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555- Physiology & Pathophysilogy > Exam 6 - Cardiac Cycle / Starling Curve > Flashcards

Exam 6 - Cardiac Cycle / Starling Curve Flashcards

1
Q

When are all valves closed

A
  • Isovolumic contraction and relaxation
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2
Q

Relationship of SV in ventricles

A
  • should be equal in a healthy person
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3
Q

Duration of cardiac cycle

A
  • Obtain HR
  • Take inverse of HR
  • Multiply by 60 to get duration of 1 cardiac cycle
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4
Q

1 Hz

A
  • 1 beat per minute
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5
Q

Time in systole and diastole

A
  • 1/3 in systole

- 2/3 in diastole

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6
Q

Length of systole

A
  • starts with A-V valve closure (isovolumic contraction)
  • ends with semi-lunar valve closure (isovolumic relaxation)
  • atrial contraction happens during systole
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7
Q

Length of diastole

A
  • starts with semi-lunar valve closure (isovolumic relaxation)
  • ends with closure of A-V valves (isovolumic contraction)
  • as HR increases…time spent in diastole decreases
    - both get shorter but diastole is sacrificed more
  • most of time spent in diastole is passive filling
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8
Q

Atrial kick contribution

A
  • 30% of the filling

- 20% of the actual SV

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9
Q

At what HR is time spent in each phase switched

A

200 bpm

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10
Q

Problems filling and ejecting can lead to….

A
  • Heart failure
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11
Q

Aortic Stenosis

A
  • effects systole

- isovolumic contraction pressure would increase

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12
Q

Aortic Insufficiency

A
  • effects diastole

- Aortic valve doesn’t close all the way at dicrotic notch

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13
Q

Mitral stenosis

A
  • effects diastole
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14
Q

Mitral insufficiency

A
  • effects systole

- more pressure in atria during systole

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15
Q

Hypertrophy

A
  • thickening of heart wall
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16
Q

Dicrotic notch

A
  • Aortic valve closing

- closes when there is no more forward flow through aorta

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17
Q

What keeps Aortic valve open at end of systole

A
  • KE of blood flow
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18
Q

A wave on wigger diagram

A
  • atrial contraction
  • atrial kick
  • small increase in atrial and ventricular pressure
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19
Q

C wave on wigger diagram

A
  • AV (mitral) valve closing and bulging into atrium
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20
Q

V wave on wigger diagram

A
  • atrial filling increases atrial pressure

- falls when mitral valve opens and releases blood into ventricle

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21
Q

S1 heart sound

A
  • beginning of systole (isovolumic contraction)
  • mitral and tricuspid valves slam shut
  • valves closing, vibrations, blood recoil….all cause noise
  • heard over apex of heart
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22
Q

S2 heart sound

A
  • beginning of isovolumic relaxation
  • aortic and pulmonary valve slam shut
    - PA after A because A has bigger pressure gradient
  • heard near end of t-wave
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23
Q

S3 and S4

A
  • not normally heard
  • heard during diastole
  • when heard it creates gallop rhythm
  • S3 heard in heart failure….S4 associated with atrial contraction
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24
Q

Left vs Right atrial and ventricular pressures

A
  • Left should be higher
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25
Q

Palliative surgery

A
  • alleviates symptoms
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26
Q

Corrective surgery

A
  • fixes problems permanently
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27
Q

Arterial-Venous O2 difference

A
  • 25% (100% arterial - 75% venous)
    • Heart takes 75% of the 100…25% left for body
  • Heart functions under aerobic only
    • if low O2….increase coronary blood flow (1:1 O2/flow ratio)
28
Q

Hypoxia

A
  • lack of O2
29
Q

Ischemia

A
  • lack of blood flow
30
Q

Diameter effect on velocity

A
  • if diameter decreases….velocity increases
31
Q

Types of heart work

A
  • Pressure work: work needed to open semilunar valves
    - work that builds up pressure
    - EXTERNAL work
    - 99% of total work
  • Volume work: work needed to eject blood
    - KE of blood flow
    - 1% of work….but can increase up to 50% w/ aortic stenosis
32
Q

Work output of heart

A
  • Pressure work + Volume work
  • amount of energy converted to work by heart for each beat
  • Increase in preload / afterload will increase work by heart
  • area under curve = stroke work output
33
Q

Minute work output

A
  • Stroke work output x HR
34
Q

Total energy output of heart

A
  • Heart external work (area under cure) + PE

- PE is work the heart could do if it were able to contract all the way to empty ventricle

35
Q

Work load of Left vs Right side

A
  • Right side is 1/6th of left
  • due to pressure difference…PVR is much lower than SVR
  • also uses 1/6th of the O2
36
Q

Energy efficiency of heart

A
  • ATP used by heart turned into heat and work
  • 20-25% efficient
    • can go as low as 5-10% with heart failure
37
Q

Diastolic pressure

A
  • Pressure at end of Diastole
  • Created by resting stretch
  • exponential curve shape due to compliance
    - high compliance at beginning….lower at end
  • optimal preload is 120-170ml…after that you get too big of increase in diastolic pressure
38
Q

Max ventricle pressure generation

A
  • 250-300 for LV

- 60-80 for RV

39
Q

Stroke volume

A
  • EDV-ESV
40
Q

Ejection fraction

A
  • SV/EDV
  • Normal is 50-70% (AHA)
  • 40% can be indicative of heart failure
41
Q

O2 consumption in diastolic phase

A
  • still happens…just less than systolic phase
42
Q

Tension developed during isometric contraction

A
  • enough to overcome afterload
43
Q

Relationship of stroke volume and fiber shortening

A
  • directly proportional
44
Q

Ejection vs shortening

A
  • As muscle fibers shorten….ejection occurs
  • Even though pressure increases due to ejection…radius of ventricle gets smaller (shortening) so overall tension decreases
45
Q

Normal CO

A
  • 5 L/min
  • changes based on moment to moment needs
  • HR x SV
  • CO is passive….meaning venous return dictates CO
46
Q

Factors that change HR

A
  • Sympathetic tone

- Parasympathetic tone (dominant controller of HR)

47
Q

Factors that will change SV

A
  • Intrinsic contractility (preload, resting stretch/tension) (+)
  • After-load (-)
  • Extrinsic contractility
48
Q

Preload and SV relationship

A
  • Increases preload increases distance fibers can shorten
  • 1 mmHg change in preload changes volume by 25 mls
  • changing EDV does not change ESV
  • no change in extrinsic contractility
49
Q

Afterload and SV relationship

A
  • increase in afterload will increase ESV
  • increase in afterload will decrease SV
  • 1 mmHg change in afterload changes SV by 0.5 ml
    - pressure change in preload affects SV more than afterload
  • EDV does not change but ESV does
  • Afterload is normally controlled tightly so normally wont see this
50
Q

Extrinsic contractility and SV relationship

A
  • increased sympathetic tone moves peak tension curve up and left
  • each fiber able to generate more tension at any given length
  • SV increases because fibers can shorten more than normal
  • ESV is decreased
51
Q

How increased contractility looks on graph

A
  • ESV moves left
  • same systolic pressure at lower systolic volume
  • increased slop of extrinsic line
52
Q

If only pre-load changes…

A
  • EDV changes proportional to preload change
    - fiber length changes same way (resting stretch)
  • ESV does not change
  • SV changes proportional to preload change
    - ability of fibers to shorten changes too
53
Q

If only after-load changes

A
  • EDV does not change
    - resting fiber length does not change
  • ESV changes (proportional to after-load change)
  • SV changes (inversely proportional to after-load change)
54
Q

If only extrinsic contractility changes

A
  • EDV does not change
  • ESV changes (inversely proportional to contractility change)
  • SV changes (proportional to contractility change)
55
Q

Estimation of contractility

A
  • End systolic pressure / End systolic volume

- can use PA to measure systolic pressure

56
Q

Volume pressure curves only show changes in what?

A
  • Stroke volume

- assuming no change in HR

57
Q

Maximum Cardiac Outputs

A
  • Max Para / No Symp: 7.5
  • No Para / No Symp: 10-11
  • No Para / Normal Symp: 12.5
  • No Para / Max Symp: 24-25
58
Q

Effects of parasympathetic on CO

A
  • Lower HR (negative chronotropic)
59
Q

Effects of sympathetic on CO

A
  • Increase HR (positive chronotropic)

- Increase SV (positive inotropic)

60
Q

Effects of arterial pressure on CO

A
  • arterial pressure is AFTER-LOAD

- more after-load will decrease SV

61
Q

Effects of filling pressure on CO

A
  • Filling pressure is PRE-LOAD

- more pre-load will increase SV

62
Q

Energy production by the heart

A
  • 70-90% from fatty acids
  • 10-30% from lactate and glucose
    • fetal cells use more lactate and glucose until few weeks old
63
Q

Myoglobin

A
  • protein in heart cells that binds with O2

- not as strong as hemoglobin

64
Q

O2 consumption by heart

A
  • remember heart uses 75% of available O2
  • of the O2 it consumes….
    • 25% used for basal metabolism… no contraction
    • 75% used for muscle contraction
      • 50% for x-bridges
      • 25% for pumping calcium
65
Q

Pressure work O2 consumption

A
  • 50% of overall cardiac O2 use
  • largest consumer of O2
  • major determinant is after-load
66
Q

Volume work O2 consumption

A
  • only 0.5% of overall cardiac O2 use

- Pressure is more costly in energy than volume

555- Physiology & Pathophysilogy (12 decks)

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