Case 1 + 2 - heart Flashcards

1
Q

Dorsal motor nucleus of the Vagus (DMNV)- nervous effect on cardiac output

A

In the medulla oblongata. When activated it inhibits the SA node which decreases heart rate, decreasing cardiac output and mean arterial pressure. Parasympathetic and mediated via vagus nerves

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2
Q

Rostral ventrolateral medulla (RVLM)- nervous effect on cardiac output

A

In the medulla oblongata. When activated by sympathetic outflow, mediated by the nerves. It stimulates the SA node causing heart rate, cardiac output and mean arterial pressure to increase. Also causes the constriction of smooth muscle in the blood vessels. Vasoconstriction increases mean arterial pressure

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3
Q

Nucleus tractus solitarius (NTS)- nervous effect on cardiac output

A

When there is an increase in blood pressure this will be detected in the baroreceptors in the ceratoid sinus and aortic arch. This will fire action potential along the Glossopharyngeal nerve and vagus nerve respectfully, to the Nucleus Tractus Solitarius (NTS) in the medulla Oblongata. This will then stimulate the DMNV to produce its effect, and inhibit the RVLM.

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4
Q

The effects of posture on arterial blood pressure

A

When you stand up blood pools in your legs and less returns to your heart, decreasing blood pressure in the aorta. This will be detected by baroreceptors which will stretch less. Less firing to the NTS, less stimulation of DMNV and less inhibiting RVLM. This will increase cardiac function, heart rate, cardiac output and finally blood pressure. Vasoconstriction also occurs due to the RVLM, this increases the resistance and blood pressure. There will be an increase in sympathetic which increases peripheral resistance, and a decrease in parasympathetic which increases heart contraction. This will readjust the blood pressure back to normal. Increasing the blood supply to the brain

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5
Q

Stopping blood loss from blood vessels

A

The smooth muscle in the blood vessel constrict when the blood vessel is broken, this increases blood pressure but reduces blood flow and blood loss. This causes nervous reflexes initiated by pain and local myogenic contraction of blood vessels. Platelets releasing thromboxane A2 and serotonin which cause vasoconstriction. The thrombin generated in the coagulation cascade triggers the endothelium to release endothelin-1 which is a vasoconstrictor. This whole process is the vascular spasm. Platelets will plug the hole

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6
Q

Blood as a pump

A

The left and right side of the heart act as two pumps. The pump on the right side of the heart send blood to the lungs, when they contract to be oxygenated. When the left ventricle contract the blood is sent around the body.

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7
Q

The walls of the heart

A

The walls of the ventricles are much thicker than the walls of the atria, because the ventricles need to develop more force when they contract, as in the left ventricle the blood needs to go around the whole body. For the right ventricle, the force generated needs to be relatively small because the blood is only going to the lungs which aren’t very far away. If too high a pressure is developed, tissue fluid would accumulate in the lungs hampering gas exchange. In the atria the blood is only going to the ventricles.

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8
Q

The walls of the arteries

A

Have a small lumen with thick walls, especially the tunica media. The walls are thick because the blood us at high pressure, so they need to be strong, so they don’t burst. There is lots of elastic fibre in the tunica media which allows walls to stretch as pulses of blood surge through at high pressure, this makes the artery wider reducing the pressure. It recoils when low pressure blood goes through so the artery becomes narrower and the pressure increases. This evens out the flow of blood.

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9
Q

The walls of the capillaries

A

They are small allowing them to get as close as possible to the cells, the walls are only one cell thick, so the oxygen does not have to diffuse far. The pressure of blood is low in the capillaries. The walls are made up of only a single layer of endothelial cells.

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10
Q

The walls of the veins

A

The vein walls are thin as blood pressure is low, so they do not have to withstand a high force. To keep blood flowing in the right direction, semilunar valves allow blood to move towards the heart and not away from it. Blood is returned in the veins by tensing muscles raising the pressure

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11
Q

Acute inflammation

A

When a tissue is damaged, the damaged cells release chemicals which are a distress signal. This causes increased blood flow and blood vessels become leaky. The distress signals also attract white blood cells to clear the germs and dead cells. Once the wound has healed, the process stops and recovery follow

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12
Q

Chronic inflammation

A

The same steps as acute inflammation but with no recovery. Leads to a negative effect on organs and tissues

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13
Q

Pulmonary arteries

A

The pulmonary trunk carries deoxygenated blood from the right ventricle. It splits into the left and right pulmonary artery which take blood to the left and right lung respectively, the blood is then oxygenated.

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14
Q

Pulmonary vein

A

The pulmonary veins take oxygenated blood from the lungs to the left atrium where its pumped to the left ventricle and then around the body through the aorta. There is a pulmonary vein on both the left and right side.

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15
Q

Mechanical events that happen during the cardiac cycle

A

1) Ventricular filling- occurs during ventricular diastole (relaxation). Pressure is low and blood flows in from the venous system
2) Atrial contraction- atrial systole, this contraction will push blood from the atrium to the ventricle
3) Isovolumetric ventricular contractions- ventricles are stimulated electrically to contract, this squeezes the blood. All valves close, pressure increases, volume doesn’t change.
4) Ventricular ejection- ventricular systole, pressure is higher than the arteries and the blood moves down the pressure gradient from the ventricles to the arteries
5) Isovolumetric ventricular relaxation- ventricles relax, all valves close, pressure decreasing, volume not changing.

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16
Q

What are the heart sounds basic

A

The valves closing due to pressure changes.

17
Q

What are the heart sounds (specific)

A

S1- closing of the microvalve, isovolumetric contraction

S2- the aortic valve closing

18
Q

Cardiac myocyte

A

A specialist type of muscle tissue in the heart. If there is a lot of calcium in the cytosol it will contract. The calcium sensor is troponin, in normal muscle cells it’s ryanodine

19
Q

How a contraction is caused in cardiac myocyte

A

An action potential causes the opening of voltage gated calcium channels. The entry of calcium causes the release of calcium from internal stores. The increase in calcium will cause the Troponin to initiate contraction. When relaxed the calcium unbinds from troponin and is exchanged with sodium. Calcium will be pumped back in the stores in the sarcoplasmic reticulum.

20
Q

Cardiac muscle

A

Striated, it branches off and connects to more then one muscle cell. They contain intercalated disks, where one myocardial muscle cell come into contact with a neighbouring muscle cell. They are packed with connexon proteins which form pores creating a direct contact between neighbouring muscles cells. These gap junctions allow the electrical impulse to pass through the heart, so the heart will contract at the same time

21
Q

Annulus fibrosis

A

Connective tissue which forms and anchors the valves, it then influences the force exerted on them. Stops the electrical charge from spreading from the atria to the ventricle. The ventricle can only contract when signalled by the SA node.

22
Q

SA node

A

Made up of pacemaker cells which initiates our heartbeat causing the mechanical contraction of the heart

23
Q

Action potential in the atria

A

At the threshold potential, in phase 0, there is an increased movement of calcium ions into the cell, this causes depolarisation as the cell is positive. In Phase 3 the calcium channels close and K+ charges exist. The loss of positive ions causes hyperpolarisation as it goes negative. In phase 4 the membrane potential goes more positive straight away. This is due to Na+ influx and calcium channels opening again. This is the prepotential and causes slow depolarisation

24
Q

What causes the action potential in the ventricle

A

Requires an external stimulus. Caused by the SA node which opens the sodium channels in the ventricular myocyte, triggering phase 1

25
Q

Action potential in the ventricle

A
  • In phase 0 the sodium channels open, causing the myocyte to become more positive and depolarise.
  • In phase 1 the sodium channels and close and the fast potassium channels open, K+ leaves the cell making it more negative.
  • In phase 2, calcium channels open and fast K+ channels close. Causing the membrane potential to stay constant. This is a plateau phase and is a sustained depolarisation prolonging the action potential
  • In phase 3 the calcium channels close and the slow potassium channels open, causing hyperpolarisation as the membrane becomes more negative.
  • At phase 4 it is at resting potential
26
Q

The ionic basis for the prepotential in atria contraction

A

In phase 4 the prepotential permits automacy, allowing the heart to beat regardless of the rest of the body. It is activated by hyperpolarisation in phase 3 and the HCN mediates If which causes slow depolarisation towards the AP threshold. It does this through Potassium ion efflux and sodium channel influx, but there is more sodium influx which causes the depolarisation. It reaches the threshold and the upstroke inactivates the HCN gated channels

27
Q

How sympathetic nerves affect atrial contraction

A

When activated it causes the release of noradrenaline which binds to beta 1 adrenoreceptors on the cardiac pacemaker and myocyte cell membranes. This increases opening of HCN channels in the pacemaker cells, increasing Na+ influx. Ca+2 channels also open causing the influx of Ca+2. All this increases the slope of prepotential in phase 4 and heart rate increases. Its starting membrane potential will be more positive meaning it will have to travel less of a distance

28
Q

How parasympathetic nerves affect atrial contraction

A

When activated cause the release of acetylcholine which binds to muscarinic cholinergic receptors. This decreases the opening of HCN channels, decreasing NA+ influx. It slows the opening of the Ca+2 channels which decreases Ca+2 influx. It opens additional ligand gated K+ channels which cause K+ efflux. All this hyperpolarises the membrane and reduces the slope of prepotential. The starting membrane will be lower meaning its more of a distance for it to travel. Less contraction of the AV node

29
Q

The electrical events of a cardiac cycle

A

Electrical activity originates in the SA node which fires spontaneously. Waves of electricity spread via gap junctions, these lead to mechanical activity. The atria contract when the calcium is released due to the electrical stimulation. The electrical impulse travels through the atria in the intermodal pathways (specialised conductive system) till it gets to the AV node. When this fires it spreads down the interventricular septum. At the apex it then spreads upwards through the Purkinje tissue and the ventricles contract from the bottom upwards There is a lag at the AV node so the atria and ventricles don’t contract at the same time