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
y descent
Mitral valve opens and blood flows into ventricle Therefore LA pressure falls
26
Changes to LA pressure-time curve in AF
Absent a waves
27
Changes to LA pressure-time curve in Tricuspid regurgitation
Giant c wave Loss of x descent Merging of v wave
28
Changes to LA pressure-time curve in AV junction block
Regular cannon a waves
29
Changes to LA pressure-time curve in Complete heart block
Irregular cannon a waves
30
Pressure-volume loop for LV
31
Valves on Pressure-Volume loop for LV
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
32
Stroke volume on Pressure-Volume loop for LV
SV = LVEDV - LVESV Left ventricular end diastolic volume - Left ventricular end systolic volume
33
Work done by LV from pressure-volume loop
Work done = Pressure x Volume Therefore Work done = area inside the loop
34
Three factors which modify the pressure-volume loop for LV
Preload Contractility Afterload
35
Preload definition
End diastolic stretch or tension of the ventricular wall Represented on pressure-volume loop as LVEDV
36
Effect of increasing preload on stroke volume
Increasing preload increases stroke volume until overdistention occurs Frank-Starling relationship
37
Elastance definition
Reciprocal of compliance Elastance = Change in pressure / Change in volume
38
Effect of increasing preload on pressure-volume loop of LV
39
Contractility definition
Intrinsic ability of heart to do mechanical work for a given preload and afterload
40
Contractility representation on pressure-volume loop of LV
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
Effect of increasing contractility on pressure-volume loop for LV
Ees has increased slope Rotated up and to the left
42
Afterload definition
Ventricular wall tension required to eject the stroke volume
43
Representation of afterload on pressure-volume loop
Slope of the straight line joining LVEDV from x axis to the end systolic pressure point on the loop Line is called Ea
44
Effect of increasing afterload on pressure-volume loop
Gradient of Ea line moves up and to right
45
Normal coronary blood flow in adults
200 - 250 ml/min 5% of cardiac output
46
O2 extraction from coronary blood flow
55 - 60%
47
O2 extraction from the rest of the body blood flow
25%
48
Coronary perfusion pressure definition (CorPP)
Driving pressure for coronary circulation Generated by difference between aortic pressure and intracardiac pressures, therefore varies throughout cardiac cycle
49
Graph of coronary blood flow during systole and diastole
50
Why is left coronary blood flow more impacted by systole and diastole than right coronary blood flow
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
Typical pulmonary artery systolic and diastolic pressures
25 / 15 mmHg
52
O2 supply to myocardium
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
Resting membrane potential definition
Transmembrane voltage that exists when an excitable cell is quiescent (not producing an action potential) Negative inside compared to Outside the cell
54
Factors which contribute to Resting membrane potential
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
Use of the Nernst equation
Calculates membrane potential for an individual ion at equilibrium
56
Use of the Goldman equation
Examines contribution of multiple ions across the membrane
57
Automaticity definition
Property of cardiac pacemaker cells in sinoatrial node Lack stable resting membrane potential - spontaneously decays towards threshold potential (pre-potential)
58
What occurs when cardiac pacemaker cells reach threshold potential
All or nothing depolarisation initiated
59
Rate of spontaneous discharge in Sinoatrial node
70-80 bpm
60
Rate of spontaneous discharge in Atrioventricular node
60 bpm
61
Rate of spontaneous discharge from ventricular cell
40 bpm
62
Maximal negative potential of cardiac pacemaker cell
- 60 mV
63
Threshold potential of cardiac pacemaker cell
- 40 mV
64
Peak positive potential of cardiac pacemaker cell
+ 20 mV
65
Duration of cardiac pacemaker cell action potential cycle
150 ms
66
Three phases in cardiac pacemaker cell action potential
Phase 4 (Pre potential) Phase 0 (Depolarisation) Phase 3 (Repolarisation)
67
Phase 4 of cardiac pacemaker cell action potential
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
Phase 0 of cardiac pacemaker cell action potential
Depolarisation Due to influx of Ca2+ ions
69
Phase 3 of cardiac pacemaker cell action potential
Repolarisation Due to inactivation of the slow Ca2+ channels and increased K+ outflow
70
Effect on action potential of sympathetic / adrenergic stimulation of cardiac pacemaker cell
Increase slope of pre-potential Hence increase heart rate
71
Effect on action potential of parasympathetic / ACh stimulation of cardiac pacemaker cell
Increase K+ efflux from cell in phase 4 Thus delays pre-potential reaching threshold Slope reduced and heart rate slowed
72
Action potential in a cardiac muscle cell defining feature
Plateau phase Calcium current extends duration of depolarisation by maintaining a positive intracellular charge
73
Maximal negative potential of ventricular muscle cell
- 90 mV
74
Threshold potential of ventricular muscle cell
- 70 mV
75
Peak positive potential of ventricular muscle cell
+ 20 mV
76
Duration of ventricular muscle cell action potential cycle
200 ms
77
Phases of ventricular muscle cell action potential
Phase 0 (Rapid depolarisation) Phase 1 (Spike) Phase 2 (Plateau) Phase 3 (Repolarisation) Phase 4 (Resting membrane potential)
78
Phase 0 of Ventricular muscle cell action potential
Rapid depolarisation Fast sodium channels open at threshold -70 mV Influx of Na+ down concentration and electrical gradient
79
Phase 1 of Ventricular muscle cell action potential
Spike Onset of depolarisation due to Na+ channel closure
80
Phase 2 of Ventricular muscle cell action potential
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
Function of plateau phase of ventricular muscle cell action potential
Provide absolute refractory period Prevents tetanic contraction
82
Phase 3 of Ventricular muscle cell action potential
Repolarisation Closure of slow-L type calcium channels Large efflux of K+ restores resting membrane potential
83
Phase 4 of Ventricular muscle cell action potential
Resting membrane potential Stable diastolic potential Maintained by differential permeability of membrane to K+ and Na+ and Sodium/Potassium ATPase
84
Ratio of differential permeability of ventricular muscle cell membrane to K+ and Na+
More permeable to K+ 100:1
85
Morphology of atrial muscle cell action potential
Similar to action potential of ventricular muscle cell but shorter duration Less extended plateau phase
86
Excitation-contraction coupling definition
Sequence of events which converts action potential to cardiac muscle contraction Link is calcium
87
Process of excitation-contraction coupling (Long but important flashcard)
88
How does Beta adrenergic stimulation generate positive inotropy
Increases calcium flow through L type calcium channels