control of ventilation Flashcards
eupnoea
normal quiet breathing
hyperpnoea
increased ventilation
tachypnoea
increased respiratory rate
hyperventilation
overventilation (PaCO2 less than normal)
hypocapnia
PCO2 less than normal
hypercapnia
PCO2 greater than normal
hypoxia
PO2 less than normal
hyperoxia
PO2 greater than normal
hypoxaemia
PO2 less than normal in blood
asphyxia
hypoxia and hypercapnia
dyspnoea
stressful breathing.
apnoea
absence of breathing
what controls ventilation
sensors -Chemoreceptors
Lung receptors
Other receptors send input to central controller
central controller - medulla oblongata and pons sends output
effector - respiratory muscles receive output from central controller
pons respiratory centers
pneumotaxic center
apneustic center
medullary respiratory center
dorsal respiratory group
ventral respiratory group
what kind of neurons are dorsal respiratory group
Inspiratory neurons
location of dorsal respiratory group
dorsomedial medulla
function of - DRG dorsal respiratory group
DRG inspiratory neurons fire inducing muscle contraction and therefore inspiration
what kind of neurons are ventral respiratory group
Both inspiratory and expiratory neurons
when does - VRG ventral respiratory group become inactive
Both sets remain inactive during quiet breathing
when does ventral respiratory group become active
Utilised when demand for ventilation is increased beyond normal (active expiration)
what neurons display pacemaker like activity
ventral respiratory group
dorsal respiratory group
pre-bötzinger complex
ventral respiratory group
dorsal respiratory group
pre-bötzinger complex can generate what types of breathing rythms
- normal breathing (fast, low amplitude)
2. Sighs (slow, large
what modifies the rhythm generated in the medulla
modified by neurons in the pons
pneumotaxic centre function
sends signals to the DRG that help silence/inhibit the inspiratory neurons
apneustic centre function
prevents the inspiratory neurons from being switched off
causes of loss of function of the pneumotaxic centre and apneustic centre
depressant drugs on the respiratory centres
cord injury
damage to motor nerves (trauma, neurological disease)
muscle diseases e.g. dystrophies
dysfunction of the respiratory apparatus i.e. restriction and obstruction
receptors in airways and lungs
stretch receptors
irritant receptors
j receptors
chemoreceptors
peripheral
central
stretch receptors function
there are nerve endings in the airway smooth muscle which are stimulated by stretch during inspiration
where do the impulse of the stretch receptors travel to
impulses travel in the vagus nerve to inhibit the inspiratory centre
Hering-Breuer inflation reflex
there are nerve endings in the airway smooth muscle which are stimulated by stretch during inspiration
the nerve impulses travel in the vagus nerve to inhibit the inspiratory centre
irritant receptors
nerve endings near the airway epithelial cells which are stimulated by noxious gases, cigarette smoke, dust and cold air
where do the impulse of the irritant receptors travel to
travel in the vagus nerve causing reflex bronchoconstriction or coughing
irritant receptors are involved in
asthma attacks
j receptors function
nerve endings near the capillaries in the alveolar walls called juxtacapillary receptors which are stimulated by pulmonary congestion and oedema
where do the impulse of the j receptors travel to
travel in the vagus nerve causing reflex apnoea or rapid shallow breathing
irritant receptors are involved in
in the rapid shallow breathing and dyspnoea of pulmonary congestion and oedema
chemoreceptors
Specialised cells that respond to changes in the chemical composition of the blood or other fluid
location of peripheral chemoreceptors
Located near the heart in the
carotid bodies - at the bifurcation of the common carotid arteries
aortic bodies - above and below the aortic arch
where do the impulses and info of peripheral chemoreceptors travel to
is carried via the vagus and glossopharyngeal nerves to the dorsal respiratory group
what does peripheral chemoreceptors respond to
increased arterial CO conc
decrease in pH
decrease arterial O2 levels
how does peripheral chemoreceptors correct the response made
send glossopharyngeal nerve to dorsal respiratory group - induce muscle contraction for inspiration
inc. ventilation
location of central chemoreceptors
medulla separate from the respiratory centres
what stimulates central chemoreceptors
by an increase in brain extracellular fluid PCO2 and H+ but not by a decrease in PO2
what is central chemoreceptors responsible for
responsible for 80% of the ventilatory response to increased PaCO2
what is the central chemoreceptors response to arterial blood H+ like and why
poor response to arterial blood H+ because of the blood-brain barrier
what chemoreceptor responds to all of the decreased PaO2
peripheral chemoreceptors
what is responsible for most the of the response to increased arterial blood H+
peripheral chemoreceptors
how can we measure ventilatory response to hypoxia and hypercapnia
changing the PaO2 and PaCO2 by inhaling hypoxic and hypercapnic gas mixtures
when a graph is drawn to indicate the relationship between ventilation and PaCO2 what do we expect to see
steep upward graph at 30 PaCO2
what does the graph steep line with ventilation and PaCO2 indicate
ventilation is sensitive to a very small change in PaCO2
what does hypocapnia cause
increased neuromuscular excitability and tetany
what does hypercapnia cause
depression of the nervous system and coma
anaemic
the PaO2 is normal but the O2 content is < normal
stagnant hypoxia
the PaO2 and O2 content are normal but O2 delivery to the tissues is reduced due to decreased blood flow
histotoxic hypoxia
the PaO2, O2 content and delivery are normal but the tissues cannot use the O2 due to metabolic poisoning e.g. cyanide poisoning
respiratory disorders are due to
decreased ventilation
decreased alveolocapillary diffusion
decreased transport
respiratory disorders caused by decreased ventilation
neurological damage, muscular disorders, obstructive and restrictive pulmonary diseases etc
respiratory disorders causes by decreased alveolocapillary diffusion
emphysema, oedema, fibrosis, atelectasis
respiratory disorders causes by decreased transport
anaemia, carbon monoxide poisoning
