Exam 3 Flashcards

1
Q

autonomic nervous system

A

two branches- sympathetic and parasympathetic
involuntary control of organ function
organ contraction, HR/BP, stress response

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2
Q

ANS in relation to daily acitivity

A

sympathetic branch- associated with stress and physical activity, mental/emotional stress, exercise
parasympathetic- associated with rest and “slow” background activity, increased digestion, lower overall activity

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3
Q

ANS neuron configuration

A

2 neuron series- preganglionic neuron and postganglionic neuron

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4
Q

where is the cell body in a preganglionic neuron

A

cell body located within CNS

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5
Q

where is the cell body of a postganglionic neuron

A

cell body is located within autonomic ganglia

 sympathetic: sympathetic chain ganglia
 parasympathetic: terminal ganglia, near or on surface of effector
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6
Q

2 neuron series sympathetic

A

start in spinal cord
preganglionic neuron goes to postganglionic neuron in sympathetic chain ganglia
postganglionic neuron goes to
effector

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7
Q

2 neuron series parasympathetic

A

start in brain stem
preganglionic neuron goes way down to postganglionic neuron at terminal ganglia
postganglionic neuron goes to effector

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8
Q

where are NTs released in 2 neuron series

A

at preganglionic to postganglionic and at postganglionic to effector

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9
Q

autonomic neurons and their NTs

A

different autonomic neurons secrete different NTs

neuron type based on the type of NT that is released

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10
Q

types of NTs released

A

cholinergic neuron

adrenergic neruon

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11
Q

cholinergic neuron releases

A

acetylcholine

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12
Q

adrenergic neuron releases

A

norepinehprine

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13
Q

receptors for specific NTs

A

cholinergic

adrengeric

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14
Q

cholinergic receptor

A

binds acetylcholine

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15
Q

2 types of cholinergic receptors

A

muscarinic

nicotinic

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16
Q

nicotinic receptor

A

on postganglionic neuron

both sympathetic and parasympathetic

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17
Q

muscarinic receptor

A

on surface of effector, mainly in parasympathetic

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18
Q

adrenergic receptor

A

binds norepinephrine and epinephrine

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19
Q

2 types of adrenergic receptors

A

alpha adrenergic receptor

beta adrenergic receptor

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20
Q

alpha adrenergic receptor

A

responds more to norepinephrine than epinephrine

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21
Q

beta adrenergic receptor

A

respond equally to norepinephrine and epinephrine

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22
Q

preganglionic neurons: NTs effects

A

preganglionic NTs secreted affects postganglionic neuron
in both sympathetic and parasympathetic
secretes acetylcholine

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23
Q

postganglionic neurons: NTs and effects

A

postganglionic NTs affect effector organs
in parasympathetic- cholinergic neurons- secrete acetylcholine in response to preganglionic stimulation
in sympathetic- adrenergic neurons- secrete norepinephrine in response to preganglionic stimulation

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24
Q

sympathetic prgn and pgn pathway

A
Prgn- cholinergic neuron
   secretes Ach
   binds to nicotinic receptor on
pgn- adrenergic neuron
   secretes norepinephrine 
   binds to alpha or beta adrenergic receptors on
effector
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25
Q

parasympathetic prgn and pgn pathway

A
prgn- cholinergic neuron
    secretes Ach
    binds to nicotinic receptor on
pgn- cholinergic neurons
    secretes Ach
    binds to muscarinic receptor on
effector
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26
Q

regulation of ANS responses

A

many effector organs have input from sym and psym divisions
1 antagonistic effects
2 coordinated response

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27
Q

antagonistic effects

A

sympathetic and parasympathetic produce opposite effects

one may have a stronger effect than the other

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28
Q

coordinated response

A

1 one division can coordinate activity of multiple different structures
2 both divisions can coordinate activity of different structures for the same purpose

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29
Q

eyes sympathetic vs parasympathetic

A

sympathetic- pupil dilation

parasympathetic- pupil constriction

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30
Q

Bronchi sympathetic vs parasympathetic

A

sympathetic- bronchodilation

parasympathetic- bronchoconstriction

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31
Q

GI tract sympathetic vs parasympathetic

A

sympathetic- decrease digestion

parasympathetic- increase digestion

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32
Q

heart sympathetic vs parasympathetic

A

sympathetic- increase HR, BP, force of contraction

parasympathetic- decrease HR, BP, force of contraction

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33
Q

blood vessels sympathetic vs parasympathetic

A

sympathetic- mostly vasoconstriction (alpha adrenergic receptors), increase BP, some vasodilation (beta adrenergic receptors)
parasympathetic- vasodilation of some blood vessels, very little effect on systemic BP

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34
Q

response to stress

A

mass activity of sympathetic division- activates adaptations to escape stressor
increase BG, HR, blood flow to muscles, respiratory rate, inhibition of non-essential activities (digestion, reproduction)
fast acting response

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35
Q

system (whole body) effects

A

more noticeable with sympathetic stimulation
some preganglionic sympathetic neurons stimulate adrenal medulla
Ach goes to adrenal medulla, adrenal medulla secretes epinephrine, epinephrine enters circulation and affects functions of other organs

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36
Q

pharmacology

A

receptor agonists

receptor antagonists

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37
Q

receptor agonists

A

drugs that bind to receptor and mimics effects of endogenous NTs
sympathomimetic drugs
parasympathomimetic drugs

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38
Q

receptor antagonists

A

drugs that bind to receptor and block effect of endogenous NTs

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39
Q

innervation of vasculature

A

nervous stimulation- motor neurons
blood vessels- capillary beds around muscle fibers, supplied and drained by arteries and veins
delivery of oxygen rich blood

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40
Q

muscle fibers

A

composed of many myofibrils

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41
Q

myofibrils

A

composed of actin myofilaments (thin filament) and myosin myofilaments (thick filament), titan

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42
Q

sarcolemma

A

plasma membrane of muslce fiber

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43
Q

sarcoplasma

A

cytoplasm of muscle fiber

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44
Q

sarcomere

A

made up of action and myosin joined end to end

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45
Q

what is the smallest contractile structure

A

sarcomere

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46
Q

a band

A

length of myosin, some overlapping of myosin and actin

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47
Q

i band

A

contain actin and z disk

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48
Q

actin structure

A

F actin- 2 strands in a helix
G actin- has an active site for binding myosin heads
troponin
tropomyosin

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49
Q

troponin

A

3 subunits, 1 binds to g- actin, 1 binds to tropomyosin, 1 has binding site for Ca++

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50
Q

tropomyosin

A

sits within indention of helix

at rest- blocks active sites of g- actin

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51
Q

myosin

A

2 myosin heavy chains forming a rod
hinge region- allows bending of myosin heads
myosin heads- capable of binding to g-actin
4 myosin light chains- attached to myosin heads, regulatory function

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52
Q

myosin heads

cross bridge formation

A

binding of myosin head and actin molecule
facilitates contraction of muscle- hinge region, bending and straightening
heads have ATPase that does ATP hydrolysis that releases energy for bending of hinge

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53
Q

sliding filament model

A

actin myofilament sliding over the myosin myofilament shortening of sarcomere this translates to muscle contraction

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54
Q

sliding filament model

relaxation

A

lengthening of sarcomere

external forces- contraction of antagonist muscle or gravity

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55
Q

neuromuscular junction/ motor end plate

A

synapse of motor neuron on muscle fiber
Ach secretion by motor neuron
Ach binds to ligand gated ion channels on muscle fiber
Na+ rushes into muscle, depolarization of muscle fiber

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56
Q

excitation- contraction coupling

A
conversion of neural signals into physical process of contraction
t-tubles
sarcoplasmic reticulum (SR)
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57
Q

steps to muscle contraction

A

neuron action potential- muscle action potential- contraction

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58
Q

t-tubules

transverse tubules

A

infoldings of sarcolema

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59
Q
sarcoplasmic reticulum (SR)
what is it
what does it store and release
A

modified smooth ER, stores Ca++, release Ca++ into sarcoplasm in response to muscle AP

60
Q

muscle fiber AP and conduction

A

AP of muscle fiber occurs at NMJ
AP propagates along sarcolemma and along t-tubules
this causes voltage gated Ca++ channels on SR to open
Ca++ flows out of SR, Ca++ binds to troponin
troponin molecules change conformation/position
this causes tropomyosin to move
active sites on G action exposed
myosin heads bind to G actin (cross bridge formation)
sliding filament and muscle contraction occurs
when complete Ca++ re enters SR, restoration of filaments to original position

61
Q

cross bridge cycling

A

repeated interaction of myosin head and actin myofilament
cross bridge formation
energy stored in myosin heads facilitate sliding filaments
ATP binds to myosin heads, head is released
ATP hydrolyzed, energy stored for next round
happens many times in a single contraction

62
Q

relaxation requires energy

A

muscle relaxation, Ach secretion at NMJ stops
stops APs along sarcolemma, stops Ca++ release from SR
movement of Ca++ back into SR, energy dependent process
Ca++ actively pumped back into SR (requires ATP)
restoration of membrane potential- Na+/K+ pump (requires ATP)

63
Q

whole muscle physiology

motor unit

A

consists of single motor neuron and all muscle fibers it innervates

64
Q

what does a motor unit respond to stimulation as

A

single unit

65
Q

what does each muscle fiber have for a motor neuron

A

action potential

66
Q

muscle twitch

A

single contraction of muscle in response to stimulus

AP in one or more of muscle fibers

67
Q

phases of muscle twitch

A

lag
contraction
relaxation

68
Q

force of contraction

A

all or none
graded muscle response
how to increase force of contraction- summation or recruitment

69
Q

all or none

force of contraction

A

threshold must be reached for contraction to occur

70
Q

graded muscle response-

force of contraction

A

different strength of contraction

71
Q

to increase force of contraction
force of contraction
summation

A

increase force via more APs

72
Q

to increase force of contraction
force of contraction
recruitment

A

increase number of muscle fibers/motor units that are contracting

73
Q

frequency summation

A

stimuli applied in quick succession before muscle fully relaxed with each stimulus tension increasing
increased frequency of APs

74
Q

complete tetnus

A

very rapid, high frequency continuous stimulation with no relaxation, causes sustained contraction of muscle

75
Q

what does increased frequency of APs do

A

Ca++ accumulating in muscle fibers

results in increased force of contraction

76
Q

types of muscle contractions

A

isometric

isotonic

77
Q

isometric muscle contraction

A

no noticeable change in length of muscle, no movement of joint
increase in tension/force in muscle during contraction

78
Q

example of isometric contraction

A

maintenance of posture

79
Q

isotonic muscle contraction

A

tension produced by muscle is constant, change in length of muscle, movement occurs

80
Q

example of isotonic muscle contraction

A

moving limbs or fingers

81
Q

types of isotonic muscle contractions

A

concentric contraction

eccentric contraction

82
Q

concentric contraction

A

working muscle shortens, tension in the muscle great enough to overcome the load

83
Q

eccentric contraction

A

working muscle lengthens, tension being maintained against the load

84
Q

fatigue

A

diminished ability to generate force

85
Q

what causes fatigue

A

reduced neural stimulation
depletion of substrates (ATP or glycogen)
accumulation of metabolites (lactic acid, Mg++, ROS) may interfere with Ca++ release from SR

86
Q

muscle fiber types and contraction

A

slow twitch

fast twitch

87
Q

slow twitch muscle fibers/ type 1

A

slower contraction, slower response to nervous stimulation, smaller fiber diameter, extensive vasculature, higher mitochondria and myoglobin concentrations, dark appearance
slow ATPase activity on myosin heads, more resistant to fatigue

88
Q

fast twitch muscle fiber/ type 2

A

faster response to nervous stimulation, fast ATPase activity on myosin heads, less vasculature, less myoglobin and mitochondria, lighter color, higher glycogen content, more susceptible to fatigue

89
Q

what muscle fiber is for endurance

A

slow

90
Q

what muscle fiber is for olympic lifting

A

fast

91
Q

heat production

A

ATP metabolism

shivering thermogenesis

92
Q

ATP metabolism

A

during muscle contraction- release of heat normal body temperature maintenance, increase with more contraction

93
Q

shivering thermogenesis

A

uncoordinated involuntary contraction of skeletal muscle, initiated by hypothalamus in response to signals from skin and spinal cord, generation of heat in response to cold air temperature

94
Q

blood cycle through heart

A
1 O2 poor blood carried in superior and inferior vena cava
2 enters RA
3 passes through tricuspid valve
4 enters RV
5 passes through pulmonary SL valve
6 carried through pulmonary arteries to lungs
7 O2 rich blood carried through pulmonary veins
8 enters LA
9 passes through bicuspid valve
10 enters LV
11 passes through aortic SL valve
12 carried to body by aorta
95
Q

coronary circulatioin

A

carries oxygen rich blood to the heart itself and drains heart of oxygen poor blood

96
Q

myocardial infraction

A

“heart attack”

necrosis of myocardium due to one or more coronary blockages

97
Q

“widow maker”

A

blockage of left anterior descending artery

98
Q

characteristics of cardiac muscle

A

cardiac myocytes

99
Q

cardiac myocytes

A

striated, rich in mitochondria, elongated and branched, excitatory and conductive, conduction of AP

100
Q

cardiac muscle functional unit

A
intercalated disk
desmosomes
gap junctions
cardiac syncytium
"all or none" principle
synctia
101
Q

intercalated disks

A

form close contact with adjacent cells

102
Q

desmosomes

A

hold contact during contraction

103
Q

gap junctions

A

free flow of cytoplasm for AP conduction

104
Q

cardiac syncytium

A

when one cell becomes excited, all cells become excited and heart contracts as one unit

105
Q

two syncytia of cardiac muscle

A

atrial syncytium

ventricular syncytium

106
Q

types of cadiac myocytes

A

contractile

autorhythmic

107
Q

autorhythmic myocytes

A
autonomic foci
sinoatrial node
atrioventricular node
bundle of his
(left and right bundle branches)
purkinje fibers
108
Q

autorhythmic foci

A

autorhythmic cells that fire at their own intrinsic rates

109
Q

what does SA node do

A

spontaneously generates APs at regular intervals of 70 BPM

110
Q

spread of excitation follows specific sequence

A

SA node fires- signal spreads across atria (.04s), atria contracts
signal delay (.11s) at AV node- allows atria to fully empty
signal reaches ventricles (.08s)
purkinje fibers stimulate ventricles to contract
force of ventricular contraction pushes blood through arteries

111
Q

heart block

A

first degree
second degree
third degree

112
Q

first degree heart block

A

impulses to ventricles slightly delayed

113
Q

first degree heart block

A

impulses to ventricles slightly delayed

114
Q

first degree heart block

A

impulses to ventricles slightly delayed

115
Q

second degree heart block

A

impulses intermittently blocked

116
Q

third degree heart block

A

no impulses from atria reach ventricles

atrial pacemaker- medical device that produces electrical signals

117
Q

action potential in contractile myocytes

A

long refractory period compared to skeletal muscle

prevention of tetanus

118
Q

what is the RMP for skeletal and contractile myocytes

A

-90 mV

119
Q

fast Na+ channels

A

respond quickly to stimulation

120
Q

L- type channels (long opening/slow)

A

respond slowly to stimulation

l- type Ca++ channels

121
Q

AP in contractile myocyte graph

A
phase 0- depolarization, 
phase 1- early repolarization
phase 2- plateau
phase 3- regular repolarization
phase 4- RMP
122
Q

phase 0

AP in contractile myocytes

A

fast Na+ channels open, Na+ rushes in

at -40 mV l- type Ca++ channels open, small steady influx of Ca++

123
Q

phase 1
early repolarization
AP in contractile myocytes

A

some K+ open briefly, K+ out

124
Q

phase 2
plateau
AP in contractile myocytes

A

l- type Ca++ open, Ca++ in, K+ open, K+ efflux

counter balance with Ca++ and K+ at 0 mV

125
Q

phase 3
regular repolarization
AP in contractile myocytes

A

Ca++ closed, K+ open, K+ out

126
Q

action potential in autorhythmic myocytes

A

never at rest, SA node “pacemaker potential”, positive drift from -60 mV to -40 mV
allows for “readiness” to fire and spontaneous depolarization

127
Q

three causes of pacemaker potential

A

1 increased influx of Na+- “funny channels” open in response to hyperpolarization, allows Na+ in, pushes up RMP
2 decrease efflux of K+- K+ channels close during hyperpolarization of AP, limiting K+ leaving cell (pushes up voltage)
3 differential influx of Ca++ ions- some Ca++ channels open before threshold, pushes voltage to threshold, once at threshold, l- type Ca++ channels open, producing AP

128
Q

AP in autorhythmic myocytes

A

threshold- -40 mV
phase 1- pacemaker potential
phase 2- depolarization
phase 3- repolariztion

129
Q

phase 1
pacemaker potential
AP in autorhythmic myocytes

A

in hyperpolarized state “funny” Na+ channels open, leads to Na+ coming into cell, closed K+ channels reduced K+ from leaving cell, as threshold approached some Ca++ channels open briefly, Ca++ moves into cell, threshold is reached

130
Q

phase 2
depolarization
AP in autorhythmic myocytes

A

l- type Ca++ channels open, Ca++ in

131
Q

phase 3
repolarization
AP in autorhythmic myocytes

A

Ca++ channels close, K+ channels open, K+ efflux

132
Q

electrocardiogram (ECG)

A

record of electrical activity of heart

electrical events correlate with physical activity

133
Q

p wave

A

atrial depolarization

onset of atrial contraction

134
Q

QRS complex

A

ventricular depolarization

onset of ventricles contraction

135
Q

t wave

A

ventricular repolarization

precedes ventricles relaxing

136
Q

fibrillation “quiver”

A

atrial fibrillation

ventricular fibrillation

137
Q

atrial fibrillation (A-fib)

A

irregular contraction of atria
compatible with life and full activity, irregular spacing of QRS complex and no p waves
treat with beta blockers (block beta-adrenergic receptors) to drop HR and reestablish SA node rhythm

138
Q

ventricular fibrillation (V-fib)

A

emergency, results in “cardiac arrest”
ventricular twitches- not proper contractions
loss of consciousness within seconds
fatal unless immediate intervention (CPR and defibrillation)

139
Q

defibrillator

A

applies strong electrical current that depolarizes most/entire heart at once, gives SA node time to re-establish normal sinus rhythm

140
Q

cardiac cycle

A

pattern of contraction and relaxation of heart chambers initiated by spontaneous AP from SA node
atria- primer pumps- push blood into ventricles
ventricles- power pumps- force blood into pulmonary system and systemic circulation
diastole- relaxation- blood fills chambers
systole- contraction, blood pushed out of chambers

141
Q

cardiac cycle

steps

A

1- passive ventricular filling- blood entering left and right ventricles through gravity
SA node
2 atrial systole- pushes rest of blood into ventricles
AV node to purkinje fibers
ventricular systole (early)- pressure increases in ventricles, causes AV valve to close, semilunar valves closed, no movement of blood
ventricular systole (late)- pressure strong enough to open SL valves, blood ejected into great arteries
ventricular diastole- ventricles relax

142
Q

intrinsic regulation of heart

A

cardiac output- amount of blood pumped per minute
stroke volume- volume of blood pumped per beat
CO= HR*SV
changes in HR and SV leads to changes in CO

143
Q

starling’s law of the heart

A

stroke volume of LV increases as volume of LV increases due to preload (stretch) of cardiac muscle
greater preload- greater force of contraction

144
Q

scenario

starling’s law of the heart

A

vigorous exercise increases venous return of blood to heart
more blood filling chambers increases preload
increased preload increases stroke volume
healthy heart muscle is like a spring

145
Q

extrinsic regulation of heart (autonomic ns)

A

PANS- vagus nerve, synpase a SA node and AV node
Ach binds to muscarinic receptors- inhibitory influences
SANS- project to heart as cardiac nerves, nerves synapse at SA node, AV node, and myocardium, NE binds to adrenergic receptors- excitatory influence,
also epinephrine from adrenal medulla binds to adrenergic receptors- excitatory influence