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

Exam 6 - Cardiac Cycle / Starling Curve Flashcards

(66 cards)

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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
Palliative surgery
- alleviates symptoms
26
Corrective surgery
- fixes problems permanently
27
Arterial-Venous O2 difference
- 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
Hypoxia
- lack of O2
29
Ischemia
- lack of blood flow
30
Diameter effect on velocity
- if diameter decreases....velocity increases
31
Types of heart work
- 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
Work output of heart
- 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
Minute work output
- Stroke work output x HR
34
Total energy output of heart
- 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
Work load of Left vs Right side
- 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
Energy efficiency of heart
- ATP used by heart turned into heat and work - 20-25% efficient - can go as low as 5-10% with heart failure
37
Diastolic pressure
- 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
Max ventricle pressure generation
- 250-300 for LV | - 60-80 for RV
39
Stroke volume
- EDV-ESV
40
Ejection fraction
- SV/EDV - Normal is 50-70% (AHA) - 40% can be indicative of heart failure
41
O2 consumption in diastolic phase
- still happens...just less than systolic phase
42
Tension developed during isometric contraction
- enough to overcome afterload
43
Relationship of stroke volume and fiber shortening
- directly proportional
44
Ejection vs shortening
- As muscle fibers shorten....ejection occurs - Even though pressure increases due to ejection...radius of ventricle gets smaller (shortening) so overall tension decreases
45
Normal CO
- 5 L/min - changes based on moment to moment needs - HR x SV - CO is passive....meaning venous return dictates CO
46
Factors that change HR
- Sympathetic tone | - Parasympathetic tone (dominant controller of HR)
47
Factors that will change SV
- Intrinsic contractility (preload, resting stretch/tension) (+) - After-load (-) - Extrinsic contractility
48
Preload and SV relationship
- 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
Afterload and SV relationship
- 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
Extrinsic contractility and SV relationship
- 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
How increased contractility looks on graph
- ESV moves left - same systolic pressure at lower systolic volume - increased slop of extrinsic line
52
If only pre-load changes...
- 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
If only after-load changes
- 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
If only extrinsic contractility changes
- EDV does not change - ESV changes (inversely proportional to contractility change) - SV changes (proportional to contractility change)
55
Estimation of contractility
- End systolic pressure / End systolic volume | - can use PA to measure systolic pressure
56
Volume pressure curves only show changes in what?
- Stroke volume | - assuming no change in HR
57
Maximum Cardiac Outputs
- 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
Effects of parasympathetic on CO
- Lower HR (negative chronotropic)
59
Effects of sympathetic on CO
- Increase HR (positive chronotropic) | - Increase SV (positive inotropic)
60
Effects of arterial pressure on CO
- arterial pressure is AFTER-LOAD | - more after-load will decrease SV
61
Effects of filling pressure on CO
- Filling pressure is PRE-LOAD | - more pre-load will increase SV
62
Energy production by the heart
- 70-90% from fatty acids - 10-30% from lactate and glucose - fetal cells use more lactate and glucose until few weeks old
63
Myoglobin
- protein in heart cells that binds with O2 | - not as strong as hemoglobin
64
O2 consumption by heart
- 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
Pressure work O2 consumption
- 50% of overall cardiac O2 use - largest consumer of O2 - major determinant is after-load
66
Volume work O2 consumption
- 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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