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nuero > cardiac cycle > Flashcards

cardiac cycle Flashcards

1
Q

what is systole

A

Ventricular contraction

Ventricles generate pressure then eject blood into the arteries

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2
Q

what is diastole

A

Ventricular relaxation

The ventricles fill with blood

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3
Q

what is the 1st phase

A

systole

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4
Q

what is teh end diastolic volume

A

maximum blood in the heart just before the ventricle start to contract

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5
Q

End-systolic volume

A

residual volume left in the heart after contracting

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6
Q

what is teh Stroke volume (mL)

A

End-diastolic volume - End-systolic volume

how much blood is ejected

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7
Q

what is a clinical indicator of heart function

A

ejection fraction

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8
Q

how to work it out

A

stroke volume/End-diastolic volume

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9
Q

normal range of ejection fraction

A

52 - 72

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10
Q

patient in heart fraction

A

30 - 35

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11
Q

what is the start of teh cardiac cycle

A

artial systole

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12
Q

how is the start shown on an ecg

A

p wave = atrial systole

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13
Q

what does the atrial contraction do

A

Atria contract to ‘top-up’ the volume of blood in ventricle

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14
Q

what may you hear in the heart of a patient with congestive heart failure, pulmonary embolism or tricuspid incompetence

A

4th heart sound

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15
Q

next stage

A

Isovolumetric contraction

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16
Q

what is it shown on ecg

A

QRS

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17
Q

which is

A

start of ventricular depolarisation

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18
Q

what is start of ventricular depolarisation

A

This is the interval between AV valves (tricuspid & mitral) closing and semi-lunar valves (pulmonary & aortic) opening
(ventricular pressure increases near the aortic pressure)

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19
Q

what is the change in volume

A

no change in volume §

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20
Q

what causes the first heat sound (lub) to occur

A

closure of AV valves

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21
Q

what sort contractions occur at this point

A

isometric

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22
Q

what is the next stage

A

rapid ejection

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23
Q

when does it begin

A

As ventricles contract pressure within them exceeds pressure in aorta and pulmonary arteries. Semilunar valves open, blood pumped out and the volumes of ventricles decrease.

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24
Q

so what marks the start of this phase

A

Opening of the aortic & pulmonary valves mark the start of this phase

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25
Q

what is the heart sound in this phase

A

no heart sound

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26
Q

what is the next stage

A

Reduced ejection

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27
Q

what does thsi phase signify

A

This phase marks the end of systole

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28
Q

what causes the semilunar valves to close

A

Reduced pressure gradient means aortic & pulmonary valves begin to close
As pressures in ventricles fall below that in arteries, blood begins to flow back causing semilunar valves to close

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29
Q

describe the changes to the ventricular volume

A

Blood flow from ventricles decreases and ventricular volume decreases more slowly

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30
Q

what causes teh t wave

A

Ventricular muscle cells repolarize producing T wave

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31
Q

what is the next stage

A

Isovolumetric relaxation

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32
Q

when do the AV valves open

A

The aortic & pulmonary valves shut, but the AV valves remain closed until ventricular pressure drops below atrial pressure.

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33
Q

what causes the Dichrotic notch

A

caused by rebound pressure against aortic valve as distended aortic wall relaxes.

34
Q

what heart sound can be heard

A

2nd - dub

35
Q

why

A

due to closing of the SL valves

36
Q

what is the rate of pressure decline in the ventricle caused by

A

rate of relaxation of the muscle fibre

regulated by ca atpases in sr membrane

37
Q

do volume change

A

no- isometric

38
Q

what stage occurs next

A

Rapid passive filling

39
Q

when do AV valves open

A

when ventricular pressure falls below the atrial presuure

40
Q

what part of ecg

A

Occurs during isoelectric (flat) ECG between cardiac cycles

no electrical activity

41
Q

what is the heart sound heard

A

3rd heart sound – usually abnormal and may signify turbulent ventricular filling
Can be due to severe hypertension or mitral incompetence (mitrial doesn;t close properly)

42
Q

what is the next stage

A

Reduced passive filling

43
Q

aka

A

This phase can be called diastasis

44
Q

what happens

A

ventricle fills more slowly

45
Q

how mcuh can V without atrial contraction

A

The ventricles are able to fill considerably without the contraction of the atria.

46
Q

next stage

A

starts again atrial systole

47
Q

how do the pressure change pattern in the right and left side of the heart compare

A

identical

48
Q

what is teh differnce in bith sides

A

Quantitatively, the pressures in the right heart and pulmonary circulation are much lower (peak of systole – 25mmHg in pulmonary artery)

49
Q

blood difference ejected

A

Despite lower pressures right ventricle ejects same volume of blood as left (it is simply pumping the same quantity of blood into a lower pressure circuit)!

50
Q

what is the pulmonary capillary wedge pressure

A

indirect estimate of left atrial pressure

gives us idea of severity of left ventricular failure

51
Q

what does an increase in left ventricular pressure cause atrial

A

increase pulminary oedema

life threating

52
Q

how to measure the left atrial pressure

A

use right side of the heart

ventriular bloon right atrium ventricle

53
Q

what happens when we reach aortic pressure

A

aortic valvue opens blood expelled from the heart

54
Q

what is preload

A

the amount of blood coming back to teh heart stretching the ventricles

55
Q

how to increase preload

A

increase in amount of blood returning to the heart

56
Q

relationship between preload and force

A

larger preload, larger stretch more force

more blood ejected

57
Q

what is the afterload

A

Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction
diastolic blood pressure

58
Q

what does the afterload cause

A

shorteing of teh muscle fibres

less able to expel blood in teh ventricles

59
Q

what represents the afterload

A

The blood pressures in great vessels (aorta and pulmonary artery) represent the AFTERLOAD

60
Q

what is ESPVR

A

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

61
Q

Increases in preload result in

A

increased stroke volume

62
Q

what is that known as

A

This is the Frank-Starling relationship

63
Q

Increases in afterload result in

A

decreased stroke volume

afterload increases, the amount of shortening of muscle fibres that occurs decreases

64
Q

when the after load increases what effect does it have on the aortic valve

A

Greater pressure required to open aortic valve
afterload is the resistance that is required to be overcome to circulate blood so high pressure aorta = higher pressure in ventricle (i think)

65
Q

what is cardiac output calculated

A

Heart rate
*
Stroke volume

66
Q

what is stroke volume affected by

A

Preload
Afterload
Contractility

67
Q

what is Contractility

A

Contractile capability (or strength of contraction) of the heart

68
Q

what is it increases by

A

Sympathetic stimulation

69
Q

how

A

Changes Ca2+ delivery to myofilaments

70
Q

What happens to PV loops during exercise?

A

(1) Increased VR (vebous return) aided by muscle and respiratory pump increases EDV
2 Main factor: Sympathetic activation of the myocytes increases ventricular contractility, that decreases end-systolic volume.
3 combacted by The increase in arterial pressure that occurs during exercise increases afterload (and can lessen the reduction in end-systolic volume but offset by large increase in contractility)

71
Q

summary

A

(4) Combination of increased cardiac contractility and increased VR generate increased SV (and EF) ejection fraction

72
Q

what is this dependent on

A

If HR increases to very high rates, diastolic filling time can be reduced and this decreases EDV

73
Q

what hormone can cause symoathetic innervation

A

Hormonal: Circulating adrenaline from adrenal gland

74
Q

nueral

A

Neural: Noradrenaline released from nerves

75
Q

how does an increase in preload shown on a pv grapgh

A

more wide- (more left ventricular volume) (increase size from the left) same pressures

76
Q

decrease preload

A

more narrow- less ventricular volume (decrease size from the left)
same pressures

77
Q

increase afterload

A

thinner and higher

thinner from the right side is squashed

78
Q

decrease afterload

A

normal

79
Q

excersize

A

Venous return increases due to venoconstriction and skeletal muscle pump, and contractility is increased via sympathetic nervous system

wider from both sides and higher

80
Q

what increases afterload

A

hypertension vasoconstriction

81
Q

increase preload

A

higher venous return

nuero (36 decks)

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