Respiratory Flashcards

1
Q

functions of respiratory system

A

homeostatic regulation of blood gases: provides O2 and eliminates CO2
filtering action: protects against microbial infection
regulates blood pH
contributes to phonation + olfaction
reservoir for blood

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2
Q

upper airways

A

nasal cavity - nostrils
oral cavity - mouth
pharynx
larynx (vocal cords)

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3
Q

lower system

A

trachea
left + right main bronchi
left + right lungs
diaphragm

thoracic wall
parietal pleura (membrane)
intrapleural fluid
visceral pleura (membrane)

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4
Q

composition of structures

A

trachea + primary bronchi = C shape cartilage + smooth muscle
bronchi = plates of cartilage + smooth muscle
bronchioles = smooth muscle

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5
Q

conducting zone

A

pathway for gas to the respiratory zone
anatomical dead space = no alveoli + no gas exchange
~150mL

trachea
bronchi
bronchioles
terminal bronchioles = smallest airway without alveoli

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6
Q

respiratory zone

A

where gas exchange occurs
contains alveoli

respiratory bronchioles (sparse alveoli)
alveolar ducts
alveolar sacs (many alveoli)

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7
Q

pulmonary structures + blood vessels

A

pulmonary artery carries low-O2 blood to alveoli (500 million)
280 billion capillaries → in contact with alveoli for gas exchange
pulmonary vein carries high O2 blood to heart

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8
Q

alveoli

A

type I alveolar cells = simple squamous epithelium
type II alveolar cell
macrophage

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9
Q

type I alveolar cells

A

involved in gas exchange
epithelial cells forming surface of alveolus
do not divide

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10
Q

type II alveolar cells

A

produce surfactant
act as progenitor cells to differentiate into type I cells

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11
Q

respiratory membrane

A

alveolus → capillary
- alveolar fluid
- alveolar epithelium (type I + II pneumocytes)
- basement membrane of alveolar epithelium
- interstitial space
- basement membrane of capillary endothelium
- capillary endothelium

very thin = easily damaged

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12
Q

respiration steps

A
  1. ventilation
  2. gas exchange in lungs
  3. gas transport
  4. gas exchange in tissues
  5. cellular respiration
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13
Q
  1. ventilation
A

breathing = exchange of air between atmosphere and alveoli by bulk flow

steps:
1. CNS sends rhythmic excitatory drive to respiratory muscles
2. respiratory muscles contract rhythmically and in organized pattern
3. changes in volume and pressures at the level of chest + lungs
4. air flows in and out

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14
Q

bulk flow

A

movement due to pressure gradient → high to low
higher pressure in atmosphere compared to lungs = inspiration
F = (P alv - P atm)/R

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15
Q
  1. gas exchange in lungs
A

exchange of O2 + CO2 between alveolar air + blood in lung capillaries by diffusion

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16
Q

diffusion

A

movement due to concentration gradient (partial pressures)

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17
Q
  1. gas transport
A

transport of O2 + CO2 through pulmonary + systemic circulation by bulk flow

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18
Q
  1. gas exchange in tissues
A

exchange of O2 + CO2 between blood in tissue capillaries and cells by diffusion

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19
Q
  1. cellular respiration
A

cellular utilization of O2 and production of CO2

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20
Q

respiratory muscles

A

pump muscles
airway muscles
accessory muscles

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21
Q

pump muscles

A

INS:
- diaphragm
- external intercostals
- parasternal intercostals

EXP:
- internal intercostals
- abdominals (4 = external + internal abdominal oblique, transverse + rectus abdominus)

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22
Q

airway muscles

A

INS:
- tongue protruders (genioglossus)
- pharyngeal + laryngeal dilators

EXP:
- pharyngeal + laryngeal constrictors

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23
Q

accessory muscles

A

INS
- sternocleidomastoid
- scalene

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24
Q

normal/quiet inspiration

A

diaphragm contracts → pushes abdomen down + expands thorax as air comes in
external intercostals + parasternal intercostals → pull ribs up and out

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25
maximal/forced inspiration
stronger contraction of diaphragm recruitment of accessory muscles → further expansion of thoracic cavity - sternocleidomastoid + scalenes move sternum up and out - pectoralis minor elevates ribs
26
normal/quiet expiration
no active contraction of resp muscles relaxation of inspiratory muscles → recoil of lungs = air moves out
27
maximal/forced expiration
abdominal muscles contract → compress organs + force diaphragm higher = push air out internal intercostal muscles contract → pull ribs down and inward
28
spirometry
pulmonary function test to determine amount + rate of inspired + expired air test lung volume + capacity use spirometer
29
tidal volume
Vt volume of air moved in/out of lungs during normal breath ~500 mL
30
inspiratory reserve volume
IRV amount of air forcefully inhaled after normal inspiration additional capacity ~3000 mL
31
expiratory reserve volume
ERV amount of air forcefully exhaled after normal exhalation ~1100 mL (smaller than IRV)
32
residual volume
RV volume of air remaining in lungs after maximal forceful expiration ~1200 mL prevents lungs from collapsing cannot be measured with spirometry
33
total lung capacity
volume of air in lungs at end of maximal inspiration Vt + IRV + ERV + RV 5000-6000 mL
34
inspiratory capacity
Vt + IRV total capacity for inspiration
35
vital capacity
Vt + IRV + ERV max vol of air that can be forcibly exhaled after maximal inspiration
36
functional residual capacity
ERV + RV vol remaining in lungs at end of normal expiration
37
total/min ventilation
total amount of air moved into respiratory system per minute = Vt x resp frequency = 0.5L x 12 brpm = ~6L/min
38
alveolar ventilation
amount of air moved into alveoli per minute less than minute ventilation depends on anatomical dead space = 0.15 L =(Vt - dead space) x resp frequency = (0.5 - 0.15 L) x 12 brpm = ~4.2 L/min dead space is constant regardless of breath size increased depth of breathing is more effective in increasing alveolar ventilation than increasing breathing rate
39
FEV1
spirometry test: forced expiratory volume in one second in healthy person: should approximate vital capacity
40
FVC
spirometry test: forced vital capacity total amount of air that is blown out in one breath after max inspiration as fast as possible ~ vital capacity
41
FEV1/FVC ratio
proportion of the amount of air that is blown out in one second normal = ~80%
42
normal resp pattern
ratio = 83% high FEV1 + high FVC
43
obstructive resp pattern
FEV1 is significantly reduced, FVC is normal/reduced = ratio <70% → reduced difficulty exhaling all air from lungs → shortness of breath slower exhalation of air due to damage to lungs or narrowing of airways high air vol in lungs after full exhalation ex. bronchial asthma, COPD, cystic fibrosis
44
restrictive resp pattern
reduced vital capacity FEV1 + FVC are reduced ratio = 90% (almost normal) cannot fill lungs completely (restricted from full expansion) due to stiffness in lungs ex. pulmonary fibrosis, neuromuscular disease, scarring of lung tissue
45
flow
F = ΔP/R proportional to pressure difference between two points inversely proportional to resistance
46
Boyle's Law
P1V1 = P2V2 for a fixed amount of an ideal gas at a fixed temp, P and V are inversely proportional
47
compression of alveoli
↓ V = ↑ P expiration
48
decompression of alveoli
↑ V = ↓ P inspiration
49
elastic recoil
- lungs have tendency to collapse - chest wall pulls thoracic cage outward at equilibrium: inward elastic recoil of lungs balances outward elastic recoil of chest wall
50
intrapleural fluid
reduces friction of lungs against thoracic wall during breathing
51
intrapleural pressure
pressure within pleural cavity fluctuates with breathing always sub-atmospheric (-) → opposing directions of elastic recoil of lungs + thoracic cage if P(ip) = P(alv) → lungs would collapse
52
alveolar pressure
pressure of air inside alveoli changes during ventilation + determines direction of air flow dynamic - directly involved in producing air flow when P alv = P atm, F=0
53
P(alv) - P(atm)
governs gas exchange between lungs and atmosphere = flow
54
transpulmonary pressure
force responsible for keeping alveoli open pressure gradient across alveolar wall: P(tp) = P(alv) - P(ip) static - does not cause airflow determines lung volume P(tp) > 0 to maintain lungs expanded in thorax (P alv > P ip)
55
inspiration
1. diaphragm + inspiratory intercostals contract 2. thorax expands 3. P(ip) becomes more subatmospheric = ↑ P(tp) 4. lungs expand 5. P(alv) becomes subatmospheric 6. air flows into alveoli
56
expiration
1. diaphragm + inspiratory intercostals relax 2. chest wall recoils inward 3. ↑ P(ip) = ↓ P(tp) - return to preinspiration value 4. lungs recoil 5. air in alveoli becomes compressed = P(alv) > P(atm) 6. air flows out of lungs
57
airway resistance
small → small ΔP is enough to cause airflow
58
resistive forces
1. inertia 2. friction
59
inertia of resp system
negligible
60
friction
1. lung tissue past itself during expansion (negligible) 2. lung and chest wall tissue surfaces past each other (reduced by IPF) (negligible) 3. frictional resistance to flow of air = 80% of total airway resistance
61
laminar airflow
gas particles move in linear fashion low resistance found in small airways (distal to terminal bronchioles)
62
transitional flow
extra energy required → produce vortices ↑ resistance found in most of bronchial tree
63
turbulent flow
highest resistance large airways (trachea, larynx, pharynx)
64
Poiseuille's law
for laminar flow resistance is proportional to viscosity of gas + length of tube inversely proportional to airway radius (^4)
65
R in small airways
each small airway has high individual resistance terminal bronchioles aligned in parallel = lower aggregated resistance combined → lowest R
66
R in disease conditions
R is determined primarily by small airways → easily occluded by: - smooth muscle contraction around airway - edema in walls of alveoli + bronchioles - mucous collecting in lumen of bronchioles
67
lung compliance
measure of elastic properties of lungs how easily lungs can expand determined by - elastic components of lungs + airway tissue (elastin + collagen) - surface tension
68
C(L)
= (ΔV)/(ΔP(tp)) change in lung volume produced by given change in P(tp) slope of pressure-volume curve ↑ C(L) = easier to expand (at given change in P(tp))
69
emphysema
↑ compliance floppy lungs due to destruction of elastin in walls of alveoli = collapse of smaller airways less elastic recoil large changes in lung vol due to little changes in P(tp) low O2 due to less SA for gas exchange
70
pulmonary fibrosis
↓ compliance collagen deposition in alveolar walls stiff lungs higher P(tp) changes are necessary to generate changes in lung volume poor gas exchange causes ↓ O2
71
surface tension
property of surface of liquid that allows it to resist external force → cohesion of molecules gives lungs elastic recoil (makes lungs collapse) decreases lung compliance
72
alveolar surface tension
air entering lungs is humidified → saturated with water water molecules cover alveolar surface cohesion of water → create surface tension = creates inward recoil → alveolar collapse decreases gas volume inside alveolar = increases pressure to prevent collapse
73
Laplace's equation
P = (2T)/r [T = surface tension] at equilibrium, tendency of increased pressure to expand the alveolus balances the tendency of surface tension to collapse the smaller the radius, the greater the pressure needed to keep alveolus inflated
74
different alveolar sizes
smaller alveoli = greater pressure → gas movement from high to low pressure = (POTENTIALLY) small alveoli collapse into larger ones do not collapse because of surfactant → lowers surface tension = similar pressure across alveoli
75
surfactant
produced by type II alveolar cells made of lipoproteins = hydrophobic + hydrophilic properties → decreases density of water molecules covering alveolar surface reduces surface tension of alveolar fluid = ↑ lung compliance stabilize alveoli against collapse
76
IRDS
infant respiratory distress syndrome born premature = under developed lungs → immature type II alveolar cells can't produce enough surfactant = ↓ O2 have abnormally low lung compliance
77
partial pressures of gases
P increases with increased motion → due to change in temperature, concentration of gas molecules
78
Dalton's Law
in a mixture of gases, each gas acts independently total pressure = sum of individual pressures
79
P atm
= P (N2) + P (O2) + P (H2O) + P (CO2) = 760 mmHg P (p) = % of air x P total 78% N2 → P (N2) = 593 mmHg 21% O2 1% H2O 0.04% CO2
80
Fick's Law
V(gas) ∝ [A/T] x D x (P1 - P2) rate of transfer of a gas through membrane (Vgas) - is proportional to: A = area of diffusion ΔP = difference in gas partial pressure between two sides D = diffusion constant - is inversely proportional to: T = thickness of membrane
81
D = diffusion constant
D ∝ (sol)/√ (MW) sol = solubility MW = molecular weight
82
diffusion of CO2 vs O2
solubility: CO2 > O2 similar molecular weights CO2 diffuses 20x more rapidly than O2 P (CO2) is higher in alveoli than atm P (O2) is higher in atm than alveoli
83
P (O2) atm > P (O2) alveoli
1. loss of O2 to blood by diffusion = ↓ P (O2) 2. mixing of inspired air with functional residual vol = ↓ P (O2) (3.) warming + humidification of air in resp tract = ↓ P (O2)
84
alveolar partial pressures
determined by - P (O2) + P (CO2) in atm - alveolar ventilation [V(A) = (V(T) - V(D)) x resp frequency] - metabolic rate - perfusion
85
increasing alveolar ventilation
= ↑ O2 intake + ↑ CO2 production = ↑ P (O2) + ↓ P (CO2)
86
increasing metabolic rate
= ↑ O2 intake + ↑ CO2 production = ↓ P (O2) + ↑ P (CO2)
87
lung perfusion
amount of blood that passes through pulmonary capillary system in the lung using O2 from alveoli + adding CO2
88
systemic circulation
high pressure system overcome high resistance to deliver blood to peripheral tissue
89
pulmonary circulation
low pressure system only deliver blood to lungs
90
ventilation/perfusion ratio
V/Q ratio balance between ventilation + perfusion one of major factors affecting alveolar (+ arterial) levels of O2 + CO2
91
V/Q matching
local perfusion decreases to match a local decrease in ventilation (+ vice versa) ↓ airflow / blood flow to region of lung ↓ P (O2) in p. blood / ↓ P (CO2) in alveoli vasoconstriction of p. vessels / bronchoconstriction ↓ blood flow / airflow diversion of blood flow and airflow away from local area of disease to healthy areas of the lung
92
ex. bronchoconstriction causes vasoconstriction
blockage of airway leads to poor gas exchange in alveoli → blood flow is diverted to better ventilated alveoli to compensate
93
perfused alveoli that are not ventilated
blocked airway → ↓P(O2) + ↑P(CO2) decreases V/Q ratio
94
ventilated alveoli that lack perfusion
blocked blood flow → ↑P(O2) + ↓P(CO2) increases V/Q ratio
95
O2 transport
arterial blood = highly oxygenated similar partial pressures of O2 and CO2 as seen in alveoli majority of O2 is bound to Hb → in RBC small amount is dissolved in plasma
96
CO2 transport
venous blood = poorly oxygenated ↓ P(O2) + ↑ P(CO2) compared to alveoli majority of CO2 is transported as bicarbonate some is bound to Hb = carbaminohemoglobin small amount is dissolved in plasma
97
O2 uptake in lungs
- diffuses from alveoli (↑[]) to p. capillary (↓[]) - dissolved in plasma - moves to RBC - binds with Hb
98
O2 delivery to tissues
- diffuses from RBC to plasma - diffuses into tissue = dissolved O2 in ISF - moves into cells - consumed in cell mitochondria
99
oxygen-hemoglobin dissociation curve
x = P (O2) - systemic venous: ↓ P(O2) - systemic arterial: ↑ P(O2) y = Hb saturation (%) - ↓ as O2 dissociates from Hb difference between Hb sat of arterial and venous = amount of O2 unloaded in tissue capillaries
100
effect of DPG concentration on Hb saturation
DPG = metabolic waste product no DPG = high sat (L) added DPG = low sat (shift curve to R) same effect seen with CO2
101
effect of temperature on Hb saturation
high metabolism increases temperature ↑t = ↓ sat shifts curve to R
102
effect of acidity on Hb saturation
high metabolic activity = high acidity (low pH = high [H+]) shifts curve to R
103
effect of fetal hemoglobin on Hb saturation
high saturation during fetal development decreases with aging adult Hb = shift curve to R
104
CO2 uptake from tissues
CO2 exits cells and is dissolved in ISF → diffuses to blood in blood = 4 pathways 1. remains in plasma as dissolved CO2 2. enters RBC and remains as dissolved CO2 3. enters RBC and binds to deoxyHb = HbCO2 4. enters RBC and reacts with H2O → carbonic acid (CA catalyst) → dissociates to HCO3- + H+ [HCO3- exits RBC; H+ increases in venous blood = ↓ pH]
105
CO2 delivery to lungs
HbCO2 dissociates → dissolved CO2 HCO3- moves back into RBC → binds with H+ → hydrolyzed into H20 + dissolved CO2 ↓[CO2] in plasma drives diffusion of dissolved CO2 from RBC into plasma → diffuses into alveoli
106
H+ transport
Hb from HbO2 + H+ from H2CO3- bind together H+ is not dissolved in RBC or plasma to maintain stable pH Hb buffers production of H+ in peripheral tissues + capillaries
107
respiratory acidosis
high [H+] as a result of ↑ P(CO2) hypoventilation causes CO2 production > CO2 elimination = ↑ P(CO2) + ↑ [H+]
108
respiratory alkalosis
low [H+] as a result of ↓ P(CO2) hyperventilation causes CO2 production < CO2 elimination = ↓ P(CO2) + ↓ [H+]
109
metabolic acidosis
high blood [H+] as a result of metabolism change is independent of changes in P(CO2)
110
metabolic alkalosis
low blood [H+] as a result of metabolism change is independent of changes in P(CO2)
111
neural control of breathing
automatic process regulated by neuronal network in pons + medulla (brainstem)
112
breathing initiation
in medulla by specialized neurons (PreBotC)
113
medullary respiratory centre
dorsal respiratory group ventral respiratory group Pre-Botzinger Complex: sets basal resp rate
114
DRG
fires during inspiration stimulates inspiratory muscles = diaphragm + external intercostals phrenic nerve → diaphragm intercostal nerves → external intercostals
115
VRG
expiration contains Pre-Botzinger Complex in upper portion = respiratory rhythm generator intercostal nerves → internal intercostals
116
pons respiratory centres
- pneumotaxic centre - apneustic centre = pontine respiratory group
117
PRG
centres help modulate activity of medullary inspiratory neurons - termination of inspiration at appropriate time - smooth transition between inspiration + expiration
118
pneumotaxic centre
descending inhibition to apneustic centre + DRG
119
respiratory rhythmicity centre
DRG + VRG send signals to one another = local regulation of each other
120
modification of breathing
by: higher structures of CNS inputs from central + peripheral chemoreceptors inputs from mechanoreceptors in lung + chest wall inputs from other peripheral receptors
121
inhibitory modification
voluntary control of breathing Hering-Breuer reflex (stretch receptors in lungs)
122
stimulatory modification
voluntary control of breathing medullary chemoreceptors carotid + aortic body chemoreceptors proprioceptors in muscles + joints receptors for touch, temp, + pain stimuli
123
peripheral chemoreceptors
carotid bodies + aortic bodies respond to changes in arterial blood: - hypoxia = ↓ P(O2) - metabolic acidosis = ↑ [H+] - respiratory acidosis = ↑ P(CO2)
124
central chemoreceptors
located in medulla respond to changes in brain extracellular fluid: - ↑ P(CO2) via associated changes in [H+]
125
hypoxia
stable ventilation between 60-120 mmHg arterial P(O2) arterial P(O2) drops below 60 → stimulation of peripheral chemoreceptors ↓ inspired P(O2) = ↓ alveolar P(O2) = ↓ arterial P(O2) ↑ firing of peripheral chemoreceptors → reflex via medullary respiratory neurons (activation of DRG + VRG to control activity of resp muscles centrally = ↑ resp rate + tidal vol) ↑ contraction of resp muscles = ↑ ventilation = return of P(O2) to normal
126
hypercapnia
stable ventilation at 40 mmHg arterial P(CO2) arterial P(CO2) increases above 40 → stimulation of central chemoreceptors (also peripheral) ↑ P(CO2) = ↑ alveolar P(CO2) = ↑ arterial P(CO2) ↑ brain extracellular fluid P(CO2) + ↑ brain extracellular fluid [H+] = respiratory acidosis ↑ firing of central chemoreceptors → reflex via medullary respiratory neurons (activation of DRG + VRG to control activity of resp muscles centrally = ↑ resp rate + tidal vol) ↑ contraction of resp muscles = ↑ ventilation = return of P(CO2) to normal
127
chemoreceptors + metabolic acidosis
H+ stimulates peripheral chemoreceptors (does not cross blood brain barrier)
128