respiratory Flashcards
respiration vs ventilation
resp = exchange gases @ alveoli
vent = movement air thru airways
plica vena cava
fold of pleura that caudal vena cava runs to heart in
what type control diaphragm
somatic - can control it bc can control breathing
importance neg press in pleural cavity
holds lungs against ribs/diaphragm
* w/o it ribs etc move but lungs don’t (= can’t breathe)
* hole in pleura = lung collapse = pneumothorax
species diffs bet pleural sacs
ruminants: L + R pleural sacs isolated = conditions limited to side of injury
dog/cat/horse: mediasteinal pleura permeable = comm = unilateral problem becomes bilateral
nares
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
turbinates
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)
where are turbinates found
- dorsal nasal concha
- ventral nasal concha
- ethmoidal conchae
passage air after nasal cavity
-> nasopharynx -> larynx -> infraglottic cavity -> trachea -> bifurcation dorsal to base heart …..
structure + role larynx
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
structure trachea
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
bronchus types
- primary to each lung
- second each supply lobe
- tert (= segmental) each supply prim lobule (bronchopulmonary segment)
CT bet lobules
peribronchial CT
* -> surface visceral pleura
* can be visible as surface marbling, e.g. pigs
tracheal bronchus
in ruminants + pigs, deviates from trachea cranial to bifurcation -> cranial lobe R lung
division systems bronchi
- 1st 6 = monopodial sys, w only small decr in diameter for small incr in cross-sectional area
- 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
airway lining
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
lobe + lobule distinction diff species
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
lobe defn
portion tiss supplied secondary bronchus
not defined external divisions
bronchus vs bronchiole
- cartilage rings dwindle -> plates then replaced sm musc (can change diameter) + elastic tiss (structure) in bronchioles
- bronchioles no submucosal glands
bronchioles <1mm diameter
terminal bronchioles
last division bronchioles before resp zone, each ending in air exchange portion lung (secondary lobule)
* no cilia
* no goblet cells
* Clara cells prod surfactant
resp zone components
- resp bronchioles w alveolar outpouchings of walls for some gas exchange
- alveolar ducts
- alveolar sacs
sm musc + elastic tiss in resp zone
no sm musc - all affected external forces
lots elastic tiss investing it = passively recoils to shape (lots expiration passive)
cells in alveoli epithelium
- type 1 alveolocytes = v thin squamous
- type 2 = cuboidal to prod surfactant (keep surface bet cells + air moist)
- macrophage to phagocytose tiny foreign particles/infectious agents past nasal + escalator -> alveoli
alveolocytes = pneumocytes
layers for gas exchange
thin = easy gas exchange
thin fluid film for O2/CO2 dissolve so can move across mems
bronchovascular bundle
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
histology resp sys
bronchial circulation
bronchial arteries from aorta -> supply lung tiss -> bronchial veins -> azygous vein
* some -> pulm circ -> LA (deoxed blood no significant effect on oxygenation blood -> bod)
why does all blood pass thru cap bed in lungs
interarterial + intervenous anastomoses in lungs but no arteriovenous
* = neoplastic cells, infectious agents sieved out + stay @ lungs = tumours spread there often
nerve supply to lungs
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)
what sends info on sensory nerves
mechanoreceptors (stretch receptors) + chemoreceptors (e.g. if irritant) -> resp centre
label
larynx
label
cross-section trachea
why so many layers to airways
complex for defence against external environ
1. aerodynamic filtration
2. mucociliary escalator
aerodynamic filtration
coiled turbinates = particles bounced to sides covered mucous = stick then cilia beat w escalator = moved out
bc turbinates covered pseudostratified w cilia + mucous
histology lower resp tract
epithelial defences gone so can gas exchange so need alveolar defences (macrophages)
histology bronchovascular bundle
blood air barrier
interstitium almost indistinguishable
how does alveolar epitheium renew
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
upper vs lower resp sys
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)
how does mucous mem change down lower resp tract
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
interlobular septa
CT walls sepping respiratory unit lobules
* consist sollagen, elastic fibres + bvs
* no in carnivores, complete in ruminants + pigs, horses have incomplete (poorly lobulated)
alveolar pores
= septal pores = openings in interalveolar septa
* lined by epithelial cells for air + macrophages pass bet alveoli
visceral pleura =?
pulmonary pleura
* squamous -> cuboidal cells overlying elastic fibres + dense irregular CT
* free surface of cells covered microvilli
* thickest parts cont collagen, bvs, lymph vessels
respiratory rate
RR
no. breaths taken 1min
resting RR
20-30brpm
horses = 10-12brpm
eupnoea
normal resting breathing
tachypnoea
increased RR
hyperpnoea
increased resp depth
dyspnoea
incr resp effort
apnoea
absence of breathing
purpose of breathing
ventilate alveoli
how to get air movement
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
result/importance neg press in pleural space
- lungs expand on inspiration
- lungs no collapse on expiration
how does inspiration happen
- diaphragm contracts + flattens caudally
- external intercostal musc run caudoventral + contract so ribs out + cranial
- = incr size thoracic cavity = decr press = air in
how does expiration happen
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
result active expiration
walls compressed so tiss recoils = neg press = passive inspiration
before active inspiration
transpulmonary press
diff bet alveolar press + intrapleural press
compliance
w equ
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
what does lung compliance depend on
- elasticity of lungs + thoracic cage
- alveoli surface tension
alveoli surface tension
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
surfactant made up of?
- phospholipids
- prots
- Ca2+
role surfactant + how works
- hydrophilic heads phospholipids dissolve in fluid lining alveoli
- tails remain in liquid layer
- reduce formation H bonds bet water mols
- = decr surface tension
O2/CO2 dissolve in fluid lining, NOT surfactant
atelectasis
w causes
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
what determines press in alveolus
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
what determines airway resistance w equ
effect incr has on resistance
radius (r), length (L), viscosity (η)
Pouseille’s: R = 8Lη/πr^4
(double radius = decr R 4-fold)
decr, incr, incr
turbulence vs viscosity
in resp they’re effectively the same
how does resistance vary bet insp + exp
peribronchial CT comms w visceral pleura so insp = lower airways distended = lower resistance to airflow
varying resistance parts resp tract
during insp
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
how alter airway radius
sm musc in walls (ANS innerv)
* symp = β2 adrenoreceptors to relax musc, dilate, decr res
* parasymp = contract musc, constr airways, incr res
asthma
bronchospasm = decr airway diameter = incr resistance
cause + effect incr turbulence
incr speed (e.g. bc larger airway)
==> incr friction bet mols = incr resistance to flow
effect smaller bronchioles
decr speed flow + laminar airflow = minimal friction = minimal resistance airflow
laminar airflow
continuous flow uniform in direction + velocity
tidal vol
vol air moved during resp cycle
* 10ml/kg in normal resting dog
normally only uses tiny bit potential vital capacity
minute ventilation
tidal vol * resp rate
* metabolic activity incr = O2 requirement incr + need expel more CO2 = need min vent incr too
residual vol
vol air remaining after full expiration due limitations compressability thoracic wall
functional residual capacity
exp reserve vol + residual vol = total amount air in lungs after normal exp at rest
how max tidal vol in peak exercise
- neck muscs used further expansion to take in inspiratory reserve vol
- abdom + internal intercostal used active exp force more air out + use exp reserve vol
graph showing respiratory vols
F + P
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
how does gas exert press
gas mols move + collide w surfaces, creating press
* mol size irrelevant - CO2 + O2 mol both exert same press
what makes gas mols move
from region high partial press that gas to region low partial press that gas down press grad
* other gases present irrelevant to gradient
partial press gas in sol
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
how does PO2 down airways change
air humidified = water vapour added = PO2 proportionately less but total press exerted by gas same
* PO2 = (atmos press - PH2O) * 0.21
what affects composition air in alveoli
- alveolar ventilation
- exchange gases - only small prop exchanged w each breath
variation concs O2/CO2 bet airways + alveoli
- PAO2 < PO2 in airways bc constant diff O2 -> blood
- PACO2 > PCO2 in airways bc diff out blood -> alveoli
all stay quite stable if composition inspired air + cent rate same
PA… = alveolar partial press
how press grads bet blood + alveoli maintained
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
ventilation:perfusion ratio
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
hyperventilation defn + result
incr ventilation at normal metabolic rate
= incr PAO2 + decr PACO2 = incr PaO2 + decr PaCO2 = hypocapnia - can cause alterations in pH
hypoventilation
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
dead space defn w types
areas ventilated but don’t participate in gas exchange
1. anatomical dead space = airways
2. functional dead space = unperfused alveoli
what air enters alveoli in inspiration
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
O2 transport
poorly soluble = can’t carry enough in plasma meet needs = need Hb
structure Hb
4 haem units each w associated globin chain
* haem = pigment mol cont Fe2+
* each ferrous ion reversibly bind 1O2
== 1 Hb can bind 4O2
globin role
polypep to prevent irreversible binding O2 -> ferrous ion so O2 can be released at tiss
* diff globin mols = diff sequence aas = diff affinity O2
blood O2 capacity
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
what determines O2 content blood
O2 capacity and PAO2 (alveolar partial press O2
cooperative binding
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
oxyhaemoglobin dissociation curve
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
effect of temp on oxyhaemoglobin dissociation curve
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
effect pH on oxyhaemoglobin dissociation curve
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
how does 2,3-DPG decr Hb affinity
binds Hb
* ruminant + some foetal Hb no bind = Hb retains higher affinity (important for maternal circ -> foetus)
methods CO2 transport in blood
- dissolved in plasma - 5% bc more soluble than O2
- carbamino compounds = combined w prots in rbc or plasma
- as bicarb ions as diffs tiss -> rbc -> carbonic acid -> dissociate (readily) (back to acid -> CO2 to exhale at lungs)
carbaminohaemoglobin
= HbCO2
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
formation + what happens to bicarb ions in blood
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
what happens to H+ formed in rbcs
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
alveolar vs extra-alveolar vessels
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
resp sys on radiograph
how does vasc resistance (+ so diameter) change
- initially decr as bronchovasc bundle CV pulls extra-aalveolar open + caps not yet compressed
- then breathe in = alveoli bigger = caps bet them squished
so w anaesthesia be careful no overinflate causing vasc resistance
pulmonary vascular resistance
(press (pulm art) - press (LA))/CO
compare pulm + systemic vasc resistance
- 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
where is pulm vasc res changed
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
neural control pulm vasculature
autonomic via pulmonary plexus + vagus
not main influence pulm flow - f(l)ight = humoral for overall vasodil
symp effect on pulm vasc
β-receptors = vasodil
α-receptors = vasoconstr
more α than β so overall effect vasoconstr
parasymp effect on pulm vasc
- release nitric oxide stims muscarinic receptors = vasodil
- direct sm musc action = vasoconstr
net overall = vasodil
humoral controls pulm vasculature
- NO from endothelial cells for vasodil due:
* parasymp stim
* bradykinin
* incr speed blood flow in vessel due shear stress, e.g. exercise - 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
control of resp
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
central pattern generator
CPG
network communicating pathways that prod appropriate resp rate + depth based on need
* rythmically activates neurones dorsal resp grp
what controls inspiration
neurones dorsal resp grp stim motor neurones -> muscs insp (diaphragm, ext intercosts)
Hering-Breuer reflex
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
control expiration
mainly passive due elastic recoil
active via neurones ventral resp grp sending impulses expiratory muscs (int intercosts, abdom)
irritant receptors
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
musc spindle stretch receptors
in resp muscs to monitor their movements + modulate strength contractions
peripheral chemoreceptors where + innerv
- carotid bodies @ division common carotid artery -> internal + external, innerv glossopharyngeal
- aortic bodies in aortic arch, innerv vagus - important foetus, not adult
in these locations bc need good blood supply
role peripheral chemoreceptors
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
central chemoreceptors
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
buffer
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
dissociation constant
pKa
pH when conc both components equal - acid + H+/base side equ
compensation acidosis/alkalosis
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
panting
fast shallow breathing - moves dead space air up + down
* worsens ventilation
weak vs strong acid/base
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
graph for respiratory acid:base imbalances
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
gross embryology
mammals
- foregut = tube then groove in floor (cranial + extends caudal)
- deepens + forms outgrowth (laryngotracheal tube)
- sepped from oes (original tube) by bilateral tracheo-oesophageal grooves
- grooves meet form tracheo-oesophageal septum so tubes sepped
- cranial laryng tube = trachea - endoderm lining -> resp epithel + mucosa + submucosal glands
- as grows caudally bifurcates -> 2 bronchial buds (principal, 1, bronchi)
- extend caudally (R midline, L lateral) -> lobar, 2, bronchi (R = 4, L = 2)
- extend caudally, dividing -> segmental, 3, bronchi
- -> further divisions
outer tube splanchnic mesoderm will become visceral pleura
pharynx forms from foregut cranial to septum
how does pulm circ become part of circ
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
angiogenesis vs vasculogenesis
angio = existing bvs grow + invest lungs
vasculo = new bv network that grows + joins existing
resp sys histological embryology stages
- embryonic
- pseudoglandular
- canalicular
- terminal sac
- alveolar
embryonic stage
histological embryology
from formation laryngotracheal groove -> formation 3 bronchi
* endoderm -> epithelium w mucosal + submucosal glands
* splanchnic mesoderm -> sm musc, cartilage, CT
pseudoglandular stage
histological embryology
- lungs extend, developing conducting branches bronchial tree
- vascularisation starts
canalicular stage
histological embryology
- 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
terminal sac stage
histological embryology
resp bronchioles -> sacs lined cuboidal epithel (air sacs forming)
* organises into type I + II alveolocytes
* production surfactant begins
alveolar stage
histological embryology
- 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
development gas exchange in foetus
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
arrangement foetal + maternal bvs
countercurrent = most efficient gas exchange
concurrent
crosscurrent = foetal going past in loops
pool = foetal dipping in + out maternal
why is foetal blood relatively hypoxic
oxed + deoxed blood mixed couple times in circ
how does foetus cope relative hypoxia
- carotid bods relatively insensitive - develop sensitivity 1st few wks life
- higher CO than adult
- higher affinity Hb for O2
how does foetal Hb have higher affinity O2
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
what happens resp sys during birth
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
changes to resp sys at birth
- hypoxia as O2 supply cut off (no placenta
- hypercapnia same reason
- decr bod temp of foetus
- 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
myoglobin
in sk musc + stores O2 - released at low cell pH, e.g. during exercise
increaasing red blood cell count (rbcc)
short term = splenic contraction
long term = erythropoeisis
* balance bc too high = incr blood viscosity = incr resistance flow = incr afterload = incr cardiac workload = heart failure
how does effect hypoxic pulm vasoconstr vary bet species
diff amounts pulm vasc sm musc
* cattle > pigs > horses > sheep > dogs
so consequences low inspired pO2 more significant cow than sheep
why does hypoxia mean decr pH
more anaerobic resp = more lactic acid = decr pH (only lil bit)
NOT bc incr PaCO2 bc lower atmos press means lower pCO2 asw
