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BIOM 3200 > Cardio-Respiratory System > Flashcards

Cardio-Respiratory System Flashcards

1
Q

What are the 3 coats that make up the walls of arteries and veins?

A 
1 - Tunica externa (connective tissue)
2 - Tunica media (smooth muscle)
3 - Tunica interna
-> Endothelium
-> Glycoproteins/connective tissues
-> Elastin
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2
Q

What are 2 key differences between arteries and veins?

A
  • Arteries have more muscle

- Veins have valves

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3
Q

Where is most blood distributed at rest?

A
  • Venous system

- Functions as a reservoir from which more blood can be added

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4
Q

Describe veins?

A
  • Able to expand as they accumulate additional amounts of blood
  • Higher compliance than arteries
  • Venous pressure is too low to return blood to heart
  • Veins pass between skeletal muscle groups which provide contractions to help move blood back (‘skeletal muscle pump’)
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5
Q

What is the average pressure in veins?

A

2 mmHg

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6
Q

What helps venous blood return to heart from abdominal and thoracic regions?

A

The act of breathing/contracting of the diaphram and pressure in the abdomen from breathing squeezes the veins to help move blood

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7
Q

How is one-way flow of blood back to the heart ensured?

A

Venous valves

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8
Q

How were venous valves discovered? By who?

A
  • A tourniquet on an arm causes blood to collect in a bulge

- William Harvey

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9
Q

Describe the arteries?

A
  • In aorta/larger arteries, there are numerous layers of elastin fibres b/n smooth muscle cells of tunica media
  • Large elastic arteries expand when pressure rises as a result of ventricles’ contraction
  • They recoil when blood pressure falls during relaxation of the ventricles
  • Small arteries/arterioles are less elastic, so diameter changes slightly
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10
Q

What drives the blood forward in arteries during the diastolic phase?

A
  • Elastic recoil
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11
Q

How many capillaries are in the body?

A

Over 40 billion

- Scarcely any cell is more than 60-80 um away from capillary

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12
Q

How does vasoconstriction/vasodilation affect capillaries?

A
  • Vasoconstriction decreases blood flow to capillary bed

- Vasodilation increases it

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13
Q

What do capillaries consist of?

A
  • The walls are composed of just endothelial cells

- They lack smooth muscle/connective tissue, making it easier to exchange materials

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14
Q

What happens at the arterial end of a capillary? The venous end?

A

Arterial end:
- BP forces fluid out of capillary to interstitial fluid
Venous end:
- Select fluid is drawn back into capillary by osmotic pressure

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15
Q

What is the formula for flow?

A

Flow = driving forces/resistance

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16
Q

What 3 factors does resistance depend on? Who determined this?

A

1 - Radius of tube/blood vessel
2 - Viscosity of blood
3 - Length of tube/blood vessel

-> Jean Leonard Marie Poiseuille

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17
Q

How does radius affect flow?

A

Decreased radius = increased resistance = decreased flow

- Vessel radius regulated by smooth muscle contraction
Contraction = decreased radius

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18
Q

How does viscosity affect flow?

A

Increased viscosity = increased friction = increased resistance = decreased flow

Increased hematocrit = increased interaction b/n RBC = increased clots = decreased radius

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19
Q

How does length affect flow?

A

Increased length = increased friction = increased resistance = decreased flow

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20
Q

Describe the pulmonary artery and vein?

A 
Pulmonary artery:
- Carries blood away from heart
- Low oxygen
Pulmonary vein:
- Carries blood to heart
- Highly oxygenated
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21
Q

Where does the nasal cavity lead to?

A

Pharynx

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22
Q

What is the pharynx?

A

A muscular passage connecting the nasal cavity with the larynx

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23
Q

What happens at the larynx?

A
  • Air is diverted toward the lungs and food is directed to the esophagus to the stomach
  • Contains the vocal cords (folds in lining tissue of larynx)
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24
Q

What are 4 physical properties of the lungs?

A

1 - Inspiration and compliance
2 - Expiration and elasticity
3 - Surface tension
4 - Lung volumes and capacities

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25
Q

What is necessary for inspiration?

A

Lungs must be able to expand when stretched (they must have high compliance)

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26
Q

What does compliance mean?

A
  • Ease with which lungs can expand under pressure

- Change in lung volume per change in transpulmonary pressure (dV/dP)

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27
Q

How does lung disease affect respiration?

A

Lung disease reduces compliance

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28
Q

What happens during inspiration?

A
  • Chest expands

- Diaphragm contracts

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29
Q

What happens during expiration?

A
  • Chest contracts

- Diaphragm relaxes

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30
Q

What is necessary for expiration to occur?

A

Lungs must get smaller when tension is released (have elasticity)

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31
Q

What is elasticity?

A

Tendency of a structure to return to its initial size after being distended

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32
Q

What allows lungs to resist distension?

A

High content of elastin proteins = very elastic

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33
Q

What causes lungs to always be in a state of elastic tension?

A

Lungs are normally stuck to the chest wall

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34
Q

When does tension increase/decrease in the lungs?

A

Increase:
- During inspiration when lungs are stretched
Decrease:
- By elastic recoil during expiration

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35
Q

What is necessary for the lungs to inflate?

A

Lungs must be attached to the inner wall of the chest cavity

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36
Q

What happens to a person who has a chest wound on one side?

A

Cannot inflate the lung on the wounded side even though they continue to ventilate

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37
Q

What causes the chest cavity to increase in volume?

A

Contraction of the diaphragm and intercostal muscles

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38
Q

What do pleural membranes do?

A
  • Make attachment of the outer lung surface to the inner surface of the chest cavity
  • Produce a mucous-rich lubricating fluid (pleural fluid) into the pleural space between 2 membranes
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39
Q

What do the pleural membranes consist of?

A
  • One membrane layer attached to the surface of the lung

- One membrane layer attached to the inner wall of the chest cavity

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40
Q

What does the pleural fluid do?

A
  • Holds the two pleural membranes together - it is the ‘glue’ that holds the lungs attached to the inner wall of the thoracic cavity
  • Lubricant that allows the lungs to slide easily within thoracic cavity as they inflate/deflate
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41
Q

What happens when the size of the thoracic cavity changes?

A

The volume of lungs changes consequently

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42
Q

What is surface tension exerted by? How?

A
  • Fluid of alveoli

- Water molecules on the inner surface of alveoli are attracted to other molecules, acting to collapse the alveoli

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43
Q

What is surfactant?

A
  • A mixture of phospholipids and hydrophobic proteins
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44
Q

What secretes surfactant?

A
  • Secreted into alveoli by type II alveolar cells
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45
Q

What is the role of surfactant?

A
  • Lowers surface tension in alveoli by disrupting interactions between water molecules
  • Prevents alveoli from collapsing during expiration
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46
Q

When is surfactant produced?

A

Late in fetal life

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47
Q

What is respiratory distress syndrome?

A

Premature babies are sometimes born with lungs that lack sufficient surfactant and alveoli collapse

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48
Q

What is tidal volume?

A

Volume of gas inspired/expired in an unforced respiratory cycle (about 500 mL)

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49
Q

What is inspiratory reserve volume?

A

Max volume of gas that can be inspired during forced breathing in addition to tidal volume

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50
Q

What is expiratory reserve volume?

A

Max volume of gas that can be expired during forced breathing in addition to tidal volume

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51
Q

What is residual volume?

A

Volume of gas remaining in lungs after max expiration

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52
Q

What is total lung capacity?

A

Total amount of gas in lungs after max inspiration

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53
Q

What is vital capacity?

A

Max amount of gas expired after a max inspiration

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54
Q

What is inspiratory capacity?

A

Max amount of gas that can be inspired after a normal tidal expiration

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55
Q

What is functional residual capacity?

A

Amount of gas remaining in lungs after a normal tidal expiration

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56
Q

What is anatomical dead space?

A
  • Where no gas exchange occurs

- Nose, mouth, larynx, trachea, bronchi, bronchioles

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57
Q

What is hemoglobin? What does it consist of?

A
  • A protein present in cytoplasm of red blood cells
  • Contains 4 heme groups, which each contain an iron molecule
  • 2 alpha and 2 beta chains
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58
Q

What is the function of hemoglobin?

A
  • Acts as an O2 shuttle from lungs to body tissues
  • Iron can chemically bind O2 and release it when cells need it
  • Acts as a CO2 shuttle from body tissues to lungs
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59
Q

What is the role of CO2 in the lungs?

A

CO2 from tissues diffuses from blood to alveoli and blood CO2 levels become low
- Increases pH

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60
Q

O2 binds Hb in what conditions?

A

High pH environment

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61
Q

What happens to pH levels in the tissues?

A
  • Blood CO2 levels are high b/c cells produce CO2 as byproduct of metabolism
  • O2 levels are low b/c it is being used by cells
  • Decreases pH
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62
Q

What determines whether O2 binds hemoglobin or O2 is released from oxyhemoglobin?

A 
Acidity of the plasma
High acidity:
- O2 is released
Low acidity:
- O2 binds Hb
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63
Q

What gas exchange by O2 occurs at the lungs?

A
  • O2 dissolves in fluid lining of alveoli, diffuses through walls of alveoli and blood capillaries into plasma
  • O2 then diffuses into RBCs and combines chemically with Hb to form oxyhemoglobin
  • Oxyhemoglobin formation occurs in lungs b/c CO2 levels are low
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64
Q

What gas exchange by O2 occurs at the tissues?

A
  • O2 is released from oxyhemoglobin (in RBC), and diffuses from RBC into body tissues
  • Dissociation of Hb/O2 occurs at tissues b/c blood CO2 levels are high
65
Q

Describe the solubility of Co2 gas?

A
  • Low solubility

- Only very little can be carried in simple solution

66
Q

What happens to CO2 when it diffuses into RBCs?

A
  • Converted into bicarbonate ion by carbonic anhydrase

- A small amount of CO2 binds chemically to Hb to make carbamino compounds

67
Q

What happens to CO2 in tissues?

A
  • Constant production of CO2 causes bicarbonate equation to go in forward direction
68
Q

What happens to CO2 in lungs?

A
  • CO2 is being lost to alveolar air sacs

- Bicarbonate equation moves in reverse direction

69
Q

If a diver goes down 10m, what happens to the partial pressures and amount of dissolved gasses in blood plasma?

A
  • They will be twice values at sea level
70
Q

What might cause serious effects to a diver’s body?

A
  • Increased nitrogen and O2 dissolved in blood plasma
71
Q

At what depth would there be permanent damage to the human lung?

A

30m

72
Q

What is the mammalian diving reflex?

A
  • Drop in heart rate (bradycardia)
  • Vasoconstriction
  • Spleen releases RBCs carrying O2
  • Increased blood volume in lungs, occupying space created by compression of air in lungs and preventing collapse
73
Q

What does SCUBA stand for?

A

Self-Contained Underwater Breathing Apparatus - air tanks

74
Q

What does the gas mix in a SCUBA tank aim to do? What do they consist of?

A
  • Avoid O2 toxicity
  • Made of normal atmospheric air
  • Commonly less nitrogen to reduce nitrogen narcosis and decompression sickness
75
Q

What is decompression sickness?

A

N2 gas bubbles form in tissues and enter blood and block small blood channels producing pain and possibly more serious damage

76
Q

How do divers prevent decompression sickness?

A

Divers ascend slowly so large amount of N2 can diffuse through alveoli and be eliminated through expiration

77
Q

What is the primary treatment of decompression sickness?

A
  • Hyperbaric oxygen therapy

- Raise blood O2 concentration

78
Q

What health consequences arise 5000 ft above sea level?

A

Acute Mountain Sickness

  • Headache (low arterial pressure stimulates vasodilation, increasing blood flow and pressure in skull)
  • With hypocapnia (reduced CO2 in blood from hyperventilation) = cerebral vasoconstriction
79
Q

What happens to health at 9000 ft above sea level?

A

Pulmonary edema

  • Shortness of breath, fatigue, confusion
  • Blood vessels constrict causing increased blood pressure in lungs
  • As a result, fluid leaks from vessels to alveoli
80
Q

What happens to health at 10000 ft above sea level?

A

Cerebral edema

  • Confusion, incoordination, hallucinations
  • Coma, death
81
Q

Describe where blood comes/goes from atria/ventricles?

A
  • Atria receive blood from venous system

- Ventricles pump blood to arterial system

82
Q

About how much blood does each ventricle pump each beat?

A

75 mL

83
Q

Which ventricle performs more work? Why? What is the result?

A
  • LV performs greater work
  • LV pumps blood further and against more pressure
  • LV wall is thicker than RV
84
Q

What are the right and left sides of the heart separated by?

A
  • Septum
85
Q

What are murmurs?

A
  • Abnormal blood flow due to septal defects
86
Q

What are the atria and ventricles separated by?

A
  • Connective tissue/fibrous skeleton which contains one-way atrioventricular (AV) valves, which prevent backflow of blood from ventricles
87
Q

What causes opening/closing of AV valves?

A
  • Pressure differences b/n atria and ventricles
88
Q

Describe the AV valve between the RA and RV?

A
  • 3 flaps

- ‘Tricuspid valve’

89
Q

Describe the AV valve between LA and LV?

A
  • 2 flaps

- ‘Bicuspid valve’ or ‘Mitral valve’

90
Q

What are semilunar valves? Where are they located?

A
  • One-way

- Located at origin of pulmonary artery and aorta to prevent backflow of blood from arteries

91
Q

What causes the opening/closing of semilunar valves?

A
  • Pressure differences between ventricles and arteries
92
Q

What is the cardiac cycle?

A
  • Repeated pattern of contraction and relaxation of the heart
93
Q

What are the 5 steps of the cardiac cycle?

A
  1. Both atria fill with blood
  2. Buildup of pressure in atria causes AV valves to open and 80% of blood flows to ventricles
  3. Atria contraction sends final 20% of blood to ventricles
  4. Simultaneous contraction of both ventricles (0.1-0.2 s later)
  5. RV sends blood to pulmonary system, LV sends blood to systemic system
94
Q

What is systole?

A
  • Phase of contraction
95
Q

What is diastole?

A
  • Phase of relaxation
96
Q

What does systole/diastole commonly refer to? Is this always the case?

A
  • Commonly refers to ventricles

- There is still an atrial systole and diastole separate from ventricular

97
Q

What is the average cardiac rate? How long does each cycle last approximately?

A
  • 75 bpm

- 0.8 s

98
Q

What is stroke volume?

A
  • Amount of blood pumped from ventricles in one heart beat

- Contraction of ventricles in systole ejects about 2/3 of blood they contain

99
Q

What is end-systolic volume?

A
  • 1/3 of initial amount of ventricles which isn’t pumped out
100
Q

What is cardiac output?

A
  • Volume of blood pumped by both ventricles per minute

- CO = HR x stroke volume

101
Q

What facilitates the heart’s pumping ability?

A
  • Electrical activity
102
Q

Which 3 specialized regions of the heart can spontaneously generate action potentials?

A
  • Sinoatrial node
  • Atrioventricular node
  • Purkinje fibers
103
Q

What is the function of the SA node? Where is it located?

A
  • Functions as pacemaker

- Located in RA, near opening of superior vena cava

104
Q

Which nerve innervates the SA node?

A
  • Vagus nerve
105
Q

What is the role of specialized cells of the AV node?

A
  • Move impulse from atria to ventricles
106
Q

How does the electrical impulse travel in the heart?

A

1 - Originate at SA node, spread to adjacent myocytes in RA and LA (via gap junctions)
2 - AV node cells move impulse from atria to ventricles
3 - Impulse continues through AV bundle (or bundle of His)
4 - Descends through interventricular septum and divides R and L into Purkinje fibers in ventricle walls
5 - Spreads from endocardium to epicardium, causing both ventricles to contract simultaneously

107
Q

Where does the bundle of His lie?

A
  • Lies within interventricular septum
108
Q

What makes purkinje fibers different from the SA/AV nodes?

A
  • Could generate own impulses if needed
109
Q

Describe the rate of conductance at each stage of electrical activity of the heart?

A
  1. Impulse starts at SA node
    - Spreads quickly
  2. Goes to AV node
    - Conduction rate slows
  3. Continues through AV bundle
    - Conduction rate increases
  4. Descends down interventricular septum, divides R and L into Purkinje fibers in ventricle walls
    - Conduction rate peaks at 5m/s
110
Q

What is the rapid conduction in the Purkinje fibers caused by?

A
  • More positive resting membrane potential and many gap junctions
111
Q

What is the electrocardiogram?

A
  • Potential differences generated by heart are conducted to body surfaces where they can be recorded by electrodes placed on skin
  • NOT single action potential
112
Q

What will be affected on an ECG as a result of myocardial ischemia?

A
  • ‘S-T elevation’

- Ventricles don’t relax as they should, so cannot fill with blood

113
Q

What can lead to bradycardia?

A
  • Hyperstimulation of right vagus nerve which innervates SA node (b/c vagus slows HR)
  • AV node and Purkinje fibers can take over if SA node isn’t functioning properly
114
Q

What are 2 other names for cardiomyocytes?

A
  • Cardiac muscle cells

- Myocardial cells

115
Q

How are cardiomyocytes arranged?

A
  • Long, rod-shaped organelles called ‘muscle fibers’
116
Q

What are muscle fibers of the cardiomyocytes made up of?

A
  • Numerous ‘myofibril’ rods which have a distinct striated pattern of alternating light and dark bands
117
Q

What are myofibrils?

A
  • Functional unit of muscle fibers
118
Q

How are myofibrils separated?

A
  • By protein structures called ‘Z-discs’

- The section b/n Z-discs is a ‘sarcomere’

119
Q

What happens to Z-discs during contraction of the cardiac muscles?

A
  • Z-discs move closer together

- Thin and thick filaments slide past one another

120
Q

What do Z-discs act as anchors for?

A
  • Thin protein filaments called ‘actin’
121
Q

What lies between the actin?

A
  • Thicker filaments of ‘myosin’
122
Q

What gives the striated pattern of myofibrils?

A
  • Overlapping of thin/thick filaments
  • Light = I-bands
  • Dark = A-bands
123
Q

Where do the Z-discs lie?

A
  • Middle of I-bands
124
Q

Where is the ‘H-zone’? What is it seen as?

A
  • In the centre of the A-band

- Narrow light band

125
Q

How are cardiomyocytes connected?

A
  • Via gap junctions

- Permits electrical impulses to be conducted from cell to cell

126
Q

What do the gap junctions of the cardiomyocytes look like when stained?

A
  • Intercalated discs
127
Q

What does contraction follow?

A

Ca2+ induced Ca2+ release
- Ca2+ enters cardiomyocyte cytoplasm through V-gated channels, then stimulates opening of the Ca2+ release channels (ryanodine receptors) in the sarcoplasmic reticulum

128
Q

What does Ca2+ from voltage-gated channels serve as?

A
  • Messenger for SR Ca2+ release channels
129
Q

What must happen in order for heart muscles to relax?

A
  • Ca2+ in the cytoplasm must be pumped back into the SR
130
Q

What are the 5 steps of excitation-contraction coupling after voltage-gated calcium channels open?

A

1 - Ca2+ diffuses from ECF to cytoplasm
2 - Ca2+ release channels on SR open
3 - Ca2+ released from SR binds to sarcomere, stimulates contraction
4 - Ca2+ ATPase pumps calcium back into SR
5 - Myocardial cell relaxes

131
Q

What does muscle contraction look like in cardiomyocytes?

A
  • Myosin filaments have angular head at one end

- Muscle contraction is caused by head attaching to actin and swiveling, moving Z-discs closer together

132
Q

Where is tropomyosin in cardiomyocytes?

A
  • Attached to actin
133
Q

What is attached to tropomyosin?

A
  • Troponin complex of 3 subunits
134
Q

What are the details of muscle contraction in myosin (3 steps)?

A

1 - When ATP is hydrolyzed to ADP, myosin head becomes activated and changes orientation
2 - Attachment of Ca2+ to troponin causes movement of troponin-tropomyosin complex, exposing binding sites to actin
3 - Myosin cross bridges can then attach to actin and undergo a ‘power stroke’

135
Q

What is cardiovascular disease?

A
  • Class of diseases involving heart/blood vessels
136
Q

What is a major contributor to CVD? What does this lead to?

A
  • Coronary artery disease, which leads to congestive heart failure
137
Q

What is congestive heart failure?

A
  • Heart doesn’t pump as efficiently
  • Ventricles are often to blame
  • Often caused by CAD and MI
  • Back-up of blood in veins forces fluid into interstitial tissue (edema)
138
Q

Is there a cure for congestive heart failure?

A
  • No known cure
139
Q

What is coronary artery disease?

A
  • Occurs when you have plaque build-up in one or more of the 3 coronary arteries
  • Blood flow to heart is restricted -> angina
140
Q

What is plaque?

A

Build-up of cholesterol, immune cells, other substances

141
Q

What is angina?

A

Chest pain

142
Q

What causes a myocardial infarction?

A
  • ‘Heart attack’
  • Build-up of plaque is sufficient to severely and chronically interrupt blood flow
  • Death of cardiomyocytes
143
Q

What does the body do to try to compensate for congestive heart failure?

A
  • Cardiac remodelling to try to pump better

- Worsens problem

144
Q

What are some common treatments for congestive heart failure?

A
  • Beta-blockers to help heart pump
  • Diuretics to remove salts and fluids
  • Late stage: surgery or heart transplant
145
Q

What are two circulating catecholamines related to heart function?

A

1 - Epinephrine

2 - Norepinephrine

146
Q

What is the role of epinephrine?

A
  • Secreted from adrenal medulla during times of stress (exercise, emotional stress, pain, heart failure)
147
Q

What is the role of norepinephrine?

A
  • 20% of total blood norepinephrine is secreted from adrenal medulla
  • Rest is spillover from sympathetic nerves innervating blood vessels
148
Q

What are 2 effects of epinephrine binding to beta-adrenergic receptors?

A
  • Increases heart rate and ionotropy (contractility)

- Vasodilation of systemic arteries and veins at low-moderate concentrations

149
Q

What is the effect of epinephrine binding to alpha-adrenergic receptors?

A
  • Vasoconstriction of systemic arteries and veins at high concentrations
150
Q

What is the effect of norepinephrine binding to beta-adrenergic receptors?

A
  • Increases heart rate and ionotropy (contractility) = increased cardiac output
151
Q

What is the effect of norepinephrine binding to alpha-adrenergic receptors?

A
  • Vasoconstriction of systemic arteries and veins at high concentrations
152
Q

What is the overall cardiovascular response to increased circulating epinephrine and norepinephrine?

A
  • Increased cardiac output and systemic vascular resistance

- Results in increased arterial blood pressure

153
Q

How is heart rate affected by activation of baroreceptors?

A
  • Decreases due to activation of baroreceptors (pressure sensors)
  • Vagal-mediated bradycardia in responses to elevation in arterial pressure
154
Q

What is the effect of blocking one adrenergic receptor?

A
  • Alters cardiovascular response

- Other adrenergic receptor can still bind catecholamines

155
Q

What is the predominant adrenergic receptor of heart?

A
  • Beta 1
156
Q

What treatment is most often prescribed for hypertension, angina, and heart failure?

A
  • Beta-blockers
157
Q

What occurs in chronic heart failure?

A
  • Vicious cycle of sympathetic activation
158
Q

What does treatment with beta-blockers do?

A
  • Inhibits progressive deterioration of cardiac function (not a cure)
159
Q

What does coffee do to cardiac function?

A
  • Caffeine stimulates CNS
  • Increases catecholamine secretion
  • Increases heart rate, stroke volume, cardiac output, blood pressure

BIOM 3200 (4 decks)

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