CONTROL AND ADJUSTMENT

OF RESPIRATION
VNA
Physiology
Centre of Preclinical Science Studies
Faculty of Dentistry
UiTM
SPECIFIC LEARNING OUTCOMES:

Control and Adjustment of Respiration:

• Describe the control of respiration.
• Describe the functions of chemoreceptors.
• Describe high altitude acclimatization on respiration.
• Describe the four type of hypoxia and their suitability for oxygen therapy.
• Describe effect of exercise on respiration.
 Introduction:
In normal healthy adults:

At rest: ≈ 200 mL of O2 is used each minute by body cells.

Several mechanisms help match
breathing effort to metabolic
demand.
During strenuous exercise: increases 15- to 20-fold.

Elite endurance-trained athletes: increases 30-fold.

 Control of respiration

➢ The size of the thorax is altered by the action of the

breathing muscles:
Respiratory center = Group of neurons • Contract: as a result of nerve impulses transmitted
from centers in the brain.
• Relax: in the absence of nerve impulses.

➢ These nerve impulses are sent from clusters of neurons

can be divided into two principal areas on the basis of located bilaterally in the brain stem.
location and function:
DRG
(1) Medullary respiratory center in the medulla oblongata
VRG
(2) the pontine respiratory group in the pons (PRG)
 (1) Medullary respiratory center in the medulla oblongata

• The medullary respiratory center is made up of two collections of neurons:

1) dorsal respiratory group (DRG)
2) ventral respiratory group (VRG)

Role of the medullary respiratory center in controlling normal quiet breathing

During normal quiet breathing:

• Neurons of the DRG generate impulses to:
1) the diaphragm via the phrenic nerves
2) the external intercostal muscles via the intercostal nerves.

• Impulses are released in bursts, which begin weakly, increase in

strength for about TWO SECONDS, and then stop altogether.

• When the nerve impulses reach the diaphragm and external

intercostals, the muscles contract and INHALATION OCCURS.
 During normal quiet breathing:
• When the DRG becomes inactive after two seconds, the
diaphragm and external intercostals relax for about
THREE SECONDS, allowing the passive recoil of the lungs
and thoracic wall.

• Normal quiet EXHALATION OCCURS.

Role of the medullary respiratory center in controlling normal quiet

breathing
 (1) Medullary respiratory center in the medulla oblongata

• The medullary respiratory center is made up of two collections of neurons:

1) dorsal respiratory group (DRG)
2) ventral respiratory group (VRG)
Role of the medullary respiratory center in controlling forceful breathing

Pre- Bötzinger complex: important in the generation of

the rhythm of breathing. This rhythm generator, is
composed of pacemaker cells that set the basic rhythm
of breathing. The exact mechanism of these pacemaker
cells is unknown. However, it is thought that the
pacemaker cells provide INPUT TO THE DRG, driving the
rate at which DRG neurons fire ACTION POTENTIALS.
 Role of the medullary respiratory center in controlling forceful breathing

• The VRG becomes activated when forceful breathing is

required, such as during exercise, when playing a wind
instrument, or at high altitudes.

• DURING FORCEFUL INHALATION: nerve impulses from

the DRG not only stimulate the diaphragm and external
intercostal muscles to contract, they also activate
neurons of the VRG involved in forceful inhalation to
send impulses to the accessory muscles of inhalation
(sternocleidomastoid, scalenes, and pectoralis minor).
Contraction of these muscles results in forceful
inhalation.

• DURING FORCEFUL EXHALATION: the DRG is inactive

along with the neurons of the VRG that result in forceful
inhalation, but neurons of the VRG involved in forceful
exhalation send nerve impulses to the accessory
muscles of exhalation (internal intercostals, external
oblique, internal oblique, transversus abdominis, and
rectus abdominis). Contraction of these muscles results
in forceful exhalation.
 (2) the pontine respiratory group in the pons (PRG)

• PRG is a collection of neurons in the pons.The neurons in

the PRG are active during inhalation and exhalation. The
PRG transmits nerve impulses to the DRG in the medulla.
The PRG may play a role in both inhalation and exhalation
by MODIFYING the basic rhythm of breathing generated by
the VRG, as when exercising, speaking, or sleeping.
 FX OF CHEMORECEPTORS

Chemoreceptor Regulation of Breathing

• Chemoreceptors: sensory neurons that are responsive to chemicals.

• GENERAL FX : Chemoreceptors in TWO locations of the respiratory system

(I) monitor levels of CO2, H+, and O2 and (2) provide input to the
respiratory center.

• TWO LOCATIONS:
1) CENTRAL CHEMORECEPTORS are located in or near the
medulla oblongata in the central nervous system.
➢ Fx: They respond to changes in H+ concentration or PCO2, or
both, in cerebrospinal fluid.
2) PERIPHERAL CHEMORECEPTORS are located in the aortic
bodies, clusters of chemoreceptors located in the wall of the arch
of the aorta, and in the carotid bodies. The chemoreceptors of the
aortic bodies are located close to the aortic baroreceptors, and the
carotid bodies are located close to the carotid sinus baroreceptors.
These chemoreceptors are part of PNS.

➢ Fx: are sensitive to changes in PO2, H+, and PCO2 in the

blood.
Case: HYPERCAPNIA (elevated CO2 in the blood)

• Normally, the PCO2 in arterial blood is 40 mmHg.

• When hypercapnia occurs:

• Central chemoreceptors: are stimulated and respond vigorously to
the resulting increase in H+ level or high PCO2.

• Peripheral chemoreceptors: are stimulated by both the high PCO2

and the rise in H+. It also respond to a deficiency of O2. When PO2
in arterial blood falls from a normal level of 100 mmHg but is still
above 50 mmHg, the peripheral chemoreceptors are stimulated.
Regulation of breathing in response to changes in blood PCO2, PO2, and pH (H) via negative feedback control.

The chemoreceptors participate in a negative feedback

system that regulates the levels of CO2, O2, and H+ in the
blood.

Increased PCO2, decreased pH (increased H+), or decreased

PO2, input from the central and peripheral chemoreceptors
causes the DRG to become highly active, and the rate and
depth of breathing increase.

Rapid and deep breathing, called hyperventilation, allows the

inhalation of more O2 and exhalation of more CO2 until PCO2
and H+ are lowered to normal.
Case: HYPOCAPNIA (reduced CO2 in the blood)

• arterial PCO2 is lower than 40 mmHg.

• Results of Deep breathing or rapid breathing.
• the central and peripheral chemoreceptors are not stimulated, and stimulatory
impulses are not sent to the DRG. As a result, DRG neurons set their own setup
until CO2 accumulates and the PCO2 rises to 40 mmHg.

• DRG neurons are more strongly stimulated when PCO2 is rising above normal
than when PO2 is falling below normal.

• As a result, people who hyperventilate voluntarily and cause hypocapnia can hold
their breath for an unusually long period.
 High altitude acclimatization on respiration

• When a person ascends to a high altitude and stay there for a longer periods, the body slowly gets
adapted to the new environment.

• The body mechanisms that undergo changes to bring an adaptation of the person to the new
environment are together called ACCLIMATIZATION.

• The adaptive changes appear within 8 hours and may take several days. The maximum height: 18000
feet. Beyond the above level, the subject needs to O2 inhalation for survival.

• Respiratory changes- to maintain normal O2 supply to the tissue at a high altitude

 RESPIRATORY CHANGES

• Low PO2 stimulates the respiratory centres via peripheral

chemoreceptors.

• Increase in pulmonary ventilation due to an increase in the rate and

depth of respiration.

• As a result, CO2 is washed off and alkalosis develops. The kidney corrects
this by excreting HCO3- into urine.

• Diffusion capacity for O2 increases.

• Vital capacity, lung volumes increase in permanent high altitude

residents.
 Types of hypoxia and their suitability for oxygen
therapy
• Hypoxia is a deficiency of O2 at the tissue level. Based on the cause, we can classify hypoxia into four types, as
follows:
(1) HYPOXIC HYPOXIA: is caused by a low PO2 in arterial blood as a result of high altitude, airway obstruction,
or fluid in the lungs.

(2) ANEMIC HYPOXIA: too little functioning hemoglobin is present in the blood, which reduces O2 transport
to tissue cells. Among the causes are hemorrhage, anemia, and failure of hemoglobin to carry its normal
complement of O2, as in carbon monoxide poisoning.

(3) ISCHEMIC HYPOXIA: blood flow to a tissue is so reduced that too little O2 is delivered to it, even though
PO2 and oxyhemoglobin levels are normal.

(4) HISTOTOXIC HYPOXIA: the blood delivers adequate O2 to tissues, but the tissues are unable to use it
properly because of the action of some toxic agent. One cause is cyanide poisoning, in which cyanide blocks
an enzyme required for the use of O2 during ATP synthesis.
OXYGEN THERAPY • Very useful in hypoxic hypoxia caused by low O2 in
the atmosphere, hypoventilation and impaired
diffusion in the lung.
• Alveolar PO2 increases by several times. This
(1) HYPOXIC HYPOXIA increases the pressure gradient between alveoli
and the blood.

• Is moderately beneficial.
• Helps in providing extra supply of O2 to tissue.
(2) ANEMIC HYPOXIA • In CO poisoning when 100% O2 is given, it facilitate not only
dissociation of CO from Hb but also increases the transport of O2
in dissolved state.

(3) ISCHEMIC HYPOXIA • Less useful.

• Doubtful.
(4) HISTOTOXIC HYPOXIA
• Tissue are unable to utilize O2.
 Effect exercise on respiration

• As cardiac output rises, the blood flow to the lungs termed pulmonary perfusion, increases as well.

• O2 diffusing capacity (fr0m alveoli to pulmonary blood) may increase threefold during maximal exercise
because more pulmonary capillaries become maximally perfused.

A greater surface area available for diffusion of O2 into pulmonary blood capillaries.
• When muscles contract during exercise, they consume large amounts of O2 and produce
large amounts of CO2.

AT THE ONSET OF EXERCISE:

• An abrupt increase in breathing is followed by a more gradual increase. The abrupt increase in
breathing is due to neural changes that send excitatory impulses to DRG.

DURING MODERATE EXERCISE:

• The more gradual increase in breathing. It is due to chemical and physical changes in the bloodstream,
including (1) slightly decreased PO2, due to increased O2 consumption; (2) slightly increased PCO2, due
to increased CO2 production by contracting muscle fibers; and (3) increased temperature, due to
liberation of more heat as more O2 is utilized.

DURING STRENUOUS EXERCISE:

• HCO3- buffers H+ released by lactic acid in a reaction that liberates CO2, which further increases PCO2.
AT THE END OF AN EXERCISE SESSION:
• An abrupt decrease in breathing is followed by a more gradual decline to the resting level.
The initial decrease is due mainly to changes in neural factors when movement stops or
slows; the more gradual phase reflects the slower return of blood chemistry levels and
temperature to the resting state.
Summary
• The respiratory center consists of a medullary respiratory center in the medulla and a pontine
respiratory group in the pons.
• The medullary respiratory center in the medulla is made up of a dorsal respiratory group (DRG),
which controls normal quiet breathing, and a ventral respiratory group (VRG), which is used during
forceful breathing and controls the rhythm of breathing.
• The pontine respiratory group in the pons may modify the rhythm of breathing during exercise,
speaking, and sleep.
• The activity of the respiratory center can be modified in response to inputs from various parts of
the body in order to maintain the homeostasis of breathing.
• These include cortical influences; the inflation reflex; chemical stimuli, such as O2 and CO2 and H+
levels; proprioceptor input; blood pressure changes; limbic system stimulation; temperature; pain;
and irritation to the airways. (See Table 23.3.)
 Thank you
VNA
Centre of Preclinical Science Studies, Faculty of Dentistry, UiTM