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Biology/Physiology > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

0
Q

What are the main components of the cardiovascular system?

A

The heart, the blood vessels (arteries, arterioles, veins, venules and capillaries) and the blood.

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1
Q

Name all the functions of the cardiovascular system

A
  1. Transports oxygen from lungs to tissues.
  2. Removes carbon dioxide from tissues and releases it in lungs.
  3. Transports nutrients from the digestive system to cells.
  4. Transports metabolic waste from tissues to excretory organs.
  5. Transports hormones from glands to target cells.
  6. Distributes metabolic heat and maintains body temperature.
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2
Q

The heart muscle contraction is similar to the contraction of which other muscle?

A

Skeletal muscle

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3
Q

Is the source of calcium for the cardiac muscle intracellular, extracellular or both?

A

Both

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4
Q

What does it mean when cells in the heart show INTRINSIC AUTOMATICITY?

A

It means they have the ability to generate heartbeat.

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5
Q

Which cells in the heart show intrinsic automaticity?

A

The SA node (sinoatrial node), the AV (atrioventricular) node and the Purkinje fibres/bundle of His.

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6
Q

What is than me given to the cells that show INTRINSIC AUTOMATICITY?

A

Autorhythmic cells

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7
Q

What is the name of the part of the heart called the primary pacemaker? It has the fastest pacemaker potential and it drives the heart.

A

The SA node

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8
Q

Put these in order of the fastest rhythm: bundle of His/Purkinje fibres, AV node and SA node. With 1 being the fastest.

A
  1. SA node
  2. AV node
  3. Purkinje fibres/bundle of His
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9
Q

How is the heartbeat initiated?

A

Electrical signals travel from the pacemaker cells to the contractile cells in the atria and ventricles via gap junctions.

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10
Q

What is the main difference between initiation of contraction in the cardiac muscle compared to the skeletal muscle?

A

The action potential in the cardiac muscle is originates from the heart’s pacemaker cells, whereas the binding of acetylcholine to the skeletal muscle (nicotinic) receptors causes contraction in the skeletal muscle.

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11
Q

What are the two main difference between action potentials in the cardiac muscle compared with the skeletal muscle.

A
  1. Action potentials in the cardiac muscle originate from pacemaker cells.
  2. Action potentials in the cardiac muscle are longer due to calcium entry.
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12
Q

Why is there a plateau in the action potential of a myocardial contractile cell?

A

This is due to a decrease in potassium permeability and an increase in calcium permeability. The combination of an influx of calcium and an effluent of potassium causes a plateau.

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13
Q

When do the calcium channels open during the action potential of a myocardial contractile cell?

A

They open at the same time when sodium channels open where the cell receives a wave of depolarisation from the pacemaker cells but they are very slow to open, so calcium only enters at the stage where potassium channels close.

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14
Q

What is the difference between fast and slow potassium channels.

A

Slow potassium channels are found both in neurons and also in cardiac contractile cells. The fast potassium channels open straight after the sodium channels close, allowing potassium out, but they are also fast to close.

The slow potassium channels open with depolarisation just like the sodium and calcium channels. But like the calcium channels, these slow potassium channels are slow to open and only open when the calcium channels are closed.

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15
Q

How long is an action potential in a neuron or skeletal muscle fibre compared with a contractile myocardial cell.

A

In a neuron/skeletal muscle fibre - 1-5msec

In a contractile myocardial cell - 200msec or more - it is very long due to the influx of calcium.

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16
Q

Why is the longer myocardial action potential caused by an influx of calcium ions important?

A

It helps prevent the sustained contraction called a TETANUS. So that the heart muscles can relax between contractions allowing the ventricles to fill with blood.

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17
Q

Why is not possible to have a tetanus in a cardiac muscle?

A

The action potential in a cardiac contractile cell, the contraction of the cell and the refractory period end almost simultaneously, so by the time the next action potential takes place, the contractile cell is almost completely relaxed, so no summation occurs, therefore tetanus cannot occur.

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18
Q

Why is it possible to achieve a tetanus in a skeletal muscle and not a cardiac muscle?

A

The action potential and refractory period in a skeletal muscle ends just as contraction begins, so if the next action potential is fired immediately after the refractory period, summation and therefore tetanus can occur.

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19
Q

What other factor aside the contraction of the cell refractory period and action potential ending simultaneously prevents a tetanus from happening in a cardiac contractile cell?

A

The long refractory period in a cardiac muscle prevents tetanus.

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20
Q

Name the two stages of an action potential of a pacemaker cell

A
  1. The pacemaker potential

2. The action potential

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21
Q

Why is the pacemaker potential important?

A

When the pacemaker potential depolarises to threshold the autorhythmic/pacemaker cell fires an action potential.

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22
Q

Why is the pacemaker potential unstable?

A

The If channels open at negative membrane potential and they are permeable to sodium and potassium. However, the sodium influx exceeds the potassium influx, so the net influx of positive charge depolarises the auto rhythmic cell.

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23
Q

Describe the process of an action potential in a pacemaker cell.

A
  1. If channels open (sodium influx is greater than potassium efflux) and so net influx of positive charge depolarises the cell to reach threshold level.
  2. At threshold level, an action potential is triggered, If channels close and calcium channels open, depolarising the cell even more.
  3. A second set of voltage gated calcium channels open due to depolarisation, and the cell is even more depolarised.
  4. Then slow transient potassium channels open, allowing potassium out, calcium channels close.
  5. Cell repolarises and at hyperpolarisation, If channels open again.
    4.
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24
Q

What is the relationship pacemaker cells and heart rate?

A

The speed at which pacemaker cells depolarise determines heart rate (the rate at which the heart contracts)

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25
Q

What is the average number of heart beats per minute?

A

60-70 beats per minute but a change in the body’s demands may change the number of heart beats per minute.

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26
Q

How does the nervous system modulate heart rate?

A

Sympathetic nervous system - releases noradrenaline/norepinephrine and speeds up heart rate by increasing the influx of calcium and influx of sodium and efflux of potassium in If channels of the pacemaker cells.

Parasympathetic nervous system - releases acetylcholine - slows rate by increasing the efflux of potassium ions and reducing the influx of calcium ions.

27
Q

How can we measure the voltage across the heart?

A

By using an electrocardiogram - where electrodes are placed across the heart to measure the voltage across the heart.

28
Q

Name the different parts of a heart beat on an electrocardiogram

A

PQRS wave

P wave shows atrial depolarisation and T wave shows ventricular depolarisation.

29
Q

Describe the cardiac cycle

A
  1. Deoxygenated blood flows into the right atrium via the superior and inferior vena cava (veins)
  2. Blood flows from the right atrium to the right ventricle through the triscuspid valve (right atrioventricular valve)
  3. The blood from the right side of the heart is pumped into the lungs where it is OXYGENATED.
  4. Oxygenated blood flows back from the lungs to the left atrium through the bicuspid valve (left atrioventricular valve)
  5. Blood is pumped from the left ventricle through the aortic valve (semilunar valve) to the aorta and then to the rest of the body.
  6. As the ventricles relax, back flow of blood is prevented by the aortic/semilunar valve closing.
30
Q

What determines the ‘lub-dup’ sound of the heart beat?

A
  1. The first heart beat is caused by the closing of the AV valves.
  2. The second heart beat is caused by the closing of the semilunar valves (which includes the aortic valve)
31
Q

Give two types of conditions where the valves are damaged

A
  1. Stenosis - where the valves are narrowed and disrupts forward flow.
  2. Leaky valves - where the valves do not shut properly to prevent back flow.
    Both conditions will have a distinct sound.
32
Q

What is stroke volume?

A

It is the amount of blood ejected from a ventricle during a single heart beat.

33
Q

What is cardiac output?

A

CO = HR x SV

It is the amount of blood pumped out by the heart in a minute.

34
Q

What does cardiac output represent in terms of the well being of a person?

A

It is a measure of heart performance.

35
Q

How much is the normal blood volume of a person?

A

5 litres

36
Q

How is cardiac output regulated?

A
  1. Intrinsic regulation - preload and afterload

2. Extrinsic regulation - autonomic nervous system (sympathetic and parasympathetic)

37
Q

Describe the preload on the heart.

A

It is the degree at which the ventricular or heart muscles STRETCH before contraction - so it is the pressure on the heart before contraction.

38
Q

Describe Frank-Starlings Law of the heart

A

It describes the relationship between end diastolic volume (EDV) (which is controlled by venous return of blood) and stroke volume.

Stroke volume indicates the force of contraction of the ventricles and EDV indicates the measure of stretching.

So as more blood fills the ventricles from the veins (venous return), the ventricles stretch, then contract more forcefully, in order to eject more blood. Therefore as EDV increases (stretching increases), stroke volume increases because the contraction force increases.

39
Q

What does preload represent?

A

An increase in myocardial work and oxygen requirement. Increased filling of the heart causes an increase in output.

40
Q

What is afterload?

A

It is the combined end diastolic volume (EDV) and arterial resistance during ventricular contraction - it is the pressure at which the heart (ventricles) is contracting against.

41
Q

What causes an increase in afterload?

A

An increase in aortic pressure causes an increase in afterload, because the aortic pressure is the pressure at which the ventricles are contracting against.

As aortic pressure increases, the ventricles have to increase the strength of their contraction, therefore they stretch even more.

42
Q

What is ventricular hypertrophy?

A

A long term increase in arterial (aortic) pressure which result in the thickening of the ventricular muscles as they are over stretched as they aim to increase the force of contraction. So they permanently expand and increase in size.

43
Q

Explain the two ways of extrinsic regulation of cardiac output.

A

NS = nervous system
1. Sympathetic NS releases noradrenaline to act on beta1 adrenergic receptors on pacemaker cells - there is an increase in calcium and sodium (from If channels) influx and therefore an increase in depolarisation so an increase in heart rate.

  1. Parasympathetic NS - releases acetylcholine to act on muscarinic receptors on pacemaker cells to increase potassium efflux and decrease calcium influx, therefore slowing down depolarisation and hyperpolarising the pacemaker cells, so decreasing heart rate.
44
Q

Aside controlling heart rate, the autonomic nervous system can control stroke volume, describe this.

A

The sympathetic nervous system also acts on the muscles (myocytes) themselves by releasing noradrenaline and adrenaline to bind to beta1 adrenergic receptors on pacemaker cells which will then activate the cAMP second messenger system.

The cAMP second messenger system will phosphorylate voltage gated calcium channels (increases calcium entry from the extracellular fluid) and phospholamban (which increases calcium entry from the sarcoplasmic reticulum).

Lastly, the sympathetic nervous system can increase venous constriction so increase venous return and therefore increase EDV and stroke volume.

45
Q

Describe the ways in which venous return can be increased

A

EDV is determined by venous return.
Contraction of veins (skeletal muscle pump), pressure changes in abdomen and thorax (respiratory pump) and sympathetic in vervain of the veins controls venous return.

46
Q

How does sympathetic innervation of the veins affect the Frank-Starlings curve?

A

It shifts the curve to the left, because sympathetic innervation allows veins to constrict, decreasing their volume and increasing their pressure so more blood is forced out and flows into ventricles (increased EDV) therefore force of contraction increases and stroke volume increases.

47
Q

Why is blood measured by mean arterial pressure?

A

Arteries retains the pressure produced by the contraction of the left ventricle in their elastic walls and this pressure is slowly released by the elastic coil of the arteries.

48
Q

What determines mean arterial pressure (MAP)?

A

MAP is directly proportional to peripheral resistance (constriction of arterioles) and cardiac output.

49
Q

What is the function of arterioles?

A

They create high resistance for arterial blood flow and therefore direct blood flow to tissues by CONSTRICTING or DILATING. Arterioles are therefore said to have VARIABLE RESISTANCE.

50
Q

What regulates the diameter of arterioles?

A

It is regulated by metabolic/local factors - a decrease in oxygen levels and a rise in carbon dioxide levels (low pH) in tissues will cause VASODILATION so that more blood flows into the working tissue to provide carbon dioxide.

Paracrine (hormones) - noradrenaline is released which causes VASODILATION of arterioles. Release of histamine and bradykinin also causes VASODILATION.

Myogenic factors - an increase in blood pressure will cause local arterioles to constrict to ensure that capillary pressure is not raised.

51
Q

Which blood vessels contain smooth muscle?

A

Arteries have a lot of smooth muscle and veins have some smooth muscle but capillaries have no smooth muscle.

52
Q

Capillaries do not have smooth muscle except for which part?

A

The precapillary sphincter

53
Q

Which blood vessels have elastic tissue?

A

Arteries have a lot of elastic tissue, veins are less elastic than arteries.

54
Q

What are precapillary sphincters?

A

They are the muscle rings that support the capillaries.

55
Q

Put these in order of the largest - arteries, arterioles and capillaries. With 1 being the largest

A
  1. Arteries
  2. Arterioles
  3. Capillaries
56
Q

What is the difference between the walls of arteries and veins?

A

Veins have thinner walls but a larger diameter, arteries have thicker walls to store pressure from the left ventricle.

57
Q

Which blood vessel is most of our blood found and what is the function of the smooth muscle in this blood vessel?

A

About 65-70% of our blood is found in the veins. Smooth muscle allows the veins to alter their capacity and thus alter the filling pressure of the heart which contributes to stroke volume.

58
Q

What is the function of valves in the veins?

A

Valves prevent back flow of blood because pressure in the veins is very low and blood prefers to flow from a high to low pressure therefore back flow of blood is preferred but valves prevent this by shutting.

59
Q

What regulates venous return?

A

The skeletal muscle pump
The respiratory pump
The sympathetic nervous system (constricts veins, to increase their pressure, therefore forcing more blood out of them and increasing venous return)

60
Q

What is the endothelium? Describe it’s functions.

A

The endothelium is a type of epithelium.
It is the lining of the blood vessels.
It prevents blood clotting and controls the passing of substances from the blood to tissues.
It always regulates VASODILATION by releasing noradrenaline to modulate the contraction of smooth muscle around blood vessels.

61
Q

What generates blood pressure?

A

Ventricular contraction.

62
Q

Describe the windkessel effect.

A

When the ventricles relax after contraction, the semilunar (aortic valve) shuts and the elastic recoil of arteries (aorta) sends blood forward to the rest of the body.

63
Q

Describe the factors that affect blood pressure.

A
  1. Changes in blood volume - via blood loss or diuretics - which will REDUCE blood pressure.
  2. Varying cardiac output.
  3. Varying peripheral resistance - hypertension is thought to be caused by an increase in peripheral resistance.
  4. Redistribution of blood within the system - constricting of veins by sympathetic stimulation to increase venous return.
64
Q

What are the two mechanisms that regulate blood pressure.

A
  1. Local mechanisms - metabolic, paracrine and myogenic responses which constrict or dilate arterioles.
  2. CNS mechanisms - Renin Angiotensin Aldosterone System (RAAS)
65
Q

What is autoregulation?

A

It is the local control of resistance in arterioles to enable changes in flow or to keep flow or pressure constant.

Biology/Physiology (7 decks)

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