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RSPT 1207 - CARDIOPULMONARY A&P
REGULATION of VENTILATION
Reference & Reading: Egan’s pp. 164-166, 298 - 305
The brain, spinal cord, subsequent nerves and nerve endings compose the Central
Nervous System (CNS). The regulation of breathing occurs within the Central
Nervous System. The CNS will receive stimuli, asses and make a decision based on
the data received and sends command along a motor nerve (neuron) to the muscles of
ventilation.
How the CNS receives stimuli:
I.
CHEMORECEPTORS – Specialized nerve structures that
“monitor” the oxygen, carbon dioxide, and H+ in the body and send signals
to the medulla in the brain to regulate breathing.
a. Central Chemoreceptors
1. Located directly on the medulla and are in contact with CSF
and not blood.
2. The blood and CSF are separated by a membrane called the
blood-brain barrier. The barrier is relatively impermeable to
H+ and HCO3 – ions, but CO2 is very permeable to the
blood-brain-barrier.
3. When CO2 moves across the blood-brain barrier, it goes
through the process of hydrolysis:
CO2 + H2O
H2CO3
HCO3- + H+
4. The H+ ions that build in the CSF as a result of hydrolysis
stimulate the central chemoreceptors increasing ventilation
almost instantly
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5. By increasing ventilation the PaCO2 reduces as will the
CO2 levels in the CSF, causing a decrease in ventilation.
6. Because of this relationship, it can be said that the central
chemoreceptors regulate ventilation through the indirect
effects of CO2 on the pH level of CSF.
7. The response of the H+ ions and the central chemoreceptors
are quite sensitive and with changes of even 2 mmHg can
trigger a change in the rate of breathing.
8. Over time in the presence of hypercapnia, the central
chemoreceptors will become blunted to the increased H+ level.
b. Peripheral Chemoreceptors
1. Located high in the neck at the bifurcation of the internal and
external carotid arteries, and also on the aortic arch.
2. Also called carotid and aortic bodies
3. This group of chemoreceptors are sensitive to :
 Decreased PaO2 (less than 60 mmHg)
 Increased PaCO2
 Decreased pH (acidosis)
4. Changes in pH must be as large as 0.05 to 0.1 before the
peripheral chemoreceptors respond
5. When the Central Chemoreceptors do not respond to
hypercapnia by increasing the minute ventilation, the
peripheral chemoreceptors will respond to hypoxemia.
6. The hypercapnic person will regulate breathing using his
hypoxic drive.
II.
Cerebral Cortex – the upper or higher part of the brain becomes involved
in the breathing pattern when a person is aware that he is having breathing
difficulties
a. SOB – When a person is aware that he is having trouble breathing
this is called Shortness Of Breath or SOB.
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1. It is not just triggered by hypercapnia, or hypoxemia, but also
by having increased WOB and fatigue associated with low
compliance or increased RAW.
2. A person who is hypoxic can feel restless, become frightened
and may decide to increase his Ve over the automatic
response from the medulla
b. Deliberate Alterations
1. The breathing pattern may be altered by the higher parts of
the brain for actions such as talking, swimming, singing, and
other activities.
2. As soon as the cerebral cortex ends the interference in
breathing for the activity the medulla will take over and
breathing will become automatic again.
How the CNS processes information:
There are two portions of the lower brain/brainstem that controls ventilation for a
person:
I.
Medulla (Oblongata) – It has been found that the main center for the
cyclical pattern for breathing occurs in the medulla. During quiet breathing
the inspiratory command fires for about 2 seconds and then 3 seconds is
allowed for exhalation. On the surface of the medulla are two areas:
a. Dorsal Respiratory Groups (DRG):
1. Contain mainly inspiratory neurons that send impulses to the
motor nerves of the diaphragm, and external intercostals
muscles.
2. Vagus and glossopharyngeal nerves send sensory impulses to
the DRG from the lungs, airways, peripheral chemoreceptors,
and joint proprioreceptors.
3. These impulses modify the basic breathing pattern in the
medulla
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b. Ventral Respiratory Groups (VRG):
1. Located on either side of the medulla and contain inspiratory
and expiratory neurons
2. Inspiratory neurons send impulses via the vagus nerve to
laryngeal and pharyngeal muscles to open vocal cords. Also
sent impulses to the diaphragm and external intercostals
muscles for inspiration
3. Expiratory neurons send impulses to the internal interscostal
and abdominal expiratory muscles for exhalation.
II.
Pons – the word “pon” literally means bridge. The Pons acts as a bridge
between the cerebral cortex and the medulla. It is not involved in rhythmic
breathing but modifies the output of the medulla.
It takes commands like “I need to swim/talk/ sing” (cerebral cortex)
Into
“Breathe now, hold now” commands (medulla)
There are two groups of neurons in the pons:
1. Apneustic Center: the function is ill-defined and can only be
demonstrated when it is isolated from the pneumotaxic center
and vagus nerves. The patient will breath with prolonged
inspiratory gasp with few exhalations.
2. Pneumotaxic Center: controls the “switch-off” point of
inspiration or the inspiratory time. Works with the Apneustic
Center to control the depth of inspiration. Strong signals
increase the RR. Weak signals prolong inspiration and
increase Vt.
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How the CNS sends commands:
The spinal cord contain the neural pathways for nerve conduction, both sensation
and motor impulses. They are along the spinal cord and lie within the protection of the
spinal cord.
I.
Sensory Nerves – Nerves that carry impulses only toward the CNS via
cranial nerves
a. Vagus Nerves – sends information to the medulla about breathing
reflexes, blood pressure and cardiac activity. It is the only nerve that
extends beyond the head and neck region, extending to the thorax and
abdomen
b. Glossopharyngeal Nerves – Sensations of breathing and blood
pressure go to the CNS via these cranial nerves.
II.
Motor Nerves – Nerves that carry impulses only away from the CNS
a. Phrenic Nerves – Breathing commands are sent along the phrenic
nerves
i. There is a right and left phrenic nerve that runs along the
mediastinum to sending motor commands to the diaphragms
ii. These nerves exit the spinal cord between C3 and C5.
Severing the spinal cord above C2 will result in complete chest
and diaphragm muscle paralysis.
b. Intercostal Nerves – These nerves enter the muscle groups between
T2 and T11 and run along the rib cage.
Breathing Controlled by Reflexes
I.
Hering-Breur Reflex
a. Generated by stretch receptors located in the airways
b. When lung inflation stretched these receptors, signals are sent via
vagus nerve to stop inspiration
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II.
Deflation Reflex
a. When there is a sudden collapse in the lung, the deflation reflex
results in hyperpnea.
b. Signal is sent via vagus nerve
III.
Head’s Paradoxical Reflex
a. When the vagus nerve is blocked, hyperinflation of the lung occurs
and causes an increase in Ve.
b. May be related to increased lung volumes during exercise, periodic
sighs during quiet breathing and baby’s first breaths.
IV.
Irritant Receptors
a. Cholinergic Reflex bronchospasm
1. Vagal sensory nerve fibers located in larger central airways.
2. Rapidly adaptive
3. Activated by tactile stimulation
 Inhaled irritants – histamine, chemicals, cigarette smoke
 Mechanical factors – dust, particulate matter
 Pulmonary congestion
4. Stimulation can result in
 Bronchoconstriction
 Hyperpnea
 Laryngospasm
 Glottis closure
 Coughing
b. Vagovagal Reflex
1. When the reflex has both sensory and motor vagal
components
2. Activated by physical stimulation of conducting airways
 Endotracheal intubation
 Airway suctioning
 Bronchoscopy
3. Stimulation can result in
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 bradycardia
 coughing
 laryngospasm
V.
J Receptors
a. Also called Juxtacapillary Receptors
b. Located next to pulmonary capillaries
c. Activated by
 Alveolar inflammatory responses – pneumonia
 Pulmonary vascular congestions – CHF
 Pulmonary edema
d. stimulation results in
 rapid, shallow breathing
 a feeling of dyspnea
 narrowing of the glottis on exhalation
Abnormal Breathing Patterns
I.
Cheyne-Stokes Breathing
a. Ve increases, reaches a “climax,” then decreases then apnea occurs.
b. A delay is present between the PaCO2 in the CNS, and the
PaCO2 in the rest of the body.
c. Usually caused by a decreased Cardiac Output (CHF) and some
brain injuries.
d. Blood flow is slow between the two areas.
e. The brain is reacting to the acidotic CSF when the lower arterial
CO2 suddenly arrives it causes apnea.
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II.
Biot’s Breathing
a. During regular breathing there is apnea
b. Similar to Cheyne-Stokes, but the Vt does not change
c. Caused by increased intracranial pressure
III.
Apneustic Breathing
a. Caused by damage to the pons.
b. Persistant Hyperventilation with prolonged inspiratory holds
followed by short exhalations
IV.
Central Neurogenic Hypoventilation
a. Respiratory Centers do not respond to ventilatory stimuli
appropriately, i.e. – does not respond to changes in acid-base
balance
b. Associated with head trauma, brain hypoxia, narcotic suppression
of respiratory center
V.
Central Neurogenic Hyperventilation
a. Persistent hyperventilation because the CNS is responding to
abnormal stimuli
b. Related to midbrain and upper pons damage
c. Associated with head trauma, sever brain hypoxia, and lack of
blood flow to brain.