CARDIOVASCULAR SYSTEM LECTURE 2

THE HEART

Right venous inlet valve

It is the tricuspid valve and this allows blood to flow into the right ventricle but not out.

Left venous inlet valve

It is the biscuspid (mitral) valve and this allows blood to flow into the left ventricle but not out.

Chordae tendinaea

It is the tendons that attach the mitral valve to the papillary muscles.

Papillary muscles

They allow the chordae tendineae to have the right amount of tension to allow the valve to close.

Pressure difference

The inlets have a much larger volume while the outlets have smaller volume as the blood ejected needs to be at high pressure.

Ratios between ventricles

The pressure ratio is 5:1 to the left ventricle as well as the wall thickness ratio which is 3:1.

Outlet valves

The aortic valve and the pulmonary valve. Both of these valves are semilunar and do not require chondae tendineae or papillary muscles due to their small nature.

Orientation of the heart

2/3 of the heart lies on the left side of the body with 1/3 on the right. The apex is points inferiorly, anteriorly, and to the left. The right and inferior border is formed mainly by the right ventricle, while the left border is formed mainly by the left ventricle and atrium. The superior border are the blood vessels or otherwise known as the base.

X-ray diagrams

A normal heart shouldn’t typically occupy more than 50% of the overall width of the chest. If it does, it suggests there is an issue concerning the heart. A common occurrence of this is known as having as a boot shaped heart'.

Boot shaped heart

Rheumatic fever that has been left untreated for too long, causing the individuals cells to attack self, especially the valve leaflets of the heart. This causes aortic stenosis and is easily preventable if rheumatic fever was treated in earlier stages.

Aortic stenosis

This restricts the blood flow in outlet valves, specifically the aortic valve. This causes the left ventricle to undergo muscle hypertrophy as they have to push blood through a smaller opening. The thickness can affect the elasticity and lose compliance as well as cause limited blood supply to the left ventricle which can lead to myocardial infraction.

Layers of the heart wall

Endocardium, myocardium, epicardium.

Layers of the pericardium

Visceral pericardium, pericardial space (serous fluid), parietal pericardium, fibrous pericardium.

Cardiac tamponade

This is when an area of myocardial infraction results in blood leak out into the pericardial space. This causes the space the inflate until it reaches maximum size where it will instead squeeze on the heart, affecting the hearts ability to fill.

Fibrous skeleton of the heart

Densely packed fibre and fat surround the mitral valve, aortic valve, and partly the tricuspid valve but not the pulmonary valve. This is to support the high pressure areas as well as have good electrical insulation via fat

Sinoatrial node

A cluster of modified cardiomyocytes found attached to the right atrium. These cells are all autorythmic so it can depolarise and depolarise on their own. This is the pacemaker of the heart and causes even atrial contractions.

Atrioventricular node

A cluster of modified cardiomyocytes found between the atria and ventricles. These cells are also autorythmic but at a slower rate (100ms delay). It then branches off into atrioventricular bundles eventually splitting into the right and left bundle branches. As it goes around the apex and the outside wall of the heart, it turns into purkinje fibres. These branches cause systole.

Cardiac cycle

Ventricular filling, atrial contraction, isovolumetric ventricular contraction (systole), ventricular ejection, and isovolumetric ventricular relaxation (diastole).

Ventricular filling

Pressure in ventricle drops below atrial pressure causing the mitral/tricuspid valves to open and fill the ventricle to 80% of its volume.

Atrial contraction

Atria contracts to fill the ventricle to 100% its volume. This is done by the SA node which causes the pressure of the atria to increase slightly. The slight increase in pressure in the atria is not big due to the thin muscle layers as we all as no valves in the pulmonary veins which can result in back flow.

Systole

Complete and even ventricular contraction. The pressure increases in the ventricles causes blood to flow into the atria however the mitral/tricuspid valves close not allowing it to happen (first heart sound). The ventricular pressure is still below the arterial pressure so blood does not push the aortic and pulmonary valves open. This lasts for about 0.05s and the ventricle is isolated from circulation during this time.

Ventricular ejection

Systole still contitunes but now ventricular pressure has exceeded arterial pressure, causing blood to open and flow through the aortic and pulmonary valves.

Diastole

The ventricle relaxes so the pressure drops cause the flow of blood to reverse in the arteries and closing the aortic and pulmonary valves (second heart sound). The ventricular pressure however is still higher than the atrial pressure so the mitral/tricuspid valves remain closed. The ventricle is once again isolated from circulation for 0.05s and the whole heart is relaxed.