Theabsoluterefractoryperiodiscausedbytheclosingofthe

excitatoryNa+channels.Thedurationoftheabsoluterefractoryperiod
isfixedwhilethatoftherelativerefractoryperiodisnot.
Theabsoluterefractoryperiodistheintervalfromthebeginningofthe
actionpotentialuntilthefiberisabletoconductanotheraction
potential.Therelativerefractoryperiodfollowsandis
thetimeperiodinwhich,althoughthecellhasnotfullyrecovered,a
small,weakactionpotentialcanbegeneratedastheresultofastrong
inputstimulus.Theabsoluterefractoryperiodisthetimeperiod
duringwhichtherapidinfluxofNa+rapidlydecreasesthenegativityof
thecardiaccell.AsVm(membranepotential)approacheszerothe
electrostaticforcepullingNa+intothecellisneutralized.The
concentrationgradientofNa+howevercontinuestopushNa+intothe
cellandthecellbeginstohyperpolarizeasVmbeginstobecome
positive.ThisclosingoftheNa+channelssignalsthebeginningofthe
absoluterefractoryperiod.Oncethesechannelsclose,theycannot
reopenforasetperiodoftime.WhenVmbecomespositivebyabout
20mV,Na+continuestotoenterthecellbecausetheconcentration
gradientoverpowerstheelectrostaticforces.Theinfluxisslow
however,andmanyoftheinactivationgateshavealreadyclosed.At
about30mV,Na+influxceases.Thechannelsremaincloseduntilthe
firsthalfofrepolarization,andthusthecellisabsolutelyrefractory
duringthisentireperiod.Noactionpotentialcanbegeneratedbythe
cellduringthistime,andthecellwillnotrespondtofurther
excitation.Thismechanismpreventssustained,tetaniccontractionof
cardiacmuscle.Tetanuswouldprecludethenormalintermittentpumping
actionoftheheartandinterruptthepatternofelectricalconduction
throughoutthecardiacmuscle.Theresultwouldbefibrulation.The
relativerefractoryperiodimmediatelyfollowstheabsoluterefractory
period,andisduetotheeffluxofK+ions.Duringthesecondhalfof
repolarization,theexcitatoryNa+channelsaremostlyreadytoopen,
andasmallweakactionpotentialcanbegenerated.However,itis
bettertowaituntilthechannelsarefullyreadybeforecontinuingwith
thenextexcitation.Fullexcitabilityisnotregaineduntilthe
cardiacfiberhasbeenfullyrepolarized.Inorderforanaction
potentialtobegeneratedduringtherelativerefractoryperiodthe
stimulusmustbegreaterthanthatwhichwouldnormallyelicita
response.Unliketheabsoluterefractoryperiod,thedurationofthe
relativerefractoryperiodcanchange.Asheartrateincreases,and
systoledecreases,theactionpotentialbecomesnarrowerduetoa
decreaseinrelativerefractoryperiod.Atrest,theheartrateslows,
andtheactionpotentialbecomeswiderastherelativerefractoryperiod
increases.Thisallowsgreateroxygensupplytoreachneedyareas
duringexerciseandotherstressconditions.Theserefractoryperiods
areimportantbecauseduringthistimethegradientconcentrationsof
importantions(Na+,K+)arerestored.Thisallowsfurtherexcitation
ofthecardiacfiber.Theresultsoftherefractoryperiodscanbeseen
intheplateauofthecardiacfiberactionpotential.

PulmonaryPhysiology

Respiratorysystemhastwoimportantsections:conductingand
respiratoryzones.Conductingzoneswhereairtravelsand
respiratoryzoneswhererespirationhappens!
Generation116conducting.1723=respiratoryzone.
Conductingzone:ciliapermitthemovementofairfasterintothe
respiratoryzone,ciliaiswherenoalveolus!Freshairpass
throughthispart,usually150mlofair.Itiscalledthe
anatomicaldeadspace.
Anatomicaldeadspacequantityofvolumepassingthroughto
alveolus.Whyistherethisdeadspace?Meansnogasexchange!
Asfreshairmovingwithaidofcilia,reachrespiratoryzone,we
reachcertainalveolusandhavegasexchange.Eachoneofalveolus
surroundedbyalveolarvesselsalsoknownaspulmonary
capillaries.Simplediffusionoxygenpassalveolustocirculation,
whereastheco2passesfromcirculationtoalveolus.
Thevolumeinsiderespiratoryzone,depends,23L.
Inspirationdiaphragmcontracting,itdescends,increasingvolume
oflungs.Whenbreathingnormallytidalvolume!
Anotherpatienthavingdiseasechestradiographybreathe
forcefullypatientinspiringcontraction!Normalbreathing
diaphragmdescend1cm,butforcefullyinspirationdiaphragm
descend10cm,thatswhenpictaken!
Theribsgoup,increasecrosssectionalareaduringinspiration.
Eachalveolisurroundedbygasbloodbarriersurfaceareaof50
100m.
LungshavepleuraFRC,openglottisrelaxrespiratorymuscles2
3cmofpressure
Elasticityandresistance,resistanceinlungsarereduced!When
inexercise,bloodreacheslungstheresistancereducedtoenhance
thecardiacoutput!
ThecontrolofrespirationCNSdorsalinspirationinmedulla
activated!Sympatheticsignals.Expirationventralexp.,expel
airtooutside.
Lungsinrespiratoryzones,containsurfactant,type2alveoli
cells,ifwedonthavesurfactantairisgonnadryproduce
collapseofalveoli.
Alveolarpressuregreaterthanarteriolepressurecollapse!
Pneumothorax!
Momentinspiring,noseciliacleanfrombadparticles.Thosecilia
preventtheseharmfulsubstancesfrompassing.
Sinusesproducemucous.Maintaindustparticles,wespeakbecause
ofthesinuses.Frontalsinusesprotectfromheadtrauma.

Tracheaissensitivetopresenceofbacteria.

Problemwiththemdecreaseproductioninunhealthypatients,and
haverespiratoryproblems!

Alveolarmarcophagestheyarepresentinlungs!Getridof
bacteriavialysosomes,killthebacteria!Lifespan1to5
weeks,onceprotectingus,movetolymphaticcirculationanddie.

Reflexesbrainisactivatedandinvoluntarilybreathhigher,
inspirationgreater,diaphragmdescend,pressureinlungsrise,
intercostalmusclespulldiaphragmdrastically,uvulaisdescend
Coughreflex!Particleintrachea,receptorssendinfotobrain,
braincoughcenterisactivated,involuntariyforceful
respiration.
Bronchoconstrictionpatientwithasthma,histamineless!Patient
notgonnalive.Leukotrieneshavepatientgreat!Forbroncho
constriction.Blockingtheproductionofleukotrienesprotect
them!
Aplacewithcontaminationbronchoconstrictionpresentasa
defensemechanism.

Aalveoli,aarteriole

Nitrogenandoxygeniswhatwebreathe!

Daltonsbarometricpressure=nitrogen+oxygen+watervapor
pressure+co2
Barometricpressureatsealevel760mmHg,subatmospheric0atm.
Cusco,highelevationhyperventilationandmoreRBCSproduction.
Doublesofventilation=80mmhg,andlower20mmhg
hypoventilation.Normalis100mmHg

Ventillation:
Spirometer- device, insert tube in mouth, subject expires
prolonged and forcefully in order to check different volumes and
capacity.
Patient expires, the bell goes up and pen goes down! The first
important volume- tidal volume- 500 ml, normal breathing!
Inspire forcefully- oscillation goes up. Expiration- goes down.
TL+IRV = inspiratory reserve capacity
TL+ERV+IRV= vital capacity
Expiration after the normal tidal volume- functional residual
capacity.
FRC= ERV+RV
Residual volume- maximum expiration, but we expire all we can
and the remaining air after forceful expiration is called residual
volume.
FRC= is part of residual volume, erv
Residual volume cant be measured by spirometer.
Pletysmograph can measure RV, FRC
TLC= VC+FRC+RV
Tlc frc, rv CANT BE measured by spirometer, but pletysmograph!
Our tidal volume 500 ml

Restrictive disease- patient cant have normal entrance of air,

smaller chest- fibrosis, ribs fractures, so lungs cant expand!
Fibrotic tissues- cant expand. Rib fractures- it hurts to expand.
Obstructive disease- hyperinflation. TLC greater than normal
lung, because of RV increases abnormally. Increase compliance,
inspiratory efforts increase!
Example- emphysema, constant smoker, destroying alveoli, can
breathe but cant breathe completely.
Obstruction of single alveolar capillary pressure, oxygen partial
pressure will be 80 instead 100, tissues have hypoxia
The role of surfactant- decrease the surface tension, which is
caused by intramolecular attractions in the surface of alveoli,
causes the tendency to collapsealveolus is like a bubble, inside
it is covered by thin layer of water, inside is filled by airwater
molecules have attraction, intramolecular attraction.the
attraction of water molecules makes circle smaller, surfactant
reduces surface tension so lungs can expand easily.
Lung when overstretched when high volume, and becomes rigid,
so compliance increases.
Giving difference between pressure and volume when inspiring
and expiring, its related to surface tension.
Compliance is change of volume over change in pressure.
Water filled lung is more compliant.we dont have air water
interface! So no surface tension
Tidal volume avg- 500 ml
Intrapleural space pressure- negative 5
Intrapleural pressure in apex and base is not the same! Because
of gravity. The chest wants to expand but lungs want to collapse.
The greater the force in opposite direction- intrapleural
pressure.the greater recoil tendency of lung the more negative
the intrapleural pressure
Alveoli in apex larger than base, more compliant in base alveoli,
less distended, -2.5.
The base of lung is better ventilated.

Problems Notes
In order for proper gas exchange to happen, ventilation and blood flow
need to match. If perfusion exceeds ventilation, the amount of oxygen
diffusing into the capillary blood and the amount of carbon dioxide
diffusing out of capillary blood are reduced. Lower than normal Po2 and
higher than normal CO2, the lower Po2 will cause vascular resistance
to rise!

A rise or fall in the oxygen saturation of hemoglobin is caused by a

decrease in the arterial O2 tension, from a low V/Q ratio,
hypoventilation or anatomical right to left shunt.
The physiological dead space includes the anatomical dead space (the
conducting airways) and the areas of the lung that are ventilated by
not perfused or poorly perfused, the areas of the lung with a high V/Q
ratio.
During inspiration respiratory muscles pull the chest wall out and the
diaphragm down and IP becomes more negative.