Cardiac cycle Flashcards

1
Q

What phases is each heart beat split into?

A

Diastole = 2/3 of each beat

Systole - 1/3 of each

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2
Q

What is diastole?

A

Ventricular relaxation - not contracting
blood is passively flowing from the left and right atrium into left and right ventricle. they fill.
4 subphases

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3
Q

Systole?

A

Ventricular contraction: Ventricles generate pressure then eject blood into arteries. ( left into the aorta, right into pulmonary artery)
3 subphases

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4
Q

What is the order of the cardiac cycle?

A
Atrial systole
isovolumetric contraction
rapid ejection
slow ejection
isovolumetric relaxation
rapid passive filling
slow passive filling
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5
Q

What is end-diastolic volume?

A

The Maximum volume of blood in the heart just before the ventricles start to contract.
Maximum relaxation, maximum filling in the heart and just before systolic period starts
120mL at rest

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6
Q

What is the end-systolic volume?

A

Amount of blood that is in the heart after contraction has been completed - essentially residual volume
50mL at rest

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7
Q

What is stroke volume?

A

The volume of blood that is expelled from the heart in any one cardiac cycle.
at rest approx 70mL

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8
Q

Stroke volume equation?

A

Stroke Volume (mL) = End-diastolic volume - end systolic volume

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9
Q

What is ejection fraction?

A

Cardiac function indicator
Stroke vol / end diastolic vol x 100 = ef %
normal range is 52-57%
heart failure could be 30-35%

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10
Q

Atrial Systole ECG

A

P wave on the ECG signifies start of atrial systole

Electrical activity stimulates atrial muscle to contract.

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11
Q

Atrial systole?

A

Atria already almost full from passive filling driven by the pressure gradient. They contract to ‘top up’ the volume of blood in the ventricle

Normally atria contraction contributes 10% of ventriculatr filling but can go up to 40% at high heart rates (when diastolic period is shortened)

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12
Q

4th heart sound?

A

an abnormal sound that may occur during atrial systole.

occurs w congestive heart failure, pulmonary embolism or tricuspid incompetence

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13
Q

Isolvolumetric contraction / Isovolumic contraction ECG?

A

QRS complex on ECG. Marks the start of ventricular depolarisation (excitation - coupling reaction)

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14
Q

What is isovolumetric contraction?

A

This is the interval between the AV valves (tricuspid and mitral) closing and semi-lunar valves (pulmonary and aortic) opening

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15
Q

What is the contraction of ventricles with no change of volume?

A

Isovolumetric contraction
(contraction without any change in volume)
Because both valves have closed

But pressure of ventricles increase to the extent of aortic pressure

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16
Q

When does the first heart sound happen and what’s the cause of it?

A

‘lub’ happens in isovolumetric contraction bc of the closure of the AV valves and associated vibrations

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17
Q

What marks the start of rapid ejection?

A

Opening of aortic and pulmonary valves.

= ejection begins when intraventricular pressure exceeds pressure within aorta and pulmonary arteries. Causing valves to open (aortic and pulmonary)

  • as blood is pumped out ventricular volume falls
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18
Q

Why is blood expelled from ventricles?

A

Because there is. pressure gradient that propels it from the ventricles into the aorta and pulmonary arteries.

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19
Q

When is maximum blood volume reached?

A

Early on in the rapid ejection phase

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20
Q

When are the max pressure of the pul artery and aorta achieved?

A

also v rapidly during rapid ejection. pressure mirrors the pressure in the ventricles

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21
Q

Is there a heart sound for rapid ejection?

A

No - valves opening doesn’t cause sound

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22
Q

When does reduced ejection occur?

A

200miliseconds after QRS complex and beginning of ventricular contraction. T wave on ECG

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23
Q

What does reduced ejection represent?

A

The end of the systole, T wave on the ECG = ventricular repolarisation occurring

24
Q

What does ventricular repolarisation do?

A

Decline in ventricular active tension and pressure. So rate of ejection and ventricular emptying falls.

As the pressure gradient falls between aorta and intraventricular pressure, aortic and pulmonary valves close. and blood flow from ventricles decrease, flow slows, ventricular volume decreases more slowly.

25
Q

What causes the semi-lunar valves to close

A

As the pressure in ventricles falls below arterial pressure, blood begins to flow back closing the valves.

26
Q

End of T wave?

A

complete repolarisation of ventricles

27
Q

What causes the second heart sound?

A

‘dub’

closure of semilunar valves and associated vibrations

28
Q

What happens to the AV valves when the aortic and pulmonary valves shut?

A

( isovolumetric relaxation )

Remain closed until ventricular pressure drops below atrial pressure * VENTRICULAR volume does not change

29
Q

How is the rate of pressure decline in the ventricles determined?

A

By the rate of relaxation of the muscle fibres = lusitropy

30
Q

What is muscle relaxation largely regulated by?

A

ATPase and calcium in the SR membrane

31
Q

What is the dichrotic notch?

A

Caused by rebound pressure against aortic valve as distended aortal wall relaxes, increasing aortic pressure for a few msecs before lowering.

  • notice on graph
32
Q

What on the ECG signifies the rapid passive filling?

A

No electrical activity : flat area after T wave

33
Q

What occurs during rapid passive filling?

A

AV valves rapidly open and blood flows from atrium to ventricles passively

34
Q

What may a 3rd heart sound be?

A

usually abnormal and may signify turbulent ventricular filling

Can be due to severe hypertension or mitral incompetence

35
Q

What is Reduced passive filling?

A

Also known as diastasis

Ventricular volume fills more slowly. To a considerable amount before atrial contraction.

  • End of diastole and cardiac cycle starts all over again after this.
36
Q

The patterns of pressure changes in the right heart are ( x ) to those of the left

A

Identical

37
Q

The pressure in the right heart and pulmonary circulation are ( x ) than left

A

Much lower

  • despite lower pressure right ventricles ejects same volume of blood as left
38
Q

What does measuring pulmonary capillary wedge pressure give a clinical measurement of?

A

Left atrial pressure

  • Gives an idea of left ventrical failure and mitral valve stenosis. These are due to increase in left atrial pressure. This tends to lead to increased pulmonary oedema
39
Q

Wha is the systemic circuit high pressure?

A

120/80 mmHg

whereas pulmonary circuit low pressure = 25/5 mmHg

40
Q

Why cannot we put a catheter in the left atrium to measure its pressure?

A

Although left ventricular pressure can be directly measured by placing a catheter within the left ventricle, it is not feasible to advance this catheter back into the left atrium.

41
Q

How do we measure pulmonary pressure or left atrial pressure?

A

Use the right side of heart, take a ventricular balloon and push that into the right atrium, ventricle and then the pulmonary artery and measure the pressures as u move from one change to other.

ra - low
rv- high
pa - also high
pcw- decreases

42
Q

What is preload?

A

amount of blood coming back to heart and stretching ventricles. (larger = larger force bc larger stretch)

43
Q

Referring to pressure loops, what does a larger preload do?

A

More blood moved into the L ventricle so more stretch occurs. And pressure increases ( larger Y axis value ) towards afterload.

44
Q

When does the ventricle encounter afterload?

A

Just after isovolumic ventricular contraction

45
Q

What pressure represents the afterload?

A

Blood pressure in the aorta and in the pulmonary artery

46
Q

Effects of increased afterload?

A

(greater diastolic pressure)

less shortening of muscle fibres and so less able to expel blood from ventricles.

When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.

Because a greater pressure is required to open the aortic valve.

volume loop gets larger in height. but narrower

  • slide 21
47
Q

What is the ESPVR?

A

End systolic Pressure-Volume line.

maximal pressure that can be developed by the ventricle at any given volume

if comp to the active/passive force graph it’d be the same as the active force

48
Q

Increases in preload result in what change in stroke volume?

A

Increases ( Frank-starling relationship )

Venous return increase = left ventricular volume increase

49
Q

How to calculate cardiac output?

A

Heart rate x Stroke volume

Stroke volume affected by preload, afterload and contractility.

50
Q

What is Contractility?

A

strength of contraction of the heart

affects stroke volume

Increased by: Sympathetic stimulation of myocytes

Extrinsic mechanism: Changes cAMP which changes Ca2+ delivery to myofilaments

51
Q

Cardiac contractility affects ( x ) of the Frank starling relationship?

A

Steepness

Can produce a ‘family’ of ESPVR lines

52
Q

As contractility increases, ESPVR lines?

A

Increase steepness

Generates more force due to more calcium to myofilaments and vice versa

53
Q

Why is exercise used to look at PV loops?

A

It is a good example of how simultaneous changes in preload, afterload and contractility affect the ventricular pressures and volumes

54
Q

During exercise, an (a) in end systolic volume and (b) in end diastolic volume leads to a (c) stroke volume

A

a - decrease

b - increase (produces an increase in stretch and increase in the force of the muscle. the increase in edv is brought about by the increase in venous return)

c - greater

55
Q

What happens to the end systolic pressure volume relationship during exercise?

A

shifts :
increase in contractility, sympathetic stimulation and symp activation = more calcium in myocytes and myofilaments. THIS DECREASES END SYSTOLIC VOLUME

56
Q

What happens during exercise that negates the positive effects?

A

Increased arterial pressure
this increases afterload
tends to lessen the reduction in systolic volume that occurs.

bUT major effect is thru sympathetic activation and the large increase in contractility overcomes the arterial pressure increase.

57
Q

What can happen to the end diastolic volume is heart rate is increased a lot?

A

Can lower it because less time is spent filling during diastole