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Anatomy II > Chapter 18- Cardiovascular System > Flashcards

Chapter 18- Cardiovascular System Flashcards

1
Q

Pulmonary Circuit

A

Any of the blood vessels that carry blood to and from the lungs
Concerned with the right side of the heart

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2
Q

Pulmonary arteries

A

Pump oxygen-poor blood from the right side of the heart to the lungs to oxygenate it
Later returns to the other side of the heart through the pulmonary veins

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3
Q

Pulmonary veins

A

Pump oxygenated blood from the lungs to the left side of the heart

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4
Q

Systemic circuit

A

Any of the blood vessels that carry blood to and from the body tissues
Devliering oxygenated blood to the tissues for exchange to occur

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5
Q

Aorta

A

OXYGENATED blood leaves the heart through aorta to go into body tissues

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6
Q

Pre and Post cava

A

Oxygen POOR returns to the heart through the precava and postcava

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7
Q

Path of the blood through the heart

A

Blood travels through all four chambers of the heart and both circuits continuously
Left- Systemic
Right- Pulmonic

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8
Q

Oxygenated blood (left- Systemic)

A

Travels through arteries to get to tissues
Through aorta

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9
Q

Deoxygenated blood (left- systemic)

A

Travels through veins to get back into the heart
through pre and post cava

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10
Q

Deoxygenated blood (right- pulmonary)

A

Arteries to get to lungs

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11
Q

Oxygenated blood (right- pulmonary)

A

Going to left
Veins to get back into the heart

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12
Q

The right side is low pressure. Why?

A

It is smaller
Just going to lungs and back

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13
Q

The left side is high pressure. Why?

A

Must generate more force/pressure because more distance is covered and requires more muscle tissue
Walls more thick
Propels blood all over

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14
Q

The heart is tipped where?

A

In the thoracic cavity
apex points to the left hip

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15
Q

Fibrous pericardium

A

Outermost portion
Fibrous tissue
Less flexible
Prevents heart from filling with too much blood
anchors heart in chest cavity
Protects heart
Bending blood vessels is like bending a hose

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16
Q

Serous Pericardium

A

Internal portion
Divides into visceral and parietal layers that form fluid filled sac around the heart
Movement to it prevents heart from rubbing against other organs/structures
Prevents rubbing away of heart walls

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17
Q

Layers of the heart wall

A

Epicardium- outermost
Myocardium- middle later
Epicardium- innermost layer

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18
Q

Epicardium

A

Visceral layer of pericardium

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19
Q

Myocardium

A

Contains cardiac muscle cells arranged in spiral bundles
The heart twists slightly as it contracts to pump blood
Propels more blood and increases force generated

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20
Q

Endocardium

A

Covers internal surfaces of the heart including the valves
Continuous with linings of major blood vessels entering and leaving the heart
A slippery slick fluid that lines the endocardium

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21
Q

2 Atria

A

Superior receiving chambers

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22
Q

Right atrium

A

Receives OXYGEN POOR blood from some part of the body
Blood enters via pre and post-cava, coronary sinus

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23
Q

Left atrium

A

Receives OXYGENATED blood from the lungs
Blood enters through pulmonary veins

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24
Q

Atrial features

A
  1. Pectinate muscle- increases contractile force of atrium without increasing the mass of the heart (Not the true muscle tissue responsible for generating force, just an add on)
  2. Auricles- Two ears sitting o the external surface of the heart (Increases the amount of blood being brought into the atrium/waiting room)
  3. Fossa ovalis- Indentation in the left atrium (new foramen ovale)
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25
Q

2 ventricles

A

Inferior pumping chambers

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26
Q

Right ventricle

A

Deoxygenated blood to lungs

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27
Q

Pulmonary trunk (artery)

A

Pumps from the heart to the lungs
FROM right ventricle

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28
Q

Left ventricle

A

Oxygenated blood to other tissues

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29
Q

Aorta

A

Pumps from heart to the rest of the body
FROM left ventricle

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30
Q

Ventricle features

A
  1. Trabeculae carnae- ridges of muscle that assist with the proper functioning of the heart valves
  2. papillary muscle- Assist in opening/closing the heart valves
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31
Q

2 heart valves

A
  1. Atrioventricular valves- prevents backflow of blood from the ventricles back into the atria
  2. Semilunar valves- Prevents backflow of blood from blood vessels into ventricles (each has 3 cusps)
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32
Q

Tricuspid valve (AV)

A

Right side
3 cusps

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33
Q

Bicuspid valve (AV)

A

Left side
2 cusps

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34
Q

Papillary muscles

A

Take up slack of chordae tendinae

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35
Q

Aortic semilunar valve

A

sits at the base of the aorta
Left ventricle pumps blood into the aorta

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36
Q

Pulmonary semilunar valve

A

Sits at the base of the pulmonary trunk/artery
Right ventricle pumps blood into the pulmonary trunk

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37
Q

Heart murmurs

A

dysfunctional heart valve(s)
Regurgitation of blood (where this occurs depends on which valve doesn’t work
Stenosis
Left side more problematic than the right
either congenital or develop later in life
Heart sound problems
Usually not dangerous, but can indicate other potentially dangerous heart conditions

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38
Q

Stenosis

A

Valves do not allow enough blood through the valve

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39
Q

Heart sounds

A

Normal- lub-dup
Heart murmur- Lub-whoosh-dup (whoosh- blood going backwards

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40
Q

“Innocent” murmurs

A

usually congenital
can disappear

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41
Q

“Abnormal” murmurs

A

Children- indicate congential heart disease (fixed w surgery)
Adults- Indicate acquired heart valve issues
Slow down the flow of blood because it’s going in the wrong direction
Treat by putting in an artificial valve

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42
Q

Blood Supply to the heart

A

Coronaries

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43
Q

Coronary circulation

A

Blood supply that provides heart tissue with nutrients

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44
Q

Left coronary artery

A

Supplies left side of the heart
Anterior interventricular artery- Supplies anterior walls of ventricles and the wall dividing the two
circumflex artery- supplies the left atrium and posterior left side

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45
Q

Right coronary artery

A

Supplies right side of the heart
Right marginal artery- supplies myocardium of lateral portion of right side of the heart
Posterior interventricular artery- supplies posterior ventricular walls

46
Q

Coronary veins

A

Drain oxygen-poor blood
pathway similar to arteries (in opp. direction)

47
Q

What do coronary veins combine to form? what does it skip?

A

Coronary sinus
(empties blood into right atrium, skips the cavas)

48
Q

Anterior cardiac veins

A

Empties into atrium (skips coronary sinus)

49
Q

Cardiac muscle cells

A

Striated and contract by the sliding filament model of contraction
Interconnected

50
Q

Intercalated discs

A

How plasma membranes are connected
Contain desmosomes and gap junctions

51
Q

Functional syncytium

A

Muscle cells contract simultaneously

52
Q

Why is functional syncytium important for the function of the heart?

A

Can pass messages from one cell to another and can communicate
Spread action potentials from one to the other
If the heart contracts whenever it wants, it impairs blood flow; must contract as a single time

53
Q

How is the large number of mitochondria important for muscle fatigue?

A

Produces a massive amount of ATP to be used for functioning

54
Q

Pacemaker cells

A

Cardiac muscle cell type
Noncontractile cells that spontaneously (NOT randomly, just independently) depolarize
Influence other types of cells
Sets the pace of the heart

55
Q

Contractile cardiac cells

A

Contractile cells that depolarize in response to pacemaker cells
Cause contraction of myocardium that pumps blood through the heart

56
Q

Pacemaker potential

A

“slow depolarization”
Na+ channels open, K+ channels close
Causes the membrane potential to be more positive (decreases potential)

57
Q

Depolarization

A

Ca2+ channels open at threshold potential (-40 mV)
Ca2+ rush into cell
Creation of action potential

58
Q

Repolarization

A

Ca2+ channels close
K+ removed from cell (gates open)
Slow sodium channels are open as well
once RMP established, the cycle begins again

59
Q

Where are pacemaker cells found? How many areas are there?

A

Nodes; 5

60
Q

Sinoatrial Node

A

Primary pacemaker of the heart
Located in the upper right atrial wall
Generates around 75 impulses/min
Depolarizes at the SA and spreads through both atria until it reaches the Atrioventricular node

61
Q

Atrioventribular node

A

Found in interatrial septum
If Sinoatrial node is dysfunctional, the AV node will take over as the primary pacemaker
Side effect- heard rate will slow
Generates around 50 impulses/min
Impulses delayed by .1 seconds because if there was no delay, the atria wouldn’t empty completely prior to contraction

62
Q

Bundle branches

A

Right and left branches in the wall that divides the arteries
Helps conduct impulses toward the apex of the heart

63
Q

Subendocardial conducting network (purkinje fibers)

A

Found at heart apex and along outer ventricle walls
Will travel up the outer ventricle walls
Depolarizes contractile cells of both ventricles
More elaborate on left side than right because many branches come off and proliferate from the one branch because the left walls are thicker
Thicker = more cardiac myocytes = more stimulation needed to get the same message

64
Q

Where are the cardiac centers found?

A

Medulla oblongata

65
Q

Cardioacceleratory center

A

Sympathetic division
postgangliionic fibers innverate sinoatrial node and atrioventricular node ,heart muscles, coronary arteries
Speeds up heart rate

66
Q

Cardioinhibitory center

A

Parasympathetic
Postganglionic motor neurons found in heart wall, innervate sinoatrial node and atrioventricular node
Slows down heart rate

67
Q

Action potentials of contractile cardiac cells

A
  1. Depolarization (Na gates open - Membrane potential from -90 to +30)
  2. Plateau phase (Ca channels open, + K too)
  3. Repolarization (Ca channels close, all K channels open to go back to resting rate)
68
Q

How does the action of Ca and K cause a plateau

A

Decreases, but very slowly because the K counteracts the Ca coming into the cell
Holds depolarization in place for a few milliseconds to create tension and move more blood
Repolarization = tension will decrease

69
Q

Electrocardiography

A

Detection of the electrical impulses generated in & transmitted by the heart

70
Q

Electrocardiogram

A

Doctors can see heart activity
produce several “waves” or complexes

71
Q

Waves of the ECG

A

P wave
QRS wave - series of spikes moving up and down
T wave

72
Q

P wave

A

Depolarization of the atria
2 atria contracting shortly after the P wave begins will go through the ventricle
Moves to AV node after depolarization is complete

73
Q

QRS

A

Depolarization of the ventricles
Peak - R
Troughs - QS
Current changes direction
Split left and right and travel up the side of the heart

74
Q

T wave

A

Repolarization of the ventricles
Wider than QRS complex

75
Q

RR interval

A

The time between subsequent heartbeats

76
Q

Junctional rhythms

A

Abnormal heartbeat
Indication is dysfunctional Sinoatrial node and atrioventricular node must take over and will slow the heart rate
Causes…
RR interval will become wider
P wave is no longer evident, heart rate slows
If there is no Sinoatrial node, you have no P wave

77
Q

Ventricular fibrillation

A

Abnormal heartbeat
Action potentials occur in highly irregular patterns in ventricles
Contractile cells no longer work as a unit
Causes fluttering in the chest where the two atria do whatever they want
Chaotic, irregular ECG deflection are seen in acute heart attack and electrical shock

78
Q

Cardiac Cycle

A

Includes all mechanical events associated with blood flow through the heart in one complete heartbeat

79
Q

Systole vs. Diastole

A

S- Period of contraction
D- Period of relaxation
Each cycle occurs 75 time per minute

80
Q

Ventricular filling

A

(mid to late diastole - heart relaxed): pressure in the heart is low
AV valves are open → blood flows freely from atria into ventricle
Atrial systole occurs: atria contract → push remaining blood into ventricle
Ventricles have end diastolic volume
At the very end of this phase → atria relax & ventricles depolarize

81
Q

End diastolic volume

A

Maximum volume of blood found in the ventricles before it contracts

82
Q

Isovolumetric contraction phase

A

Systole
Same volume contraction
Ventricles begin to contract due to depolarization→ pressure in ventricles rises quickly
AV valves close, SL valves are not yet opened
Blood volume remains constant
Pushing in on the blood that is stored in them - blood isn’t going anywhere

83
Q

Why is blood not ejected from the ventricles during isovolumetric contraction phase?

A

All valves are closed so blood cannot leave, just push on it

84
Q

Ventricular ejection

A

Systole
Blood flows from ventricles into aorta and pulmonary trunk
Right ventricle - pulmonary artery - lungs
Pressure will drop off

85
Q

Isovolumetric relaxation

A

Early diastole
Ventricles relax, ventricular pressure drops rapidly
End systolic volume reached: volume of blood remaining in the ventricles
SL valves close → ventricles are closed off again (but now nearly empty)
Prevents a heart murmur where blood flows back

86
Q

Cardiac Output

A

The total amount of blood pumped by ventricle in a single minute
Cardiac output (Stroke volume) x (heart rate)
You’re heart pumps all of your heart’s blood volume

87
Q

Stroke Volume

A

EDV - ESV
Volume of blood pumped out by ventricles with each beat
Directly correlated with force of ventricular contraction
Close to 0
Stronger heart = stronger stroke volume
Adult average is around 70 mL of blood per minute

88
Q

Heart rate

A

Beats per minute
The average for an adult is 75 beats/min

89
Q

What happens to Cardiac Output when stroke volume increases? Heart rate? Both? In what circumstances would this happen?

A

Cardiac output increases when either stroke volume or heart rate increases
Physical exercise, certain hormones, etc.

90
Q

Maximal cardiac output

A

The maximum amount of blood that can be pumped in a single minute
The total amount is dependent on the level of physical fitness
Less fit = lower maximal cardiac output (20/25 L/min)
More fit = higher maximal cardiac output (35 L/min)
If you exercise more frequently, you are training your heart to pump more efficiently

91
Q

Individuals who are more physically fit vs. less physically fit

A

More = higher maximum cardiac output BC their bodies require more oxygen and nutrients
Less = lower maximum cardiac output

92
Q

Preload

A

Changing EDV
Stretch of sarcomeres just prior to contraction
Will increase the force of contraction during systole

93
Q

How are sarcomeres stretched?

A

Preloading with blood stretches out the walls and cells of the walls

94
Q

Frank-starling Relationship

A

Increasing the total volume of blood at the end of diastole will increase strength of contraction during systole
More preload –> stronger contraction –> increased amount of blood moved

95
Q

Changing ESV- Two ways

A

Contractibility - intrinsic strength of the ventricle independent of loading conditions
“Afterload”- forces that oppose blood ejection from the ventricles dependent on the resistance created by blood vessels

96
Q

What happens to end systolic volume when contractibility increases? Why?

A

It will force more blood out of the ventricle, decreasing the amount of blood in the ventricle
To increase contractibility, increase calcium release

97
Q

How does resistance affect the ability to pump blood?

A

Moving up against the wall
Prevents blood from leaving the ventricles coming from the blood vessels
The more blood leaving the venctricle, the more blood before it contracts creating a stronger contraction
Dilate blood vessels = less resistance (bigger tube)
Contract blood vessels = greater resistance (narrower tube)
ik this doesn’t make any sense page 13 chapter 18

98
Q

What happens to ESV when afterload is increased?

A

ESV increases because you are increasing resistance because it makes it more difficult to pump blood into the ventricles

99
Q

Autonomic nervous system regulation of heart rate

A

Sympathetic - NE released and SA node fires faster = faster heartbeat (higher contractibility)
Parasympathetic - ACCL released

100
Q

Vagal Tone

A

Heart rate is slower than it would be if the vagus nerve did not innervate
Cutting the vagus nerve would increase heart rate to 100 beats/min

101
Q

Hormones

A

Epi and Norepi- Increase Heart rate and contractibility
Thyroxine- thyroid hormone that increases metabolic rate and body heat

102
Q

Ions

A

Plasma electrolyte imbalances can increase/decrease heart rate substantially

103
Q

Hypocalcemia vs. Hypercalcemia

A

Calcium
Hypo- decrease heart rate
hyper- increase heart rate (faster contraction)

104
Q

Hypokalemia vs. Hyperkalemia

A

Potassium
Hypo- Weakened/feeble heartbeat
Hyper- DANGEROUS; Excessively high potassium levels causing cardiac arrest

105
Q

Other factors affecting heart rate

A

Age (declines with age)
Biological sex (females have higher rate than males)
Exercise/physical fitness (increased fitness = decreased heart rate)
Body temp (higher body temp = higher Heart rate)

106
Q

Congestive heart failure

A

The inefficiency of blood pumping by heart to body tissues
Usually a progressive condition

107
Q

Causes of congestive heart failure

A

Coronary atherosclerosis- fatty buildup that clogs coronary arteries
Hypertension- persistent high blood pressure in the arteries forcing the heart to work harder
Multiple myocardial infections (heart attacks) causes buildup of scar tissue
Dilated cardiomyopathy- ventricles stretch out and myocardium deteriorates

108
Q

Pulmonary congestion

A

Left side fails, right side normal

109
Q

Pulmonary edema

A

Filling of lungs with fluid and will not move through systemic circuit fast enough causes improper amount of gas exchange

110
Q

Peripheral congestion

A

Right side fails

111
Q

What happens if one side fails?

A

Puts undue stress on the other side and heart will eventually fail
treatment- remove excess fluid, decrease blood pressure, increase contractility of defective side

Anatomy II (4 decks)

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