AUTONOMIC NERVOUS SYSTEM

12/24/2012
1


Respiratory centers in brain
stem establish a rhythmic
breathing pattern
Automatic breathing is
generated by a rhythmicity
center in medulla oblongata
that directly controls muscles
of respiration
Insert fig. 16.25

Medullary respiratory
center
 1- Dorsal respiratory group
(DRG)
 2- Ventral respiratory group
(VRG)
1- Dorsal respiratory group
(DRG) consists mostly of
 Inspiratory neurons that drive
inspiration
 (i.e when DRG fire,
inspiration takes place, when
they stop firing, expiration
takes place).
 DRG has important
interconnection with VRG.

Medullary respiratory center
 1-Dorsal respiratory group (DRG) &
 2-Ventral respiratory group
(VRG) composed of:
 Inspiratory neurons
 Expiratory neurons; that inhibit
inspiratory neurons
 VRG (both inspiratory & expiratory neurons)
remain inactive during normal quiet
breathing.
 VRG called by DRG during periods when
demands for ventilation are increased
 Only during active (forceful) expiration,
expiratory neuron fire from VRG &
stimulate expiratory muscles (the abdominal
& internal intercostal muscles).
(Remember normal
expiration is passive).

Medullary respiratory
center
 Dorsal respiratory group (DRG) &
 Ventral respiratory group (VRG)
 Pre-Bötzinger complex
 Widely believed that they
generate respiratory rhythm &
drive DRG inspiratory neurons
firing
 It displays pace-maker activity
causing self induced action
potential.

Activities of medullary
rhythmicity center is influenced
by centers in pons
 1- Pneumotaxic center (upper
pons)
 2- Apneustic center (lower
pons)

Activities of medullary rhythmicity
center is influenced by centers in
pons
 1- Pneumotaxic center (upper
pons)
 antagonizes apneustic center,
inhibiting inspiration
 i.e It sends message to DRG
neurons to stop inspiration,
so that expiration can take
place, therefore, regulates
inspiration & expiration.
 (i.e limit duration of
inspiration & letting
expiration occur normally)
 Dominates over apneustic
center

Activities of medullary rhythmicity center
is influenced by centers in pons
 1- Pneumotaxic center
 2- Apneustic center
(lower pons)
 Promotes inspiration by
stimulating inspiratories in
medulla
 Provides extra boost
(=enhancement) to inspiratory
drive
 When Pneumotaxic center is
damaged; causes Apneusis (deep
prolonged inspiration interrupted
by brief expiration).
 Apneustic center is free to act in
absence of Pneumotaxic center



Inspiratory neurons in medullary center stimulate
spinal motor neurons that innervate respiratory
muscles
We breathing rhythmically in & out during quiet breathing
because of alternate contraction & relaxation of inspiratory
muscles (diaphragm & external-intercostal muscles)
Expiration is passive & occurs when inspiratories are
inhibited (means when these neurons are not firing,
inspiratory muscles relax & expiration takes place).

Conscious breathing involves direct control by the
cerebral cortex via corticospinal tract

Automatic breathing is
influenced by activity of
chemoreceptors that monitor
blood PCO2, PO2, & pH (= H+)
 1- Central chemoreceptors
are in medulla
 2-Peripheral
chemoreceptors are in large
arteries near
 heart (aortic bodies)
sends
impulse to respiratory center in medulla via
vagus (=X) cranial nerve.
 & in carotids (carotid bodies)
sends impulse to respiratory center in
medulla via glassophyrangeal (=IX) cranial
nerve .

Chemoreceptors modify ventilation to
maintain normal CO2, O2, & pH levels
◦ PCO2 is most crucial because of its effects on blood
pH
 H2O + CO2  H2CO3  H+ + HCO3-


Hyperventilation causes low CO2 (hypocapnia)
Hypoventilation causes high CO2 (hypercapnia)

1- Brain (= central)
chemoreceptors are
responsible for greatest
effects on ventilation
 Are sensitive to
changes in blood PCO2
directly because of the
resultant changes in
the pH of cerebrospinal
fluid
 H+ can't cross bloodbrain barrier (BBB) but
CO2 can, which is why
it is monitored & has
greatest effects

1- Brain (= central)
chemoreceptors are
responsible for greatest effects
on ventilation
 Increased H+ in brain ECF
directly stimulates central
chemoreceptors
 PCO2 level more than 7080mmHg directly depresses the
central chemoreceptors &
respiratory center & produce
severe respiratory acidosis.
 Decreased PO2 < 60 mmHg
in arterial blood – depresses
central chemoreceptors &
respiratory center except
peripheral chemo-Rs
 Rate & depth of
ventilation adjusted to
maintain arterial PCO2
of 40 mm Hg

2- Peripheral chemoreceptors
 Do not respond directly to PCO2
 i.e sensitive to changes in blood PCO2 indirectly, because of
the consequent changes in blood pH, only respond to H+
levels
(as a result of ↑H+ levels)

Low blood PO2 (hypoxemia) has little affect on ventilation
 PO2 has to fall to about half normal (= 50-60 mmHg)
before ventilation is significantly affected (because of safety
margin in %Hb saturation afforded by plateau portion of O2-Hb curve. Hb still
90% saturated at arterial PO2 of 60 mmHg)
 Does influence chemoreceptor sensitivity to PCO2 & pH
(i.e drop in PO2 also stimulate breathing indirectly by
increasing chemoreceptor sensitivity to PCO2 & pH)
 Increased PCO2 in arterial blood– weakly stimulates
peripheral chemoreceptors.
 Increased H+ ion in arterial blood– stimulates peripheral
chemoreceptors indirectly by increases in blood CO2
 Increased H+ ion in arterial blood – CAN NOT cross BBB,
therefore, does not affect central chemoreceptor
 Peripheral chemo-Rs play major role in adjusting
ventilation in response to change in arterial H+
conc. without any change in PCO2.
 i.e PCO2 is normal & arterial H+ increased or
decreased resulted from non—CO2 generating acid.
 Arterial H+ conc. increases during diabetes mellitus
because excess H+-generating ketoacidosis
abnormally produced & added to blood.
 A rise in arterial H+ stimulate ventilation by means
of Peripheral chemo-Rs & thus play important role
in regulating body’s acid –base balance.

Lungs have receptors that influence brain respiratory
control centers via sensory fibers in vagus
◦ Unmyelinated C fibers are stimulated by noxious
substances such as capsaicin (a colorless irritant chemicals
found in various capsicums that gives hot peppers their hotness)

 Causes apnea followed by rapid, shallow breathing
◦ Irritant receptors are rapidly adapting; respond to
smoke, smog, & particulates
 Causes cough
Hering-Breuer reflex is mediated by stretch receptors
activated during inspiration when tidal volume become
more than 1 liter e.g. during exercise
 Inhibits respiratory centers via vagus nerve to prevent over
inflation of lungs
What Happens When We Hold the Breath
Voluntarily?
 Hypoventilation causes high CO2 (hypercapnia)
 Powerful influence of central chemo-Rs on respiratory center is
responsible for your inability to deliberately hold your breath
more than 1min
 When we hold our breath, metabolically produced high CO2 &
resultant increase in H+ ion in ECF of brain.
 That’s stimulates central chemoreceptors which overrides
voluntary inhibitory input to respiration & stimulates respiratory
center in medulla, therefore, breathing resumes despite
attempts to prevent it.
 During this period of holding, PO2 does not fall below 60 mmHg
to cause stimulation of peripheral chemoreceptors, therefore, it
is central effect.