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chp 18 power point Flashcards

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Biology 101 flashcards
1
Q

the sac containing the heart

A

pericardium

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2
Q

3 layers that form the heart

A

epicardium
myocardium
endocardium

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3
Q 
inflammation of the pericardium
painful
may damage the lining tissues
may damage myocardium
is what disease
A

pericarditis

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4
Q

a buildup of pericardial fluid, or
bleeding into the pericardial cavity
may result in cardiac failure

A

cardiac tamponade

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5
Q

Interatrial septum separates

A

atria

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6
Q

Interventricular septum separates

A

ventricles

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7
Q

Left ventricular wall is much thicker because

A

it must pump blood throughout the body and against gravity

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8
Q

Right atrium (RA) - receives what kind of blood

A

deoxygenated

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9
Q

Right atrium (RA) - receives deoxygenated blood from three sources

A

superior vena cava (SVC)
inferior vena cava (IVC)
coronary sinus (CS)

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10
Q

Right ventricle (RV) pumps to lungs via

A

Pulmonary Trunk (PT)

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11
Q

what sends deoxygenated blood from the heart to the lungs for gas exchange
right and left branches for each lung
blood gives up CO2 and picks up O2 in the lungs

A

pulmonary arteries

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12
Q

What send oxygenated blood from the lungs to the heart

A

Pulmonary veins (PV) -

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13
Q

what receives blood from PV

pumps to left ventricle

A

left atria

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14
Q

what sends oxygenated blood to the body via the ascending aorta

A

left ventricle

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15
Q

duplication of supply routes and anastomoses (crosslinked connections)
is what

A

Collateral circulation

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16
Q

Myocardium has its own

A

blood supply

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17
Q

simple diffusion of nutrients and O2 into the myocardium is impossible due to

A

its thickness

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18
Q

Heart can survive on how much of normal arterial blood flow

A

10-15%

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19
Q

first branches off the aorta

A

arteries

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20
Q

blood moves more easily into the myocardium when it is what between beats -> during diastole

A

relaxed

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21
Q

what first branches off the aorta
blood moves more easily into the myocardium when it is relaxed between beats  during diastole
blood enters coronary capillary beds

A

arteries

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22
Q

what carries deoxygenated blood from cardiac muscle is collected in the coronary veins and then drains into the coronary sinus
deoxygenated blood is returned to the right atrium

A

Coronary veins

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23
Q

Compromised coronary circulation due to

A
  • emboli: blood clots, air, amniotic fluid, tumor fragments
  • fatty atherosclerotic plaques
  • smooth muscle spasms in coronary arteries
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24
Q

-ischemia (decreased blood supply)
-hypoxia (low supply of O2)
-infarct (cell death)
are due to

A

circulation

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25
Q

classic chest pain

is

A

Angina pectoris

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26
Q

pathology causes pain is due to myocardial ischemia – oxygen starvation of the tissues
tight/squeezing sensation in chest
labored breathing, weakness, dizziness, perspiration, foreboding

A

Angina pectoris

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27
Q

pathology often during exertion - climbing stairs, etc.
pain may be referred to arms, back, abdomen, even neck or teeth
silent myocardial ischemia can exist

A

angina pectoris

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28
Q

heart attack

A

Myocardial infarction (MI)

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29
Q

what pathology causes thrombus/embolus in coronary artery
some or all tissue distal to the blockage dies
if pt. survives, muscle is replaced by scar tissue

A

Myocardial infarction (MI)

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30
Q

Long term results

of myocardial infarction

A

size of infarct, position
pumping efficiency?
conduction efficiency, heart rhythm

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31
Q

electrically charged oxygen atoms with an unpaired electron

A

oxygen free radicals

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32
Q

indiscriminately attack molecules: proteins (enzymes), neurotransmitters, nucleic acids, plasma membrane molecules

A

radicals

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33
Q
  • re-establishing blood flow may damage tissue

- further damage to previously undamaged tissue or to the already damaged tissue

A

Reperfusion damage

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34
Q

what has dense connective tissue covered by endocardium

A

valves

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35
Q
  • thin fibrous cords

- connect valves to papillary muscles

A

AV valves

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36
Q

when pressure low do valves open or close

A

open

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37
Q

with contraction, pressure increases

papillary muscles contract and

A

pull valves together

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38
Q

Function to prevent backflow of blood into/through heart

A

valves

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39
Q

Open and close in response to changes in pressure in heart

A

valves

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40
Q

Four key valves

A

Four key valves: tri- and bi-cuspid (mitral) valves between the atria and ventricles and semi-lunar valves between ventricles and main arteries

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41
Q

also close the entry points to the atria

A

valves

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42
Q

Separate the atria from the ventricles

A

bicuspid (mitral) valve – left side

tricuspid valve – right side

43
Q

valves with feathery edges

A

tricuspid and bicuspid

44
Q

in the arteries that exit the heart to prevent back flow of blood to the ventricles

A

semilunar valves

45
Q

a semilunar valve that does not close properly is called

A

incompetent

46
Q

a semilunar valve that is hardened, even calcified, and does not open correctly is called

A

stenosis

47
Q

-near instantaneous depolarization is necessary for efficient pumping

A

cardiac muscles Contractile cells

48
Q

-much longer refractory period ensures no summation or tetany under normal circumstances

A

cardiac muscles Contractile cells

49
Q

opening fast Na+ channels does what

A

initiates depolarization near instantaneously in cardiac action potential

50
Q

opening CA++ channels while closing K+ channels does what

A

depolarizes and contributes to sustaining the refractory period

51
Q

closing Na+ and Ca++ channels while opening K+ channels does what

A

restores the resting state

52
Q

long absolute refractory period permits

A

forceful contraction followed by adequate time for relaxation and refilling of the chambers

53
Q

inhibits summation and tetany

A

long absolute refractory period

54
Q

what kind of membranes does the heart have

A

leaky

55
Q

the fact that the membrane is more permeable to K+ and Ca++ ions helps explain

A

why concentration changes in those ions affect cardiac rhythm

56
Q
  • spontaneously depolarize

- creates autorhythmicity

A

pacemaker potentials

57
Q

cardiac cells repeatedly fire spontaneous action potentials

A

Autorhythmic cells

58
Q

the conduction system

A

Autorhythmic cells:

59
Q

origin of cardiac excitation

fires 60-100/min

A

SA node

60
Q

-AV bundle (Bundle of His)
-R and L bundle branches
-Purkinje fibers
make up

A

conduction system

61
Q

It’s as if the heart had only two motor units

A

: the atria and the ventricles

62
Q
  • irregular rhythms: slow (brady-) & fast (tachycardia)

- abnormal atrial and ventricular contractions means

A

Arrhythmias

63
Q

-rapid, fluttering, out of phase contractions – no pumping
-heart resembles a squirming bag of worms
means

A

Fibrillation

64
Q

-abnormal pacemaker controlling the heart
-SA node damage, caffeine, nicotine, electrolyte imbalances, hypoxia, toxic reactions to drugs, etc.
means

A

Ectopic pacemakers (ectopic focus)

65
Q

-AV node damage - severity determines outcome
-may slow conduction or block it
mean

A

Heart block

66
Q

SA node damage (e.g., from an MI)

A
  • AV node can run things (40-50 beats/min)

- if the AV node is out, the AV bundle, bundle branch and conduction fibers fire at 20-40 beats/min

67
Q

once action potentials reach the AV bundle, conduction is

A

rapid to rest of ventricles

68
Q

conduction slows

allows atria time to

A

finish contraction and to better fill the ventricles

69
Q

basic rhythm of the heart is set by the

A

internal pacemaker system

70
Q

pathway of the internal pacemaker

A

central control from the medulla is routed via the ANS to the pacemakers and myocardium

71
Q

parasympathetic input for extrinsic control of the heart

A

acetylcholine

72
Q

sympathetic input - for extrinsic control of the heart

A

norepinephrine

73
Q

measures the sum of all electro-chemical activity in the myocardium at any moment

A

Electrocardiogram

74
Q

Cardiac Output =

A

= Heart Rate x Stroke Volume

75
Q

Amount of blood pumped by each ventricle in 1 minute

A

Cardiac Output

76
Q

Cardiac Output is

A

variable

77
Q

Cardiac Reserve =

A

maximal output (CO) – resting output (CO)

78
Q

average individuals have a cardiac reserve of

A

4X or 5X CO

79
Q

trained athletes may have a cardiac reserve of

A

7X CO

80
Q

heart rate does not increase to the

A

same degree

81
Q

stroke volume -

A

EDV – ESV

82
Q

EDV

A

End Diastolic Volume
Volume of blood in the heart after it fills
120 ml

83
Q

ESV

A

End Systolic Volume
Volume of blood in the heart after contraction
50 ml

84
Q

Each beat ejects about what percentage of the blood in the ventricle

A

60%

85
Q

Most important factors in regulating SV:

A

preload, contractility and afterload

86
Q

the degree of stretching of cardiac muscle cells before contraction

A

preload

87
Q

increase in contractile strength separate from stretch and EDV

A

contractility

88
Q

pressure that must be overcome for ventricles to eject blood from heart

A

Afterload

89
Q

increasing/decreasing fiber length does what

A

increases/decreases force generation

90
Q

Length-Tension relationship?

A

fiber length determines number of cross bridges

cross bridge number determines force

91
Q

How is fiber length determined/regulated?

A

Fiber length is determined by filling of heart – EDV (End Diastolic Volume)

92
Q

Factors that effect EDV (End Diastolic Volume)

A

anything that effects blood return to the heart) increases/decreases filling

93
Q

Increases/decreases SV

A

Cardiac muscle

94
Q

– Frank-Starling Law of the Heart

A

preload

95
Q

Length tension relationship of heart

A 
Length = EDV (End Diastolic Volume)
Tension = SV (stroke volume)
96
Q

Sympathetic Stimulation increases the number

A

of cross bridges by increasing amount of Ca++ inside the cell

97
Q

Sympathetic nervous stimulation (NE) does what to the heart

A

opens channels to allow Ca++ to enter the cell

98
Q

Positive Inotropic Effect increase

A

increase the force of contraction without changing the length of the cardiac muscle cells

99
Q

if blood pressure is high, it is

A

difficult for the heart to eject blood

100
Q

more blood remains in the chambers after each beat

A

Afterload

101
Q

heart has to work harder to eject blood, because of

A

the increase in the length/tension of the cardiac muscle cells

102
Q

Intrinsic Regulation of Heart Rate

A

Pacemakers

Bainbridge effect

103
Q

Increase in EDV increases HR

Filling the atria stretches the SA node increasing depolarization and HR

A

Bainbridge effect

104
Q

Extrinsic regulation of Heart Rate

A 
Autonomic Nervous System
Sympathetic - norepinephrine
Parasympathetic – acetyl choline
hormones – epinephrine, thyroxine
ions (especially K+ and Ca++)
body temperature
age/gender
body mass/blood volume
exercise
stress/illness

Bio 2 (20 decks)

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