1 Chapter 5 Respiration Liu Yuhong Department of Physiology Ji Ning Medical College E-mail:...

1

Chapter 5 Respiration

Liu Yuhong Department of PhysiologyJi Ning Medical College

E-mail: [email protected]

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The gas exchange between the body and the external environment is named respiration.

The goales of respiration are:

uptake oxygen (O2)

output carbon dioxide(CO2)

3

Respiration is consisted of three major functional events:

①

④③②

gas transport

CO2O2

5

atria

ventricle

6

Section A Organization of the Respiration System

nose

bronchioles

alveolus

7

Nasal Cavity

Nose

Mouth

Bronchus

Bronchiole

Alveolus

Diaphragm

Throat

(pharynx)

Windpipe (Trachea)

Left lungs

Ribs

9

sternum

ribs

diaphragm

external intercostal

muscles internal intercostal muscles

abdominal muscles

The thorax/chest

Expand

Recoil

10

• When intercostal muscles contract or relax, the volu

me of chest expand or recoil, then the volume of lun

gs expand or recoil. Why?

11

• Pleural cavity is made up of two layers of pleura.One is

visceral layer stick to the surface of lung and the other is

parietal layer stick to thorax .

• There is only little liquid in the pleural cavity but not gas.

• The effect of this layer of liquid is :（ 1 ） The power between liquid molec

ules pastes two layers of pleura to make them tightly.

（ 2 ） Lubrication effect between two layers of pleura.

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Section B Pulmonary ventilation

Pulmonary ventilation is the gas exchange process between lungs and environment.

13

Mechanics of Pulmonary Ventilation:Mechanics of Pulmonary Ventilation:

Two factors:

• One is the power to push gas flowing.• The other is resistance to prevent gas flowing.

• The former must overcome the latter , and then

pulmonary ventilation can be completed.

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Ⅰ Ⅰ the force that causesthe force that causes Pulmonary VentilationPulmonary Ventilation

1. Respiratory movement

Thoracic expansion and contraction caused

by respiratory muscles are named respiratory

movement. (inspiration, expiration)

15

• Muscles of inspiration : diaphragm and

external intercostal muscles

• Muscles of expiration : internal intercostal muscles

and abdominal muscles

Eupnea

deep breathing

16

The Process of eupnea:

Inspiration: inspiration muscles contract thoraxes expand lungs expand lung volumes increase intrapulmonary pressure decreases gas enters lungs

Expiration: diaphragm and external intercostal muscles relax thorax recoils lung recoils intrapulmonary pressure increases gas is removed.

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patternspatterns :

Abdominal breathing

Thoracic breathing

Eupnea

deep breathing

Normal quiet breathing is accomplished almost entirely by movement of the diaphragm.

Breathing caused primarily by the movement of external intercostal muscles.

Breathing at rest is calm.

Respiratory movement is greatly enhanced.

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2. intrapulmonary pressure

Intrapulmonary pressure is the pressure in pul

monary alveoli.

Intrapulmonary pressure is equal to atmosphe

ric pressure when apnea , vocal cord is open.

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At the first of inspiration, lung volume increases an

d intrapulmonary pressure decreases below atmosph

eric pressure. Air enters alveoli under the pressure di

fference. Intrapulmonary pressure increases as the in

creasing of gas in lung. At the last of inspiration, intr

apulmonary pressure is equal to atmospheric pressur

e and the air flow stops.

22

At the first of expiration, lung volume decreases an

d intrapulmonary pressure increases until it exceeds

atmospheric pressure. Air outflows lungs and intrap

ulmonary pressure decreases by and by. Intrapulmo

nary pressure is equal to atmospheric pressure at th

e last of expiration.

23

Artificial respiration: once respiration stops, int

rapulmonary pressure can be changed factitiously .

Pressure difference between intrapulmonary pres

sure and atmospheric pressure can be created to

maintain pulmonary ventilation .

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Intrapleural pressure is u

sually negative pressure.

At the end of expiration o

f eupnea,the pressure is a

bout -5~ -3mmHg.

At the end of inpiration o

f eupnea, the pressure is

about -10~ -5mmHg.

3. Intrapleural pressure

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Intrapleural pressure ＝ intrapulmonary pressure － lungs recoil

At the end of respiration or inspiration, intrapulmonary pressure equals atmospheric pressure

intrapleural pressure= － lungs recoil

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If pleura breaks, pleural cavity will be open to

atmosphere and air will enter pleural cavity . This

is called pneumothorax. At this time , two layers o

f pleura separate and lungs contract for the elasti

c recoil.

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Power of Pulmonary Ventilation (Summary)

Expansion and contraction of respiration muscles e

xpansion and contraction of thoracic cage (lungs c

hange with the moving of thoracic cage)lung volumes

change pressure differences between lung volume

and atmospheric pressure gas enters or is removed

out of lungs.

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Ⅱ Ⅱ Resistances to Pulmonary Ventilation Resistances to Pulmonary Ventilation

one is elastic resistance (70 ％ ) （ the main resistance of eupnea ）

elastic resistance of lung

elastic resistance of thorax

the other is non- elastic resistance( 30 ％ )

airway resistanceinertial resistanceviscous resistance of organization

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1. Elastic Resistance and Compliance

The ability of an elastic structure to resist stretching or distortion is named elastic resistance.

Compliance is the expandability of elastic tissue when acted on by foreign forces.

Relationship between compliance and elastic resistance C ＝ 1 / R

☆

☆

☆

Compliance is inversely proportional to elastic resistance, that is, the larger the compliance, the less elastic properties, and vice versa.

E.g. an elastic band

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（（ 11 ）） Elastic Resistance of Lungs and ComplianceElastic Resistance of Lungs and Compliance change of lung volume （△ V ）lungs compliance ＝ change of transpulmonary pressure （ △P ）

transpulmonary pressure is the difference between intrapulmonary pressure and pleural pressure.

(L/cmH2O)

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injector

Water manometer

Connect tracheal intubation

Three-way tap

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① Lung static compliance diagram

• If curve slope is large , it means the compliance is large and the elastic resistance is small.

• If curve slope is small, it means the compliance is small and the elastic resistance is large.

transpulmonary pressure(cmH2O)

Lu

ng

vo

lum

e c

ha

ng

e

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②Specific compliance

Specific compliance = Measured lung compliance

（ L/cmH2O ） / Total lung capacity （ L ）

adultinfant

Lung compliance

Total lung capacity

Specific compliance

Lung compliance is also influenced by the total capacity of the lung.

35

③ Source of lungs elastic resistance

a. The elastic recoil power of lungs elastic recoil power

surface tension

bead

liquid layer Alveolar surface tension

b. The recoil power caused by surface tension between the liquid layer of inner alveoli and gas in alveoli.

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Retraction force can be calculated by Formula Laplace .

Retraction force P = 2T / r

T ： surface tension dyn/cm

r ： alveoli radius （ cm ）

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(2) Pulmonary Surfactant

DPPC

DPPC is an important p

ulmonary surfactant in the

the liquid layer of inner al

veoli, DPPC binding to a

polipoprotein exist as lip

oprotein.

liquid layer Alveolar surface tension

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• DPPC is synthesised by alveoli cells.Ⅱ

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physiological effect of pulmonary surfactant

（ 1 ） Lower alveolar surface tension and reduce inspiration

resistance.

（ 2 ） Accommodate surface tension and stable alveolar pres

sure.

（ 3 ） The effect of suction is reduced. Reduce the producin

g of alveolar liquid and prevent pulmonary edema.

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development of Pulmonary surfactant

occurent from cyesising 25 － 30 weeksat the high point in cyesising 40 weeks

Premature may get respiratory distress syndrome even to death for deficiency of pulmonary surfactant and formation of pulmonary atelectasis.

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2. non-elasrtic resistance

Learn by yourself.

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Ⅲ Pulmonary Volume and Capacities

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• Tidal Volume(TV) : amount of air inhaled or exhaled in one quiet breathing. 500mL

• Inspiratory reserve volume (IRV) : the maximum extra volume of air that can be inspired over and above the normal tidal volume. 1500-2000mL

1. Pulmonary Volume

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● Expiratory reserve volume (ERV ): the maximum extra volume of air that can be exspired by forceful expiraton after the end of a normal tidal expiraton . 900-1200mL● RV(residual volume): amount of air remaining in the lungs after maximum expiraton. 1000-1500mL

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2. pulmonary capacities

● Inspiratory Capacity (IC):maximum amount of air that can be inhaled after a normal tidal expiration. = TV + IRV 2000 － 2500 mL

● Functional residual capacity (FRC): amount of air remaining in the lungs after a normal tidal expiration .

= RV+ERV 2500 mL

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• vital capacity (VC ): amount of air that can be exhaled with maximum effort after maximum inspiration. = TV+ IRV +ERV ♀ 2500 ♂3500mL

• total lung capacity (TLC): maximum amount of air that lungs can contain.=RV+VC

3500 － 5000 mL

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• timed vital capacity (TVC)• expired 80% of all vital capacity at the first second• expired 96% of all vital capacity at the second second• expired 99% of all vital capacity at the third second

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3. lung ventilation volume

Minute ventilation volume=

Tidal Volume×respiratory rate 6-8L

Maximal voluntary ventilation :70 － 120L/min

It is expressed ventilation reserve.

500ml 12-18 times/min

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4.Dead space and Alveolar Ventilation

dead space

anatomic dead space

alveolar dead space

physiologic dead space:

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150 150150

2500

2500 2500150

350

the end of inspiration

the end of exspiration

500150350

inspiration exspiration

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alveolar ventilation = (tidal volume- dead space)× resp

iratory rate

（ 500mL － 150mL ） ×12 次 / 分 =350 ×12= 4200 L

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respiratory rate

（（ time/mintime/min ））tidal volume

（（ mlml ））ventilation volume

（（ ml/minml/min ））alveolar ventilation

（（ ml/minml/min ））

1616 500500 80008000 56005600

88 10001000 80008000 68006800

3232 250250 80008000 32003200

If tidal volume decreases half, respiratory rate increases double. Minute ventilation volume keeps constant, but alveolar ventilation will decrease greatly. Considering as ventilation efficiency of slow and deep respiration is higher than fast and light respiration.

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Section C Gas exchange

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Ⅰ principle of gas exchange

gas diffusion:

Gas molecules move freely among one another. The

result is gas molecules diffuse from high-pressure area

toward low-pressure area. The process is called gas diff

usion.

Exchange of gas in alveoli and tissues are physical d

iffusion processes .

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The volume of gas diffusion in unit time is called diffusion rate. It is effected by the following factors

D∝△P*T*A*S

d*√MW

△P is the pressure difference between the two ends of the

diffusion pathway, T is the temperature, A represents the

cross-sectional area of the pathway, S is the solubility of t

he gas, d is the distance of diffusion, MW stands for the m

olecular weight of the gas.

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1. Gas partial pressure difference: gas partial pressure diff

erence is larger—diffuses faster

2. Gas molecular weight and solubility:

when solubility is high, it diffuses fast

when molecular weight is large,it diffuses slowly.

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3. Diffusion area of alveolar membrane : when diffu

sion area of alveolar membrane is large,it diffuses fas

t

★diffusion area of alveolar membrane is 40m2 in no

rmal quiet state.

★ diffusion area of alveolar membrane is 70m2 duri

ng sports.

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4. Diffusion distance—thickness of alveolar membrane(inverse ratio relationship)

★ Pulmonary fibrosis

★ Pulmonary edema

5. Temperature of fluid increases

Solubility increases—Diffuses fast

Averages 0.6 μm

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Ventilation/perfusion ratio is the rate between alveolar ventilation and pulmonary blood flow.

VA: alveolar ventilation per minuteQ : pulmonary perfusion per minute

VA/Q (value of normal quiet state) ＝ 4.2L/5L ＝ 0.84

If blood flow decreases and gas exchange are normal--the exchange total amount decreases. Soalveolar ventilation and blood flow must keep anappropriate ratio.

6. Ventilation /Perfusion Ratio(VA/Q )

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★ventilation /perfusion ratio increases:it means partial alveolar gas can not exchange fully with the blood =physiological dead space increases.

★ventilation /perfusion ratio decreases:it means partial blood flow through hypoventilation alveoli. They can not get fully exchange. And it equals functional arteriovenous shunt.

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When normal adult is standing, every part of lung V

A / Q is not well-distributed

Apex of lung : VA descent/Q descent, Q descenting

is more obvious. ratio rises(more than 3)

Base of lung: VA descents/Q rises, ratio descents

(0.6).

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7. pulmonary diffusion capacity

When all kinds of gas is under unit partial pressure difference,the gas volume(ml) passing through respiratory membrane per minute is called pulmonary diffusion capacity. It is the physiological index to test the diffusion ability of respiratory membrane.

DL

V

PA PB

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CO2 diffusibility/ O2 diffusibility= √O2 molecular

weight/ √CO2 molecular weight=√32/√44 ＝ 5.6/6.

6

But because CO2 solubility/ O2 solubility= 0.592/0.0

244=24.3/1.0(Herry’s law ）CO2 diffusion velocity/ O2 diffusion velocity =

（ 5.6/6.6 ） × （ 0.592/0.0244)=20.6/1.0 From all above ,we know that the diffusion velocity of CO2 is much more than that of O2. There is no diffusion disturbance of CO2 in clinical.

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Ⅱ Pulmonary gas exchange

PO2 of mixed venous blood is 5.32 kPa （ 40mmH

g ） is lower than 13.82 kPa （ 104mmHg ） of alveo

lar gas. O2 in alveolar gas diffuses to blood. PO2 in bloo

d rises gradually until it is almost equal to PO2 in alveol

ar gas.

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PCO2 of mixed venous blood is 6.12kPa （ 46mmH

g ） It is higher than 5.32 kPa （ 40mmHg) of alveol

ar gas. CO2 in blood diffuses to alveolar gas. PCO2 in bl

ood descents gradually until it is almost equal to PCO2 i

n alveolar gas.

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Ⅲ Tissues Gas Exchange

72

Section D Gas Transport

Ⅰ Existing forms of O2 and CO2 in the blood

chemical combination(primary)

physical dissolution(medium)two forms

O2 physical dissolution combination physical dissolution O2

lung tissue

CO2 CO2 physical dissolutioncombination physical dissolution

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Ⅱ oxygen transportation

oxygen transportation

98.5 ％ binding to Hb

1.5 ％ physical dissolution

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Maximum capacity of hemoglobin binding with O2 (in every 100ml blood ) is named oxygen capacity.

When normal Hb is in 15g/100ml blood , 1g Hb

binds with 1.34ml O2.

Oxygen capacity= 15×1.34 ＝ 20ml

The volume of hemoglobin binding with oxygen (in fact or really) is called oxygen content.

arterial blood: 20ml O2

venous blood: 15ml O2

76

The percentage of oxygen content to oxygen capaci

ty is called oxygen saturation.

oxygen content

oxygen capacity

In arterial blood, oxygen content equals 20ml and o

xygen saturation is 100%.

In venous blood , oxygen content equals 15ml and o

xygen saturation is 75%.

×100%)(=

77

form

O2 partial pressure is higher(lung)

Hb ＋ O2 HbO2

O2 partial pressure is lower(tissues)

reduction 、 royal blue oxygenation 、 red

break

relaxationtension

（一）

78

character

1. Reversible binding. Without enzyme. Fast. Effected b

y PO2.

2. O2 binds with Fe2+ of hemoglobin . The iron value is

permanent. So the process is called oxygenation but n

ot oxidation.

PO2↑

PO2↓HbO2Hb + O2

79

3. Globin of hemoglobin is made up of two αpeptide chains

and two β peptide chains . There is a protoheme molecul

ar on each peptide chain including a Fe2+. Each Fe2+ bind

s with an O2 . So each hemoglobin can bind with four O2.

Fe

80

4. O2 can facilitate binding or releasing.

In lungs, increasing of PO2 promotes combination.

In tissues, decreasing of PO2 promotes releasing.

PO2↑

PO2↓HbO2Hb + O2

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5. The binding or releasing curves of Hb and O2 appear S

form.This is related to the allosterism effect of Hb.

Hb binds with O2—salt bond breaks, R form

Hb releasing with O2—salt bond forms,T form

The affinity of T form to O2 is smaller.

The affinity of R form to O2 is larger.

relaxationtension

Hb HbO2

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（二） oxygen dissociation curve

The curve reacts the relationship of PO2 and saturation of oxygenation Hb .

83

oxygen dissociation curve character

1. Superior segment of curve: PO2 60 － 100mmHg.

Slope is flat.

Partial pressure of oxygen c

hanges greatly. But oxygen sa

turation changes little—even

PO2 of environment or alveoli

descents, oxygenation saturat

ion will maintain high level.

84

Significance:

Hemoglobin amortizati

on function: even blood

itself of environment ox

ygen change greatly, tis

sue PO2 still remain in n

ormal range.

• PO2 descents in plateau

85

2. Middle segment of curve PO2 60 － 40mmHg is the p

art that HbO2 releases O2.

e.g. venous blood PO2 level

86

3. Inferior segment of curve . PO2 10 － 40mmHg . Th

e slope is steep.

PO2 descents a little. It makes oxygen saturation desc

ent greatly. This is benefit to supplying oxygen for tissue activity.

87

（三） factors effect oxygen dissociation curve

T increases, the concentration of H+, CO2, 2 ，3-DPG rises, pH descents . Curve move to right. Oxygen saturation descents and dissociation increases.

And vice versa.

88

2 ， 3 － DPG is a kind of organophosphate in RBC.

缺氧、贫血 hypoxia, anemia

长时间运动 long time sports

RBC 2 ， 3DPG increases

89

factors effect oxygen dissociation curve

90

Ⅲ Transportation of CO2

transportation of CO2

physical dissolution（ 5% ）

combination（ 95% ）

bicarbonate（ 88% ）

Carbaminohemoglobin（ 7% ）

92

（一） Transport in bicarbonate pattern

character:

1. Reaction is reversible. But it need the help of enzyme(C

A).

2. Conjugation or dissociation is decided by partial pressure

difference of CO2.

3. There is the transfer of Cl － in the reaction.

93

（二） Transport in carbaminohemoglobin pattern

in tissues

HbNH2+CO2 HbNHCOOH

lung

HbNHCOO －＋ H ＋

94

character

1. Reaction is reversible and need not the help of enzyme.

2. Conjugation or dissociation is decided by the

oxygenation effect of Hb.

Much Deoxy Hb binds with CO2.

Little Hb binds dissociation is much.

3. The effect of partial pressure difference is not obvious.

in tissues HbNH2+CO2 HbNHCOOH lung HbNHCOO- ＋ H+

carbaminohemoglobin

95

Section E Regulation of Respiration

96

Ⅰ respiratory center Respiratory center is composed of several groups

of nerve cells which produce and regulate respirator

y movement in central nervous system.

97

Lumsden experiment in year 1923 Cross-cut site Patterns of respiration Patterns of respiratory movement after cutting vagus nerve

Between pons Normal Deeper and slowerand midbrainIn the middle Deeper and slower Apneusisof ponsBetween Pons Anomalo-respiration Pant respirationand medullaBetween medulla Respiration arrests Respiration arrests and spinal cord

98

Conclusion:

Superior part of pons -- pneumotaxic respiratory center

medulla --basic respiratory center

spinal cord--primary respiratory center

99

Regulation of Cerebral Cortex to Respiration

1. Liberty Regulation and Creation of

respiration Conditioned reflex.

2. Coordination with the process of la

nguage activity.

Clinical: Descending pass of spinal c

ord pro-Lateral funiculus is damage

d.---Autonomous breathing arrests.

Regulate through voluntary breathin

g. Use breathing machine during sl

eeping . Oden’s curse

100

Ⅱ Formation of Respiratory Rhythm

vagi

101

Reversion inhibition theory(part neuronal cir

cuit feedback and controling theory)

1 ） Central inspiratory activity

2 ） inspiratory off-switch mechanism central inspirato

ry activity inspiration-initiative process

expiration-passive -process

102

3 ） The mechanism of changing from expiratory phase

to inspiration—there are probably a group of cutting of

f expiratory neurs.

Imagining the process of expiration phase is probabl

y controled by a mechanism of inhibiting inspiration a

bility during respiration phase. The ability degree of th

is mechanism is getting weaker during the expiration p

hase.once reaching the critical level, the inhibition of i

nspiration ability is relieved and the next inspiration w

ill begin.

103

Ⅲ Reflex Control of Breathing

Respiratory movement can be regulated , accelerate

d or inhibited by all kinds of stimulus to the body.

104

（一） Chemical Control of Breathing

1 . Chemoreceptor

（ 1 ） peripheral chemoreceptor

Carotid body and aortic body: stimulated when PCO2

in blo

od increases, PO2 in blood decr

ease, H+ Concentration in blood increase.

105

(2) central chemoreceptor

106

Abdomen Lateral of central chemoreceptor feel the stimulation of H+ change in the Cerebra Spinal Fluid.

character

a. Not feel the stimulation of deficiency of O2.

b. H+ in the blood has no effect to it. For it is

difficult to pass the blood brain barrier.

107

c. The sensibitity to CO2 is higher than that to peripheral chemoreceptor. But the latent period of reaction to sudden change of PCO2

in the arterial blood is longer

than that of the peripheral chemoreceptor.

d. Utility stimulant is not CO2 itself but the increase of H+ caused by CO2.

109

2. Regulation of CO2 、 H+ 、 O2 to respiration（ 1 ） Influence of CO2 to respiration

a. Act indirectly to central chemoreceptor(main pathway)

b. Act directly to peripheral chemoreceptor.

The sensibitity of central chemoreceptor to H ＋ is about 25 times of that of peripheral chemoreceptor.

110

air PCO

2

Arterial PCO2

peripheral chemoreceptor

diffuses across

blood-brain barrier

Brain extracellular fluid PCO2

Brain extracellular fluid [H+]

( CO2+H2O H2CO3 HCO3- + H+ )

CA

central chemoreceptor

Medullary inspiratory neurons

Ventilation increases

80%

+

+

+

+

“+”: exciting

111

（ 2 ） Effect of O2 to respiration

1 ） character

a. Hypoxia stimulation act through peripheral chemorecep

tor. If the inputing of peripheral chemoreceptor is cut, th

e stimulation effect disappear.

b. The direct effect of hypoxia to center is light inhibition.

112

2 ） The pathway of hypoxia regulating respiration

The main pathway is acting directly on peripheral

chemoreceptor and inputting impulse.respiration ce

nter is excited.

113

（ 3 ） Effect of H+ to respiration

1 ） Increasing H+ or decreasing pH can faster respiration.

It is the effective stimulator to chemoreceptor.

2 ） Pathway of H+ regulating respiration

a. H+ in blood increases—excites peripheral chemorecepto

r mainly

b. H+ in Cerebra Spinal Fluid increases-- excites central c

hemoreceptor . Because H+ is very difficult to diffuses

across the blood-brain barrier, so brain extracellular fl

uid [H+] increased very little.

115

（ 4 ） Interface of PCO2 、 H+and PO2 effect respiration

1 ） PCO2 does main role in normal respiration regula

tion.

2 ） When any of the three factor changes ,it can induce the continued change of the other factors.and it can change the respiration effect of the first factor changing .

3 ） Hypoxia and increasing of H+ concentration can strengthen the stimulation effect of PCO2 increasing

to respiration.

116

150 150150

2500

2500 2500150

350

the end of inspiration

the end of exspiration

500150350

inspiration exspiration

117

the alveolar ventilation reaction of changing any of the factors of PCO2

， PO2， PH in Arterial blood but not control

ing the other two factors

118

PCO2

PO2

summary

central

chemoreceptor

peripheral chemoreceptor

119

Ⅳ Pulmonary Stretch Reflex

Inflation of the lungs caused inhibition of ins

piration, while collapse of the lungs enhanced in

spiration. This reflex is termed Pulmonary Stret

ch Reflex.

120

reflex

• Reflex arc

stimulation

receptor afferent nerve center efferent nerve effector

response

122

Pulmonary Pulmonary

inflation reflex deflation reflex

Part of sensor Smooth muscle of bronchus and bronchiole

Stimulation property dilatate diminish

Effect relax(expiration) Shrink(inspiration)

Significance Urge inspiration urge expiration change

change into expiration into inspiration promptly, promptly,inhibit too deep inhibit too expiration. or too long inspiration.

1 Chapter 5 Respiration Liu Yuhong Department of Physiology Ji Ning Medical College E-mail:...

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