The Left Ventricle - Much thicker than the right ventricle as it needs to contract more powerfully to pump blood all around the body. The right side only pumps to the blood.
Ventricles have thicker walls than atria as they have to push blood out of the heart, whereas atria only has to push to ventricles - a much shorter distance.
Atriventricular valves - link the atria to the ventricles and stop blood flowing back into the atria when the ventricles contract.
Semi-lunar valves - link the ventricles to the pulmonary artery and aorta, and stop blood flowing back into the heart after the ventricles contract.
The cords - attach the AV valves to the ventricles to stop them being forced up into the atria when the ventricles contract.
The valves only open one way, whether they are open or closed depends on the pressure of the heart chambers. High pressure - forces open, low pressure - forced shut.
Cardiac muscle is myogenic (it can contract and relax without recieving signals). It starts in the sino-atrial node (SAN) which is in the wall of the right atrium. It acts as a pacemaker which sets the rhythm of the heartbeat by sending out regular waves of electrical activity to the atrial walls. The electrical impulse can travel to the left atria via the interatrial septum. This causes the right and left atria to contract at the same time. A band of non-conducting tissue prevents the impulse travelling directly to the ventricles. Instead they travel to the atrio-ventricular node (AVN). Before anything else happens there is a slight delay to make sure the atria have finished contracting so the ventricles can contract. The imoulse travels to the Bundle of His which are a group of muscle fibres responsible for conducting the waves to the purkinje fibres. These are finer muscle fibres in the right and keft ventricle walls. They carry the wave into the musclular walls of the right and left ventricle causing them to contract simultaneously from the bottom up.
Cardiac Output = Stroke Volume x Heart Rate
Atrial Systole - Ventricles are relaxed. The atria contract, decreasing the volume of the chamber and increasing the pressure inside the chamber. This pushes the blood into the ventricles. There is a slight increase in ventricular pressure and chamber volume as the ventricles recieve the ejected blood from the contracting atria.
Ventricular Systole - The atria relax. The ventricles contract decreasing their volume and increasing the pressure. The pressure becomes higher in the ventricles than in the atria, which forces the AV valves shut to prevent back-flow. The pressure in the ventricles is also higher than in the aorta and pulmonary artery. This forces open the semi-lunar valves and blood is forced out into these arteries.
Diastole - Atria and ventricles both relax. The higher pressure in the aorta and pulmonary artery forces shut the semi-lunar valves to prevent backflow into the ventricles. Blood returns to the heart and the atria fill again due to the high pressure in the vena cava and pulmonary vein. This starts to increase the pressure in the atria. As the pressure in the ventricles continues to relax, the pressure falls below the pressure of the atria and so the AV valves open. This allows blood to passively flow into the ventricles from the atria. The atria contract and the whole process starts again.
Atheroma - The wall of an artery is made up of several layers, the inner lining is the endothelium and is usually smooth and unbroken. If damage occurs, white blood cells and lipids from the blood, clump together under the lining to form fatty streaks. Over time, more of these build up and harden to form a fibrous plaque called an atheroma. This partially blocks the lumen of the artery and restricts blood flow, causing blood pressure to increase.
Thrombosis - An atheroma plaque can burst the lining of the artery which damages the artery wall and leaves a rough surface. Platelets and fibrin accumulate at the site of damage and form a blood clot (thrombus). This can cause a complete blockage of the artery, or it can become dislodged and block a blood vessel elsewhere in the body. Debris from the rupture can cause another blood clot to form further down the artery.
Aneurysm - Atheroma plaque damages and weakens arteries. They also narrow arteries, increasing blood pressure. When blood travels through a weakened artery at high pressure, it may push the inner layers of the artery through the outer elastic layer to form a balloon like swelling - aneurysm. This can burst, causing a haemorrhage. If in the brain, can cause a stroke.
Myocardial Infarction and Factors Affecting CHD
The heart is supplied with blood from the coronary arteries. This blood contains the oxygen needed by the heart muscle to carry out respiration. If a coronary artery become completely blocked off, an area of the heart will be cut off from its blood supply, depriving the heart of oxygen.
High blood cholesterol and poor diet - If the blood cholesterol is high then there are more fatty deposits in the blood. High density lipo-proteins make up an atheroma, so there is an increased risk of this happening. It could block the flow of blood causing a myocardial infarction. High diet in fat, increased cholesterol levels. High salt increases blood pressure.
Smoking - Carbon monoxide binds with haemoglobin and reduces the amount of oxygen trnsported in the blood, so reduces amount of oxygen available. If heart does not recieve as much then can lead to heart attack. Nicotine makes blood more viscous so harder to pump around. Also decreases amount of anti-oxidants in the blood which are important for protecting cells from damage. Fewer of these, more likely for cell damage, leading to atheroma.
High blood pressure - Increases risk of damage to artery wall, increases risk of atheroma forming, increases blood clot formation, resulting in heart attack.