SGU Physiology - Respiratory

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SGU Physiology Final - Respiratory System

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

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

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