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Kin 426 > 2: Cardiac Pump Function > Flashcards

2: Cardiac Pump Function Flashcards

1
Q

what important differences is there between myocardial cells and skeletal muscle cells

A

morphological and functional differences

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2
Q

what is quite similar between myocardial cells and skeletal muscles

A

contractile elements

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3
Q

what is each skeletal and cardiac cell made up of

A

sarcomeres (from z line to z line) that contain thick filaments composed of myosin (in A band) and thin filaments containing actin

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4
Q

where do thin filaments extend from

A

point where they are anchored to z line (through I band) to interdigitate with thick filaments

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5
Q

how does shortening occur for both type of muscle

A

by sliding filament mechanism as in skeletal muscle

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6
Q

what is sliding filament mechanism

A

actin filaments slide along adjacent myosin filaments by cycling of the intervening cross-bridges, thereby bringing z lines together

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7
Q

what is crucial to force produced by muscle cells

A

how much overlap you have at start point

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8
Q

less crossbridging

A

harder to create force-tension relationships

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9
Q

what is the striking difference between cardiac and skeletal muscle

A

semblance of a syncytium in cardiac muscle with branching interconnecting fibers (structure of how heart arranged cellularly)

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10
Q

why is the myocardium not a true anatomic syncytium

A

laterally the myocardial fibers are separated from adjacent fibers by their respective sarcolemmas and end of each fiber is separated from its neighbor by intercalated disks

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11
Q

intercalated disks

A

at end of each fiber, dense structures that are continuous with sarcolemma

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12
Q

even though cardiac muscle is not a true syncytium

A

it functions like one

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13
Q

how does cardiac muscle function like a syncitium

A

a wave of depolarization followed by contraction of entire myocardium (all or none response) occurs when a suprathreshold stimulus is applied to any one site

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14
Q

if stimulate heart muscle anywhere

A

will stimulate a depolarization across entire heart

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15
Q

what is disadvantage of acting like syncitium

A

rogue depolarization events where it it outside of normal SA node
can cause arythmias or interruptions

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16
Q

as wave of excitation approaches the end of a cardiac cell, the spread of excitation to next cell depends on

A

electrical conductance of the boundary between the two cellls

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17
Q

what is present in intercalated disks between adjacent cells

A

gap junctions (nexi) with high conductances

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18
Q

what do the gap junctions do

A

mediate conduction of the cardiac impulse from one cell to next

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19
Q

what are the gap junctions made up of

A

connexons, hexagonal structures that connect the cytosol of adjacent cells

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20
Q

what does each connexon serve as

A

low resistance pathways for cell-to-cell conduction
connect cytosol from cell-to-cell

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21
Q

what do cardiac and fast skeletal muscle fibers differ in

A

number of mitochondria in the two tissues

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22
Q

how much mitochondria are in fast skeletal muscle fibers

A

relatively few

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23
Q

why is there few mitochondria in fast skeletal muscle

A

called on for short periods of repetitive or sustained contractions and can metabolize anaerobically and build up a substantial O2 debt

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24
Q

how much mitochondria in cardiac muscle

A

very rich in mitochondria

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25
Q

why is cardiac muscle rich in mitochondria

A

contracts repetitively for a lifetime and requires a continuous supply of O2

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26
Q

why is heart intolerant to anaerobic metabolism

A

brief interruption in oxygen causes instant pain

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27
Q

what does the large numbers of mitochondria do for heart

A

rapid oxidation of substrates with the synthesis of ATP can keep pace because of large numbers of mitochondria

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28
Q

what do large numbers of mitochondria contain

A

respiratory enzymes necessary for oxidative phosphorylation (need to maintain)

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29
Q

how is heart provided with adequate O2 and substrate for metabolism

A

myocardium is endowed with a rich capillary supply, about one capillary per fiber

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30
Q

what does one capillary per fiber create

A

short diffusion distances

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31
Q

what do short diffusion distances form capillary to RBCs allow for

A

O2, CO2, substrates, and waste material can move rapidly between myocardial cell and capillary

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32
Q

what are sarcolemmal invaginations

A

myocardium has deep invaginations of the sarcolemma into the fiber at the z lines

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33
Q

what does the sarcolemmal invaginations allow for

A

exchange of substances between capillary blood and myocardial cells

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34
Q

the sarcolemmal invaginations constitute

A

the transverse-tubular, T-tubular system

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35
Q

the T-tubular lamina (surface area)

A

are continuous with the bulk interstitial fluid

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36
Q

what do T-tubules play a key role in

A

excitation-contraction coupling (facilitating readily available Ca++)

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37
Q

what does the human heart consist of

A

two pumps in series

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38
Q

what does the “right heart” consist of

A

right atrium and right ventricle, that pumps venous blood to the pulmonary circulation

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39
Q

what does the “left heart” consist of

A

left atrium and left ventricle, that pumps oxygenated blood into the systemic circulation at relatively high pressure

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40
Q

what are the atria

A

thin walled, low pressure chambers that function more as large reservoir conduits of blood for their respective ventricles than as important pumps for the forward propulsion of blood

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41
Q

where are ventricles formed and originate

A

formed by a continuum of muscle fibers that originated from the fibrous skeleton at the base of the heart (mostly around the aortic orifice)

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42
Q

Base of the heart

A

where atria and ventricles connect

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43
Q

what do the fibers of the ventricle sweep toward

A

the apex of the epicardial surface and also pass toward the endocardium as they gradually undergo 180 degree change in direction to lie parallel to epicardial fibers and form endocardium and papillary muscles

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44
Q

at the apex of the heart the fibers

A

twist and turn inward to form papillary muscles

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45
Q

at the base and around the valve orifices

A

the fibers form a thick, powerful muscle that not only decreases ventricular circumference for ejection of blood but also narrows the AV valve orifices as an aid to valve closure

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46
Q

what does the 180 degree change in direction of the fibers allow

A

for muscle contraction to squeeze

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47
Q

endocardium and epicardium

A

inside and outside

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48
Q

when unravel heart

A

fold out in a long hollow tube

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49
Q

tricuspid valve

A

valve between the right atrium and right ventricle is made up of the three cusps

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50
Q

mitral valve

A

valve between the left atrium and left ventricle and has two cups

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51
Q

two cusps=

A

two parts

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52
Q

the total area of the cusps of each AV valve is approximately

A

twice that of their respective AV orifices

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53
Q

why is the total area of the cusps twice the area of their orifices

A

so that there is considerable overlap of the leaflets in the closed position

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54
Q

what are attached to the free edges of these valves

A

chordae tendinae

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55
Q

chordae tendinae

A

fine, strong ligaments

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56
Q

where do the chordae tendinae arise from

A

the powerful papillary muscles of the respective ventricles and prevent eversion of the valves during ventricular systole `

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57
Q

what do semilunar valves not have

A

chordae tendinae

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58
Q

2 atrioventricular valves

A

tricuspid valve
mitral valve

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59
Q

semilunar valves

A

valves between the right ventricle and the pulmonary artery and between the left ventricle and the aorta

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60
Q

what do the semilunar valves consist of

A

3 cuplike cusps attached to the valve rings

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61
Q

what do the cusps of semilunar valves do at end of the reduced ejection phase of ventricular systole

A

there is brief reversal of blood flow toward the ventricles that snaps the cusps together and prevents regurgitation of blood into the ventricles

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62
Q

what do the cusps of semilunar valves do during ventricular systole

A

the cups do not lie back against the walls of the pulmonary artery and aorta but float in the bloodstream approximately midway between the vessel walls and their closed position

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63
Q

what are behind the semilunar valves

A

sinuses of valsava, small outpocketings of the pulmonary artery and aorta

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64
Q

what develops between the sinuses of valsalva and the cusps of semilunar valves

A

eddy currents develop that tend to keep the valve cusps away from the vessel walls

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65
Q

what is behind the right and left cusps of the aortic semilunar valve

A

the orifices of the right and left coronary arteries

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66
Q

what would happen if there were no sinuses of Valsalva and the eddy currents developed therein

A

the coronary ostia could be blocked by the valve cusps

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67
Q

2 semilunar valves

A

aortic valve
pulmonary valve

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68
Q

annulus fibrosus

A

fibrotic ring around valves

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69
Q

why does regurgitation happen

A

poor seal of mitral and tricuspid
causes a murmur

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70
Q

problem with regurgitation

A

if not enough going forward and some going back the ventricle will stretch and can enlarge

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71
Q

ectopic foci

A

AP events that are not part of normal conductance pathway for transmitting AP from SA node throughout atria

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72
Q

when can ectopic foci occur

A

when atria stretched out, such as from regurgitation

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73
Q

what can ectopic foci underpin

A

atrial fibrillation, rogue electrical signals, not contracting synchronously

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74
Q

progression of regurgitation to atrial fibrillation

A

regurgitation
atrial remodeling
ectopic foci
atrial fibrillation

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75
Q

when can regurgitation be worse for people with it

A

with exercise
more blood from left atrium to pulmonary bed can cause elevated pressure and alter ventilation causing shortness of breath

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76
Q

what does pericardium consist of

A

a visceral layer that adheres to the epicardium and a parietal layer that is separated from visceral layer with thin layer of fluid

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77
Q

what does the fluid between the parietal and visceral layer provide

A

lubrication for the continuous movement of the enclosed heart (limit friction)

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78
Q

what does the pericardium strongly resist

A

a large, rapid increase in cardiac size because its distensibility is small (can still remodel)

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79
Q

what does the pericardium play a role in

A

preventing sudden overdistention of the chambers of the heart

80
Q

with congenital absence of pericardium or after its surgical removal

A

cardiac function is within physiological limits

81
Q

with the pericardium intact what does an increase in diastolic pressure in one ventricle cause

A

increases the pressure and decreases the compliance of the other ventricle

82
Q

what is it called when increase in diastolic pressure in one ventricle causes increase in pressure in other

A

pericardial mediated ventricular interaction

83
Q

steps of pericardial mediated ventricular interaction

A
  1. increase left ventricular EDV
  2. increase EDP
  3. will stretch pericardium on left side of heart (fibrous not stretchy)
  4. Pericardium will move inward toward right side of heart
  5. RV squished, volume decreased because left side pulling on it
84
Q

how long is pericardial mediated ventricular interation

A

usually occurs over a couple beats and then stabilizes

85
Q

what can occur is LV enlarges (e.g., heart failure)

A

LV can chronically stretch pericardium
restricts RV, reduced EDV
not reduced EDV on left side

86
Q

what is role of pericardium

A

controlling volume of heart
increase in volume in one side will decrease compliance in other side therefore decreasing its EDV

87
Q

what are the 2 types of stress that are stimulus for hypertrophication

A

volume loading or pressure loading

88
Q

volume loading

A

increased EDV
- Can be healthy within limits (aerobic and strength trained individuals)

89
Q

pressure load

A

after load (e.g., hypertension) chronically pushing

90
Q

when LV dilates during diastole and becomes spherical; as in heart failure what happens

A

it is less efficient
more energy is required (greater wall tension) for the distended heart to eject the same volume of blood per beat than for the normal undilated heart (more MVO2)

91
Q

Laplace’s law states

A

tension in the wall of the vessel equals teh transmural pressure difference times the radius of the vessel

92
Q

transmural pressure difference

A

pressure across the wall, or distending pressure, (delta)P

93
Q

what can the laplace relationship be applied to

A

to the distended and spherical heart if correction is made for wall thickness

94
Q

Laplace’s law equation

A

T= delta P x r/2w

95
Q

T

A

wall stress (force/area)

96
Q

delta P

A

transmural pressure

97
Q

r
w

A

radius
wall thickness

98
Q

why is 60 beats per minute better than 80

A

slower HR is consuming less O2, pumping more per beat, lower MVO2

99
Q

for someone with heart failure why do they have higher HR

A

for same volume of blood, higher O2 requirement

100
Q

what does larger heart experience

A

more wall stress

101
Q

wall stress inversely proportional to

A

wall thickness

102
Q

increase wall stress

A

decrease wall thickness

103
Q

why does heart wall thicken

A

hypertrophy to protect from stress

104
Q

why do giraffes have really thick heart walls

A

the hydrostatic pressure from the fluid above the heart puts pressure on it
really thick walls because pressure from neck
wall stress lower because thick walls

105
Q

contraction of heart is triggered by

A

spread of electrical excitation throughout the syncytium of muscle cells

106
Q

what is the strength of contraction of each cardiac cell determined by

A

the chemical processes linking or “coupling” this excitation to acto-myosin cross bridge cycling (excitation-contraction coupling)

107
Q

what does excitation contraction coupling determine

A

contractility of heart

108
Q

for normal excitation-contraction coupling what does the heart require

A

optimal concentrations of Na+, K+, Ca++

109
Q

in absence of Na+

A

the heart is not excitable and will not beat because the AP depends on extracellular Na+

110
Q

the resting membrane potential is independent of

A

Na+ gradient across the membrane

111
Q

contractility

A

for a given stimulus, how quickly does it contract

112
Q

contractility is defined by

A

rate of contraction
caused by Ca++

113
Q

e-c coupling

A

for how much electrical will cause mechanical

114
Q

what does a moderate reduction in extracellular K+ do

A

has little effect on myocardial excitation and contraction, but it flattens the T-wave of the electrocardiogram

115
Q

what does a severe reduction in extracellular K+ produce

A

weakness, paralysis, and cardiac arrest

116
Q

low K+
high K+

A

low T wave
high T wave

117
Q

what is T wave apart of

A

repolarization
athletes have massive T waves

118
Q

large increases in extracellular K+ produce

A

dysrhythmias, depolarization, loss of excitability of myocardial cells, and cardiac arrest in diastole

119
Q

what is essential for cardiac contraction

A

Ca++
determines magnitude of contractility

120
Q

removal of Ca++ from extracellular fluid results

A

in decreased contractile force and eventual arrest in diastole

121
Q

what is poor contractility generally caused by

A

issue of Ca++ handling

122
Q

an increase in extracellular Ca++

A

enhances contractile force

123
Q

very high Ca++ concentrations induce

A

cardiac arrest in systole (rigor)

124
Q

what does amount of Ca++ available determine

A

contractility

125
Q

free intracellular Ca++ concentration is responsible for

A

the contractile state of the myocardium

126
Q

during the plateau (phase 2) of AP, what increases

A

Ca++ permeability of the sarcolemma

127
Q

How does Ca++ enter the cell

A

through voltage-dependent L-type channels in the sarcolemma and in the T-tubules (allows more to come in)

128
Q

how do L-type (long lasting) channels open

A

need electrical stimulation

129
Q

opening of Ca++ channels is facilitated by

A

phosphorylation of the channel proteins by a cyclic adenosine monophosphate (cAMP) - dependent protein kinase

130
Q

what is the primary source of extracellular Ca++

A

interstitial fluid
some may also be bound to sarcolemma

131
Q

what is not sufficient to induce contraction of myofibrils

A

the amount of Ca++ that enters the cell from extracellular space

132
Q

what does the Ca++ that enters through extracellular space do

A

serves as trigger (trigger Ca++) to release Ca++ from the intracellular Ca++ stores in SR

133
Q

how does the intracellular Ca++ leave the SR

A

through calcium release channels called ryanodine receptors

134
Q

What else are ryanodine receptors called

A

channel protein, foot protein or junctional processes of SR

135
Q

why is it called ryanodine receptor

A

because it binds ryanodine avidly

136
Q

what happens after the process of Ca++ induced Ca++ release

A

the cytosolic free Ca++ increases and the Ca++ binds to the protein troponin C

137
Q

what does the Ca++-troponin complex interact with

A

tropomyosin to unblock active sites between the actin and myosin filaments

138
Q

what does unblocking the active sites between actin and myosin allow for

A

cross-bridge cycling and hence contraction of the myofibrils (systole)

139
Q

what determines strength of contraction

A

amount of Ca++ available

140
Q

what happens during CV disease when less Ca++ channels are open

A

availability of Ca++ channels for Ca++ to come into cell
less contraction of heart

141
Q

mechanisms that raise systolic Ca++

A

increase the developed force

142
Q

mechanisms that lower Ca++

A

decrease the developed force

143
Q

what is developed force

A

rate of contraction over time

144
Q

source of catecholamines

A

sympathetic stimulation

145
Q

what do catecholamines do

A

increase Ca++ entry into the cell by phosphorylation of the Ca++ channels via a cAMP-dependent protein kinase

146
Q

what do the catecholamines enhance

A

myocardial contractile force

147
Q

what else do catecholamines do

A

elicit a limiting action by decreasing the sensitivity of the contractile machinery to Ca++ by phosphorylation of troponin I

148
Q

what happens when sensitivity to Ca++ decreases

A

less Ca++ needed for greater contraction when exposed to increased Ca++

149
Q

an increase in systolic Ca++ is also achieved by

A

increasing extracellular Ca++ or decreasing the Na+ gradient across sarcolemma

150
Q

how can the sodium gradient be reduced

A

by increasing the intracellular Na+ or decreasing extracellular Na+

151
Q

what increases intracellular Na+

A

cardiac glycosides

152
Q

how do cardiac glycosides increase intracellular Na+

A

inhibit the Na-K pump which results in an accumulation of Na+ in cells

153
Q

what does the elevated cytosolic Na+ from inhibiting NA-K pump do

A

reverses the Na+-Ca++ exchanger so that less Ca++ is removed from the cell
this Ca++ is store in SR

154
Q

how does lowered extracellular Na+ reduce the sodium gradient

A

results in reduction of Na+ reduction into cell and hence less exchange of Na+ for Ca++

155
Q

how is developed tension diminished

A

reduction in extracellular Ca++

156
Q

causes of reduction of extracellular Ca++

A

increase in Na++ gradient across sarcolemma
administration of Ca++ blockers that prevent Ca++ from entering myocardial cell

157
Q

what happens at end of systole with Ca++

A

influx ceases and the SR is no longer stimulated to release Ca++

158
Q

what does the SR do after systole

A

takes up Ca++ by means of an ATP-energized Ca++ pump that is regulated by phospholamban

159
Q

when is phospholamban’s inhibition of the Ca++ pump relieved

A

when phospholamban is phosphorylated by cAMP-dependent protein kinase

160
Q

what does phosphorylation of troponin I do

A

inhibits the Ca++ binding of troponin C

161
Q

what happens when Ca++ is inhibitted from binding to troponin C

A

permits tropomyosin to again block the sites for interaction between the actin and myosin filaments and relaxation (diastole) occurs

162
Q

what is strength of relaxation dependent on

A

catecholamines
phosphorylation

163
Q

inotropy

A

strength of contraction

164
Q

lusitropy

A

strength of relaxation

165
Q

why do we want heart that relaxes quickly

A

increased filling
if poor relaxation it will impede EDV and mitigate frank starling effect

166
Q

what do catecholamines enhance

A

inotropy and lusitropy

167
Q

cardiac contraction and relaxation are both accelerated by

A

catecholamines and adenylyl cyclase activation

168
Q

how does catecholamines and adenylyl cyclase activation increase contraction

A

resulting increase in cAMP activated cAMP-dependent protein kinase which phosphorylates the Ca++ channel is the sarcolemma
allows greater influx of Ca++

169
Q

how does catecholamines and adenylyl cyclase activation accelerate relaxation

A

by phosphorylating phospholamban, which enhances Ca++ uptake by the SR and by phosphorylating troponin I, which inhibits Ca++ binding of troponin C

170
Q

phosphorylation of cAMP-dependent protein kinase serve to

A

increase both speed of contraction and relaxation

171
Q

Ca++ that enter cell to initiate contraction must be

A

removed during diastole

172
Q

how is the Ca++ that enter cell to initiate contraction removed during diastole

A

primarily by exchange of 3 Na+ for 1 Ca++
also from cell by pump that uses ATP to transport Ca++ across sarcolemma

173
Q

why is heart failure a syndrome

A

constellation of signs and symptoms

174
Q

what can a patient with heart failure have

A

dilated heart, low cardiac output, fluid retention, high venous pressure, an enlarged liver, and peripheral edema

175
Q

how can symptoms of heart failure be treated

A

diuretic and drugs that block the neurohumoral axis (sympathetic nervous and renin-angiotensin systems)

176
Q

what does diuretic do

A

decreases extracellular fluid volume, thereby lessening the volume load (preload) on heart and reducing venous pressure, liver congestion and edema

177
Q

what are drugs that block the neurohumeral axis

A

ace inhibitor (angiotensin converting enzyme)
ARB’s (angiotensin receptor antagonists)
Beta blockers (B-adrenergic receptors)

178
Q

what do Ace inhibitors and ARB’s do

A

block production or action of angiotensin II to reduce afterload
interfere with structural remodeling (hypertrophy)

179
Q

what do beta blockers do

A

block B-adrenergic receptors to reduce HR and energy expenditure
interfere with the structural remodeling (hypertrophy)

180
Q

why is digoxin sometimes used

A

inhibits Na-K pump to increase intracellular Ca++ stores, enhancing contractility
last thing to keep heart going

181
Q

why do people begin to retain fluid

A

to increase EDV and normalize CO

182
Q

when is renin-angiotensin system activated

A

when low CO
increases fluid in body

183
Q

how do ace inhibitor and ARB’s reduce afterload

A

increase pressure
cause resistance arterioles to contract

184
Q

tortion

A

twist scaled to size of heart

185
Q

although myocardium is made of individual cells with discrete membrane boundaries, how do cardiac myocytes in ventricles contract

A

almost in unison
same in atria

186
Q

myocardium functions as a

A

syncytium with an all or non response to excitation

187
Q

cell-to-cell conduction occurs through

A

gap junctions that connect the cytoplasm to adjacent cells

188
Q

because of myofibril orientation, during systole

A

the apex twists in one direction and base twists in the opposite to aid with ejection of blood

189
Q

exercise potentiates

A

the systolic twisting effect

190
Q
A
191
Q

the influx of Ca++ from interstitial fluid during excitation triggers

A

the release of Ca++ from the SR

192
Q

the free cytosolic Ca++ activates

A

contraction of the myofilaments (systole)

193
Q

relaxation (diastole) occurs as a result of

A

uptake of Ca++ by SR, by extrusion of intracellular Ca++ by Na+-Ca++ exchange, and to a limited degree by Ca pump

194
Q

endocardial fibers

A

oriented in right handed helix (top left to bottom right)

195
Q

epicardial fibers

A

oriented in left handed helix (bottom left to top right
dominated rotational motion because of its lever arm

196
Q
A

Kin 426 (4 decks)

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