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MIDS 197 > Ch 4 Hemodynamics > Flashcards

Ch 4 Hemodynamics Flashcards

1
Q

The cardiac cycle is divided into how many phases hemodynamically?

A

7

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2
Q

List the 7 cardiac phases?

A

-Atrial systole
-IVCT
-Rapid ejection
-Reduced ejection
-IVRT
-Rapid filling
-Reduced filling

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3
Q

What happens in phase 1 atrial systole?

A

-P wave represents atrial depolarization, atrial contraction occurs shortly after
-Atria pressure increases (causes valves to open, a wave on graph)
-Blood moves through AV valves + into ventricles
-LV pressure rises due to increased volume
-Onset of QRS representing ventricular depolarization

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4
Q

What valves are open in phase 1 atrial systole?

A

AV valves open, semilunars closed

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5
Q

Does a mechanical function occur before or after the electrical stimulation?

A

After, always need electrical stimulation first before a mechanical function can occur

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6
Q

Where blood flows, what happens to pressure?

A

Pressure increases where blood goes

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7
Q

Are valves open or closed in phase 2 IVCT?

A

All closed

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8
Q

What happens in phase 2 IVCT?

A

-Beginning of systole (aka end diastole) represented with QRS, ventricular depolarization
-LV pressure keeps rising as muscle tension + contraction intensifies
-Isovolumetric b/c no change in ventricular volume (MV + AV closed)
-LA pressure increases as MV bulges into LA + continues pulmonary venous return (c wave on graph)
-Hear S1 due to MV closure

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9
Q

Which valves are open in phase 3 rapid ejection?

A

Semilunar valves, AV remain closed

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10
Q

What happens in phase 3 rapid ejection?

A

-LV pressure exceeds aortic pressure causing AoV to open + begin rapid ejection of blood from LV into AO
-LV volume rapidly decreases
-Peak systolic pressure reached in this phase (120 systolic BP # for systemic circulation)
-Atrial pressure remains stabilized

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11
Q

If we see mmHg in a question, what should we think right away?

A

Know it is a pressure gradient question

(mmHg = mm of mercury)

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12
Q

What valves are open in phase 4 reduced ejection?

A

Semilunar valves still open, AV still closed

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13
Q

What happens in phase 4 reduced ejection?

A

-LV still contracting but at slower rate until T wave occurs (ventricular repolarization)
-Ventricular pressure drops below AO pressure
-AO pressure goes down as well
-Outward flow still occurs due to kinetic energy of blood from LV propelling blood into AO still
-AoV closes, ending ventricular systole
-LA pressure slowly starting to increase

(think ventricles live high + atria live low)

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14
Q

Are valves open or closed in phase 5 IVRT?

A

All closed (causing equal pressure)

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15
Q

What happens in phase 5 IVRT?

A

-Onset of diastole (aka end systole) seen at end of T wave
-LV pressure falls rapidly due to relaxation, ventricular repolarization (T wave)
-Ventricular volumes remain constant due to all valves being closed
-LA pressure increases (v wave on graph) due to increasing volume of blood from pulmonary veins
-S2 sound occurs from AoV closure

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16
Q

What valves are open in phase 6 rapid filling?

A

AV valves open, semilunars closed

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17
Q

What happens in phase 6 rapid filling?

A

-LV pressure falls below LA, causing MV to open + allow rapid passive filling to occur
-Rapid filling of LV is due to the LA already being maximally filled when that MV opens
-Ongoing relaxation of LV causing a suction effect
-LA pressure decreases once MV opens, then levels off due to continuous flow from pulmonary veins

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18
Q

On m-mode of MV, what do each peaks represent?

A

1st E peak: 80% of blood from LA that passively fills LV (phase 6/7)

2nd A peak: 20% of blood from atrial kick as LA contracts
(phase 1)

(MV wants to close, but the atrial kick keeps it open a little longer which produces that second peak)

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19
Q

Phase 6 rapid filling correlates to which letter on m-mode of the MV?

A

E

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20
Q

What valves are open in phase 7 reduced filling?

A

AV valves still open, semilunars still closed

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21
Q

What happens in phase 7 reduced filling?

A

-Passive ventricular filling almost completed
-Referred to as period of ventricular diastasis (diastole)
-Ventricles continue to fill with blood + expand
-Ventricles become less compliant causing intraventricular pressure to rise

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22
Q

What happens after phase 7?

A

Cycle repeats again

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23
Q

Why is it important to know the normal pressure values in the heart?

A

To diagnose certain types of cardiac disease + dysfunction

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24
Q

List the pressure values for each chamber, the PA + AO?

A

RA: 4
RV: 25/4
PA: 25/10
LA: 8
LV: 120/8
AO: 120/80

(atria + ventricles must have similar diastolic values so that the atria can overcome the pressure in the ventricles in order to open the valve to allow blood to flow into the ventricles)

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25
Q

Pressure higher on left or right side?

A

LEFT (b/c systemic circulation)

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26
Q

The higher top number of the 2 pressure values represents what?

A

Systolic pressure (peak pressure during ejection)

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27
Q

The lower bottom number of the 2 pressure values represents what?

A

Diastolic pressure (end of diastole for ventricles + great arteries)

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28
Q

Notice how the atria only has 1 pressure value, what does this represent?

A

Average pressure in atria across cardiac cycle

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29
Q

Differentiate stroke volume + cardiac output?

A

SV: volume of blood ejected from LV in systole during 1 HEART BEAT (cardiac cycle)

CO: volume of blood the heart pumps out during 1 MINUTE

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30
Q

Cardiac output formula?

A

SV x HR

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31
Q

What is the normal CO range in a resting adult?

A

5-6 L/min

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32
Q

What affects CO?

A

Main:
-HR + SV

Others:
-preload (venous return, EDV)
-afterload (forward arterial resistance)
-inotropy (contractility)

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33
Q

What is ejection represented in?

A

%

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34
Q

What is hypervolemia?

A

Increased fluid volume

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35
Q

What is preload?

A

Volume of blood in ventricles at end of diastole (end diastolic pressure)

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36
Q

List 3 factors that increase preload?

A

-Hypervolemia
-Regurgitation of valves
-Heart failure

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37
Q

What stretches in preload before contraction?

A

Initial stretch of cardiac myocytes

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38
Q

What 3 things is preload determined by?

A

-Ventricular end diastolic volume (stretches LV)

-Ventricular end diastolic pressure (how much gas is left in tank)

-Ventricular compliance (how well can the ventricle relax/contract)

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39
Q

The pressure generated at a given volume is determined by what?

A

The compliance of the ventricle

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40
Q

Define the ratio of compliance?

A

Change in volume / change in pressure

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41
Q

List an example that would cause an increase + decrease in compliance?

A

Increase: dilated (loose) ventricle
Decrease: hypertrophic (stiff) ventricle

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42
Q

Is it easier to fill ventricles that are more or less compliant?

A

More compliant (willing to do so)

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43
Q

Would a heart with increased compliance have a higher or lower preload?

A

Higher - b/c has higher fluid volume in ventricles

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44
Q

What is afterload?

A

Pressure LV must overcome to eject blood through AoV to circulate blood throughout body

(load against which the heart must contract to eject blood)

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45
Q

Afterload is proportional to what?

A

Average arterial pressure

46
Q

The greater the aortic pressure, the greater or weaker the afterload on the LV?

A

Greater

47
Q

The greater the pulmonary pressure, the greater or weaker the afterload on the RV?

A

Greater

48
Q

What kinds of issues could lead to increased aortic or pulmonary pressures?

A

AO: hypertension
Pulmonary: COPD

49
Q

List 2 factors that increase afterload?

A

-Hypertension
-Vasoconstriction (narrowing blood vessels)

50
Q

Does an increase in afterload cause an increase or decrease in cardiac workload?

A

Increase

51
Q

What is the Frank Starling law/mechanism (rubber band theory)?

A

The more the stretch, the bigger contraction

52
Q

What is a sarcomere?

A

Basic contractile unit of a myocyte (muscle fiber)

53
Q

What does the frank starling law describe?

A

-Relationship b/w initial length of myocardial fibers + force generated by contraction

-Relationship b/w sarcomeres + tension of muscle fibers

54
Q

If the tension in the muscle fiber is greatest, will this cause a big or small force of contraction?

A

Greatest force of contraction

(think if we stretch out a rubber band as far as we can, it will fly across the room due to the biggest contraction)

55
Q

If the sarcomeres are closer together, will this cause an increase or decrease in contraction?

A

Decrease - b/c less tension + strength

56
Q

Frank starlings law observes that ventricular output increases as preload (end diastolic pressure/volume) increases or decreases?

A

Increases

(think more blood is being pumped out due to increased volume in ventricles at end diastole)

57
Q

The greater the ventricular diastolic volume, will the myocardial fibers stretch more or less in diastole?

A

More!

(think of balloon filling up + stretching)

58
Q

The more the myocardial fibers are stretched, the greater OR weaker the tension in the muscle fibers? What then happens to the force of contraction of the ventricle?

A

Greater stretch = greater tension = greater contraction

59
Q

What is a ventricular wall stress used to estimate?

A

The afterload on individual cardiac fibers within the ventricle

60
Q

Define ventricular wall stress?

A

It is the average tension the individual muscle fibers in the ventricular wall must generate to shorten against the developed intraventricular pressure

(think the sarcomeres must create tension so they can contract against the pressure)

61
Q

What represents wall stress?

A

Sigma

62
Q

Does afterload increase OR decrease when pressures in the ventricles is elevated during systole + by ventricular dilation?

A

Afterload is increased

63
Q

Does changes in preload affect tension? What is their relationship?

A

Yes! They are proportionately related!

(increase in preload = increase in tension)

64
Q

Define tension?

A

The ability of the muscle to develop force

65
Q

What is total tension?

A

-Passive tension + active tension
-Is the tension during contraction

66
Q

What is active tension?

A

Total tension - passive tension

(difference b/w total + passive tension curves)

67
Q

Maximum active tension of a cardiac myocyte corresponds to a sarcomere length of what?

A

2.2 micrometers

68
Q

Is preload EDV or ESV?

A

EDV - end diastolic volume

69
Q

Give an example of how we can apply the length tension relationship to the heart?

A

Length: ventricular volume (preload)
Tension: ventricular pressure

70
Q

As preload (EDV) increases, will pressure increase OR decrease in order for the ventricle to contract?

A

Increase

71
Q

Does increased afterload cause an increased OR decreased velocity of fiber shortening?

A

Decreased velocity - increased ventricular pressure causes shortening + decreases our SV

(think slower velocity b/c we can not pull the rubber band back as much, meaning it does not go very far)

72
Q

Does decreased afterload cause an increased OR decreased velocity of fiber shortening?

A

Increased velocity - less ventricular pressure allows for more ventricular stretching + a more forceful contraction

(think faster velocity b/c we can crank our rubber band back, meaning it will go very far)

73
Q

Is afterload + velocity proportionately related?

A

No! Inversely related

74
Q

Explain how increasing venous return affects preload + stroke volume?

A

Increases preload + SV

(more stretch = greater force of contraction = more volume ejected)

75
Q

Explain how decreasing venous return affects preload + stroke volume?

A

Decreases preload + SV

(less stretch = less force of contraction = less volume ejected)

76
Q

Is preload, stroke volume + venous return proportionately or inversely related?

A

Proportionately

77
Q

What do pressure volume (PV) loops measure?

A

-Direct real time cardiac function
-Plots real time ventricular pressure against ventricular volume

78
Q

Do PV loops use a qualitative or quantitative approach?

A

Quantitative

79
Q

Do PV loops determine the contractility of the heart independently OR dependently of preload + afterload?

A

Independently

80
Q

With PV loops, where is the PV catheter inserted into the heart?

A

Into RV/LV - measures all load-dependent data for every cardiac cycle

81
Q

What is the end systolic pressure volume relationship (ESPVR)?

A

The max pressure that can be generated by the ventricle at any given LV volume

82
Q

What is the end diastolic pressure volume relationship (EDPVR)?

A

Passive filling curve for the ventricle

83
Q

The slope of the EDPVR is the reciprocal of what?

A

Ventricular compliance

84
Q

Is afterload + SV proportionately or inversely related?

A

Inversely related

85
Q

As afterload increases, what happens to SV?

A

Decreases

(unable to pump out as much blood b/c ventricle can’t contract as well due to higher pressure/afterload)

86
Q

As afterload decreases, what happens to SV?

A

Increases

(ventricle is able to have a strong contraction + eject more blood out due to less pressure/afterload)

87
Q

Does higher afterload create more work for the ventricles?

A

Yes!

-less blood ejected due to less contraction (fiber shortening)
-reduced SV + higher end systolic volume
(b/c not ejecting as much blood out)

88
Q

Does the width of the PV loop increase or decrease with a higher afterload?

A

Decrease

89
Q

Does lower afterload create less work for the ventricles?

A

Yes!

-muscle fibers (ventricle) able to contract better
-increases SV + lower end systolic volume
(b/c ejecting more blood out)

90
Q

Does the width of the PV loop increase or decrease with a lower afterload?

A

Increase

91
Q

What occurs at a constant end diastolic volume, in regards to afterload + SV?

A

-Increased afterload (AO pressure)
-Decreased SV
-Increasaed ESV

92
Q

Does increased venous return increase OR decrease the width of the PV loop?

A

Increase

93
Q

When do the ventricles contract in regards to preload + afterload?

A

-When preload increases, causing more rapid fiber shortening
-When afterload is held constant (same ESV)

94
Q

If venous return increases, what happens to the force of contraction + the SV?

A

They both also increase - due to increased fluid volume

95
Q

Does Drank Starling ensure that the output of both ventricles will match over time?

A

Yes!

(RV output increases venous return to LV, causing LV output to increase as well)

96
Q

What is inotropy?

A

Known as the force of contraction (contractility)

97
Q

Changes in inotropy are caused by what?

A

Cellular mechanisms that alter myosin ATPase activity, at a given sarcomere length

98
Q

Give an example of an inotropic agent that increases the contractility of the heart?

A

Norepinephrine

99
Q

What is the most important factor that influences ventricular inotropy?

A

Sympathetic nervous system

100
Q

What is a hormone/neurotransmitter that the sympathetic nervous system releases?

A

Norepinephrine - it binds to B1 adrenoceptors in myocytes causing a positive inotropic effect in the atria + ventricles

101
Q

Does elevated epinephrine + norepinephrine have positive inotropic effects similar to sympathetic activation?

A

Yes

102
Q

During exercise our HR rises, what happens to our hearts filling time + our SV?

A

-Less filling time
-Lower SV

(less blood leaving heart b/c ventricles don’t have much time to fill when our heart beats faster)

103
Q

Increased inotropy (contractility) by sympathetic activation causes a greater OR weaker force of contraction?

A

Greater

(maintains SV despite lower EDV)

104
Q

An increase in inotropy causes an increase OR decrease in SV?

A

Increase

105
Q

A decrease in inotropy causes an increase OR decrease in SV?

A

Decrease

106
Q

Does inotropy + SV have an inverse or proportionate relationship?

A

Proportionate/congruent relationship

107
Q

What happens to the PV loop width when there is higher contractility, increased SV + lower ESV?

A

Increased PV width (b/c increased pressure + volume in ventricle)

108
Q

What happens to the PV loop width when there is lower contractility, decreased SV + higher ESV?

A

Decreased PV width (b/c decreased pressure + volume in ventricle)

109
Q

Do changes in inotropy change our EF?

A

Yes!

110
Q

Does increased inotropy cause an increased EF?

A

Yes - due to increased ventricular pressure

111
Q

Can the ventricles generate increased pressure at any given volume?

A

Yes - to a certain degree

MIDS 197 (15 decks)

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