Physiology of RS 2

8/9/2019 Physiology of RS 2

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The Respiratory System: Gas

Exchange and Regulation of Breathing


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Diusion of Gases

Partial Pressure of Gases (Pgas)

• Concentration of gases in a mixture (air

• Gases mo!e from areas of high partial pressure to

areas of lo" partial pressure• #o!ement of gases also occurs $et"een cells and

the $lood in the capillaries

• #o!ement of gases occurs $et"een $lood in the

pulmonary capillaries and the air "ithin theal!eoli – #o!ement of gasses is $y diusion across the

respiratory mem$rane of the al!eoli


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Dalton%s &a" of 'artial'ressure•

Each gas in a mixture (air tends to diuseindependently of all other gases – xygen does not interfere "ith car$on dioxide

diusion or !ice !ersa

• Each gas diuses at a rate proportional to itspartial pressure gradient until it reachese)uili$rium – This allo"s for t"o*"ay tra+c of gases in the lungs

and in the $ody tissues

• The total pressure exerted $y a mixture ofgases is the same as the sum of the pressureexerted $y each indi!idual gas in the mixture

– 'air , '-. / '. / '0.


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• The partial pressure of a gas is the pressure exerted$y each gas in a mixture and is directly proportional toits percentage in the total gas mixture (0enry%s &a"

• Example: 1tmospheric 1ir

• 1t sea le!el2 atmospheric pressure is 345 mm0g

– 1ir is 6378 -itrogen• The partial pressure of nitrogen ('-. is:

– 5937 x 345 mm0g , '-. , ;< mm0g

– 1ir is 6 .=8 xygen

• The partial pressure of oxygen ('. is:

– 59.= x 345 mm0g , '. , =45 mm0g

– 1ir is 6 595>8 car$on dioxide

• The partial pressure of car$on dioxide ('C. is:

– 59555> x 345 mm0g , 'C. , 59< mm0g9

'artial 'ressure:1tmospheric 1ir


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•

Composition of the partial pressuresof oxygen and car$on dioxide in thepulmonary capillaries and al!eolarair: – 'ulmonary arterial capillary $lood

• 'C. of pulmonary capillary $lood is >

mm0g

• '. of pulmonary capillary $lood is >5mm0g

– 1l!eolar air:

• 'C. of al!eolar air is >5 mm0g

• ' of al!eolar air is =5> mm0g

'artial 'ressure: 1l!eolar 1ir


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Solu$ility of Gases in a&i)uid• The a$ility of a gas to dissol!e in "ater

• ?mportant $ecause . and C. are

exchanged $et"een air in the al!eoli and

$lood ("hich is mostly "ater• E!en "hen dissol!ed in "ater2 gases exert

a partial pressure

•

Gases diuse from regions of higherpartial pressure to"ard regions of lo"erpartial pressure


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Gas Exchange in the &ungs

• Gas exchange occurs $y diusion across therespiratory mem$rane in the al!eoli

• xygen diuses from the al!eolar air intothe $lood

– 1l!eolar air '. , =5> mm0g

– 'ulmonary capillaries '. , >5 mm0g

• Car$on dioxide diuses from the pulmonary

capillary $lood into the al!eolar air – 'ulmonary capillaries 'C. , >4 mm0g

– 1l!eolar air 'C. , >5 mm0g


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Gas Exchange in Respiring Tissue• Gas partial pressures in systemic

capillaries depends on the meta$olicacti!ity of the tissue

•xygen concentrations – Systemic arteries '. , =55 mm0g

– Systemic !eins '. , >5 mm0g

• Car$on dioxide concentrations – Systemic arteries 'C. , >5 mm0g

– Systemic !eins 'C. , >4 mm0g


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Transport of Gases in the Blood:.•

;78 of . is transported in com$ination "ithhemoglo$in molecules (;78

– .8 of . is dissol!ed and transported in the plasma

• 0emoglo$in (0$ – 1 protein found in RBCs

– . $inds loosely to 0$ due to its molecular structure

• 0emoglo$in consists of four polypeptide chains – Consists of > glo$in molecules2 each of "hich is $ound to

a heme group

– The heme group contains an iron molecule2 "hich is thesite of . $inding

• Each 0$ molecule is a$le to carry > molecules of.


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• . $inds temporarily2 or re!ersi$ly2 to 0$

• xyhemoglo$in (0$.

– 0$ / . , 0$.

– 0$ attached to four . molecules is

saturated

– Saturated 0$ is relati!ely unsta$le and

easily releases . in regions "here the'. is lo"

• Deoxyhemoglo$in (00$

– 00$ , 0$ / .

Transport of Gases in the Blood:.


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The 0emoglo$in*xygenDissociation Cur!e

• Descri$es the relationship $et"eenthe aterial '. and 0$ saturation

• The 0$* . Dissociation Cur!e plots thepercent saturation of 0$ as a function of

the '.


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Hb Saturation• @ull saturation

– 1ll four heme groups of the 0$ molecule in the $lood

are $ound to .

• 'artial saturation – -ot all of the heme groups are $ound to .

• 0$ saturation is largely determined $y the '.

in the $lood• 1t normal al!eolar '. (=5> mm 0g2 0$ is

;39 * ;78 saturated


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Hb Unloading of O2

• @actors that increase . unloading

from hemoglo$in at the tissues: – ?ncreased $ody temperature

• Decreases 0$ a+nity for .

– Decreased $lood p0 (the Bohr eect• 0/ ions $ind to 0$

– ?ncreased arterial 'C. (the Car$amino eect


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The Bohr Eect•

Based on the fact that "hen . $inds to 0$2certain amino acids in the 0$ moleculerelease 0/ ions

– 0$ / . A 0$. / 0/

– 1n increase in 0/ (a decrease in p0 pushes thereaction to the left2 causing . to dissociate from

0$

• 0$ a+nity for . is decreased "hen 0/ ions

$ind to 0$2 therefore . is unloaded from 0$• 0/ concentration increases in acti!e tissues2

"hich facilitates . unloading from 0$ so that

it may $e utilied $y the acti!e tissues


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• Based on the fact that C. may $ind

to 0$

– 0$ / C. A 0$C.

– 1n increase in 'C. pushes the reaction

to the right2 formingcar$aminohemoglo$in (0$C.

• 0$C. decreases 0$ a+nity for . – This decreases . transport in the $lood

• The car$amino eect is one methodof trans ortin C in the $lood

The Car$amino Eect


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• These factors are all present duringexercise and ena$le 0$ to release

more . to meet the meta$olicdemands of "oring tissues – $ody temperature , 0$ a+nity for

.

– 0/ ions ( p0 , 0$ a+nity for .

– arterial 'C. , 0$ a+nity for .



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Transport of Gases in the Blood:C.CO2 may be transported in the blood by…

• Dissol!ing in the plasma

• Dissol!ing as $icar$onate

• Binding to 0$ (car$aminohemoglo$in


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Transport of Gases in the Blood:C.

CO2 Dissoled in Plasma

• C. is !ery solu$le in "ater

• 6 * 48 of C. in the $lood is dissol!ed in

plasma

• The partial pressure gradient $et"een thetissues and $lood allo"s C. to easily

diuse from the tissues into the plasma• The amount of C. dissol!ed in the plasma

is proportional to the partial pressure of C.


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Transport of Gases in the Blood:C.C. as Bicar$onate (0.C


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Transport of Gases in the Blood:C.CO2 bound to Hb

(!arbaminohemoglobin)• Car$aminohemoglo$in

– C. attached to a hemoglo$in molecule

– 0$ / C. A 0$C.

• 6 * 78 of C. is $ound to 0$ in RBCs

• C. diuses into RBCs and $inds "ith theglo$in component (not the hemecomponent of 0$ for transport to thelungs


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C. Exchange and Transport in

Systemic Capillaries and eins

"he Chloride Shift• C. may $e transported as 0$C. or 0.C<

– 0/ ions or $icar$onate may accumulate in RBCs

• 0$ functions as a $uer for 0/ ions – 0$ $inding to 0/ ions forms 00$ as a $uer so that

RBCs do not $ecome too acidic

– 0$ / 0/ A 00$

• The $icar$onate ion (0.C


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The Eect of . on C. Transport

"he Haldane e#e!t• &oadingHInloading of C. onto 0$ is directly related to:

• = The partial pressure of C. ('C.

– ?n areas of high 'C.2 car$aminohemoglo$in forms

–

This helps unload C. from tissues• . The partial pressure of . ('.

– ?n areas of high '. (such as in the lungs2 the amount of

C. transported $y 0$ decreases

– This helps unload C. from the $lood

•


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Central Regulation of entilation

• The purpose of !entilation is todeli!er . to and remo!e C. from

cells at a rate su+cient to eep up

"ith meta$olic demands• Breathing is under $oth in!oluntary

and !oluntary control –

-ormal $reathing is rhythmic andin!oluntary

– 0o"e!er2 the respiratory muscles may$e controlled !oluntarily


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-eural Control of Breathing $y #otor-eurons

• The $rainstem generates $reathingrhythm

• Signals are deli!ered to therespiratory muscles !ia somaticmotor neurons

• 'hrenic ner!e – ?nner!ates the diaphragm

• ?ntercostal ner!es – ?nner!ate the internal and external

intercostal muscles


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• Central control of respiration is notcompletely understood

•

Research indicates that respiratorycontrol centers are located in the$rainstem

• Respiratory control centers includeJ –

#edullary Rhythmicity 1rea of the medullao$longata

– 'neumotaxic 1rea of the pons

– 1pneustic Center of the pons

Generation of the Breathing Rhythm $y the Brainstem


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#edullary Rhythmicity 1rea

• ?ncludes t"o groupsof neurons: – Dorsal Respiratory

Group

– entral RespiratoryGroup


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"he Dorsal $espiratory Group • The medullary inspiratory center• @unctions to generate the $asic respiratory rhythm

– The respiratory cycle is repeated =. * = timesHminute• Dorsal neurons ha!e an intrinsic a$ility to spontaneously

depolarie at a rhythmic rate• Kuiet $reathing * ?nhalation

– The dorsal inspiratory neurons transmit ner!e impulses!ia the phrenic and intercostal ner!es to the diaphragmand external intercostal muscles

– Lhen these muscles contract2 the lungs Mll "ith air• Kuiet $reathing * Exhalation

– Lhen the dorsal inspiratory neurons stop sendingimpulses2 expiration occurs passi!ely as the inspiratorymuscles relax and the lungs recoil


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"he %entral $espiratory Group• The medullary expiratory center

• @unctions to promote expiration during

forceful $reathing• ?f the rate and depth of $reathing increases

a$o!e a critical threshold2 it stimulates aforceful expiration

• The !entral expiratory neurons transmit ner!eimpulses to the muscles of expiration – The internal intercostals

– The a$dominal muscles



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'neumotaxic 1rea

• ?ncludes t"o groupsof neurons: – 'ontine Respiratory

Group

– The Central 'atternGenerator


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'neumotaxic 1rea

"he Pontine $espiratory Group • @acilitates the transition $et"een

inspiration and expiration

• Regulates the depth or the extent ofinspiration

• Regulates the fre)uency of respiration


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'neumotaxic 1rea

"he Central Pattern Generator• 1 net"or of neurons scattered $et"een the pons and the

medulla – Exact location of these neurons is unno"n

•

Coordinates the control centers of the $rainstem• Regulates the rate of $reathing

• Regulates the length of inspiration – 1!oid o!er*inNation of the lungs

•

Regulates the depth of $reathing – pneumotaxic output , shallo"2 rapid $reathing – pneumotaxic output , deep2 slo" $reathing


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'eripheral ?nput to RespiratoryCenters

• Receptors and reNexes monitor and respondto stimuli

• @eed information (input to the Central'attern Generator

• ?nput recei!ed fromJ – Chemoreceptors

– 'ulmonary stretch receptors• Detect lung tissue expansion and may protect lungs

from o!er inNation through the 0ering*Breuer reNex – ?rritant receptors

• Detect inhaled particles (dust2 smoe and triggercoughing2 sneeing2 or $ronchiospasm


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'eripheral ?nput to RespiratoryCenters: Chemoreceptors

Peripheral Chemore!eptors• Detect chemical concentration of $lood and

cere$rospinal Nuid

• &ocation: – Carotid sinus

– 1t its $ifurcation into the internal and external carotid arteries

– Connected to medulla $y aerent neurons in theglossopharyngeal (C- ?O ner!e

• Chemical concentration of the $lood is mostimportant

– Changing le!els of C.2 .2 and p0 of the $lood

– Sensiti!e to lo" arterial . concentrations ($elo" 45

mm0g


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• 'eripheral chemoreceptors are !ery sensiti!eto changes in arterial p0

• arterial p0 ( 0/ ion concentration occurs:

– Lhen arterial C. le!els increase

– Lhen lactic acid accumulates in the $lood

• Therefore2 arterial p0 is the most po"erful

stimulant for respiration• Lhen . concentration is lo"2 !entilation

increases



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Central !hemore!eptors• Sensiti!e to 0/ ion concentration in cere$rospinal

Nuid

• &ocated in the medulla "ithin the $lood*$rain$arrier

• C. is a$le to diuse across the $lood*$rain $arrier

and com$ine "ith "ater to form car$onic acid –

This reaction releases 0/

ions in the cere$rospinal Nuid – C. then com$ines "ith "ater in cere$rospinal Nuid to

form car$onic acid

• Stimulation of these central chemoreceptorsincreases respiration rate2 thus increasing $lood p0

to homeostatic le!els



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Chemoreceptor reNexes•

Chemoreceptors maintain normal le!els ofarterial C. through chemoreceptor reNexes

• ?ncreased C. , increased concentration of0/ ions ( p0 –

This stimulates the chemoreceptors• Decreased $lood p0 can $e caused $y

– Exercise and accumulation of lactic acid

– Breath holding

– ther meta$olic causes

• arterial p0 causes the respiratory system toattempt to restore normal $lood p0 $yJ – !entilation to decrease C. le!els

– This results in an increase in p0 to normal le!els

Conscious Control of


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Conscious Control ofBreathing•

Control o!er respiratory muscles is !oluntary – Therefore2 $reathing patterns may $e consciously

altered

• oluntary control is made possi$le $y neural

connections $et"een higher $rain centers(the cortex and the $rain stem

• oluntary control includesJ – 0olding your $reath

–

Emotional upset – Strong sensory stimulation (irritants that alter

normal $reathing patterns


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Distur$ances in Respiration

Hyperpnea• 1n in the arterial C. concentration "ith a

resultant in CS@ Nuid p0

• This condition stimulates theJ –

Central chemoreceptors2 and – #edullary respiratory centers

• Stimulates an increase in !entilation

Hyperentilation• #ore C. is exhaled resulting in arterial C.

concentration

• This returns arterial p0 to normal le!els

Th R i t S t i 1 id B


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The Respiratory System in 1cid*Base0omeostasis

&!id'ase Disturban!es in lood• The a!erage p0 of $ody Nuids is 399 – The p0 of !enous $lood and extracellular Nuid is

39


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Th R i t S t i 1 id B


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The Respiratory System in 1cid*Base0omeostasis

• Respiratory centers located in the$rainstem help regulate p0 $y controllingthe rate and depth of $reathing

•

Respiratory responses to changes in p0are not immediate2 it re)uires se!eralminutes to modify p0

• Respiratory responses to changes in p0are almost t"ice the $uering po"er ofall the chemical $uers com$ined


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Physiology of RS 2

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