PHYSIOLOGY OF CONTROL OF
BREATHING
Prof. Sultan Ayoub Meo
MBBS, M.Phil, Ph.D (Pak), M Med Ed (Dundee), FRCP (London),
FRCP (Dublin), FRCP (Glasgow), FRCP (Edinburgh)
Professor and Consultant, Department of Physiology,
College of Medicine, King Saud University, Riyadh, KSA
REGULATION OF RESPIRATION
Respiration
is
regulated
by
three
mechanisms:
Nervous regulation
Chemical regulation
Peripheral chemoreceptor control system.
different
NERVOUS REGULATION
• Dorsal respiratory group
• Ventral respiratory group
• Pneumotaxic center
• Apneustic center
NERVOUS REGULATION
NERVOUS REGULATION
Controls automatic
breathing.
Consists
of
interacting
neurons
that
fire
either
during
inspiration
(I
neurons)
or
expiration
(E neurons).
NERVOUS REGULATION
I neurons: Located primarily in dorsal respiratory group
(DRG):
Regulate activity of phrenic nerve.
Project to and stimulate spinal interneurons that
innervate respiratory muscles.
E neurons: Located in ventral respiratory group (VRG):
Passive process.
Controls motor neurons to the internal intercostal
muscles.
E neurons inhibit the I neurons.
Rhythmicity of I and E neurons may be due to
pacemaker neurons.
NERVOUS REGULATION
Apneustic center:
Promote inspiration by stimulating the I neurons in
the medulla.
Pneumotaxic center:
Antagonizes the apneustic center.
Inhibits inspiration.
DORSAL RESPIRATORY GROUP
OF NEURONS
Dorsal
respiratory
group
of
neurons
are
located
bilaterally in the dorsal portion of the medulla oblongata
in / close to the nucleus of the tractus solitarius.
Dorsal group of neuron is made up of I neurons.
They receive afferents from the air ways and carotid and
aortic bodies which terminate in the nucleus of tractus
solitarius.
DORSAL RESPIRATORY GROUP
OF NEURONS
Functions:
On stimulation initiate normal inspiration
Rhythmically discharges inspiratory signals
Inspiratory signals begin weekly and increase in ramp fashion
for 2 seconds, then cease for next 3 seconds and then begin
another cycle.
VENTRAL RESPIRATORY GROUP
OF NEURONS
Ventral respiratory group of neurons extend through the
nucleus
ambigus
and
nucleus
retroambigus
in
the
ventrolateral part of the medulla oblongata.
The ventral group has
[E] neurons at its caudal end
[I] neurons in its mid portion
[E] neurons at its rostral ends.
The neurons in the rostral end of this group appear to inhibit
[I] neurons during expiration.
FUNCTIONS OF VENTRAL RESPIRATORY
GROUP OF NEURONS
Ventral respiratory group neurons are inactive during
normal quiet respiration.
Normal quiet breathing is caused by repetitive
inspiratory signals from the dorsal respiratory group,
transmitted mainly to the diaphragm. Expiration results
from the elastic recoil of the lungs.
These neurons provide active role / strong discharge
during forceful expiration.
PNEUMOTAXIC CENTER
Pneumotaxic center located dorsally in the nucleus
parabrachialis of the upper pons, transmits impulses to the
inspiratory area.
Functions: Transmit signals to the dorsal inspiratory areas
to switch off the inspiratory ramp signals, controlling the
duration of the filling phase of the lungs. When these
signals are strong inspiration lasts for 0.5 sec. When weak,
inspiration lasts as long as 5 seconds, filling the lungs with
excess air.
Stimulation of the pneumotaxic center limits the period of
inspiration, It increases the rate of respiration
APNEUSTIC CENTER
Apneustic center: Situated in lower pons.
Functions: It send signals to the dorsal respiratory group
of neurons to prevents the switch off of inspiratory ramp
signals
Stimulation of this centre prolongs the period of
inspiration.
An increase in the duration of inspiration result in a deeper
and more prolonged inspiratory effort.
The rate of respiration becomes slow because of the
greater depth of inspiration
CHEMICAL REGULATION OF
RESPIRATION
CHEMICAL REGULATION OF
RESPIRATION
Respiratory system maintain the concentration of CO2 and O2
CO2 is most important stimulus for regulating respiratory
rate.
Effects of H+ and CO2 on the chemosensitive area:
Effects of blood H+ ions: H+ ions that provide the important
stimulus for regulating the rate of respiration, blood H+ ions
cannot effect the chemosensitive area alone because it
cannot cross the blood brain barrier and blood C.S.F barrier.
Effects of blood CO2: Blood CO2 can cross the blood brain
and blood C.S.F barriers, CO2 in blood combines with H2O to
form carbonic acid. This CO2+H2O form
H2CO3
CHEMICAL REGULATION OF
RESPIRATION
Carbonic acid rapidly dissociates into H+ ions and
bicarbonate (HCO3-) ions.
Increase in CO2 will increase the H+, but on the other
hand a decrease in CO2 will cause a decrease in H+
ions. H+ ions stimulate the chemosensitive areas.
Chemoreceptors
2 groups of chemo-
receptors that monitor
changes in blood PC02,
P02, and pH.
Central: Medulla.
Peripheral:
Carotid and aortic bodies.
Control breathing
indirectly via sensory
nerve fibers to the
medulla (X, IX).
PERIPHERAL CHEMORECEPTORS
PERIPHERAL CHEMORECEPTORS
PERIPHERAL
CHEMORECEPTORS
Effects of oxygen: The peripheral chemoreceptors detect
changes in PO2. The arterial PO2 falls from 104 mm Hg,
impulses from these receptors are carried to the brain via the
vagus and glossopharyngeal nerves, result in an increased
rate and depth of respiration.
Effect of decreased pH (increased H+ ions): Increased
alveolar ventilation lowers the PCO2 in the arterial blood and
reduces the amount of acid, which tends to return the arterial
pH to normal.
PERIPHERAL
CHEMORECEPTORS
Effects of CO2:
CO2
stimulates the peripheral
chemoreceptors.
Peripheral chemoreceptors are stimulated by decreased or
increased CO2, increased H+ ion concentration, and
decreased
pH
and
low
O2.
When
peripheral
chemoreceptors are stimulated, the impulses transmitted
from these receptor sites to the dorsal inspiratory area
causes the switch off of the inspiratory ramp signals. Since
the period of inspiration becomes limited there is an
increase in the rate of respiration.
CHEMORECEPTOR CONTROL
Central chemoreceptors:
More sensitive to changes in arterial PC0 .
2
H20 + C02
H+ cannot cross the blood brain barrier.
C02 can cross the blood brain barrier and will
form H2C03.
Lowers pH of CSF.
Directly stimulates central chemoreceptors.
CHEMORECEPTOR CONTROL
Peripheral chemoreceptors:
Are not stimulated directly by changes in arterial
PC0 .
2
H20 + C02
H2C03
H+
Stimulated by rise in [H+] of arterial blood.
Increased [H+] stimulates peripheral
chemoreceptors.
CHEMORECEPTOR
BREATHING
CONTROL
OF