Dr.

Farrukh Majeed
Department of Physiology
doctorfarrukhmajeed@gmail.com
 Nervous and Chemical
regulation of respiration and
respiratory reflexes
 Learning Objectives

At the end of this lecture students should be able

to:
• Describe respiratory centers and nervous regulation
of respiration.
• Discuss chemical control of respiration and
chemoreceptors.
• Discuss respiratory reflex and other factors that
affect respiration and sleep apnea
• Understand regulation of respiration during exercises
Who controls your respiration you or your
brain?
 Control of respiration

1)
2)
Neural Chemical
Control
Control

3) Other mechanisms that serve other purposes

 Respiratory
centers

Medullary Pontine
 Medullary respiratory center

Dorsal respiratory Ventral respiratory

group (DRG) group (VRG)
neurons neurons
 Pons

Pons
Pneumotaxic center
respiratory
Apneustic center
centers

Respiratory Pre-Bötzinger
control complex
centers in
brain stem
Dorsal respiratory
Medullary group
respiratory
center Ventral respiratory
group Medulla
Dorsal respiratory group (DRG) neurons

Consists of inspiratory neurons

Which terminate on motor neurons

that supply inspiratory muscles
 Inspiratory muscles

External
Diaphragm
intercostals

Phrenic nerve Intercostal nerves

Cell bodies located in the spinal cord

 Generation of respiratoty rhythem
Neurons in pre-Potzinger complex
Neurons in pre-Potzinger complex
Display self-induced action potentials
Are responsible for
causing
the basic rhythm of ventilation
rhythmic firing of inspiratory neurons of DRG
 Dorsal Respiratory Group
( Inspiratory Center )
 

Sets basic rhythm by spontaneously initiating inspiration.

 
DRG neurons fire ( for 2 seconds ) DRG neurons stop
firing (3 seconds )
 
 
message to inspiratory muscles inspiratory muscles relax
 
 
contraction of these muscles elastic recoil of chest and lungs
 
 
Inspiration Expiration
 

 
This automatic rhythmic firing produces the normal resting breathing rate
( 12-15 breaths per minute ).
 Ventral respiratory group
(VRG) neurons

Consists of inspiratory neurons

and expiratory neurons

Both of which remain inactive

during normal quiet breathing
 VRG respiratory neurons
are stimulated by DRG respiratory
neurons during periods when
demands for ventilation
are increased
During active expiration

DRG respiratory neurons

Stimulate VRG respiratory neurons

Stimulate Expiratory muscles

Active Expiration occurs

 DRG has special
interconnections with VRG

VRG is brought into action

when the demands for
ventilation increase

Thus VRG plays role in

active expiration

VRG is called into play by DRG as an ‘overdrive’ mechanism

 Pontine centers

Pneumotaxic Apneustic
center center
 Pons

Pons
Pneumotaxic center
respiratory
Apneustic center
centers

Respiratory Pre-Bötzinger
control complex
centers in
brain stem
Dorsal respiratory
Medullary group
respiratory
center Ventral respiratory
group Medulla
Exert ‘fine-tunning’
influences over the
medullary center
For normal and smooth
inspirations and
expirations
 The Pneumotaxic center
sends impulses to DRG
that ‘switch off’ the
inspiratory neurons

duration
of inspiration is
limited

The apneustic center

prevents the inspiratory
neurons from being
switched off

It thus prolongs
inspiratory drive
 Pneumotaxic center
is dominant over the
apneustic center Without pneumotaxic center
prolonged inspiratory gasps
occur interrupted by
very brief expirations

This abnormal pattern

of breathing is
apneusis
Hering - breuer reflex

Increased tidal volume

as in exercise triggers
Hering-Breuer reflex to
prevent over inflation
of the lungs
 Hering - breuer reflex

Stretching of Activation of
 Tidal volume
the lungs stretch receptors

Inspiration Inspiratory
 Tidal volume neurons inhibited
stops
 Sleep apnea
Subconscious breath holding
for a short time

Usually during deep sleep

The subject
may have respiratory arrest
and may die
Sudden Infant Death Syndrome (SIDS)

A form of sleep apnea in very young

infants for no apparent reason

The infant is found dead while sleeping

in his or her crib

This condition is also known as

‘Crib Death’
 Control of respiration

1) 2)
Neural
Control
Chemical
Control

3) Other mechanisms that serve other purposes

Then
The it
medullary
respondsrespiratory
by sending
center
signalsreceives
to the respiratory
information
about
musclesthetobody’s
adjustneeds
the rate
for
and depth
gas exchange
of ventilation
 The signals
which  ventilation

 PCO2  PO2
 H+

These factors operate through chemoreceptors

 Chemoreceptors

Central Peripheral
Located in the medulla carotid bodies bifurcation of the
in the vicinity of the common carotid arteries
respiratory center aortic bodies  arch of aorta
Changes in PCO2 , PO2 and pH are corrected
Changes in PCO2 , PO2 and pH

Chemoreceptors

Medullary respiratory center

respiratory muscles

Changes in breathing pattern

 Role of PO2 in Respiration

PO2 mediates its effects

on respiration through
peripheral
chemoreceptors

peripheral
chemoreceptors
respond only when the
arterial PO2 is
 60 mm Hg
Role ofUpPO 2 in Respiration
to PO 60 mm Hg, 2
Hb is still 90%
saturated

100
Percent saturation of hemoglobin

80
Therefore peripheral Plateau
chemoreceptors
60
serve as an
phase

40 emergency mechanism

20
in dangerously low
arterial PO2 states
0 20 40 60 80 100

PO 2 mm Hg Abro
 Relieves
Arterial PO2 <60 mm Hg

Emergency
life-saving No
mechanism effect
on
Medullary
Peripheral Central
respiratory
chemoreceptors chemoreceptors
center

 Ventilation

Arterial PO2
 Role of PO2 in Respiration

Sudden severe drop in PO2

(Below 20mmHg)

Depress the brain

causes loss of consciousness
and death in 4 min
 Roleperipheral
of PO2 chemoreceptors
in Respiration
respond to the PO2 of the blood,
NOT the total O2 content
of the blood

In conditions like CO poisoning and anemia, the

total O2 content of the blood can be reduced
but the arterial PO2 remains normal

Thus respiration is not stimulated although

the person may die from cellular O2 deprivation
 Role of PCO2 in Respiration
Any minor change in PCO2

brings appropriate changes in ventilation

 ventilation to
 arterial PCO2 eliminate excess
CO2

 ventilation to
 arterial PCO2 accumulate reduced
CO2
Role of PCO2 in Respiration

Central chemoreceptors
Arterial
Arterial
PCO2PCO
is the ismost
do not monitor CO2 itself but they
2
important
monitored
regulator
by of
central
ventilation
are sensitive to changes in CO2
under
chemoreceptors
resting conditions
induced [H ] in the ECF
+
 arterial PCO2  Brain ECF PCO2 CO2 + H2O

H2CO3

Weakly  Brain ECF [H+] H+ + HCO3 -

+ +
In brain ECF
Peripheral + Central
chemoreceptors chemoreceptors

Medullary
respiratory
center

 arterial PCO2  Ventilation

Who controls your respiration you or your
brain?
 Breathing Breath holding
resumed (voluntarily)

Voluntary control to
hold breath overridden  Arterial PCO2

Stimulates
respiratory  [H+] in ECF
center
 Voluntary breath holding from
center in cerebral cortex

Excitatory inputs from

central chemoreceptors
stimulated by H+
generated by ↑ CO2

Inspiratory neurons
in DRG
(rhythmically firing)

Medulla

-٨ ++

Spinal cord - Phrenic nerve Diaphragm

PCO2  70 - 80 mm Hg

Depression of respiratory
center
 Chronic lung disease

Hypoventilation

 PCO2 PO2  60 mm Hg

 ECF[H+]
+ +
Central Peripheral
chemoreceptors chemoreceptors

 Ventilation
 Serious chronic lung disease

Hypoventilation

 PCO2 PO2  60 mm Hg

H2CO3 = ↑HCO3 - + H  ECF [H+]

 ECF [H ]
+


Central
chemoreceptors
no more affected
Peripheral
chemoreceptors

 Ventilation

In these cases O2 should be administered carefully as hypoxic

drive to ventilation is the only and prime stimulus
Summary
 Reading material
• Guyton 13th edition chapter 41 page no-
• Sherwood 9th edition page no: