC’s move into artery wall.
3. Cholesterol accumulates, a deposit builds up (called an atheroma).
4. Calcium tissue and fibrous tissue build up> causing a hard swelling (called a plaque) on the inner lining of the artery.
5. Wall elasticity is reduced.
6. Plaque= artery becomes narrow.
7. Heart finds it difficult to pump blood around body= rise in blood pressure.
8. Dangerous positive feedback builds up.
• Plaque= leads to high blood pressure= makes it likely that further plaques will form.
• Arteries become narrow and cannot supply enough blood to bring oxygen and nutrients to the tissues.
o Tissues can no longer function properly= leads to symptoms
FACTORS WHICH INCREASE CVD
THE RISK OF CVD CAN BE REDUCED BY:
• Stopping smoking
• Maintaining a resting blood pressure below 140/85mmHg
• Maintaining low blood cholesterol level
• Maintaining a normal BMI/ low waist-to-hip ratio
• Taking more physical exercise
• Moderate or no use of alcohol
CHOLESTEROL
• Cholesterol is not soluble in water so needs to combine with proteins to form= Lipoproteins
• Evidence shows a correlation between increased cholesterol levels and death rate
• Low fat diet which avoids saturated fats reduces total blood cholesterol
• HDLs reduce blood cholesterol deposition= high level of HDLs is good
CONFLICTING EVIDENCE
• Studies prove a positive correlation between fat consumption and CHD mortality rates.
• it has been proposed that regular moderate consumption of alcohol= protective defense against CHD.
o wine has antioxidants.
o this prevents oxidation of LDLs.
OTHER RISKS:
SALT
• A high salt diet can cause the kidneys to retain water.
• Higher fluid levels in the blood = result in elevated blood pressure with the associated CVD risks.
STRESS
• Evidence that CHD is sometimes linked to poor stress management.
• Increased stress can result in:
o Release of adrenaline which causes arteries + arterioles to constrict.
o This can lead to high BP.
• Stress can lead to overeating.
o E.g. increased alcohol consumption and a poor diet.
ALCOHOL
• Heavy drinking can lead to high blood pressure, contributes to obesity and an irregular heartbeat.
• Excess alcohol consumption can lead to:
o Direct tissue damage- to liver, brain and heart.
o This increases the risk of CVD.
ROLE OF ANTIOXIDANTS
• Unstable radicals in the body during reactions result when an atom has an unpaired electron.
• They are highly reactive and can damage many cell components.
• Vitamin C can protect against radical damage.
• Wine also contain chemicals which have antioxidant properties and help stop platelets from sticking together.
REDUCING BLOOD CHOLESTEROL LEVELS
• Untargeted screening and dietary advice have little influence on people as they:
o Underestimate the risk or
o Are unwilling to make lifestyle changes
• Cholesterol lowering drugs e.g. statins quickly reduce the risk of heart disease and stroke.
• In patients who have CVD statins can reduce the risk of heart attack by 33%.
• In people who do not have CVD but have elevated cholesterol levels, statins lower total and LDL cholesterol by more than 20%.
• HOWEVER, statins can increase the risk of developing cancers.
o E.g. gastrointestinal and respiratory cancers
• The benefit of statins does outweigh the risk.