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Kin 426 > 2.2 > Flashcards

2.2 Flashcards

1
Q

what determines the strength of cardiac contraction

A

preload

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2
Q

for an isolated strip of ventricular cardiac muscle or an isolated papillary muscle in experiment, what is preload

A

force (load) on the muscle prior to its being activated to contract

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3
Q

what does preload apply

A

tension to the muscle and stretches it passively to a new length

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4
Q

by addition of very large afterload what may muscle have to do

A

may be forced to contract isometrically and muscle will not be able to lift

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5
Q

by addition of very large afterload why may muscle not be able to lift

A

isometrically contract because further lengthening that would be caused by afterload is prevented with a physical stop

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6
Q

upon electrical stimulation what does muscle do

A

contracts isometrically and develops max active force of which it is capable from that initial length

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7
Q

what does increasing preload do

A

always stretches muscle further, causing both increased initial length and greater active force development to a point

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8
Q

total tension within muscle at peak of contraction is

A

sum of the passive tension and active tension

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9
Q

when contractility is increased

A

active tension and total tension are greatly increased

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10
Q

what can increase contractility

A

norepinephrine

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11
Q

what is largely unaffected when contractility is increased

A

passive tension
thus increase in total tension is due entirely to greater active tension

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12
Q

reduction in contractility

A

results in reduced total tension
largely due to decreased active tension development

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13
Q

example of something that reduces contractility

A

pharmacologic block of L-type Ca++ channels

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14
Q

heart that had heart attack that LV moves toward atria and enlarges

A

trying to increase SV and preload

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15
Q

decreased contraction from too much length is analogous to

A

right limb of frank starling method

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16
Q

how decrease contractility

A

block Ca++ into cell or block B adrenergic receptors

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17
Q

as increase length of papillary muscle

A

force development increases to a certain point

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18
Q

when stretched too much

A

force development goes down
same as descending limb of frank starling curve

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19
Q

in the heart, preload is

A

stress exerted on the ventricle during diastole

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20
Q

what can preload in heart be represented by

A

laplace equation for a thick walled sphere

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21
Q

what is laplace equation

A

wall stress is inverse to wall thickness

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22
Q

explanation of use of laplace equation for preload in hear

A

increased preload, increases pressure which increases wall stress
ventricle with bigger EDV will have more wall stress

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23
Q

what can muscle be characterized by

A

a passive length-tension relationship

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24
Q

how is the passive length-tension relationship obtained

A

measuring length at different preloads

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25
Q

what is critical to the performance of the heart (preload)

A

fact that active tension generated by cardiac muscle rises steeply with increasing initial muscle length
allows heart to contract more strongly if it is stretched by greater volume of blood prior to contraction

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26
Q

definition of contractility

A

change in pressure over change in time

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27
Q

why does heart contract more strongly if stretched by greater volume of blood

A

more stretch, steeper slope
rise/run

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28
Q

when is the developed force maximal

A

when cardiac muscle begins its contractions at initial sarcomere length of 2.2 um

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29
Q

what develops maximal developed force at 2.2um

A

at this length there is optimal overlap of thick and thin filaments and max number of possible cross-bridge attachments

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30
Q

in cardiac muscle when does level of contractile activation increase significantly

A

over range of 1.8 to 2.0 um sarcomere length, accounts for steep rise in active force

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31
Q

when is developed force of cardiac muscle less than the max value

A

when sarcomeres are stretched beyond the optimal length because myofilaments overlap less hence reducing cross bridge cycling (descending limb)

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32
Q

what happens at very short sarcomere lengths

A

the thin filaments overlap each other in central region of sarcomere, diminishing contractile force

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33
Q

what is starting at very short sarcomere lengths analogous to

A

doing bicep curl and starting at top

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34
Q

what is a mechanism not present to the same extent in skeletal muscle

A

stretch of cardiac cells enhances the affinity of troponin C for Ca++, thus resulting in binding of greater amount of Ca++ to troponin C and formation of greater number of cross-bridges

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35
Q

why does stretch cause more binding

A

bind more readily the more stretched out (not in skeletal)

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36
Q

the mechanism responsible for this greater affinity of troponin

A

remains to be determined

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37
Q

what is one concept for the mechanism responsible for this greater affinity of troponin

A

the thick and thin filaments are brought closer to each other as the diameter of the muscle fiber narrows during stretch because cell maintains constant volume
- if closer maybe less distance for Ca++ to move

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38
Q

what may help in the stretch problem in the concept for the mechanism

A

the protein, titin, may help in process, in that it forms a scaffold to which actin and myosin filaments bind

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39
Q

what is another feature different from that of skeletal muscle

A

is amount of Ca++ released from SR in cardiac muscle increases with increasing sarcomere length

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40
Q

as enhance preload

A

it will facilitate greater release of Ca++

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41
Q

what kind of phenomenon is amount of Ca++ increasing with increasing sarcomere length

A

this is time-dependent
developing slowly over many beats, after the sarcomere length has been increased

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42
Q

what contributes to the length dependence of cardiac muscle contraction from 1.8 to 2.2 um

A

three cellular mechanisms

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43
Q

what are the 3 mechanisms that contributes to length dependence of cardiac muscle contraction from 1.8 to 2.2

A
  1. changes in myofilament overlap, similar to those in skeletal muscle (contractile start point)
  2. increased activation as a result of greater chemical affinity to troponin C for Ca++
  3. increased activation as a result of greater release of Ca++ from the SR
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44
Q

afterload determined the

A

velocity of cardiac muscle shortening

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45
Q

a strip of cardiac muscle, and the intact heart, also experiences

A

an additional load (force) against which it must contract, after it is activated

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46
Q

what does afterload determine

A

the velocity with which the muscle can shorten

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47
Q

in the intact heart what does afterload represent

A

left ventricular ejection in the aorta
- velocity of blood as moves through aorta

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48
Q

during ejection what is the afterload represented by

A

the impedance (resistance) blood faces due to aortic and intraventricular pressures, which are virtually equal to each other

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49
Q

the afterload is

A

the stress (wall stress) applied to the ventricle during ejection of blood

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50
Q

if theres stiff aorta

A

high impedance

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51
Q

stretchy aorta

A

low impedance

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52
Q

if the afterload is such that muscle can generate enough force to lift the load

A

then the muscle contracts isometrically until it generates enough force to lift the afterload, after which it can begin to shorten

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53
Q

the velocity of shortening is maximal (V0) for

A

no afterload

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54
Q

when does velocity of shortening decrease to zero

A

when force (load) is too great for the muscle to lift at all (F0) (i.e., an isometric contraction)

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55
Q

what increases the velocity of shortening at every level of afterload

A

norepinephrine

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56
Q

what constitutes the cardiac cycle

A

a period of cardiac muscle relaxation, diastole, and a period of contraction, systole

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57
Q

what is contraction of ventricles referred to as

A

ventricular systole

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58
Q

what is stroke volume into the aorta determined by

A

strength and velocity of the left ventricular contraction

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59
Q

what are 3 important determinants of stroke volume

A
  1. myocardial contractility (i.e., e-c coupling processes)
  2. preload (sarcomere length)
  3. magnitude of afterload
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60
Q

what do these 3 factors determine

A

the strength and velocity of myocardial contraction

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61
Q

hearts that do not squeeze well

A

do not do well with afterload

62
Q

ventricular systole

A

isovolumic contraction

63
Q

what does the onset of ventricular contraction coincide with

A

the peak of the R wave of the ECG and the initial vibration of the first heart sound

64
Q

R wave

A

not ventricular contraction but the signal for it
indicative of electrical event not mechanical
corresponds to rise in Ventricular pressure

65
Q

where is onset of ventricular contraction indicated on ventricular pressure curve

A

earliest rise in ventricular pressure after atrial contraction

66
Q

phase between start of ventricular systole and opening of semilunar valves is termed

A

isovolumic contraction because the ventricular volume is constant during this brief period

67
Q

what happens between start of ventricular systole and opening of semilunar valves

A

when ventricular pressure rises abruptly

68
Q

what happens the moment ventricular pressure exceeds aorta

A

aortic valve opens

69
Q

what marks the onset of ejection phase

A

opening of semilunar valves

70
Q

what can the opening of semilunar valves that marks onset of eject can be subdivided into

A
  1. an earlier, shorter phase (rapid ejection)
  2. a later, longer phase (reduced ejection)
71
Q

rapid ejection phase is distinguished from reduced ejection phase by

A
  1. sharp rise in ventricular and aortic pressures that terminate at peak ventricular and aortic pressures
  2. a more abrupt decrease in ventricular volume
  3. a greater aortic blood flow
72
Q

what does the sharp decrease in left atrial pressure curve at onset of ejection results from

A

the descent of the base of the heart and stretch of the atria

73
Q

during reduced ejection period

A

blood flow from aorta to the periphery exceeds ventricular output, and therefore aortic pressure declines

74
Q

throughout ventricular systole, the blood returning to atria

A

produces a progressive increase in atrial pressure

75
Q

during approximately the first third of ejection period

A

left ventricular pressure slightly exceeds aortic pressure and flow accelerates (continues to increase)

76
Q

during last two thirds of ejection period

A

reverse holds true, aortic pressure exceeds left ventricular pressure

77
Q

the reversal of ventricular-aortic pressure gradient is in presence of what

A

continued flow of blood form left ventricle to the aorta (caused by momentum of forward blood flow)

78
Q

what is the reversal of ventricular-aortic pressure gradient a result of

A

the storage of potential energy in the stretched arterial walls, which produces a deceleration of blood flow into the aorta

79
Q

the peak of the flow curve coincides

A

in time with the point at which the left ventricular pressure curve intersects the aortic pressure curve during ejection
v > A to V < A

80
Q

Thereafter the switch of pressure gradient

A

flow decelerates (continues to decrease) because the pressure gradient has been reversed (A > v)

81
Q

With right ventricular ejection there is

A

shortening of the free wall (lateral surface) of the right ventricle and lateral compression of the chamber

82
Q

shortening of the free wall of the right ventricle

A

descent of the tricuspid valve ring

83
Q

with left ventricular ejection

A

little shortening of the base to apex axis and ejection is accomplished mostly by compression of left ventricular chamber
- some reduction in volume by shorten but majority by circumference reduced

84
Q

in venous pulse, a wave

A

caused by atrial contraction

85
Q

in venous pulse, c wave

A

by the impact of the adjacent common carotid artery and to some extent by transmission of a pressure wave

86
Q

in c wave what is pressure wave created by

A

abrupt closure of the tricuspid valve in early ventricular systole

87
Q

in venous pulse, v wave

A

by pressure of blood returning from the peripheral vessels and the abrupt opening of the tricuspid valve

88
Q

what happens when blood coming to atria from inferior and superior venae cavae

A

some comes back because no valve

89
Q

p wave

A

atrial depolarization

90
Q

QRS complex

A

ventricular depolarization

91
Q

t wave

A

ventricular repolarization

92
Q

ventricular diastole

A

isovolumic relaxation

93
Q

what is isovolumic relaxation the onset of

A

lengthening of sarcomere
starting to relax without changer in volume
driven by pressure

94
Q

what does aortic valve closure produce

A

the notch on descending limb of aortic pressure curve and the second heart sound (with some vibrations)

95
Q

aortic valve closure marks

A

ends of ventricular systole

96
Q

isovolumic relaxation

A

phase between the closure of the semilunar valves and the opening of the AV valves

97
Q

what is isovolumic relaxation characterized by

A

a fall in ventricular pressure without a change in ventricular volume

98
Q

start of diastole

A

mitral opening
isovolumic relaxation

99
Q

mitral valve closure

A

onset of systole
ventricular contraction

100
Q

aortic valve closure

A

end of systole
early diastole

101
Q

when does major part of ventricular filling occur

A

immediately on opening of the AV valves
when blood that had been returned to atria during the previous ventricular systole is abruptly released into the relaxing ventricles (pressure lower in V than A)

102
Q

rapid filling phase

A

major part of ventricular filling

103
Q

onset of rapid filling phase is indicated by

A

decrease in left ventricular pressure below left atrial pressure, resulting in opening of mitral valve

104
Q

rapid flow of blood from atria to relaxing ventricles produces

A

a decrease in atrial and ventricular pressures and a sharp increase in ventricular volume

105
Q

rapid filling phase is followed by

A

phase of slow filling
diastasis

106
Q

diastasis

A

blood returning from periphery flows into the right ventricle and blood from lungs into the left ventricle

107
Q

the small, slow ventricular filling of diastasis is indicated by

A

a gradual rise in atrial, ventricular, and venous pressures and in ventricular volume

108
Q

onset of atrial systole occurs

A

soon after beginning of the p wave of ECG (atrial depolarization)

109
Q

what happens during atrial systole

A

transfer of blood from atrium to ventricle made by the peristalsis-like wave of atrial contraction completes the period of ventricular filling

110
Q

atrial systole is responsible for

A

the small increases in atrial, ventricularm and venous (a wave) pressures as well as ventricular volume

111
Q

throughout ventricular diastole, atrial pressure

A

barely exceeds ventricular pressure, indicating a low-resistance pathway across the open AV valves during ventricular filling

112
Q

p wave

A

electrical event for atrial contraction not mechanical event

113
Q

atrial contraction can force blood

A

in both directions because there are no valves at junction of venae cavae and right atrium or at junctions of pulmonary veins and left atrium

114
Q

why does little blood go back into the venae cavae and pulmonary veins during brief atrial contraction

A

because of the inertia of the inflowing blood

115
Q

what does atria serve as

A

reservoir, conduit, pump

116
Q

what does atria serve as if have afib

A

only conduit

117
Q

what is atrial contraction not essential for

A

ventricular filling

118
Q

when can atrial contraction not essential for ventricular filling be oberserved

A

in atrial fibrillation or a complete heart block

119
Q

what is atrial contraction’s contribution governed by

A

heart rate and structure of AV valves

120
Q

at slow heart rates

A

filling practically ceases toward end of diastasis, and atrial contraction contributes like additional filling

121
Q

during tachycardia (elevated HR)

A

diastasis is abbreviated, and atrial contribution can become substantial, especially if it occurs immediately after rapid filling phase when AV pressure gradient is max

122
Q

increased EDV contribution of atria

A

is higher during exercise
10-20% EDV during exercise comes form atrial contribution

123
Q

should tachycardia become so great as to encroach on rapid filling phase

A

atrial contraction becomes very important in rapidly propelling blood to fill ventricle during brief period of cardiac cycle

124
Q

if the period of ventricular relaxation is so brief that filling is seriously impaired

A

even atrial contraction cannot prevent inadequate ventricular filling

125
Q

what can the reduction in CO from ventricular relaxation being so brief result in

A

syncope (fainting)

126
Q

if CO bottomed out what could have caused

A

squeeze function or filling is impaired

127
Q

if atrial contraction occurs simultaneously with ventricular contraction

A

no atrial contribution to ventricular filling can occur
mitral valve should close with V contracting

128
Q

in ventricular contraction the preload is

A

stress (pressure) in the ventricle, prior to contraction, that stretches myocardial cells

129
Q

in ventricular contraction the afterload is

A

the aortic pressure against which the left ventricle ejects the blood

130
Q

wiggers diagram

A

simultaneous recording of left atrial, left ventricular, and aortic pressures
ventricular volume; hear sounds; and ECG through cardiac cycle

131
Q

pressure-volume relationships examine

A

the relationship between pressure and volume in the hear during each cardiac cycle

132
Q

why are examining pressure volume relationships useful

A

this relationship reflects the properties and conditions of the myocardial cells, and also relationship provides hemodynamic characterization of the heart

133
Q

effects of changes in … are revealed in resulting changes in stroke volume (pressure volume relationships)

A

preload, afterload, and cardiac contractility on stroke volume

134
Q

pressure volume relationships can be recorded in

A

humans and can be useful for evaluating cardiac function and other CV parameters

135
Q

left ventricular pressure-volume loop

A

relationship between left ventricular pressure and left ventricular volume throughout entire cardiac cycle

136
Q

how does the heart twist during contraction

A

base of heart twists in one direction, apex is twisting in opposite direction

137
Q

summation of apical and base rotation is

A

twist of the heart

138
Q

what does the twist do to the ventricles

A

reduce the surface area and heart will shorten

139
Q

what does reduction of surface area cause

A

ejection of blood

140
Q

during rest, peak twist occurs at

A

time of ejection

141
Q

what does heart have to do after twist

A

recoil and untwist

142
Q

what gives heart recoil

A

titin gives the springy structure
when contracting, titin is compressed

143
Q

at maximal untwist

A

mitral valves open and pulls blood in

144
Q

as heart untwists in diastole how does it pull blood in

A

heart springs back so quickly it generates suction in LV
generates a pressure gradient from apex to base
pulls blood from apex to base

145
Q

what is pressure called in ventricle from apex to base

A

IVPG intraventricular pressure gradient

146
Q

the greater the untwisting

A

the greater the suction

147
Q

during exercise

A

peak twist is greater

148
Q

greater the untwisting during exercise

A

greater the recoil and IVPG

149
Q

what increases for exercise

A

the magnitude of untwisting

150
Q

what is the advantage of greater untwisting during exercise

A
  • more filling in shorter time
  • during exercise diastole is shorter, left ventricle filling time shortens
  • greater untwisting and suction cause greater EDV in shorter time
  • more relaxing if more twisting
151
Q

speckle tracking

A

allows experimenters to track how the heart tissue moves

152
Q

what underpins twisting and untwisting

A

compression of titin that springs back to facilitate untwisting

Kin 426 (4 decks)

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