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Anatomy II > heart physiology > Flashcards

heart physiology Flashcards

1
Q

T/F the heart needs neural stimulation and neurotransmitters to depolarize

A

false! the heart generates its own ability to depolarize and contract

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2
Q

autorhythmic cells

A

noncontractile cells within contractile cells within muscles of the heart

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3
Q

pacemaker potentials

A

self-regulated action potentials in the heart

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4
Q

how do autorhythmic cells initiate and spread impulse

A

they are leaky-
Na can easily move in, K cannot easily move out

they are connected with desmosomes to neighboring cells- when they depolarize, it quickly spreads

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5
Q

T/F auto rhythmic cells have unstable resting potentials

A

true

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6
Q

autorhythmic cell location

A 
SA node
AV node
Bundle of His
Bundle Branches
Purkinje Fibers
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7
Q

how do we change rate at which heart beats

A

nervous connections

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8
Q

SA Node

A

main controller of electricity in heart

sits atop R atrium; just beneath where coronary sinus empties

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9
Q

“pacemaker of the heart”

A

SA node

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10
Q

AV Node

A

depolarizes; signal transfers from AV node all the way to apex of heart
sits atop inter ventricular septum

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11
Q

bundle of His

A

site of autorhythmic cells

splits to R and L sides of heart (splits higher or lower depending on person)

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12
Q

bundle branches

A

branches of bundle of his; go right or left

contain autorhythmic cells

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13
Q

Purkinje fibers

A

fibers coming off Bundle of His branches

send electrical impulse to muscle cells; end up in papillary muscles

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14
Q

2 clusters of neurons in medulla that send reflexes to heart

A

cardioaccelatory center

cardioinhibitory center

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15
Q

cardioaccelatory center

A

sends sympathetic nervous impulses to heart
sympathetic nerve fibers use norepinephrine as NT –> norepinephrine causes autorhymic cells to depolarize and HR increases

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16
Q

cardioinhibitory center

A

sends parasympathetic nervous impulses to heart

parasympathetic nerve fibers use acetylcholine –> ACh hyper polarizes SA node cells, then slows down and HR decreases

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17
Q

ECG (electrocardiogram)

A

graphic recording of electrical events of the heart

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18
Q

deflection waves

A

what we see in an ECG

includes P wave, QRS complex, and T wave

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19
Q

P Wave

A

represents wave of depolarization in atria

SA node has depolarized and made pacemaker potential that’s spread through atria

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20
Q

QRS Complex

A

represents depolarization of ventricles

2 things happening, only 1 shown (repolarization of atria not shown)

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21
Q

T Wave

A

represents repolarization of ventricles

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22
Q

how can we see if there are problems with the heart’s conduction pathway?

A

looking at timing between intervals in ECG

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23
Q

PR interval

A

time between start of P wave and start of R wave

represents movement of electrical impulse through atria down

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24
Q

heart sound and what is it generated by?

A

Lub-Dup; generated by valves closing

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25
Q

“Lub” is caused by what

A

AV valve closure

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26
Q

“Dup” is caused by what

A

SL Valve closure

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27
Q

murmur

A

extraneous or abnormal heart sound

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28
Q

pathological murmur

A

murmur related to malfunctioning of heart valves

valves may not be closing all the way

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29
Q

cardiac cycle

A

systole and diastole of both atria plus systole and diastole of both ventricles

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30
Q

systole

A

phase of contraction

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31
Q

diastole

A

phase of relaxation

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32
Q

blood pressure

A

pressure that blood exerts on arteries as it leaves the heart
generated by pressure difference

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33
Q

why is bp higher on left side?

A

left wall much more muscular and thick because it has to push blood to entire body

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34
Q

why is bp lower on right side

A

so lung tissue won’t be damaged

so blood flows slow enough for adequate gas exchange

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35
Q

cardiac output

A

amount of blood that leaves ventricles per minute

produce of stroke volume and heart rate

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36
Q

stroke volume

A

amount of blood that leaves heart per beat

difference between amount of blood in ventricles before and after systole

end diast. volume - end syst. volume

37
Q

cardiac reserve

A

difference between max CO and normal CO

38
Q

how high can max CO go

A

20-25 mL/min

39
Q

avg SV for healthy people my age

A

70 mL/b

40
Q

avg HR for healthy people my age

A

75 bpm

41
Q

how do we increase the amount of blood pumping through the heart

A

cardiac reserve

42
Q

end diastolic volume

A

when ventricles are most relaxed and full; just before contraction

43
Q

end systolic volume

A

blood that’s left behind in ventricle after it contracts

44
Q

factors affecting stroke volume

A

stretch of cardiac muscle (starling law of heart)
contraction strength NOT due to stretch
arterial pressure

45
Q

how does stretch of cardiac muscle affect stroke volume

A

when cardiac muscle tissue is stretched (by blood), it contracts with increased force
greater blood in ventricle (preload) means greater force of contraction

46
Q

preload

A

amount of blood in ventricles before they contract

directly proportionate with contraction strength

47
Q

how does contraction strength not due to stretch affect stroke volume

A

norepinephrine changes rate of contraction and amount of calcium allowed into muscle cell
increases force of contraction

48
Q

how does arterial pressure affect stroke volume

A

blood moves in response to pressure differences

higher pressure of arteries causes pressure difference to not be as high, so decreases blood out

49
Q

afterload phenomenon

A

higher pressure of arteries causes pressure difference to not be as high, so decreases blood out

50
Q

factors that affect HR

A 
sympathetic nervous system
parasympathetic nervous system
adrenal medulla production of epinephrine
thyroid production of thyroxine
BP changes (baroreceptors)
ionic imbalances
age
sex
exercise
temperature
51
Q

how does norepinephrine affect HR

A

speeds up HR

52
Q

how does acetylcholine affect HR

A

slows down HR

53
Q

how does adrenal medulla production of epinephrine affect HR

A

speeds up HR suddenly

54
Q

how does thyroid production of thyroxine affect HR

A

speeds up HR gradually/sustained

55
Q

how does bp change (baroreceptors) affect HR

A

changes speed at which heart contracts

when bp incr, change in pressure is detected by baroreceptors –> send signal to heart to beat faster

56
Q

how does ionic imbalance affect HR

A

ion imbalance can incr or decr HR based on what is imbalanced

depolarization of tissues requires ion movement

57
Q

how does age affect HR

A

HR decreases as you age

58
Q

how does gender affect HR

A

female HR > male HR

59
Q

how does exercise affect HR (short and long term)

A

short term- HR increases when exercising because muscles need more O2 delivered

long term- resting HR decreases with continued long term exercise

60
Q

how does temperature affect HR

A

HR is higher when you have a fever

61
Q

vagal tone

A

reduction in heart’s rate of contraction due to stimulation from vagus nerve

62
Q

if we were able to disconnect heart from all nerves, what would HR be? what is it actually?

A

100 bpm; 75 bpm

63
Q

how does vagal tone make the heart slow down?

A

parasympathetic nervous impulses from cardioinhibitory center travel from medulla oblongata and cause hyper polarization of SA node

64
Q

where do parasympathetic fibers that slow down the heart run?

A

along cranial nerve 10 (vagus nerve)

65
Q

why do we have vagal tone?

A

so we can increase HR even more in case of emergency

66
Q

tachycardia

A

abnormally high resting HR

>100 bpm

67
Q

bradycardia

A

abnormally low resting HR

<60 bpm

68
Q

congestive heart failute

A

dangerously low cardiac output

69
Q

factors that could cause CHF

A

coronary atherosclerosis
high BP
myocardial infarction
dilated cardiomyopathy

70
Q

coronary atherosclerosis

A

blockages within coronary artery

decreases diameter of vessels, which decreases CO (heart doesnt have enough energy to pump strongly)

71
Q

how does high blood pressure cause CHF

A

high blood pressure in aorta reduces “ejection fraction” coming from heart

72
Q

high blood pressure

A

diastolic over 90

73
Q

how does myocardial infarction cause CHF

A

as blood supply is decreased to heart muscle, myocardium loses its ability to contact

74
Q

dilated cardiomyopathy is usually due to:

A

valve failure

75
Q

dilated cardiomyopathy

A

eventually, if we have high bp or low HR and blood is allowed to continue to pool in ventricles, ventricles stretch too much
ventricles so stretched that they don’t respond with increased contraction –> they just get loose and weak

76
Q

the heart is developed from which embryonic structure?

A

mesoderm

77
Q

heart development

A
  1. originates as 2 endothelial tubes
  2. tubes fuse into single chambered “heart” by day 23
  3. early chambers formed by day 25
  4. D-looping and structural changes divide heart into separate chambers and change orientation by day 46
78
Q

D-looping of heart

A

heart makes rightward circle until it is upside down during development

79
Q

foramen ovale

A

connection of 2 atria through interatrial septum

right up until birth, 2 atria are connected by this

80
Q

why are atria connected in utero?

A

fetus doesn’t have to do gas exchange until it is born bc it gets all oxygenated blood from mom

81
Q

ductus arteriosus

A

connection between pulmonary trunk and aorta that seals at birth

82
Q

ductus arterioles becomes ______

A

ligamentum arteriousum

83
Q

T/F no blood goes to lungs before birth

A

false- some blood goes to lungs to supply them with blood (but no oxygenation is taking place there)

84
Q

age related changes of heart

A

valve sclerosis
decreased cardiac reserve
fibrosis of myocardium
atherosclerosis

85
Q

valve sclerosis

A

cusps of heart valves accumulate deposits –> so cusps do not close right –> leakage –> decreased CO

86
Q

how to decrease risk of valve sclerosis

A

eat lipids and Calcium

87
Q

decreased cardiac reserve due to aging

A

as you age, you get sedentary, and cardiac reserve decreases

88
Q

fibrosis of myocardium

A

as you age you get sedentary, so unused heart muscle converts to fibrous CT (cannot contract)

Anatomy II (17 decks)

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