Lecture no.23
16-3-2011
physiology
regulation of respiration
we will talk about “control of breathing”
 Control of breathing aims to maintain normal O2 and CO2 in the
blood.
We have : respiratory center system(respiratory controller system)
“which maintain homeostasis of co2 and o2”
Therefore if u
alveolar ventilation then Po2 will up tO 150mmHg
(plateau).
-Increase ventilation means “hyperventilation”
The purpose of hyperventilation is to make the composition of alveolar
air close to the composition of atmospheric air>>>(O2
and CO2
PAO2
)
PACO2
PACO2
P A O2
V
 Which means the more ventilation
co2 “coz ur push out co2 from ur body” .
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the less the alveolar
Lecture no.23
16-3-2011
physiology
regulation of respiration
You make the alveolar air near the atmospheric air “so the co2 is low”
VA
PCO2
THE EFFECT OF CO2 ON VENTILATION
More co2>>more ventilation( pco2 >>>>ventilation
)
 In the blood when co2 is high this will stimulate the respiratory
controller system to drive ventilation more,therefore you push co2
out more.
 If p02 decreases in the blood there is an increase in ventilation to
return po2 normal in the blood…
(
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po2>>>>>>
ventilation )
Lecture no.23
16-3-2011
regulation of respiration
physiology
1 : 100% ventilation
2: double ventilation “hyperventilation”
.5: 50% ventilation “hypoventilation
N.B: po2 with vA is not linear relation
 WE NOTICE THAT:
When PO2 increases in the bld more than 100 mmHg , it will not
suppress V.(so 100 is the level that if pco2 reach it ,V is not
affected means there is no contenious decreasing on v) .
But if pco2 increases >>>v will
increase “vice versa”
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Lecture no.23
16-3-2011
regulation of respiration
Note that when p02 reach 60mmHg >>>> steap decline starts. ”steap curve”
If Po2 < 60 mmhg …
STOP
>>>there is “
HB”
HB “in RBcs” tells Po2 that : if u get down below 60 “I start loosing control”
So if po2 < 60 “HB START TO LOOSE CONTROL”
When po2 fall down from 100 to 60 >>> HB still holding po2 “not releasing 02)
90% : 18ml O2( 100%: 20 ml o2>>>15g × 1.34 )
From 18ml ,cells need only 5 ml (25% × 20) …so u still in agood shape
 When (p02 < 60 mmHg),,HB says: don’t worry >>
So HB works …and respiratory center is at rest up to now .
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physiology
Lecture no.23
16-3-2011
regulation of respiration
physiology
keep ur respiratory center at rest ,don’t stimulate the respiratory
center>>don’t do any hyperventilation >> don’t overload ur respiratory
muscle “ I’m here I’m in a good shape”
 If po2 < 60 ,it will affect :
1. HB>>> bcoz o2 decrease.
2. CNS (there is asite which starts making firing impulses)
Note : there is no contact between HB(its kinetic ,allosteric, interaction
behavior and conformational changes …) & the respiratory center .
Note : Respiratory neurons start working only if Po2 < 60 mmHg.
_________________________________________________________
summarization
 The purpose of resp.center is maintaining po2,pco2 in the arterial
bld gases>>>>> when we say,,we also involve H2, bcoz:
CO2 + H2O
H2CO3
HCO3- +H+
***CO2,is considered as an acid even it hasn’t (H+)
NOW we can say that resp.system controls:
1. Po2
2.pco2
3.H2
Q: What stimulate the resp.crnter?
A: - PO2, PCO2, H2
Q: Which do you think is a major controller or
stimulator for the respiratory center, is it the (O2)
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a g e(CO2)???
Lecture no.23
16-3-2011
regulation of respiration
physiology
 From (PO2 –HB) dissociation curve, we notice that if PO2 decreases
from 100 to 60, it won’t affect>>>bcoz the curve isn’t
linear>>>>>>>This means that O2 is NOT the major controller.
BUT>>>> CO2:
- The curve is linear, so any
in PCO2 ,will be accompanied with
in PO2 concentration .
V
PCO2
- IN hyperventilation>>>>>
CO2
- IN hypoventilation>>>>>>
CO2
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pco2
VA
Lecture no.23
16-3-2011
regulation of respiration
physiology
IN the Lung:
Hyperventilated:
PO2
,,,, PCO2
apex
Base
Hypoventilated
PO2


,,,PCO2
When the contents of apex & base are mixed in the left
ventricle as the follow:
- If po2 in apex =130, po2 in base = 50>>>>>>the net po2 isn’t
((130+50)/2)>>>the result will be closer to 50!!
So : we notice that the hyperventilation lung is unable to
correct the hypoventilated lung>>>bcoz the shape of (O2HB)
Curve isn’t linear , its sigmoidal.
However……if the:
PCO2 in apex =30,PCO2 in base= 50>>>>the net is (40)>>the
curve is linear.
so :
1. CO2 can correct itself (self compensatory).
2. Any
or
in PCO2 can affect the resp.center in order
to maintain CO2.
 NOW,we can give an explanation for why PO2=95??
)21 ‫(هدا السؤال ساله الدكتور في محاضرة‬
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Lecture no.23
16-3-2011
regulation of respiration
physiology
Respiratory controller system:
 It s in the medulla oblongata...
 There are two groups of diffused neurons(in the respiratory
crnter):
1. Dorsal respiratory group(DRG)
2. Ventral respiratory group(VRG)
 AT normal quiet breathing:
-DRGs are working(active)>>>they send impulses to the
phrenic neurons which located between (C3-C5)cervical
(precervical 5) so it will be stimulated then>>>> it will
stimulate the resp.muscles like Diaphragm .
-VRGs are silent
DRGs
1.inspirastory neuron
(I)
2. AT normal quiet
breathing:
working(active)
3. they send impulses to
the phrenic neurons which
located between (C3C5)cervical (precervical 5)
so it will be stimulated
then>>>> it will stimulate
the resp.muscles like
Diaphragm .
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VRGs
1. inspiratory & expiratory
(I&E)
2. silent .
3. they can stimulate
accessory inspiratory &
expiratory muscle
(internal intercostals&
abdominal musle)
Lecture no.23
16-3-2011
regulation of respiration
physiology
Note: if the collapsing tendency of the lung decreases like in (
COPD),where the elastic fibers are destroyed …now expiration is
active .
Pherinc neurons >>>>they lack automaticity ,they lack intrinsic
ability to make there own AP.
 During exercise ,u may have both the VGR & DGR >BOTH r
working
 In the medullary in different area,not with the
respiratory center there is collection of neuron sensitive
to chemicals (chemosensetive neurons)>>this chemical is
H2.
 Above the medulla is the PONS,in the pons we have 2
accessory respiratory center
One in the lower third of the pons we called it “Apneustic
center”
The other in the upper one third we called it “Pneumatoxic
center”
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Lecture no.23
16-3-2011
regulation of respiration
physiology
If we ask someone to stop his breath , ventilation
(decrease)>>>CO2 WILL (INCREASE).
 From the cortex there is an inhibitory effect ..which inhibit
neuron (pherinc)….then it will stop working >>no muscle
contraction >>>no breathing >>co2 will increase in bld.
 Co2 reaches 50mmHg and bcoz co2 doesn’t have barrier so it will
enter CSF >>where co2 combines to water (co2 + H2O-----> H2CO3---- HCO3- +H+
 H+ >>>stimulate chemosensetive area in the medulla >>>its going to
stimulate DGR>>>DGR will make strong stimulus on pherinc neuron.
 So until now:
The pherinc neuron is under 2 different stimuli , one
from the cortex(inhibitory),and the other from the
medulla( stimulatory)
The medullary stimuli is stronger than the cortical and
thus stimulation of the diaphragm occur,therefore its
not possible to anyone to suicide through stop
breathing.
*respiratory centers send sensory neurons
(chemoreceptor) to sense po2 mainly and less exert to
co2,H,in the aorta and carotid artery.
So the sensory will go to aorta (the largest).
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Lecture no.23
16-3-2011
regulation of respiration
physiology
Po2=100,A
Po2=40,V
Po2=40
Po2=40
ARTERY
The cell must sense the artery ,although it is surrounded by
interstitial po2=40
In this work there is amiraculous manner
Cells
“chemoreceptor”
The carotid & aortic bodies measure the chemoreceptor(po2)
3shan n5le el po2 elm7ee6 bl cell like el po2 elmwjood in the arterial
aspect of the capillary 9ar fe m9’a3fe in arterial bld 3shrat elmrrat >>>
mshan heek r7 tkoon el p02 mo 40 r7 tkoon btw 95-100 y3ne like el po2
in artery
****HOE DOESE THE INTERSTITIAL PO2 BECOME HIGH THAN
NORMAL??
1. Making the cells (don’t consume o2) metabolically inactive>>but
this way cant be applied ,bcoz the cell which we talk about is the
most active cell
2. Increase bld supply to this cell in which the cells whatever
consume the result is (what is the left = what is dilever).
 The cells which have chemoreceptor these cells start 2
sending AP and stimuli to CNS (medulla),only if the po2 <
60mmHg so these cells don’t respond if the po2 is btw 60100….although these cells dn’t know about HB and its
compliant.
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Lecture no.23
16-3-2011
regulation of respiration
physiology
 Pco2 start affecting centrally
 Po2 start affecting peripherally
Ventilation during exercise
Exercise>>> ventilation
What stimulate ventilation during exercise or wt stimulate the
RSS during it???
PCO2
exercise
VA
During exercise the curve is shifted upward
At rest if VA=1(100%),pco2= 40mmHg
At exercise If the VA is doubled 5 times ,then the pco2 is also
40 this is bcoz as we know >>
during exercise when amount of co2 “delivery “
amount of co2 “washed out” will
the
too.
So ABG of pco2 still constant.
- What drive muscle to contract during exercise ?
- When stimuli come to muscle ,it also go to respiratory
center >>>so when joints move >>they send impulse to the
respiratory center to increase po2 ventilation.
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Lecture no.23
16-3-2011
regulation of respiration
physiology
 For comatose person if he starts moving his legs he start
hyperventilation
 So the same stimuli which drive muscle to contract ...they
stimulate the ventilation tooo
IF u go to high attitude place the % of po2
still constant”21%” but po2 will decrease
then the peripheral stimulus will make
more ventilation then co2 will decrease>>>
this will suppress R.C SO there is 2 diff.
“opposing stimuli”
Co2
O2
>>>>suppression of R.C
>>>>STIMULATION
Henderson-Hasselbalch Equation:
PH=6.1 + log (HCO3-/PCO2)
- Any decrease in pco2 >>>increase in pH then the kidney
starts excreating Hco3- in the urine so PH will back to
normal.(no alkalosis neither acidosis)>>>there is no H+
inhibitory effect >>>so ventilation will increase.
DONE BY:SUMAYA T. SHHADA
This sheet is dedicated to my sisters:
DR. Safeya shhada
Aseel Dasan,Sumaya A.odeh,Aya Mhfooz,Nour
Saddouq,Bayan saleh,Banan Mteir,Majd
Madani,Rawan Hamdan,Rasha Al3wazim
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