Oxygen Concentration and Partial
Pressure in the Alveoli
 The oxygen concentration in
the alveoli, and its partial
pressure is controlled by:
1.
The rate of absorption
of oxygen into the
blood
2. The rate of entry of
new oxygen into the
lungs by the
ventilatory process.
Rate of alveolar
ventilation.
CO2 Concentration and Partial
Pressure in the Alveoli
 Determined by two
factors:
 First, the alveolar PCO2
increases directly in
proportion to the rate of
carbon dioxide excretion
 Second, the alveolar
PCO2 decreases in
inverse proportion to
alveolar ventilation.
By
Dr. Mudassar Ali Roomi (MBBS, M.Phil.)
Assist. Prof. Physiology
Control of respiration
Two types:
1. Nervous control of respiration
2. Chemical control of respiration
Control of repiration
Components:
 Sensors

gather information
 Central controller

integrate signals
 Effectors

muscles
Respiratory centre
 Located bilaterally in
medulla oblongata and pons.
 Composed of
1. Dorsal Respiratory Group
(DRG)
2. Ventral Respiratory
Group (VRG)
3. Pneumotaxic center
4. Apneustic center
Respiratory centre
Pre-Botzinger complex (pre-BOTC)
 A collection of pace-
maker cells at the upper
end of Dorsal Respiratory
Group (DRG)
 Synaptic connection with
DRG
 Function: Discharges
rhythmic respiratory
signals
Dorsal Respiratory Group (DRG)
 Extends most of the length of M.
oblongata
 LOCATION: Neurons located in
nucleus of tractus solitarius and
additional neurons in reticular
substance of medulla
 vagus and glossopharyngeal nerve
terminates at Nucleus of tractus
solitarius
 Both nerves – afferent nerves for resp.
signals to center
 Pace maker neurons send ramp signals
to inspiratory muscles in a Rhythmic
fashion
 Ramp signals controlled by
(a) Pneumotaxic center
(b) Stretch receptors in the
lungs
Significance of ramp signals
 No gasping
 Smooth inflation of lungs
Full cycle of respiration
5 seconds
 2sec inspiration
 3 sec expiration
 Fibers from respiratory
center (DRG) reach the
motor neurons in spinal
cord between C3 & C5 to
form phrenic nerve
 Complete lesion of spinal
cord above C3 will stop
the breathing
 Lesion after C5 will not
affect the respiration
The Hering-Breuer Inflation Reflex
 Muscular portions of the walls of the bronchi and bronchioles throughout
the lungs have stretch receptors
 Transmit signals through the vagi into the dorsal respiratory group of
neurons when the lungs become overstretched.
 Switches Off the inspiratory ramp and thus stops further inspiration
 These signals affect inspiration in much the same way as signals from the
pneumotaxic center
 It also increases rate of respiration
The Hering-Breuer Inflation Reflex
 This reflex is activated when tidal volume increases to
more than three times normal
 Therefore, this reflex appears to be mainly a protective
mechanism for preventing excess lung inflation
Lung “J Receptors.”
 Location: In the alveolar walls in
juxtaposition to the pulmonary
capillaries
 Stimalation: Stimulated especially
when the pulmonary capillaries
become engorged with blood or
 Example: When pulmonary
edema occurs in such conditions as
congestive heart failure.
 Their excitation may give the
person a feeling of dyspnea.
Ventral Respiratory Group (VRG)
 LOCATION: Ventral part of medulla
 Two nuclei
 (1) Nucleus Ambiguus rostrally
 (2) Nucleus Retroambiguus caudally
 Both types of neurons –
INSPIRATORY & EXPIRATORY
 Center remain inactive during quite
breathing
 Active only in increased pulmonary
ventilation, during which signal from
DRG spill over to VRG
 Stimulation of accessory inspiratory
muscles & expiratory muscles
Pneumotaxic
Center
 Location: Upper part of Pons
 Function: Switches off Ramp
Signal
 Controls rate and duration of
Inspiratory ramp signals
 Strong stimulation may reduce
Inspiratory phase to 0.5 sec
respiratory rate ↑ to 30 – 40/min
 Weak stimulation may ↑
Inspiratory phase to 5sec or
more respiratory rate ↓ to 3-5/
min
Apneustic Center
 Located in lower part of pons
 Function: Prevent inspiratory
neurons from being switched
off → prolonged inspiration
 Shortens expiration
 Such Respiration called –
apneusis
CHEMICAL CONTROL OF
RESPIRATION
Following chemical stimuli stimulate the respiration:
1. Excess CO2
2. Excess Hydrogen ion
3. Decreased Oxygen
Central chemosensitive area

Stimulated by CO2 & H+ .Oxygen have no effect
Peripheral chemoreceptors

Stimulated by O2. CO2 & H+ has little effect
Location of Chemosenstive area
 Located bilaterally
beneath the ventral surface
of medulla
 Hydrogen ions are only
the main direct stimulus
for these group of neurons
Decreased Stimulatory Effect of Carbon Dioxide After the
First 1 to 2 Days
 CO2 has a potent acute effect on controlling respiratory
drive but only a weak chronic effect after a few days of
adaptation.
 Mechanism of adaptation: Renal readjustment of the
hydrogen ion by increasing the blood bicarbonate, which
binds with the hydrogen ions in the blood and
cerebrospinal fluid to reduce their concentrations
Acclimatization of chemoreceptors
 Mountain climbers have found that when they ascend a
mountain slowly
 Over a period of days rather than a period of hours
 They breathe much more deeply and therefore can
withstand far lower atmospheric oxygen concentrations
than when they ascend rapidly
 The reason is within 2 to 3 days, the respiratory center in the
brain stem loses about four fifths of its sensitivity to changes in
Pco2 and hydrogen ions.
 Therefore, the excess ventilatory blow-off of carbon dioxide
that normally would inhibit an increase in respiration fails to
occur
 Low oxygen can drive the respiratory system to a much higher
level of alveolar ventilation than under acute condition
 The alveolar ventilation often increases 400 to 500 per cent
after 2 to 3 days of low oxygen
Peripheral Chemoreceptor
 Carotid bodies through
Hering N to
Glossopharyngeal N
 Aortic Bodies through
Vagus N to DRG
 Both bodies are supplied
by special minute
arteries direct from the
arterial trunk
Stimulation of the Chemoreceptors by Decreased
Arterial Oxygen
Effect of Carbon Dioxide and Hydrogen Ion Concentration on
Chemoreceptor Activity
They have a weak effect but stimulation by way of the
peripheral chemoreceptors occurs as much as five times as
rapidly as central stimulation
Regulation of Respiration During
Exercise
PERIODIC BREATHING
An abnormality of respiration
 CHEYNE-STOKES BREATHING
is characterized by slowly waxing and waning
respiration occurring about every 40 to 60 seconds
mechanism :
 Overbreathes decrease CO2 & increase
O2 in pulmonary blood
 It takes several seconds before the
changed pulmonary blood can be
transported to the brain and inhibit the
excess ventilation
 Overventilated for an extra few seconds.
 Therefore, when the overventilated
blood finally reaches the brain
respiratory center
 The center becomes depressed an
excessive amount
 Then the opposite cycle begins and cycle
repeats
CHEYNE-STOKES
BREATHING
Under normal conditions, this mechanism is highly Damped
But in two conditions it occurs
1. Long delay occurs for transport of blood from the lungs
to the brain seen in severe cardiac failure
2. Increased negative feedback gain in the respiratory
control areas seen in brain damage
Biot Breathing / Cluster respiration:
 Alternate periods of
Respiration & Apnea, but
transition of one period
to other is abrupt, not
gradual.
 CAUSES:
Meningitis
2. Disease affecting
medulla.
1.
Sleep Apnea
 Absence of spontaneous
breathing
 Occur during normal sleep
TYPES
1. Obstructive Sleep
Apnea
2. Central Sleep Apnea
Obstructive Sleep Apnea
 most commonly occurs in older, obese persons
1. Narrow pharyngeal passage, and relaxation of these muscles during sleep
causes the pharynx to completely close so that air cannot flow into the
lungs.
2. The snoring proceeds, often becoming louder, and is then interrupted by a
long silent period during which no breathing (apnea) occurs.
3. decreases in PO2 and increases in PCO2, which greatly stimulate
respiration.
4. This, in turn, causes sudden attempts to breathe, which result in loud snorts
and gasps followed by snoring and repeated episodes of apnea.
5. excessive daytime drowsiness as well as other disorders, including
increased symphatetic activity
Central Sleep Apnea (CSA)
 CAUSES:
damage to the central respiratory centers
2. abnormalities of the respiratory neuromuscular apparatus
3. Cessation of the ventilatory drive during Sleep
4. Strokes
1.
Treatment of CSA:
 Respiratory stimulants may be helpful.
 Ventilation with CPAP at night is usually necessary.