Control of respiratory functions.
Sleep apnea syndrome
Dariusz Nowak
Appropriate rate of alveolar ventilation and lung
perfusion
maintain the relative stable oxygen pressure (PO
2
),
carbon dioxide pressure (PCO
2
) in the arterial blood
PO
2
85-100 mm Hg
PCO
2
35-45 mm Hg
receptors (chemoreceptors)
nerves
respiratory center
effectors
Respiratory center
Localization bilateral , in medulla oblongata and
pons.
Dorsal respiratory group
Ventral respiratory group
Pneumotaxic center
Apneustic center
Chemosensitive area
Respiratory center – dorsal
respiratory group
• Sensory terminal of vagus and glossopharyngeal nerves
Signals from peripheral chemoreceptors
baroreceptors
various type receptors in the lung
• Generates basal rhythm of respiration
2 second inspiratory signal
3 second breake (no inspiratory signal) – passive expiration
Control of inspiratory signal:
A/ rate of signal increase (velocity and strenght of one
breathe)
B/ point at which signal is ceased – frequency of respiration
Respiratory center – pneumotaxic center
• Limits the duration of inspiration
• Increases the respiratory rate
Controls the „switch-off” time-point of
inspiratory signal
Respiratory rate 40 breaths/min or 3
breath/min
Strong or weak pneumotaxic signal.
Respiratory center- ventral respiratory
group
• Inactive during normal quiet respiration
• Active when high levels of pulmoary
ventilation are required (e.g. during exercise)
• Contributes to both heavy inspiration and
expiration (impulses to abdominal muscles)
Respiratory center – apneustic center
• Sends signals to dorsal respiratory group
• Prevents or retards the „switch-off” the
inspiratory signal
• Controls the intensity of inspiration , allows
full inspiration
Additional way controlling
respiration
Hering-Breuer inflation reflex
• Strech receptors (located in muscle wall of bronchi and
bronchioles)
• Vagus nerve
• Dorsal respiratory group
Lungs become overstreached – hyperinflation
Signals act on dorsal respiratory group to „switch-of” inspiratory
signal
Reflex stops further inspiration and increases respiratory rate
(like the pneumotaxic center)
• In humans prevents excessive lung inflation ( reflex is
activated when TV > 1.5 l)
Control of ventilation
We know how the respiratory rate
and the intensity (quiet , deep) of
inspiration and expiration is
controlled
What is the mechanism controlling
current respiratory pattern to
match the ventilatory (metabolic
needs) of our body ?
Chemoreceptors
• Central chemoreceptors – chemosensitive area (in medulla)
• Peripheral chemoreceptors located in carotid and aortic bodies
• [H
+
] – directly stimulates respiratory center via central receptors
• PCO
2
also directly stimulates respiratory center
• PO
2
acts only via peripheral chemoeceptors
Changes in blood PCO
2
or [H
+
]
↓
Chemosensitive area
↓
other parts of respiratory center
↓
increased lung ventilation
chemoreceptors
• [H
+
] does not cross blood-brain barrier
• [H
+
] is the main stimulator ot the chemosensitive
area
• CO
2
rapidly diffuses through b-b barrier
What is the role of CO
2
?
Low buffering capacity and low protein concentration
in the fluid surrounding chemosensitive area
Under normal conditions (healthy subject) [H
+
] and
CO
2
contribute to 80% of impulses responsible for
respiratory drive
20 % - oxygen (PO
2
)
Respiratory center adaptation to
increased PCO
2
Prolonged increase in blood PCO
2
• Stimulation is highest during first few hours after
increase in PCO
2
• Then it decreases to about 20% of the initial (maximal)
value ( after 1 or 2 days)
Why ?
Due to buffering function of the kidneys
• Increase in blood bicarbonate levels
• Diffusion of bicarbonate through blood cerebrospinal fluid
barrier
• Binding of H
+
by bicarbonates in the close neighborhood
of the chemosensitive area
What is a consequence of
adaptation to increased pCO
2
?
Patient with severe chronic respiratory
insufficiency (e.g. With pulmonary emphysema
or COPD)
Has hypercapnia and hypoxemia
Decreased pO
2
is the major factor stimulating
respiratory center
How can we treat patient with oxygen ?
Low flows
Low O
2
concentrations
Why O
2
is not important as CO
2
in
stimulation of respiratory centre under
normal conditions ?
• Hemoglobin saturation is almost total in PO
2
range 60 – 100 mmHg
• Changes of PO
2
from 60 to 100 mmHg have no
significant influence on O
2
content in the
blood and O
2
delivery to tissues.
Thus CO
2
is the most important variable
responsible for respiratory drive regulation
under normal conditions.
Peripheral chemoreceptor
system
localization:
Aortic bodies – along the aorta arch
Carotid bodies – bifurcation of the common carotid artery
• Very high blood flow through these bodies
• They are exposed continously to arterial blood O
2
(PAO
2
)
• Respond to changes in PAO
2
( decrease) and to a
lesser extent to PCO
2
and [H
+
]
• Hihgly senstive to PAO
2
in the range 60 to 30 mmHg
• Why ??
Peripheral chemoreceptors
• PCO
2
– mediated stimulation via peripheral
receptors is 7-8 times lower than that via
chemosensitive area
• But the onset of stimulation occurs 5 times
rapidly
• Increases rapidity of ventilatory response to
CO
2
when we start exercise
Regulation of respiration during
exercise
• Mean arterial PO
2
, PCO
2
and pH remain almost
normal during exercise
What stimulates intense ventilation during exercise ?
• Brain ; motor impulses to muscles are collaterally
transmitted to neurons in respiratory center
• movement of arms and legs ; excited
proprioreceptors (in joints and muscles) transmit
impulses to respiratory centre
• Hypoxia in the muscles during exercise – afferent
nerve signals to respiratory centre ?
• Changes of PCO
2
and PO
2
between expiration and
inspiration ?
Voluntary control of
respiration
• Talking
• Singing
• Eating
• Defecation
Voluntary hypoventilation or hyperventilation
• Not mediated through respiratory center in the
medulla
• Pathway: cortex , spinal tract ,spinal neurons ,
muscles
Depressant of the respiratory center
• Morphine
• Pentobarbital
• Sleep
Alveolar hypoventilation – chemosensitive areas
reveal decreased response to CO
2
Upper airways muscles relaxation – increase in
the airflow resistance