How can we help?

You can also find more resources in our Help Center.

110 terms

SGU Physiology - Respiratory

SGU Physiology Final - Respiratory System
STUDY
PLAY
conducting zone
the airways of hte lungs, have no gas exch, Fx = warm, clean humidify
Respiratory zone
the alveoli w/ large cross-sec A that participate in gas exch (vs conducting)
Type I pneumocytes
alveolar cells w/ large SA and very thin memb
Type II pneumocytes
alveolar cells w/ surfactant storage granules
external intercostals
lift ribs up and out to inc thoracic volume during insp
internal intercostals
pull ribs down and to dec thoracic vol during exp
760mm Hg
1atm = 100kPa in mmHg
1.33 cm H2O
1mm Hg in H2O
water
component of air that increases from 0% to 6% upon entering your trachea
Ptp (transpulmonary pressure)
elastic recoil, transmural pressure across the alveolus = Pa-Pip
Pcwr (chest wall recoil pressure)
Pip - Patm
FRC (functional residual capacity)
RV + ERV, vol in lungs after norm exp, relaxed state, Ptp = Pcwr, where total pulmonary vasc resist is lowest
IC (inspiratory capacity)
TLC - FRC
FVC (forced vital capacity)
IRV + Vt + ERV
FEF25-75
flow rate between 25-75% of FVC
RV (residual volume)
volume in lungs after forced exp
obstructive lung disease
clinical: char by dec FEV1,dec FEV1:FVC (<0.8), dec FEF25-75, inc compliance, ex: COPD, bronchitis, emphysema, asthma
restrictive lung disease
clinical: char by dec FEV1, norm FEV1:FVC (0.8), dec FVC, norm FEF25-75, dec compliance ex: fibrosis
compliance
change in volume for a given change in pressure, high in COPD, low in fibrosis
elastance
1/compliance, high in restrictive (-> low compliance -> low FRC), low in obstructive
surfactant
phospholipids secreted by Type II pneumocytes, inc SA -> dec [suractant] -> inc ST -> dec C
atelectasis
collapsing of alveoli due to increased compliance
R (resistance)
8nL/(pie*r^4) = deltaP/Q
Re (reynolds)
2rvd/n
Q (flow)
deltaPpie*r^4/(8nL)
Cdynamic (dynamic lung compliance)
(deltaV/t) /(deltaP/t), dec w/inc airway R
He Dilution
method to calc FRC - V2 = V1 ([He]i/[He]f - 1)
pethysmography
method to calc FRC, able to account for obstructive lung diseases - 1) calc Vt w/ Boyle's law, 2) FRC = P4*Vt/deltaP
Ve (minute ventilation)
Vt * frequency
anatomic dead space
V that does NOT contribute to gas exch (conducting airways)
alveolar dead space
V in ventilated regions that should but are NOT contrib to gas exch)
physiological dead space
total DS = anatomic + alveolar DS
fowler method
meas anatomic DS via single breath N2 washout
bohr method
meas physiological DS via CO2 expired: Vd/Vt = (PaCO2-PeCO2)/(PaCO2)
RER
CO2 exp / O2 insp
RQ
CO2 produced / O2 consumed
alveolar ventilation equation
Va = VeCO2*0.863/PACO2
alveolar gas equation
PAO2 = PIO2 - (PACO2/R) = O2 insp - alveolar (meas via arterial) CO2 / R (norm 0.8 for norm diet)
hypercapnia (hypercarbia)
high CO2 in bl
eupnea
normal breathing
hypopnea
dec Va due to dec CO2 produced
nitrogen
makes up most of atm, ~78%
O2
makes up ~20% of atm
CO2
makes up 0.3% of atm
PairwayO2
where PO2 = 149mmHg
PAO2
105mmHg
PIO2
159mmHg
PatmN2
590mmHg
PatmCO2
0.23mmHg
PaO2
40mmHg
PvO2
100mmHg
PaCO2
40mmHg
SaO2a
75%
SaO2v
97%
HCO3
22-28 M (PA or PV)
pH
7.35-7.45 (PA or PV)
alveolar blood vessels
open at low lung volumes since they are not being compressed by alveoli
extra-alveolar vessels
open at high lung volumes since low Pip pulls them open by radial tension
Zone I
Pa > Ppa > Ppv, no flow
Zone II
Ppa > Pa > Ppv, restricted flow driven by Ppa - Pa diff, 50:50 dist:recruit
Zone III
Ppa > Ppv > Pa, highest flow driven by Ppa - Ppv diff, 70:30 dist:recruit
Zone IV
tiny zone at base of lung where Pip is less neg => inc extra-alveolar R => less Q than III
anatomical shunt
ex: bronchial circ, congenital heart defects, when some deox bl joins the ox bl at the PV -> LA, gen non-path
physiological shunt
ex: pneumothorax, V/Q mismatch, when large areas of lung are not ventilated -> deox bl in PV -> LA
bronchial circulation
takes 2-5% of CO to supply conducting airways, returns to PV as deox bl => anatomical shunt
Fick's Law
Vgas = AD/Th * deltaP
D (diffusivity)
Solubility/sqrt(MW)
O2 transfer time
time RBC spends to cross length of pulm capp ~0.75s (0.25s to ox, 0.5s capp reserve t)
DL (diffusing capacity)
AD/Th = VCO / PACO
diffusion limited
O2 supply lim by very slow ventilation, meas w/ CO
perfusion limited
O2 supply lim by supply to tissues, meas w/ N2O
O2 content
1.36Hbsat/maxsat
SaO2
(O2content - dissolved) / max = [100*(PO2)^2.8] / [P50^2.8 + PO2^2.8]
Henry's Law
[O2]dissolved = solubility PO2 = 0.003mmHg/dL PO2
1.36
g O2 that 1g of Hb can carry
cherry red
color of Ox or CO bl
dark red
color of deOx bl
blue
color of crab bl (due to Cu vs Fe)
tense state
state of Hb w/ low O2 affinity
relaxed state
state of Hb w/high O2 affinity, exhibits +coop
P50
PO2 to get 50% of Hb bound to O2, dec P50 = inc O2 affinity
right shift
effect of inc CO2 -> inc pH (Bohr fx), inc 2,3BPG, inc Temp on SaO2 curve/p50
Bohr effect
right shift of SaO2 curve in response to inc CO2 in tissues
2,3 BPG
causes rights shif of SaO2, made in response to chronic hypoxia
buffering power
H+ add before pH changes
Kassirer-Bleich Equation
mod of HH eq: [H+] = 24*CO2/[HCO3-]
incremental CO2
the small rise in [CO2] after being picked up by the tissues since not that much is expirated as you may think
Haldane effect
ibl dec CO2 carrying capacity when PO2 inc in lungs due to Hb-O2 driving off HbCO2
isopleths
keep 1 var const, change oth on graph
chloride (hamburger) shift
CA in RBC forms HCO3- -> exits via Cl-/HCO3- exchanger -> dec [Cl-]bl
buffer line
transverse line on Davenport dia that represents [HCO3-] if pH and PCO2 don't change
Davenport diagram
graphical representation of CO2 + H2O <-> H2O <-> H+ + HCO3-
respiratory acidosis
clinical: inc PCO2 -> inc HCO3- -> dec pH, ex: COPD
metabolic acidosis
clinical: dec pH -> dec HCO3-, no change in PCO2
apex
part of lung char by high resting vol, small Pip gradient (small vol inc w/insp), low ventilation
base
part of lung char by small resting vol, large Pip gradient (large vol inc w/insp), high ventilation
central chemoreceptors
loc on ventral medulla, sense PCO2 (within 3mmHg of set point) via H+ in CSF -> strong resp drive
peripheral chemoreceptors
include aortic arch (X) + carotid body (IX) Rs that sense change in PCO2, PO2, pH
carotid body chemoreceptors
very strong peripheral chemoreceptors, IX afferents, high metab activity (4x brain), bl supply 40x of brain, can be fine-tuned by ANS activity in order to inc medulla stim to inc resp drive
glomus cells
clusters w/ supporting sustentacular glia that are the sensory cells of the carotid and aortic bodies, responds to dec PO2 by closing O2sensitive K_ chans -> open VG Ca2+ chans -> send NTs to medulla (via IX for carotid or X for aortic)
DRG (dorsal respiratory group)
part of medulla active during inspiration
VRG (ventral respiratory group)
part of medulla active mainly for forced expiration (and some inspiration)
apneustic center
lower pontine resp group, allows longer medullary ramp input
pneumotaxic center
upper pontine resp group, turns off inspiration -> inc Va
cough reflex
mech/chem irritate -> upper airway chemRs -> X -> X -> cough, brochoconstrict
sneeze reflex
mech/chem irritate -> nasalRs -> V (olfactory) -> sneeze
Hering-Breur reflex
inflate/deflate lung -> stretch/J Rs -> X -> stop/start insp
pulmonary stretch receptors
sense inc Ptp -> stim expiratory off-switch
J receptors
aka juxtapulmonary cappillary or C-fiber endings, fire in response to lung injury, onver infl, edema, embolism (alveolar C fibers) or inflamm (bronchial C fibers) -> rapid shallow breathing, bronchoconstrict
hystersis
shift in P-V loop when inflating vs deflating = any phys char w/diff properties