PULMONARY PHYSIOLOGY

(everything from Watkins/Delaneys notes is in here, but theres some extra stuff from the physio for dummies text)
INTRODUCTION
Lung respiratory and conducting ones
!espiratory one " respiratory bronchioles, alveolar ducts # sacs
$onducting one " bronchioles, bronchi, trachea
%lveoli have largest cross&sectional area
'ronchioles have smooth muscle # cartilage
() divisions of branches into ever smaller conduits
*ucous&secreting, ciliated cells line conducting one air+ays, Large particles stop at nose, smaller
ones caught in cilia, finest particles (like asbestos) make it into alveoli
-as exchange can be divided into four functional components.
/entilation " movement of air into lungs (need pump to generate flo+, pipes slo+ do+n flo+ " !)
0erfusion " movement and distribution of blood through pulmonary circulation
Diffusion " movement of 1
(
and $1
(
across air&blood barrier or alveolar&capillary membrane
$ontrol of breathing " process of regulation of gas exchange to meet metabolic needs of moment
!espiratory 2uotient, !3 4 $1
(
produced 4 (55 ml/min, 4 5,6 (average)
$1
(
consumed (75 ml/min,
$arb !3 4 8, fat !3 4 5,9, protein !3 4 5,6
% 4 alveolar
a 4 arterial blood
v 4 venous blood
:on&respiratory functions of respiratory system.
(upper air+ay includes nose, paranasal sinuses, naso& and oropharynx, larynx)
8) route for +ater loss, heat elimination (+arms, moistens air so alveoli dont dry out " oxygen and
carbon dioxide cant diffuse across a dry membrane)
() enhances venous return (respiratory pump)
)) helps normalie p; by altering amount of $1
(
(;
<
&producing) exhaled
=) enables speech, singing, other vocaliation " larynx " vocal cords act as >vibrator
7) defends against inhaled foreign matter (filters particulates or microbes via mucous coat
propelled to+ards larynx by ciliary action, cough reflex, sneee reflex, immunoglobulins " both
locally produced and brought into lung from other sites)
?) removes, activates/deactivates various materials passing through pulmonary circulation (i,e,,
turns prostaglandins off, angiotensin @@ on)
9) nose " sense of smell
RESPIRATORY MECHANICS
)55 million alveoli in lungs " 5,) mm in diameter
total surface area of lungs is about 97 m
(
(sie of tennis court)
0ulmonary 0hysiology, (
collateral ventilation " airflo+ bet+een adAacent alveoli (via pores of Kohn)
pleuris " inflammation of pleural sac (painful Bfriction rubC)
atmospheric pressure 4 9?5 mm;g at sea level, decreases as altitude increases
intra!alveolar pressure (intrapulmonary pressure) +ill e2uilibrate +ith atmospheric pressure
intrapleural pressure (intrathoracic pressure) 4 97? mm;g " vacuum (called >&=)D closed cavity
EEnegative intra&alveolar, intrapleural pressures provide driving force for inhaling/exhaling
transmural pressure " pressure across surface of lungs, 4 0
alveolus
& 0
pleural space
F+o forces hold thoracic +alls # lungs in close apposition
(cant expand thorax +ithout expanding lungs)
8) intrapleural "lui#$s co%esiveness (like +ater bet+een t+o slides)
() trans&ural pressure 'ra#ient (most important)
intra&alveolar pressure 4 9?5 mm;g, pushes out against intrapleural p, of 97? mm;g
atmospheric pressure 4 9?5 mm;g, pushes in against intrapleural p,
:either chest +all nor lungs are in their resting position (both are actively pushing against space)
0leural space has slightly negative pressure because chest is pulling out, lungs are pulling in, and
theres no extra fluid to fill expanded space
Pneu&ot%ora( " air enters pleural cavity, pressure e2ualies +ith atmospheric pressure, transmural
pressure gradient is gone G lungs collapse, thoracic +all springs out
'efore inspiration " respiratory muscles are relaxed, no air is flo+ing, intra&alveolar p, 4 atm, p,
*aAor inspirator &uscles (diaphragm, external intercostals) contract G thoracic cavity enlarges
HDiaphragm is innervated by p%renic nerveD dome&shaped at rest, contracts # pulls do+n,
!esponsible for 97I of enlargement of thoracic cavity during inspiration, $ontraction of external
intercostals enlarges cavity in lateral and %0 dimensions (elevate ribs +hen contracting)J
%s lungs expand, pressure #ecreases )to *+, &&H'- G air "lo.s in
(alveolar pressure is negative during inhalation, positive during exhalation)
Intrapleural pressure #rops to *+/ &&H' (ensures that lungs +ill be fully expanded)
EELung expansion is not caused by movement of air into lungs,
With deeper contractions, contract diaphragm and external intercostals more forcefully # contract
accessor inspirator &uscles (K$*, scalenes, alae nasi, small muscles of neck/head) to raise
sternum # first ( ribs
%t end of inspiration " inspiratory muscles relax, diaphragm is dome&shaped again, rib cage falls
because of gravity once external intercostals relax, chest +alls # stretched lungs recoil G volume
decreases, pressure increases )to *01 &&H'- 2 air "lo.s out
During 2uiet breathing, expiration is passive (due to elastic recoil of lungs " no muscular/energy
expenditure), +hereas inspiration is al+ays active,
During heavy breathing " active e(piration " contract a3#o&inal &uscles (increase intra&
abdominal pressure G pushes diaphragm up G increases intrathoracic pressure), internal
intercostal &uscles (pull ribs do+n+ard, in+ard) G lungs are emptied more forcefully,
During forceful expiration, intrapleural pressure exceeds atmospheric pressure, but lungs dont
collapse because intra&alveolar pressure increases, too (= mm;g pressure gradient stays same)
0aralysis of intercostal muscles doesnt affect breathing much, but paralysis of diaphragm 4 cant
breathe, 0hrenic nerve is $)&$7, so patients +ith paralysis from neck do+n can still breathe,
%ir flo+
L
0ulmonary 0hysiology, )
Mlo+, / 4 N0/!
N0 4 pressure gradient bet+een atmosphere and alveoli
R is pri&aril #eter&ine# 3 ra#ius
!esistance of total air+ays circuit depends on O, length, cross&sectional area of conducting air+ays,
Pach ter&inal 3ronc%iole has greater resistance to flo+ than trachea, but because of vast cross&
sectional area, their overall contri3ution to total R is less t%an t%at o" central air.as (since
bronchioles are arranged in parallel),
@n healthy patient, overall respiratory system has extremely lo+ !
Laminar vs, turbulent flo+
Mlo+ can be laminar (lo+ flo+ rate) or turbulent (fast flo+ rate)
@n small air+ays, flo+ is usually laminar
Mor la&inar "lo., ! 4 6Ql (0oiseuilles La+) Q 4 viscosity, l 4 length
Rr
=
Tur3ulent "lo. has different properties " driving pressure is proportional to s2uare of flo+ (4
5
)
Furbulence is most likely to occur +ith %i'% velocit6 lar'e #ia&eter,
/olume of inflation of lung has important effect on air+ay resistance
0ressure 4 (vol,/compliance) < flo+ E resistance 0 4 pressure re2uired to breathe
$hronic obstructive pulmonary disease ($10D)
:arro+ing of lumina of lo+er air+ays, When air+ay ! increases, larger N0 must be present to
maintain same airflo+, Pxpiration is more difficult than inspiration " B+heeeC as air is forced out
through narro+ed passages, @n normal patients, smaller air+ays collapse " further outflo+ stops
only if lung volume is very lo+ (lungs can never be completely emptied)
$hronic bronchitis " triggered by fre2uent exposure to cigarette smoke, pollution, other allergens,
%ir+ay lining thickens, mucous production increases, ciliary mucous elevator is immobilied by
irritants, @ncreased mucous G bacterial infections
%sthma " obstruction due to 8) thickening of +alls b/c of inflammation, histamine&induced edema,
() plugging of air+ays by very thick mucous, )) air+ay hyperresponsiveness " trigger&induced
spasms (allergens, irritants, infection), *ost common chronic childhood disease,
Pmphysema " collapse of smaller air+ays, breakdo+n of alveolar +alls (irreversible), $an happen
because of 8) excessive release of trypsin from alveolar macrophages as defense against cigarette
smoke irritants (lungs normally protected by S
8
&antitrypsin, but can be over+helmed), () genetic
inability to produce S
8
&antitrypsin
(asthma and emphysema start in small air+ays " difficult to detect " >silent air+ays)
%mount of inspired air that makes it to alveoli depends on.
EEKtrength of pump (muscles)
EE%ir+ay resistance (frictional resistance, 65I total !)
EEPlasticity/compliance
EEFissue resistance " frictional resistance of lungs and chest +all ((5I total !)
EE@nertance " energy must be expended to set system in motion
(:eed to overcome stiff/elastic recoil, frictional resistance, and inertance)
0ulmonary elasticity
8) elastic recoil " returning to preinspiratory volume at end of inspiration
0ulmonary 0hysiology, =
() co&pliance " measure of distensibility, magnitude of change in volume for given transmural N0
Defined by slope of pressure&volume curve for lungs " curve is steep in normal operating range
(only at very lo+/high volumes does curve flatten), Nor&al co&pliance is 577 c&8&l H
5
O,
Different compliance for expiration/inspiration b/c of surfactant " %steresis, Static co&pliance is
measured +ithout airflo+D #na&ic co&pliance is measured during airflo+, (poor compliance 4
stiff lung, restrictive disease 4 more +ork to breathe)
0ulmonary elastic behavior depends on.
8) $F in lungs has lots of elastic "i3ers (arranged in mesh+ork)
() alveolar sur"ace tension
+ater molecules +ant to be close together " resist expansion of surface area (the greater the
surface tension, the less compliant the lung), @f alveoli +ere lined +ith +ater alone, surface tension
+ould be so great, air+ays +ould collapse,
pul&onar sur"actant (lipid&protein mixture) lo.ers sur"ace tension because +ater&
surfactant attraction is not as strong as +ater&+ater G increases pulmonary compliance, reduces
lungs tendency to recoil, 0roduced by tpe II pneu&octes
La0laces La+ 0 4 (F/r 0 4 in+ard&directed collapsing pressure, F 4 surface tension
Kmaller air+ays are more likely to collapse than large ones because of greater surface tension
(smaller r), but surfactant is more effective at lo+ering surface tension in smaller air+ays (less
spread out), Kurfactant stabilies small alveoli,
EEPvidence of these t+o factors of lung elastic recoil is found in differing pressure&volume
characteristics of saline&filled vs, air&filled lungs (saline&filled are easier to stretch than air&filled)
Tou can have separate pressure&volume curves for chest +all, lungs " combine to get one for total
respiratory system, F+o structures are in series, interdependent " force re2uired to inflate lung
e2uals sum of pressure difference across lung and across chest +all,
Inter#epen#ence of neighboring alveoli " surrounding alveoli resist collapse of another alveolus,
Respirator Distress Sn#ro&e )RDS- " not enough type @@ cells to make surfactant
Work of 'reathing
:ormally only re2uired on inspiration
Kubdivided into co&pliance .or9 (to expand lungs against lung/chest +all elastic forces)D tissue
resistance .or9 (to overcome viscosity of lung/chest +all)D air.a resistance .or9
Work 4 0 E /
*easurements of Lung /olumes
:!+; of total energy expended by body goes to breathing (heavy exercise " can increase 75&fold)
in obstructive lung disease, up to )5I of bodys energy expenditure is for breathing " even at restU
3uiet breathing " (,(55 ml (expiration) " (,955 ml (inspiration) tidal volume 4 755 ml
Ti#al volu&e )T4 or 4
T
- " 755 ml at rest, %mount entering/leaving lungs during one breath, %s
tidal volume increases, intrapleural and intra&alveolar pressures decrease in direct proportion,
Inspirator reserve volu&e )IR4- " ),555 ml, extra air you can breathe in, using inspiratory
muscles (beyond normal tidal volume)
Inspirator capacit )IC- " ),755 ml, @$ 4 F/ < @!/
0ulmonary 0hysiology, 7
E(pirator reserve volu&e )ER4- " 8,(55 ml, extra air you can breathe out, using expiratory
muscles (beyond normal tidal volume)
Resi#ual volu&e )R4- " 8,=55 ml, amount that cant be expired from the lungs (can measure +ith
tracer like helium)
<unctional resi#ual capacit )<RC- " (,755 ml, /olume of lungs after normal passive expiration,
M!$ 4 P!/ < !/
4ital capacit )4C- " =,?55 ml, *aximum volume change possible, /$ 4 @!/ < F/ < P!/
Total lun' capacit )TLC- " ?,555 ml, FL$ 4 /$ < !/
<orce# vital capacit )<4C- " total volume expired from maximum inspiration to maximum
expirationD normal range is 65&8(5I normal tidal volume,
<orce# e(pirator volu&e in 1 secon# )<E4
1
- " maximum volume that can be expired in one
second, MP/
8
4 65I /$ (normal)
Ma(i&u& &i#!e(pirator "lo. rate )MME<R- " <E<
5+!*+
" forced expiratory flo+ over middle
half of the M/$, gives us most information about small air+ays (V(mm diameter)
Pea9 e(pirator "lo. rate )PE<R- = <E<
&a(
" highest expiratory flo+ achieved, $an only be
measured from flo+/volume curve
Kpirometry
Kpirometer " air&filled drum floating in +ater, 'reathe into drum " records volume changes on
spirogram, *ost lung volume subdivisions can be measured directly from spirogram
trapped gas +ithin lung must be measured either by gas dilution method or by body
plet%s&o'rap%, Lung volumes can also be measured by x&ray " plani&etr
Spiro&etr can measure F/, @!/, @$, P!/, /$ (others measured indirectly, calculated)
<orce# vital capacit )<4C- maneuver " take in deepest breath possible, breathe out as much as
possible, Data can be displayed as volume vs, time or as flo+ vs, volume
if air+ays resistance is normal, MP/
8
W 95I
M/$
O3structive ventilator #e"ect " decreased air flo+ through tubes, normal tidal volume, $an be
from 8) upper air+ays diseaseD () peripheral air+ays disease (from asthma, cystic fibrosis, chronic
obstructive bronchitis, bronchiectasis)D or )) pulmonary parenchymal disease (emphysema),
Restrictive ventilator #e"ect " normal flo+, normal !, but small vital capacity, M/$, MP/
8
are
reduced (in ratio to each other), $an be chest +all, pleural, space&occupying intra&thoracic lesion,
extra&thoracic conditions (obesity, pregnancy, ascites), or interstitial lung disease, !eduction in
lung volumes belo+ 65I of predicted values,
Pxamples of lung volumes being smaller than predicted (restrictive defect).
Mibrosing (scarring) " increased elastic recoil
Diseases of chest +all (kyphoscoliosis) " increased elastic recoil
Diseases of the pleural space (pleural effusion) " compress lung
Fests of gas exchange function of lungs
Arterial 3loo# 'as #eter&ination (%'-s) " measurement of dissolved tensions of $1
(
and 1
(
as
+ell as p; of sample of arterial blood
Pulse o(i&etr " photometric measurement of saturation of hemoglobin +ith 1
(
, (non&invasive)
D
L
CO " diffusing capacity of lung for carbon monoxide, usually done by >sin'le 3reat%$ &et%o#
(D
L
$1
sb
), D
L
$1 is affected by factors other than characteristics of gas exchange membraneD
membrane thickness and increased surface area reduce D
L
$1,
/entilation (/ " ventilation, 3 " perfusion)
0ulmonary 0hysiology, ?
/olume of air breathed in and out in one minute
Respirator )&inute- ventilation6 4
?
4 F/ (ml/breath) E f, respiratory rate (breaths/min)
%t rest. ?,555 ml 4 755 E 8( (0 L air breathed in and out per min,)
With exercise, can increase (7&fold, to 875 L/min,
F/ is more important than respiratory rate +hen minute ventilation increases
Dea# space )4
D
- " volume of air&filled space incapable of gas exchange +ith blood
@Anato&ical #ea# space " 875ml, volume of conducting air+ays ()75ml used for gas exchange)
(e2ual to individuals lean body +eight in pounds)
Alveolar ventilation6 4
A
?
4 (F/ " /
D
, dead space) E f, respiratory rate
%t rest. =,(55 ml 4 (755&875) E 8(
%lveolar ventilation is about 7 L per minute 4 cardiac output (excellent transfer of gases)
:ormal respiratory rate is 15!1+ 3reat%s8&inute
EEif you breathe deeply # slo+ly, respiratory ventilation can stay same but alveolar ventilation
increases
EEif you breathe shallo+ly # rapidly, respiratory ventilation can stay same but alveolar ventilation
decreases (even to ero)
Pach tidal breath does not completely fill/empty an alveolus " reservoir o" 'as >store#$ .it%in
alveoli thats only gradually replenished, /olume 4 :6777 &l " prevents fluctuation in alveolar gas
tensions +ith each tidal breath,
(alveolar ventilation is more important measurement than respiratory ventilation, since thats +here
gas exchange is done)
alveolar 'as eAuation. 0
%
1
(
4 M
i
1
(
(0
'
" 0
;(5
) & (0
%
$1
(
/!)
solving for conditions at sea level # ! 4 5,6. 0
%
1
(
4 5,(8(9?5&=9) " (=5/5,6)
0
%
1
(
4 855
o3structive lun' #isease " easy to fill lungs, hard to empty
FL$ is normal
M!$, !/ are increased
/$, MP/
8
, MP/
8
//$I are decreased
restrictive lun' #isease " lungs are less compliant than normal
FL$, @$, /$ are decreased
!/ is normal
MP/
8
//$I is normal or even increased
Increasin' ti#al volu&e is most efficient +ay to increase alveolar ventilation (increase
respiratory rate and alveolar ventilation increases some+hat, but dead space is also increased)
:ot all alveoli are e2ually ventilated +ith air, perfused +ith blood G alveolar #ea# space
(minimal in healthy patients, but can be lethal) ventilated, but dont participate in gas transfer
p%siolo'ic #ea# space " sum of anatomical # alveolar dead space
lo.er re'ions o" lun' are 3etter ventilate# t%an upper BonesC
gravity is largely responsible, pleural pressure is more negative at top of thoracic cavity "
greater distending pressure for alveoli at top of lungs (top alveoli are larger in sie), alveoli on
bottom vs, top operate on different parts of a pressure&volume curve
lo.er re'ions o" lun' are 3etter per"use# t%an upper BonesC
0ulmonary 0hysiology, 9
gravity is primary determinant, hydrostatic pressure gradient from top to bottom b/c lo+est
point in lung is )5 cm belo+ highest point pressure gradient of )5 cm +ater 4 () mm;g (87
mm;g above heart, 6 mm;g belo+ heart)
0erfusion conditions in lung divided into three ones (a4pulm,art, %4intra&alveolar, v&pulm,vein)
Done 1E P
a
F P
A
collapse of vessel before it crosses alveolusD no for+ard flo+D doesnt exist in
normal lungs " might occur if person has hemorrhaged ('0, intravascular volume are lo+)
Done 5E P
a
G P
A
G P
v
flo+ driven by difference bet+een arterial/alveolar pressureD primary area
of distension, recruitment of vessels during exercise
Done :E P
a
G P
A
6 P
v
G P
A
continuous for+ard flo+ through distended vessels,
*atching of ventilation to perfusion
there is not perfect matching of ventilation to perfusion in most alveoli, non&uniform distribution of
both results in alveolar units +ith varying ratios of ventilation to per"usion )48H-
alveoli at ape( are overall poorly ventilated, perfused, but relatively better ventilated than perfused
4 high //3 ratio
if no perfusion but good ventilation, alveolar gas tensions +ill be same as in trachea (0
%
1
(
4 875,
0
%
$1
(
4 5), :o effect on do+nstream gas tensions " part of dead space, 'ut if there is some
degree of perfusion 0
%
1
(
+ill be high, 0
%
$1
(
+ill be lo+
alveoli at 3ase are +ell ventilated, perfused, but better perfused than ventilated 4 lo+ //3 ratio
if no ventilation, but some perfusion, alveolar gas tensions in unit +ill be same as those in mixed
venous blood (no fresh air being added), 0
%
1
(
+ill be lo+, 0
%
$1
(
+ill be high (blood exiting
capillary +ill be lo+ in 1
(
, high in $1
(
)
units +ith lo. 48H ratios %ave 'reater e""ect on overall 'as e(c%an'e since they receive greater
proportion of total pulmonary blood flo+,
% %i'% 48H unit can$t co&pensate "or i&pact o" lo. 48H unit because its at flat part of K&
shaped oxygen&hemoglobin dissociation curve " raises 01
(
, +hich results in more dissolved 1
(
, but
not much more ;b1
(
%ny rise in PCO
5
in arterial 3loo# stimulates respiratory centers to increase alveolar ventilation
removal of $1
(
through alveolar units +ith better //3 ratios, 1verventilation of these units
cant raise 0
a
1
(
since they are operating on flat upper portion of oxygen&;b saturation curve
*easurement of //3 mismatch
alveolar!arterial 'ra#ient " 0(%&a)D1
(
or %&a gradient " refers to pressure difference for 1
(

bet+een alveolar conditions and arterial blood, *easurement of inefficiency of oxygen transfer,
EEmeasurement of %&a exists even in normal patients, contributed to by 8) ventilation&perfusion
mismatch in normal lung, () small amount of shunt caused by bronchial, Fhebesian circulations,
EE%&a gradient can be calculated using alveolar gas e2uation to calculate expected ideal 0
%
1
(
,
measure actual 0
a
1
(
,
EE:ormal %&a gradient varies +ith age " rough estimate is (7I of persons age in years
EE@f %!a 'ra#ient is %i'%er than normal, due to.
increased //3 mismatch
increased shunt fraction
markedly abnormal diffusion of oxygen " rare clinically b/c of free diffusion of 1
(
, $1
(
0ulmonary 0hysiology, 6
4enous a#&i(ture " proportion of blood flo+ing through true right&to&left shunts or
hypoventilated lungs (units +ith lo+ //3 ratios) " &easure o" .aste# per"usion, $alculated from
variation of shunt e2uation.
3
va
4 $
i
1
(
& $
a
1
(
3
F
$
i
1
(
& $
v
1
(
P%siolo'ic #ea# space " proportion of ventilation to both anatomic dead space and hypoperfused
lung (high //3 ratios) " &easure o" .aste# ventilation, $alculated from e2uation.
/
D
4 0
a
$1
(
& 0
P
$1
(
/
F
0a$1
(
:ormal /
D
//
F
ratio during resting breathing is 5,( " 5,)7
-as Pxchange
CO
5
an# O
5
are exchanged via si&ple #i""usion " no active transporters " passively move do+n
partial pressure gradients,
When bulk movement of air ceases at terminal bronchioles, oxygen moves to+ards alveolus by
diffusion, carbon dioxide diffuses a+ay from alveolus,
ideal gas la+. 0/4n!F n 4 O moles of gas, ! 4 gas constant, F 4 absolute temperature
Iole$s La.. as volume of gas increases, pressure decreases
:ormal atmospheric air 4 9XI :
(
, (8I 1
(
, a little $1
(
, pollutants, etc,
Fotal atmospheric air pressure 4 9?5 mm;g, of +hich 9XI is from :
(
, (8I from 1
(
, etc,
0artial pressure of oxygen, P
O5
is nor&all 107 &&H' (or torr)
P
N5
is nor&all 077 &&H' P
CO5
is nor&all 7C7: &&H'
%lveolar 0
1(
W pulmonary capillary 0
1(
, so more oxygen goes into blood (diffuses until e2ual),
%lveolar 0
1(
V atmospheric 0
1(
because 8) air is +armed to )9Y$ # saturated +ith +ater once it
entersD +ater vapor adds =9 mm;g partial pressure, essentially >diluting partial pressure of other
gases, () air inspired is mixed +ith lots of old, BdeadC air (M!$), 1nly 18* o" total alveolar air is
replace# .it% eac% 3reat% (V87I alveolar air is BfreshC),
%verage alveolar 0
1(
is 855 mm;g, remains nearly constant throughout cycle (as does blood 0
1(
, as
does oxygen in blood available to tissues)
%verage alveolar 0
$1(
is =5 mm;g, also fairly constant
%verage arterial 0
1(
is 855 mm;g, 0
$1(
is =5 mm;g
'lood entering pulmonary capillaries is systemic venous blood (via pulmonary arteries),
systemic venous blood 0
1(
4 =5 mm;g, 0
$1(
4 =? mm;g
1
( expelled from lungs
4 1
( extracted, used by tissues
During exercise, venous blood 0
1(
can drop to )5 G increases N0 at alveoli G more 1
(
diffuses
from alveoli into blood,
1ther factors influencing rate of gas transfer
0artial pressure gradients are the main factor determining rate of gas transfer, but there are others,
Sur"ace area
during exercise, pulmonary bp increases b/c of increased cardiac output G forces open
many of previously closed pulmonary capillaries G increases surface area for gas exchange
emphysema " K% reduced because many alveolar +alls are lost " fe+er, larger chambers
(same +hen part of lung is collapsed or +hen part of lung is surgically removed)
Jall t%ic9ness
pulmonary edema " increased interstitial fluid bet+een alveoli and pulmonary capillaries,
caused by pulmonary inflammation or left&sided congestive heart failure
0ulmonary 0hysiology, X
pulmonary fibrosis " replacement of delicate lung tissue +ith thick fibrous tissue in response
to certain irritants
pneumonia " inflammatory fluid accumulation in/around alveoli, (viral/bacterial/aspirating
food)
increasing tidal volume increases surface area by stretching alveolar +alls, and makes +alls thinner,
$linical measurement of diffusion characteristics of alveolar&capillary membrane done by test
called >#i""usin' capacit "or car3on &ono(i#e )DLCO-C
%lveolar&capillary membrane has vast surface area (95 m
(
) +ith very short distance (5,7 microns)
for diffusion, Laers o" separation 3et.een air an# 3loo#.
8) fluid layer lining alveolus, containing surfactant
() alveolar epithelium " mostly type @ cells
)) epithelial basement membrane
=) interstitial space bet+een t+o basement membranes
7) capillary basement membrane " may be fused +ith epithelial '* (in +hich case
interstitial space is a potential space)
?) capillary endothelial cell membrane
Di""usion coe""icient
!ate of gas transfer is proportional to diffusion coefficient, D (related to solu3ilit K MJ)
D is proportional to (solubility)/(s2, root *W)
D for $1
(
is (5x D for 1
(
because $1
(
is far more soluble in body, Master diffusion rate is offset
by $1
(
s smaller N0 (? mm;g) than 1
(
(?5 mm;g), so CO
5
K O
5
#i""usion &ore or less
eAuili3ratesC @n diseased lung, 1
(
transfer is more seriously impaired than $1
(
transfer because of
the difference in diffusion coefficient,
0ulmonary caps and systemic caps are only t+o places in circulation +here gas exchange occurs,
%rterial systemic capillary blood. 0
1(
4 855 mm;g, 0
$1(
4 =5 mm;g
/enous systemic capillary blood. 0
1(
4 =5 mm;g, 0
$1(
4 =? mm;g (same as tissue conditions)
Fhe more actively the cell is metaboliing, the more cellular 0
$1(
rises, 0
1(
drops " more 1
(
diffuses
from blood into cells, more $1
(
diffuses from cells into blood,
:et diffusion of oxygen is from alveoli into blood, then from blood into tissues ($1
(
" opposite)
GAS TRANSPORT
1xygen is present in blood in t+o forms
total 1
(
content in arterial blood is 57 &l O
5
8177 &l 3loo#
0hysically dissolved in plasma " only 8,7I, because oxygen is not very soluble in body fluids
5,55) ml 1
(
/855ml blood can be dissolved for each mm;g of pressure, so nor&al #issolve# O
5

content o" 3loo# is 7C: &l O
5
8177 &l, Fissue 1
(
consumption is (75 ml/min at rest, so need extra
+ay to transport 1
(
,
0
1(
is related to oxygen dissolved, not oxygen bound to ;b
$hemically bound to hemoglobin (;b) " X6,7I 1,C* &l O
5
8177 &l 3loo#
;b < ;b1
(
(reversible)
!educed hemoglobin oxyhemoglobin
;b binds reversibly +ith 1C:/ &l O
5
per 'ra& o" H3, :ormal ;b content 4 87 grams
0ulmonary 0hysiology, 85
0
1(
determines ;b saturation
Pach ;b molecule has = Me, is capable of binding to = 1, Bfully saturatedC if = 1 are bound,
0
1(
of blood is most important factor determining I;b saturation (related to H1
(
dissolvedJ)
La. o" &ass action
if blood 0
1(
is increased (i,e,, in pulmonary caps), reaction shifts to right, get more ;b1
(
,
if blood 0
1(
is decreased (i,e,, in systemic caps), ;b1
(
dissociated, releases its oxygen,
1
(
&;b dissociation curve is K&shaped, not linear,
at 0
1(
4 855 mm;g, ;b, is X9,7I saturated
even at 0
1(
4 ?5 mm;g, ;b, is X5I saturated
from ?5&9?5 mm;g 0
1(
, ;b, saturation only changes 85I & provides margin of safety in 1
(
&
carrying capacity of blood, Pven if 0
1(
falls to ?5 mm;g (high altitudes, stuck in a vault,
pathological conditions), body can maintain high I;b saturation, *ixed venous blood carries
substantial amount of 1
(
" reserve +hich can be unloaded under extreme conditions (exercise),
at 0
1(
4 =5 mm;g, ;b, is 97I saturated (resting systemic capillaries, venous blood)
;b saturation decreases as cell metabolism increases
from 0
1(
4 5&?5 mm;g, a small drop leads to a steep drop in I;b saturation,
during strenuous exercise, up to 67I of ;b, gives up its oxygen
pulse oximeter can non&invasively measure ;b saturation
utiliBation coe""icient & I of ;b that gives up its oxygen as it passes through tissue capillaries,
:ormal value 4 5+;, can increase up to L+; #urin' e(ercise,
;emoglobin as a storage unit
EE;b, acts as Bstorage depotC for oxygen " removing oxygen from solution as soon as it enters
blood from alveoli, (+hen oxygen is bound to ;b,, it doesnt count to+ards 0
1(
), 1nce ;b is
saturated as much as it can be for that 0
1(
, then 1
(
coming into blood increases 0
1(
until it
e2uilibrates +ith alveoli,
EE;b, also helps get oxygen into tissues
0
1(
of systemic blood (X7 torr) is higher than tissue 0
1(
(=5 torr), so 1
(
diffuses across, 0
1(
drops G
;b has to release oxygen G 0
1(
increases, Diffusion continues until ;b cant unload more oxygen,
0
v
1
(
4 =5 torr until it reaches pulmonary capillary beds,
tissue 0
1(
is affected by rate of blood flo+ past tissues # rate of tissue metabolism,
;b plays role in total 2uantity of oxygen blood can pick up in lungs or drop off in tissues,
@f ;b levels are reduced by 75I (i,e,, +ith anemia), 1
(
&carrying capacity of blood drops by 75I,
1ther factors affecting ;b&1
(
affinity
0
1(
is most important factor affecting ;b&1
(
, but there are othersZ
M P
CO5
" shifts 1
(
&;b curve to right (less ;b1
(
at a given 0
1(
)
N pH (increased acidity) " shifts 1
(
&;b curve to right $1
(
;
(
$1
)
exercising muscles make more carbonic acid, lactic acid G forces ;b1
(
to unload more 1
(

at these tissues
Io%r e""ect " $1
(
# ;
<
can combine reversibly +ith ;b at site other than 1
(
binding site " reduces
1
(
affinity, @mportant in enhancing oxygenation of blood in lungs, releasing oxygen at tissues,
M te&perature " shifts 1
(
&;b curve to right (exercising muscles generate heat, demand more 1
(
)
EE%bove three factors are only in systemic capillaries, ;b has higher affinity for oxygen in
pulmonary capillaries than in systemic capillaries,
0ulmonary 0hysiology, 88
@nside !'$s, 56:!3isp%osp%o'lcerate )IPG- binds reversibly to ;b and re#uces O
5
a""init,
(,)&'0- is produced during !'$ metabolism, 0roduction gradually increases if ;b is chronically
undersaturated (+hen ;b1
(
is lo+ " high altitudes, anemia, some circulatory/respiratory diseases)
Kince (,)&'0- is present throughout circulation, it not only increases ;b1
(
s ability to unload
oxygen at the tissues, but it decreases its ability to load 1
(
from alveoli, (shifts curve to right)
$arbon monoxide poisoning
;bs affinity for binding to $1 is (=5x that for oxygen, ;b$1 4 carboxyhemoglobin
Pven small amounts of $1 make cells 1
(
&starved,
$arbon dioxide
$1
(
is transported in the blood in ) +ays
total $1
(
content in arterial blood is +, &l O
5
8177 &l 3loo#
8) physically dissolved " depends on 0
$1(
, normal 0
v
$1
(
4 =7 torrD normal 0
a
$1
(
4 =5 torr,
+; of $1
(
in arterial blood is dissolved (85I in venous blood),
() bound to ;b ;b$1
(
4 carbaminohemoglobin, +; of $1
(
in arterial blood ()5I in
venous blood), $1
(
binds to terminal amine groups of blood proteins " to 'lo3in part of ;b,
not heme part, ;b has greater affinity for $1
(
than ;b1
(
(;b1
(
becomes ;b at tissues,
picks up $1
(
)
)) transported as bicarbonate (;$1
)
&
) " ,7; in arterial blood (?5I in venous blood)
taking place rapidly, in !'$s, +ith car3onic an%#rase catalying first reaction.
CO
5
O H
5
7 H
5
CO
:
H
O
O HCO
:
!
;$1
)
&
is more soluble in blood than $1
(,

!'$ has ;$1
)
[
$l
&
carrier that passively facilitates diffusion of these ions (in opposite directions),
*embrane is relatively impermeable to ;
<
, so ;$1
)
&
diffuses alone,
;$1
)
&
diffuses out into plasma, $l
&
diffuses into !'$ 4 c%lori#e s%i"t
*ost ;
<
thats left behind binds to ;b (reduced ;b has greater affinity for ;
<
than ;b1
(
) " ;b
helps keep acid&base balance bet+een arterial # venous blood,
Hal#ane e""ect " removing 1
(
from ;b increases its ability to pick up $1
(
, ;
<
'ohr effect # ;aldane effect feed into one another
\ $1
(
, \ ;
<
\ 1
(
release
\ 1
(
release \ $1
(
, \ ;
<

CO
5
#issociation curve " depicts relationship bet+een 0
$1(
and total content of $1
(
in blood,
curve is much steeper than that for oxygen, =I volume of $1
(
is exchanged during normal
transport of $1
(
from tissues to lungs,
Respirator e(c%an'e ratio )R- " ratio of $1
(
output to 1
(
uptake,
! 4 /
$1(
/
1(
]nder normal resting conditions, =ml $1
(
. 7 ml 1
(
5,6 (65I)
PULMONARY ILOOD <LOJ
0hysiologic anatomy of pulmonary circulation
high flo+ (7L/min), lo+ pressure (87 mm;g), lo+ resistance (8&( mm;g/L/min) circuit
0ulmonary 0hysiology, 8(
pul&onar arter extends only 7 cm above !/ before dividing, /essels are thin&+alled,
distensible " can accommodate most of stroke volume of !/,
pul&onar capillaries form a dense net+ork in alveolar +alls " air spaces are nearly completely
surrounded by flo+ing blood, (large surface area for gas exchange, short air&blood barrier)
s&all pul&onar veins collect oxygenated blood from capillaries, run bet+een lobules, form four
lar'e pul&onar veins
0ressures in pulmonary circulation
pul&onar arter
systolic pressure averages (7 mm;g, diastolic pressure averages 6 mm;g,
mean pulmonary arterial pressure is 87 mm;g
distribution of blood in lung is not complex " only need enough pressure to lift blood to top of lung
+ork re2uired of !/ is much less than L/ !/ is less muscular than L/
pulmonary capillary pressure is estimated using "lo.!#irecte# pul&onar arter )S.an!GanB-
cat%eter to measure back pressure from L%, :ormal Bpul&onar capillar .e#'e pressureC
)PCJP- @ + &&H', Hhelps determine L% filling pressure (+ould be elevated +ith stenotic mitral
valve, left&sided congestive heart failure)J
pul&onar capillaries are surrounded by gas " subAected to pressure shifts occurring +ithin
alveolar spaces during ventilation, K+ings in alveolar pressure may affect flo+ pressure in caps,
if alveolar pressure is higher than pressure in capillary, it +ill collapse
pressure difference bet+een inside, outside of vessel 4 trans&ural pressure
larger pulmonary arteries, veins (Be(tra!alveolarC) are subAected to much lo.er pressures than
alveolar (smaller) vessels " pulled open as lung expands on inspiration
pul&onar vascular resistance )P4R- 4 input pressure " output pressure
blood flo+
0/! is about one!tent% t%at o" sste&ic circulation (8,9 mm;g/L/min), !esistance doesnt need
to be so high since there is no demand to regulate blood flo+ to various vascular beds/organs,
Lungs have mechanisms to 9eep pressures lo., With exercise, 3 through lungs increases several
fold, but pressure doesnt rise because 0/! decreases (via recruit&ent and #istension of air+ays)
as lung inflates, alveolar, extra&alveolar vessels are stretched,
'lood volume of lungs
normal blood volume of lungs is =75 ml (95ml in capillaries)
pulmonary vessels act as reservoir, accommodate up to t+ice as much blood volume,
volume of blood in lungs varies +ith intrathoracic p, " high intrathoracic pressure expels
blood from lungsD L/ failure causes pooling of blood in lungs rise in pulmonary p,
Mactors affecting vascular resistance
Passive c%an'es in vascular resistance
pulmonary arterial pressure (0%0) increase 0/! decreases
L% pressure increases 0/! decreases
blood volume increases 0/! decreases
transpulmonary pressure increases 0/! increases
Active c%an'es in vascular resistance " vessels are reactive because of smooth muscle in +alls
/asoconstriction.
0ulmonary 0hysiology, 8)
alveolar %po(ia " most potent stimulus causing vasoconstriction (adaptive mechanism to
match best ventilation +ith best perfusion) 0/! increases
aci#e&ia " 0/! increases
humoral substances " %ista&ine, prosta'lan#in <
5a
/asodilation.
humoral substances " AC%, prosta'lan#in E
1
, nitric o(i#e, 3ra#9inin
EE%:K stimulation has no effect on human 0/!
A##itional "unctions of pulmonary circulation
blood volume storage " change from standing to lying posture
filtration " stray blood clots
metabolic " biologic activation (angiotensin @ to @@ by %$P), inactivation (bradykinin,
serotonin, 0-P
8
, 0-P
(
, 0-M
(S
)
CONTROL O< RESPIRATION
B0acemakerC activity for respiration is in respiratory control centers of brain, Neural control o"
respiration includes.
8) factors responsible for alternatin' inspiration8e(piration r%t%& (match body needs)
() factors that re'ulate &a'nitu#e (rate, depth) of ventilation
)) factors that &o#i" respirator activit to serve ot%er purposes
both voluntar (i,e,, +ith speech) # involuntar (i,e,, sneee/cough) control,
Fhe &e#ullar respirator center is the primary respiratory control centerD provides output to
respiratory muscles, F+o other centers, in pons, apneustic center6 pneu&ota(ic center "
influence output from primary center,
$ell bodies for neuronal fibers of phrenic, intercostals nerves are in spinal cord, @mpulses from
&e#ullar center terminate there sti&ulate nerves "or inspirator &uscles, When neurons
are not firing, inspiratory muscles relax and expiration occurs,
Me#ullar respirator center
EDorsal respiratory group (D!-) " nucleus tractus solitariusD mostly inspirator neurons,
terminate on motor neurons that supply inspiratory muscles (initial processing station for feedback
from peripheral sensors)
E/entral respiratory group (/!-) " nucleus retroambiguusD 3ot% inspiratory # expiratory neurons
" both remain inactive during 2uiet breathing, $alled into play by D!- as >overdrive mechanism,
Pspecially important in active expiration, 1nly during active expiration do impulses travel to
expiratory muscles,
-eneration of respiratory rhythm comes from rostral ventro&e#ial &e#ulla, near upper (head)
end of /!-, Drives rate at +hich inspiratory neurons fire, !hythm starts +ith latent period of
several seconds, follo+ed by %0s, +hich crescendo over a fe+ seconds " leading to >ramp pattern
of inspiratory muscle activity,
0ontine centers exert >fine tuning influences on medullary center ensure normal, smooth
breathing, influence timing of s+itching bet+een inspiration # expiration, 0neumotaxic center
(upper pons) sends impulses to D!- to >turn o""$ inspirator neurons, %pneustic center (lo+er
0ulmonary 0hysiology, 8=
pons) prevents inspiratory neurons from being turned off, 1f the t+o, the pneumotaxic center
dominates, Without pneumotaxic >brakes, apneusis 4 prolonged inspiratory gasps +ith very brief
interrupting expirations, (can occur +ith severe brain damage)
$ortex " involved in voluntary control of respiration
;ypothalamus, limbic system " can alter pattern of breathing, i,e,, affective states like fear, rage,
!espiratory effects of brainstem transections (see page = of notes for diagram)
Erostral to pons (top) " little e""ect on spontaneous respiratory rhythm
E&i#!pontine" eliminates neurons associated +ith pontine respiratory group, removing tonic
excitation, resulting in slo.e# "reAuenc, increase# ti#al volu&e, 4a'us is also transected here "
input from lung stretch receptors is lost, resulting in apneusis
Eponto&e#ullar transection " irre'ular 3reat%in' pattern o" 'aspin' (loss of vagal afferents
has no effect)
Etransection o" spinal cor# " eliminates all descending drive, results in apnea
Kensors
Central c%e&oreceptors
near ventral surface of medulla in vicinity of exit of X
th
and 85
th
$:s
distinct from respiratory center neurons
bathed in brain P$M, respond to changes in H;
<
J (composition of P$M determined by $KM, local
blood flo+, and local metabolism)
$KM contains less protein than blood 4 poorer buffering capacity, change in 0
$1(
+ill change p;
of $KM more than it changes p; of blood,
Perip%eral c%e&oreceptors
$arotid bodies (most important), aortic bodies
!espond primarily to #ecreases in P
O5
" less so to decreases in p;, increases in 0
%
$1
(
,
When 0
a
1
(
falls belo+ 855 torr, rapid responseD 3elo. 07 torr " dramatic response
Glo&us cells in receptor release catec%ola&ines t%at sti&ulate 'lossop%arn'eal nerves
Pul&onar stretc% receptors
%ir+ay smooth muscle
Discharge in response to distension of the lungD activity sustained +ith lung inflation
@mpulse travels in vagus
;ering&'reuer reflex " +hen /
F
W 8 L (during exercise, etc,), pulmonary stretch receptors in small
muscle of air+ays are activated %0s travel through afferent nerve fibers to medullary center,
inhibit inspiratory neurons, (negative feedback to keep lungs from being over&inflated)
Irritant receptors
'et+een air+ay epithelial cells
Ktimulated by noxious gases, cold air, particulates
@mpulses travel in vagus, leading to bronchoconstriction, hypernea
PQR receptors
^uxta&capillary receptors in alveolar&capillary membrane
@mpulses travel in vagus rapid, shallo+ breathing
0ulmonary 0hysiology, 87
Ktimulated in interstitial lung disease or pulmonary edema
1ther receptors
E:ose and upper air+ay receptors " respond to mechanical, chemical stimuli (like irritant receptors
in lo+er air+ays)
E^oint, muscle receptors " impulses from moving limbs may be part of stimulus to increase minute
ventilation
E-amma system " muscle spindles in intercostals, diaphragm that sense elongation of these
muscles, strengthen contraction
E%rterial baroreceptors " increased systemic '0 can cause reflex hypoventilation, apnea,
(decreased '0 hyperventilation)
H;
<
J in brain P$M is primary regulator of ventilatory magnitude
%rterial blood gases are held very constant in normal range by varying magnitude of ventilation to
match bodys needs for oxygen uptake/carbon dioxide removal, Kignals sent to medullary
respiratory center sends signals to adAust rate/depth of ventilation,
Decreased arterial oxygen, increased carbon dioxide does stimulate ventilation, but H;
<
J is more
important,
!esponse to CO
5
6 P
a
CO
5
is &ost i&portant factor in control of ventilation under normal
conditions, 0
a
$1
(
is &aintaine# .it%in : torr +hen a+ake
/entilatory response to 0
a
$1
(
is reduced by sleep, increasing age, genetic factors, athletic training,
Central c%e&oreceptors are main playersD peripheral chemoreceptors play minor role
!esponse to 1
(
" minor role in control of normal ventilation, except at high altitudes
becomes important in chronic hypoxemia
!esponse to p; " difficult to separate from response to 0
$1(
Decreased 0
1(
*onitored by peripheral chemoreceptors " carotid/aortic bodies, :ot sensitive to modest changes
in 0
1(
, %rterial 0
1(
must be V ?5 mm;g (=5I reduction) for chemoreceptors to send afferent
impulses to medullary inspiratory neurons, (happens +ith severe pul&onar #isease6 re#uce#
at&osp%eric pressure), ]ntil you get to ?5 mm;g, youre still in plateau range of ;b&1
(

dissociation curve (safe), @f it +erent for peripheral chemoreceptors, the lo+ 0
1(
+ould depress
respiratory centers stop breathing, $hemoreceptors respond to 0
1(
, not oxygen content,
Ane&ia6 CO poisonin' " 0
1(
is normal, but total 1
(
is too lo+,
@ncreased 0
$1(
0
$1(
is most important input regulating magnitude of ventilation under resting conditions, $hanges
in alveolar ventilation have immediate, pronounced effect on arterial 0
$1(
(unlike 0
1(
), Pven slight
alterations from normal 0
$1(
induce significant reflex, @ncreased 0
$1(
increased ventilation,
Caroti#8aortic 3o#ies are onl .ea9l responsive to c%an'es in P
CO5
, Central c%e&oreceptors
in medulla are sensitive to c%an'es in CO
5
!in#uce# SH
O
T (not sensitive to $1
(
itself),
''' is permeable to $1
(
, so increased arterial 0
$1(
increased brain P$M 0
$1(
increased H;
<
J
stimulates central chemoreceptors increases ventilation by stimulating respiratory centers,
0ulmonary 0hysiology, 8?
H
O
can$t per&eate III " reason central chemoreceptors dont respond to H;
<
J in plasma, @f you
hold your breath W 8 minute, $1
(
builds up, H;
<
J in brain P$M builds up, increased 0
$1(
&;
<

stimulant to respiration overrides voluntary input to respiratory centers, and breathing resumes,
4er %i'% CO
5
levels #irectl #epress entire 3rain, including respiratory centers (like lo+ 1
(

does), @f you increase 0
$1(
up to 95&65 mm;g, ventilation increases to blo+ it off, A3ove L7
&&H'6 respirator neurons are #epresse# respirator aci#osis, (!eason +hy, in closed
environments like space shuttle/submarine, you need something to remove $1
(
, pump in 1
(
,)
With some kinds of COPD" prolonged hypoventilation elevated 0
$1(
and reduced 0
1(
, ]sually
synergistic " sum of stimulatory inputs is greater than individual, 'ut in some severe cases, patient
loses sensitivit to %i'% P
CO5
C 0rolonged high H;
<
J in brain P$M allo.s ti&e "or HCO
:
!
to cross
III and buffer/neutralie ;
<
, 'rain P$M H;
<
J seems normal, and body is una+are of high 0
$1(
,
Level of ventilation is unusually lo+, considering high 0
$1(
, @n this case, hypoxic 1
(
drive to
increase ventilation becomes primary respiratory stimulus,
H;
<
J in arterial blood
Aortic8caroti# 3o# c%e&oreceptors are %i'%l responsive to c%an'es in SH
O
TC %ny change in
0
$1(
leads to change in H;
<
J (in both arterial blood # brain P$M), @ncreased H;
<
J in arterial blood
stimulates ventilation, though central chemoreceptors are more important stimulant, Arterial SH
O
T
can c%an'e .it%out increase# P
CO5
" i,e, during diabetes mellitus because of increased keto acids
in the blood, Fhe peripheral chemoreceptors sensitivity to changes in H;
<
J serves to regulate the
acid&base balance,
Pxercise increases ventilation " +hy_
%lveolar ventilation can increase up to (5&fold +ith exercise, Tet,
0
1(
stays the same, or even increases a little,
0
$1(
stays the same, or even decreases a little
During &il#8&o#erate e(ercise6 SH
O
T #oesn$t increase because $1
(
is held constant, With %eav
e(ercise, though, SH
O
T increases 3ecause o" lactic aci# buildup (from anaerobic metabolism),
/entilation increases +ithin a fe+ seconds of exercise " not long enough for changes in arterial
blood gases to stimulate it, *echanism for its increase is poorly understood, 0ossible reasons are.
8) re"le(es "ro& 3o# &ove&ents " Aoint/muscle receptors excited during muscle contraction
stimulate respiratory centers (reason even passive movement increases ventilation)D
() increase# 3o# te&perature " energy generated during muscle contraction is converted to heat
(same reason increased ventilation accompanies fever)D
)) epinep%rine release from adrenal medulla increases during exerciseD
=) i&pulses "ro& cere3ral corte(, especially at onset, to respiratory center # muscles
/entilation can be influenced by other factors, beyond 1
(
/$1
(
EProtective re"le(es " sneeing, coughing, govern respiratory activity temporarily,
EPain reflexly stimulates respiratory center,
EE&otional e(pressions " laughing, crying, sighing, groaning,
E!espiratory system reflexly inhibited during s.allo.in',
0ulmonary 0hysiology, 89
ECere3ral corte( allo+s for voluntary control of breathing " sends impulses directly to motor
neurons in spinal cord that supply respiratory muscles, (Tou can voluntarily hyper& or
hypoventilate to a certain point,)
Local controls on smooth muscle of air+ays, arterioles
**If alveolus has too much blood compared to air
1
(
level in alveolus and surrounding tissues falls belo+ normal (blood is extracting more 1
(
from
alveolus), Decrease# SO
5
T 2 vasoconstriction 2 re#uce# 3loo# "lo.
**If alveolus has too much air compared to blood
Increase# SO
5
T 2 vaso#ilation 2 increase# 3loo# "lo.
(opposite of effect in systemic circulation, +here decreased H1
(
J leads to vasodilation)
%s a result of $1
(
# 1
(
local controls, little air/blood is +asted G most efficient exchange possible
%:K can modestly adAust air+ay sie
'ronchomotor tone is provided by smooth muscle in air+ay +alls,
Paras&pat%etic c%oliner'ic neurons on &uscarinic receptors (2uiet, relaxed situation)
promotes 3ronc%oconstriction (via smooth muscle contraction)
%$h, methacholine, humoral substances (histamine), decrease in 0
%
$1
(
S&pat%etic a#rener'ic neurons on bronchiolar 3eta receptors cause 3ronc%o#ilation to ensure
maximum airflo+ +ith minimum resistance (more oxygen available),
$irculating catecholamines " epinephrine, isoproterenol
`
(
adrenergic receptors (albuterol " `
(
agonist)
Work capacity
'est single predictor of a persons +ork capacity is maximum volume of 1
(
the person can use per
minute to oxidie nutrients for energy production, 4 &a(i&al o('en consu&ption6 &a( 4O
5
,
;ave person exercise until exhausted " measure volume of air, 1
(
, $1
(
content, /1
(
depends on
respiratory system, circulatory system, muscles,
!espiratory states +ith abnormal blood gas levels/abnormal breathing patterns
Asp%(ia " oxygen starvation of tissues (lack of 1
(
in air, respiratory impairment, or inability of
tissues to utilie oxygen)
Canosis " blueness of skin from insufficiently oxygenated blood in arteries
Eupnea " normal breathing
Hpernea " increased pulmonary ventilation to meet increased metabolic needs (exercise)
Hperventilation " increased pulmonary ventilation in excess of metabolic needs
0
$1(
a, get respiratory alkalosis (anxiety, fever, aspirin poisoning) voluntary or involuntary
Hpocapnia " belo+ normal $1
(
level in arterial blood, caused by hyperventilation
Hpoventilation " underventilation in relation to metabolic re2uirements
0
$1(
\, get respiratory acidosis
Hpercapnia " excess $1
(
in arterial blood, caused by hypoventilation
Hpo(ia" insufficient 1
(
at cellular level, inade2uate tissue oxygen deliveryD determined by cardiac
output, oxygen content of arterial blood, tissue oxygen uptake,
%nemic hypoxia. reduced 1
(
&carrying capacity of blood (decreased !'$s, ;b in !'$s, or
$1 poisoning) P
O5
is nor&al6 3ut O
5
content is too lo.
$irculatory hypoxia. (stagnant hypoxia) too little oxygenated blood delivered to tissues, can
be restricted to one area (local vascular spasm/blockage) or generalied (congestive heart
0ulmonary 0hysiology, 86
failure, circulatory shock) arterial P
O5
6 O
5
content nor&al6 3ut not enou'% 3loo# reaches
cells,
;istotoxic hypoxia. inability of cells to utilie oxygen available to them (cyanide poisoning)
;ypoxic hypoxia. caused by 8) respirator &al"unction involving inade2uate gas
exchange (normal alveolar 0
1(
, but reduced arterial blood 0
1(
) or () exposure to %i'%
altitu#e8su""ocatin' environ&ent (alveolar # arterial 0
1(
are reduced),
Hpo(e&ia " reduction in tension of oxygen dissolved in blood (reduced 0
a
1
(
), @f severe enough,
leads to ;b desaturation reduced $a1
(
Respirator arrest " permanent cessation of breathing
Su""ocation " 1
(
deprivation as result of inability to breathe oxygenated air,
Hpero(ia " above normal 0
1(
D impossible if breathing normal atmospheric air at sea level,
'reathing supplemental oxygen can increase alveolar and arterial 0
1(
" total 1
(
content isnt
changed much since ;b +as already X9,7I saturated, @f 0
1(
is too high o('en to(icit (brain
# retinal damage)
'iots breathing " a series of breaths of e2ual depth irregularly alternating +ith period of apnea
(seen most often in &enin'itis)
%pneustic breathing " prolonged inspiratory gasps (seen in %ea# trau&a, neurolo'ic #isor#ers)
$heyne&Ktokes " gradual increase in depth, sometimes rate, to a maximum, follo+ed by gradual
decrease, resulting in apnea, Ccles are :7 secon#s to 1 &inute in length, (seen in severe
%po(e&ia, at %i'% altitu#es +hile asleep, in severe %eart #isease or 3rain #a&a'e)
%pnea " transient cessation of breathingD during sleep, ventilation decreases # central
chemoreceptors are less sensitive to arterial 0
$1(
(especially during !P* sleep), Kleep apnea " may
stop breathing for a fe+ seconds or up to 8&( minutes 755 times per nightU
1bstructive " cessation of ventilation due to intermittent obstruction of the pharynx by the
tongue during sleep, $entral controller output is increased,
$entral " intermittent cessation of central controller output cessation of ventilation
Kudden infant death syndrome (K@DK) " (&= month old babies, often +ith poorly developed carotid
bodies, Kleeping on stomach, exposure to nicotine increases chances,
Dyspnea " difficult/labored breathingD people have subAective sensation that they are not getting
enough air, feel shortness of breath even though their 0
$1(
, 0
1(
may be normal, $an be from
anxietyD increased +ork of breathing due to restrictive/obstructive factors
$onditions at high # lo+ altitudes
Mountain cli&3in' " %t 85,555 feet, 0
1(
falls into steep part of 1
(
&;b dissociation curve " ;b
saturation rapidly declines as you go above 85,555 feet (not in plateau range anymore), %t 86,555
feet, atmospheric pressure 4 )65 mm;g, 0
1(
4 =7 mm;g, Acute &ountain sic9ness " hypoxic
hypoxia, hypocapnia&induced alkalosis ($1
(
blo+n off more rapidly than produced),
Deep sea #ivin' " atmospheric pressure doubles at )5 feet belo+ sea levelU *ore :
(
dissolves in
tissues nitro'en narcosis (Brapture of the deepC), %t 875 feet under " euphoric, dro+sy, %t
)75&=55 feet under " lose consciousness (oxygen toxicity),
@f you ascend too 2uickly " #eco&pression sic9ness (Bthe bendsC), :
(
forms bubbles as it 2uickly
converts from solution into gas,