Respiration Flashcards

1
Q

What are the four processes of respiration?

A
  1. Pulmonary ventilation –> movement of air in and out of lungs
  2. External respiration –> O2 and CO2 exchange between lungs and blood
  3. Transport –> O2 and CO2 in blood
  4. Internal respiration –> O2 ad CO2 between systemic blood vessels and tissues
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2
Q

What are the major organs of the upper respiratory tract? (3)

A
  1. Nose and nasal cavity
  2. Paranasal sinuses
  3. Pharynx
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3
Q

What are the major organs of the lower respiratory tract? (4)

A
  1. Larynx
  2. Trachea
  3. Bronchi and branches
  4. Lungs and alveoli
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4
Q

What is the dividing point between the upper and lower respiratory tract?

A

The interface between the larynx and pharynx

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5
Q

What are the two regions of the nose and what are they formed by?

A
  1. External nose
  • formed by bones: maxillary, frontal, and nasal
  • Formed by hyaline cartilages: septal, minor and major alar
  1. Nasal cavity
  • formed by bones: ethmoid, vomer, maxilla and palatine
  • formed by cartilage: septal cartilage (divides midline)
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6
Q

What is the function of the nose?

A
  • produces mucus
  • filters, warms, and moistens incoming air
  • resonance chamber for speech
  • receptors for sense of smell
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7
Q

What is the Nasal vestibule and what is it’s purpose?

A

Nasal cavity superior to the nostrils → lined with vibrissae to filter coarse particles from inspired air

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8
Q

What is the function of paranasal sinuses?

A

Lighten the skull; may also warm, moisten and filter incoming air

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9
Q

What is the function of the pharynx?

A

Passageway for food and air, also facilitates exposure of immune system to inhaled antigens

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10
Q

What is the function of the larynx?

A
  • air passageway
  • prevents food from entering the lower respiratory tract
  • voice production
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11
Q

What is the function of the trachea?

A

Air passageway that cleans, warms and moistens incoming air

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12
Q

What is the bronchial tree and what is it’s function?

A

Bronchial tree = left and right main bronchi that subdivide into lobar and segmental bronchi and bronchioles

Function: air passageways connecting trachea with alveoli; cleans, warms and moistens incoming air

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13
Q

What is the function of the alveoli?

A

Main sites of gas exchange

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14
Q

What type of epithelium makes up the walls of the alveoli?

A

Simple squamous epithelium

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15
Q

What are the two pleurae associated with lungs, what do they cover and what is their purpose?

A

Parietal pleura lines the thoracic cavity

Visceral pleura covers external lung surfaces

Function: produce lubricating fluid and compartmentalize lungs

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16
Q

Which structure of the lungs has direct contact with blood?

A

Alveoli

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17
Q

What are the alae?

A

structure that binds the nostrils laterally to the face

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18
Q

What is the dorsum nasi?

A

Anterior margin of the nose

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19
Q

What bones form the external nose?

A
  1. Nasal bone (forms bridge)
  2. Frontal bone (forms root)
  3. Maxillary bone (laterally)
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20
Q

What is the type of cartilage in the nose and the names of cartilages that make up the nose?

A

HYALINE CARTILAGE

  1. Septal cartilage
  2. Lateral processes of septal cartilage
  3. Minor alar cartilages (laterally)
  4. Major alar cartilages (apex)
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21
Q

What forms the roof of the nasal cavity?

A

ethmoid and sphenoid bones

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22
Q

What forms the floor of the nasal cavity?

A

Hard and soft palate (bone and muscle respectively)

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23
Q

What is the name of the opening where the nasal cavity turns into the nasopharynx?

A

Posterior nasal apertures (choanae)

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24
Q

What is the difference between the nasal conchae and the nasal meatus?

A

Conchae → scroll-like mucosa covered projections that protrude medially from each lateral wall of nasal cavity

Meatus → groove inferior to each concha

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25
Q

What is rhinitis and where does an infection spread?

A

Rhinitis = inflammation of nasal mucosa

Nasal mucosa is continuous with mucosa of respiratory tract so infections spread from nose → throat → chest

*can also spread to tear ducts and paranasal sinuses causing blockage of sinus pathways

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26
Q

How does a sinus headache happen?

A

Blockage of sinus pathways can lead to absorption of air, producing a vacuum

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27
Q

What is the anatomical position of the pharynx and what does it connect?

A

Runs from base of skull to vertebra C6

Connects nasal cavity and mouth to larynx and esophagus

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28
Q

Which tonsils are found in the nasopharynx?

A

Pharyngeal tonsils (adenoids)

Pharyngotympanic tubes (auditory tubes)

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29
Q

What type of epithelium lines the nasopharynx?

A

pseudo-stratified columnar epithelium

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30
Q

What structures close the nasopharynx during swallowing?

A

Soft palate and uvula

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31
Q

What tonsils are located in the orsopharynx?

A

Palatine tonsils (in lateral walls of fauces)

Lingual tonsil (posterior surface of tongue)

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32
Q

What type of epithelium lines the laryngopharynx?

A

Stratified squamous (non-keratinized)

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33
Q

What is Waldeyer’s ring?

A

Shows the position of the tonsils and whether or not they are off midline

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34
Q

What happens when adenoids are infected and swollen?

A

Blocks air passage in nasopharynx making it necessary to breathe through the mouth

When they are chronically enlarged, sleep and speech may be disturbed

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35
Q

What are the two zones of the lower respiratory system and what is their function?

A

1 - Conducting zone: conduits that transport gas to and from gas exchange sites (cleanses, warms and humidifies air)

2 - Respiratory zone: site of gas exchange (made of microscopic structures)

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36
Q

What is the anatomical position of the larynx?

A

3rd to 6th cervical vertebra

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37
Q

What are the three functions of the larynx?

A
  1. Provides patent airway
  2. routes air and food into proper channels (trachea vs esophagus)
  3. Voice production
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38
Q

What are the 9 cartilages in the larynx?

A

1 - Thyroid cartilage (contains laryngeal prominence)

2 - Cricoid cartilage (ring shaped)

3 & 4 - Arytenoid cartilage (paired)

5 & 6 - Cuneiform cartilage (paired)

7 & 8 - Corniculate cartilages (paired)

9 - Epiglottis

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39
Q

What type of cartilage is the epiglottis made from?

A

Elastic (recall that the E structures are elastic)

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40
Q

What are the two vocal ligaments and what are their functions?

A
  1. Vocal folds: vibrate to produce sound as air rushes from lungs
  2. Vestibular folds: help to close the glottis during swallowing (no part in sound production)
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41
Q

What is the glottis?

A

opening between vocal folds

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42
Q

What cartilages are attached by the vocal ligaments?

A

Arytenoid cartilages attached to thyroid cartilage

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43
Q

Why do vocal ligaments appear white?

A

there are no blood vessels

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44
Q

What determines loudness and pitch of speech?

A

Loudness → force of air from lungs

Pitch → length and tension of vocal cords

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45
Q

What structures “shape” sound into language?

A

muscles of:

  • pharynx
  • tongue
  • soft palate
  • lips
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46
Q

What is laryngitis and what is it caused by?

A

Laryngitis = inflammation of vocal folds causing them to swell, interfering with vibrations (changes to vocal tone causing hoarseness)

Often caused by viral infections, overuse, dry air, bacterial infections, tumours on folds or irritating chemicals

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47
Q

What are the three layers of the wall of the trachea and what are they made of?

A
  1. Mucosa: ciliated pseudo-stratified epithelium (contains goblet cells)
  2. Submucosa: connective tissue supported by C-shaped cartilage rings (contains seromucous glands)
  3. Adventitia: connective tissue (outermost layer)
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48
Q

What is the trachealis?

A

Smooth muscle fibers that connect posterior parts of cartilage rings and contract during coughing to get rid of mucus

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49
Q

What is the Carina?

A

Last tracheal cartilage which is found at the point where the trachea branches into the two main bronchi

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50
Q

What is special about the Carina’s mucosa?

A

It is highly sensitive and violent coughing will be triggered if any foreign object makes contact with it

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51
Q

How many orders of branching do air passages undergo?

A

23

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52
Q

What is the difference in the right and left primary bronchi?

A

The right primary bronchus is wider, shorter, and more vertical than the left so there is a higher chance of things going in there by accident

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53
Q

What do the primary bronchi branch into and is there a difference between the right and left?

A

Primary bronchi branch into lobar/secondary bronchi; 3 on the right and 2 on the left

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54
Q

What do the lobar bronchi branch into?

A

Segmental/tertiary bronchi

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55
Q

What classifies a branch as a bronchiole?

A

When they are less than 1mm in diameter, they do not contain cartilage

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56
Q

What is the size of a terminal bronchiole?

A

less than 0.5mm

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57
Q

What are the 3 major changes that occur in the conducting zone?

A
  1. Support structures change: cartilage rings become irregular plates and elastic fibers replace cartilage in the bronchioles
  2. Epithelium type changes: pseudo-stratified columnar becomes cuboidal, cilia and goblet cells become more sparse
  3. Smooth muscle increases: allows bronchioles to provide substantial resistance to air passage
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58
Q

Where does the respiratoy zone begin?

A

Terminal bronchioles → respiratory bronchioles → alveolar ducts → alveolar sacs (clusters of alveoli)

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59
Q

What is the respiratory membrane?

A

Blood-air barrier made of alveolar and capillary walls along with their fused basement membranes (super thin ~0.5um which allows for gas exchange)

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60
Q

What makes up the alveolar walls?

A

Simple squamous epithelium and cuboidal type II alveolar cells which secrete surfactant and antimicrobial proteins → surfactant reduces surface tension

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61
Q

What are the 3 significant features of alveoli?

A
  1. Surrounded by fine elastic fibers and pulmonary capillaries
  2. Alveolar pores equalize air pressure throughout lung and provide alternate route in case of blockage
  3. Alveolar macrophages keep alveolar surfaces sterile (carried to throat and swallowed)
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62
Q

What divides into bronchopulmonary segments and how many are there on the left and right lungs?

A

The lobes of the lung (recall 3 on right and 2 on left) divide into bronchopulmonary segments (10 on right and 8-10 on left)

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63
Q

What separates the bronchopulmonary segments?

A

Connective tissue septa

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64
Q

What is a lobule and what does it look like?

A

Smallest subdivision of the lungs that is visible to the naked eye; looks like hexagonal segments served by bronchioles and their branches

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65
Q

What makes the lungs elastic and spongy?

A

Stroma, elastic connective tissue

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66
Q

How many segments are in each lobe of the lungs?

A

Right superior lobe - 3

Right middle lobe - 2

Right inferior lobe - 5

Left superior lobe - 4

Left inferior lobe - 5

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67
Q

What are the two circulations that provide blood to the lungs and what types of systems are they?

A
  1. Pulmonary circulation - low pressure, high volume system
  2. Bronchial circulation - high pressure, low volume (part of systemic circulation)
68
Q

What is the difference between pulmonary and bronchial arteries?

A

Pulmonary arteries deliver systemic venous blood from heart to the lungs to be oxygenated

Bronchial arteries provide oxygenated blood to lung tissue (supply all lung tissue except for the alveoli)

69
Q

What plexus innervates the lungs and what are the actions of the different fibers found in it?

A

Nerves enter through the pulmonary plexus on lung root

Parasympathetic fibers → bronchoconstriction

Sympathetic fibers → bronchodilation

Visceral sensory fibers → sense in the lungs

70
Q

What is the function of pleural fluid?

A

Fills the pleural cavity and provides lubrication and surface tension that assists in expansion and recoil of lungs

71
Q

What is Pleurisy and what happens to a person who has it?

A

Pleurisy = inflammation of pleurae often resulting from pneumonia

Inflamed pleura become rough and friction causes stabbing pains when breathing; excess liquid may be produced causing excessive amounts of fluid which may exert pressure on lungs

72
Q

What is pleural effusion?

A

Fluid accumulation in pleural cavity

73
Q

What is atmospheric pressure?

A

Pressure exerted by air surrounding the body → 760 mm Hg at sea level = 1 atm

74
Q

What is intrapulmonary pressure (P pul) and how does it compare to atmospheric pressure?

A

Pressure in the alveoli → fluctuates with breathing and eventually equalizes with atmospheric pressure

75
Q

What is intrapleural pressure (P ip) and how does it compare to atmospheric pressure?

A

Pressure in pleural cavity → ALWAYS a negative pressure usually ~4mmHg less than P pul

76
Q

How and why is excess fluid pumped out of the pleural cavity?

A

Excess fluid is pumped out by the lymphatic system because if fluid accumulates, a positive P ip pressure develops and the lung will collapse

77
Q

What are the two inward forces that promote lung collapse?

A
  1. Lungs natural tendency to recoil from elasticity → lungs always try to assume the smallest size
  2. Surface tension of alveolar fluid pulls on alveoli to try and reduce their size
78
Q

How is a negative P ip maintained?

A

Strong adhesive force between the parietal and visceral pleurae

79
Q

What is transpulmonary pressure?

A

Transpulmonary pressure = (P pul - P ip)

This is the pressure that keeps the lung spaces open and prevents collapse; greater transpulmonary pressure, the larger the lungs will be

80
Q

What would P ip have to be equal to for the lungs to collapse?

A

P ip = P pul

P ip = P atm

P ip MUST be negative to keep lungs inflated

81
Q

What is atelectasis?

A

Collapsed lung

82
Q

What is Boyle’s law?

A

Relationship between pressure and volume of a gas

→ gasses fill the container they are in

→ Pressure (P) varies inversely with volume (V)

→ P1V1 = P2V2

83
Q

What is the process of quiet inspiration?

A

Active process involving inspiratory muscles:

  1. Diaphragm: contracts, moves inferiorly and flattens, increasing thoracic volume
  2. Intercostals: external intercostals contract, lift rib cage up and out, increasing thoracic volume
  3. Lungs are pulled out/stretched with thoracic cage (P pul drops by ~1mmHg and P ip lowers to ~6mmHg less than P atm)
  4. Air flows into the lungs down its pressure gradient until P pul = P atm
84
Q

What extra muscles are activated in forced deep inspirations?

A

Accessory muscles:

→ scalenes

→ sternocleidomastoid

→ pectoralis minor

→ erector spinae help straighten thoracic curve

85
Q

What is the process of quiet expiration?

A

Passive process:

  1. inspiratory muscles relax, thoracic cavity volume decreases and lungs recoil
  2. volume decrease causes intrapulmonary pressure (P pul) to increase by +1 mmHg
  3. P pul > P atm so air flows out of lungs down its pressure gradient until P pul = P atm
86
Q

What is the difference between quiet and forced expiration?

A

Quiet is a passive process

Forced is an active process that uses:

→ oblique & transverse abdominal muscles

→ internal intercostal muscles

87
Q

Describe intrapulmonary pressure during expiration and inspiration.

A

Intrapulmonary pressure = P pul

Pressure inside lung decreases as lung volume increases (inspiration)

Pressure inside lung increases as lung volume decreases (expiration)

88
Q

Describe intrapleural pressure during inspiration and expiration.

A

Pleural cavity becomes more negative during inspiration (~6mmHg less than P pul)

Pleural cavity returns to initial value during expiration (~ -4 mmHg)

89
Q

What are the three factors that influence the ease of air passage and amount of energy required for ventilation?

A
  1. Airway resistance
  2. Alveolar surface tension
  3. Lung compliance
90
Q

What is the relationship between flow, pressure and resistance?

A

F = deltaP/R

where deltaP = pressure gradient between atmosphere and alveoli (2 mmHg or less during quiet breathing - moves 500 mL of air)

91
Q

Why is airway resistance usually insignificant?

A
  1. Diameters of airways in the first part of the conducting zone are very large
  2. Progressive branching or airways as they get smaller increases the total cross-sectional area
92
Q

Where does airway resistance happen?

A

Medium sized bronchi

93
Q

Is there any resistance in the terminal bronchioles?

A

no, diffusion drives gas movement there

94
Q

What is surface tension?

A

The attraction of liquid molecules to one another at a gas-liquid interface

→ tends to bring liquid molecules closer together and reduce contact with gas molecules

→ resists forces that would increase the SA of a liquid

95
Q

What is surfactant?

A

Detergent-like lipid and protein complex that helps to reduce surface tension of alveolar fluid → made by type II alveolar cells and prevents alveolar collapse

96
Q

What is IRDS and how is it treated?

A

IRDS = Infant Respiratory Distress Syndrome; where there is insufficient quantity of surfactant in premature infants

Treated by spraying natural or synthetic surfactant into newborn’s air passages (severe cases may require mechanical ventilation)

97
Q

How might one develop bronchopulmonary dysplasia?

A

Surviving mechanical ventilation

98
Q

What is lung compliance?

A

Measure of change in lung volume that occurs with given change in transpulmonary pressure (measure of lung stretchiness)

99
Q

Why is lung compliance usually high?

A
  1. Distensibility of lung tissue
  2. Surfactant, which decreases alveolar surface tension
100
Q

What is the difference in lung compliance in those with emphysema versus fibrosis?

A

Emphysema → higher lung compliance than normal

Fibrosis → lower lung compliance than normal

101
Q

How do you calculate lung compliance?

A

CL = delta V/ (P pul - P ip)

Where CL = lung compliance

Delta V = change in lung volume

(P pul - P ip) = change in transpulmonary pressure

102
Q

What can decrease lung compliance?

A
  • nonelastic scar tissue replacing lung tissue (fibrosis)
  • Reduced surfactant production
  • Decreased flexibility of the thoracic cage
103
Q

What is Tidal Volume?

A

The amount of air moved into and out of lungs with each breath

104
Q

What is Inspiratory reserve volume (IRV)?

A

Amount of air that can be forcibly inhaled beyond tidal volume

105
Q

What is expiratory reserve volume (ERV)?

A

Amount of air that can be forcibly expelled from the lungs

106
Q

What is residual volume?

A

Amount of air that always remains in the lungs → needed to keep alveoli open

107
Q

What is inspiratory capacity?

A

TV + IRV

108
Q

What is functional residual capacity?

A

RV + ERV

109
Q

What is vital capacity?

A

TV + IRV + ERV

110
Q

What is total lung capacity?

A

Sum of all lung volumes

TV + IRV + ERV + RV

111
Q

What is the general trend in the difference between lung volumes in men and women?

A

Generally, men have higher lung volumes other than tidal volume which is the same ~500mL

112
Q

What is anatomical dead space?

A

Air that remains in passageways and does not contribute to gas exchange (~150mL)

113
Q

What is alveolar dead space?

A

Space occupied by non-functional alveoli due to collapse or obstruction

114
Q

What is obstructive pulmonary disease characterized by?

A

Increased airway resistance, ex. bronchitis

TLC, FRC and RV may increase because of hyperinflation of lungs

115
Q

What is restrictive pulmonary disease characterized by?

A

Reduced TLC due to disease or exposure to environmental agents (ex, tuberculosis or fibrosis)

VC, TLC, FRC, and RV decline because lung expansion is compromised

116
Q

What is forced vital capacity?

A

Pulmonary function test measuring amount of gas forcibly expelled after taking a deep breath

117
Q

What is forced expiratory volume (FEV)?

A

Amount of gas expelled during a specific time interval of FVC

→ FEV1 is the amount of air expelled in the first second

118
Q

What is the trend seen for normal, obstructive, and restrictive breathing in respect to FEV1?

A

normal → 80% of FVC

Obstructive → less than 80% of FVC

Restrictive → 80% or more of FVC

119
Q

What is minute ventilation?

A

Total amount of gas that flows into or out of the respiratory tract in 1 minute (only a rough estimate of respiratory efficiency)

120
Q

What is alveolar ventilation rate?

A

AVR = flow of gasses into and out of alveoli during a particular time

*better indicator of effective ventilation compared to minute ventilation

121
Q

How do you calculate AVR?

A

AVR = frequency (breaths/min) * (TV - dead space) (ml/breath)

122
Q

What can cause an increase or decrease in Alveolar ventilation?

A

Increase → increasing the TV

Decrease → rapid, shallow breathing

123
Q

What is the difference between internal and external respiration?

A

Internal → diffusion of gasses between blood and tissues

External → diffusion of gasses between blood and lungs

124
Q

What happens to the partial pressure of a gas at high altitudes versus low altitudes?

A

high → pressures decline

low → pressures increase

125
Q

What does Henry’s Law describe?

A

For gas mixtures in contact with liquids:

  • each gas will dissolve in the liquid in proportion to it’s partial pressure
  • At equilibrium, partial pressures in the two phases will be equal
  • Amount of each has that will dissolve depends on:
    • solubility
    • temperature (higher temperature, lower solubility)
126
Q

What are the three things that influence gas exchange during external respiration?

A
  1. Partial pressure gradients & gas solubility
  2. Thickness & SA of respiratory membrane
  3. Ventilation-perfusion coupling
127
Q

What is ventilation-perfusion coupling?

A

Matching of alveolar ventilation with pulmonary blood perfusion

128
Q

How is adequate oxygenation of blood ensured if blood flow increases by 3x?

A

The O2 partial pressure gradient is steep (venous blood 40mmHg and alveolar PO2 104 mmHg)

So, equilibrium is reached across the membrane in 0.25 seconds but it takes an RBC 0.75 seconds to travel from the start to end of the pulmonary capillary

129
Q

How does CO2 cross the membrane if the partial pressure gradient is not as steep as O2?

A

CO2 is 20x more soluble so it diffuses in equal amounts

130
Q

What is the thickness and surface area of the respiratory membrane?

A

Thickness → 0.5-1 um

SA → 40x the surface area of skin

131
Q

What would happen if the effective thickness of the respiratory membrane increases dramatically?

A

0.75 second transit time of the RBC may not be enough to fully oxygenate blood resulting in oxygen deprivation

132
Q

What is the difference between perfusion and ventilaton?

A

Perfusion = blood flow reaching alveoli

Ventilation = amount of gas reaching alveoli

*perfusion and ventilation rates must be matched for optimal, efficient gas exchange

133
Q

How does the partial pressure of oxygen and carbon dioxide control perfusion and ventilation?

A

perfusion → changes alveolar diameter; where alveolar O2 is high, arterioles dilate, where it is low, arterioles constrict

ventilation → changes bronchiolar diameter; where alveolar CO2 is high, bronchioles dilate, where alveolar CO2 is low, bronchioles constrict

134
Q

Why isn’t perfusion-ventilation balanced across all alveoli?

A
  1. Regional variations from the effects of gravity on blood and air flow
  2. Unventilated areas caused by alveolar ducts plugged with mucus
135
Q

What are the two ways that O2 is carried in blood?

A
  1. 1.5% dissolved in plasma
  2. 98.5% bound to each iron in Hb
136
Q

What are the factors that influence hemoglobin saturation?

A
  1. PO2
  2. Temperature, Blood pH, PCO2, concentration of bisphosphoglycerate → can all modify the structure of Hb and decrease it’s affinity for O2
137
Q

How does PO2 influence hemoglobin saturation in arterial and venous blood?

A

Arterial: PO2 is 100mmHg and contains 20mL O2/100mL of blood; Hb is 98% saturated and further increases in PO2 produces minimal increase in O2 binding

Venous: PO2 is 40 mmHg and Hb is still 75% saturated

138
Q

What is the venous reserve?

A

Oxygen remaining in venous blood that can still be used (recall that Hb in venous blood is still 75% saturated)

139
Q

What is described in the Bohr effect?

A

As cells metabolize glucose, they use O2 which causes:

increase in PCO2 and H+ in capillary blood → weakens O2-Hb bond resulting in O2 unloading

Heat production in active tissue directly and indirectly decreases Hb affinity for O2

140
Q

What happens to the oxygen-saturation curve when the body temperature is lower versus higher than normal?

A

lower → curve shifts to the left, higher affinity for O2

higher → curve shifts to the right, lower affinity for O2

141
Q

What happens to the oxygen-saturation curve when there is increased CO2 versus decreased CO2?

A

Increased → curve shifts right, lower binding affinity

Decreased → curve shifts left, higher binding affinity

142
Q

What is hypoxia?

A

Inadequate O2 delivery to tissues

143
Q

What is the difference between anemic, ischemic, histotoxic and hypoxemic hypoxia?

A

Anemic → few RBCs, abnormal or too little Hb

Ischemic → impaired or blocked circulation

Histotoxic → cells unable to use O2

Hypoxemic → abnormal ventilation; pulmonary disease

144
Q

Why is CO so dangerous to inhale?

A

Hb has 200x greater affinity for CO as compared to O2

145
Q

What are the three forms of CO2 transported in the blood?

A
  1. 7-10% dissolved in plasma
  2. 20% bound to globin in Hb (carbaminohemoglobin)
  3. 70% transported as bicarbonate ion in plasma
146
Q

What is the Haldane effect?

A

Lower PO2 and Hb-O2 saturation allows more CO2 to be carried by Hb

Process encourages CO2 exchange at tissues and lungs

147
Q

What is the purpose of carbonic acid-bicarbonate buffering system?

A

helps blood resist changes in pH

148
Q

What are the neural control centers for respiration?

A

Pontine respiratory centers

Medullary respiratory centers (2 areas: ventral respiratory group and dorsal respiratory group)

149
Q

What is the role of the Ventral Respiratory Group (VRG)?

A

VRG = network of neurons in brain stem that extends from spinal cord to pons-medulla junction

Sets eupnea (normal respiratory rate and rhythm) at 12-15 breaths/min

Inspiratory neurons excite diaphragm and external intercostals via phrenic and intercostal nerves, respectively

Expiratory neurons inhibit inspiratory neurons

150
Q

What is the role of the Dorsal Respiratory Group (DRG)?

A

DRG = network of neurons located near root of cranial nerve IX

Integrates input from peripheral stretch and chemoreceptors and sends it to VRG; not much else is known

151
Q

What is the role of the pontine respiratory centers?

A

Influence and modify activity of VRG; smooth transition between inspiration and expiration, modifies rhythms during speaking and sleep

152
Q

What is apneustic breathing and what is it caused by?

A

Apneustic breathing = prolonged inspirations

caused by lesions in the pontine respiratory centers

153
Q

What is the most widely accepted hypothesis of the generation of respiratory rhythm?

A

Reciprocal inhibition of two sets of interconnected pacemaker neurons in the medulla generates rhythm; each neuron set controls the other to ensure rhythm

154
Q

What are the four factors influencing breathing rate and depth?

A
  1. chemical (most important)
  2. influence of higher brain centers
  3. pulmonary irritant reflexes
  4. inflation reflex
155
Q

What is the influence of the partial pressure of O2 on breathing rate and depth?

A

Peripheral chemoreceptors in aortic and carotid bodies sense arterial O2 levels and declining PO2 normally only has a slight effect on ventilation

→ you need a substantial drop in arterial PO2 to stimulate increased ventilation (drop to 60mmHg)

→ only indirectly effects breathing by influencing peripheral chemoreceptor sensitivity to changes in PCO2

156
Q

How does pH influence breathing rate and depth and what is it mediated by?

A

Mediated by peripheral chemoreceptors

decreased pH → respiratory system increases respiratory rate and depth

157
Q

How do hypothalamic and cortical controls in higher brain centers effect breathing rate and depth?

A

Hypothalamic → act through limbic system; change in body temp changes rate, holding breath while in anger or gasping with pain

Cortical → signals from cerebral motor cortex that bypass medullary controls; voluntary breath holding

158
Q

How do pulmonary irritant reflexes influence breathing rate and depth and what are some of those irritants?

A

Receptors in bronchioles respond to irritants by reflexive constriction of air passages. triggers cough in trachea or sneeze in nasal cavity

Irritants include dust, accumulated mucus, and noxious fumes

159
Q

What is the Hering-breuer reflex?

A

Hering-Breuer reflex = inflation reflex

Mechanical stretch receptors in plurae and airways are stimulated by lung inflation and send inhibitory signals to medullary respiratory centers to end inhalation and allow expiration

→ protective response rather than normal mechanism

160
Q

What is hyperpnea?

A

Increased ventilation in response to metabolic needs → can increase 10-20 fold

161
Q

What are the 3 neural factors for increase in ventilation during exercise?

A
  1. Psychological stimuli: anticipation of exercise
  2. Cortical motor activation of skeletal muscles and respiratory centers
  3. Excitatory impulses to respiratory centers from proprioceptors in moving muscles, tendons, joints
162
Q

What is the key feature and other common features of COPD?

A

Key → decrease in ability to force air out of lungs

Other: history of smoking, dyspnea, coughing, frequent pulmonary infections, patients develop hypoventilation, respiratory acidosis and hypoxemia

163
Q

What is emphysema and what are the 3 consequences of the disease?

A

Emphysema = permanent enlargement of alveoli and destruction of alveolar walls, decreased lung elasticity

  1. Accessory muscles now required for breathing; 10-15% more energy needed to breath than normal
  2. Trapped air causes hyperinflation, flattens diaphragm and causes expanded barrel chest
  3. Damaged pulmonary capillaries lead to enlarged right ventricle
164
Q

What are the causes, results, symptoms and risk factors for chronic bronchitis?

A

Caused by inhaled irritants resulting in:

→ excessive mucus

→ mucosa of lower respiratory pathways become inflamed and fibroses

→ obstructed airways impairing lung ventilation and gas exchange

Symptoms: frequent pulmonary infections

Risk factors: smoking, environmental pollutants

165
Q

What is asthma, what causes it and what are the characteristic symptoms?

A

Asthma = active inflammation of airways followed by bronchospasm; caused by interleukins, IgE and recruitment of inflammatory cells

Characteristics: acute episodes, coughing, dyspnea, wheezing and chest tightness

166
Q

What is cystic fibrosis, what causes it and what are the treatments used to treat it?

A

Cystic fibrosis = most common lethal genetic disease where viscous mucus clogs passageways leading to bacterial infections

Caused by abnormal Cl- membrane channel protein so Cl- transport function is compromised

treated by mucus-dissolving drugs, antibiotics, and inhalation hypertonic saline to thin mucus