Respiratory Phys Flashcards

1
Q

respiratory physl is the study of

A

how oxygen is brought into the lungs and delivered to tissue and how carbon dioxide is removed

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2
Q

what are 6 functions of the respiratory system?

A

homeostatic regulation of blood gases, protect from microbial infection, regulate blood pH, phonation (speech), olfaction, blood reservoir

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3
Q

what 3 structures comprise the upper resp. system?

A

nasal/oral cavities, pharynx, larynx

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4
Q

what is after the larynx?

A

trachea

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5
Q

what 6 structures comprise the lungs?

A

bronchi->bronchioles->alveoli, smooth muscle, connective tissue, pulmonary circ.

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6
Q

what is the larynx?

A

the vocal cords

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7
Q

what are the 3 sections of the pharynx?

A

naso, oro and laryngopharynx

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8
Q

what is anterior and posterior to the trachea and primary bronchi?

A

anterior: C-shape cartilage
posterior: smooth muscle

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9
Q

what changes from the primary bronchi to the bronchi of the lungs?

A

C-shaped cartilage to plates of cartilage (smooth muscle remains)

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10
Q

what changes from the bronchi to the bronchioles?

A

only smooth muscle (no cartilage)

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11
Q

what are the 2 zones of the airways beyond the larynx?

A

conducting and respiratory zone

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12
Q

what is the conducting zone?

A

area where gas is brought to gas exchanging region (no alveoli/gas-exchange - “anatomical dead space”)

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13
Q

what is the respiratory zone?

A

where gas exchange occurs (alveoli)

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14
Q

what is the smallest airway without alveoli?

A

terminal bronchioles

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15
Q

what airway occasional has alveoli?

A

respiratory bronchioles (after terminal)

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16
Q

where is generation 0 and 23 of the resp system?

A

0: trachea
23: alveolar sacs

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17
Q

what incr and decr w each generation level? (2, 2)

A

incr: # of branches, SA (cross sectional area)
decr: diameter and length

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18
Q

what are the alveoli?

A

tiny, thin-walled, capillary-rich sacs in lungs where gas exchange occurs

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19
Q

approx. how much blood do capillaries in lungs contain at rest and exercise?

A

70 mL and 200 mL

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20
Q

what are type 1 alveoli?

A

flat, epithelial cells

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21
Q

what are 2 functions of type 2 alveoli?

A

produce surfactant, act as progenitor cells

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22
Q

how can type 2 alveoli act as progenitor cells?

A

multiply and divide to replace damaged type 1 alveoli

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23
Q

what is the alveolar surfactant and its function?

A

detergent-like substance made of lipoproteins; reduces surface tension of alveolar fluid

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24
Q

how long is needed for gas exchange to occur at the level of the alveoli?

A

0.75 (RBC passes through pulmonary capillary system/2-3 alveoli)

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25
Q

what must O2 and CO2 diffuse through?

A

respiratory memb

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26
Q

what are the 6 layers of the respiratory memb?

A

alveolar fluid/surfactant, alveolar epi., basement memb of alveolar epi., interstitial space, basement memb of capillary endothelium, capillary endothelium

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27
Q

what is a con of having a thin resp memb.?

A

easily damaged

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28
Q

what is a pneumocyte?

A

alveolar cell

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29
Q

what are the 5 steps of repsiration?

A

ventilation, gas exchange in alveoli, gas transport, gas exchange at tissues, cellular utilization of gases

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30
Q

what is ventilation?

A

exchange of air between atmosphere and alveoli by bulk flow (O2 in, CO2 out)

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31
Q

what occurs during gas exchange in alveoli?

A

O2 and CO2 exchange btwn alveolar air and capillary blood by diffusion

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32
Q

what occurs during gas transport throughout the body?

A

O2 and CO2 circulate through pulmonary and systemic circ by bulk flow

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33
Q

what occurs during gas exchange in tissues?

A

O2 and CO2 exchange btwn blood in capillaries and tissue cells by diffusion

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34
Q

what occurs during cellular utilization of gases?

A

O2 is used and CO2 is released

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35
Q

how is ventilation produced? (4)

A
  1. CNS sends rhythmic excitatory drive to resp. muscles
  2. resp. muscles contract rhythmically
  3. changes in V and P allow for gas movement
  4. air flows in and out
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36
Q

what are 3 categories of resp. muscles?

A

pump, airway and accessory muscles

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37
Q

what do the pump muscles do?

A

make changes in P and V at level of lungs

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38
Q

where are the airway muscles?

A

upper airways (keep them open)

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39
Q

what are the INS (4) and EXP (2) upper airway muscles?

A

INS: tongue protruders (Genioglossus), alae nasi, pharyngeal and laryngeal dilators
EXP: pharyngeal and laryngeal constrictors

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40
Q

what do the accessory muscles do?

A

facilitate respiration during exercise

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41
Q

what are 2 INS accessory muscles?

A

sternocleidomastoid, scalene

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42
Q

what are the INS and EXP pump muscles?

A

INS: diaphragm, external and parasternal intercostals
EXP: internal intercostals, abdominals

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43
Q

what are the 5 INS muscles?

A

acc: sternocleidomastoid, scalene
pump: diaphragm, external and parasternal intercostals

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44
Q

what are the 5 EXP muscles? (4 abd.)

A

pump: internal intercostals, external and internal abd. oblique, transversus adb., rectus abd.

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45
Q

what is the diaphragm?

A

dome-shaped muscle that flattens during INS

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46
Q

what occurs when the diaphragm contracts?

A

forces abdominal contents down and forwards, widens rib cage, incr V of thorax

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47
Q

where are the external intercostals?

A

within the rib cage

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48
Q

what occurs when the external intercostals contract?

A

pull ribs upward, incr V of thorax (bucket handle motion)

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49
Q

where are the parasternal intercostals?

A

near sternum

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50
Q

what occurs when the parasternal intercostals contract?

A

pull sternum forward and incr anterior-posterior dimension of rib cage (pump handle motion)

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51
Q

what are the 4 abdominal muscles?

A

external oblique, internal oblique, transversus admonius, rectus abdominis

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52
Q

when are the expiratory pump muscles active?

A

deeper, faster breathing (exercise) to return lungs to resting position

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53
Q

what occurs when the internal intercostals contract?

A

pull rib cage down, decr thoracic V

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54
Q

what occurs when the scalenes contract?

A

elevate upper ribs, incr thoracic cavity

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55
Q

where are the scalenes?

A

attached on upper rib cage

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56
Q

where are the sternocleidomastoids?

A

connected to sternum

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57
Q

what occurs when the sternocleidomastoids contract?

A

raises sternum

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58
Q

when are the accessory INS muscles active?

A

during exercise or heavy respiration (little contribution to quiet/rest breathing)

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59
Q

what do muscles do during rest INS?

A

diaphragm contracts, external and parasternal intercostals pull ribs up and out

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60
Q

what do muscles do during forced resp. INS?

A

stronger diaphragm contraction, accessory muscles recruited (incr thoracic V)

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61
Q

what occurs during rest EXP?

A

no active contraction of resp muscles (diaphragm relaxes)

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62
Q

what do muscles do during forced resp. EXP?

A

abd. muscles contract, pushing abd. contents up and diaphragm higher, internal intercostals contract and push rib cage down (decr thoracic V)

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63
Q

what is obstructive sleep apnea?

A

reduction in upper airway patency during sleep (snoring, apneas, sleep disturbances) due to decr muscle tone or anatomical defects

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64
Q

what 2 regions are involved in the filtering action of resp?

A

conducting zone/”mucociliary escalator” and macrophages in alveoli

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65
Q

what 2 cells that line trachea are a part of the “mucociliary escalator”?

A

goblet (mucus-producing) and ciliated cells

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66
Q

what do the cells of the “mucociliary escalator” do?

A

entrap inhaled biological and inert particles and remove them from airways

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67
Q

what is periciliary fluid?

A

fluid produced by ciliated cells that forms the Sol layer (low viscosity/density)

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68
Q

what do goblet cells produce?

A

mucus that forms patchy gel layer above sol layer (high viscosity & elasticity)

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69
Q

how is mucus w/ trapped particles removed?

A

cilia movements (downward-nasopharynx, upward-trachea) bring mucus towards eso.

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70
Q

what is the last defense to inhaled particles?

A

macrophages in alveoli (phagocytosis)

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71
Q

what occurs when silica dust and asbestos are inhaled?

A

macrophages cannot digest these particles and die, producing chemotactic factors that recruit fibroblasts and cause pulmonary fibrosis

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72
Q

what is spirometry?

A

pulmonary function test to determine amount and rate of inspired and expired air

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73
Q

what is a spirometer?

A

device used to measure V of air inspired and expired by lungs (amount and rate/time)

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74
Q

what cannot be measured by a simple spirometry test? (3)

A

residual V, functional residual capacity, total lung capacity

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75
Q

what is the tidal V (TV)?

A

V of air moved in OR out of lungs during each resp cycle

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76
Q

what is the expiratory reserve V (ERV)?

A

max. amount of air that can be expelled after a normal expiration (max. voluntary expiration)

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77
Q

what is the inspiratory reserve V (IRV)?

A

max. amount of air that can be inhaled after a normal inspiration (max. voluntary inspiration)

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78
Q

what is the residual volume (RV)?

A

V of air remaining in lungs after max. expiration (cannot be expired or measured w spirometer)

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79
Q

what is RV =?

A

RV = FRC - ERV

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80
Q

what is atelectasis?

A

complete/partial lung/lobe collapse when alveoli become deflated/collapse (RV)

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81
Q

what are lung capacities?

A

sum of 2 or more lung volumes

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82
Q

what is vital capacity (VC)?

A

max. V of air forcibly exhaled after max. inspiration

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83
Q

how do you calculate VC?

A

VC = TV + ERV + IRV

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84
Q

what is inspiratory capacity (IC)?

A

max. V of air that can be forcibly inhaled

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85
Q

what do you calculate IC?

A

IC = TV + IRV

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86
Q

what is functional residual capacity (FRC)?

A

V of air remaining in lungs at end of normal expiration

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87
Q

how do you calculate FRC?

A

FRC = RV + ERV

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88
Q

what is total lung capacity (TLC)?

A

V of air in lung at end of max. inspiration

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89
Q

how do you calculate TLC?

A

TLC = FRC + TV + IRV = VC + RV

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90
Q

what cannot be measured by a spirometry test?

A

RV, FRC and TLC (contain RV)

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91
Q

what is tidal volume (Vt)?

A

total amount of air inspired at each breath (~500mL)

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92
Q

what is total/minute ventilation

A

total amount of air moved in and out of resp. system per min.

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93
Q

how do you calculate total/min ventilation?

A

Vt x resp. frequency (breaths per min, bpm)

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94
Q

what is alveolar ventilation (Va)?

A

amount of air moved into alveoli per min

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95
Q

what is the anatomical dead space (Vd)?

A

area in upper resp. system that contains air wo/ gas exchange (conduction zone, ~1/3, 150mL)

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96
Q

who do you calculate alveolar ventilation?

A

Va = (Vt - Vd) x freq. (bpm)

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97
Q

does V in anatomical dead space change with breath size?

A

no, it is constant

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98
Q

what is the most effective way to breathe to incr alveolar ventilation?

A

incr depth (decr bpm) rather than incr bpm (decr depth)

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99
Q

what is FEV1?

A

forced expiratory V in 1 second (FVC in 1s)

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100
Q

what is FVC?

A

forced vital capacity, total V of air that is blown out after max. INS as fast as possible (VC = IRV + TV + ERV)

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101
Q

what is FEV1/FVC?

A

proportion of air that is blown out in 1s

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102
Q

normal V for FVC

A

~5.0L

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103
Q

what does a patient with obstructive lung disease have trouble with?

A

exhaling all the air from their lungs (slower)

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104
Q

what 3 diseases are associated with obstructive breathing?

A

bronchial asthma, chronic obstructive pulmonary disease, cystic fibrosis

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105
Q

what is the most reduced w obstructive breathing patterns?

A

FEV1 (and FEV1/FVC ratio)

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106
Q

what drugs are used to reduce bronchospasms with asthma?

A

B2 adrenergic agonists

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107
Q

what does a patient with restrictive lung disease have trouble with?

A

cannot fully inhale/expand their lungs

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108
Q

what might cause restrictive lung patterns?

A

lung and chest stiffness, weak muscles, or damaged nerves

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109
Q

what is reduced with restrictive lung patterns?

A

FVC and FEV1

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110
Q

what appears normal with restrictive lung patterns?

A

FEV1/FVC ratio (both are reduced)

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111
Q

what 3 diseases are associated with restrictive breathing?

A

lung fibrosis, neuromuscular diseases, or lung tissue scarring

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112
Q

what can be measured using the helium dilution method?

A

FRC (RV + ERV)

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113
Q

what features of helium makes it useful for the gas dilution technique?

A

not taken up by vascular system (insoluble in blood) and can stay contained in lungs (reach equilibrium after a few breaths)

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114
Q

what do the variables in C1V1 = C2(V1 + V2) correspond to? (Helium test)

A

C1, V1: initial conc. and V of He in machine
C2: [He] at equilibrium after a few breaths (lungs + machine)
V2: FRC (V of He in lungs)

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115
Q

what does the helium dilution method only measure?

A

communicating gas or ventilated lung volume

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116
Q

what are the static properties of the lungs?

A

mechanical properties when no air is flowing (maintain chest and lung V)

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117
Q

what 4 properties are associated w static mechanics of ventilation?

A

intrapleural P (Pip), transpulmonary P (Ptp), static lung compliance, ST of lungs

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118
Q

what 3 properties are associated w dynamic mechanics of ventilation?

A

alveolar P (Palv), dynamic lung compliance, airway and tissue R

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119
Q

what is bulk flow?

A

movement of gas btwn high to low P

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120
Q

what is Boyle’s Law?

A

for fixed amount of ideal gas kept at constant temp, P and V are inversely proportional (P1V1=P2V2)

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121
Q

how does expiration demonstrate Boyle’s Law?

A

compression: decr V and incr P, air flows out

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122
Q

how does inspiration demonstrate Boyle’s Law?

A

decompression: incr V and decr P, air flows in

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123
Q

what is different btwn Boyle’s Law and the resp system?

A

not a sealed container (open to atm), air moves by bulk flow

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124
Q

what is the formula for bulk flow?

A

F = ΔP (= Palv - Patm) / R

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125
Q

what is the pleura?

A

thin double-layered envelope that cushions btwn lungs and thoracic wall+diaphragm

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126
Q

what does the visceral pleura cover?

A

external surface of lung

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127
Q

what does the parietal pleura cover?

A

thoracic wall and superior face of diaphragm

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128
Q

what separates the visceral and parietal pleura?

A

intrapleural fluid (~10 mL, 5-35 um)

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129
Q

what does the intrapleural fluid do?

A

allows visceral and parietal pleura to move around while breathing (decr friction)

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130
Q

how does the elastic recoil of lungs and chest wall balance eachother?

A

lung: tendency to collapse (inward)
chest: tendency to expand (outward)
(not directly attached, intrapleural space)

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131
Q

what is the transpulmonary P (Ptp) responsible for?

A

keeping alveoli open (P gradient)

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132
Q

what does the intrapleural P act as?

A

relative vacuum

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133
Q

how does the Pip act as a vacuum?

A

negative P keeps lungs inflated (always < Patm)

134
Q

what would occur if Pip = Palv?

A

lungs would collapse (elastic recoil)

135
Q

what is Ptp =?

A

Palv - Pip

136
Q

why is Ptp always > 0?

A

Pip is negative and subtracted so the double negative makes Ptp positive (ensures lungs are expanded in thorax)

137
Q

are Ptp and Palv static or dynamic parameters?

A

Ptp: static (doesn’t cause airflow but determines lung V)
Palv: dynamic (determines airflow)

138
Q

what occurs during an INS effort? (8)

A

CNS sends excitatory drive to INS muscles, contract, incr thoracic V, Pip becomes more neg, Ptp incr (= Palv - -Pip), lungs expand, Palv decr, air flows into alveoli/lungs

139
Q

what occurs during an EXP effort? (8)

A

INS muscles relax, chest wall recoils, Pip returns to pre-INS value (incr), Ptp decr, lungs V decr, air in alveoli compresses, Palv incr (> Patm), air flows out of lungs/alveoli

140
Q

what is airway R usually?

A

small (small ΔP generates flow ~1 mmHg)

141
Q

what 2 forces can cause R?

A
  1. inertia of resp system

2. friction

142
Q

btwn what 3 structures can there be R?

A
  1. btwn different alveolar sacs (within lungs)
  2. btwn lung and chest wall (decr by interpleural fluid)
  3. btwn air and airways (80%)
143
Q

what is laminar flow?

A

gas moves linearly (in small airways)

144
Q

what is transitional flow?

A

intermission btwn laminar and turbulent flow (branches in bronchial tree, incr R)

145
Q

what is turbulent flow?

A

not smooth or laminar (large airways: trachea, larynx, pharynx, high velocity and R)

146
Q

what does Poiseuille’s law state for laminar flow? (R)

A

R is proportional to viscosity and length but inversely proportional to radius^4 (highest in small airways)

147
Q

how does R vary in the tracheal bronchiol tree

A

low at medium-sized bronchi, decr in resp zone

148
Q

what is R for a healthy subject approx?

A

1.5 cm H20/L/s

149
Q

what is the R in the upper, large and small airways?

A

upper: 0.6
large: 0.6
small: 0.3

150
Q

why is R highest in upper and larger airways if r is bigger?

A

airflow is turbulent or transitional in these airways, R is highly sensitive to non-laminar flow

151
Q

how is R calculated for airways in series vs parallel?

A

series: R = R1 + R2…
parallel: 1/R = 1/R1 + 1/R2…

152
Q

how does airways being aligned in parallel contribute to low terminal R?

A

each small airway has a high individual R but the sum of all the reciprocal Rs is much lower (large airways in series, incr sum of Rs)

153
Q

what airways contribute most to R in diseased ppl? 3 reasons why?

A

small airways; smooth muscle contraction, edema (alveoli and bronchioles), mucus (bronchioles)

154
Q

what is compliance?

A

measure of the elasticity and distensibility of the lungs

155
Q

what is the formula for compliance?

A

C = ΔV / VPtp

156
Q

what are the y and x axis for compliance?

A

∆Vlung vs ∆Ptp

157
Q

what is dynamic vs static compliance?

A

w or wo airflow

158
Q

how is static compliance measured?

A

at FRC (end of EXP)

159
Q

does emphysema vs pulmonary fibrosis have higher or lower compliance than normal?

A

emphysema: higher (stretched/ruptured alveoli)

pulmonary fibrosis: lower (collagen=stiff)

160
Q

what does dynamic compliance measure?

A

lung stiffness and airway R against which distending forces have to act (≤ static C)

161
Q

what is hysterisis?

A

a system whose response depends on its current state and its HISTORY

162
Q

what are the 4 regions of P-V graph when inflating a collapsed lung w incr Ptp? (Vl = lung volume)

A
  1. stable Vl: hard to inflate collapsed airways
  2. exponential Vl: airways open and Vl incr
  3. linear Vl: expansion of open airways (Pip more neg)
  4. Vl plateaus: max Vl, compliance decr
163
Q

how is the P-V loop diff in normal vs collapsed lungs?

A

much smaller and less hysteresis

164
Q

how is hysteresis apparent in the lungs?

A

different INS and EXP compliance curves (easier to keep inflated lungs open vs collapsed/narrowed)

165
Q

what 2 factors determines lung compliance?

A
  1. elastic components

2. surface tension

166
Q

where is elastin and collagen localized in the lungs? (3)

A

alveolar walls, around blood vessels and bronchi

167
Q

what 2 components influence the elastic components of the lungs and how?

A
  1. elastin (extensible)

2. collagen (inextensible)

168
Q

what contributes more to lungs elastic behaviour: fiber elongation vs fiber arrangement?

A

geometrical arrangement of fibers

169
Q

what does the degeneration of elastin and collagen w ageing cause?

A

decr lung compliance

170
Q

what causes emphysema? effects?

A

elastin destruction (alveolar destruction); incr lung compliance w less elastic recoil (little ΔPtp = large ΔV)

171
Q

what causes pulmonary fibrosis? effects?

A

collagen deposition in alveolar walls; decr lung compliance (high Δ Ptp required for ΔV)

172
Q

surface tension occurs where in the lungs?

A

air-water interface in alveoli

173
Q

what effect does incr ST have on lung compliance?

A

decr (2/3 of lung compliance)

174
Q

what is surface tension?

A

measure of the attractive/cohesive forces that pull water’s surface molecules together at an air-liquid interface (H-bonds)

175
Q

how is the P-V curve of liquid-filled lungs different than a deflated lung?

A

curve is steeper, no hysteresis, lower inflation pressures

176
Q

how does alveolar ST influence lung compliance?

A

water molecules line internal surface of alveoli which creates inward recoil, incr P creates outward F that balances inward ST F

177
Q

what is Laplace’s equation? ind and dep variables?

A

P = 2T/r; P: dep, r: ind, T: constant (ST)

178
Q

what is the effect of different sized alveoli in the lungs?

A

where ST is constant, smaller r have higher P (small alveoli want to collapses so air can move from high P to lower P/large alveoli)

179
Q

why don’t smaller alveoli collapse due to incr P?

A

surfactant in fluid that lines alveoli

180
Q

what alveolar cells produce surfactant?

A

type 2

181
Q

what are 3 benefits of having surfactant in the alveoli?

A
  1. decr ST of alveolar fluid
  2. incr compliance
  3. stabilizes alveoli
182
Q

what are 3 components of alveolar surfactant?

A

phospholipids (dipalmitoyl-phosphatidylcholine, phosphatidylcholine), surfactant apoproteins, Ca ions

183
Q

how does surfactant reduce ST of water in alveoli?

A

amphiphilic phospholipids arrange btwn water molecules (hydrophobic: towards air) and reduces H-bonding

184
Q

how does surfactant stabilize alveoli?

A

prevents small alveoli from collapsing as thickness of surfactant incr w/ decr in SA and thus decr ST (T) vs larger alveoli (P is equalized and no bulk flow)

185
Q

what issue do premature infants have w/ their alveoli?

A

lack surfactant, decr compliance and incr work to breathe (infant resp distress, IRDS)

186
Q

what areas of the lungs have highest vs lowest ventilation (when standing)?

A

hightest: bottom
lowest: top

187
Q

why does the bottom of the lungs have the highest ventilation?

A

gravity pulls lungs down, decr neg Pip (incr P), less F pulling lungs open, alveoli start more deflated and receive more INS air

188
Q

what is the relationship btwn ventilation vs Pip?

A

for the same change in Pip, the change in ventilation is greatest at the base than apex of lungs (logarithmic)

189
Q

what 2 factors incr P of a gas? (not V)

A

temp, [gas]

190
Q

what does Daltons Law state?

A

in a mixture of gases (air), each gas operates independently (Pt is sum of all Pp)

191
Q

how do you calculate Pp of a gas?

A

% of gas in mixture -> decimal/fraction x Pt

192
Q

what does Fricks Law state? V/t = (A/T) * D * (P1 - P2)

A

rate of transfer of a gas through a sheet of tissue/time is proportional to A (area), D (diffusion constant), diff in Pp of gas and inversely proportional to thickness (T)

193
Q

what is D (diffusion constant)?

A

amount of gas transferred btwn alveoli and blood/time (diffusion)

194
Q

does CO2 or O2 have greater solubility in liquids?

A

CO2

195
Q

what is D also proportional to?

A

solubility (D = Sol/√MW)

196
Q

what does Henry’s Law state?

A

amount of gas that dissolves in a liquid is proportional to Pp of gas in equilibrium w that liquid

197
Q

if Pp of gas is same as in liquid, what also determines amount of gas in liquid?

A

solubility ([gas] in liquid = P x Sol)

198
Q

if Po2 = Pco2, how will the [gas] in liquid differ?

A

[co2] > [o2] as it has incr solubility

199
Q

does O2-Hb contribute to Pp?

A

no, no longer “dissolved in solution” and doesnt contribute to Pp

200
Q

why is the Pp of water higher in the alveoli than the atmosphere?

A

air is warmed and humidified in alveoli by mucus membranes

201
Q

why is Po2 in air > Po2 in alveoli? (3)

A
  1. warming/humidification incr Ph2o and decr Po2
  2. O2 diffuses to blood
  3. INS air mixes w/ FRV (decr Po2)
202
Q

how does altitude affect Po2 in alv?

A

is inversely proportional to alv Po2 (incr = decr alv Po2 )

203
Q

how does alveolar ventilation (Va) affect alveolar Po2?

A

incr Va, incr gas exchange until Po2 in atm ≈ alv (incr Po2 in alv)

204
Q

how does metabolic rate affect Po2 in alveoli?

A

incr MR, incr o2 consumption in tissues, decr Po2 returning to alv, decr Po2 in alv

205
Q

what other/4th factor affects alveolar Po2 and Pco2?

A

perfusion

206
Q

how does Pco2 in atm affect Pco2 in alv?

A

barely, Pco2 in atm/INS air is very small

207
Q

how does alveolar ventilation (Va) affect alveolar Pco2?

A

incr Va, decr Pco2 (co2 diffuses from blood to alveoli, exhaled)

208
Q

how does metabolic rate affect Pco2 in alveoli?

A

incr MR, incr co2 production in tissues, incr co2 returning to alv, incr Pco2 in alv

209
Q

what % of the capillary length does majority of gas exchange btwn alveoli and blood occur?

A

~30% (first thrid)

210
Q

why is it advantageous for gas exchange to occur in the first third of the capillary?

A

allows more length of capillary to be available for gas exchange if needed (diseased ppl)

211
Q

whats the difference btwn pulmonary and systemic circulation btwn P and R?

A

sys: high P, high R (fight gravity)
pulm: low P, low R (fragile system)

212
Q

why does the pulm circ system have low P and R?

A

low P: only needs to pump blood to top of lungs, avoid rupturing resp memb or edema formation
low R: shorter and wider vessels (Poiseuille’s law)

213
Q

what allows the pulm circ to have high compliance vessels? (3)

A

lots of arterioles w/ low resting tone, thin walls w/ little smooth muscle, can dilate w/ incr BP

214
Q

can time for blood to pass through pulm capillaries be reduced?

A

yes, (0.75s to 0.3s) when CO incr

215
Q

what is the V/Q ratio?

A

ventilation/perfusion is the balance btwn ventilation and gas exchange in alveoli and pulm capillaries

216
Q

what is perfusion?

A

gas exchange btwn alveoli and pulm capillaries (O2 from alv into circ, CO2 from circ into alv)

217
Q

how does high ventilation affect Po2 and Pco2?

A

alv levels approach atm levels (incr O2, decr CO2)

218
Q

how does high perfusion affect Po2 and Pco2?

A

alv levels approach venous levels (decr O2, incr CO2)

219
Q

what is the cause and effect of a high V/Q ratio?

A

cause: capillary occlusion
effect: alveolar dead space (Vd)

220
Q

what is alveolar dead space?

A

regions of lungs w/ high V/Q, over ventilated/underperfused, no gas exchange btwn alv and capillary

221
Q

what is the cause and effect of a low V/Q ratio?

A

cause: airway occlusion
effect: shunt

222
Q

what is a shunt?

A

portion of venous blood that doesn’t get oxygenated/not available for gas exchange and returns to arterial blood

223
Q

how is regional lung perfusion measured?

A

inject patient w/ mixture of saline solution and radioactive Xenon while patient holds breath

224
Q

where is lung perfusion greatest?

A

base (bottom)

225
Q

what does lung perfusion depend on? (2)

A

gravity, posture

226
Q

where is V/Q ratio highest and lowest in lungs?

A

highest: base
lowest: apex

227
Q

what are the V/Q ratios in the base and apex of lungs vs basal/ideal V/Q?

A

base: 0.6x (decr V/Q: decr Po2, incr Pco2)
apex: 3x (incr V/Q: incr Po2, decr Pco2)

228
Q

what mechanism matches low ventilation w/ decr perfusion?

A

pulmonary hypoxic vasoconstriction (due to decr Po2)

229
Q

what mechanism matches low perfusion w/ decr ventilation?

A

bronchoconstriction (due to decr Pco2)

230
Q

what do homeostatic mechanisms do to match ventilation and perfusion?

A

divert blood and airflow in local/diseased area to healthy areas of lung (vasoconstriction/bronchoconstriction)

231
Q

How is O2 primarily carried in the blood?

A
  1. Dissolved (2%)

2. Bound to Hb (98%)

232
Q

What are the 4 Hb chains called?

A

Globins (2 a, 2 B)

233
Q

What is a heme group?

A

Porphyrin ring structure w/ ferrous iron (2+) that binds O2 (4/Hb)

234
Q

what is the approx. Po2 in systemic arterial vs venous blood? in mmHg

A

arterial: 100 mmHg (towards tissues)
venous: 40 mmHg (away from tissues)

235
Q

what % of Hb is saturated in systemic arterial vs venous blood?

A

arterial: 97.5%
venous: 75%

236
Q

what % of O2 from Hb is dropped off in the tissues?

A

25%

237
Q

what is O2 capacity?

A

max. amount of O2 that can be combined w/ Hb

238
Q

what is Hb saturation?

A

% of available Hb binding sites w/ O2 attached

239
Q

what equation calculates % Hb saturation?

A

(O2 combined w/ Hb ÷ O2 capacity) x 100

240
Q

does 100% Hb saturation mean high O2 V in blood?

A

no, if V of Hb is low, V of O2 is also low

241
Q

what is the most important determinant of Hb saturation?

A

Arterial Po2

242
Q

what 3 factors alter the O2 dissociation curve?

A

pH, Pco2, temperature

243
Q

what causes the sigmoidal shape of the O2 dissociation curve?

A

cooperative binding (allostery)

244
Q

what is cooperative binding (in context of Hb)?

A

when 1 O2 binds, Hd undergoes conf change from tense (T) to relaxed (R) state that facilitates further binding of O2 (exposes Fe in heme group)

245
Q

where on the O2 dissociation curve are the steep and plateau areas? in mmHg

A

steep: 10-60 mmHg
plateau: 60-100 mmHg

246
Q

what is the significance of the steep portion of the O2 dissociation curve? (40-60 mmHg)

A

incr O2 dissociation w/ small decr in Po2

247
Q

what is the significance of the steep portion of the O2 dissociation curve? (10-40 mmHg)

A

incr metabolic rate (decr Po2) further facilitates O2 delivery into tissues

248
Q

what is the significance of the plateau portion of the O2 dissociation curve? (60-100 mmHg)

A

conditions that decr alv Po2 and thus arterial Po2 won’t affect Hb saturation (% bound to O2 is still high)

249
Q

what is anemia?

A

decr Hb in blood (100% sat is still less O2 than normal)

250
Q

what is polycythemia?

A

incr Hb in blood or incr V of blood that incr Hb (100% sat is more O2 than normal)

251
Q

what is the effect of CO poisoning on O2-Hb dissociation curve?

A

reduction in O2-Hb binding by 33% (CO-Hb) and change from sigmoidal to log shape of curve

252
Q

how much more affinitive is CO for Hb than O2?

A

200x

253
Q

what does the log shape of the O2-Hb dissociation curve bcse of CO poisoning indicate?

A

decr O2 unloading to tissues as lower Po2 is required

254
Q

how does incr in Po2blood affect equil btwn deoxy and oxy-Hb?

A

(use Le Chatelier’s principle)
incr in Po2: incr oxy-Hb
decr in Po2: incr deoxy-Hb (favors unloading)

255
Q

what does shifts to the right vs left of the O2-Hb dissociation curve mean for O2 aff for Hb?

A

right: decr O2 aff for Hb (incr unloading)
left: incr O2 aff for Hb

256
Q

what 4 factors shift O2-Hb dissociation curve to the right?

A

incr in temp, Pco2, [DPG] and [H+]

257
Q

where does DPG come from?

A

end product of RBC metabolism

258
Q

what are 3 causes for incr [DPG]?

A

chronic hypoxia, high altitudes, chronic lung disease

259
Q

what 3 forms is CO2 carried in blood?

A

dissolved (in plasma or RBC), bicarbonate (maj.) or carbamino compounds (both in RBC)

260
Q

what enzyme catalyzes the rxn of CO2 + H20 -> H2CO3?

A

carbonic anhydrase (CA)

261
Q

what is carbonic acid?

A

H2CO3

262
Q

what does carbonic acid react to form?

A

H+ and HCO3-

263
Q

what is HCO3-?

A

bicarbonate

264
Q

what is the chloride shift?

A

bicarbonate export from RBC is balanced w/ Cl import to maintain elec. neutrality

265
Q

what molecule facilitates the exchange of HCO3- and Cl- in RBCs?

A

anion exchanger

266
Q

what maintains elec. neutrality in blood so more HCO3- can exit RBCs?

A

incr in [H+] (decr pH)

267
Q

what does combination of CO2 w/ amino groups (globins) in Hb produce?

A

carbaminohemoglobin

268
Q

is an enzyme required to form carbaminohemoglobins?

A

no

269
Q

does deoxy-Hb or oxy-Hb have a higher aff for CO2?

A

deoxy-Hb

270
Q

what is the effect of CO2 binding to deoxy-Hb?

A

decr [deoxy-Hb] shifts equil. to favor more O2 dissociation

271
Q

what is the benefit of CO2 incr Hb-O2 dissociation?

A

aids O2 unloading in tissues

272
Q

how does CO2 transfer into alv due to diff Pco2 affect HCO3- and Hb?

A

promotes HCO3- (from plasma and RBC) and Hb-CO2 conversion to dissolved CO2

273
Q

what occurs to the H+ from carbonic acid breakdown in RBCs when HCO3- exits to plasma?

A

H+ reacts w/ Hb

274
Q

does deoxy-Hb or oxy-Hb have a higher aff for H+?

A

deoxy-Hb

275
Q

what is the benefit of H+ bound to Hb and not dissolved in plasma or RBC?

A

Hb acts as a buffer for pH (prevents acidity)

276
Q

how does Hb act as a buffer at peripheral tissues?

A

O2 drop off forms deoxy-Hb and CO2 pick up forms HCO3- and H+ which reacts w/ deoxy-Hb

277
Q

how does the equil for HCO3- vs Hb act at the lungs?

A

HCO3- binds to H+ so Hb-H+ favors dissociation and O2 can bind to deoxy-Hb

278
Q

what causes respiratory acidosis?

A

hypoventilation: incr CO2 production wo/ CO2 elimination so Pco2 incr and H+ conc incr

279
Q

what causes respiratory alkalosis?

A

hyperventilation: incr CO2 elimination wo/ CO2 production so Pco2 decr and H+ conc decr

280
Q

what is metabolic acidosis?

A

incr H+ in blood (ind. of Pco2)

281
Q

what is metabolic alkalosis?

A

decr H+ in blood (ind. of Pco2)

282
Q

what system controls rhythm of breathing?

A

CNS

283
Q

what brain structure initiates breathing?

A

medulla (specialized neurons)

284
Q

what structures/receptors modify breathing? (5)

A

higher brain centers (NTs), central and peripheral chemoreceptors, lung stretch receptors, proprioceptors (in muscles/joints), touch/pain/temp. receptors

285
Q

neuronal networks must establish an _________ rhythm for contraction of resp muscles

A

automatic

286
Q

what 3 groups in the brainstem contain resp neurons?

A

pontine, dorsal, and ventral resp groups

287
Q

which resp neuron group generates INS and EXP rhythm?

A

ventral resp group (VRG) in medulla

288
Q

what group in the VRG initiates INS rhythmic activity?

A

PreBotzinger complex (PreBotC)

289
Q

what does the PreBotC excite? via what pathway?

A

INS resp muscles; polysynaptic

290
Q

what group in the VRG initiates EXP rhythmic activity?

A

Parafacial resp group (pFRG)

291
Q

what does the pFRG excite? via what pathway?

A

EXP resp muscles; polysynaptic

292
Q

neuronal networks adjust breathing rhythm to accomodate what 4 bodily changes?

A

metabolic demands (Po2, Pco2, pH), mechanical conditions (posture, pregnancy), non-ventilatory behaviours (speaking, eating) and pulmonary/non-pulmonary diseases

293
Q

PreBotC and pFRG neurons drive activity in ________ neurons that excite _____ neurons to rhythmically contract resp muscles

A

premotor and motor

294
Q

for INS, the PreBotC activates premotor neurons in the ______ VRG (2 regions)

A

rostral and parahypoglossal region, pXII

295
Q

premotor rostral VRG neurons can excite _______ motor neurons in ______ spinal cord and contract the __________ (2 pathways)

A

PHRENIC/thoracic, CERVICAL/thoracic, DIAPHRAGM/ext. intercostals

296
Q

premotor parahypoglossal/pXII VRG neurons excite _____ motor neurons in the ________ to control the _______ and ______ _________ ________

A

cranial, medulla, tongue and upper airway muscles (larynx)

297
Q

for EXP, the pFRG activates premotor neurons in the _____ VRG

A

caudal

298
Q

premotor caudal VRG neurons can excite _______ motor neurons in the spinal cord and contract the __________ ____________ and __________ muscles (2 pathways)

A

THORACIC/lumbar, INTERNAL INTERCOSTALS/abdominal

299
Q

are the thoracic motor neurons that innervate INS and EXP muscles the same?

A

no, different motor neuron pool

300
Q

t/f: tidal volume and resp rate are fixed

A

f: can incr or decr based on activation or inhibition of resp networks

301
Q

what can alter arterial Po2 and Pco2? (4)

A

sleep, exercise, talking and panting

302
Q

what is hypoxia and hypercapnia?

A

hypoxia: low Po2
hypercapnia: high Pco2

303
Q

what is the similar effect of hypoxia, hypercapnia and acidosis?

A

incr in ventilation (incr Po2, decr Pco2 and incr pH)

304
Q

what are chemoreceptors?

A

specialized structures that sense changes in Po2, Pco2 and H+/pH (have a key role in chemical control of ventilation)

305
Q

where are the peripheral chemoreceptors? (2)

A

carotid and aortic bodies

306
Q

t/f: the carotid and aortic bodies are the same as the carotid and aortic sinuses

A

f: carotid and aortic bodies (chemoreceptors) and sinuses (baroreceptors) are different structures w/ different roles

307
Q

what are carotid and aortic bodies (peripheral chemoreceptors) most sensitive to?

A

hypoxia (low arterial Po2)

308
Q

what are 4 characteristics of the carotid bodies?

A

extremely small, chemosensitive, highly vascularized, high metabolic rate

309
Q

what allows the carotid bodies to have virtually same Po2, Pco2 and pH as systemic arteries even though they have a very high metabolic rate?

A

blood flow/perfusion&raquo_space; metabolic rate

310
Q

what are the 2 types of cells in the carotid bodies?

A

type 1: glomus cells

type 2: sustentacular cells

311
Q

what is the function of the glomus cells?

A

chemosensitive cells that drive ∆ventilation w/ ∆Po2 in arteries (also sensitive to Pco2 and H+/pH)

312
Q

what is the function of the sustentacular cells?

A

act as support in CB

313
Q

what are 4 characteristics of glomus cells that make them neuron-like?

A

have V-gated ion channels, depolarization causes APs, have intracellular vesicles w/ NTs, stimulation causes release of NTs

314
Q

what do NTs from glomus cells released in the CB stimulate?

A

glossopharyngeal nerve (CN IX) afferents

315
Q

what do glossopharyngeal nerve (CN IX) afferents innervate and cause?

A

dorsal/ventral resp group in brainstem (PreBotC and pFRG) to incr resp drive to muscles and incr ventilation

316
Q

glomus cells ____ firing rate in response to low Po2

A

incr

317
Q

at what Po2 range (in mmHg) are peripheral chemoreceptors most sensitive?

A

<60 mmHg (stable btwn 60-120: normal physl levels)

318
Q

decr in Po2 <60 mmHg will ____ ventilation

A

incr (drastic)

319
Q

what occurs when peripheral chemoreceptors incr firing with low INS Po2? (<60 mmHg)

A

reflex via medullary resp neurons (activate DRG and VRG neurons in medulla) to centrally control activity of respiratory muscles by incr resp rate and tidal volume

320
Q

what occurs when INS Pco2 incr? (5)

A

incr alv Pco2 reverses diffusion grad and causes UPTAKE of alv Pco2 and incr arterial Pco2 which will incr ventilation

321
Q

a range of what Pco2 will causes large changes in ventilation? (in mmHg)

A

40-46 mmHg (very sensitive)

322
Q

where are central chemoreceptors?

A

close to surface of medulla (close contact to blood vessels and cerebrospinal fluid)

323
Q

what 3 regions regions of the medulla contain central chemoreceptors?

A

rostral (anterior), intermediate and caudal (posterior)

324
Q

where are 2 other chemosensitive sites in the brain?

A

medullary raphe and hypothalamus

325
Q

what % of central vs peripheral chemoreceptors are responsible for response to hyercapnia?

A

70% central

326
Q

what 2 resp groups respond to hypercapnia to change ventilation?

A

dorsal (DRG) and ventral resp group (VRG)

327
Q

what is the process for peripheral chemoreceptor detection of hypercapnia? (start w/ inc alv Pco2) (9)

A

incr alv Pco2, incr art Pco2, incr art [H+] (as CO2 reacts w/ H2O), peri. chemoreceptors incr firing, glossopharyngeal nerves excite DRG and VRG (PreBotC and pFRG), incr resp muscle contractions, incr ventilation (resp. f and TV), alv and art Pco2 return to normal and art [H+] returns to normal

328
Q

what is the process for central chemoreceptor detection of hypercapnia? (start w/ inc alv Pco2) (10)

A

incr alv Pco2, incr art Pco2, incr brain ECF Pco2, incr brain ECF [H+], central chemoreceptors incr firing, excite VRG (PreBotC and pFRG), incr resp muscle contractions, incr ventilation (resp. f and TV), alv, art, and brain ECF Pco2 return to normal, brain ECF [H+] returns to normal

329
Q

what is the step response to metabolic acidosis? (start w/ incr production of non-CO2 acid) (9)

A

incr production of non-CO2 acid, incr arterial [H+], peripheral chemoreceptors incr firing, reflex via medullary resp neurons, resp muscles incr contractions, incr ventilation, decr alv Pco2, decr art Pco2, arterial [H+] returns to normal

330
Q

why can hypercapnia but not metabolic acidosis be controlled by central chemoreceptors?

A

CO2 can easily cross BBB and react w/ H2O to produce H+ but H+ from met. acidosis cannot easily cross BBB (no CO2)

331
Q

how does strenuous exercise cause hyperventilation?

A

incr in lactic acid causes metabolic acidosis which is detected by peripheral chemoreceptors to incr ventilation