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SEMESTER 1
Body Systems
control of breathing
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Cards (13)
TWO KEY TASKS OF BREATHING
establish
automatic
rhythm
adjust the rhythm to accommodate:
metabolic
(arterial blood gases + pH),
mechanical
(postural change) and
episodic
non-ventilatory behaviours (e.g. speaking sniffing, eating)
Under normal conditions:
O2-
rate of absorption is matched to delivery
CO2-
rate of generation is matched to removal
Balance achieved by:
changes
in blood flow and oxygen delivery --> local
changes
in depth and rate of respiration --> central
Complexities:
no single pacemaker generating basic
rhythm
of breathing
no single
muscle
devoted to the pumping of air
LOCAL CONTROL OF GAS TRANSPORT
PO2
and
PCO2
in active tissue
decreased PO2
-->
increased O2
delivery
increased PO2 -->
vasodilation
-->
increased
blood flow --> increased O2 delivery and CO2 removal
LUNG
PERFUSION
decreased
PO2 -->
vasoconstriction
--> decreased blood flow
direct blood to areas of
higher
PO2
ALVEOLAR
VENTILATION
increased PCO2 -->
broncoconstriction
--> air flow
direct
airflow
to area of
higher
PCO2
CENTRAL CONTROL OF VENTILATION
SENSORS-
central
+
peripheral
chemoreceptors and mechanoreceptors
CENTRAL CONTROLLER-
respiratory
centres In the
pons
and
medulla
EFFECTORS- muscles of
ventilation
AIM is to keep arterial
PCO2
and
PO2
as constant as possible
SENSORS
central chemoreceptors-
medulla
change in
pH
hypercapnia
no effect of hypoxia
peripheral chemoreceptors-
aortic
and
carotid
body
hypoxia
hypercapnia
change in
pH
mechanoreceptors-
lung
receptors
respond to
stretch
rapidly
+
slowly
adapting receptors
c-fibres
receptos
FACTORS INFLUENCING RATE AND DEPTH OF BREATHING
changing body
demands
(e.g exercise)
altitude-
acute mountain sickness
disease
changing levels of
CO2
,
H+
,
O2
, in the
arterial
blood
CENTRAL CHEMORECEPTROS
just beneath the
ventral
surface of the
medulla
close to the entry of
VIII
and
XI
cranial nerves
stimulated by acidic or high
PCO2
in the CSF
increased PCO2 -->
decreased
ph -->
increased
ventilation -->
decreased
PCO2
CO2 crosses the blood-brain barrier as its
lipid
soluble (CSF is only
weakly
buffered)
PERIPHERAL CHEMORECEPTORS
detect changes in
PO2
,
PCO2
and
pH
outside the
brain
carotid
body at bifurcation of
carotid
arteries
innervated by
carotid
sinus nerve
aortic
bodies above and below aortic arch
innervated bt
vagus
if PO2 increases, (e.g. breathing oxygen-rich gas mixtures) -->. generates
free radicals
leading to
coma
and
death
if PO2 decreased:
arterial PO2 must drop below
60
mmHg before ventilation is increased
central
chemoreceptors switch off
peripheral
chemoreceptors increase breathing rate
MECHANORECPTORS: SLOW ADAPTING- STRETCH RECEPTORS
located in
visceral pleura
,
bronchioles
and
alveoli
innervated by fibres of
vagus
nerve
over
inflation -->
increased
discharge -->
inhibition
of respirate centres
response = hiring
Breuer
reflex
MECHANORECEPTOR-
RAPID ADAPTING-
IRRITANT RECEPTOR
located in airway epithelia (close to mucosa)
noxious
gases (smoke/ dust/ cold air) --> increased
discharge
--> bronchoconstriction
shape the ventilatory pattern and protecting the airway
initially fire
rapidly
but then soon
decreases
their fire rate
response to
coughing
reflex
MECHANORECEPTOR- C-FIBRES
located in
alveoli
wall (close to
capillaries
) and conducting
airways
(
bronchial mucosa
)
chemical
/
mechanical
stimuli --> increased
discharge
-->
bronchoconstriction
+
rapid shallow
breathing +
mucus secretion
response is
defence
mechanism
RHYTHMICITY CENTRE-
medulla
controls automatic breathing
interacting neurons that fire during inspiration (I neurons) and expiration (E neurons)
PNEUOTAXIC AND APNEUSTIC CENTRES- pons
modifies firing pattern of medullary centres
I neurons in DRG --> regulate activity of phrenic nerve --> sets rhythm and stimulates muscles of quiet inspiration
E neruons in VRG --> passive process
activation of E neruons inhibit I neurons