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respiratory Flashcards

1
Q

respiration vs ventilation

A

resp = exchange gases @ alveoli
vent = movement air thru airways

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2
Q

plica vena cava

A

fold of pleura that caudal vena cava runs to heart in

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3
Q

what type control diaphragm

A

somatic - can control it bc can control breathing

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4
Q

importance neg press in pleural cavity

A

holds lungs against ribs/diaphragm
* w/o it ribs etc move but lungs don’t (= can’t breathe)
* hole in pleura = lung collapse = pneumothorax

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5
Q

species diffs bet pleural sacs

A

ruminants: L + R pleural sacs isolated = conditions limited to side of injury

dog/cat/horse: mediasteinal pleura permeable = comm = unilateral problem becomes bilateral

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6
Q

nares

A

outer part nostril where air enters
* protection from invasion foreign mat

interior rostral nasal cavity lined stiff hairs for further protection

horse = expandable for incr air floe bc can’t breathe thru mouth

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7
Q

turbinates

A

scrolls bone lined vascular mucosa w mucous glands
* splits nasal cavity into 4 interconnected passageways = meati (single meatus)
* warms (-> core body temp), humidifies + cleans air - bc mucosa v mucousy (protect against infection)

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8
Q

where are turbinates found

A
  • dorsal nasal concha
  • ventral nasal concha
  • ethmoidal conchae
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9
Q

passage air after nasal cavity

A

-> nasopharynx -> larynx -> infraglottic cavity -> trachea -> bifurcation dorsal to base heart …..

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10
Q

structure + role larynx

A

interconnected cartilages that move (inc epiglottis), lined mucous mem
* connects pharynx + trachea
* protect lower airways
* involved swallowing, coughing, eructation/vomming/rumination
* open + close w breathing so paralysis = vocal fold -> centre + no open = resistance airflow

epiglottis involved diverting food mat airway -> oes

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11
Q

structure trachea

A

incomplete rings cartilage (fibro, framework), w ends joined trachialis musc
* sometimes flat cartilage + long musc = sticks trachea on inspiration = difficult breathe
* carnivores = musc on outside, everything else = on inside

exterior CT layer, tubular, ciliated mucosal lining w mucous glands

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12
Q

bronchus types

A
  1. primary to each lung
  2. second each supply lobe
  3. tert (= segmental) each supply prim lobule (bronchopulmonary segment)
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13
Q

CT bet lobules

A

peribronchial CT
* -> surface visceral pleura
* can be visible as surface marbling, e.g. pigs

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14
Q

tracheal bronchus

A

in ruminants + pigs, deviates from trachea cranial to bifurcation -> cranial lobe R lung

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15
Q

division systems bronchi

A
  1. 1st 6 = monopodial sys, w only small decr in diameter for small incr in cross-sectional area
  2. then equal sys -> 2 daughter bronchi equal size to each other = large incr cross-sectional area (double each time)
    * = air travelling slower + less turbulent by end
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16
Q

airway lining

A

pseudostratified ciliated columnar epithelium w goblet cells + submucosal glands
* cilia beat together for mucous -> pharynx -> swallow = protective mucociliary escalator function
* remove foreign mat + microbes that bypassed upper airway defences

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17
Q

lobe + lobule distinction diff species

A

bounding gait need greater freedom movement = more external sep bet lobes (dog lots, horse nope)

dogs = lobule divisions not visible, pigs = v visible CT marbling

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18
Q

lobe defn

A

portion tiss supplied secondary bronchus

not defined external divisions

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19
Q

bronchus vs bronchiole

A
  • cartilage rings dwindle -> plates then replaced sm musc (can change diameter) + elastic tiss (structure) in bronchioles
  • bronchioles no submucosal glands

bronchioles <1mm diameter

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20
Q

terminal bronchioles

A

last division bronchioles before resp zone, each ending in air exchange portion lung (secondary lobule)
* no cilia
* no goblet cells
* Clara cells prod surfactant

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21
Q

resp zone components

A
  • resp bronchioles w alveolar outpouchings of walls for some gas exchange
  • alveolar ducts
  • alveolar sacs
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22
Q

sm musc + elastic tiss in resp zone

A

no sm musc - all affected external forces

lots elastic tiss investing it = passively recoils to shape (lots expiration passive)

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23
Q

cells in alveoli epithelium

A
  1. type 1 alveolocytes = v thin squamous
  2. type 2 = cuboidal to prod surfactant (keep surface bet cells + air moist)
  3. macrophage to phagocytose tiny foreign particles/infectious agents past nasal + escalator -> alveoli

alveolocytes = pneumocytes

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24
Q

layers for gas exchange

A

thin = easy gas exchange

thin fluid film for O2/CO2 dissolve so can move across mems

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25
Q

bronchovascular bundle

A

bronchus w bronchial artery + vein running alongside w CT tiss around (part pleura)
* breathe + change press pleural space = pleura moves, all connected = bundles open + reduced resistance blood/air flow

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26
Q

histology resp sys

A
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27
Q

bronchial circulation

A

bronchial arteries from aorta -> supply lung tiss -> bronchial veins -> azygous vein
* some -> pulm circ -> LA (deoxed blood no significant effect on oxygenation blood -> bod)

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28
Q

why does all blood pass thru cap bed in lungs

A

interarterial + intervenous anastomoses in lungs but no arteriovenous
* = neoplastic cells, infectious agents sieved out + stay @ lungs = tumours spread there often

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29
Q

nerve supply to lungs

A

symp + parasymp from pulmonary plexus
1. vagus nerve for parasymp supply, directly innervating airways
2. symp only innervates bvs, effects on airway sm musc via (nor)adrenaline in blood on β2 adrenoreceptors (indirect)

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30
Q

what sends info on sensory nerves

A

mechanoreceptors (stretch receptors) + chemoreceptors (e.g. if irritant) -> resp centre

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31
Q

label

A

larynx

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32
Q

label

A

cross-section trachea

purple dots in submucosa = inflammatory cells (surveillance/ inflammation)
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33
Q

why so many layers to airways

A

complex for defence against external environ
1. aerodynamic filtration
2. mucociliary escalator

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34
Q

aerodynamic filtration

A

coiled turbinates = particles bounced to sides covered mucous = stick then cilia beat w escalator = moved out

bc turbinates covered pseudostratified w cilia + mucous

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35
Q

histology lower resp tract

A

epithelial defences gone so can gas exchange so need alveolar defences (macrophages)

'chicken wire'
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36
Q

histology bronchovascular bundle

A
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37
Q

blood air barrier

A

interstitium almost indistinguishable

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38
Q

how does alveolar epitheium renew

A

type 1 pneumocytes can’t divide so if damaged just type 2 (no good for gas exchange) - they divide then specialise
* so type 2 essential for mucous asw as maintenance

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39
Q

upper vs lower resp sys

A

upper = nose + pharynx
lower = larynx, trachea, bronchi, lungs

  • stratified squamous -> pseudostratified ciliated columnar epithelium w goblet cells
  • upper = cilia down towards pharynx, vus up towards pharynx (both so can be swallowed)
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40
Q

how does mucous mem change down lower resp tract

A

after tertiary bronchi pseudo -> ciliated columnar w some goblet cells -> w/o goblet -> non-ciliated simple cuboidal (terminal bronchioles) -> simple squamous

from terminal bronchioles inhaled particles removed by macrophages

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41
Q

interlobular septa

A

CT walls sepping respiratory unit lobules
* consist sollagen, elastic fibres + bvs
* no in carnivores, complete in ruminants + pigs, horses have incomplete (poorly lobulated)

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42
Q

alveolar pores

A

= septal pores = openings in interalveolar septa
* lined by epithelial cells for air + macrophages pass bet alveoli

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43
Q

visceral pleura =?

A

pulmonary pleura
* squamous -> cuboidal cells overlying elastic fibres + dense irregular CT
* free surface of cells covered microvilli
* thickest parts cont collagen, bvs, lymph vessels

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44
Q

respiratory rate

RR

A

no. breaths taken 1min

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45
Q

resting RR

A

20-30brpm
horses = 10-12brpm

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46
Q

eupnoea

A

normal resting breathing

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47
Q

tachypnoea

A

increased RR

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48
Q

hyperpnoea

A

increased resp depth

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49
Q

dyspnoea

A

incr resp effort

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50
Q

apnoea

A

absence of breathing

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51
Q

purpose of breathing

A

ventilate alveoli

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52
Q

how to get air movement

A

due press changes in alveoli
1. for inhalation: gen press < atmospheric (by expand thoracic cavity)
2. for exhalation: gen press > atmos (= decr size thoracic cavity) then air out until alveolar press = atmos

bet breaths no movement air (insp + exp pauses) = press in alveoli = atmos press

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53
Q

result/importance neg press in pleural space

A
  1. lungs expand on inspiration
  2. lungs no collapse on expiration
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54
Q

how does inspiration happen

A
  1. diaphragm contracts + flattens caudally
  2. external intercostal musc run caudoventral + contract so ribs out + cranial
  3. = incr size thoracic cavity = decr press = air in
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55
Q

how does expiration happen

A

usually passive from elastic recoil lungs + muscs so press incr + air out
* some species = active phase, also in exercise =:
1. internal intercostals (cranioventral) = ribs caudal + in
2. abdom muscs contract = abdom contents up = diaphragm domes
3. = thorax decr size = alv press incr = exp

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56
Q

result active expiration

A

walls compressed so tiss recoils = neg press = passive inspiration

before active inspiration

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57
Q

transpulmonary press

A

diff bet alveolar press + intrapleural press

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58
Q

compliance

w equ

A

degree to which change in transpulmonary press leads to change in lung vol

C = change in vol/change in press

altered in disease state + if obese

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59
Q

what does lung compliance depend on

A
  1. elasticity of lungs + thoracic cage
  2. alveoli surface tension
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60
Q

alveoli surface tension

A

resp zone surfaces lined fluid facilitate dissolution + diffusion gases + water mols form H bonds at water-air interface, creating surface tension
* = decr SA = resists lung expanion = decr lung compliance

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61
Q

surfactant made up of?

A
  • phospholipids
  • prots
  • Ca2+
62
Q

role surfactant + how works

A
  1. hydrophilic heads phospholipids dissolve in fluid lining alveoli
  2. tails remain in liquid layer
  3. reduce formation H bonds bet water mols
  4. = decr surface tension

O2/CO2 dissolve in fluid lining, NOT surfactant

63
Q

atelectasis

w causes

A

collapsed alveoli due inadequate surfactant
1. premature neonates inadequate prod surfactant = severe dyspnoea
2. in adults sigh = stim release surfactant so prevention sigh =…
3. prolonged general anaesthesia w inadequate ventilation

64
Q

what determines press in alveolus

A

radius (r) + surface tension (T)

P = 2T/r

= smaller alv, higher press, air small -> large = small collapse

SO
all alv same amount surfactant = conc higher in small = surface tension decr relatively more = press equiv

65
Q

what determines airway resistance w equ

effect incr has on resistance

A

radius (r), length (L), viscosity (η)

Pouseille’s: R = 8Lη/πr^4
(double radius = decr R 4-fold)

decr, incr, incr

66
Q

turbulence vs viscosity

A

in resp they’re effectively the same

67
Q

how does resistance vary bet insp + exp

A

peribronchial CT comms w visceral pleura so insp = lower airways distended = lower resistance to airflow

68
Q

varying resistance parts resp tract

during insp

A

lower airways dilated (CT comm) = upper higher resistance
* so mouth breathe to incr A + decr resistance
* horses = obligate nasal breathers = distensible nares + can decr size bvs in nasal passageways to decr resistance

69
Q

how alter airway radius

A

sm musc in walls (ANS innerv)
* symp = β2 adrenoreceptors to relax musc, dilate, decr res
* parasymp = contract musc, constr airways, incr res

70
Q

asthma

A

bronchospasm = decr airway diameter = incr resistance

71
Q

cause + effect incr turbulence

A

incr speed (e.g. bc larger airway)
==> incr friction bet mols = incr resistance to flow

72
Q

effect smaller bronchioles

A

decr speed flow + laminar airflow = minimal friction = minimal resistance airflow

73
Q

laminar airflow

A

continuous flow uniform in direction + velocity

74
Q

tidal vol

A

vol air moved during resp cycle
* 10ml/kg in normal resting dog

normally only uses tiny bit potential vital capacity

75
Q

minute ventilation

A

tidal vol * resp rate
* metabolic activity incr = O2 requirement incr + need expel more CO2 = need min vent incr too

76
Q

residual vol

A

vol air remaining after full expiration due limitations compressability thoracic wall

77
Q

functional residual capacity

A

exp reserve vol + residual vol = total amount air in lungs after normal exp at rest

78
Q

how max tidal vol in peak exercise

A
  1. neck muscs used further expansion to take in inspiratory reserve vol
  2. abdom + internal intercostal used active exp force more air out + use exp reserve vol
79
Q

graph showing respiratory vols

A
80
Q

F + P

A

F = fraction of gas mix made that gas, e.g. FO2 = 21%

P = partial press that gas (press exerted by gas w/in mix), e.g. PO2 = 0.21 * atmos press

81
Q

how does gas exert press

A

gas mols move + collide w surfaces, creating press
* mol size irrelevant - CO2 + O2 mol both exert same press

82
Q

what makes gas mols move

A

from region high partial press that gas to region low partial press that gas down press grad
* other gases present irrelevant to gradient

83
Q

partial press gas in sol

A

gas mols dissolve in contact w water
* incr partial press = more dissolves
* mols also come out of sol to re-enter gas phase
* no. mols of given gas entering + leaving sol in given time equal = dynamic equilibrium = partial press gas in sol = partial press in gas phase

CO2 more soluble than O2

84
Q

how does PO2 down airways change

A

air humidified = water vapour added = PO2 proportionately less but total press exerted by gas same
* PO2 = (atmos press - PH2O) * 0.21

85
Q

what affects composition air in alveoli

A
  • alveolar ventilation
  • exchange gases - only small prop exchanged w each breath
86
Q

variation concs O2/CO2 bet airways + alveoli

A
  1. PAO2 < PO2 in airways bc constant diff O2 -> blood
  2. PACO2 > PCO2 in airways bc diff out blood -> alveoli

all stay quite stable if composition inspired air + cent rate same

PA… = alveolar partial press

87
Q

how press grads bet blood + alveoli maintained

A

use O2 + prod CO2 by respiring tiss then both diff bet alv + blood until equilibrium reached

PO2 in tiss < PaO2 (in arterioles) so O2 -> tiss
* opp for CO2

88
Q

ventilation:perfusion ratio

A

determines equilibrium CO2 + O2 reach
* correct equilib relies on correct vent + perf
* low VA:Q underventilated + overperfused - narrowed/obstructed airways
* high VA:Q = overventilated + underperfused - disease, recumbency so press on bvs from other organs

range across lungs, e.g. caudodorsal lung lobes preferentially perfused

89
Q

hyperventilation defn + result

A

incr ventilation at normal metabolic rate
= incr PAO2 + decr PACO2 = incr PaO2 + decr PaCO2 = hypocapnia - can cause alterations in pH

90
Q

hypoventilation

A

decr PAO2 + incr PACO2 = decr PaO2 (hypoxia) + incr PaCO2 (hypercapnia)
* risk during general anaesthesia so need monitor
* outside GA variations PaCO2 uncommon bc CO2 v soluble = can move bet alveoli + over-vent compensate under-vent but O2 no sol = no move = no compensate = hypoxia common

91
Q

dead space defn w types

A

areas ventilated but don’t participate in gas exchange
1. anatomical dead space = airways
2. functional dead space = unperfused alveoli

92
Q

what air enters alveoli in inspiration

A

dead space gas fills alveoli before fresh air
* dead space air conts proportion exhaled air from last breath = lower pO2 + higher pCO2
* exacerbated by shallow breathing

93
Q

O2 transport

A

poorly soluble = can’t carry enough in plasma meet needs = need Hb

94
Q

structure Hb

A

4 haem units each w associated globin chain
* haem = pigment mol cont Fe2+
* each ferrous ion reversibly bind 1O2

== 1 Hb can bind 4O2

95
Q

globin role

A

polypep to prevent irreversible binding O2 -> ferrous ion so O2 can be released at tiss
* diff globin mols = diff sequence aas = diff affinity O2

96
Q

blood O2 capacity

A

max O2 that lood leaving lungs could carry
* 1g Hb can carry 1.36ml O2
* mammalian blood = [Hb] 150g/L so 1L 200ml O2 if all Hb bound

97
Q

what determines O2 content blood

A

O2 capacity and PAO2 (alveolar partial press O2

98
Q

cooperative binding

A

when O2 binds to haem, affinity other binding sites for O2 incr
AND
as O2 starts dissociate 1 site, other sites’ affinity decr = unloading facilitated

99
Q

oxyhaemoglobin dissociation curve

A

Hb never 100% saturated w/in normal pO2

avg tiss pO2 = 40mmHg = 75% dissociation - rest = reserve if needed, e.g. exercise

anaemia = O2 content decr but Hb saturation same = oximeter no identify

sigmoid
100
Q

effect of temp on oxyhaemoglobin dissociation curve

A

incr temp = to right = decr affinity Hb for O2
* active tiss prods more heat = need more O2 = Hb releases it (easier O2 offload)
* vice versa

101
Q

effect pH on oxyhaemoglobin dissociation curve

A

decr pH due incr pCO2 or incr 2,3-DPG (prod metabolism) = more active tiss = decr Hb affinity for O2 = easier unload O2 = more released

102
Q

how does 2,3-DPG decr Hb affinity

A

binds Hb
* ruminant + some foetal Hb no bind = Hb retains higher affinity (important for maternal circ -> foetus)

103
Q

methods CO2 transport in blood

A
  1. dissolved in plasma - 5% bc more soluble than O2
  2. carbamino compounds = combined w prots in rbc or plasma
  3. as bicarb ions as diffs tiss -> rbc -> carbonic acid -> dissociate (readily) (back to acid -> CO2 to exhale at lungs)
104
Q

carbaminohaemoglobin

= HbCO2

A

vast majority carbamino compounds in blood (in rbcs)
* CO2 binds more readily deoxyHb than oxyHb so offloading O2 facilitates loading CO2 at tiss so active + offload more O2 = more space for more CO2
* vice versa in lungs

105
Q

formation + what happens to bicarb ions in blood

A

formed in rbc then diffs out -> plasma = electrochem grad = exchanged for Cl- = chloride shift
* reaction reversed at lungs as CO2 exhaled so grad to reform it

106
Q

what happens to H+ formed in rbcs

A

can’t diffuse out = buffered H+
* buffered by Hb to maintain pH
* deoxyHb greater affinity than oxy so at tiss Hb dissociates O2, deoxy binds H+ = press grad CO2 -> H+/HCO3- + vice versa to convert -> CO2 + exhale at lungs where more O2

107
Q

alveolar vs extra-alveolar vessels

A

alveolar = caps running in alveolar septa, participate gas exchange

extra-alveolar = move blood to + from lungs (bronchovasc bundle)

dorsocaudal region lung norm best ventilated = preferentially perfused

108
Q

resp sys on radiograph

A
109
Q

how does vasc resistance (+ so diameter) change

A
  1. initially decr as bronchovasc bundle CV pulls extra-aalveolar open + caps not yet compressed
  2. then breathe in = alveoli bigger = caps bet them squished

so w anaesthesia be careful no overinflate causing vasc resistance

110
Q

pulmonary vascular resistance

A

(press (pulm art) - press (LA))/CO

111
Q

compare pulm + systemic vasc resistance

A
  • pulm lower
  • pulm = caps contribute significantly, sys = arterioles
  • means arterial pulsations systemic transferred -> caps so pulm cap flow pulsatile instead

caps v lil signif sys, vs arterioles v lil signif pulm

112
Q

where is pulm vasc res changed

A

pulm arteries/arterioles cont sm musc in walls - contract/relax
* amount varies bet species so intensity vasoconstr varies
* relax = dilate = decr PVR
* contract = constr = incr PVR

controlled by balance neural + humoral

113
Q

neural control pulm vasculature

A

autonomic via pulmonary plexus + vagus

not main influence pulm flow - f(l)ight = humoral for overall vasodil

114
Q

symp effect on pulm vasc

A

β-receptors = vasodil
α-receptors = vasoconstr
more α than β so overall effect vasoconstr

115
Q

parasymp effect on pulm vasc

A
  • release nitric oxide stims muscarinic receptors = vasodil
  • direct sm musc action = vasoconstr

net overall = vasodil

116
Q

humoral controls pulm vasculature

A
  1. NO from endothelial cells for vasodil due:
    * parasymp stim
    * bradykinin
    * incr speed blood flow in vessel due shear stress, e.g. exercise
  2. alveolar hypoxia for vasoconstr to maintain VA:Q by diverting blood to well-ventilated alveoli
    * problem if hypoxia generalised, e.g. altitude, bc then all constr = incr afterload = heart failure
117
Q

control of resp

A

automatic + rhythmic, adjusted w/o conscious input but degree conscious control (won’t allow to detriment tho)
* pacemaker neurones in pre-Botzinger complex in medulla oblongata

118
Q

central pattern generator

CPG

A

network communicating pathways that prod appropriate resp rate + depth based on need
* rythmically activates neurones dorsal resp grp

119
Q

what controls inspiration

A

neurones dorsal resp grp stim motor neurones -> muscs insp (diaphragm, ext intercosts)

120
Q

Hering-Breuer reflex

A

pulm stretch receptors in lung send impulses -> pons just rostral medulla oblongata stop stim insp + prevent overinflation lung
* incr in frequency impulses signals degree inflation
* important in exercise

121
Q

control expiration

A

mainly passive due elastic recoil

active via neurones ventral resp grp sending impulses expiratory muscs (int intercosts, abdom)

122
Q

irritant receptors

A

in epithelial lining airways, stimmed:
1. contact foreign mat
2. deformation airways

stim protective mechs against further invasion, e.g. cough, incr mucous secr, bronchoconstr, shallow breathing

123
Q

musc spindle stretch receptors

A

in resp muscs to monitor their movements + modulate strength contractions

124
Q

peripheral chemoreceptors where + innerv

A
  1. carotid bodies @ division common carotid artery -> internal + external, innerv glossopharyngeal
  2. aortic bodies in aortic arch, innerv vagus - important foetus, not adult

in these locations bc need good blood supply

125
Q

role peripheral chemoreceptors

A

monitor PaO2 from dissolved in plasma (= accurate), PaCO2, arterial [H+]
* pO2 decr = glomus cells depol = a pots -> resp centre incr ventilation
* O2 not much effect until below 60-70mmHg but Hb no dissociate much before then so chill

anaemic = PaO2 seems fine bc dissolved same but not enough Hb carry enough

126
Q

central chemoreceptors

A

v sensitive, only monitor PaCO2 as most important factor affecting resp + PaO2 less sensitive as Hb saturation stays so high
* CO2 crosses blood:brain barrier -> HCO3-/H+ - detect [H+] in cerebrospinal fluid + impulses resp centre incr vent
* incr arterial [H+] no effect as can’t cross blood:brain barrier

127
Q

buffer

A

sys that can bind or donate H+ ions + so alter pH
* acid, prots (Hb), NH3

obey law of mass action - incr conc 1 component + equ moves opp direction

128
Q

dissociation constant

pKa

A

pH when conc both components equal - acid + H+/base side equ

129
Q

compensation acidosis/alkalosis

A

if cause is respiratory, compensation metabolic (kidneys) + vice versa
* acidosis = need remove H+ = incr resp rate/depth + secr in intercalated (alkalosis compensation)
* alkalosis = need add H+/remove bicarb = decr resp rate/depth + absorb H+ in intercalated

can be partial or full - full when pH completely back to normal

all abt moving equ one way or other

130
Q

panting

A

fast shallow breathing - moves dead space air up + down
* worsens ventilation

131
Q

weak vs strong acid/base

A

strong = dissociates completely in water - useless as buffer as no remove anything from sol, e.g. HCO3-

weak dissociates incompletely = most bound stay bound, e.g. H2CO3 holds on so time convert -> CO2 + H2O

132
Q

graph for respiratory acid:base imbalances

A

uncompensated = lil incr/decr in HCO3- bc 1 HCO3- for every H+ when H2CO3 dissociates
compensated = big incr/decr due renal compensation as synthed + absorbed or secreted

133
Q

gross embryology

mammals

A
  1. foregut = tube then groove in floor (cranial + extends caudal)
  2. deepens + forms outgrowth (laryngotracheal tube)
  3. sepped from oes (original tube) by bilateral tracheo-oesophageal grooves
  4. grooves meet form tracheo-oesophageal septum so tubes sepped
  5. cranial laryng tube = trachea - endoderm lining -> resp epithel + mucosa + submucosal glands
  6. as grows caudally bifurcates -> 2 bronchial buds (principal, 1, bronchi)
  7. extend caudally (R midline, L lateral) -> lobar, 2, bronchi (R = 4, L = 2)
  8. extend caudally, dividing -> segmental, 3, bronchi
  9. -> further divisions

outer tube splanchnic mesoderm will become visceral pleura

pharynx forms from foregut cranial to septum

134
Q

how does pulm circ become part of circ

A

cardiac tube developed already w venous end ventral to foregut
= mesoderm in contact w endoderm foregut so connex bet heart + lungs can develop
1. angiogenesis
2. vasculogenesis

don’t know which of 2 - probs bit of both

135
Q

angiogenesis vs vasculogenesis

A

angio = existing bvs grow + invest lungs
vasculo = new bv network that grows + joins existing

136
Q

resp sys histological embryology stages

A
  1. embryonic
  2. pseudoglandular
  3. canalicular
  4. terminal sac
  5. alveolar
137
Q

embryonic stage

histological embryology

A

from formation laryngotracheal groove -> formation 3 bronchi
* endoderm -> epithelium w mucosal + submucosal glands
* splanchnic mesoderm -> sm musc, cartilage, CT

138
Q

pseudoglandular stage

histological embryology

A
  • lungs extend, developing conducting branches bronchial tree
  • vascularisation starts
lung section
139
Q

canalicular stage

histological embryology

A
  • airway lumens enlarge
  • resp bronchioles form - bigger spaces
  • caps come into contact w epithelium in bronchioles

start of resp part developing, as opposed just ventilation before

lung section
140
Q

terminal sac stage

histological embryology

A

resp bronchioles -> sacs lined cuboidal epithel (air sacs forming)
* organises into type I + II alveolocytes
* production surfactant begins

141
Q

alveolar stage

histological embryology

A
  • caps associate closely w alveolar lining = form blood air barrier
  • type II proliferate so surfactant production incr
  • diff -> type 1 = thin-walled squamous appearance

incomplete at birth + continues post-natally

142
Q

development gas exchange in foetus

A

early embryo = diffusion but quickly insufficient so placentation to bring maternal + foetal circulations close for gas exchange
* microvilli in placenta = high SA, incr Rogas exchange

143
Q

arrangement foetal + maternal bvs

A

countercurrent = most efficient gas exchange
concurrent
crosscurrent = foetal going past in loops
pool = foetal dipping in + out maternal

144
Q

why is foetal blood relatively hypoxic

A

oxed + deoxed blood mixed couple times in circ

145
Q

how does foetus cope relative hypoxia

A
  1. carotid bods relatively insensitive - develop sensitivity 1st few wks life
  2. higher CO than adult
  3. higher affinity Hb for O2
146
Q

how does foetal Hb have higher affinity O2

A

ruminants = foetal Hb unresponsive 2,3DPG
primates = foetal Hb reduced interaction 2,3DPG
horses/pigs = no foetal Hb BUT foetal rbcs have lower [2,3DPG]

all reduce dissociation of Hb from O2

147
Q

what happens resp sys during birth

A

as foetus develops alveoli expand due fluid in them
* process birth squeezes some fluid out + remainder reabsorbed into lymphatic + bvs

= C-section more likely have fluid in lungs

148
Q

changes to resp sys at birth

A
  1. hypoxia as O2 supply cut off (no placenta
  2. hypercapnia same reason
  3. decr bod temp of foetus
  4. sensory stim, e.g. mum licking, us rubbing

== 1st breath w lots effort (intra-alveolar press 60mmHg below atmos press) -> fluid out, lungs open, air in
* lungs inflate, pleura moves, bronchovasc budnles open = decr pulm vasc resistance = blood no diverted = pulm gas exchange starts

born premature = no much surfactant = surface tens = hard breathe = give surfactant in trachea

149
Q

myoglobin

A

in sk musc + stores O2 - released at low cell pH, e.g. during exercise

150
Q

increaasing red blood cell count (rbcc)

A

short term = splenic contraction

long term = erythropoeisis
* balance bc too high = incr blood viscosity = incr resistance flow = incr afterload = incr cardiac workload = heart failure

151
Q

how does effect hypoxic pulm vasoconstr vary bet species

A

diff amounts pulm vasc sm musc
* cattle > pigs > horses > sheep > dogs

so consequences low inspired pO2 more significant cow than sheep

152
Q

why does hypoxia mean decr pH

A

more anaerobic resp = more lactic acid = decr pH (only lil bit)

NOT bc incr PaCO2 bc lower atmos press means lower pCO2 asw

NSF (22 decks)

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