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Anaesthetic FRCA Primary - eLFH Physiology > eLFH - Cardiovascular Physiology Part 1 > Flashcards

eLFH - Cardiovascular Physiology Part 1 Flashcards

1
Q

Cardiac cycle definition

A

Time taken to complete one systole and one diastole

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2
Q

Ratio of cycle spent in systole vs diastole

A

At rest one third systole, 2 thirds diastole

At faster heart rates ratio approaches 50:50

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3
Q

Normal peak LV pressures

A

120 mmHg

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4
Q

Normal peak RV pressures

A

25 mmHg

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5
Q

Total volume ejected into aorta per cycle (stroke volume)

A

70 ml

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6
Q

Pressure-time curve for LV, Aorta, LA and ECG

A
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7
Q

How would pressure- time curve differ for RV compared to LV

A

Same morphology as LV curve but at much lower pressures

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8
Q

Pressure-time curve for LV, Aorta and LA with key processes labelled

A

Explanations of each follows

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9
Q

Atrial systole

A

Pressure from atrial ejection of blood into ventricular cavity

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10
Q

Mitral valve closes

A

Atrial systole completes ventricular filling

Pressure in LV > LA

MV closes

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11
Q

Isovolumetric contraction

A

Both mitral and aortic valves closed

Pressure in LV increases until exceeds aortic pressure and AV opens

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12
Q

Aortic valve opens

A

AV opens at ~ 80 mmHg

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13
Q

Ejection

A

Ventricular ejection into aorta as LV pressure > aortic pressure

Initially ejection is rapid and then slows

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14
Q

Aortic valve closes

A

As ejection continues, LV pressure falls

AV closes once aortic pressure > LV pressure

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15
Q

Isovolumetric relaxation

A

Both MV and AV closed

Steep fall in pressure

Metabolically active process

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16
Q

Mitral valve opens

A

As LV pressure falls below LA pressure, MV opens and passive ventricular filling begins

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17
Q

Why does aortic pressure fall during diastole after aortic valve closes

A

Run off of blood into the vascular tree

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18
Q

What causes dichrotic notch on aortic pressure trace

A

Elastic recoil of aortic walls

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19
Q

Percentage of LV filling from atrial contraction vs passive filling

A

30% atrial contraction

70% passive filling

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20
Q

Left atrium pressure-time curve with key waves identified

A

Explanation of each follows

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21
Q

a wave

A

Atrial contraction

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22
Q

c wave

A

Small increase in LA pressure as isovolumetric contraction bulges back of the closed mitral valve

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23
Q

x descent

A

As ventricle contracts, pulls fibrous atrio-ventricular rings towards the apex of the heart

This comparatively lengthens the atria and causes pressure in LA to fall

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24
Q

v wave

A

LA pressure rises due to venous return accumulating in atria during systole whilst mitral valve remains closed

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25
Q

y descent

A

Mitral valve opens and blood flows into ventricle
Therefore LA pressure falls

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26
Q

Changes to LA pressure-time curve in AF

A

Absent a waves

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27
Q

Changes to LA pressure-time curve in Tricuspid regurgitation

A

Giant c wave
Loss of x descent
Merging of v wave

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28
Q

Changes to LA pressure-time curve in AV junction block

A

Regular cannon a waves

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29
Q

Changes to LA pressure-time curve in Complete heart block

A

Irregular cannon a waves

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30
Q

Pressure-volume loop for LV

A
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31
Q

Valves on Pressure-Volume loop for LV

A

A = MV open
B = MV closes
B to C = Isovolumetric contraction
C = AV opens
C to D = Ejection
D = AV closes
D to A = Isovolumetric relaxation

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32
Q

Stroke volume on Pressure-Volume loop for LV

A

SV = LVEDV - LVESV

Left ventricular end diastolic volume - Left ventricular end systolic volume

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33
Q

Work done by LV from pressure-volume loop

A

Work done = Pressure x Volume

Therefore Work done = area inside the loop

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34
Q

Three factors which modify the pressure-volume loop for LV

A

Preload

Contractility

Afterload

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35
Q

Preload definition

A

End diastolic stretch or tension of the ventricular wall

Represented on pressure-volume loop as LVEDV

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36
Q

Effect of increasing preload on stroke volume

A

Increasing preload increases stroke volume until overdistention occurs

Frank-Starling relationship

37
Q

Elastance definition

A

Reciprocal of compliance

Elastance = Change in pressure / Change in volume

38
Q

Effect of increasing preload on pressure-volume loop of LV

39
Q

Contractility definition

A

Intrinsic ability of heart to do mechanical work for a given preload and afterload

40
Q

Contractility representation on pressure-volume loop of LV

A

Shown by slope of the end systolic pressure line - angle of the end systolic pressure point with the x axis

This contractility line is called Ees

41
Q

Effect of increasing contractility on pressure-volume loop for LV

A

Ees has increased slope
Rotated up and to the left

42
Q

Afterload definition

A

Ventricular wall tension required to eject the stroke volume

43
Q

Representation of afterload on pressure-volume loop

A

Slope of the straight line joining LVEDV from x axis to the end systolic pressure point on the loop

Line is called Ea

44
Q

Effect of increasing afterload on pressure-volume loop

A

Gradient of Ea line moves up and to right

45
Q

Normal coronary blood flow in adults

A

200 - 250 ml/min

5% of cardiac output

46
Q

O2 extraction from coronary blood flow

47
Q

O2 extraction from the rest of the body blood flow

48
Q

Coronary perfusion pressure definition (CorPP)

A

Driving pressure for coronary circulation

Generated by difference between aortic pressure and intracardiac pressures, therefore varies throughout cardiac cycle

49
Q

Graph of coronary blood flow during systole and diastole

50
Q

Why is left coronary blood flow more impacted by systole and diastole than right coronary blood flow

A

Left coronary vessels are exposed to considerable transmitted pressure from LV during systole

Leads to left coronary compression

Left coronary blood flow almost ceases during systole

Transmitted intra-cavity pressures are much lower on the right so right coronary blood flow is less affected by cardiac cycle

51
Q

Typical pulmonary artery systolic and diastolic pressures

A

25 / 15 mmHg

52
Q

O2 supply to myocardium

A

Immediate endocardial layer on inner surface of ventricles obtains O2 directly via diffusion from blood within the ventricle cavity

Rest of heart muscle relies on coronary perfusion

53
Q

Resting membrane potential definition

A

Transmembrane voltage that exists when an excitable cell is quiescent (not producing an action potential)

Negative inside compared to Outside the cell

54
Q

Factors which contribute to Resting membrane potential

A

3Na+/2K+ ATPase pump (net loss of one positive ion per pump cycle)

Differential permeability of membrane to K+ and Na+

‘Held’ negatively charged molecules inside the cell (Donnan effect)

55
Q

Use of the Nernst equation

A

Calculates membrane potential for an individual ion at equilibrium

56
Q

Use of the Goldman equation

A

Examines contribution of multiple ions across the membrane

57
Q

Automaticity definition

A

Property of cardiac pacemaker cells in sinoatrial node

Lack stable resting membrane potential - spontaneously decays towards threshold potential (pre-potential)

58
Q

What occurs when cardiac pacemaker cells reach threshold potential

A

All or nothing depolarisation initiated

59
Q

Rate of spontaneous discharge in Sinoatrial node

60
Q

Rate of spontaneous discharge in Atrioventricular node

61
Q

Rate of spontaneous discharge from ventricular cell

62
Q

Maximal negative potential of cardiac pacemaker cell

63
Q

Threshold potential of cardiac pacemaker cell

64
Q

Peak positive potential of cardiac pacemaker cell

65
Q

Duration of cardiac pacemaker cell action potential cycle

66
Q

Three phases in cardiac pacemaker cell action potential

A

Phase 4 (Pre potential)

Phase 0 (Depolarisation)

Phase 3 (Repolarisation)

67
Q

Phase 4 of cardiac pacemaker cell action potential

A

Pre potential - no stable resting membrane potential

Slow decrease in membrane permeability to K+ so positive charge slowly build up within cell

RMP -60 mV moves to threshold -40 mV

Slope of phase 4 determines heart rate

68
Q

Phase 0 of cardiac pacemaker cell action potential

A

Depolarisation

Due to influx of Ca2+ ions

69
Q

Phase 3 of cardiac pacemaker cell action potential

A

Repolarisation

Due to inactivation of the slow Ca2+ channels and increased K+ outflow

70
Q

Effect on action potential of sympathetic / adrenergic stimulation of cardiac pacemaker cell

A

Increase slope of pre-potential

Hence increase heart rate

71
Q

Effect on action potential of parasympathetic / ACh stimulation of cardiac pacemaker cell

A

Increase K+ efflux from cell in phase 4

Thus delays pre-potential reaching threshold

Slope reduced and heart rate slowed

72
Q

Action potential in a cardiac muscle cell defining feature

A

Plateau phase

Calcium current extends duration of depolarisation by maintaining a positive intracellular charge

73
Q

Maximal negative potential of ventricular muscle cell

74
Q

Threshold potential of ventricular muscle cell

75
Q

Peak positive potential of ventricular muscle cell

76
Q

Duration of ventricular muscle cell action potential cycle

77
Q

Phases of ventricular muscle cell action potential

A

Phase 0 (Rapid depolarisation)

Phase 1 (Spike)

Phase 2 (Plateau)

Phase 3 (Repolarisation)

Phase 4 (Resting membrane potential)

78
Q

Phase 0 of Ventricular muscle cell action potential

A

Rapid depolarisation

Fast sodium channels open at threshold -70 mV
Influx of Na+ down concentration and electrical gradient

79
Q

Phase 1 of Ventricular muscle cell action potential

A

Spike

Onset of depolarisation due to Na+ channel closure

80
Q

Phase 2 of Ventricular muscle cell action potential

A

Plateau

Small but sustained current of Ca2+ into cell
Through slow-L type calcium channels

Opening triggered as action potential passes -35 mV with timed inactivation

81
Q

Function of plateau phase of ventricular muscle cell action potential

A

Provide absolute refractory period

Prevents tetanic contraction

82
Q

Phase 3 of Ventricular muscle cell action potential

A

Repolarisation

Closure of slow-L type calcium channels

Large efflux of K+ restores resting membrane potential

83
Q

Phase 4 of Ventricular muscle cell action potential

A

Resting membrane potential

Stable diastolic potential
Maintained by differential permeability of membrane to K+ and Na+ and Sodium/Potassium ATPase

84
Q

Ratio of differential permeability of ventricular muscle cell membrane to K+ and Na+

A

More permeable to K+ 100:1

85
Q

Morphology of atrial muscle cell action potential

A

Similar to action potential of ventricular muscle cell but shorter duration

Less extended plateau phase

86
Q

Excitation-contraction coupling definition

A

Sequence of events which converts action potential to cardiac muscle contraction

Link is calcium

87
Q

Process of excitation-contraction coupling

(Long but important flashcard)

88
Q

How does Beta adrenergic stimulation generate positive inotropy

A

Increases calcium flow through L type calcium channels

Anaesthetic FRCA Primary - eLFH Physiology (13 decks)

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