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BS - Cardiovascular System > Cardiac Haemodynamics > Flashcards

Cardiac Haemodynamics Flashcards

1
Q

What happens when the ventricles are 70% full with blood?

A

The atria contract in atrial systole

The pressure in the atria increases and forces blood into the ventricles

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2
Q

How is the first heart sound created?

A

As ventricles begin to contract, ventricular pressure exceeds atrial pressure

The atrioventricular valves close - the first heart sound

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3
Q

What happens after the atrioventricular valves have closed?

What type of contraction is this?

A

Both sets of heart valves are closed so pressure rapidly builds in the contracting ventricles

This is an isovolumetric contraction as there is no change in volume

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4
Q

What happens when ventricular pressure exceeds pressure in the aorta?

A

The aortic valve opens and blood is ejected into the aorta

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5
Q

What happens to ventricular pressure in diastole?

A

Ventricular pressure falls as blood enters the aorta

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6
Q

How is the second heart sound created?

A

When ventricular pressure falls below aortic pressure, the aortic valve closes

This creates the second heart sound

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7
Q

What happens when ventricular pressure drops below atrial pressure?

A

The atrioventricular valves open

Blood flows from the atria into the ventricles

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8
Q

What is different in a cardiac action potential compared with skeletal muscle and neuronal action potentials?

A

There is a key role for calcium in the cardiac action potential

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9
Q

What is the resting potential of cardiac muscle?

A

-90 mV

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10
Q

What happens during phase 0 of the cardiac action potential?

A

Rapid influx of sodium ions causes depolarisation

Membrane potential reaches + 10 mV

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11
Q

What happens during phase 2 of the cardiac action potential?

A

Rapid influx of calcium ions leads to initiation of the contraction

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12
Q

What happens during phase 3 of the cardiac action potential?

A

Potassium ions leave the cell and it repolarises

After repolarisation it returns to its resting state

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13
Q

What is significant about there being a lot of variability between cardiac myocytes?

A

variability helps to contribute to the geometric shape of the left ventricle

This allows different parts of the ventricle to contract in different ways

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14
Q

What is the state of troponin and tropomyosin before contraction of cardiac muscle?

A

Troponin and tropomyosin form a complex that blocks the myosin binding site on the actin filament

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15
Q

What happens during systole in relation to contraction?

A

Calcium ions arrive inside the sarcoplasm and bind to troponin

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16
Q

What happens when calcium ions bind to troponin?

A

They move the troponin-tropomyosin complex and expose the myosin binding site on the actin filament

The myosin head binds to the actin filament and forms a cross-bridge

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17
Q

How does contraction result from cross-bridge formation?

A

The myosin heads dock in and exert a pulling action on the actin

This results in a contraction

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18
Q

What can usually be detected in heart attack patients?

A

Troponin leaks out of the myocyte, and this can be detected

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19
Q

How much ATP is used by myocardial cells daily?

A

6 kg

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20
Q

What is stored within ATP?

How can this be converted into mechanical energy?

A

Chemical energy is stored within ATP

It is hydrolysed to release a phosphate group, and is converted to ADP

This process converts it into mechanical energy

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21
Q

What does converting ATP into mechanical energy mean for the myocardium?

A

It results in force generation and myofilament shortening

This process transforms basic mechanical energy into a useful hydraulic function for the whole organ

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22
Q

Concerning the hydraulic function of the heart, what happens when wall stress increases?

A

Fluid pressure in the chamber is raised

Left ventricular pressure exceeds aortic pressure and the aortic valve opens

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23
Q

Concerning the hydraulic function, in which ways do the myocardial fibres thicken?

Why does this happen?

A

There is both:

  1. longitudinal filament shortening
  2. circumferential thickening

This leads to a complex geometric reconfiguration that reduces LV chamber diameter

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24
Q

What is the purpose of reducing LV chamber diameter?

A

It causes further blood to be displaced from the ventricle into the circulation

This increases ejection fraction

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25
Q

Concerning hydraulic function, what happens to the ventricular muscle when the ventricle contracts?

A

The muscle becomes shorter and thicker

This increases ejection pressure

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26
Q

Why is the hydraulic function of the heart creating a high pressure important?

A

The system in which blood is propelled has inherent resistance as it branches out into increasingly small and dense vessel networks

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27
Q

What does branches of the arteries becoming smaller contribute to?

A

Systemic vascular resistance

28
Q

What needs to be done in order to overcome increased systemic vascular resistance?

A

The cardiac output needs to be maximised through effective power generation in the pump

29
Q

Why is the diastolic period essential?

A

It allows the electric system to repolarise

It allows the myocardium to relax and the heart to fill with blood

30
Q

What other things occur during the diastolic period?

A
  1. aortic valve shuts
  2. coronary sinuses fill with blood
  3. myocardium receives oxygen and glucose to allow more ATP to be generated
31
Q

What is cardiac functional reserve?

A

It is the capacity of the heart to augment performance on demand

The heart needs to pump at rest, but also needs to be able to cope with higher demands

32
Q

During which conditions may it be necessary to utilise cardiac reserve?

A
  1. exercise
  2. intercurrent illness
  3. pregnancy
  4. fluid overload
33
Q

What is the equation for cardiac output?

A

cardiac output =

heart rate x stroke volume

34
Q

What is the equation for cardiac reserve?

A

cardiac reserve =

maximal cardiac output - cardiac output at rest

35
Q

Which 2 mechanisms are used to increase cardiac reserve?

A
  1. increasing heart rate

2. increasing stroke volume

36
Q

What is the effect of sympathetic innervation on increasing heart rate?

A

It increases SA node depolarisation

This leads to more frequent action potentials in the heart

This increases conduction through the AV node and bundle of His

37
Q

How does adrenaline act to increase the heart rate?

A

It increases the heart rate through action on adrenergic receptors

This is B1 agonism

38
Q

What mechanisms are used to increase stroke volume?

A

Stroke volume is increased through sympathetic activity

Stroke volume also depends on preload

39
Q

How does the sympathetic nervous system act to increase stroke volume?

A

It causes prolonged opening of Ca+ channels, so more Ca2+ enters cells

This enhances calcium action in excitation-contraction coupling mechanisms

This leads to increased contraction of cardiac muscle cells

40
Q

How does stroke volume change with sarcomere length?

A

As sarcomere length increases, there is more Ca2+ influx

The tension within the sarcomere increases

This causes an increased stroke volume

41
Q

What is meant by cardiac muscle having a much smaller window of activity than skeletal muscle?

A

Small changes in cardiac sarcomere length result in large variations in tension

42
Q

On the tension-sarcomere length graph, what is the situation at physiological stretch?

A

Ventricular sarcomere length is on the ascending limb

Stretching the left ventricle will aid contraction

43
Q

What does left ventricle end-diastolic volume determine?

A

It determines how stretched the left ventricle is

44
Q

What is preload?

A

The load on the ventricle before it contracts

45
Q

Why can more contraction occur as the left ventricle becomes more stretched?

A

As the muscle stretches, the diameter of the myofibril is reduced

The thick and thin filaments are closer together

More myosin heads can interact with actin

46
Q

What does Starling’s Law of the heart state?

A

The energy of contraction is a function of the length of the muscle fibre

47
Q

According to Starling’s Law of the heart, what happens to stroke volume as preload increases?

A

As preload increases, stroke volume increases

There is more interaction between the filaments and the myofibrils

48
Q

Why does an increased preload lead to an increased stroke volume?

A

venous return always correlates with cardiac output

exercise and other demands lead to increased venous return, which allows augmentation of stroke volume

49
Q

Why does venous return always correlate with cardiac output?

A

It equilibrates the right and left heart output

Left ventricular cardiac output is the same as right ventricle preload

50
Q

What is on the x and y axis of the Frank-Starling curve?

A

y axis - stroke volume

x axis - LVEDP which is the same as preload

51
Q

what causes the dynamic Frank-Starling curve to shift to the left and right?

A

Shifts to left during exercise and pharmacological stimulation

Shifts to the right during myocardial loss and pharmacological depression

52
Q

In which direction does sympathetic stimulation shift the Frank-Starling curve?

What is the mechanism behind this?

A

To the left

Noradrenaline and adrenaline stimulate cAMP

This means that more calcium can enter the cell and there is greater cross-bridge formation in sarcomeres

53
Q

What is ejection fraction?

A

The amount of blood that is ejected from the ventricle with each contraction

(during each systole)

54
Q

What is the equation for ejection fraction?

A

ejection fraction =

stroke volume + end-diastolic volume

55
Q

What is physiological ejection fraction and how does this change during exercise?

A

physiological ejection fraction is 50 - 75%

during exercise, ejection fraction can reach 90%

56
Q

What would show reduced ejection fraction?

A

a failing heart

57
Q

In heart failure, what do the following conditions lead to?

i - diseased myocardium

ii - ischaemia

iii - viral infections/alcohol

iv - increased afterload

A

i - myocardium contracts less

ii - scarred myocardium

iii - wall-thinning

iv - chronic high-output

58
Q

How does the body try to compensate for a failing ventricle?

A

Over-activation of the sympathetic nervous system to increase the heart rate

The renin-angiotensin-aldosterone system also kicks in

59
Q

How do the measures to compensate for a failing ventricle work over time?

A

They initially increase the preload

Eventually left ventricular stretch exceeds physiological levels and it moves to the descending limb of the sarcomere tension curve

The heart cannot increase stroke volume as the muscle is not working

60
Q

How is the Frank-Starling curve shifted in left ventricular failure and why?

A

to the right

Even though preload is increasing, the stroke volume is decreasing

61
Q

How are the lungs affected by heart failure?

A

Left ventricular failure leads to the lungs filling with fluid

The fluid leaks into the interstitial spaces and eventually the alveoli

62
Q

How can alveolar ventilation be optimised in heart failure?

A

High-flow oxygen

63
Q

What is used to relax pulmonary vessels in heart failure?

What is the purpose of this?

A

Morphine

This reduces the preload and takes the strain off the left ventricle

It helps to remove some fluid from the lungs

64
Q

what is morphine used for in heart failure?

A

To relax the pulmonary vessels

It also helps with breathing and pain

65
Q

What is furosemide used for in heart failure?

A

It takes some fluid off the lungs to help with breathing

It also reduces the preload

66
Q

Why is it important to used furosemide to help with breathing in heart failure?

A

Helping with breathing helps to improve oxygen saturation

BS - Cardiovascular System (20 decks)

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