Enrico Tiepolo
Respiratory control
Respiratory activity is regulated by control centers located in the brain stem.
They operate based on inputs from aortic and carotid chemoreceptors (through the vagus and
glossopharyngeal nerves, respectively), lung stretch receptors (vagus) and chemo- receptors in the
CNS itself. This information converges mostly to the nucleus tractus solitarii in the medulla.
At rest, the respiration is obtained by an intermittent
activation of the diaphragm. Efferent control is handled by the
dorsal respiratory group in the medulla, that drives a
graded contraction of the diaphragm by generating a ramp of
action potentials (i.e., spikes at a gradually increasing frequency
that produce a slowly mounting contraction of the muscle).
The ramp autonomously stops, but can be ended by inputs
from the pneumotaxic center (a group of neurons in the
pons that stop contraction of the diaphragm and therefore
inspiration by inhibiting the neurons in the dorsal respiratory
group) or from lung stretch receptors located in the bronchial
smooth muscle (through the vagus: Hering-Breuer reflex), both of
which act through the apneustic center and also decrease
the respiratory rate, by prolonging the expiration phase (passive, due to lung elastic recoil).
When forced respiration is required, the ventral respiratory group intervenes to control both
the inspiratory and the expiratory phase. Forced inhalation involves, in addition to the diaphragm,
contraction of the external (and parasternal) intercostal muscles that pull up the ribs, expanding the
anteroposterior diameter of the thorax, and of the sternocleidomastoid and scalene muscles that
raise the ceiling of the thorax expanding the vertical diameter.
Forced exhalation also involves muscles of the thoracic cage (internal intercostals: note, EXternal
for INspire, INternal for EXpire), but most work is performed by the abdominal muscles (mainly
rectus abdomini) that push the viscera against the diaphragm forcing its ascent.
The signals controlling respiration
The main stimulus that enhances respiratory activity is blood pH, which is related to blood pCO2 (at
least in the short term). Changes in respiratory activity (and ventilation) rapidly affect blood pH.
• Arterial pH is sensed by chemoreceptors in aortic arch and carotid glomi.
• Chemoreceptors are also present in the CNS, and they also sense pH, but CSF pH, which is not
necessarily equal to arterial pH, as the blood brain barrier is not permeable to protons and bicarbonate
(charged).
This set up is particularly important, clinically: if pTUG rises due to respiratory problems, plasma
pH falls (doubling the pCO2 lowers the pH by 0.3 units) and chemoreceptor elicit a respiratory
response; if this does not manage to correct the pCO2, normal pH will be restored by a
corresponding increase in plasma bicarbonate (increase in alkali reserve) (remember that pH depends
on the ratio bicarbonate/CO2). The peripheral chemoreceptors will not sense the
hypercapnia (high pCO2) anymore, but CO2 freely diffuses to the CNS and its increased
concentration will lower the CSF pH, maintaining a persistent activation of CNS
chemoreceptors, which offer the persisting stimulus for the needed hyperventilation.
165 Body At Work II
Respiratory control
Respiratory activity is regulated by control centers located in the brain stem.
They operate based on inputs from aortic and carotid chemoreceptors (through the vagus and
glossopharyngeal nerves, respectively), lung stretch receptors (vagus) and chemo- receptors in the
CNS itself. This information converges mostly to the nucleus tractus solitarii in the medulla.
At rest, the respiration is obtained by an intermittent
activation of the diaphragm. Efferent control is handled by the
dorsal respiratory group in the medulla, that drives a
graded contraction of the diaphragm by generating a ramp of
action potentials (i.e., spikes at a gradually increasing frequency
that produce a slowly mounting contraction of the muscle).
The ramp autonomously stops, but can be ended by inputs
from the pneumotaxic center (a group of neurons in the
pons that stop contraction of the diaphragm and therefore
inspiration by inhibiting the neurons in the dorsal respiratory
group) or from lung stretch receptors located in the bronchial
smooth muscle (through the vagus: Hering-Breuer reflex), both of
which act through the apneustic center and also decrease
the respiratory rate, by prolonging the expiration phase (passive, due to lung elastic recoil).
When forced respiration is required, the ventral respiratory group intervenes to control both
the inspiratory and the expiratory phase. Forced inhalation involves, in addition to the diaphragm,
contraction of the external (and parasternal) intercostal muscles that pull up the ribs, expanding the
anteroposterior diameter of the thorax, and of the sternocleidomastoid and scalene muscles that
raise the ceiling of the thorax expanding the vertical diameter.
Forced exhalation also involves muscles of the thoracic cage (internal intercostals: note, EXternal
for INspire, INternal for EXpire), but most work is performed by the abdominal muscles (mainly
rectus abdomini) that push the viscera against the diaphragm forcing its ascent.
The signals controlling respiration
The main stimulus that enhances respiratory activity is blood pH, which is related to blood pCO2 (at
least in the short term). Changes in respiratory activity (and ventilation) rapidly affect blood pH.
• Arterial pH is sensed by chemoreceptors in aortic arch and carotid glomi.
• Chemoreceptors are also present in the CNS, and they also sense pH, but CSF pH, which is not
necessarily equal to arterial pH, as the blood brain barrier is not permeable to protons and bicarbonate
(charged).
This set up is particularly important, clinically: if pTUG rises due to respiratory problems, plasma
pH falls (doubling the pCO2 lowers the pH by 0.3 units) and chemoreceptor elicit a respiratory
response; if this does not manage to correct the pCO2, normal pH will be restored by a
corresponding increase in plasma bicarbonate (increase in alkali reserve) (remember that pH depends
on the ratio bicarbonate/CO2). The peripheral chemoreceptors will not sense the
hypercapnia (high pCO2) anymore, but CO2 freely diffuses to the CNS and its increased
concentration will lower the CSF pH, maintaining a persistent activation of CNS
chemoreceptors, which offer the persisting stimulus for the needed hyperventilation.
165 Body At Work II
